DR Tourkey Note New Edition MRCS

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SPINE AND LIMBS
CERVICAL VERTERAE
◌Other than the fracture , what are the abnormal signs in this radiograph:
1- abnormal alignment(the distance between the dens and the lateral masses of c1 on both sides is
not equal).
2- prevertebral soft tissue swelling due to fracture edema.
MRCS OSCE REVISION GUIDE 3rd EDITITION 1 1

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◌Ligaments attached to the odontoid process:

- transverse Atlantal ligament.
- Apical odontoid ligament.
- Alar ligament.
Type of Atlanto axial joint: synovial pivot.
◌Ligaments between C1 and C2:

- ant. Atlanto axial ligament.
- Post. Atlanto axial ligament.
- Transverse ligament.
1st spinous process to be felt: of C7 (has a long spine = vertebra prominence). Demonstrate it on
the subject.
Q:Why we can not feel the upper spinous processes?
A: As they are short, bifid and attached to the nuchal ligament.
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MRCS OSCE REVISION GUIDE 3rd EDITITION 3
◌Atypical cervical vertebrae and the atypical features:

C1(atlas): no body , no spine.
C2(axis): body projects upwards to form the ofontoid process, thick spine.
C7(vertebra prominence): very long spine, smaller foramen transversium.
Q:How many vertebrae make the spinal column? How many spinal nerves?
A: 7 cervical. 8 cervical.
12 thoracic. 12 thoracic.
5 lumbar 5 lumbar.
5 fused sacral. 5 sacral.
3 fused coccygeal. 1 coccygeal.
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LUMBAR VERTERAE
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Infective endocarditis
INTERVERTEBRAL FORAMEN
◌The root of each spinal nerve.
◌Dorsal root ganglion.
◌The spinal artery of the segmental
artery.
◌Communicating veins between the
internal and external plexuses.
◌Recurrent meningeal (sinu-vertebral)
nerves.
◌Transforaminal ligaments.
LUMBAR PUNCTURE
◌Level of the lumbar puncture:
L4/L5 (at the supracrestal line).
◌Layers to pass through:
- skin,sc fat, fascia.
- Supraspinous ligament.
- Interspinous ligament.
- Ligamentum flavum.
- Epidural space.
- Dura matter.
- Arachinoid matter.
- CSF
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◌IV disc anatomy:

Internal nucleus pulposus surrounded by fibrocartilagenous
annulus fibrosus.
Degenerative changes in disc : spondylosis
Type of IV joint: secondary cartilagenous joint.
◌Movement on lumbar vertebrae: Flexion, extension, lateral

flexion.
◌Level of the spinal cord in newborn and adult: L3 ( at birth) ,

L1/2(adult).
◌Contents of the spinal canal below L2: filum terminnale and cauda
equina
◌Location of the paravertebral venous plexus:

- anterior external vertebral venous plexus, the small system around
the vertebral bodies.
- posterior external vertebral venous plexus, the extensive system
around the vertebral processes.
- anterior internal vertebral venous plexus, the system running the length of the vertebral canal anterior
to the dura.
- posterior internal vertebral venous plexus,the system running the length of the vertebral canal posterior
to the dura.
Tumours metastatising to the spine:

-Lung - 31% -Breast - 24%
-GI tract - 9% -Prostate - 8%
-Lymphoma - 6% -Melanoma - 4%
-Unknown - 2% -Kidney - 1%
-Others including multiple myeloma - 13%
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Demonstrate on a living subject :
- hyoid bone(c3)
- cricoid cartilage(c6)
- roots of brachial plexus
- posterior triangle
◌Structures found at c6:

- termination of the pharynx and begining of the oesphagus.
- Termination of the larynx and begining of the trachea.
- Entry of the vertebral artery to the foramen
transversium.
- Intermediate tendon of omohyoid crosse the carotid sheath.
- Middle thyroid vein emerging from the thyroid gland.
- Inferior thyroid artery entering the thyroid gland.
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UPPER LIMB
BRACHIAL PLEXUS
Where are parts of brachial plexus found:

- roots: exits from iv foramina between scalenus ant. And medius
- Trunks: base of the post. Triangle of the neck behind the 3rd part of subclavian artery
- Divisions: behind middle 1/3 of the clavicle
- Cords : related to the 2nd part of axillary artery
Erb’s paralysis Klumbek's paralysis

◌Damage to the uppert nerve roots (c5,c6) ◌ Injury to lower trunk ( C8,T1).
◌Motor affection: ( waiter's tip deformity) ◌Motor affection: (claw hand deformity).
-Paralysis of arm abductors( supraspinatous + deltoid) ----- -Paralysis of all intrinsic muscles of the hand(muscle
-> arm adduction. wasting and loss of fine finger movements)
-Paralysis of arm external rotators( infraspina- tous -Paralysis of wrist and finger flexors( weak
+teres minor) ------> arm internal rotation. wrist and finger flexion)
-Paralysis of forearm flexors and supinators -Hyperextension of MCP joints(unopposed action of
(biceps ,brachialis, brachioradialis) -------> forearm the extensor digitorum by impaired lumbricals and
extension and pronation. interossei)
-Paralysis of extensor carpi radialis longus-à - Flexion of PIP (unopposed action of flexor digitorum
wrist flexion superficialis by lumbricals and interossei)
◌Sensory affection: loss of sensation of radial ◌Sensory affection: loss of senastion over ulnar
side of arm and forearm. border of forearm and hand.
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BONES OF THE UPPER LIMB
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◌Articulate humerus, radius and ulna:

-Capitulum of the humerus + radial head.
-trochlea of the humerus +trochlear notch of
the ulna.
-olecranon of the ulna+ olecranon fossa of
the humerus
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Scaphoid bone blood supply:

It receives its blood supply pri-
marily from lateral and distal
branches of the radial artery,
via palmar and dorsal branches.
These provide an "abundant" sup-
ply to middle and distal bone,
but neglects the proximal portion,
which relies on retrograde flow.
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MEDIAN AND ULNAR NERVES
◌Median nerve sensory distribution in the

hand:
a) lateral 2/3 of the palm of the hand.
b) lateral (radial) three and a half digits on the
palmar side.
c) dorsum of the tips of index, middle and
thumb.
◌Median nerve motor distribution in hand :
LOAF muscles:
lateral 2 lumbricals
opponenece polics
abductor policis brevis
flexor policis brevis
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C/p of ulnar nerve injury at wrist: ( complete claw hand)
- Clawing of the 4th and 5th digits ( paralysis of the medial lumbricals and interosseii).
- Loss of sensation of the medial 1/3 of the palmar and dorsal aspects of hand and fingers.
◌Why ulnar paradox: In proximal ulnar nerve

injuries, there will be paralysis of the
medial 1/2 of the FDP which will decrease flexion of the IP joints
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CARPAL TUNNEL
Attachments of flexor retinaculum:
◌Proximal: pisiform+ tubercle of scaphoid

◌Distal: hook of hamate + trapezium
◌Structrues passing through carpal tunnel:

- 4 tendons of flexor digitorum superficialis.
- 4 tendons of flexor digotorum profundus.
- 1 tendon of flecor policis longus.
- 1 tendon of flexor carpi radialis.
- Median nerve.
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ID
-Ulnar art.
- Radial art.
-Superficial palmar
arch.
◌Superficial palmar arch: formed mainly by the arch of the superficial division of the ulnar artery
and is completed by the superficial palmar branch of the radial artery.
MOVEMENTS OF THE THUMB
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Q:Where are tendons of FDS and FDP insert?

FDS: splitted tendon on both sides of the middle phlanax.
FDP: passes throgh the splitted tendon of FDS to be inserted into the terminal phalanx.
Q:How to test FDP?

A:By fixing the PIP
Q:How to test FDS?

A:adjacent digits must be held in extension, in order to eliminate FDP
motion in adjacent fingers, which otherwise might give the impression of
FDS motion in the examined finger.
Q:How to test ulnar artery( allen' s test)?

A: -Elevate the hand and ask the patient to make a fist for 30
sec..
- Apply pressure on both ulnar and radial aa. to occlude both.
- While still elevated, open the hand, it should be blanched.
- Release pressure over the ulnar artery, colour should return in 7
seconds.
Q:When you are doing power grip of the hand, what is the role of radial nerve?
A:Radial nerve supplies wrist extensors which give mechanical advantage to power grip by synergistic
activity which cause more efficient flexion of the digits.
Q:Why hand grip is powerful in extension than flexion?

A:Because the flexor muscles in extension position is in a state of tension than in flexion position, so contraction
in this position is more powerful
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1: Extensor digitorum tendon. 2: Extensor indicies tendon.

3: intertendinous connections . 4: 1st dorsal interosseus muscle.
5: radial styloid process. 6: ulnar styloid process.
7: Extensor carpi ulnaris. 8: abductor digiti minimi
◌Tendon attached to pisiform : flexor carpi ulnaris.
◌1st dorsal interosseus :

-Origin: from the first metacarpal.
-Insertion: into the lateral side of extensor expansion of index finger.
-Action: abduction of index finger.
Q:What makes extensor tendons attached to the phalanges?

A:Extensor expansion
Q:What is the function of intertendinous connections?
A: - create space between extensor tendons.
- redistribute force between tendons.
- coordinate extension of fingers.
- stabilize MCP joint.
ANATOMICAL SNUFF BOX

◌Boundaries:
-Anterolateral: tendons of : - abductor policis longu - extensor
policis brevis.
-Posteromedial: tendon of. Extensor policis longus.
Insertion of EPL: dorsum of the base of the terminal phalanx of

the thumb
Insertion of EPB: dorsum of the base of the proximal phalanx of
the thumb.
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FOREARM MUSCLES
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CUBITAL FOSSA
◌Boundaries:
- superolateral:
bravhioradialis muscle.
- Medially: pronator teres.
- Floor: brachialis.
Contents:(M-L)
- Median nerve
- Brachial artery
- Biceps tendon
◌Strucutres passing in spiral groove:

- radial nerve, profunda brachii
vessels.
◌C/p of radial nerve injury at the spiral groove:

- paralysis of wrist extensors ------> wrist drop.
- Paralysis of finger extensors ------> finger drop.
- Loss of sensation in the 1st web space.
Median nerve injury at elbow:
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◌Supracondylar fracture humerus:
Associated injuries:
-Brachial artery injury( absent distal pulses).
- Anterior interosseus nerve injury( unable to flex the interphalangeal joint of his thumb and the distal
interphalangeal joint of his index finger).
- Ulnar nerve injury ( claw hand).
- Radial nerve injury ( wrist drop,finger drop).
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ROTATOR CUFF MUSCLES

◌Supraspinatous:
-Origin:
supraspinous fossa.
-Insertion:
greater tubrosity.
-N. Supply:
suprascapular n.
◌Infrainatous:
-Origin:
infraspinous fossa.
-Inserion:
greater tubrosity.
-N.supply:
suprascapular n.
◌Teres minor:
-Origin: upper 2/3
of lateral border of
scapula. ( dorsal
aspect)
-Insertion:
greater tubrosity
-N.supply: axillary
n.
◌Subscapularis:
-Origin: sbscapular
fossa.
-Insertion:
lesser tubrosity.
-N.supply: upper
and lower
subscapular n.
◌Shoulder joint abduction:

- Supraspinatous ( 0-15).
- Deltoid ( middle fibres) 15-90.
- Trapezius and serratus anterior ( over 90).
which will require upward rotation of the scapula with lateral rotaion of the humerus
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Factors decreasing the stability of the shoulder joint:

1- shallow glenoid cavity
2- lax capsule with few ligaments
3- inferior aspect is not supported due to the presence of quadrangular space
◌The main stabilizer of the shoulder joint is the rotator cuff
muscles.
QUADRANGULAR SPACE
◌sup.: teres minor.

◌Inf.: teres major.
◌Lat.: Surgical neck of humerus.
◌Med.: long head of triceps.
◌Contents: axillary n.--post. Circumflex humeral
vessels.
AXILLARY NERVE
Motor : deltoid + teres minor.

Sensory: skin to the lower half of deltoid ( badge
area).
Injury: inability to abduct the shoulder over 15, loss
of sensation over the badge area.
AXILLARY ARTERY
◌Divided by pectoralis minor to 3 parts: [ screw the
lawyer save a patient]
- 1st part: medial to pectoralis: superior thoracic
artery.
- 2nd part: behind the pectoralis: thoracoacromial,
lateral thorcic.
- 3rd part: lateral to pectoralis: ( subscapular,
ant.circuflex humeral, post, circumflex humeral).
◌Muscles inserted in bicepital groove : ( lady bw 2

majors)
- teres major: ( medial lip).
- Latismus dorsi(floor).
- Pectoralis major( lat. lip).
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BICEPS MUSCLE
◌Origin:
- long head : ( supraglenoid tubercle).
- Short head ( coracoid process).
◌Insertion:
- biceptal tendon into radial tubrosity.
◌Relation to tendon:
-Median nerve , brachial aa.( medially).
-Radial nerve ( lateral).
◌N.supply: musculocutaneous nerve.
TRICEPS MUSCLE
◌Origin:
-Long head: infraglemoid tubercle.
-Lat . Head: anove the spiral groove.
-Med. head: below the spiral groove.
◌Insertion: Olecranon.
◌N.supply: radial nerve.
UPPER LIMB RELEXES
1. Biceps reflex (C5/6) – located in the antecubital fossa -tap your finger overlying the biceps tendon.
2. Triceps reflex (C7) – place forearm rested at 90º flexion.
3. Supinator reflex (C6) – located 4 inches proximal to base of the thumb.
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◌Surface marking of coracoid

process:
-Medial 3/4 and Lateral 1/4 of the
clavicle
-1 cm below that point.
◌Structures attached to the coracoid process:

1- ligaments: coracoclavicular- coracohumeral- coravoacromial.
2- muscles: pectoralis minor( insertion)'- coracobrachialis( origin)- short
head of biceps( origin).
PECTORALIS MAJOR
◌Origin :
-Clavicular head: from the medial half of
the anterior surface of the clavicle.
-Sternocostal head: ant. Surface of the
sternum- upper 6 costal cartilages- EOA.
◌Insertion: Lateral lip of bicepital groove.
◌Nerve supply: medial ( c8-T1) and
lateral pectoral nerve ( c5-c7)
◌Action:
- adduction and medial rotation of the
arm( the whole muscle).
- Clavicular head: flexion of the arm.
- Sternocostal head: extends the flexes
arm.
- Acts as accessory respiratory muscle by
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elevating the ribs.
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TRAPEZIUS MUSCLE
◌Origin: ext.occipital protuberance,superior nuchal

line ,spinous process of c7, spinous processes of all
thoracic vertebrae.
◌Insertion: lateral 1/3 of clavicle,medial acromion,
aponeurosis over the spine of the scapula
◌N.supply: spinal accessory n.
SERRATUS ANTERIOR MUSCLE
◌Origin: 9-10 slips from the 1st to 8 th ribs.

◌Insertion: Medial border of scapula.
◌N.supply:Long thoracic nerve of bell( c5,c6).
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LOWER LIMB
ARCHES OF THE FOOT
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Q:What are the components of the Medial Longitudinal arch?

A:◌Bones - calcaneum, talus, navicular, all 3 cuneiforms, medial 3
metatarsals.
◌Ligaments – short , long plantar ligaments and spring ligaments.
◌Muscles - flexor hallucis longus, peroneus longus, tibialis anterior and posterior.
Q:What are the components of the Lateral Longitudinal arch?
A:◌Bones - Calcaneum, cuboid and lateral 2 metatarsals.
◌Ligaments - long and short plantar ligaments.
◌Muscles - peroneus longus and brevis, short plantar muscles
Q:What are the components of the Transverse arch?
A:◌Bones - the bases of all 5 metatarsals (each foot actually forms one half of
an arch).
◌Muscles - peroneus longus
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CHAPT
◌ID ligaments on the medial and lateral aspects of the ankle:

◌Attachements of deltoid ligament:
-Superior: medial malleolus
-Inferior: 1- tubrosity of the navicular. 2- spring ligament. 3- neck of talus. 4- sustanecukum tali.
5- body of talus.
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Q:What movements occur at the subtalar joint?
A:Inversion and eversion of the foot occur at the subtalar joint.

Q:Which muscles perform these actions?
A:Inversion - Tibialis anterior and posterior (with some help from the extensor and flex or
hallucis longus muscles).
Eversion - Peroneus longus and brevis.
Q:What are the bones forming ankle joint: ( synovial-hinge)?

A:Trochlear surface of talus, lower end of tibia and fibula.
Q:What are the movements of ankle joint?
A:◌Plantar flexion: gastrocnemius ,soleus. Plantaris. + tibialis post. , flexor didgitorum
longus, flexor jalicius longus.
◌Dorsiflexion: tibialis ant., extensor halicius longus, extensor digitorum longus, proneus tertius.
Q:Ankle joint is most stable in dorsiflexion why?
A :The most stable position of the ankle is in dorsiflexion. As the foot moves into dorsiflexion,
the talus glides posteriorly and the wider anterior portion of the talus becomes wedged into the
ankle mortise. As the ankle moves into plantarflexion, the talus glides anteriorly and the ankle
less stable, some “wobble” (small amounts of abduction, adduction, inversion, and eversion) is
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Q:What is the type of inferior talofibular joint?

A: syndsmosis
Associated injury in syndesmotic fracture: fractures lateral mallelus
Q:Where to palpate dorsalis pedis and post. Tibial A.?
A:Lateral to the EHL tendon---- halfway between the post.border of the
medial mallelus and tendoachilles.
◌Structures passing behind the medial malleolus: (TOM DOES VERY
NICE HATS)
- tibialis post . Tendon. - flexor digitorum longus tendon. - post. Tibial
vessels.
- Post. Tibial nerve. - FHL tendon.
◌Demonstrate the foot pulses on this actor:

-The dorsalis pedis pulse is found between the first two metatarsal bones.
-The posterior tibial pulse is found 2-3cm below and behind the medial malleolus.
ARTERIES OF THE FOOT
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Q:What muscles make the achilles tendon?

A:Three muscles insert into the Achilles or calcaneal tendon:
-Soleus.
-Gastrocnemius.
-Plantaris.
ID tendons on the dorsum of the foot

Leg compartments
Interosseus membrane: separates anterior from

posterior
Anterior intermuscular septum :

Separartes anterior from lateral
Transverse intermuscular septum :

Separates superficial post. From deep post.
Posterior intermuscular septum :

Separates the posterior from latetal
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Q:On an actor demonstrate how you would test the knee and ankle reflexes?
A:Knee reflex: The foot should be unsupported, relaxed and off the ground. The thigh should be
fully exposed.
-Test by tapping the patellar tendon with a tendon hammer. You are looking for reflex contraction
of the quadriceps muscles.
Ankle reflex: The foot should be pointing laterally, be flexed, and relaxed. the leg should be fully
exposed.
-Test by tapping the Achilles tendon with a tendon hammer. You are looking for reflex
contraction of the calf muscles.
Q:What nerve roots do these reflexes originate from?

A: -Ankle: S1.
-Knee: L3/4.
Q:What movement is ankle dorsiflexion?
A:Dorsiflexion is the upwards movement of the foot in relation to the leg.
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Q:At what joint does dorsiflexion occur?
A:At the ankle joint between the tibia/fibula and the
talus.
Q:What muscles are involved in dorsiflexion?

A:Muscles of the anterior compartment of leg are involved:
-Tibialis anterior.
-Extensor hallucis longus.
-Extensor digitorum longus.
-Peroneus tertius.
Q:How would you demonstrate ankle plantarflexion?

A:Plantarflexion is the downwards movement of the foot in relation to the leg.
Q:What muscles are involved?

A:Both the superficial and deep posterior compartments of the leg are involved
◌Superficial posterior compartment:
-Gastrocnemius.
-Soleus.
-Plantaris (only weak participation).
◌Deep posterior compartment:
-Flexor hallucis longus.
-Flexor digitorum longus.
-Tibialis posterior.
-Popliteus.
Q:What action occurs when tibialis anterior and tibialis posterior contract together? At what
joint does this occur?
A:Ankle inversion.
Inversion and eversion both occur at the subtalar joint.

Q:What muscles are responsible for ankle eversion?and what nerve innervates them?
A:Peroneus brevis and peroneus longus, The superficial peroneal nerve.
Q:What motor and sensory function is lost with damage to the superficial peroneal nerve?
A:Inability to evert the foot and loss of sensation over the dorsum of the foot, apart from the
first web space, which is innervated by the deep peroneal nerve.
Q:Common peroneal (fibular) nerve injury:
A:This is a relatively common injury because of its superficial and vulnerable position as it
winds around the neck of the fibula. Dorsiflexion (extensor muscles) and eversion (the
peronei) are lost; the foot drops and becomes inverted. There is sensory loss over the
dorsum of the foot
Q: How would you recognise compartment syndrome in the lower leg?

A:Compartment syndrome is an emergency that presents with pain out of proportion to the
injury sustained, in someone with a swollen leg, particularly acute on passive stretching of the
ankle. There may be paraesthesia,
pulselessness and paralysis, all late signs and suggestive of impending limb necrosis.
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Describe the blood supply to the

head of the femur head:
The majority of the blood supply to
the head of the femur is from
retinacular arteries, which arise as
ascending cervical branches from
the extracapsular arterial
anastomosis. This is formed
posteriorly by the medial femoral
circumflex artery and anteriorly
from branches of the lateral femoral
circumflex artery with minor
contributions from the superior and
inferior gluteal arteries.
There is also supply from the artery of the ligamentum teres, also know as the artery of the round
ligament of
the femoral head (a branch of the obturator artery).
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Infective endocarditis 2
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FEMORAL TRIANGLE Www.Medicalstudyzone.com
Base: inguinal ligament

Medial border: medial margin of the adductor longus muscle
Lateral border: medial margin of the Sartorius muscle
Floor:
*medially: pectineus and adductor longus
*laterally: iliopsoas
Contents: (FROM LATERAL TO MEDIAL)

- femoral nerve
- femoral artery
- femoral vein
- deep inguinal lymph nodes and lymphatics
Femoral artery can be palpated in the femoral triangle midway

between the ASIS and the pubic symphysis
FEMORAL SHEATH
The femoral sheath is a funnel-shaped, fascial tube of varying length (usually 3 to 4 cm) that passes deep
to the inguinal ligament and encloses proximal parts of the femoral vessels and creates the femoral canal
medial to them .
The sheath is formed by an inferior

prolongation of the transversalis and
iliopsoas fascia from the abdomen/greater
pelvis. The femoral sheath does not enclose
the femoral nerve. The sheath terminates
inferiorly by becoming continuous with the
tunica adventitia, the loose connective tissue
covering of the femoral vessels.
The femoral sheath is subdivided into three

compartments by vertical septa of
extraperitoneal connective tissue that extend
from the abdomen along the femoral vessels.
The compartments of the femoral sheath are
lateral compartment : for the femoral artery
. Intermediate compartment: for the femoral vein
. Medial compartment: which constitutes the femoral canal.
FEMORAL CANAL
The femoral canal is the smallest of the three compartments. It is short and conical and lies between the medial wall of the femoral sheath
and the femoral vein. The femoral canal • Extends distally to the level of the proximal edge of the saphenous opening
• Allows the femoral vein to expand when venous return from the lower limb is increased or when increased intraabdominal pressure causes
a temporary stasis in the vein.
• Contains loose connective tissue, fat, a few lymphatic vessels, and sometimes a deep inguinal lymph node ( Cloquet node)
• The base of the femoral canal, formed by the small ( approximately 1 cm in diameter) proximal opening at its abdominal end, is the femoral
ring .
The boundaries of the femoral ring are as follows: laterally, a femoral septum between the femoral canal and the femoral vein; posteriorly, the
superior ramus of the pubis covered by the pectineal ligament; medially, the lacunar ligament; and anteriorly, the medial part of the inguinal
ligament.
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ADDUCTOR CANAL
Hunter's canal, also known as the subsartorial or adductor canal, runs from the apex of the
femoral triangle to the popliteal fossa.(adductor hiatus)
Boundaries:
-Anterolaterally :Vastus
medialis.
-Anteromedially/Roof
:Sartorius .
-Posteriorly : Adductor
longus and magnus.
Contents:
-Femoral artery and vein.
- Saphenous nerve.
-Nerve to vastus
medialis.
Q:What is the surface marking of the adductor hiatus?

A:The adductor hiatus lies 2/3rds along the line between the ASIS and the adductor tubercle of the
femur.
POPLITEAL FOSSA
◌Boundaries:
- upper medial: semimebrnosus and semitennosus.
- Upper lateral: biceps femoris.
- Lower medial: medial head of
gastrocnemius.
- Lower lateral : lateral heaad of
gastrocnemius.
◌Contents ( superficia to deep):
- common peroneal nerve.
- Tiibial nerve.
- Politeal vein.
- Popliteal artery.
- Lymph nodes: they receive from a
small area of the skin above the heel
and from the deep structures of the
calf
◌DD of lump from popliteal fossa:

- backer's cyst. - pop. Artery
aneurysm. - lipoma
- Schwanoama. - Popliteal vein
varicosities
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Q:Where does the iliotibial tract attach?

A:The Iliotibial tract is attached to the anterolateral iliac tubercle of
the iliac crest proximally and the lateral condyle of the tibia distally.
Q:What muscles insert onto it?
A:Gluteus maximus and tensor fasciae lata muscles insert onto
the iliotibial.
Q:What is its clinical significance?

A:The iliotibial tract stabilises the knee in extension and in partial
flexion. It is important in walking and running.
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Q:What clinical sign is evident with weakness of gluteus medius and minimus?
A:A Trendelenburg gait or a positive Trendelenburg test.
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66
1 53
PATHOLOGY CHAPTER
Q:What is the surface markings of the sciatic nerve?
-The surface marking of the sciatic nerve is a curved line drawn

from 2 points: halfway between the posterior superior iliac spine
to the ischial tuberosity to halfway between the ischial tuberosity
and the greater trochanter.
Q:What is the course of the sciatic nerve?
The sciatic nerve runs inferolaterally under cover of the gluteus maximus,
midway between the greater trochanter and the ischial tuberosity . It
descends from the gluteal region into the posterior thigh, where it lies
posterior to the adductor magnus and deep (anterior) to the long head of
the biceps femoris.
Q:What variations do you know with regard

to the sciatic nerve exiting the pelvis?
the sciatic nerve is composed of the tibial (L4-s3) and common fibular
(L4-s2) nerves, which usually enter the gluteal region bound in a
common connective tissue sheath (A). In some cases (12%), the two
nerves enter the gluteal region separately: the tibial nerve at the inferior
border of piriformis and the common fibular nerve pierces piriformis (B).
In another variation (0.5%), the common fibular nerve enters the gluteal
region along the superior border of the muscle and the tibial nerve along
its inferior border (C).
51
54 ANATOMY
Www.Medicalstudyzone.com 2
Q:What is the nerve related to ASIS?

A:Lateral cutaneous nerve of the thigh
◌Meralgia parathetica:
A painful mononeuropathy of the lateral femoral cutaneous nerve (LFCN), it is commonly due to focal entrapment of
this nerve as it passes through the inguinal ligament
VASCULAR LACUNA
◌Vascular lacuna : is an anatomical structure placed behind/below the inguinal
ligament. Lacuna vasorum is medially, while muscular lacuna is laterally.
◌Contents of lacuna vasorum (order from medial part):
-Deep inguinal lymph nodes.
-Femoral vein.
-Femoral artery.
-Femoral branch of the genitofemoral nerve.
◌Contents of lacuna musculorum:
-Femoral nerve.
-Iliopsoas.
-Lateral femoral cutaneous nerve.
52
54
TRUNK AND THORAX

T TRTRUUY
-ID branches supplying GIT
1
◌ABDOMINAL AORTA Www.Medicalstudyzone.com
Surface markings:
[Course T12-L4]
T12 ------- >4 cm above transpyloric plane in midline.
L4 --------- > supracristal line in midline.
Transpyloric plane : halfway between the jugular notch and the upper border of pubic symphysis
Branches of abdominal aorta:
Vertebral level Single branches Paired branches

T12 Coeliac trunk Rt.+ Lt. Inf. phrenic aa.
L1 Superior mesentric Rt. + lt. Middle supra-renal
a. aa
L2 ---------- Rt. + lt. Renal aa.
L3 Inferior mesenteric Rt. + lt. Gonadal aa.
a.
L4 Median sacral a. Rt. + lt. Common iliac aa
Posteior branches > 4 pairs of lumbar arteries from the back of aorta opposite each vertebral
level (L1-L4) plus the median sacral artery.
Ant.relations: -celiac trunk and branches,

- body of the pancreas
- SMA
- 3rd part of duodenum
- root of mesentry,
- splenic vein,
- left renal vein
2
◌
◌ID branches on abdominal aortogram :
A:Abdominal aorta G:common hepatic

B:Rt.common iliac H:SMA
C:Lt.Common iliac I:gastroduodenal a
D:Lt. Renal a. J:Lt. Hepatic a.
E:Rt. renal a. K:Rt. hepatic a.
F:splenic a. L: IMA
◌ID AAA on CT angiography ----------> saccular.

Infrarenal AAA.
◌Define aneurysm: abnormal dilatation of an artery.
◌pathogenesis: median cystic necrosis (trueaneurysm),
post- traumatic (false aneurysm).
◌Causes(risk factors):
-HTN secondary to astherosclerosis secondary to
smoking.
-Marfan syndrome.
-Syphilis.
-Bicuspid aortic valve.
◌Dissecting aneurysm: separation of the layers of

the arterial wall with propagation of dissection
proximally and distally
3
INFERIOR VENA CAVA:
◌Tributaries: (L5-T8)
T8: paired inferior phrenic veins.
T8: hepatic veins (3).
L1: right suprarenal
vein.
L1: renal veins.
L2: right gonadal
vein.
L1-L5: lumbar
veins.(3rd and 4th
lumnar veins)
L5: common iliac veins (origin).
◌ID RT,LT gonadal veins, iliac vessels :
4
◌Renal veins( ant. relations) :

-Rt side: 2nd part of duodenum
-Lt side: body of pancreas,SMA,splenic vein
SPLEEN
◌ID
-Blood supply: art > splenic art. ( from the celiac trunk).
Venous > splenic vein to SMV to portal vein
-related ribs: opposite 9th,10th,11th ribs.
-Structure to warry during splenectomy: tail of the pancreas.
-Describe the course of splenic aa:

Arises from the coliac trunk ----> passes to the left above the upper border of the pancreas >
behind the stomach separated from it by the lesser sac-----> lienorena. Ligament > ends by
giving up terminal branches inside the hilum of the spleen.
It supplies: stomach ,pancreas and spleen
5
PANCREAS
◌Parts: head.neck.body and tail.
◌Islet cells produce:

-Alpha cells: glucagon.
-Beta cells: insulin.
-D cells: somatostatins.
◌blood supply: (3 sources)

1-Superior pancreaticoduodenal aa( from gastrduodenal
aa)
2-Inferior pancreaticoduodenal aa ( from SMA)
3-Pancreatic branches ( from splenic aa)
◌ducts:
1- main pancreatic duct : drains head,body and tail > opens into
major duodenal papilla.
2- accessory pancreatic duct: drains the uncinate process >
opens into minor duodenal papilla.
◌vessels encounterd during whipple:

Abdominal aorta,SMA, Lt.renal vein, sup. and inf. pancreatico duodenal aa., splenic vein ,SMV,portal
vein
◌ligament connecting the tail of pancreas with the spleen: lienorenal ligament.
◌devolopment of pancreas: arises from 2 buds:

1- the ventral bud: arises from the hepatic diverticulum and it gives rise to the lower part
of the head and uncinate process.
2- the dorsal bud : arises from the dorsal aspect of the duodenum and gives rise to
upper part of the head, neck, body and tail.
6
LIVER
◌the 1st. 2 organs injured in stab epigastrium:

-Liver ( lt. Lobe)
-stomach
Q: What demarcates lef t and right lobe ?

A: Anatomical: -falciform ligament (ant.), fissure for
ligamentum teres and ligamentum
venosum (posteroinferiorly)
Surgical: a line passing from IVC to the fossa of GB
Q: what art.of the celiac trunk supplies both liver

and stomach ?
A: hepatic art.( runs in the free border of lesser omentum to porta hepatis)
Venous drainage: hepatic veins to IVC
◌porta hepatis: strucures open in:

Ant.: Rt. and Lt.. Hepatic
ducts
Intermediate: hepatic art.
Post. : portal vein
◌Ligament supporting:
1- Falciform ligament ( to the diaphragm and AAW)
2- Lesser omentum ( to the stomach and 1st part of
duodenum)
3- Rt. and Lt. Triangular ligament ( to the diaphragm)
4-Upper and lower coronary ligament ( to the diaphragm)
7
GALL BLADDER
Surface marking: at the angle between the 9th costal cartilage and the lateral margin of
the rectus sheath.
Q: Why shoulder pain in cholecystitis ?

A: An inflamed GB may irritate the diaphragm
Roots of phrenic nerve that supply the diaphragm as the same as the supraclavicular
nerve supplying the shoulder tip.
STOMACH
PARTS: fundus,body,pylorus
BLOOD SUPPLY:
Art.:
-Lt. Gastric a. From celiac trunk
-Rt. gastric a. From hepatic a.
-Lt. Gastroepiploic from splenic a.
-Rt. Gastroepiploic from gastroduodenal from
hepatic a.
-Short gastric a. From splenic a.
Venous:
- Lt.gastric+ rt. gastric vv > portal vein
- Lt. Gastroepiploic+ short gastric vv.>splenic
vein
-.Rt. gastroepiploic v > SMV
8
DUOENUM
◌consists of 4 parts
-peritoneal relations:
The first part of the duodenum lies within the peritoneum but its other parts are retroperitoneal.
-blood supply:
1-superior pancreatico duodenal artery ( from
gastroduodenal)
2-inferior pancreatico duodenal artery ( from SMA)
3- branches from hepatic, right gastric, right gastroepiploic and supraduodenal arteries.
◌Relations of the different parts of the duodenum :
First part
-Anteriorly: Quadrate lobe of the liver and gallbladder.

-Posteriorly: Portal vein, gastroduodenal artery, and common bile duct (CBD).
-Superiorly: Epiploic foramen being divided from it by the portal vein and bile duct.
-Inferiorly: Head and neck of the pancreas.
Second part
-Anteriorly: Gallbladder and right lobe of the liver, transverse colon, transverse
mesocolon(commencement), and coils of the small intestine.
-Posteriorly: Right kidney and right renal vessels, right edge of the inferior vena cava (IVC), and
right psoas major muscle.
-Medially: Head of the pancreas.
-Laterally: From below upward, ascending colon, right colic flexure, and right lobe of the liver.
9
Third part
-Anteriorly: Root of the mesentery, superior mesenteric vessels, and coils of the jejunum.
-Posteriorly: Right psoas major, right ureter, IVC, abdominal aorta, and right gonadal vessels.
-Superiorly: Head of the pancreas with its uncinate process.
-Inferiorly: Coils of the jejunum.
Fourth part
-Anteriorly: Transverse colon and transverse mesocolon.

-Posteriorly: Left psoas major muscle, left sympathetic chain, left gonadal vessels, and inferior
mesenteric vein.
-Superiorly: Body of the pancreas.
-On to the left: Left kidney and left ureter.
-On to the right: Upper part of the root of mesentery
Major duodenal papilla: It’s a well

marked conical projection on the
posteromedial wall and situated 8-10 cm
distal to the pylorus. On its peak starts
the common hepatopancreatic duct
(created by the unification of bile and
main pancreatic ducts).
10
APPENDIX
◌Positions:
-Retrocecal,Pelvic,Subcecal,Pre-ileal,Post-ileal.
◌blood supply:
-appendicular art. From ileocolic art. Appendicular vein to SMV
Q: why appendicitis pain is referred to umblicus ?
A: Pain initially starts in the perimubilical region as visceral pain

from the appendix is conveyed in nerve fibres entering the
spinal cord at the T10 level (the T10 dermatome covers the level
of the umbilicus). Irritation of the parietal peritoneum by an
inflamed appendix later on causes localisation of pain to the RIF
URINARY BLADDER
◌ID
-Art Supply: sup. and inf. vesical arteries from the internal iliac art.
-Venous drainage: to vesical venous plxus to internal iliac vein.
◌Nerve supply to detrusor m.:

-Sympathetic: inhibit contraction of
the muscle (from L1,L2)
-Parasympthetic: stimulate
contraction of the muscle (from S2-
S4)
◌most common bladder cancer:

TCC,SCC, mixed,adenocarcinoma.
-c/p of bladder cancer:,painless
hematuria.
Q: risk factors of bladder

cancer
A: aniline dyes,smoking,b-naphthalamine, s.hematobium
Q: how does ureter enters the bladder ?

A: at the base of the bladder at the corner of the trigone.
◌Peritoneal relations of the bladder:
-covers the superior surface and the upper part of the post Surface
◌Layers encounterd during suprapubic catheterization:

Skin ,sc tissue,scarpa’s ,linea alba,fascia transversalis,preperitoneal fat
◌post. Relations of the bladder:

-Male: rectovesical pouch+ 2 vas defrens+ terminal part of the 2 ureters.
-Female: vesicouterine pouch+ terminal part of the 2 ureters. 11
ID on a plastic model : uterus,fallopian tubes, ovaries, douglaspouch, ceacum, terminal ileum and
appendix
DIAPHRAGM
◌Attachements:
Origin:
STERNAL COSTAL VERTEBRAL
Rt. crus(upper 3L)
Lt. Crus(upper 2L)
Median arcuat lig.
(Bw 2 crurae)
Xiphoid process(back) Inner surface of the lower 6 Medial arcuate lig (Bw the
costal cartilages crus&transverse process of L1)
lateral arcuate lig.
(Bw the transverse process of
L1& the 12 th rib)
Insertion: in the central tendon.
12
Openings:
VENA CAVAL OESPHAGEAL AORTIC

T8 T10 T12
Central tendon Right crus Behind median arcuate
ligament
IVC+ rt. phrenic n. Oesphagus+ 2 vagi Aorta,azygous,thoracic duct
13
EXTERNAL OBLIQUE MUSCLE
◌origin: outer surface of the 5th to 12th rib.

◌Insertion: xiphoid process,linea alba,pubic tubercle,anterior half of iliac crest
◌Nerve supply: lower 6 thoracic nerves (T7-T12) and subcostal nerve
◌Directions of fibres: downwards ,forwards and medial.
INTERNAL OBLIQUE MUSCLE
◌Origin: lumbar fascia,iliac crest,ing.ligament.

◌Insertion: inferior borders of 10th-12th ribs, linea alba, pubis via conjoint tendon
◌Nerve supply: lower 6 thoracic nerves,subcostal nerve, first lumbar nerve
◌Directions of fibres: upwards ,forwards and medial.
14
INGUINAL CANAL:
◌boundaries:
-ant. Wall: skin,sc,EOA,Internal oblique m.( lateral 1/3)
-Post. Wall:
conjoint tendon
Fascia transversalis
Reflected part of inguinal ligament
-Roof: lower arched fibres of int. oblique and transversus abdominis m.
-Floor: grooved surface of the ing. Ligament
OESPHAGUS:
Begins: at the lower border of cricoid cartilage(c6).
Ends: at the cardiac opening of the stomach opposite T11
Blood supply
Arterial Venous
Neck: inferior thyroid a. Neck: inferior thyroid vein.
Thorax: branches from aorta. Thorax: azygous veins.
Abdomen: lt.gastric a.+ inferior Abdomen:azygous vein(systemic) Lt.gastric

phrenic a. vein(portal).
◌Cells lining: stratified squamous epithelium.
◌Barret’s oesphagus: columnar metaplasia with increased

risk of developing adenocarcinoma
◌Achalasia: Esophageal achalasia is an esophageal motility

disorder involving the smooth muscle layer of the esophagus
and the lower esophageal sphincter (LES). It is characterized
by
incomplete LES relaxation, increased LES tone, and lack of
peristalsis of the esophagus
15
◌Microscopic picture of achalasia: hypetrophied musculature with absence of myentric plexus.
◌Lymphatic drainage :
- Cervical: deep cervical L.ns.
- Thoracic : post. Mediastinal L.ns.
- Abdomen: lt. Gastric L.ns.
Q: what makes an indent on the oesophagus ?

A: lt bronchus- aortic arch- lt. Atrium.
◌Complications of perforated oesphagus: mediastinitis.
16
THORAX
Q: How many cusps have the pulmonary valve?

A: 3
◌Vertebral level of the pulmonary valve: T6.

Level of pulmonary trunk division: T5
Q: Where to auscultate pulmonary valve ?

A: second ICS left parasternal edge.
17
Azygous vein:
◌Tributaries:
-right sup. intercostal vein
-hemiazygous and accessory
hemiazygous
- pericardial veins
- mediastinal veins
- lower right post. Intercostal veins
- eosphageal veins
- bronchial veins
◌Branches of ascending aorta:

Rt. and left coronary arteries arising from the aortic sinus opposite the aortic valve.
SYMPATHETIC TRUNK
◌Where preganglionic fibres come from > the corresponding spinal nerves T1-L2
Q: What connects it to the spinal nerves?

A: ganglion+ white ramus communicans + grey ramus
Q: How sympathetic nerves leave the sympathetic chain?

A:
1- Through the spinal nerves.
2- Forming plexuses around
blood vessels(cardiac and
pulmonary plexuses, greater
splanchanic nerve , lesser
splanchanic nerve).
18
LUNGS
◌ID main bronchus.
◌ID Structures passing through the hilum of lung:
-pulm.vein, superior division(most. Ant.).
-pulm. arterty
- rt. and lt. Main bronchus(most. Post.).
-bronchial art. And vein.
-lymph nodes.
- autonomic nerves.
◌Pulmonary ligament:
Pleural fold that connects the mediastinal surface of the lung and the
pericardium to allow expansion of pulm. Veins with increased blood flow.
19
◌ID surface anatomy of the lung on the skeleton:
-Apex: curved line from the stenoclavicular joint to 3 cm above the junction bw the medial 1/3
and the intermediate 1/3 of clavicle.
-Ant. Border: sternoclavicular joint to the xiphisternal joint behind the lateral border of the
sternum lt lung deviates laterally from the sternum at the 4 th costal cartilage to form the
cardiac notch.
- Inferior border: line drawn bw 6th rib MCL,8th rib MAL,10 th rib vertebral column.
- Post. Border: transverse process of C7 to transverse process of T 10.
- Hilum: oppsite T5,T6,T7.
- Carina: at the level of T4.
Q: How many bronchopulmonary segments in each lung?

A: 10.
Q: What is the nerve relation anterior and posterior?

A: Phrenic nerve , sympathetic chain.
Q: Describe the course of a clot from deep veins of the calf to pulmonary artery?
A: Pop. Vein--- femoral vein----EIV ---- CIV ---- IVC ---- right atrium ---- AV valve pulmonary
valve
---- pulmonary artery.
◌Nerve supply of the intercostal muscles: intercostal nerves and their collateral branches
20
21
◌Subclavian steal syndrome:

Retrograde flow of blood flow down to the vertebral art. Due to stenoocclusive disease in the
subclavian artery proximal to the vertebral artery, This will lead to brainstem ischemia on arm
excercise.
◌Thoracic outlet syndrome:

Compression of the neurovascular bundle (brachial plexus subclavian art.) between the scalenus
medius and scalenus ant > neurological and vascular symptoms in the arm.
◌Show on the skeleton where to put a chest tube: 5th ICS mid axillary line.
Q: Why bradycardia after chest tube insertion?

A: due to irritation of the vagus nerve.
POSTERIOR MEDIASTINUM
Boundaries:
Ant: pericardium+ vertical part of the
diaphragm 9
Post.: lower 8 thoracic vertebrae (T5-
T12)
On each side: mediastinal pleura
Contents:
.Thoracic aorta
.Thoracic duct
• Posterior mediastinal lymph nodes
• • Azygos and hemi-azygos veins
• • Esophagus
• • Esophageal plexus
• • Thoracic sympathetic trunks
• Thoracic splanchnic nerves 22
HEAD AND NECK

ANATOMY
THYROID GLAND
◌Arterial supply:
- Superior thyroid art. from ECA supplies the
superior part.
- Inferior thyroid art. from thyrocervical trunk
from subclavian art. supplies the inferior part.
-Thyroida ima art.(10%) from the aortic arch.
◌Venous drainage :
- Superior thyroid vein to IJV.
- Middle thyroid vein to IJV.
- Inferior thyroid vein to lt. brachiocephalic vein.
◌Lymphatic drainage :
To (pre-laryngeal,pre-tracheal,para-tracheal,upper and lower deep cervical,brachiocephalic ) lymph nodes.
Infrahyoid Muscles
◌Deep: sternothyroid,thyrohyoid.
◌Superficial: sternohyoid , omohyoid.
◌Nerve supply: all parts by ansa cervicalis c1 to c3 except for thyrohyoid which is innervated by c1.
◌Action: depress the hyoid bone and larynx during swallowing and speaking.
1 MRCS OSCE REVISION GUIDE 3rd edition

ANATOMY Www.Medicalstudyzone.com
HEAD AND NECK
N.B: Vertebral level of thyroid cartilage: c4.
Q: Why thyroid moves up with deglution?
A: As the thyroid gland present within the pretracheal fascia which is attached to the thyroid
cartilage and hyoid bone , when the diagastric muscle contract it pulls the hyoid bone
upward which pulls the the thyroid cartilage which pulls the pretrachea fascia with its
contents.
Commonly injured nerves during thyroidectomy

◌ELN (close to the superior thyroid art.)
◌RLN( close to the inferior thyroid art.)
◌Cervical sympathetic chain ( lateral ligature of the inf. Thyroid artery trunk causing ischemia
induced neural damage).
-Papillary thyroid cancer is the only type to spread lymphatically

-Cell origin of medullary carcinoma > parafollicular c cells.
◌Late complications of thyroidectomy: hypothyroidism , hypocalcemia.
LARYNX
◌Nerve supply:
Motor ---- > all laryngeal muscles are supplied by RLN except for cricothyroid m.
Which is supplied by
ELN (branch of SLN) from the vagus.
Sensory----- >Above vocal cord > ILN (from SLN).
Below vocal cord - > RLN (from vagus).
◌Attachements of vocal cords:
Ant ---- > thyroid cartilage.
Post ---> arytenoid cartilage.
Lat ---- > laryngeal m.
Med ---- > free border.
◌ Oppening vocal cords: by the 2 post. Cricoarytenoids by externally
rotating the arytenoids.
◌ Closing the larynx during swallowing: : by lateral
cricoarytenoid m.
◌ Tensing vocal cords: by the 2 cricothyroid
◌ Cricothyrodotomy - > crcothyroid membrane ( between
the thyroid and cricoid cartilages)

Www.Medicalstudyzone.com ANATOMY
HEAD AND NECK
PARATHYROID GLAND
◌Location: on the post. aspect of the thyroid gland 2 on each side.
◌Hormone secretion: parathormone which plays a role in cacium homeostasis.
◌Embryology: inferior parathyroid-- > 3rd branchial arch with the thymus.
Superior parathyroid -- > 4 th branchial arch.
◌Blood supply: inferoir thyroid artery.
RLN
◌Supplies all laryngeal muscles except cricothyroid m. And gives sensory innervation of the
mucuous membranes of the larynx below the vocal cords.
◌Unilateral injury may lead to :
- Partial: dyspnea on effort
- Complete: hoarsness of voice
◌-Bilateral injury may lead to :
-partial ( midline ) -- > respiratory compromise.
-full (half abducted) -- > the patient will not be able to speak or cough.
SKULL
◌Age at which cranial sutures ossify: by 18 to 24 months.
◌If fused at birh; craniosynostosis.
◌Mastoid bone develops: by the age of 2 years.
◌Diploic veins: veins found in the skull that drain the diploic space to the dural venous sinus.

◌Pterion:
-Bones forming: frontal,parietal,temporal,sphenoid.
-Clinical signficane: middle meningeal art. runs behind and injury here may lead to extradural
hematoma.
◌Muscles attached to the styloid process:

-styloglossus. -stylohyoid. -stylopgaryngeus.
THE TEMPROMANDIBULAR JOINT (TMJ)
◌Type: bi-arthroidal (condyloid) hinge joint.

◌Articulating surfaces:
- The mandibular fossa.
- Articular tubercle (from the squamous part of the temporal bone).
- Head of mandible.
◌Movements :
- Opening : diagastric, lateral ptrygoid, genihyoid, mylohyoid.
- Closing.
- Protrusion.
- Retrusion.
- Side to side.
TEMPORALIS MUSCLE
◌ Blood supply: deep temporal arteries ( ant.and

post.) from maxillary artery.
Q: What supplies the scalp over the temporalis

muscle?
A: Superficial temporal artery from ECA

HEAD AND NECK

Causes of lytic skull lesions:

-lytic skeletal metastasis. -multiple myeloma. - paget's disease.
-sarcoidosis. -osteomyelitis. -hemangioma.

HEAD AND NECK
THE SKULL FORAMINA

Middle cranial fossa:
The middle cranial fossa consists of three

bones – the sphenoid bone and the
two temporal bones.
Its boundaries are as follows:
• Anteriorly and laterally it is bounded by

the lesser wings of the sphenoid bone.
These are two triangular projections of
bone that arise from the central sphenoid
body.
• Anteriorly and medially it is bounded by
the limbus of the sphenoid bone. The
limbus is a bony ridge that forms the
anterior border of the chiasmatic sulcus (a
groove running between the right and left
optic canals).
• Posteriorly and laterally it is bounded by
the superior border of the petrous part of
the temporal bone.
• Posteriorly and medially it is bounded by the dorsum sellae of the sphenoid bone. This is a large superior
projection of bone that arises from the sphenoidal body.
• The floor is formed by the body and greater wing of the sphenoid, and the squamous and petrous parts of
the temporal bon
The middle cranial fossa consists of a central portion, which contains the pituitary gland, and two lateral
portions, which accommodate the temporal lobes of the brain.
Posterior cranial fossa:
The posterior cranial fossa is comprised of three bones: the occipital bone and the two temporal bones.
It is bounded as follows:
• Anteriorly and medially it is bounded by the

dorsum sellae of the sphenoid bone. This is
a large superior projection of bone that arises
from the body of the sphenoid.
• Anteriorly and laterally it is bounded by the
superior border of the petrous part of
the temporal bone.
• Posteriorly it is bounded by the internal surface
of the squamous part of the occipital bone.
• The floor consists of the mastoid part of the
temporal bone and the squamous, condylar and
basilar parts of the occipital bone.
The posterior cranial fossa houses the brainstem

and cerebellum.

HEAD AND NECK
Q:What is the cranial nerve tracks on the clivus?

A:Abducent nerve
Q: What is the name of the juve-

nile structure that form the clivus?
A: spheno-occipital synchondrosis.
- Type of growth plate in clivus: hyaline cartilage.
- Fusion of the spheno-occipital synchondrosis: initiates in girls at 12-13 years, and in boys at 14-15
years and is complete by 17-18 years
lateral frontal diagonal basilar

skull fracture:
bones involved:
frontal bone,sphenoid bone,

temporal bone, parietal bone
Begnin tumours of the posterior cranial fossa:

Hemangioblastoma, acoustic neuroma, Ependymoma and ependymoblastoma.
CHAPTER

CAVERNOUS SINUS
◌There are 2 cavernous sinuses each lying laterally on either side of the sella turcica.
◌Draining blood from: -sup. ophthalmic veins + facial vein.
-emisary veins from ptrygoid plexux.
-sphenoparietal sinuses.
◌Drains blood to: -superior and inferior petrosal sinuses.
-IJV.
- intercavernous sinus.
◌Contents:
- occulomotor n.
- ICA.
- trochlear n.
- abducent n.
- ophthalmic n.
- maxillary n.
CAVERNOUS SINUS THROMBOSIS:

The facial veins make clinically important connections with the
cavernous sinus through the superior ophthalmic veins. Blood
from the medial angle of the eye, nose, and lips (dangerous
area) usually drains inferiorly into the facial vein. However,
because the facial vein has no valves, blood may pass
superiorly to the superior ophthalmic vein and enter the
cavernous sinus. In people with thrombophlebitis of the facial
vein, pieces of an infected thrombus may extend into the
cavernous sinus, producing thrombophlebitis of the cavernous
sinus.
Signs of thrombosis: - painful swelling of the eye.
- 3rd,4th,5th,6th cranial palsies.
- gradual loss of vision.

HEAD AND NECK
DURAL VENOUS SINUSES


HEAD AND NECK
TT
TONGUE
ONGUE
◌Nerve supply(general + taste):
-Post 1/3: general plus taste >
glossopharyngeal nerve.
-Ant. 2/3: general----> lingual nerve Taste>
chorda tympani nerve.
◌Extrinsic muscles: stylo,hyo,palato,geni
(glossus)
◌Muscle retracting the tongue: styloglossus.
-Nerve supply: all by hypoglossal nerve except
for the palatoglossus by vagus nerve.
FACIAL NERVE
Intra-cranial Course:
origin between pons and medulla -----

> IAM--------------------- > facial canal
(petrous part of temporal bone) - > exit through
the stylomastoid foramen
Branches in face:
( temporal,zygomatic,buccal,marginal,
mandibular,cervical)
Muscle supplied by facial nerve in ear:

Stapedius muscle
Type of facial nerve palsy occuring in Acoustic

neuroma: LMNL
Difference between UMNL and LMNL facial palsy?

In upper motor neuron lesion upper part of face will be spared, only lower part will be affected but in
lower motor neuron lesion both upper and lower part of face will be affected
Q:Why patients with acoustic neuroma hears

Voices louder on the affected side ?
As the facial nerve may be involved as it passes with the vestibulochoclear nerve through IAM.
This will cause parlysis of the stapedius muscle which will cause wider oscillation of the
stapes, resulting in heightened reaction of the auditory ossicles to sound vibration
(hyperacusis).

TRIANGLES OF THE NECK
◌Anterior triangle:
-Post.: ant.border of the sternomastoid. -Ant.: midline of the neck.
-Sup.:lower border of the mandible Divided by( diagastric m.+ sup. belly of omohyoid )to: diagastric ,
carotid,muscular,1/2 submental triangles.
◌Posterior triangle:
Post.:ant.border of the trapzius. -Ant.: post.boder of sternomadtoid.
-Inf.:middle 1/3 of clavicle.
SPINAL ACESSORY NERVE
◌Surface anatomy: it crosses the post.triangle of neck between the point of the junction
between upper 1/3 and lower 2/3 of the sternomastoid to the junction between upper 2/3 and
the lower 1/3 of the trapezius
◌Supplies:-trapezius( shrug the shoulder).
-Sternomastoid ( turns the head to the contralateral side)

HEAD AND NECK
GREAT AURICULAR
NERVE
◌Supply: (c2-c3)
- skin over the angle of the mandible.
- skin over the parotid gland.
- skin of the lower 1/2 of the auricle.


HEAD AND NECK
EXTERNAL CAROTID ARTERY
◌course: -Begining > one of the 2

terminal branches of CCA at the
upper border of the thyroid
carilage (c4).
-Termination >Behind the
neck of the mandible inside
the parotid gland by dividing
into
superficial
temporal and
maxillary
branches.
◌Nerve passing ant.to it:Hypoglossal
nerve.
◌Branches: Some American Ladies
Found Our Pyramids Most
Satisfactory.
-superior thyroid a.
-ascending pharyngeal art.
-lingual art.
- facial art.
-occipital artery.
-post. Auricular.art.
-maxillart art.
superficial temporal art.
◌carotid body: on the post.aspect of the bifurcation of CCA contains

chemoreceptors sensitive to changes in PH.
◌carotid sinus: the carotid sinus is a dilated area at the base of the internal carotid artery
just superior to the bifurcation of the internal carotid and external carotid at the level of the
superior border of thyroid cartilage. It contains baroreceptors for maintaining blood
pressure.

PATHOLOGY
PAROTID GLAND
◌surface anatomy:
-upper end: curved line from the head of the
mandible to the center of mastoid bone.
-posterior border: straight line from the center
of the mastoid process to a point 2 cm below
and behind the angle of the mandible.
-Ant. Border: aline from the tragus of the ear
to the center of the
posterior border of the
masseter then to the point
2 cm below and behind the
angle of the mandible.
PAROTID DUCT
◌surface anatomy: the middle 1/3 of a line
drawn between intertragic notch to the middle
of the philtrum,
opens by piercing buccinator m.oppsite the
upper 2nd molar tooth.
◌ Blood supply: arterial >branches from ECA

within the gland.
Venous > to the
retromandibular vein.
◌Parasympathetic ganglion supplying

parotid: otic ganglion.
◌Structures passing through:

1-facial nerve and its branches.
2- retromandibular vein formed by the union of maxillary vein and sperficial temporal vein.
3- external carotid artery with its 2 terminal branches( maxillary artery and superficial
temporal art.)
4- auriculotepmoral nerve.
5- deep parotid lymph nodes
Parasympathetic supply to the parotid gland:
Inferior salivary nucleus-> glossopharyngeal

nerve->tympanic nerve->tympanic plexus->lesser
petrosal nerve->
Lesser petrosal nerve->otic ganglion-
>auriculotempral nerve

HEAD AND NECK
.
◌Type of parotid salivary secretions: serous.
◌DD of parotid lump:-infection(parotitis,mumps).

-obstructed duct( calculus or ext. compression).
-Neoplasm(pleomophic adenoma,wartin tumour).
-Deep parotid lymph nodes.
◌Frey syndrome: the aberrant regeneration of the

postganglionic secretomotor parasympathetic nerve fibers,
which are carried in the auriculotemporal nerve from the otic
ganglion to the parotid to the severed postganglionic
sympathetic fibers that supply the sweat glands of the skin . As a
result, sweating, dermal flush, or both occur in the distribution of
the auriculotemporal nerve during salivary stimulation.
◌Lymphatic drainage : to deep,and superficial parotid

lymph nodes.
SUBMANDIBULAR GLAND
Submandibular duct -----> opens in the floor of the mouth on either side of the lingual
frenulum (sublingual papilla)
Submandibualr gland type of secretion----> mucous+serous
Nerves at risk of injury on submandibular gland excision:
.lingual nerve.(above )
.hypoglossal nerve ( below)----->

deviation of the tongue to the affected side
on protrusion
.marginal mandibular branch of facial

nerve.(incision should be 4cm below the
mandible)

PATHOLOGY

ANATOMY Www.Medicalstudyzone.com 2
HEAD AND NECK
NEUROANATOMY
Arterial supply of the brain:
ID vessels on cerebral MRA:

PATHOLOGY
◌Signs of MCA infarct:

-hemiplegia of the lower 1/2 of the contralateral face
-hemiplegia of the contralateral upper and lower extrmities
- aphasia if in the dominant hemisphere
- id MCA aneurysma
- if ruptured will lead to subarchinoid haemorrhage

HEAD AND NECK
Vertebral artery:
◌Crosses transversly across the post.arch of the atlas

◌Vertebral artery: .enters the skull through the foramen magnum
◌Vertebral artery course:

Inside the skull, the 2 vertebral arteries pass upwards , forwards and medially in the
subarachinoid space to reach the anterior aspect of the medulla oblongata, then they unite
together at the lower border of the pons to form the basilar artery.
Q:What the vertebral artery and basilar artery supply in the brain?
A:The vertebrobasilar arterial system perfuses the medulla, cerebellum,
pons, midbrain, thalamus, and occipital cortex.
BOUNDARIES OF THE MIDDLE EAR
◌Roof of the middle ear: tegmen tympani.

◌How middle ear infections cross the skull: by direct erosion of tegmen tympani It may
also spread to mastoid air cells causing mastoiditis.
◌C/ p of meningism: photophobia, neck stiffness, fever.

SUBARACHNOID SPACES /CISTERNS

ANATOMY Www.Medicalstudyzone.com 2
HEAD AND NECK

ARNOLD CHIARI MALFORMATION
It is a condition affecting the brain. It consists of a downward displacement of the cerebellar tonsils through the
foramen magnum causing non-communicating hydrocephalus as a result of obstruction of cerebrospinal fluid (CSF)
outflow.
MENINGIOMA
ID parasagittal meningioma.
Where it arise from: it arises from the arachnoid "cap" cells of the
arachnoid villi in the meninges.
What structure it may compress: superior sagittal sinus.
What area of the brain is affected: motor area 4.
What is the patient will be presented by: monoparesis of the
contralateral lower limb.

HEAD AND NECK
GBM
Type of contrast: Gadolinium
What is meant by ring enhancement : is an abnormal radiologic sign on MRI or CT scans obtained using radiocontrast.
On the image, there is an area of decreased density, surrounded by a bright rim from concentration of the enhancing
contrast dye. This enhancement may represent breakdown of the blood-brain barrier and the development of an
inflammatory capsule
Differential diagnosis :
MAGIC DR or DR MAGIC
M: metastasis
A: abscess
G: glioblastoma
I: infarct (subacute phase)
C: contusion
D: demyelinating disease
R: radiation necrosis or resolving hematoma


HEAD AND NECK PATHOLOGY
occulomotor nerve
◌Muscles supplied by
occulomotor nerve :
- superior rectus m.
- Levator palpebrae
superioris
- Sympathetic fibres to
Muller's muscle
- Inferior rectus m.
- Inferior oblique
- Medial rectus
- Sphincter pupillae
CHAPTER
◌Paralysis of oculomotor nerve leads to :

-The eye will be displaced outward
and displaced downward; outward
because the lateral rectus
(innervated by the sixth cranial
nerve) maintains muscle tone in
comparison to the paralyzed medial
rectus.
The eye will be displaced
downward, because the superior
oblique (innervated by
the fourth cranial or trochlear nerve),
is unantagonized by the paralyzed
superior rectus, inferior rectus and
inferior oblique.
-The affected individual will also
have a ptosis, or drooping of the
eyelid, and mydriasis (pupil dilation).
Q:What is the exact structure on which the occulomotor nerve is pressed against?
A:Petrous part of the temporal bone ( attached border of tentoruim cerebel
TENTORIUM CEREBELLI
The tentorium cerebelli is a horizontal projection of the meningeal dura mater that covers and
separates the cerebellum in the posterior cranial fossa from the posterior parts of the cerebral
hemispheres.

Attachements:
- Posteriorly : to the occipital bone along the grooves for the transverse sinuses.
- Laterally, it is atthitached to the superior border of the petrous part of the temporal bone,
ending anteriorly at the anterior and posterior clinoid process.
-The anterior and medial borders of the tentorium cerebelli are free, forming an oval opening in
the midline (the tentorial notch), through which the midbrain passes.
FALSE LOCALISING SIGN:

Neurological signs are described as “false localizing” if they reflect dysfunction distant or remote from the expected
anatomical location of pathology
This most commonly occurs in abducent nerve palsy due to increased ICP

PATHOLOGY
INFECTIVE ENDOCARDITIS
◌ Definition: inflammation of the endocardial surfaces of the heart including heart valves which is caused
by certain micro organisms.
Q: why rheumatic heart and valve replacement patients are more susceptible to IE?
A: Blood usually flows smoothly over valves, when these valves are damaged as in RH or valve
replacement, there will be an increased chance for bacterial colonization on damaged tissues.
Diagnosis
◌ Dukes criteria
- 2 major criteria.
- Or 1 major + 3 minor criteria.
- Or 5 minor criteria.
Major criteria
◌ major blood culture criteria:
- 2 blood cultures positive for micro organisms typically
found in patients with IE.
- Blood cultures persistently positive for one of these
micro organisms drawn 12 hours apart.
- 3 or more separate blood cultures drawn at least 1 hour
apart.
◌ major echocardiographic criteria:

- Valve vegetations.
- Myocardial abscess.
- New partial dehiscence of a prothetic valve.
Minor criteria
◌ predisposing factor: known cardiac lesion or iv drug abuser.
◌ Fever: > 38°C.
◌ Vascular problems: Arterial emboli, Janeway lesions, conjuctival hge.
◌ Immunological proplems: Glomerulonephrits, Roth’s spots, Osler’s nodes.
◌ Positive blood cultures that doesn’t meet the criteria above.
◌ Echocardiographic findings consistent with IE that does not meet the criteria above.
1
CHAPTER
Common organisms
- Viridans strept or staph.
- Coagulase nagative staph.
- Enterococi.
- Hacek group of micro organisms (oropharyngeal commensals):
(Haemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens, and
Kingella species.)
◌ Signs in hand:
- Osler’s nodes: painful, raised ,red lesions due to immune complex deposition.
- Janeway lesions : non painful ,nodular or macular red lesions due to septic emboli which deposit bacteria
forming microabscesses.
- Splinter hemorrhages: tiny blood clots under nails.
TREATMENT
◌ IV antibiotics depending on culture and sensitivity for 6 weeks
(IV ceftriaxone and vancomycin).
◌ Restrictions:
- Valves do not have specific blood supply so antibiotics can not
reach.
- Organisms lie inside the vegetations.
- Bacteria forms a biofilm (glycocalyx covering) that shields them from antibiotics.
◌ Note that: If IE occurs in tricuspid valve in younger persons ----- > right-sided heart failure.
◌ If no response to medical treatment: Valve replacement or heart transplantation but remember matching
should be done before heart transplantaion (HLA antigen) and if not matched (type 1 ------ > graft rejection).
Q: How to prevent graf t rejections?
A: Immunosuppresant therapy ---- > tacrolimus, mycophenolate, steroids.
◌ Side effects of long term steroid:
- opportunistic bacterial and viral infections such as EBV, CMV ----- > leukemia,lymphoma.
- Cushinoid features: obesity, m.weakness, hirsutism, striae.
- Cardiovascular: fluid retention, hypertension.
- Endocrine: DM.
- musculoskeletal: osteoprosis.AVN, proximal myopathy.
Q: After valve replacement, why on warfarin?
A: To prevent thromboembolism.
◌ Mechanism of action of warfarin: Vit. K antagonist thus inhibiting clotting factors 2, 7, 9 and 10.
◌ Warfarin Reversal: Vit. K, FFP, PCC.
Q: How to monitor?
A: To prevent thromboembolism.
◌ Note that: Right-sided vegetations (tricuspid valve IE) = IV drug abuser
2
DIVERTICULITIS AND ENDOMETRIOSIS
◌ Stem: (LIF pain + peritonism ----> ruptured diverticulitis ----> Hartman’s procedure ---- > histopath.
----> diverticulitis + endometriosis).
PATHOPHYSIOLOGY OF DIVERTICULOSIS
- Colonic diverticula result from the unique structure of the
colonic muscularis propria and elevated intraluminal pressure in
the sigmoid colon. Where nerves, arterial vasa recta, and their
connective tissue sheaths penetrate the inner circular muscle
coat, focal discontinuities in the muscle wall are created. In
other parts of the intestine these gaps are reinforced by the
external longitudinal layer of the muscularis propria, but, in the
colon, this muscle layer is gathered into the three bands termed
taeniae coli. Increased intraluminal pressure is probably due to
exaggerated peristaltic contractions, with spasmodic
sequestration of bowel segments, and may be enhanced by diets
low in fiber, which reduce stool bulk, particularly in the sigmoid
colon.
Q: What is the Cause of diverticulitis in diverticular
disease?
A: Obstruction of diverticula leads to inflammatory changes, producing diverticulitis and peridiver-
ticulitis. Because the wall of the diverticulum is supported only by the muscularis mucosa and a
thin layer of subserosal adipose tissue, inflammation and increased pressure within an obstructed
diverticulum can lead to perforation.
Q: How neutrophils migrate to the site of infection?
A: - margination and rolling along the vessel
wall.
- firm adhesion to the endothelium.
- transmigration between endothelial cells.
- migration in interstitial tissues toward a
chemotactic stimulus
.
3
Q: How did endometriosis got the colon?

A:
◌ Theories are as follows:
- The regurgitation theory: proposes that
endometrial tissue implants at ectopic sites via
retrograde flow of menstrual endometrium.
Retrograde menstruation through the fallopian
tubes occurs regularly even in normal women and
can explain the distribution of endometriosis within
the peritoneal cavity.
- The vascular and lymphatic dissemination theory :
holds that endometrial tissue from the uterus can
“spread” to distant sites (e.g., bone, lung, and
brain) via blood vessels and lymphatic channels.
- The metaplastic theory: suggests that
endometrium arises directly from coelomic
epithelium (meso- thelium of pelvis or abdomen),
from which the müllerian ducts and ultimately the
endometrium itself originate during embryonic
development.
Q: Is endometriosis can increase the risk of cancer?

A: Yes, especially ovarian cancer (3.5 fold risk increase).
Q: Why endometriosis causes pain?
A: Because of intrapelvic bleeding and peri-utetine adhesions.
Q: Few days later developped LIF collection, why?
A: Retained collection (pelvic abcess).
Q: What antibiotics to give?
A: - amoxycillin clavulinic (1.2 g BD for 7 days) to cover G+ve organisms.
- gentamycin (80 mg BD for 3 days) to cover G-ve organisms.
- clindamycin (600 mg BD for 5 days) to cover anaerobes.
4
AORTIC STENOSIS
◌ Causes:
Q: What are causes of sudden death in AS?

A: Aortic dissection and MI.
Q: Aortic valve endocarditis, after a while weakness in Arm?

A: Thromboembolism which lead to cerebrovascular stroke.
Q: Which coagulation system will not be affected by warfarin?
A: Intrensic pathway.
Thromus definition:
Solid material formed of the constituents of blood in flowing blood
Q: If metallic valve replacement was done and the patient developped
IE, why the valve should be removed?
A: - The valve will be a septic focus.

- The valve will be dehiscent.
Q: What If we found micrscopic branching hyphae on a removed metallic valve?
A:
◌ This is fungal infection:
- Candida.
- Aspergillus.
- Microsporum.
- Trichophyton.
- Epidermophyton.
5
GASTRIC CARCINOMA
◌ Gastrectomy with splenectomy, pathology report.

◌ Stem: Surgery done -----> histopath ---- > signet ring carcinoma.
◌ 2 major risk factors for gastric cancer:
- H. pylori infection, chronic atrophic gastritis.
- Intestinal metaplasia.
- Pernicious anemia.
- Adenomatous polyps more than 2 cm.
- Previous gastric surgery.
- HNPCC
- FAP.
Pathology report discussion with the family in 4 simple lines

◌ This is cancer of the stomach.
◌ With incomplete resection.
◌ With high possibility of recurrence.
◌ The patient will require further resection and chemotherapy.
Q: 7-10 days later the patient had axillary vein thrombosis, what prediposes to that?
A: hypercoagulable state in malignancy.
Q: 6 months later came with ascites, derranged liver functions, hepatic mets/
mention 2 pathological tests to do?
A: - Ascites tap and cytology.
- Liver biopsy from mets.
- FNAC from the left supravlavicular lymph node.
- Tumour marker: CA72-4
TREATMENT
◌ Feeding jeujnostomy.
◌ Palliation of ascites by repeated tapping.
◌ Pain relief using opioids.
◌ palliative chemotherapy.
6
Polycystic kidney disease

◌ Stem: ADPK going for bilateral nephrectomy due to
intractable abdominal pain.
◌ Gross pathology: Enlargement of the kidney with multiple

cyst formations.
◌ Mode of inheritence: Autosomal dominant condition due to
mutations in 2 genes; PKD1, PKD2.
◌ Pathogenesis of cyst formation:

- The cells of the renal tubules divides repeatedly until causing
an out-pocketing of the tubular wall with the formation of a
saccular cyst that fills with fluid derived from glomerular
filtrate that enters from the afferent tubule segment.
Progressive expansion eventually causes most of the
emerging cysts to separate from the parent tubule, leaving an
isolated sac that fills with fluid by transepithelial secretion. This isolated cyst expands relentlessly as a
result of continued. proliferation of the mural epithelium together with the transepithelial secretion of
sodium chloride and water into the lumen.
◌ Other organs in the abdomen causing cyst formation: Liver, ovaries, pancreas, spleen.
COMPLICATIONS
◌ renal failure
◌ Infection.
◌ Hypertension.
7
Associated lesion in the brain

- Cerebral aneurysm.
Type of matching before transplant

◌ ABO blood matching.
◌ HLA matching: Human Leucocyte Antigens. HLAA, HLA-B and HLA-DR are the most important. They are
proteins located on the surface of WBC.
Types of graft rejections

◌ Hyper-acute rejection:
- Due to presence of recipient antibodies against the donor tissue.
- Occurs within minutes.
- There is complement activation, clumping of red blood cells and platelets leading to interstitial hemor-
rhage.
- Kidney swells and becomes discolored.
- Nephrectomy must be performed on transplanted organ.
◌ Acute rejection:
- Classified as accelerated if it occurs in the first week.
- Acute if it occurs within first 100 days.
- T cell mediated with diffuse lymphocytic infiltration, arteritis and tubulitis Can be reversed with high
dose steroids
◌ Chronic rejection:
- Occurs months to years after transplant.
- T-cell mediated process resulting from the foreign MHC (looking like) a self MHC carrying an anigen
- There is intimal thickening and graft vessels fibrosis
Q: What types of malignancy occuring with immunosupression?

A: Malignancy: this is 5 times greater than the normal population. Most commonly squamous cell
carcinoma of skin, cervix, basal cell carcinomas, lymphoma and Kaposi’s sarcoma..
SICKLE CELL DISEASE AND BRAIN TUMOUR
◌ Stem: lady known to have sickle cell didease, had head injury, CT done and a temporal mass of 3.8 cm
accidentally discovered.
Q: What is sickle cell disease?

A: Sickle cell disease is a common hereditary hemoglobinopathy caused by a point mutation in
β-globin that promotes the polymerization of deoxygenated hemoglobin,that leads to the replace-
ment of a glutamate residue with a valine residue. The abnormal physiochemical properties of the
resulting sickle hemoglobin (HbS) are responsible for the disease. leading to red cell distortion,
hemolytic anemia, microvascular obstruction, and ischemic tissue damage.
8
COMPLICATIONS
◌ Vaso-occlusive crisis: Triggered by infection, dehydration, acidosis, affecting the bones (painful bone cri-
sis as in hand-foot syndrome), lungs( acute chest syndrome), brain (stroke and reti-
nopathy), spleen (autosplenectomy).
◌ Sequestrtion crisis: In children, massive entrapment of sickle cell in the spleen will lead to rapid splenic
enlergement and hypovolemic shock.
◌ Aplastic crisis: Due to infection of red cell progenitors by parvo-virus.
◌ Chronic tissue hypoxia: Organ damage (spleen, heart, kidney and lungs).
◌ Increased susptibility of infection with encapsulated organsims.
Mechanism of autosplenectomy
◌ In early childhood, the spleen is enlarged up to 500 gm by red pulp congestion, which is caused by the
trapping of sickled red cells in the cords and sinuses. With time, however, the chronic erythrostasis leads to
splenic infarction, fibrosis and progressive shrinkage, so that by adolescence or early adulthood only a small
nubbin of Fibrous splenic tissue is left; this process is called autosplenectomy.
Q: What are the surgical relevance of sickle cell disease?

A: - gall stones.
- autosplenectomy.
- avascular bone necrosis.
- autosplenectomy.
- osteomyeitis.
- pulmonary hypertension.
- heart failure.
Q: Why the patient is immunocompromised?

A: Because of autosplenectomy with increased susptibility of infection with encapsulated organ-
sims.
MOST COMMON BRAIN TUMOUR IN ELDERLY

◌ High-grade:
- Gliomas, glioblastoma multiforme and medulloblastomas.
◌ Low-grade:
- Meningiomas.
- Acoustic neuromas.
- Neurofibromas.
- Pituitary tumours.
- Pineal tumours.
- Secondaries
Manifestations of brain tumours

◌ The presentation will depend on location and rate of growth but includes features of a space occupying
lesion and raised intracranial pressure (ICP) ---> Headache, which is typically worse in the mornings. Nausea
and vomiting.
9
◌ Progressive focal neurological deficits, eg, diplopia associated with a cranial nerve defect, visual field de-
fect, neurological deficits affecting the upper and/or lower limb. Cognitive or behavioural symptoms.
◌ Symptoms relating to location of mass - eg, frontal lobe lesions associated with personality changes,
disinhibition and parietal lobe lesions might be associated with dysarthria. Papilloedema (absence of papil-
loedema does not exclude a brain tumour).
Q: What if the tumour lef t untreated?

A: Increased ICP with resultanat brain herniation,conization and death
Important notes
◌ Biopsy showed squamous cells: Metastatic SCC.
◌ Possible primary sources: SCC of skin, lung, oesphagus, nasopharynx and cervix.
◌ Post biopsy had wound infection: Commonly by staph. aureus.
◌ Wound discharge showed glucose: CSF communication.
POLYTRAUMA AND TRANSFUSION
◌ Stem: Hepatitis C patient ----> trauma -----> blood loss ----> splenectomy and transfusion ----- > DIC.
◌ DIC Definition: It is a pathological consumptive coagulopathy due to activation of the coagulation and
fibrinolytic systems which leasds to formation of microthrombi in many organs with the
consumption of the clotting factors and platlets.
◌ DIC is Characterised by:
- Widespread hemorrhage.
- Thrombocytopenia, decreased fibrinogen and increased FDPs.
Functions of the platelets

◌ Platelets contribute to the hemostatic process in two different ways; firstly, through their adhesive and
cohesive functions that lead to the formation of a hemostatic plug and secondly, they can activate coagula-
tion mechanisms.
Q: How platlets are formed from bone marrow?

A: From megakaryocytes by fragmentation
Q: Why this patient has bleeding tendency?

A: Because of the liver affection.
Q: What are very late manifestations of HCV?
A: cirrhosis and HCC.
Q: What activates intrinsic and extrinsic pathways?
A: - Intrinsic pathway is activated by vessel injury which will lead to activation of factor XII.
- Extrinsic pathway is activated by tissue thromboplastin released by the damaged cells.
Q: How to test for intrinsic and extrinsic pathways?

A: - aPTT tests for intrinsic pathway.
- PT tests for extrinsic pathway and the common pathway.
10
Hypersenstivity reactions
◌ Type 1:
- This is due to mast cell degranulation mediated by IgE. The reaction is almost immediate.
- Examples include anaphylaxis, atopy and asthma.
◌ Type 2:
- Due to antibodies directed towards antigens present on the surface of cells.
- Examples include transfusion reactions and autoimmune haemolytic anaemia.
◌ Type 3:
- Due to the formation of antibody-antigen complexes (immune complex mediated).
- Examples include SLE.
◌ Type 4:
- Delayed hypersensitivity reaction mediated by T-lymphocytes. Takes 48-72 hours to see the effects.
- Examples include contact dermatitis.
◌ Type 5:
- Due to formation of stimulatory autoantibodies in autoimmune conditions.
- Examples include Graves’ disease and myasthenia gravis.
Q: What is the percentage of WBCs in packed RBCs?

A: < 1x106 leucocytes in the pack
Q: What is Life span of RBCs?

A: 120 days.
Q: What tests to do before blood transfusion?

A: ABO and Rh.
Q: What is GXM?
A: - Group cross matching: to test donor red cells against recepient serum to detect any poten-
tial incompatibility through which antibodies in recipient cause hemolysis to donor cells.
- Antigen in cross matching: A,B
Stages of bone healing

◌ Hematoma formation: (mass of clotted blood) at fracture site. Tissue in fracture site swells, very
painful, obvious inflamation, and bone cells are dying.
◌ Fibrocartilaginous callus: developes over a 3 to 4 week period. This process involves:
- Capillary growth in the hematoma.
- Phagocytic cells invading and cleaning-up debri in injury site.
- Fibroblasts and osteoblasts migrating into site and beginning reconstruction of bone.
- Note that: The fibrocartilaginous callus serves to splint the fracture.
◌ Bony callus: begins forming after 3 to 4 weeks after injury and is prominent 2 to 3 months following the
injury. Continued migration and multiplying of osteoblasts and osteocytes results in the fibrocartilaginous
callus turning into a bony callus.
◌ Remoldeling: any excess material of the bony callus is removed and compact bone is laid down in order
to reconstruct the shaft. Remoldeling is the final stage.
11
Q: What are Effects of prolonged immotility on bone?

A: Loss of bone density and increased risk of osteoprosis.
Q: Infected implant, why you should remove?

A: Septic focus.
Q: What the 1st test to do?
A: Wound swab for culture and sensitivity.
Q: What is PVL staphs aureus?
A: Panton–Valentine leukocidin (PVL) is a cytotoxin— one of the β-pore-forming toxins. The pres-
ence of PVL is associated with increased virulence of certain strains (isolates) of Staphylococcus
aureus. It is present in the majority of community-associated Methicillin-resistant Staphylococcus
aureus.
Q: What is the effect of this cytotoxin?
A: PVL creates pores in the membranes of infected cells and is the cause of necrotic lesions involv-
ing the skin or mucosa, including necrotic hemorrhagic pneumonia.
MEN 1 SYNDROME
STEM: Man with parathyroidectomy and pancreatic mass
◌ Hyperplasia definition: Increase in the No. of cells in tissue or organ in response to a stimulus.
Q: How many parathyroid glands mostly affected?

A: The 4 glands.
◌ Microscopic picture of hyperplasia:

- Microscopically, the most common pattern seen is that of chief cell hyperplasia, which may involve the
glands in a diffuse or multinodular pattern.
- Less commonly, the constituent cells contain abundant water-clear cells (water-clear cell hyperplasia).
- In many instances there are islands of oxyphils, and poorly developed, delicate fibrous strands may en
velop the nodules.
12
Q: The patient developped stupor, confusion and hypoglycemia( 1.2 mmol/l)

Why do you think?
A: Insulinoma that’s derived from β-cell of islets of langerhan’s.
Q: What other causes of unresponsive hypoglycemia do you know?
A: - Abnormal insulin sensitivity.
- Diffuse liver disease.
- Inherited glycogenoses,
- Ectopic production of insulin by certain retroperitoneal fibromas and fibrosarcomas.
C/P OF INSULINOMA
◌ Clinical manifestations:
- Confusion, stupor, and loss of consciousness. (blood glucose 2.5 mmol/L) or less.
- These episodes are precipitated by fasting or exercise
- Promptly relieved by feeding or parenteral administration of glucose.
◌ Biochemical diagnosis:
- High circulating levels of insulin (>10 µU/mL).
- High insulin-to-glucose ratio
Q: What do you suspect as another pathology in this patient?

A: Pituitary adenoma (MEN 1).
Q: What are the 3 gene mutations in insulinoma?
A: - MEN1, which causes familial MEN syndrome, type 1, also is mutated in anumber of sporadic neuro
endocrine tumors.
- Loss-of-function mutations in tumor suppressor genes such PTEN and TSC2 (which result in activa-
tion of the oncogenic mammalian TOR (mTOR) signaling pathway.
- Inactivating mutations in two genes, alpha-thalassemia/mental retardation syndrome, X-linked
(ATRX) and death-domain associated protein (DAXX), which have multiple cellular functions, includ-
ing telomere maintenance.
Q: What is double hit hypothesis?

A: Like all genes, tumor suppressor genes may undergo a variety of mutations however, most
loss-of-function mutations that occur in tumor suppressor genes are recessive in nature. Thus, in
order for a particular cell to become cancerous, both of the cell’s tumor suppressor genes must be
mutated. This idea is known as the “two hit” hypothesis.
Q: What is telomere?
A: A telomere is a region of repetitive nucleotide sequences at each end of a chromosome, which
protects the end of the chromosome from deterioration or from fusion with neighboring chromo-
somes.
Q: What is apoptosis?
A: Programmed cell death.
13
PROSTATE CANCER
◌ Stem: A man with BPH, poor urine stream and low back pain.
Q: How to take a prostate biopsy?

A: Trus guided from: midlobe parasagittal plane at( the apex, the midgland, and the base) bilaterally.
Q: Why multiple biopsies?

A: - There is often only a scant amount of tissue available for histologic examination in needle biopsies.
- Malignant glands may be admixed with numerous benign glands.
- Moreover, the histologic findings pointing to malignancy may be subtle (leading to underdiagnosis).
- There are also benign mimickers of cancer that can lead to a misdiagnosis of cancer.
Q: How to differntiate between rectum and prostate cells in a needle biopsy?

A: - Using immunohistochemical marker; α-methylacyl-coenzyme A-racemase (AMACR).
- CEA (in rectal cells).
Q: What are the gene mutations involved in pathogenesis of prostate cancer?

A: The most common acquired genetic lesions in prostatic carcinomas are TPRSS2-ETS fusion genes
and mutations or deletions that activate the PI3K/AKT signaling pathway.
Q: How can you judge the scuccess of radical prostatectomy?

A: - Fall in the level of PSA below detectable levels within 4-6 weeks.
- High PSA after prostatectomy > I should consider
recurrence.
Q: Why PSA is not reliable?

A: - PSA is organ specific, but not cancer specific.
- Although serum levels of PSA are elevated to a lesser extent in BPH than in prostatic carcinomas,
there is considerable overlap.
- Other factors such as prostatitis, infarction of nodular hyperplasias, instrumentation of the prostate,
14 and ejaculation also increase serum PSA levels.
Q: What is the grading system?
A:
◌ Gleason score:
- It grades prostate tumors from 2 – 10, 10 being the most abnormal and therefore the most likely to
spread.
- The pathologist allocates a number from 1-5 for the most common histological pattern in the speci-
men, then does the same for the second most common pattern.
- The sum of these two numbers gives the Gleason score.
Q: One test to exclude bony Mets?

A: Alkaline phosphatase.
Q: What kind of metastases and why?

A: Sclerotic. Due to increased bone deposition due to increased osteoblastic activity.
Q: Post operative, patient developed fever, dusky red urine...?
A:
◌ Why? UTI.
◌ Which of the blood components will rise? WBCs; neutrophils.
◌ What are the most common organisms? E-coli.
Q: What are the cells producing testosterone?

A: Leydig cells.
Q: What is the rational in treating prostste cancer by bilateral orchidectomy?

A: Androgen depriviation, as the growth and survival of prostate cancer cells depends on andro-
genes which bind to the androgen receptor (AR) and induce the expression of pro-growth and
pro-survival genes.
15
BASAL CELL CARCINOMA
◌ Lesion: Pearly papule with a central ulcer with rolled in (inverted) edges.
Q: Why the surrounding skin is red?

A: Due to the presence of dilated subepidermal blood vessels (telengectassias).
Q: Most propable diagnosis?
A: BCC.
Q: What is natural history of BCC?
A: Indolent with slow progression locally destructive but limited potential to metastasis (never
invades blood or lymphatic vessels)
Q: What is your concern in pathology report?
A: Deep margin involvement.
Q: How would you manage a patient with deep margin involvement?
A: Re-excision.
TREATMENT
◌ Surgical:
- Curettage and Electrodissecation: scraping away the tumour and stopping bleeding with cautery.
- Excision with primary closure, flaps, grafts, and secondary intention healing excision margin of 4 mm
around the tumour is recommended where possible.
- Cryotherapy (with liquid nitrogen), but can’t obtain tissue biopsy.
- Mohs micrographic surgery: Serial tangential horizontal sections are taken andexamined histologically
until all margins are clear.
16
◌ Radiotherapy:
- Topical photodynamic therapy - δ-aminolaevulinic acid made up in a 20% emulsionand applied topi-
cally, Tumour tissue absorbing this porphyrin metabolite becomes photosensitive with its conversion to
protoporphyrin IX and subject to photodestruction when exposed to light, usually in the wave length
range 620-670 nm.
- Topical fluorouracil 5%.
- Topical imiquimod 5%.
Q: How to prevent recurrence of deep margin involvement during re-operation?

A: If recurrent, go for Moh’s micrographic surgery (frozen section).
Q: Skin graf t placed for patient and subsequently had graf t failure...?
A:
◌ Why? Wound infection.
◌ What is the most common organism? Staph. aureus.
◌ What is MRSA? Methicilin-resistant Staphylococcus aureus.
MRSA WOUND INFECTION MANAGEMENT
◌ Abscess: I&D.
◌ Outpatient: Antibiotics; oral as clindamycin, amoxicillin plus tetracyclin or tmp/smx and linezolid.
◌ Inpatient:
- Vancomycin dose to target trough level 7-14 days.
- Linezolid 600 mg twice daily, PO or IV 7-14.
- Daptomycin 4 mg/kg once daily 7-14.
- Telavancin 10 mg/kg once daily 7-14.
- Clindamycin 600 mg IV or 300 mg PO 3 times daily.
- Decolonization with mupirocin nasal or chlorhexidine for body decolonization.
Infection control of MRSA

◌ Measures apply to all patients, regardless of MRSA status:
- High standards of hand decontamination are required to minimise the risk of cross infection.
- Hands should be decontaminated before and after every patient contact.
- Handwashing should be with liquid soap and water.
- Alcohol hand rub may be used as an alternative.
- Maintain high standards of aseptic techniques.
- Maintain high standards of ward cleanliness.
- All linen should be handled in accordance with Trust Laundry Policy.
- All waste should be disposed of in accordance with Trust Policy.
- Re-usable equipment must be decontaminated before use on another patient.
- Decontamination and Disinfection Guidelines should be followed.
- Antibiotics should be used in accordance with Trust Antibiotic Guidelines.
- Minimise inter-ward transfer of patients.
- Avoid overcrowding of patients.
- Maintain adequate and appropriately skilled nursing and other staff levels.
17
◌ The following additional precautions should be used for all MRSA positive patients:
- Place patient in a single room.
- If a side room is unavailable, may be managed in ward bays next to a sink following agreement with the
Infection Control Team.
- If a number of MRSA positive patients are present, these may be managed in a cohort.
- This should only occur following discussion with the Infection Control Team
- Wear gloves and disposable plastic aprons when handling the patient or having contact with their imme-
diate environment.
- All waste should be regarded as clinical waste and to be disposed of in yellow waste bags
- All linen to be treated as contaminated/infected and to be disposed of in an inner red alginate bag or
alginate seamed/stitched bag placed within a white plastic outer.
- Gowns may be required where extensive contact with the patient is anticipated.
Q: After exicision, the patient developed regional lymphadenopathy...?

A:
◌ FNAC done revealed (lymphocytes, PMNL, histocytes, cells with an bilobed nuclei).
◌ Interpretation: Reed-Sternberg cells (owl eye appearance) ---- > Hodgkin’s lymphoma.
◌ Mechanism of lymphatic spread:
1- Embolization
2- permeation
18
Q: What is the most common parotid benign swelling?

A: Pleomorphic adenoma.
Q: What is the meaning of pleomorphic?

◌ Remarkable histologic diversity.
◌ pleomorphic adenoma appearance: Benign tumors that consist of a mixture of ductal (epithelial) and
epithelial cells, and therefore they show both epithelial and mes-
enchymal differentiation.
Clinical signs of malignancy

◌ Facial nerve affection.
◌ Rapid increase in size.
◌ Fixity to the underlying structures.
◌ Invasion of the overlying skin.
Q: Types of parotid tumours?
Q: What are features of malignant cells?

A:
◌ Invasion: Malignant cells do not respect tissue boundaries, and can be seen infiltrating or invading into
surrounding structures.
◌ Increased mitotic rate: Malignant cells will often have increased numbers of mitoses.
◌ Differentiation and Anaplasia: Normal cells are usually structured in a particular way that corresponds
with their function. This is known as differentiation. Malignant cells may
become less differentiated as part of their path to malignancy. This is
known as anaplasia.
- Well differentiated maligant cells show features similar to the parent tissue. For example, well differ
entiated adenocarcinoma cells will tend to form gland-like structures; well differentiated squamous
cell carcinomas may show intercellular bridging or keratin formation.
- Poorly differentiated cells have lost most of their resemblance to the parent tissue, which may be dif-
ficult to identify without special staining techniques. Anaplastic cells have no resemblence to their
parent tissue, and usually indicate a veryaggresive malignancy.
19
Anaplastic Features
◌ Loss of normal tissue architecture: Normal cells are usually arranged in an orderly fashion. Epithelial
cells often have polarity, with their nuclei at a specific location. Malignant cells lose this architecture and
are arranged haphazardly.
◌ Pleomorphism: Malignant cells may show a range of shapes and sizes, in contrast to regularly sized nor-
mal cells. The nuclei of malignant cells are often very large (often larger than the entirety of a normal cell)
and may contain prominent nucleioli.
◌ Hyperchromatic nuclei: The nuclei of malignant cells typically stain a much darker colour than their nor-
mal counterparts.
◌ High nuclear-cytoplasmic ratio: The nuclei of malignant cells often take up a large part of the cell com-
pared with normal cell nuclei.
◌ Giant cells: Some malignant cells may coalesce into so-called giant cells, which might contain the genetic
material of several smaller cells.
Q: What is the best test to differentiate between begnin and malignant cells?
A: FNAC.
Q: What are Difference between cytology and histology?
A: - Cytology is the study of cellular structure and function.
- Histology is the study of tissue under the microscope.
Q: How to rule out malignany intraoperative?

A: Frozen section.
On FNAC:
◌ If you find: lymphocytes, langerhan's giant cells > granuloma.
◌ If you find: epithelioid cells with brown cytoplasm > malignant melanoma.
◌ If you find: lymphoid cells with pleomorphism > lymphoma.
◌ High senstivity test:
- The ability of a test to correctly identify those with the disease (true positive rate).
◌ High specificity test:
- The ability of the test to correctly identify those without the disease (true negative rate).
20
◌ Stem: Patient with leg operation with an implant for 3 years and got infected.
◌ Common organisms:
21
Pathogenesis of osteomyelitis
◌ inflammation and suppuration:
◌ Suppuration:
22
◌ Necrosis (sequestration):
◌ New bone formation:
◌ Resolution:
23
Q: Why pus may burst through the bone?

A: Due to increased intraosseus pressure due to increased osmolarity which occurs due to tissue
breakdown.
Q: Why the fixing plate should be removed?

A: As It has become a spetic focus.
Q: SCC developed in the sinus, why?

A: Due to chronic irritation.
- Differential diagnosis of swollen knee: -OA -Septic arthritis -Gouty arthritis

- Single bedside test to do: Aspiration
- Tests to be done on the aspirate: Culture and sensitivity . Cytology . Chemical analysis
-Type of crystals in Gouty arthritis: monosodium urate crystal
-In chronic osteomyelitis, what is sequence of events by which the draining sinus can develop SCC:
Chronic irritation ---- Hyperplasia ----- Dysplasia ----- Carcinoma
-sequestrum: piece of dead bone that has become separated during the process of necrosis from normal or
sound bone. It is a complication (sequela) of osteomyelitis.
-Involcrum: Reactive woven or lamellar bone depositions forming a shell of living tissue around a sequestrum
TREATMENT
◌ Antibiotic therapy: Blood cultures are taken and high-dose intravenous antibiotics, active against Staph-
ylococcus aureus, Streptococci and Gram-negative rods such as Escherichia coli are
given. Cephalosporins, co-amoxiclav or a combination of Flucloxacillin and gentami-
cinmay be used.
◌ Supportive treatment for pain and dehydration.
◌ Splintage of the limb.
◌ Surgical drainage: if there is no response to antibiotics for 2 days.
◌ Stem: Young female was cycling developed pain in her thigh soon as she put her foot on the ground. Xray
showed fracture shaft femur with hypodense shadow.
Q: What is pathological fracture?

A: Bone fracture which occurs without adequate trauma and is caused by a pre-existent pathologi-
cal bone lesion.
◌ Causes:
- Neoplastic: Malignant tumours either primary (multiple myeloma) or metastatic.
- Non-neoplastic: Osteoprosis, osteomyelitis, Paget’s disease and bone cyst.
24
Possible primary sites for metastasis
- Breast.
- Prostate.
- Lung.
- Thyroid.
- Kidney.
Q: Fixation was done, how to check malignancy?

A: Bone biopsy.
Q: Pathology report: typical bland appearance (follicular cells), what is the primary site?
A: Thyroid gland.
Q.What are other sites of ectopic thyroid tissues other than head and neck and thorax?
A:ovarian and testicular teratoma
Q: We have done FNAC of the thyroid but unable to differentiate cancer, why?
A: Malignancy is determined by capsular and vascular invasion which need histology rather than a
cytology to confirm.
Q: What investigations to do to confirm thyroid Mets?

A: Radioactive iodine scan.
Q: Which thyroid cancer will show no response to iodine uptake?

A: Medullary thyroid cancer as its origin is from parafollicular C cells, so it is not of a follicular origin.
Q: If a patient is O +ve, what test to do prior to blood transfusion?

A: ABO, Rh group cross matching.
Q: If the patient is telling you his group, you will still do cross matching and why?
A: Yes, to determine if the recipient has preformed antibodies against any antigens on the donor's
cells.
Define hemolysis:
Rupture(lysis) of RBC’S and release of their contents(cytoplasm) in the surrounding fluid
(blood,plasma)
COMPLICATIONS
- Acute hemolytic reactions.

- Febrile non-hemolytic transfusion reaction.
- Delayed hemolytic transfusion reactions.
- Transfusion related acute lung injury.
25
◌ Stem: Patient with dysphagia, smoker, GERD with 20 pounds loss of weight.
Q: What is the normal oesophagus lining?

A: Non keratinized stratified squamous epithelium.
Q: What is the most probable diagnosis?
A: Cancer oesophagus.
Q: What are the etiological factors of cancer oesophagus in this patient?
A: - Chronic GERD.
- Smoking.
Q: What is the effect of prolonged GERD?

A: Chronic GERD leads to the development of Barret’s oesphagus with increased risk of developing ade-
nocarcinoma.
Q: Which test to do for this patient?

A: Endoscopy plus EUS with FNAC.
Q: What will the obtained cells tell you?

A: - Stage.
- Grade.
- Immuonohistochemistry.
Q: What is the stain used in immunohistochemistry?

A: Cytokeratin.
Q: Pathology report showed Barret’s oesphagus...?

A:
◌ Definition: Columnar metaplasia of the stratified squamous epithlium of the oesophagus.
◌ Type of lining: Columnar epithelium.
◌ Type of cancer: Adenocarcinoma
26
.
◌ Staging: TNM (T2, N1)
27
If there's pleural effusion

◌ Causes:
- Spread of cancer cells to pleura.
- Lung metastases.
- Obstruction of the thoracic duct.
◌ Pathological test to do:
- Effusion cytology.
◌ Treatment: palliative treatments
- Thoracentesis.
- Indwelling pleural catheters (IPCs).
- Pleurodesis.
- Pleuroperitoneal shunting (PPS).
28
Q: Developped enlargement of a supraclavicular lymph node...?

A:
◌ Investigation: FNAC.
◌ Features under the microscope: Metastatic adenocarcinoma with tumor cells having hyperchro-
matic eccentric nuclei and intracytoplasmic vacuolation.
Q: What are investigations of MI?

A: ECG, troponin and CK-MB.
Q: What is troponin?
A: A complex of three regulatory proteins (troponin C, troponin I, and troponin T) that is integral to
muscle contraction. It's found in cardiac muscle (myocardium) and skeletal muscle.
MEN2 SYNDROME
MEN2 M
◌ Stem: Female with thyroid nodule and elevated calcitonin levels.
Q: What is the best single test to diagnose?

A: FNAC.
Q: Pathology report of FNAC showed malignant cell featuresand amyloid deposits,

immunohistochemistry stains positive with calcitonin and stains negative for thyroxine...?
A:
◌ What type of cancer? Medullary thyroid cancer.
◌ Why? Amyloid deposits and calcitonin positive on IHC.
◌ Cell source: Parafollicular C cells.
◌ What is IHC in simple words? It is a method of localizing specific antigens in tissues or cells based on
antigen antibody recognition.
◌ How it works? The antibodies are usually linked to an enzyme or a fluorescent dye. When the antibod-
ies bind to the antigen in the tissue sample, the enzyme or dye is activated, and the anti-
gen can then be seen under a microscope.
◌ Type of Ag- Ab reaction in IHC? Complement fixation.
◌ Note that: If the pathology report shows size, No. of positive lymph nodes (2-6), then you've to do TNM.
Q: If the patient developed hypertension, what do you think she might have?
A: Pheochromocytoma.
29
◌ Plasma:
- Free metanephrines.
- Catecholamines.
- Catecholamines stimulation test.
◌ Urine:
- Fractionated metanephrines.
- Total metanephrines.
- Catecholamines.
- VMA.
◌ Imaging:
- Ultrasound.
- CT.
- MRI.
- MIBG scintigraphy.
- PET/CT.
Q: If this condition was familial, what other condition you suspect?

A: Parathyroid hyperplasia.
Q: What is the treatment of medullary thyroid cancer?
A: Total thyroidectomy with block neck dissection.
30
Types of MEN syndromes, oncogene mutation and mode of inheritance
◌ Stem: Middle aged man with RIF pain, surgery was done, revealed dilated appendix (looks like mass), and
histopathology revealed appendicular abscess plus 6mm appendicular mass involving the mucosa
and the muscularis layers.
Abscess
◌ Definition: Abscess is focal collection of pus that may be caused by seeding of pyogenic organisms into a
tissue or by secondary infections of necrotic foci.
◌ Structure: Abscess typically has a central, largely necrotic region rimmed by a layer of preserved neutro-
phils, with a surrounding zone of dilated vessels and fibroblast proliferation indicative of at-
tempted repair.
Q: How neutrophils migrate to the site of inflammation?

A: The neutrophils first roll, then become activated and adhere to endothelium, then transmigrate
across the endothelium, pierce the basement membrane, and migrate toward chemo-attractants
emanating from the source of injury.
Q: What are the blood tests to identify the inflammation?

A: ESR, CRP and white blood cells count.
31
Q: What is carcinoid tumor?

A: Slowly-growing type of neuroendocrine tumor originating in the cells of the neuroendocrine
system.
Q: Where it is most commonly found?
A: Small intestine, appendix (terminal third) and they can also be found in the rectum, stomach
and lung.
Q: What is its origin?

A: Enterochromaffin (EC) cells (also known as Kulchitsky cells) in the crypts of Liberkuhn.
Q: What does it release?

A: Serotonin (5-HT), bradykinins, prostaglandins, tachykinins, substance P and histamine.
◌ Periodic abdominal pain.

◌ Manifestations of carcinoid syndrome:
- Cutaneous flushing.
- Diarrhea and malabsorption.
- Cardiac manifestations: Valvular heart lesions, fibrosis of the endocardium.
- Wheezing or asthma like syndrome: Due to bronchial constriction.
Q: How does it spread?

A: Cells produce a significant amount of beta-catenin, which enables the tumor cell adhesion, thus
promoting metastasis.
Q: What is most common metastatic site?

A: The liver.
Q: Why a person with heavy mets in liver has symptoms than with primary tumour?
A: That's because most of the blood circulation from the gastrointestinal tract must pass through
the liver before it reaches the rest of the body. The liver has strong enzymes that break down and
neutralize most of the excess serotonin and other substances produced by the carcinoid tumors,
preventing them from reaching tissues where they can cause symptoms. When carcinoid tumours
metastasize to the liver, the substances they overproduce can more easily reach the bloodstream,
and reach tissues where they can cause symptoms.
◌ Chromogranin A (CgA) testing in the blood (protein secreted from carcinoid tumour cells).
◌ 5-Hydroxyindoleacetic Acid (5-HIAA) testing in 24h urine (by product of serotonin).
◌ Pathological diagnosis: Immunohistochemistry stains positive for chromogranin B.
32
NASOPHARYNGEAL CARCINOMA
◌ Carcinoma definition: Carcinoma is a type of cancer that develops from epithelial cells.
Q: What are the differences between Benign and malignant cells?

A:
◌ Benign and malignant tumors can be distinguished from one another based on the degree of differenti-
ation, rate of growth, local invasiveness and distant spread.
◌ Benign tumors resemble the tissue of origin and are well differentiated; malignant tumors are
poorly or completely undifferentiated (anaplastic).
◌ Benign tumors are slow-growing, whereas malignant tumors generally grow faster.
◌ Benign tumors are well circumscribed and have a capsule; malignant tumors are poorly circum-
scribed and invade the surrounding normal tissues.
◌ Benign tumors remain localized to the site of origin, whereas malignant tumors are locally inva-
sive and metastasize to distant sites.
Q: What is the mechanism of radiotherapy?

A: Ionizing radiation works by damaging the DNA of cancerous tissue (base damage, single-and
double-strand breaks, and crosslinks between DNA and protein) leading to cellular death.
33
Q: What are the SI units of radiotherapy?

A:
◌ Curie (Ci): Exposure.
◌ Gray (Gy): Absorption.
◌ Sievert (Sv): Dose.
Risk factors for nasopharyngeal carcinoma

◌ Gender: Twice as often in males as it is in females.
◌ Ethnicity and race: Most common in southern China (including Hong Kong), Singapore, Vietnam, Malay-
sia, and the Philippines. It is also fairly common in Northwest Canada and Greenland.
◌ Diet: Consumption of salted fish containing carcinogenic volatile nitrosamines.
◌ Infection with the Epstein-Barr virus.
◌ Genetic factors.
◌ Family history.
◌ Tobacco and alcohol use.
Q: Patient had an oral lesion, swab showing hyphae, what is the diagnosis?
A: Candida.
Q: What are the risk factors for that patient for oral candidiasis?
A: - As a complication of radiotherapy or chemotherapy.
- Being a diabetic.
Q: What are the routes of spread of nasopharyngeal carcinoma?

A: - Lymphatic spread..
- Local invasion.
Q: Where to spread locally?
34
Q: What are the common lymph node tumours?

A: - Lymphoma (Hodgkins and Non-Hodgkins).
- Leukemia.
- Metastatic.
Q: How will you investigate for mets in lymph nodes?

A:
◌ Tissue biopsy: FNAC, excisional biopsyand sentinel biopsy for histopathological assessment with or
without immunohistochemistry.
◌ Imaging modalities: Ranging from ultrasound scan, CT scan, MRI and PET-CT.
◌ Stem: PR bleeding diagnosed as hemorrhoids, colonoscopy done revealed adenocarcinoma with melano
sis coli, biopsied, histopathology revealed lesion ip to muscularis layer.
◌ Dukes staging of colorectal cancer:
Define melanosis coli:

is a disorder of pigmentation of the wall of the colon, often identified at the time of
colonoscopy. It is benign, and may have no significant correlation with disease.
Define adenoma:
term adenoma is generally applied to benign epithelial neoplasms producing
gland patterns and to neoplasms derived from glands but not necessarily
35
Q: What are hemorrhoids?
A: Swollen or inflammed anal cushions.
◌ The anal cushions function normally when they are fixed to their proper sites within the anal canal by
fibromuscular ligaments, which are the anal remnants of the longitudinal layer of the muscularis propria
from the rectum (Treitz's ligaments).
◌ When these submucosal fibres fragment (as by prolonged and repeated downward stress related to
straining during defecation), the anal cushions are no longer restrained from engorging excessively with
blood and may result in bleeding and prolapse.
Acute thrombosis results from sudden raised pressure causing

rupture of the vascular plexus leading to a blood clot at the anal verge.
◌ Any activity requiring excessive abdominal straining such as over-
exercising can cause this.
Q: Why coronary arteries get thrombosed?

A: Due to coronary artery atherosclerosis.
Q: How coronary arteries get atherosclerosis?

A: - Endothelial injury—and resultant endothelial dysfunction—
leading to increased permeability, leukocyte adhesion,
and thrombosis.
- Accumulation of lipoproteins (mainly oxidized LDL and
cholesterol crystals) in the vessel wall.
- Platelet adhesion.
- Monocyte adhesion to the endothelium, migration into the
intima, and differentiation into macrophages and foam cells.
- Lipid accumulation within macrophages, which release inflammatory cytokines.
- Smooth muscle cell recruitment due to factors released from
activated platelets, macrophages, and vascular wall cells.
- Smooth muscle cell proliferation and ECM production.
36
Q: What are risk factors of atherosclerosis?
Q: What is the function of thrombus?

A: A thrombus is a healthy response to injury intended to prevent bleeding.
Q: How is thrombus formed?

A: - An atheromatous plaque is suddenly disrupted by intra-plaque hemorrhage or mechanical forces,
exposing sub-endothelial collagen and necrotic plaque contents to the blood.
- Platelets adhere, aggregate, and are activated, releasing thromboxane A2, adenosine diphosphate
(ADP) and serotonin—causing further platelet aggregation and vaso-spasm .
- Activation of coagulation by exposure of tissue factor and other mechanisms adds to the growing
thrombus.
Within seconds of vascular obstruction, aerobic glycolysis ceases, leading to a drop in adenosine triphos-
phate (ATP) and accumulation of potentially noxious metabolites (e.g., lactic acid) in the cardiac myocytes
◌ The functional consequence is a rapid loss of contractility, which occurs within a minute or so of the
onset of ischemia. Ultrastructural changes (including myofibrillar relaxation, glycogen depletion, cell and
mitochondrial swelling) also become rapidly apparent.
◌ These early changes are potentially reversible. Only severe ischemia lasting at least 20 to 40 minutes
causes irreversible damage and myocyte death leading to coagulation necrosis.
- utes, the thrombus can evolve to completely occlude the coronary artery lumen.
37
◌ Stem: Forearm abscess.

◌ Definition: Focal collection of pus that may be caused by seeding of pyogenic organisms into a tissue or
by secondary infections of necrotic foci.
Q: What is present inside abscess?

A: Central and largely necrotic region rimmed by a layer of preserved neutrophils, with a surround-
ing zone of dilated vessels and fibroblast proliferation indicative of attempted repair.
Q: What are organisms causing abscess?

A:
◌ Bacterial: Staph. aureus and Strept. pyogenes.
◌ Non-bacterial: Fungal, viral and parasitic.
Q: One simple test to detect the cause of abscess, what is it?

A: Gram stain.
Q: What is the cause of fever in abscess?
A: Fever is produced in response to substances called pyrogens (TNF, IL-1) that act by stimulating
prostaglandin synthesis in the vascular and perivascular cells of the hypothalamus.
Q: What is cellulitis?
A: A spreading bacterial infection of the skin affects the dermis and subcutaneous fat characterized
by redness, warmth, swelling and pain.
Q: what is the difference between abscess and cellulitis?
38
Q: When to give Antibiotic in abscess?

A: Antibiotics are indicated if the abscess is not localised (e.g. evidence of cellulitis) or the cavity is
not left open to drain freely.
Q: What are giant cells?

A: - These are multinucleated cells derived from the fusion of multiple activated macrophages to form
granuloma.
Q: What is the most common cause of granuloma?

A:
◌ Tuberculosis:
- Causative agent: Mycobacterium TB.
- Type of stain: Ziehl–Neelsen stain (Acid fast stain).
Q: What changes you see in lymph node affected with inflammation?

A: Reactive follicular hyperplasia.
◌ Stem: 65 year-old man with type 2 diabetes on oral medications, presented with perianal abscess and
went for I&D.
Q: What are the types of DM and describe the pathogenesis of each?

A:
◌ The vast majority of cases of diabetes fall into one of two broad classes:
- Type 1 diabetes (T1D) : is characterized by an absolute deficiency of insulin secretion caused by pan-
creatic beta cell destruction, usually resulting from an autoimmune attack. Type 1 diabetes accounts
for approximately 10% of all cases.
- Type 2 diabetes (T2D): is caused by a combination of
peripheral resistance to insulin action and an
inadequate compensatory response of insulin secretion
by the pancreatic beta cells (relative insulin deficiency).
Approximately 80% to 90% of patients have type 2
diabetes.
Q: What is the function of insulin and what are other

hormones affecting
blood glucose level?
A: The principal metabolic function of insulin is to
increase the rate of glucose transport into certain
cells in the bod
39
Insulin metabolic effects
◌ Carbohydrates:
Increases the uptake of glucose into various tissues.
Stimulates glycogenesis in many tissues, but especially the liver.
Stimulates hepatic generation of glucose-6-phosphate from glucose.
◌ Proteins:
Enhances the uptake of amino acids into peripheral tissues.
Stimulates protein synthesis –for this reason, insulin can be regarded as one of the growth
hormones.
◌ Fats:
Stimulates lipid uptake into cells.
Other hormones affecting blood glucose level
◌ All of them increase blood glucose level:
- Glucagon.
- Catacholamines: epinephrine and norepinephrine.
- Glucocorticoids: most important being cortisol.
- Somatotrophin: a pituitary hormone.
Q: What are the preoperative precautions for diabetic patient?/

how to prevent intraoperative hypoglycemia?
A: - Patients with diabetes must be prioritized in the operating list.
- Routine overnight admission is not necessary.
- Starvation time should be no more than one missed meal.
- Analgesia and anti-emetics should be used to enable early return to diet and usual insulin regime.
- Insulin infusions should only be used if a patient is expected to miss more than one meal.
- 0.45% sodium chloride with 5% glucose and 0.15% or 0.3% KCl is the recommended IV fluid.
- Capillary blood glucose should be measure hourly during and after the any surgical procedure.
- The WHO surgical safety checklist should identify all diabetic patients.
- The target blood glucose should be 6-10 mmol/L (acceptable range 4-12 mmol/ L).
Q: What are the Immediate and late postoperative complications?

A:
◌ Immediate:
- Hyper or hypoglycemia.
- Dehydration with electrolytes imbalances.
- Hyperglycemic hyperosmolar syndrome.
- DKA.
◌ Late:
- Infection.
- Sepsis.
- Impaired wound healing.
Q: Postoperatively, who you will involve in care of this patient?

A: Endocrinologist.
Q: What do you think this patient might need if his DM not well controlled
on oral medications?
A: Conversion to insulin therapy.
40
[ STEM: lady known to have ulcerative colitis and on surveilliance colonoscopy found to have a lesion less than 1cm in sigmoid colon.]
What is ulcerative colitis: inflammatory bowel disease affecting the colon in the form of colitis with
charcteristic ulcers
* What is TNF :
It is a cytokine involved in systemic inflammation and in making up the acute phase reaction
* Role of TNF in IBD:
TNF and other immune mediated signals direct epithelia to increase tight junctions permeability which increase
the flux of luminal bacterial components which activates innate and adaptive immune responses
what drugs antagonize TNF:

- Infliximab - Adalimumab - Cetrulizumab
mechanism of action of these drugs?

Monoclonal IgG1 antibody to TNF-α
why they are used as a treatment of UC? They are called ( biologics), used mainly in steroid refractory UC cases and for
treatment of extra intestinal manifestations
41
picture of a tumour eroding through the muscularis layer + 1/4 positive node
What will you offer this lady: total colectomy Why? The whole colon is suscepitible
. Describe adenoma carcinoma sequence:

. Stepwise accumulation of mutations of oncogenes and tumour suppressor genes:
. 1- loss of APC ( tumour suppressor gene) ----> hyperplasia
. 2- k-ras (oncogene) mutation-/----> dysplasia
. 3- loss of p 53 ( tumour suppressor gene) --> adenocarcinoma
42
. How proto-oncogenes and tumour supressor genes act?

. Proto-oncogenes: normal cellular genes whose products promote cell proliferation
. Oncogenes: mutated or overexpressed versions of proto-oncogenes that function autonomously, having lost
dependence on normal growth promoting signals
. Tumour supressor genes (p53, APC) : normal genes whose absence can lead to development of cancer, they act as : -
gatekeepers: inhibit proliferation or promote the death of cells with damaged DNA
. Function of KRAS:
.
The KRAS gene provides instructions for making a protein called K-Ras that is
part of a signaling pathway known as the RAS/MAPK pathway. The protein
relays signals from outside the cell to the cell's nucleus. These signals instruct
the cell to grow and divide (proliferate) or to mature and take on specialized
functions (differentiate). The K-Ras protein is a GTPase, which means it
converts a molecule called GTP into another molecule called GDP. In this way
the K-Ras protein acts like a switch that is turned on and off by the GTP and
GDP molecules. To transmit signals, it must be turned on by attaching
(binding) to a molecule of GTP. The K-Ras protein is turned off (inactivated)
when it converts the GTP to GDP. When the protein is bound to GDP, it does
not relay signals to the cell's nucleus.
Function of P53:
DNA damage and other stress signals may trigger the increase of p53 proteins,
which have three major functions: growth arrest, DNA repair and apoptosis
(cell death). The growth arrest stops the progression of cell cycle, preventing
replication of damaged DNA. During the growth arrest, p53 may activate the
transcription of proteins involved in DNA repair. Apoptosis is the "last resort" to
avoid proliferation of cells containing abnormal DNA.
Function of APC :
encodes a factor that negatively regulates the WNT pathway in colonic epithelium by promoting the formation of a
complex that degrades β-catenin
43
44
STEM: a young lady with endometriosis concerned that her father fied of a cancer at an early stage . , she had a
colonoscopy just now
ID a picture of FAP : multiple polyps the largest one is about 7mm and ulcerated
Def.: autosomal dominant condition chacterised by loss of APC tumour supressor gene on the long arm of
chromosome 5 leading to development of hundreds of adenomas with 100% risk of cancer by the age of 30
Classification of polyps: - non -neoplastic : hamartomatous, metaplastic
- Inflammatory: pseudopolyps ad in ulcerative colitis
- Neoplastic: villous(40%), tubulovillous(20%), tubular( 5%)
Malignant potential of adenomas depend on: 1- type of adenoma

2- diameter of adenoma: < 1 cm ---> 5%
> 2 cm----->20 %
3- degree of dysplasia
Extracolonic manifestations: in the related gardener syndrome ( mandibular osteomas,desmoid tumours,

sebaceous cyst) and Turcot syndrome
Management: prophylactic near total colectomy by the age of 25
If the patient is having a child 2 y , what is your advice: Colonoscopic screening by the age of 12
Define endometriosis:
Endometriosis is defined by the presence of “ectopic” endometrial tissue at a site outside of the uterus
Definitions:
Dysplasia: disordered cellular development charcterised by inreased mitosis,pleomorphism without the ability to
invade the basement membrane Severe dyplasia= carcinoma in situ
Abscess: collection of pus surrounded by granulation or fibrous tissue Pus: collection of neutrophils plus dead or
45 dying micro organisms
Ulcer: a lesion in the mucous membrane or the skin resulting from the gradual distingration of surface epithelial
cells
Secondary intention: secondary healing by repithelization and contraction
Life style modifications to reduce risk of cancer colon : - eat much fibres - Limit alcohol - Reduce fat intake
- Stop smoking
T.B
[ A young indian lady came back from a foreign travel with cervical lymphadenopathy, LOW, Night sweating]
diff.:Hodgkin’s lymphoma ( more in this age group and involves cervical lymph nodes more commonly) or TB
Which labs you will send her sputum to : microbiology + cytology labs
what are the tests of TB? sputum examination ( culture, ziel-neelson stain) .
Mantoux test
PCR to differentiate mycobacteria t.b from other species
quantiferon ( interferon gamma assays)
FNAC of lymph node
How to label the sputum specimens: Category -B UN3373 Where to put: in a biohazard bag
Organism of T.B: mycobactetium T.B
other mycobacteria: mycobactetia avium complex (MAC)---> disseminated infection in immunocompromised

patients
what are the culture media for mycobacteria:

- solid media: lowenstein jensen media, middle brooke media
- Liquid media: BACTEC/MIGT ( mycobacteria growth indicator tube)
* how long to culture: 1-8 weeks
* What type of protein deposition: amyloid
* Given the FNAC result: necrotic tissue, histocytes, giant cells -----> TB
* what are giant cells: cells formed by fusion of several cells (usually histocytes) often forming a granuloma
Ex. : langerhan's giant cells, Reed sternberg cells
Public health concern/ community concerns 1- notify the consultant in communicable disease control (CCDC)
2-Avoid work in food factory
3-Use mask during sneezing or coughing
4-takes DOTS anti -TB therapy
Contact tracing: the identification and diagnosis of persons who may have come into contact with an infected
person
What is your advice to contacts: councelling,screening and treatment of other family members
Granuloma: A granuloma is a structure formed during inflammation that is found in many diseases. It is a collection
of immune cells known as macrophages. Granulomas form when the immune system attempts to wall
off substances it perceives as foreign but is unable to eliminate.
46
Other Causes of granuloma: leprosy, schistomiasis, sarcoidosis,crhon's , rhematoid arthritis,crohn’s disease
GB cancer + pseudomembranous colitis:

[ cholecystectomy+ surgical site infection]
Causes:
- The most important risk factor associated with gallbladder carcinoma is gallstones (cholelithiasis), which are present in
95% of cases. Presumably, gallbladders containing stones or infectious agents develop cancer as a result of chronic
inflammation, a known enabler of malignancy in several organs .
- Carcinogenic derivatives of bile acids also are suspected to play a role.
- Primary sclerosing cholangitis is also a risk factor.
Spread:
liver( segment 5), cbd, stomach, dudenum, porta hepatis lymph nodes
Pathology:
Carcinomas of the gallbladder show two patterns of growth: infiltrating and exophytic.
- The infiltrating pattern is more common and usually appears as a poorly defined area of
diffuse wall thickening and induration.
- The exophytic pattern grows into the lumen as an irregular, cauliflower mass, but at the
same time invades the underlying wall
Most carcinomas of the gallbladder are adenocarcinomas. About 5% are squamous cell
carcinomas or have adenosquamous differentiation
◌ Surgical site infection in POD3 with yellowish discharge ---------- > actinobacilus ( sulphur granules)
Q: What is the most common organism causing surgical site infection?

A: Staph. Aureus
◌ Organisms causing necrotising fascititis:
- group A streptcocci( strept. Pyogenes)
- Staph. Aureus
- Clostridium perferngines
- Bacteroides fragilis
- MRSA
Diagnosis :
◌ cellulitis,crepitus
Laporatory: LRINEC( laporatory risk indicator for necrotising fascititis) Score
>= 6 -------------- > necrotising fascititis is highly considered
1-crp >= 150 4points 2-
wbc < 15 0 points
15-25 1 point
> 25 2 points
3- HB > 13.5 0 points
11-13.5 1 point
< 11 2 points
4- Na < 135 2 points
5- creat. > 141 2 points
6- glucose > 10 1 point
47
Pathology :
extensive necrosis with thrombosis of blood vessels
Management :
1- hemodynamic support according to CCrISP protocol
2- surgical debridement
3- antibiotics according to culture and sesntivity
Q: Who to involve in care?

A: ITU specialist, palstic surgeon
◌ Post. Operative bloody diahrrhaea:

- Pseudomembranous colitis
- Bowel ischemia
- Stress ulcer
- Infective gastroenteritis
Pathogenesis of PMC:
Pseudomembranous colitis is often triggered by antibiotic therapy that disrupts the normal microbiota
and allows C. difficile to colonize and grow. The organism releases toxins that disrupt epithelial function.
The associated inflammatory response includes characteristic volcano-like eruptions of neutrophils from
colonic crypts that spread to form mucopurulent pseudomembranes.
48
MALIGNANT MELANOMA METS:

Stem: a patient known to have hypothyroidism with a hard swelling in her right inguinal region ,her
GP sent her for biopsy
◌ DD:
Inguinal lymph nodes receive lymphatic drainage from the lower extremities and skin of the lower
abdomen, genitals, and perineum.
◌ Infections associated with inguinal lymph nodes are as follows:

- Cellulitis of the lower extremities
- Venereal infections - Syphilis, chancroid, herpes simplex virus infection, lymphogranuloma venereum
◌ Malignancies associated with inguinal lymph nodes are as follows:

- Lymphomas
- Metastatic melanomas from lower extremity primary site
- Squamous cell carcinomas from genital primary site
◌ Results of histopath: Revealed malignant melanoma.
Q: What are types of malignant melanoma?

A: Melanomas are divided into 5 main types, depending on their location, shape and whether they grow
outward or downward into the dermis:
1- Lentigo maligna: usually occur on the faces of elderly people .
2- Superficial spreading or flat melanoma: grows outwards at first to form an irregular
pattern on the skin with an uneven color.
3-Desmoplastic melanoma: is a rare malignant melanoma marked by non-pigmented lesions on sun-
exposed areas of the body . Acral melanoma: occurs on the palms of the hand, soles of the feet, or
nail beds .
4-Nodular melanomas: are lumpy and often blue-black in color and may grow faster and
spread downwards.
Satellite lesion: it is a form of local spread of malignant melanoma by contiguity

and continuity leading to pigment spreading to the surrounding area
Epithelioid melanoma: Epithelioid cells are large and round with abundant
eosinophilic cytoplasm, prominent vesicular nuclei and large nucleoli. They most
commonly arise in superficial spreading and nodular melanomas
Q: Where would you examine this lady?
A:- primary sites: Whole lower limb including nail beds and soles
- Metastatic sites: chest , abdomen and brain
Q: How to treat this lady?

A: Excision of the primary lesion with safety margin plus block inguinal lymph node dissection plus
49 radiotherapy.
Q:How can you know the phenotype of the tumor?

A: By immunohistochemistry
Recent histopathological studies of lymph node in metastatic melanoma other

than IHC: genetic mutation studies(BRAF gene)
Q:Post operative the wound is red and swollen , culture was done revealed diplococci?
A: Examples of gram-negative diplococci are Neisseria sp., Haemophilus, Moraxella catarrhalis,
Acinetobacter, and Brucella. Examples of gram-positive diplococci would be Streptococcus
pneumoniae and enterococcus.
Q:Next the patient got toxemia with rapidly spreading infection? What do you think?
A: Necrotising fasciitis
Q:What is SIRS?
A: Manifestations of SIRS include, two or more of the following:
- Body temperature less than 36 °C (96.8 °F) or greater than 38 °C (100.4 °F)
- Heart rate greater than 90 beats per minute
- Tachypnea (high respiratory rate), with greater than 20 breaths per minute; or, an arterial
partial pressure of carbon dioxide less than 4.3 kPa (32 mmHg)
- White blood cell count less than 4000 cells/mm³ (4 x 109 cells/L) or greater than 12,000 cells/
mm³ (12 x 109 cells/L); or the presence of greater than 10% immature neutrophils (band
forms). Band forms greater than 3% is called bandemia or a “left-shift.”
- Hyperglycemia (blood glucose >6.66 mmol/L [120 mg/dL]) in absence of diabetes mellitus
- Altered mental state
Q:What happens to lung in SIRS?
ARDS
Q:Define ARDS?
A: diffuse alveolar damage and lung capillary endothelial injury
50
MALIGNANT MELANOMA METASTASES

◌ Definition : malignant neoplasm of melanocytes
◌ Skin conditions associated with melanoma:

- Xeroderma pigmentosa
- Albinism
- giant congenital pigmented naevus
- Fitz patric skin type 1
- Dysplastic neavus , multiple nevi
◌ Other risk factors of malignant melanoma:

- hutchinson’s melanotic freckles
- Immunocomprimised patients
- Past history of melanoma
- Red hair, sun exposure
◌ Comment on the pathology report:

- Size
- Breslow thickness: measured in mm. From the top of stratum granulosum to the deepest point of tumour involvement
- Depth of invasion ( clark’s levels)
- Ulceration, mitoses, lymphovascular invasion
- Immunohistochemistry staining
Q:How to diff. MM from SCC?

A: Melanoma: arise from the lower layer of the epidermis from any part of the body
SCC : arise from upper and mid layer of epidermis with keratin pearl formation usually on sun exposed areas
◌ Poor prognostic factors:

- increased tumour thickness( Breslow thickness)
- Increased depth of invasion
- Type of melanoma: Nodular , amelanotic melanoma
- Prescence of ulceration
- Prescence of lymphatic or perineural invasion
- Prescence of regional or distant metastsis
◌ Genes responsible for familial MM:

- CDKN2A and CDK4
Q:Lesion excised , Breslow thickness 1.5 mm, margins 0.5 cm , what to do?
A: Re- exision
◌ Management:
excision + safety margin
Size of the safety margin is based on the Breslow thickness
> 1mm= 3 cm margin
Q:What to do to ensure adequate margins ?

A: Frozen section,Moh’s microsurgery
51
◌ Post excision the patient developped regional lymphadenopathy:

Management:
FNAC
whole body CT
Post excision the patient developped painful swelling of the arm + dyspnea > axillary vein
thrombosis > pulmonary embolism
◌ Risk factors for thrombosis:

Virchow’s triad : hypercoagulable state, venous stasis, endothelial injury
◌ Management:
- CTPA
- SC LMWH if the patient is hemodynamically stable
- thrombolysis or embolectomy ( massive embolism)
Breast cancer
Q: What can you recognize in mammogram ?

A: Speculated mass+ microcalcifications
Q: what other tests to do ?

A: Tissue biopsy ( tru-cut ,FNAC)
◌ most common type of breast cancer:

Invasive duct carinoma
◌ exision----> pathology report --- > what to look for:

-type of cancer
-No.of positive lymph nodes
-Margins status
- HER2 receptors status
- ER/PR receptor status
52 - Ki 67 proliferation index
◌ One microscopic test to do before LD flap :

- culture and senstivity of MRSA.
◌ Her2: transmembrane epidermal growth factor and it is overexpressed in 20% of breast cancer
cases and associated with bad prognosis
◌ Herceptin: ( trastazumab) causes antibody mediated destruction of cells overproducing HER2
3times weekly for 12 months .
Q:What else in management ?

A: radiotherapy, chemotherapy, hormonal therapy
◌ Hormonal therapy:
Premenopausal: tamoxifen ( 20mg /d ) for 5 years
Postmenopausal: aromatase inhibitors ( anastrazole) to prevent peripheral conversion to oestrogen
Peptic ulcer disease+ hyperparathyroidism:

[gastric ulcer----> hematemsis ---> OGD ----> peptic ulcer, biopsied] + hypercalcemia
◌
Definition:
ulcer: a local defect of the mucous membrane or the skin due to gradual distingration of the
surface epithelial cells.
◌ Risk factors of PUD:

- H-pylori infection
- NSAID’s
- Smoking
◌ H- pylori: gram negative microaerophilic spiral bacteria found in the stomach
◌ CLO test: ( campylobacter like organism) :

It depends on urease production by H-pylori
A gastric mucosal biopsy is taken during gastrosopy and is placed in a medium containing
urea and an indicator such as phenol red,urease production by H-pylori converts urea to
ammonia which increase pH changing the colour ( yellow to red)= positive test.
Q: How H- Pylori can survive in acidic medium ?

A: H. pylori survives in acidic conditions by producing urease, which catalyzes hydrolysis of urea
to yield ammonia thus elevating the pH of its environment.
53
Q: Mechanism by which H-pylori can colonize the stomach?

A:
1-Flagella, which allow the bacteria to be motile in viscous mucus
2- Urease, which generates ammonia from endogenous urea, thereby elevating local gastric
pH around the organisms and protecting the bacteria from the acidic pH of the stomach
3- Adhesins, which enhance bacterial adherence to surface foveolar cells
4- Toxins, such as that encoded by cytotoxin-associated gene A (CagA), that may be involved
in ulcer or cancer development by poorly defined mechanisms
- These factors allow H. pylori to create an imbalance between gastroduodenal mucosal defenses
and damaging forces that overcome those defenses.
Q:Type of gastric cancer that can be caused by H-Pylori?

A: Adenocarcinoma
◌ Eradication of H-pylori:
7 days twice daily of :
- Full dose of ppi+ metronidazole 400 mg+ clarithromycin 250mg
or
- Full dose of ppi+ amoxycillin 1g + clarithromycin 500mg
◌ Other causes of hematemesis in this patient:

Hypercalcemia-----> incresaed gastrin release ----- > incraesed hcl production
◌ Common causes of hypercalcemia:

- Malignancy
- hyperparathyroidism(PTH adenoma)
- Renal failure
◌ Cause of UTI in this patient: renal stones
Q:How to localise parathyroid glands ?

A: sestamibi scan, frozen section
Q:What is frozen section ?

A: is a pathological laboratory procedure to perform rapid microscopic analysis of a specimen.
Q: How the specimen is fixed ?

A: The surgical specimen is placed on a metal tissue disc which is then secured in a chuck and
frozen
rapidly to about –20 to –30 °C. The specimen is embedded in a gel like medium called OCT and consisting
of poly ethylene glycol and polyvinyl alcohol.Subsequently it is cut frozen with the microtome portion of
the cryostat, the section is picked up on a glass slide and stained (usually with hematoxylin and eosin, the
H&E stain).
Q: Why we can not use paraffin based histopathology intraoperatively?

A: As it takes a week for paraffin to embed through the tissues
Q: How many platelets present in packed RBC’s?

54
A: No platelets in packed RBC’s
◌ Histopathology report:
1 gland 0.2 g chief cells
3 glands ranging from 0.08 to 0.09 g oxiphilic cells and fat cells
◌ Interpret: parathyroid adenoma in one gland with involution to the other glands
◌ Histology of parathyroid adenoma:

parathyroid adenomas are mostly composed of uniform, polygonal chief cells with small,
centrally placed nuclei . At least a few nests of larger oxyphil cells are present as well;
uncommonly, adenomas are composed entirely of this cell type (oxyphil adenomas).A rim of compressed,
non- neoplastic parathyroid tissue, generally separated by a fibrous capsule, is
often visible at the edge of the adenoma
Q:Where to find parathyroid gland if you do not see them in the normal position ?
A: the superior mediastinum
As the thymus originates from the third pharyngeal pouch ,it occasionally drags the inferior glands down
to the mediastinum
Treatment of parathyroid adenoma:

exicsion
◌ Types of hyperparathyroidism:
1ry ---- > parathyroid adenoma( hypercalcemia)
2ry ---- > chronic renal failure( hypocalcemia)
3ry ---- > chronic stimulation of parathyroid gland due to hypocalcemia in 2ry hyperparathyroidism
leading to overactivation ( hypercalcemia)
Treatment of hypercalcemia:
- hydration
- forced direusis
- Bisphosphanates: i.v pamidronate
- Calcitonin
55
Testicular teratoma
[35 y man with left groin mass+single palpable testis]
On ultrasound , lt groin mass turned to be undescended testis with solid and cystic compnents----
> tissue diagnosis-----> pathology report ----- > comment:
-Teratoma
-Positive margins
-Lymphovascular invasion
-T4, Nx,Mx
Q: Define cryptorchidism A:
Cryptorchidism is a complete or partial failure of the intra-abdominal testes to descend into the scrotal
sac and is associated with testicular dysfunction and an increased risk of testicular cancer.
Q:How does undescended testis contribute to increased risk of testicular cancer?

A: The cryptorchid testis carries a 3- to 5-fold higher risk for testicular cancer, which arises from foci of
intratubular germ cell neoplasia within the atrophic tubules.
Q:What will be your management ?

A:- Ct abdomen and pelvis
- Satging
- Discuss in MDT
- orchiectomy+ chemotherapy
- RPLND ( if nodal disease)
◌ Discuss pathology report with family in 3 simple lines:

-This is cancer in the testis
-With incomplete resection
-With lymphatic spread
Q:Where teratoma spread to first

A: to the para-aortic lymph nodes
Q: Where does it spread to next ?

A: locoregional
56
Serological markers:
biologic markers include HCG, AFP, and lactate dehydrogenase
value of serum markers is fourfold:
• In the evaluation of testicular masses
• In the staging of testicular germ cell tumors. For example, after orchiectomy, persistent
elevation of HCG or AFP concentrations indicates stage II disease even if the lymph nodes appear
of normal size by imaging studies.
• In assessing tumor burden
• In monitoring the response to therapy. After eradication of tumors there is a rapid fall in serum
AFP and HCG. With serial measurements it is often possible to predict recurrence before the pa-
tients become symptomatic or develop any other clinical signs of relapse.
◌ Post - operative developped hematoma, mention stages of hematoma resolution:

- Lysis of the clot by macrophages (about 1 week)
- Growth of fibroblasts from into the hematoma (2 weeks)
- After few months developped small pneumothorax---- > lung metastasis
◌ Define metastasis: survival and growth of cells at a site distant from their primary origin
Q: 1year later the patient came with para-aortic lymph node compressing renal artery and
vein + SOB + PE Why PE in this patient?
A: - hypercoagulable state
- Venous stasis
Q: What is choriocarcinoma and what is its tumour marker?

A: Choriocarcinoma is a highly malignant form of testicular tumor. Histologically the tumors con-
tain two cell types, syncytiotrophoblasts and cytotrophoblasts
Tumour marker is B-HCG.
Q: What is the common tumour in this age group?

A: Seminoma
◌ Non–Hodgkin lymphoma is the most common testicular tumor in men older than 60 years.
Q: Histopath showed papillary thyroid tissue and GIT adenocarcinoma, why?

A: Teratoma has the 3 germ cell lines
57
Temporal arteritis
60 y old female with headache and skull tenderness on mastication, transient loss of vision.
◌ Biopsy from the temporal artery-------- > giant cell arteritis( granulomatous pan- arteritis with
mono-nuclear cell infiltrates)
Q: Describe the pathological changes in microscopic picture

A: MORPHOLOGY
- Involved arterial segments develop intimal thickening (with occasional thromboses) that
reduces the luminal diameter
- Classic lesions exhibit medial granulomatous inflammation centered on the internal

elastic lamina that produce elastic lamina fragmentation.
- there is an infiltrare of T cells (CD4+ > CD8+) and macrophages.
- Although multinucleated giant cells are seen in approximately 75% of adequately
biopsied specimens, granulomas and giant cells can be rare or absent
- Inflammatory lesions are only focally distributed along the vessel and long segments of
relatively normal artery may be interposed
One simple blood test to prove: ESR ( elevated).
◌ Why blindness: ophthalmic artery involvment

◌ Treatment ---- > corticosteroids.
Q: One year later developped fracture NOF why ?

A:
1- AVN
2- osteoprosis
Q: Why osteoprosis in this patient ?

A: steroid therapy , post-menopausal
◌ Pathological changes in osteoprosis:

- histologically normal bone that is decreased in quantity.
- postmenopausal osteoporosis the increase in osteoclast activity affects mainly bones or
portions of bones that have increased surface area, such as the cancellous compartment
of vertebral bodies. The trabecular plates become perforated, thinned, and lose their
interconnections , leading to progressive microfractures and eventual vertebral collapse
◌ Mechanism by which corticosteroids cause osteoprosis:

- direct inhibition of osteoblast formation
- direct stimulation of bone resorption
- inhibition of GIT calcium absorption
- Stimulation of renal calcium losses
- Inhibition of sex steroids
58
◌ Other causes of pathological fracture:

- skeletal mets
- paget’s disease
- Multiple myeloma
◌ Multiple myeloma :
Is a plasma cell neoplasm commonly associated with lytic bone lesions, hypercalcemia,
renal failure, and acquired immune abnormalities.it produces large amounts of igG
55% or igA 25%.It is the most common primary bone tumour in elderly
Diagnosis
- punched-out lytic skull lesions on x-ray
- M spike on protein electrophoresis
- Ig light chains in urine ( Bence Jones proteins)
- CRAB :
.HyperCalcemia (corrected calcium >2.75 mmol/l, >11 mg/dL)
.Renal insufficiency attributable to myeloma
.Anemia (hemoglobin <10 g/dl)
.Bone lesions (lytic lesions or osteoporosis with compression fractures)
Bence Jones protein:

Are monoclonal globulin proteins or immunoglobulin light chain found in the urine,The
proteins are produced by neoplastic plasma cells. Bence Jones proteins are present in 2/3 of
multiple myeloma cases.
◌ Concerns if going to surgery: Addisonian crisis
◌ How to prevent:
- increase the patient steroid dose prior to surgery
- Convert to i.v hydrocortisone
◌ The patient went for THR , died in POD1 suddenly ------------> fat embolism
59
Gangrene+ mesothelioma
[ worker,smoker, toe gangrene, ]
◌ Define gangrene:
Gangrene (or gangrenous necrosis) is a type of necrosis caused by a critically insufficient blood supply
◌ Define necrosis:
accidental” and unregulated form of cell death resulting from damage to cell membranes and loss
of ion homeostasis
◌ Pathogenesis of necrosis:
Severe/prolonged ischemia: severe swelling of mitochondria, calcium influx into mitochondria and
into the cell with rupture of lysosomes and plasma membrane. Death by necrosis and apoptosis
due the release of cytochrome c from mitochondria
◌Define atherosclerosis:
Pathological process of the vasculature in which an artery wall thickens as a result of accumulation of
fatty materials such as cholesterol
◌ Risk factors: smoking,HTN,D.M, family history, Increased LDL
◌ Patient developed cough------> one bedside test to do : sputum analysis

xray---------> pleural plaque
Pleural plaques, the most common manifestation of asbestos exposure, are well-circumscribed
plaques of dense collagen that are often calcified
Significance: increased malignancy risk of mesothelioma and lung adenocarcinoma
Q: Give one classification of lung cancer

60
A: adenocarcinomas (most common), squamous cell carcinoma, large cell carcinoma, and
Q: Now the patient is presented with Mets, poorly differntiated, how to tell its epithelial origin?
A: Immunohistochemistry
Q: If the tumour was epidermal growth factor positive, what will be the chemotherapeutic
agent?
Tyrosine kinase inhibitors
61
(APPLIED SURGICAL SCIENCES

AND CRITICAL CARE)
ACUTE PANCREATITIS
◌ Stem: 45 year-old male diagnosed and managed for acute pancreatitis 2 weeks later, now having tachy-
cardia,tachypnea and SOB.
◌ Differentials:
- Acute relapsing pancreatitis.
- Acute cholecystitis.
- Ascending cholangitis.
- Pancreatic peseudocyst.
Q: The patient is tachypnic, why?

A: - Abdominal pain.
- Pressure by pseudo cyst.
- ARDS.
1
scORING sYsTEMS
◌ Glascow criteria: PANCREAS
- Pao2 < 8 kpa (10-13).
- Age > 55
- Neutrophils > 15.000
- Calcium < 2 mmol (after 48h).
- Renal ( urea) > 16 (2.5-6.7) mmol/L.
- Enzymes (LDH) > 600 (after48h).
- Albumin < 32 g/L (after 48h).
- Sugar (glucose) > 10 mmol/L.
◌ At least 3 of the above = severe episode = ITU admission.
◌ Ranson's criteria:
◌ Balthazar CT scoring system:

- Pancreas.
- Enlargement of pancreas.
- Inflammatory changes in pancreas and peripancreatic fat.
- Ill-defined single peripancreatic fluid collection.
- Two or more poorly defined peripancreatic fluid collections.
◌ Apache 2:
2
Pathophysiology of hypocalcemia
◌ In early phase: Autodigestion of mesenteric fat by pancreatic enzymes and release of free fatty acids,
which form calcium salts, transient hypoparathyroidism and hypomagnesaemia.
◌ Later stages: Due to complication by sepsis, which will lead to increased circulating catecholamines
which will cause a shift of circulating calcium into the intracellular compartment leading to
relative hypocalcemia. This causes increased PTH secretion by negative feedback loop lead-
ing to further increase in intracellular calcium overload.
Pathophysiology of hyperglycemia
◌ Pancreatic enzymes destroy β cells of islets of langerhans ---> increase in serum glucose.
cT FINDINGS IN ACUTE PANCREATITIS

◌ Edema.
◌ Fat strandings.
◌ Collection.
◌ Necrosis.
◌ Abscess.
◌ Pseudocyst.
MANAGEMENT of NUTRITION
◌ TPN is usually needed in severe cases.

◌ Recently, there is growing trend towards early institution of enteral feeding with a nasojeujenal tube.
◌ Take into account:
- Premorbid nutritional status.
- Current nutritional needs.
- Estimated return to normal feeding.
COMPLICATIONS
◌ Hypovolemic shock.
◌ Haemorrhagic pancreatitis (grey turner sign and cullen's sign).
◌ ARDS,SIRS, sepsis and MOF.
◌ Pseudocyst formation.
Functions of the pancreas

◌ Endocrine: Cells of ilets of langerhans
- α cells: Glucagon.
- β cells: Insulin.
- δ cells: Somatostatins.
- PP cells: Pancreatic polypeptide.
◌ Exocrine: Pancreatic enzymes (digestion of fat ,carbohydrates and proteins)
- Enterokinase (trysinogen ---> trypsin).
- Lipase and amylase.
3
Cause of normal amylase in pancreatitis

◌ Too early or too late: It returns back to normal levels 48 h after the onset of the attack, it doesn't cor-
relate with the severity of pancreatitis and it is not specific for pancreatitis.
Causes of acute pancreatitis

◌ Gall bladder stone.
◌ Alcoholism.
◌ Abdominal trauma.
◌ Post ERCP.
◌ Hyperparathyroidism.
◌ Viral infection (mumps).
◌ Drugs (thiazide direutics).
◌ Idiopathic
Pseudocyst
◌ Definition: Collection of amylase rich fluid enclosed in a wall of fibrous or granulation tissue It requires 4
weeks or more from the onset of the attack
◌ Symptoms: Epigastric swelling, dyspepsia,vomiting and mild fever.
COMPLICATIONS
◌ Rupture (into bowel or peritoneum).
◌ Infection.
◌ Bleeding from splenic vessels.
◌ Cholangitis.
◌ CBD obstruction.
◌ Portal vein thromosis.
Management
◌ RCV line for:
- Rehydration( because of the fluid sequestration and 3 rd space loss)
- Monitoring
- TPN
◌ Pain management: According to WHO analgesic ladder (no morphine and no NSAIDs)
- Epidural analgeisa is a good option.
- PCA.
◌ Nasogastric tube and urinary catheter.
◌ Octreotides ( somatostatins) to decrease pancreatic secretions.
◌ Antibiotics.
◌ IV ppi to prevent stress ulcers and erosive bleeding.
◌ Management of pseudocyst:
- > 6 weeks, > 5 cm and > thick cyst wall ---- > internal drainage: cystogastrostomy, cystdudonostomy with
biopsy of the cyst wall to rule out malignancy.
4
sURGICAL FEEDING OPTIONS
◌ Stem: Lady with crohn's ---> ileocecal resection ----> POD4 anastmotic leakage ---- > defunctioning
ileostomy.
Q: What does AXR show?

A: Small bowel dilatation (stack of coins appearance).
Q: What may be the cause in this patient?
A: Stricture.
Feeding options
◌ Types of non-parentral feeding:
- Oral, nasogastric, nasojeujenal, percutaneous endoscopic gastrostomy and jeujonostomy.
◌ Nasojeujenal tube:
- Smaller in diameter (more prone to kinking).
- Needs endoscopic guidance for placement.
- Bypass the Stomach (less liability to pneumonia).
◌ Complications of enteral feeding:
- Tube related: kinking, misplacement, migration,infection (sinusitis) and aspiration pneumonia.
- Feed related: Diarrhae, nausae, vomiting, refeeding syndrome, fluid and electrolyte imbalance and
deranged liver functions.
◌ Complications of parentral feeding:
- Line related: Infection, thrombosis, pneumothorax and hemothorax.
- Feed related: fluid and electrolyte imbalance and hypo- or hyperglycemia.
5
TPN
◌ Indications:
- General critical illness: Severe malnutrtion (> 10 % weight loss), multiple trauma sepsis with MOF and
severe burns.
- Gut proplems: Enterocutaneous fistula, short bowel, IBD and radiation enteritis.
◌ Routes of administration:
- Central line or PICC.
◌ Types of electrolytes in TPN:
- Sodium chloride, calcium chloride, potassium chloride and magnesium chloride.
◌ Complications:
- Hypo-and hyperglycaemia.
- Hyperlipidaemia.
- Hyperchloraemic metabolic acidosis (if there is an excess of chloride).
- Hyperammoniaemia, e.g. if there is liver disease or a deficiency of L-glutamine and arginine.
- Essential fatty acid deficiency.
- Ventilatory problems due to excess production of CO2 if too much glucose is used in the mixture. In the
ventilated critically ill patient, the amount of glucose given in 24 hours may have to be restricted to 5 g/kg.
- Other complications include infection, from line sepsis, and thromboembolic phenomena, due to mi-
cro-embolic formation at the IV cannula site.
- The most potent risk is that of the re-feeding syndrome, particularly in the chronically malnourished.
- Gut atrophy: Due to the absence of trophic signals released in response to luminal nutrients, during reg-
ular feeding which will lead to bacterial translocation.
Q: How it is given?
A: In a central line because of high osmolarity (must be < 900 mosm/L).
Q: What are the Components?
A: Water, carbohydrates (50%), lipids (30%) ,proteins, vitamins, nitrogen and trace elements.
Q: From which sources may the energy requirements be satisfied?

How much energy does each of these provide?
A:
◌ The predominant sources of energy are from carbohydrates and lipid, but protein catabolism also
yields energy:
- Fats provide 9.3 kcal/g of energy.
- Glucose provides 4.1 kcal/g of energy.
- Protein provides 4.1 kcal/g of energy.
Q: What are the disadvantages of using glucose as the main energy source?
A:
◌ The problems of glucose are:
- Glucose intolerance: As part of the stress response, critically unwell patients are often in a state of hy-
perglycaemia and glucose intolerance. Therefore, if glucose is the only source of energy, patients will
not receive their required daily amount due to poor utilisation of their energy source
- Fatty liver: The excess glucose occurring as a consequence of the above is converted to lipid in the
liver, leading to fatty change. This may derange the liver function tests
6
- Respiratory failure: The extra CO2 released upon oxidation of the glucose may lead to respiratory fail-
ure and increased ventilatory requirements.
- Relying solely on glucose may lead to a deficiency of the essential fatty acids.
- Therefore, ∼ 50% of the total energy requirement must be provided by fat.
EPIDURAL
◌ Lobectomy using thoracic epidural ---> hypotension, bradychardia, desaturation, upper limb parasthsia.
◌ Differentials:
- High epidural block.
- Distributive shock 2ry to epidural.
- Paralysis of intercostal muscles.
- Paralysis of diaphragm.
- Hemothorax or pneumothorax.
- Post operative hypovolemic shock.
Q: Why patient having bradycardia?

A: High epidural block---> blocking of the cardioaccelerator fibres (sympathetic fibres) from T1-T5
----> unopposed parasympathetic action of the vagus nerve.
MANAGEMENT PLAN
◌ Call the operating consultant and anathesia consultant.

◌ Sit the patient upright.
◌ 100% O2.
◌ Stop any injections in the epidural catheter.
◌ Rule out any concomitant hypovolemic shock.
◌ Epinehrine , phenylepherine, metaraminol (inotroic agents).
◌ Atropine (chronotroic agent).
Factors affecting epidural efficency

- Level of injection.
- Dosage.
- Type of medications.
- Vasoconstrictors.
- Posture.
- Age, height and weight.
Q: Why epidural?
A: - Post operative analgesia.
- Improves outcomes.
Q: How to test the level of the block?
A: Using temperature sensation (ice packs) or ethyl
chloride spray
Q: Why we use temperature Sensation not pinprick?
A: Painful, bleeding, infection 7
Q: How to differntiate high epidural block from hypovolemic shock?

A: - Eidural: Warm and pink periphries (due to vasodilatation) bradychardia.
- Hypovolemia: Cold clammy peripheries and tachycardia.
GAsTRIC OUTLET OBSTRUCTION
◌ Causes:
- Begnin: Pyloric stenosis secondry to cronic peptic ulceration.
- Malignant: Gastric or pancreatic carcinoma.
◌ ABG: Metabolic alkalosis.
◌ Biochemical abnormalities:
- Metabolic alkalosis.
- Hypocholeremia due to loss of chloride in the vomitus.
- Hypokalemia due to increased aldosterone in response to hypovolemia.
Q: Why bicarbonate is increased?

A: - Here will be increased uptake of bicarbonates in renal tubules in response to loss of chloride
in order to maintain electrochemical neutrality.
- Reduction of pancreatic juice secretion due to loss of acid load in the duodenum, pancreatic
juice is rich in bicarbonates which will be retained.
Q: Why paradoxical acuduria?
A: - Hyponatremia ---> stimulation of angiotensin aldosterone system ---> more Na+ and H 2O
reabsorption in exchange of H+ and K+ ---> hypokalemia and the urine becomes acidic due to
the prescence of H+.
8
Q: Why hyponatremia?
A: In metabolic alkalosis, kidneys excrete more NaHCO3 to reduce blood alkalinity---> hyponatremia.
Hyponatremia
◌ Management: Normal saline 0.9% with K+ supplementation.
◌ Clinical picture: Confusion, agitation, fits and reduced GCS.
◌ Causes:
- Depletional: Siarrhea, direutics and burns.
- Dilutional: Heart failure and post-operative over adminstration of 5% glucose.
- Endocrine: Addison's disease and hypothyroidism.
- Pseudohyponatrmia: Multiple myeloma.
- SIADH.
ATRIAL FIBRILLATION AND RUPTURE VIScus
◌ CXR and ECG.
Chest x-ray comment items

◌ Check patient details: First name, surname, date of birth.
◌ Check orientation, position and side description: Left, right, erect, ap, pa, supine, prone.
◌ Check additional information: Inspiration, expiration.
◌ Check for rotation: Measure the distance from the medial end of each clavicle to the spinous process of
the vertebra at the same level, which should be equal.
◌ Check adequacy of inspiration: Nine pairs of ribs should be seen posteriorly in order to consider a chest
x-ray adequate in terms of inspiration.
◌ Check penetration: One should barely see the thoracic vertebrae behind the heart.
◌ Check exposure: One needs to be able to identify both costophrenic angles and lung apices.
◌ Identify the pathology in CXR ---> air under the diaphragm.

◌ Identify the pathology in ECG ---> AF (there is no p waves), irregular rhythm.
◌ Count the heart rate in ECG ---> count the No. of QRS in 30 blocks and multiply it by 10.
9
Q: Why it is different from recorded by the automatic machine?

A: Because automatic machine can not measure irregularity (because AF causes inadequate heart
contraction resulting in a small volume pulse).
Q: What is the cause of AF in this patient?
A: Hypokalemia and sepsis.
MANAGEMENT of Af
◌ Cardioversion: Chemical ( amiodarone), DC shockGive 300 mg of amiodarone in a large vein over 10–20
minutes and repeat the shock, followed by 900 mg over 24 hours.
◌ Anticoagulation: Unfractionated heparin 70 units /kg as a bolus then 15 units / kg/ h till adjusting APTT
to 40-60 seconds.
Differntials of perforated viscus

◌ Ruptured diverticulum.
◌ Perforated DU.
◌ Ischemic bowel.
◌ Necrotising enterocolitis.
Q: What is other cause of abdominal pain in this age group?

A : myocardial infarction
Q: How to consent in such case?

A: Patient is confused, I will proceed for the operation for the patient best interest with 2 consul-
tant signature on the consent.
PREOPERATIVE AORTIC sTENOSIS
◌ Pathophysiology of aortic stenosis:

- Fixed cardiac output -----> limited coronary blood supply----- > can not respond to decreased afterload
which may occur with anathesia or blood loss.
- Coronary perfusion pressure = systemic diastolic art. Pressure - LVED pressure.
◌ Clinical picture of aortic stenosis:
- Symptoms: Syncope, anginal pain, dyspnea, orthopnea and paroxysmal nocturnal dyspnea.
- Signs: Pulse (pulsus alternans, narrow pulse pressure), paradoxical splitting of S2 and ejection Systolic
murmur (right 2nd IC space on right sternal border).
◌ ID (ECG):
- +ve lead 1, + ve lead avL.
- -ve lead 2, -ve lead avF.
- Left axis deviation = left ventricular hyperatrophy.
10
Q: How to calculate HR based on this ECG?

A: 300/No. of large squares between two R-R intervals.
Q: What are the complications of aortic stenosis?
A: - LVH.
- HTN.
- CHF.
- VT, VF.
- Angina.
Q: What is the Investigation?

A: 2D echocardiography.
Q: What to do?
A: - Inform the consultant and the anathesist.
- Cancel the operation.
- Call the operating theatre to cancel listing.
- Explain to the patient.
- Discuss in MDT.
Q: If this patient had a bladder cancer, will you proceed to bladder

surgery or valve surgery first?
A:
◌ This will depend on the severity of aortic stenosis:
- Normal aortic valve surface area is 2.5-3.5 cm2.
- < 1cm2 = severe stenosis = transvalvular gradient > 40mm.h.
11
RESPIRAToRY ACIDOSIS
Q: How CO2 is transported in the blood?

A: - Carbaminogroup (20%): between the CO2 and proteins or peptides most of which with the globin
portion of Hb.
- Dissolved CO2 (10%).
- Bicarbonate (70% ):
Carbonic
anhydrase Inside RBCs Alveoli
H›O + CO› H›COs H+ + HCOs−
HCOs --- > Diffuses out of red cell to the plasma.

H+ -- > Binds to Hb.
◌ Chloride shift: Chloride diffuses into the red cell to maintain cellular balance.
Q: Why still no metabolic compansation?

A: Kidney takes time to react.
Q: What type of respiratory failure is that?

A: Type 2 (hypercapnia).
Q: How does morphine act?

A: By binding to mu receptors on the respiratory center causing respiratory depression.
Q: Why PaO2 is in normal range?

A: Because FiO2 is 0.6 = 60%.
Management: (ITU)
◌ ABC
◌ Ensure adequte oxygenation by humidified O2
◌ Ensure adequte ventilation either non- invasive or invasive ( entubation and invasive respiratory support
or CPAP)
◌ Management of the underlying cause.
◌ Morphine antagonist: (NALOXONE)
- Dose: 0.4 -2 mg IV intially and repeat every 2-3 min. If no response to a maximum dose of 10 mg
- Side effects: nausea, vomiting, sweating, tachycardia, abdominal cramps, pulmonary edema and cardiac
arrest.
◌ ITU admission is indicated for multi-organ mechanical support:
- Respiratory: Mechanical ventilation and non-invasive ventilation.
- Renal: Continuous haemofiltration and intermittent haemodialysis.
- Cardiac: Advanced cardiac output monitoring and inotropic support.
- Neurological: Intracranial pressure monitoring.
12
RUPTURED AAA (HYPoTHERMIA)
◌ Perioperative hypothermia: Under anaesthesia hypothermia is defined as a core temperature less

than 36°C.
Q: How to measure core temperature?

A: Oral, axillary, tympanic membrane, rectal and oesphageal.
◌ Risk factors:
- Major surgery.
- Exposed surgery.
- Massive blood transfusion.
- Combined general and regional anesthesia.
- Preoperative temp. Less than 36°C.
◌ Aetiological factors for perioperative hypothermia include:
- Abolished behavioural responses (shivering).
- Increased heat loss through radiation in the operating theatre.
- Increased heat loss through evaporation from body surfaces and open cavities.
- Cooling effect of cold anaesthetic gases.
- Hypothalamic function altered by anaesthetic agents decreasing heat production.
- Reduced metabolic heat production.
- Reduced muscle activity.
◌ Ways of heat loss:
- Radiation (50%).
- Evaporation.
- Conduction
- Convection
- Specific: Vasodilatation, cold anesthetic gases and i.v fluids and depressed hypothalamic function and
muscle relaxants which will prevent shivering.
cOMPLICATIONS
◌ Cardiovascular: Decreased cardiac output (anaesthetised), arrhythmias, vasoconstriction, ECG shows in-
creased PR interval and wide QRS complex.
◌ Respiratory: Increased pulmonary vascular resistance and V/Q mismatch, decreased ventilator drive.
Increased gas solubility.
◌ Renal: Decreased renal blood flow and glomerular filtration rate, cold diuresis.
◌ Haematological: Reduced platelet function and coagulation, increased fibrinolysis, increased haematocrit
and left shift of oxygen dissociation curve.
◌ Metabolic: Reduced basal metabolic rate, metabolic acidosis, insulin resistance and hyperglycaemia.
◌ Gastrointestinal/hepatic: Reduced gut motility.
◌ Neurological: Reduced cerebral blood flow and impaired conscious state leading to coma.
13
Q: How to prevent thsese complications?

A:
◌ Nice guidelines:
- Theatre temperature is maintained at 21°C.
- Warm i.v and irrigation fluids are used.
- Patient exposed only as needed.
- Postoperative the patient should not leave the recovery room to the ward until core temperature is
above 36°C.
- Bair hugger.
Types of blankets used in prevention of hypothermia : space blankets
DIC
◌ Definition: It is a pathological consumptive coagulopathy due to activation of the coagulation and fibri-
nolytic systems, activation of the latter leads to formation of microthrombi in many organs
with the consumption of the clotting factors and platlets.
◌ Characterised by:
- Widespread hemorrhage.
- Thrombocytopenia, decreased fibrinogen and increased FDPs.
◌ Cause of DIC in this patient:
- Severe hemorrhage, massive blood transfusion and hypothermia.
◌ Treatment of DIC:
- FFP, platelets and cryoprecipitates.

A: Hematology consultant.
INDICATIONS of PLATELET TRANSFUSION
◌ Platelet loss, consumption or dysfunction.

◌ any cause of thrombocytopaenia, e.g. <50 × 10 9, disseminated intravascular coagulation (DIC) and
post-cardiopulmonary bypass.
◌ Shelf life: 5 days.
Stages of hemostasis
◌ Vasoconstriction: smooth muscle contraction by local reflexes, thromoxane A2 and serotonin released
from activated platelets.
◌ Platelet activation: Adherence, aggregation anf plug thrombin.
◌ Coagulation: Intrinsic and extrinsic pathway -----> fibrinogen ----- > fibrin.
14
Massive blood transfusion

◌ Replacement of more than 50% of the patient's blood volume in 12-24 hours.
◌ Complications:
- Fluid overload.
- Electrolyte disturbances: Hyperkalemia due to K+ leakage from the stored RBCs and hypocalcemia due
to chelation of Ca+2 by citrate.
- ARDS (TRALI).
- Thromocytopenia: stored blood has decreased No. Of functioning platelets.
- Hypothermia.
- Coagulopathy: stored blood rapidly loses functions of the labile factors V and VIIIc.
MEAsuREs To REDUCE BLOOD Loss INTRA-OPERATIVE
◌ Cell savers.
◌ Hypotensive technique.
◌ Good hemostasis.
EARLY PosT OPERATIVE COMPLICATIONS of AAA REPAIR
◌ Colonic ischemia.
◌ Renal failure.
◌ Sexual dysfunction.
◌ Spinal cord ischemia.
BuRNS AND ARDS
◌ Calculate the surface area of the burn according to Wallace rule of nines.
15
MANAGEMENT (ABC)
◌ Airway: Look for signs of airway burns and inhalational injury as it may cause airway edema. Consider
intubation of there airway edema.
◌ Breathing and ventilation: Ensure that adequete ventilation can be achieved as tracheal or pulmonary
burns can impair effective gas exchange, also full thickness chest burns can
impeded chest expansion.
◌ Circulation; 2 large bore cannulae and fluid resuscitation by crystaloids usisng (PARKLAND FORMULA):
- Any patient > 15% TBSA.
- Any child > 10%.
- Volume of crystalloids (ml) = 4 X % TBSA X patient weight ----- > divided into 2 halfs; 1/2 in the first 8
hours and 1/2 in the subsequent 16 hours.
◌ Consider C.V line and urinary catheter.
Q: Why not to give colloids in burn?

A: Because of the increased capillary permeability occurring during the first 24 h, colloids will pass
to the extravascular space, exert an oncotic effect, and cause a paradoxical augmentation of the
third space.
Q: How do you assess the adequacy of fluid therapy?
A:
◌ A number of clinical parameters may be used:
- Clinical measures of the cardiac index includes peripheral warmth, capillary refill time and urine out-
put.
- Central venous pressure and its response to fluid challenges.
- Core temperature, e.g. rectal temperature.
- Haematocrit (HCT), which determines the plasma volume and the red cell mass. This is unreliable if
there has been a recent transfusion or haemolysis.
ARDS
◌ Definition: Acute respiratory failure and non cardiogenic pulmonary edema which will lead to hypoxemia
and decreased lung compliance refractory to O2 supply.
◌ Charcterised by:
- Diffuse pulmonary infiltrates on CXR.
- Normal PAWP (< 18 mm.Hg).
- PaO2/ Fio2 < 26.6
◌ Pathophysiology: Two phases are recognised in ALI/ARDS
- An acute phase, characterised by widespread destruction of the capillary endothelium, extravasation of
protein-rich fluid and interstitial oedema with extensive release of cytokines and migration of neutro-
phils; the alveolar basement membrane is also damaged, and fluid seeps into the airspaces, stiffening
the lungs and causing ventilation/perfusion mismatch.
- A later reparative phase, characterised by fibroproliferation, and organisation of lung tissue. If resolution
does not occur, disordered collagen deposition occurs leading to extensive lung scarring.
16
MANAGEMENT
◌ Management of the initial predisposing insult:

- Respiratory support:
○ Low tidal volume: This lung protective strategy protects the lungs from over distension and prevents
the release of inflammatory mediators.
○Moderate PEEP –Used to prevent lung injury and improve oxygenation. Lower doses are generally
preferred to minimise cardiovascular compromise and risk of pulmonary oedema.
○ Prone positioning –This has been found to significantly improve oxygenation (up to 65%).
○ High frequency oscillation –This lung protective mode of ventilation includes low positive pressure
together with high respiratory rates. It prevents ventilator-assisted lung injury.
○ Inverse ratio ventilation
○ Extracorporeal membrane oxygenation (ECMO): Can be used for profound refractory hypoxaemia. No
significant advantage has been identified although its role in combination therapy is under investiga-
tion. Major bleeding is the potential complication.
- Pharmaclogical support:
○ Low dose steroids: Certain studies have identified improved oxygenation and survival with steroid
therapy. However it is recognised that therapy should not be commenced 2 weeks after the onset of
ARDS due to the increased risk of infection and mortality
○ Inhaled nitric oxide/prostacyclin: Both treatments cause pulmonary vasodilation, reducing pulmonary
hypertension and improving gaseous exchange.
○ Antibiotics: These should be administered in cases of infective causes after obtaining the appropriate
cultures.
◌ Haemodynamic management: Studies have reported the benefit of conservative fluid management
maintaining a low central venous pressure. This reduces the pressure in
the pulmonary microvasculature.
◌ Nutrition: Enteral nutrition should be commenced after 48–72 hours of mechanical ventilation. A low
carbohydrate, high fat formula containing anti-inflammatory and vasodilating agents such as
eicosapentaenoic and linoleic acids.
PNEUMOthoRAx AND CV LINE INSERTION
17
sYsTEM foR READING CXR

◌ The ABCDE mnemonic is a useful one when trying to ensure that the examination of a chest X-ray is
a systematic one:
- A-airway.
- B-bone.
- C-cardiac.
- D- diaphragm.
- E&F-equal (lung) fields
- G- gastric bubble.
- H-hilum and mediastinum.
- I also have to add the T which stands for technicals.
Types of pneumothorax
◌ Simple Vs tension. Primary Vs secondary. open versus closed
◌ Difference between tension and simple pnemothorax:

- In Tension pneumothorax:
○ Trachea and mediastinum is shifted to the opposite side.
○ tachycardia and hypoxia.
○ Emergency situation requiring urgent needle thoracostomy in 2nd ICS midclavicular line then tube
thoracostomy in the 5th ICS midaxillary line.
○ There is continuous entry of air through a one way valve.
Safe triangle of insertion of chest tube

- Ant.: Lateral border of pectoralis major.
- Post.: Mid-axillary line.
- Inf.: A line drawn from the nipple line backwards.
INDICATIONS of CENTRAL LINE INSERTION
◌ Monitoring of fluid balance and fluid resuscitation.

◌ TPN.
◌ Certain fluids and medications (K+ rich fluids).
◌ Failed peripheral venous access.
◌ Hemodialysis.
◌ Transvenous cardiac pacing.
cOMPLICATIONS of CENTRAL VENOUS LINE INSERTION

◌ Infection and thrombosis (DVT).
◌ Air embolism.
◌ Arterial puncture: hemorrhage, pseudoaneurysm, hemothorax).
◌ Pneumothorax.
◌ Left IJV canulation: damage of the thoracic duct ---> chylothorax.
◌ Perforation of right atrium---- > cardiac tamponade.
◌ Arrythmias. 18
NICE guidlines for insertion

◌ Insertion under ultrasound guidance.
◌ Post procedure radiograph for:
- Position of the radioopaque tip in SVC just superior to its entry in RA.
- Pneumothorax.
TECHNIQUE foR INSERTION of CENTRAL VENOUS LINE (IJv)
◌ Anatomical landmarks: mastoid process, carotid pulse and the depression between the two heads of ster-
nocleidomastoid immediately above the clavicle.
◌ locate clavicle and the 2 heads of sternomastoid.
◌ In the center of the triangle formed by the previous land marks , palpate the carotid artery and insert the
needle lateral to it.
◌ The needle is directed at 30 angle towards the patient in the coronal plane aiming towards the ipsilateral
nipple.
◌ Aspirate as the needle advances ,once the blood is aspirated, cannulate the vein with seldinger technique.
◌ Suture the line in place.
◌ Removal technique:
- Head down to prevent air embolism.
◌ Sites for inserting a central venous line:
- IJV, subclavian vein, femoral vein and PICC (peripherally inserted central catheter).
Q: What is the organism causing infection?

A: Staph. epidermidis.
Q: How to prevent line infection?

A:
◌ Perform hand hygiene.
◌ Apply appropriate skin antiseptic.
◌ Ensure that the skin prep agent has completely dried before inserting the central line.
◌ Use all five maximal sterile barrier precautions:
- Sterile gloves.
- Sterile gown.
- Cap.
- Mask.
- Large sterile drape.
◌ Once the central line is in place: Follow recommended central line maintenance practices Wash my
hands with soap and water or an alcohol-based handrub before and
after touching the line.
◌ Remove a central line as soon as it is no longer needed. The sooner a catheter is removed, the less
likely the chance of infection.
19
sTEROIDS
◌ Stem: RA patient on steroids/immunomodulators.

◌ Layers of adrenal cortex: GFR
- Zona glomerulosa: Aldosterone.
- Zona fasiculata: Cortisol.
- Zona reticularis: Sex hormones.
◌ Actions of aldosterone: (mineralocorticoid)
- Na+ reabsorption and K+ excretion in DCT and collecting ducts.
- Water balance: Salt and water retention.
- Acid base balance: Metabolic alkalosis (excretion of K+)
◌ Actions of cortisol:
- Anti-insulin effect: Increase blood glucose.
- Stimulate gluconrogenesis: Increase blood glucose.
- Stimulate protein synthesis in the liver.
- Stimulate lipolysis.
- Metabolic effect as aldosterone.
- Anti inflammatory effect.
- Immunosupressive effect.
- Control body strss response.
◌ Hypothalamic pit. Adrenal axis:
20
Advice to patients starting steroids

◌ They should not stop the drug suddenly , the drug shoud be tappered off slowly.
◌ Make doctors aware that they are on steroids if they are admitted to hospital or prior to surgery (carry
steroid card, wear medicalert bracelet).
◌ There is increased possibility for infection, delayed wound healing.
◌ Steroids may lead to osteoprosis with incraesd risk of fractures.
◌ Steroids may lead to wight gain.
◌ Steroids incraese blood sugar, if diabetic you will encounter poor glycemic control, if not you can
develop diabetes.
◌ Steroids can lead to muscle weakness.
◌ Steroids can lead to mood or behviour changes.
◌ Steroids incrase the risk of peptic ulcers, do not take NSAIDs.
Addisonian crisis
◌ It is acute reduction of the circulating steroids due to:
- Primary: Addisons disease; adrenal supply of cortisol can not meet the body requirements.
- Secondary: to trauma, surgery, infection: exogenous steroids are suddenly stopped rayher than being
tappered off.
◌ Cardinal features:
- Abdominal pain.
- Nausea, vomiting.
- Unexplained shock.
- Hyponatremia, hyperkalemia.
◌ Management:
- CCRISP protocol.
- ABC protocol.
- IV steroids.
- Adjust metabolic disturbances.
◌ Prevention:
- Increase the patient steroid dose prior to surgery.
- Convert to IV steroids.
CALCIUM HOMEosTASIS
◌ Stem: Post thyroidectomy hypocalcemia, calcium 1.8---- > pod 4 0.7.

◌ Causes of post-thyroidectomy hypocalcemia:
- Removal of parathyroid glands.
- Ischemia of parathyroid glands.
◌ Calcium transport in the blood:
- 45% bound to plasma proteins.
- 50% unbound and ionised.
- 5% is associated with anions such as citrate and lactate.
21
◌ Physiologic role of calcium in the body:

- Muscle contraction.
- Nerotransmitter and nueromodulator.
- Activation of some enzymes.
- Glycogen metabolism.
- Cell division.
- Mineralization of bone.
- Blood coagulation.
◌ Hormones involved in Ca+2 homeostasis:
- PTH: (increases calcium)
○ Bone: Increases the synthesis of enzymes that break down bone matrix to release calcium and phos-
phate into the circulation. It also stimulates osteocytic and osteoclastic activity, leading to pro-
gressive bone reabsorption
○ Renal: Increases renal phosphate excretion while reducing renal calcium loss. It also stimulates 1-α
hydroxylase activity in the kidney, increasing 1,25 dihydroxy-vitamin D 3 (calcitriol), thus indi-
rectly increasing calcium absorption.
- Vitamin D3: (calcitriol)
○ Bone: Calcitriol increases both serum calcium and the calcification of bone matrix. It stimulates osteo-
blastic proliferation and protein synthesis.
○ Renal: It promotes calcium and phosphate reabsorption.
○ Gastrointestinal: It enhances gut absorption of calcium and phosphate
- Calcitonin:
○ Bone: Inhibits bone resorption through inhibition of osteoclastic activity if serum calcium >2.6 mmol/L.
○ Renal : Stimulates the excretion of sodium, chloride, calcium and phosphate.
Q: How vitamin D3 is formed?

A:
UV in skin Liver
Cholesterol Cholecalciferol 25,hydroxycholecalciferol
1-a hydroxylase in kidneys

1,25 dihydroxycholecalciferol
sIGNS of HYPoCALCEMIA
◌ Neurological: Irritability manifest as peripheral and circumoral parathesiae.
◌ Muscular: Cramps.
◌ Tetany: Spasms.
◌ Chvostek's sign: Twitching of the facial muscles on tapping of the facial nerve anterior to the tragus.
◌ Trousseau's sign: Tetanic spasm of the hand upon tapping the median nerve following blood pressure
cuff-induced arm ischaemia.
Q: Which muscle are you worried about in tetany?
A: Laryngeal muscle for the fear of laryngeospasm.
Q: Which muscle are you worried about in tetany?
A: - Commencement of cardiac monitoring.
- Fluid resuscitation Give 10 ml of 10% calcium gluconate IV, followed by 10–40 ml in a saline infusion
over 4–8 hours.
22
PAIN MANAGEMENT
◌ Stem: Post operative pain, drug chart ---- > had only panadol and arcoxia (selective COX 2 inhibitor).
PATIENT MANAGEMENT AFTER THIS DRUG CHART
◌ IMMEDIATE MANAGEMENT:
- In the critically ill patient in pain, patient assessment is vital. It should follow the same CCrISP system
of assessment as in any other circumstance:
○ Airway: Start at the beginning by checking that the patient has a patent airway.
○ Breathing: Check the respiratory rate, pattern and depth of breathing. Is your patient’s respiratory
function impaired by inadequate analgesia? Can he or she cough and expectorate properly
to avoid problems later?
○ Circulation: Tachycardia should not automatically be assumed to be caused by pain–there is com-
monly an underlying cause. A persistent tachycardia or hypertension caused by inade-
quate analgesia may potentiate the development of myocardial ischaemia, particularly in
the patient who is already hypoxaemic.
○ Disability: It is important to assess whether the method of analgesia is contributing to the patient’s
clinical deterioration. Particular attention should be paid to the patient’s level of conscious-
ness as decreasing conscious level is an early indicator of opioid toxicity.
◌ FULL PATIENT ASSESSMENT:
- Chart review; If pain relief is felt to be contributing to the patient’s deterioration, the drug charts
should be reviewed with the following questions in mind:
○ is effective analgesia prescribed?
○ is effective analgesia being given?
○ is the treatment appropriate for this patient?
◌ History and systemic examination.
◌ Investigations: Serial ABG analysis and chest X-rays.
◌ Decide and plan:
- If pain relief is adequate and the patient is improving then continue and review. If pain relief is inade-
quate determine why:
○ is it due to failure of the method of analgesia?
○ is it due to incorrect implementation of the method chosen?
○ is it due to the development of a surgical complication?
◌ liase with acute pain multidisplinary team (acute pain services); multidisciplinary acute pain team consist-
ing of surgeons, anaesthetists, nursing staff and pharmacists.
Side effects of opioids

◌ Respiratory depression (apnea).
◌ Confusion.
◌ Hypotension.
◌ Nausea and vomiting.
◌ Pin-point pupil.
◌ Itching.
◌ Constipation.
23
Q: What is the pain pathway?

A:
- Pain is transmitted via fast A-delta fibers (sharp pain) and slower C fibers (dull pain) to lateral
spinothalamic tract then to the thalamus.
24
Patient-controlled analgesia: (PCA)

◌ It's a syringe pump connected IV to allow the patient to self adminster boluses of morphine.
◌ Overdosage is avoided by limiting both the size of the bolus and the frequency of adminstration.
◌ A lock-out time is set within which pressing the button again will not result in a bolus of analgesia.
◌ One-way valve preventing backflow of opiates into the infusion chamber which may lead to over dose
when re-delivered.
◌ Proplems:
- Patient has to be alert and oriented to be able to use it.
- Can break down, run out of battery.
- Sleep disturbance.
- Not suitable for patients who are confused or who are unable to press the demand button for physical
reasons.
- Limits patient mobility.
COMPLICATIONS of PAIN
◌ CVS: increased HR, increased BP, Increased myocardial consumption ---> MI.
◌ GIT: Delayed gastric empying, reduced bowel motility ---> paralytic ileus.
◌ Respiratory: Limit chest movements leading to atelctasis, retained secretions nd pneumonia.
◌ MSK: Immobility leading to DVT.
HYPoTHYROIDISM
◌ Stem: A lady with a neck swelling, lethargy and malaise.

◌ Labs show: Low T3 and low T4 with high TSH and anemia.
◌ Hypothalamic pit. thyroid axis:
25
◌ Difference between T3 and T4:

- T3 is more biologically active, less protein binding capcity.
- T4 is in vitro inactive, more protein binding capcity.
◌ Synthesis of T3 and T4:
- Iodide ions enters the thyroid follicular cell by active pumping.
- Iodide is converted to iodine by TOP.
- Iodine combines with tyrosine forming: monoiodotyrisine (MIT) and diiodotyrosine (DIT).
- MIT + DIT = T3 (triiodotyrosine).
- DIT + DIT = T4 (tetraiodotyrosine).
◌ Type of anemia in this case:
- Macrocytic anemia = pernicious anemia (lack of absorption of vit. B12 due to antiparietal cell antibodies
leading to lack of intrinsic factor).
◌ Causes of hypothyroidism:
- Primary:
○ autoimmune (Hashimoto's).
○ iatrogenic (thyroidectomy, carbimazole).
○ transient thyroiditis (Dequervian's thyroiditis).
○ iodine deficiency.
○ infiltrative (amyldosis, sarcoidosis).
- Secondary:
○ to TSH defciency.
sIGNS of HYPoTHYROIDISM
◌ Weight gain.
◌ Memory loss.
◌ Cold intolerance.
◌ Constipation.
◌ Myxedema.
◌ Bradychardia.
◌ Muscle weakness.
◌ Pretibial edema.
Q: Patient with hypothyroidism not compliant to medications comes for an emergency

surgery, what are the risks?
A: - Myxedema coma.
- Delayed recovery from anasthesia.
- Cardiac arrythmia.
- You have to involve endocrionolgist in care and anasthesia consultant.
Q: How to increase patient compliance with the treatment?

A: - To make the dose of replacement in the early morning.
- Make the dose single not divided.
- Involve carer or a family member.
- Regular follow up visits.
- Emphasize that relapse is inevitable if therapy is interrupted.
26
EXTRADURal HEMATOMA
◌ Stem: RTA ----> GCS 15 ----> 2 episodes of Vomiting ----> amnesic events ---- > GCS 8.
◌ Biconvex shape, hyperdense.
◌ Midline shift.
◌ Compression on the ventricles.
Q: When to consider CT brain for trauma?

A:
◌ High Risk Criteria:
- GCS < 15 at 2 hours post-injury.
- Suspected open or depressed skull fracture.
- Any sign of basilar skull fracture:
○ Hemotympanum.
○ Racoon Eyes.
○ Battle's Sign.
○ CSF oto-/rhinorrhea.
- ≥ 2 episodes of vomiting.
- Age ≥ 65.
- Any head injury in anticoagulated patient.
◌ Medium Risk Criteria:
- Retrograde Amnesia to the event ≥ 30 minutes.
- "Dangerous" Mechanism:
○ Pedestrian struck by motor vehicle.
○ Occupant ejected from motor vehicle.
○ Fall from > 3 feet or > 5 stairs.
◌ Normal value of ICP: (7-15 ) mmHg (supine).
27
◌ Ways to measure:
Q: What is the danger of lumbar puncture in increased ICP?

A: Herniation and conning.
Pathophysiology of increased ICP

◌ Monoro-Kellie hypothesis:
- The skull is fixed box containing 3 components; Brain (80%), blood (10%) and CSF (10% ).
- ICP/ volume relationship is governed by these 3 components
- Increase in volume in one component may result in compansatory decrease in the volume of another
component in order to prevent rise in ICP (compensation)
- However, once the ICP has reached around 25 mmHg, small increases in brain volume can lead to
marked elevations in ICP; this is due to failure of intracranial compliance (decompensation) leading to
brain herniation.
28
◌ Lucid interval:
- A temporary improvement in a patient condition after traumatic brain injury after which the condition
deteriorates with rapid decline of consciousness.
- During this period, blood accumulates in the extradural space leading to increaes in ICP leading to cere-
bral edema
- CPP= MAP - ICP
- MAP auto-regulation range is between 50 - 150 mmHg to maintain a constant cerebral blood flow in
cases of traumatic brain injury, this will be disruption of MAP autoregulation ---- > cerebral ischemia.
C/P of INCREASED ICP

◌ Headache.
◌ Nausea and vomiting.
◌ Papiledema.
◌ Fall in GCS:
- Pressure symptoms (hematoma).
- Ischemia (loss of autoregulation of MAP).
◌ Dilated pupil (occulomotor nerve palsy)
◌ Defect in lateral gaze (abducent nerve palsy).
◌ Cushing's triad involves an increased systolic blood pressure, a widened pulse pressure, bradycardia and
irregular respiratory pattern.
29
MANAGEMNENT
◌ ABC
◌ Indications for intubation include:
- GCS ≤ 8
- Risk of raised ICP due to agitation (i.e. sedation required).
- Inability to control/protect the airway or loss of protective laryngeal reflexes.
- A fall of 2 or more points in the motor component of the GCS.
- In order to optimise oxygenation and ventilation.
- Seizures.
- Bleeding into mouth/airway.
- Bilateral fractured mandible.
◌ Management of raised ICP:
- Improving venous drainage from the brain:
○ Elevation of the head of the bed to 30°.
○ Good neck alignment: head in the neutral position.
○ Ensuring ties holding the endotracheal tube in place do not compress the neck veins. Alternatively
tape the tube using "trouser-legs".
○ Where possible immobilise the patient’s cervical spine with sandbags and tape rather than restrictive
neck collars.
- Reducing cerebral oedema:
○ Use mannitol (an osmotic diuretic) 0.5-1g/kg (= 5-10ml/kg of 10% or 2.5-5ml/kg of 20% mannitol).
Some unit use small aliquots of hypertonic saline as an alternative.
○ Use frusemide (a loop diuretic) 0.5-1mg/kg.
○ Maintain serum Na+ in the range 140-145mmol/l.
- Reduction of the cerebral metabolic rate for oxygen:
○ Close temperature regulation. Avoid hyperthermia, but do not actively induce hypothermia.
○ Use of sedation and anaesthetic drugs. Ensure that the patient is appropriately sedated and has
received adequate analgesia.
○ If the patient has a witnessed seizure loading with an anticonvulsant, usually phenytoin 18mg/kg,
should be considered.
○ In cases of intractable raised ICP, a thiopentone infusion can be used to reduce the cerebral metabolic
rate to a basal level. This is identified on EEG monitoring as "burst supression".
- Reducing intracranial blood volume:
○ Hyperventilation can be used to reduce the PaCO2 as a temporary measure, but cerebral ischaemia
may result if this is prolonged.
○ The final resort if ICP remains raised is to perform a decompressive craniectomy.
- Reducing CSF volume:
○ In a neurosurgical centre, use of an external ventricular drain (EVD) allows drainage of CSF to relieve
raised ICP.
Advantages and disadvantages of whole body CT:

* early diagnosis * Improves survival rates
* high radiation exposure * not cost effective
30
DIVERTICULAR ABsCEss AND SEPTIC SHOCk
◌ Stem: Old lady, critically ill, with LIF pain and tendeness.
◌ DD:
- Diverticulitis.
- Sigmoid volvulus.
- Gastroentrits.
- Acute constipation.
- Pelvic tumour.
- Ureteric colic.
◌ Interpret ABG, FBC:
- Metabolic acidosis with partial compansation.
- Increased total lecocytic count.
◌ Shock definition: Shock is circulatory failure resulting in inadequate organ perfusion, e.g. cannot meet the
metabolic demands.
Q: What kind of shock this patient having?

A: Septic shock.
◌ Shock definition:
- This is the presence of sepsis associated with hypotension (systolic BP <90 mmHg) or hypoperfusion
resulting in organ dysfunction despite adequate fluid resuscitation (or the requirement for inotropes),
e.g. persisting lactic acidosis, decreased urine output and altered GCS.
Q: Basic principles of management of septic shock?

A:
◌ Circulatory support: to maintain the cardiac index and oxygen delivery to the tissues
- Use IV fluids, e.g. colloids and crystalloids such as 0.9% saline.
- Inotropes may be required to increase the systemic vascular resistance.
◌ Respiratory support:
- Non-invasive or invasive ventilation may be required for the management of ARDS and respiratory
failure.
◌ Renal support: to ensure that the urine output is >0.5 ml/kg/h
- Dopamine or a furosemide infusion may be required to support the failing kidney.
- Cardiac support helps maintain the renal perfusion pressure.
- Renal replacement therapies may also be required.
◌ Nutritional support:
- May be enteral or parenteral. Enteral nutrition helps maintain mucosal integrity and reduce bacterial
translocation.
◌ Antimicrobials:
- During the early phases there is empirical use of broad spectrum antibiotics and surveillance of infec-
tion, but in the latter stages, agents are targeted to grown microbiological sensitivities from general,
e.g. blood, and local sources.
Q: CT confirmed the presence of diverticular abscess, what are the management options?
A:
◌ Open drainage:
- Advantages:
○ proper drainage with peritoneal toilet. ○ has the ability to make a stoma if needed.
- Disadvantages: liability of wound infection. ○ genral increase in morbididty
31
◌ Image guided aspiration:

- Advantages:
○ no wound infection. ○ less hospital stay. ○ possbilty to leave peg-tail catheter for repeated.
○ darinage abd administration of antibiotics.
- Disadvantages:
○ less adequate drainage. ○ does't have the ability to make a stoma.
PREGNANT LADY UNDERGOING oPEN CHOLE
◌ Stem: 34 weeks undergoing open chole for necrotising cholecystitis, BP is decreasing, HR is decreasing,
reversed telendenberg position, combined GA, epidural, the operation is taking longer duration
than expected).
◌ Benefits and risks of this patient undergoing this operation:
- Benefits: control of infection which may lead to sepsis and induction of pre-term labor.
- Risks: IUFD, DVT (long duration) and pre-term labor.

A: Neonatologist (in case of pre-term labor), ITU registrar, obstetrician, anaesthesiologist.
Q: Where to manage this case post-operative?
A: Obstetric HDU.
Q: Why blood pressure is decreasing?
A: - Compression of IVC by the uterus which will decrease the venous return which will decrease pre-
load thus decreasing the cardiac output.
- Reversed telendenberg position.
Definitions
◌ Pre-load:
- is the end diastolic volume that stretches the right or left ventricle of the heart to its greatest dimen
sions or it's the amount of myocardium that has been stretched at the end of diastole.
◌ Shock:
- Shock is circulatory failure resulting in inadequate organ perfusion, e.g. cannot meet the metabolic demands.
Q: What will be the body response to decreased blood pressure?

A:
◌ The autonomic response is due to decreased venous return (preload) which causes a drop in cardiac
output and arterial pressure by the Frank-Starling mechanism.
◌ Reflexes:
- Baroreceptors stimulate sympathetic activity producing a compensatory tachycardia, increased stroke
volume and peripheral vessel constriction (↑ SVR). This increases the cardiac output and maintains
blood pressure.
32
◌ Hormones :
- Catecholamines: the adrenal medulla is stimulated by pain and injury and releases hormones to cause
peripheral vessel constriction, e.g. noradrenaline (↑ SVR).
- Mineralocorticoids: the adrenal cortex releases hormones to stimulate salt and water retention, e.g.
cortisol to increase the blood pressure The reduction in the circulating volume, and increased sympa-
thetic activity, stimulates renin release from the macula densa of the juxtaglomerular apparatus of the
kidney, e.g. renin–angiotensin–aldosterone (RAA) cascade. A resultant increase in salt and water reten-
tion helps to restore circulating volume over several hours.
Q: What are Baroreceptors?

A: Mechanoreceptors located in the carotid sinus and in the aortic arch. Their function is to sense
pressure changes by responding to change in the tension of the arterial wall. They are supplied by
sinus nerve of Hering, which is a branch of cranial nerve IX (glossopharyngeal nerve).
Q: What are the factors affecting venous return?

A: - Muscle contraction: Rhythmical contraction of limb muscles as occurs during normal locomotory
activity (walking, running, swimming) promotes venous return by the muscle pump mechanism.
- Decreased venous compliance: Sympathetic activation of veins decreases venous compliance,
increases central venous pressure and promotes venous return indirectly by augmenting cardiac
output through the Frank-Starling mechanism, which increases the total blood flow through the
circulatory system.
- Respiratory activit: During respiratory inspiration, the venous return increases because of a de-
crease in right atrial pressure.
- Vena cava compression: An increase in the resistance of the vena cava, as occurs when the thoracic
vena cava becomes compressed during a Valsalva maneuver or during late pregnancy, decreases
return.
- Gravity: decreses venous return.
Q: Can you name some devices used in mechanical DVT prophylaxis may be used to
improve circulatory parameters in this patient?
A: Intermittent pneumatic compression devices, TEDS (thromboembolic deterrent stockings).
Q: What can be done to improve the preload of this patient?

A: Fluids, inotropic and vasopressor agents.
Actions of inotropes
◌ Adrenergic agonists: Adrenaline, noradrenaline, isoprenaline increase the systemic vascular resistance
(SVR) through vasoconstriction, heart rate, stroke volume and resultant cardiac output to increase the
systolic blood pressure.
◌ Dopaminergic agents (with some adrenergic activity): dopamine, dobutamine, dopexamine increase the
heart rate, stroke volume and resultant cardiac output and contractility to increase the blood pressure, but
depending on dose, decrease the SVR to produce vasodilatation
33
POLYTRAUMA
◌ Stem: RTA.
MANAGEMNENT
◌ Airway and cervical spine control:

- Assesment:
○ Speaking to the patient if can speak ---- > secure airway.
○ Can not speak : (1) Look in the mouth for FB or in the face for maxillofacial injuries. (2) listen to abnor-
mal breath sounds stridor or hoarsness. (3) feel the breath on your cheek.
- Management:
○ Chin lift or jaw thrust.
○ Remove any FB in the mouth.
○ Oro-naso pharyngeal airway.
○ Cricothyrodtomy.
○ Trachestomy.
○ Endotracheal entubation.
○ Immobilise the cervical spine by hard collar or sandbag or tape.
◌ Breathing:
- Assesment:
○ Inspection of any obvious chest injuries: (1) Open wounds, flail segment. (2) Count R.R. (3) symmetri-
cal chest wall movement.
○ Palpation: (1) Central trachea. (2) Surgical emphysema.
○ Percussion and auscultation: For obvious hemo or pneumothorax.
- Management:
○ High flow O2 via non rebreath mask.
○ Needle thoractomy or chest tube.
○ Occlusive dressing for open pneumothorax.
Q: Comment on the following CXR.

A: Pneumothorax, rib fracture and surgical emphysema.
Q: How will you manage this?
A: Urgent needle thoracostomy in the 2nd ICS mid-clavicular line then chest tube insertion.
34
Q: Now, patient is shocked, how will you manage the circulation?

A:
◌ Assesment:
- Pulse rate and character.
- Blood pressure.
- Class of hemorrhagic shock.
35
◌ Management:
- Stop any obvious source of bleeding
- Gain venous access by 2 large bore cannulae
- Take blood for FBC, glucose, U&E.
- Cross match for 4 units of blood
- Commence i.v fluid resuscitation with 2 litres of crysytalloid.
- Consider blood transfusion if no response to fluids.
Q: How will you monitor the response?

A: - Heart rate.
- Blood pressure.
- Capillary refill time.
- Urine output.
- Mental status.
Q: Comment on the following CT.

A: - There is a liver tear.
- Grades of liver tear:
Management of liver tear

◌ Conservative: Blood transfusion, monitoring of the hemodynamic status of the patient.
◌ Surgical:
- Damage control: Perihepatic packing.
- Repair
- Resection
36
Q: Is CT was a good investigation of this patient?

A: No, patient is hemodynamically unstable, FAST was the investigation of choice.
◌ Note that: The four classic areas that are examined for free fluid are the perihepatic space (also called
Morison's pouch or the hepatorenal recess), perisplenic space, pericardium and the pelvis.
oBSTRUCTIVE JAUNDICE
◌ Stem: Epigastric pain, nausea,vomiting ,diarrhea, increases ALT, AST, ALP, GGT, urobilinogen undetectable
in urine.
◌ Normal bilirubin level: 3-30 umol/L.
◌ Apparent jaundice ---> 35 umol/L.
Q: Why clotting derranged?

A: - Liver synthesize most of the clotting factors.
- Vit. K required to activate factors 2,7,9,10.
- In severe liver damage and biliary obstruction there will be decreased absorption of Vit. K.
- This will lead to increased prothrombin time.
Q: What is alkaline phosphatase?

A: - Increases in cholestasis to a far greater extent than ALT, AST.
- Located in the epithelium of bile canaliculi.
- Present also in bone and placental tissue.
- ALT and AST are present in hepatocytes and their increase is suggestive for liver damage rather than
obstructive jaundice.
- ALT> AST in liver pathology.
Bile
◌ Function of bile:
- Emulsification of fat into micelles thus provides a greatly increased surface area for the action of the
enzyme pancreatic lipase.
◌ Constituents of bile:
- Water.
- Cholesterol.
- Lecithin (a phospholipid).
- Bile pigments (bilirubin & biliverdin).
- Bile salts and bile acids (sodium glycocholate & sodium taurocholate).
- Small amounts of copper and other excreted metals.
37
Q: How does bile salts help in emulsification of fat?

A: Bile salt anions are hydrophilic on one side and hydrophobic on the other side; consequently, they
tend to aggregate around droplets of lipids (triglycerides and phospholipids) to form micelles, with the
hydrophobic sides towards the fat and hydrophilic sides facing outwards. The hydrophilic sides are nega-
tively charged, and this charge prevents fat droplets coated with bile from re-aggregating into larger fat
particles.
Q: What is bilirubin conjugated to?

A: The liver conjugates it with glucouronic acid by the enzyme glucuronyltransferase.
Bilirubin metabolism
◌ Congugated bilirubin goes into the bile and thus out into the small intestine. Though most bile acid is
resorbed in the terminal ileum to participate in enterohepatic circulation, conjugated bilirubin is not ab-
sorbed and instead passes into the colon.
◌ There, colonic bacteria deconjugate and metabolize the bilirubin into colorless urobilinogen, which can
be oxidized to form stercobilin: these give stool its characteristic brown color.
◌ 10% of the urobilinogen is reabsorbed into the enterohepatic circulation to be re-excreted in the bile.
Some of this is instead processed by the kidneys, coloring the urine yellow.
Q: What is urobilinogen? How it is formed?

A: It is a by product of bilirubin metabolism formed in the intestine by gut flora.
Q: What is the enterohepatic circulation?
A: Reabsorption of bile salts from the terminal ileum and return them back to the liver (95%).
Q: How to correct clotting abnormality?
A: - IV Vit. K.
- Fresh frozen plasma.
- Prothrombin complex concentrates.
- Consult hematologist.
Q: What are other investigation you want to do?

A: Abdominal ultrasound.
Q: If you find a CBD stone, what to do?
A: ERCP.
Q: What if the patient had fever, pain, chills?
A: Ascending cholangitis.
38
Causes of jaundice
◌ Pre-hepatic:
- Hemolytic anemias:
○ Hereditary spherocytosis.
○ G6PD.
○ Sickle cell disease.
- Congenital defects:
○ Gilbert syndrome.
○ Crigler-Najjar syndrome.
◌ Hepatic:
- Viral hepatitis.
- Drug induced.
- Chronic autoimmune hepatitis.
- Wilson's disease.
◌ Post-hepatic (obstructive):
- Gall stones.
- Sclerosing cholangitis.
- Cholangiocarcinoma.
- Cancer head pancreas.
39
PULMONARy EDEMA (FLUID oVERLoAD)
◌ Stem: Post-operative patient, fluid chart + vitals chart = taken crystalloids plus colloids about 7 litres, 4
litres of them are normal saline, now he is tachycadiac, hypertensive, desaturated, oliguric.
Q: What are your expected physical findings?

A: - Congested neck veins.
- Puffiness of face.
- Lung crepitations.
- Confusion.
MANAGEMNENT
◌ ABC.
◌ Stop all IV fluids.
◌ Commence high flow O2.
◌ IV frusemide.
◌ GTN infusion if systolic BP > 100.
◌ Liaise with ITU registeration.
◌ Request CXR.
◌ Request ABG and elctrolytes.
◌ Request ECG.
◌ Chest X-ray findings in pulmonary edema:

- A: Alveolar edema (bat wing or butterfly).
- B: kerley B lines.
- C: Cardiomegaly.
- D: Dilated prominent upper lobe vessels.
40
Q: Why this patient is in high risk of MI?

A: Tachycardia decreases diastole time which decrease coronary filling, also it increaes cardiac load.
Q: What is the minimal UOP?
A: In adults, the minimum acceptable urine output is 0.5 ml/kg/h.
Q: Can you explain why is the patient oliguric?
A: - The most common cause is due to the physiological stress response to surgery in the first 24–36
hours post-operatively. This is due to circulating glucocorticoids and mineralocorticoids inducing salt
and water retention.
- Surgical trauma and various anaesthetic gases also stimulate the release of vasopressin from the
posterior pituitary, stimulating post-operative solute-free water retention.
- Congestive heart failure with low renal perfusion.
Q: What are the fluids given to this patient?

A:
◌ Crystalloids and collids:
- Amount of Na in 0.9 % saline: 150 mmol/L.
- Amount of Na in Hartman's solution: 131 mmol/L.
◌ Daily requirement of Na and K:
- Na: 1-2 mEq/kg.
- K: 0.5 - 1 mEq/kg.
Prevention
◌ Insert a CV line , monitoring the central venous line.
◌ Monitoring UOP.
◌ Report to the hospital incident reporting system.
◌ Better training of junior staff.
INOTROPEs AND VAsOPREssORs
◌ Inotrope: Drug increases cardiac contractility.

◌ Vasopressor: Drug increases vasoconstriction, MAP.
◌ Both are acting through autonomic nervous system.
◌ Receptors acting on:
- Adrenergic alpha 1 receptors: (Vessel wall, heart) -----> vasoconstriction, inotropic.
- Adrenergic beta 1 receptors: (Heart) ----- > inotropic, chronotropic, minimal vasoconstriction.
- Adrenergic beta 2 receptors: (Vessel wall) ---- > vasodilatation.
- D1, D2 receptors: (kidneys) -----> direusis.
◌ Indications:
- Hypotension refractory to fluid resuscitation.
- Low cardiac output states.
- Low SVR.
41
Shock
◌ Definition: Inadequete tissue perfusion to meet metabolic requirement.
◌ SIRS:
- Criteria: (2 or more)
○ Temp. > 38 c or < 36.
○ RR > 20.
○ PaCO2 < 4.3.
○ Pulse > 90/min.
○ WBCs > 11 or < 4.
◌ Sepsis: SIRS + documented infection.
◌ Septic shock: Sepsis with organ hypoperfusion leading to organ dysfunction despite fluid replacement.
Q: Which inotrope to be used in septic shock?

A: - Noradrenaline (alpha 1 effect).
- Dopamine (D1, D2, alpha effect).
Q: How would you monitor?

A:
◌ Maintain MAP = 65 mm.Hg to maintain end organ perfusion:
- Maintain UOP.
- Optimize intra abdominal perfusion pressure.
◌ Monitor blood pressure and heart rate.
◌ Central venous pressure monitoring.
Definitions
◌ MAP:
- Average blood pressure during a single cardiac cycle (CO x SVR) + CVP.
◌ Preload:
- The amount of the myocardium that has been stretched at the end of diastole.
◌ Starling law of the heart:
- The force of the myocardial contraction is directly proportional to the myocardial fiber length, so the stroke
volume of the heart (SV) = the volume of blood ejected from the heart during systole is directly proportional
to the end diastolic volume (EDV) = the voume of the blood entering the heart during diastole.
Q: How is blood pressure controlled?

A: Through baroreceptors located in the aortic arch and carotid sinus. BP= CO X SVR.
Q: When does blood pressure increases?
A: Stretching of baroreceptors ---- > reflex reduction in the vasoconstriction and reduction in heart
rate ----> decrease in SVR, CO ---- > decrease in BP.
Q: When does blood pressure decreases?
A: Baroreceptors are less stretched ----- > increase in vasoconstriction and increase in heart
rate ----> increase in SVR, CO ----- > increase in BP.
42
ITU ADMIssION CRITERIA

◌ Patient requiring or likely to require advanced respiratory support (endotracheal entubation and mechan-
ical ventilation).
◌ Patients requiring support for 2 or more failing organ systems:
- Respiratory: Ventilation, CPAP.
- Renal: Hemodialysis.
- Cardiac: Inotropic support.
- Neurological: ICP monitoring.
◌ Patient requiring 1:1 nursing care.
ENTERocUTANEoUs fISTULA
◌ Definition: Abnormal communication lined by granulation tissue between the skin and gastrointestinal
tract.
◌ Predisposing factors:
- Intestinal anastomosis.
- Crohn's disease.
- Infection.
- Cancer.
- Irradiation.
- Ischemia.
◌ Complications of ECF:
- Sepsis.
- Malnutrition.
- Fluid and electrolyte imbalance.
MANAGEMENT (SNAP)
◌ Sepsis control.
◌ Nutritional support.
◌ Anatomical assessment.
◌ Adequate fluid and electrolyte replacement.
◌ Protect skin to prevent excoriation.
◌ Plan (conservative, surgical):
- Management of fistulas requires an MDT approach following initial resuscitation and stabilisation with
an ABCDE approach, which is particularly pertinent in patients with high-output fistulas.
- For nutritional support, one would liaise with a dietician asking him to recommend a TPN regimen that
adequately meets the patient's calorific needs.
- To ensure adequate fluid and electrolyte replacement, one would arrange bloods tests with the U&Es
guiding electrolyte replacement, and WCC and CRP acting as a measure of inflammation or infection.
- Imaging such as an MRI, CT or US scan of the abdomen can exclude an underlying collection or abscess.
- With conservative management, 60% of fistulae will close spontaneously when sepsis is controlled and
distal obstruction is relieved.
43
- Surgical management is normally delayed until after a trial of conservative measures has been undertak-
en; however, peritonitis with ongoing sepsis will require more urgent surgical intervention. In general
terms the aim of surgery is to excise the fistula tract with resection of the bowel involved and anastomo-
sis or exteriorisation of the remaining bowel, followed by delayed anastomosis.
◌ Imaging:
- CT abdomen and pelvis with contrast.
- Fistulogram:
○ To delineate the track length.
○ Locating the fistula.
○ Locating any distal obstruction.
◌ Fluid management:
- High output fistula: TPN
○ Nutritional assessment are normally performed by a dietician. It is based on a patient’s body weight
and how unwell they are. The energy requirement is 25-30 kcal/kg/day for a normal person and 45-55
kcal/kg/day for a patient following extensive trauma. In addition the protein, fats, glucose, electrolytes
and fluids are calculated and adjusted based on regular blood tests.
Factors preventing spontaneous healing

◌ Distal obstruction.
◌ Malignancy.
◌ Infection.
◌ Radiation.
◌ Crohn's disease.
◌ Malnutrition.
◌ High output.
TURP sYNDROME
◌ Post TURP confused, hypoxic and hypotensive.

◌ Possible causes:
- TURP syndrome.
- Effects of analgesia and sedation.
- Hyponatremia.
- Blood loss.
- Cerebrovascular disease.
◌ Definition: Dilutional hypotonic hypervolemia due to the use of glycine rich hypotonic irrigation solution
which will be absorbed leading to severe dilutional hyponatremia (glycine is used instead of
saline because isotonic solutions limit diathrmy use).
◌ C/P:
- Restlessness.
- Confusion.
- Blurred vision.
- Intial HTN followed by hypotension.
- HF.
- Pulmonary edema.
44
◌ Causes of confusion:
- Hyponatrmia: cerebral edema.
- High ammonia: glycine is broken down to ammonia in the liver.
◌ Cause of hypoxia:
- Pulmonary edema.
MANAGEMENT
◌ ABC according to CrISP protocol.

◌ Stop the opeartion if ongoing and prevent futher irriagation by hypotonic fuid.
◌ Cosider entbation according to the consiousness level.
◌ Order ABG and electrolytes.
◌ Correct hypothermia using bair hugger, infusion of warm fluids.
◌ Fursemide to correct fluid overload.
◌ Refer to HDU.
◌ Replacement of sodium but not more than 10 mmol/day.
Q: Will you give hypertonic Saline?

A: If Na+ is < 110 mmol/L, I will give 250-500 ml of 3% saline through a central line but not more than
10 mmol/L.
Q: What are other system can be affected by TURP?

A: Cardiac system.
Direutics
◌ Furesmide:
- Site of action: thick ascending limb of loop of henle.
- Mechanism: inhibits Na/K pumb thus preventing NaCl absorption, so the distal convluted tubules.
- It tries to prserve Na+ and lose K+.
◌ Other direutics:
- Osmotic diruetics: mannitol (osmosis).
- Thiazide direutics: DCT (inhibit Na reabsorption).
- K+ sparing direutics: spironolactone (aldosterone antagonist) acts on DCT on Na/K pumps.
- Amiloride (binds to Na+ channel at DCT).
cRUSH INJURY
◌ Compartement syndrome + rhabdomyolysis.

◌ Stem: Leg crushed for few hours in 28 years old male, left unobserved on ortho ward.
◌ Blood: AKI, urine dipstick.
◌ Labs of rhabdomyolysis:
- Increased creatine kinase (CK) > 5 times the normal.
- Incraesed lactate, LDH, creatinine.
45
- Electrolyte disturbances:
○ Hyperkalaemia (and metabolic acidosis with an increased anion gap).
○ Hypocalcaemia.
○ Hyperphosphataemia.
○ Hyperuricaemia.
- Myoglobinuria suggested by positive dipstick to blood in the absence of haemoglobinuria (red cells on
microscopy).
◌ C/P of compartment syndrome:
- Worsening pain: This may be out of proportion to the injury.
- Paraesthesia: Especially loss of two-point tactile discrimination.
- Clinical signs: Tense and swollen compartments.
- Sensory loss.
- Pain on passive stretchingLoss of regional pulses, which is a late sign.
◌ Normal compartment pressures (0-15 mm.Hg), >30 = indication of fasciotomy.
◌ Treatment:
- 4 compartment fasciotomies through 2 incisions as an emergency procedure.
Q: Acute renal failure, why?

A: - Acute tubular necrosis due to the nephrotoxic effect of myoglobin precpitating in the renal tubules.
- Note that myoglobin is the O2-binding protein found in muscles.
Rhabdomyolysis
◌ Definition: The release of potentially toxic muscle cell components into the systemic circulation.
◌ Causes:
- Blunt trauma to skeletal muscle, e.g. crush injury.
- Prolonged immobilisation on a hard surface.
- Massive burns.
- Strenuous and prolonged spontaneous exercise, e.g. marathon running.
- Hypothermia.
- Hyperthermia due to malignant hyperpyrexia.
- Acute ischaemic and reperfusion injury, e.g. clamp on an artery during surgery.
- Drugs, e.g. statins, fibrates, alcohol.
◌ Management :
- Fluid resuscitation: ensure good hydration to support urine output > 300 ml/h using IV crystalloid until
myoglobinuria has ceased.
- Diuretics, e.g. mannitol, may also be used.
- Alkalinisation : sodium bicarbonate infusion has been used to limit myoglobin-induced tubular
injury in the presence of acidic urine. It alkalinises the urine > 6.5 pH.
- Electrolyte disturbances : particularly hyperkalaemia.
fLUID MANAGEMENT PosTOPERATIVELY
◌ Stem: 48 year old lady presented by persistent hypotension and tachycardia post operative
THR/Hartman’s procedure, transferred to the ward 3:00 Pm, hypotensive and tachycardiac 70/30 at
2:00 Am.
46
◌ Fluid chart: 2X250 ml bolus with small improvement initially.

◌ Explain the fluid chart: Persistent hypotension and tachycardia with 2 fluid challenges and nothing in
between.
Q: Is that adequate?
A: No.
Q: How would you manage this case?
A: In view of response to previous fluid challenges, I will do more fluid challenges and monitor the
response.
Q: What is the formula of fluid challenge?
A: 500 ml crystalloids over 10-30 min. And monitor the fluid responsiveness.
Q: The patient is on 2 hours monitoring, is that adequate?

A: No, he should be monitored hourly.
Q: Who to notify and when?
A: I will notify my consultant when no response to multiple fluid challenges.
Q: How blood pressure is calculated?
A: Blood pressure (BP) is the product of the cardiac output (CO) and the systemic vascular resis-
tance (SVR). The CO is the product of the heart rate (HR) and stroke volume (SV).
Q: How to increase blood pressure?
A: Inotropic support and fluids to increase CO, vasopressor agents to increase SVR.
Q: What is the hormonal response to surgery and trauma?
47
Q: What are the mechanisms by which the kidneys increase osmolarity

in the renal medulla?
A:
◌ Countercurrent multiplier mechanisms:
- It is an efficient way of concentrating the urine over a relatively short distance along the neph-
ron with minimal energy expenditure.
- It occurs through the loop of henle in the juxtamedullary nephrons.
- Countercurrent system produces medullary hypertonicity (multiplier system by loop of Henle)
and maintained by (exchanger system by vasa recta).
- It occurs by repetitive reabsorption of NaCl by the thick ascending limb of loop of Henle and the
continued inflow of new NaCl from the PCT into the loop of Henle.
Mechanism of action of ADH

◌ Increases the reabsorption of solute-free water by the collecting duct.
◌ NaCl reabsorption by the thick ascending limb of Henle thus increasing the concentration of the interstitium
around the loop of Henle, this enhances the nephron’s ability to reabsorb water.
48
Q: What are the actions of renin angiotensin aldosterone system (RAAS)?
P ERFORATED GAsTRIc ULCER
◌ Stem: Middle aged man, OA, NSAIDs, peritonism.

◌ Comment on CXR: Air under diaphragm.
◌ The most likely diagnosis: Perforated gastric ulcer or duodenal ulcer.
◌ Risk factors of perforation:
- NSAIDs.
- H. pylori.
- Steroids.
- Previous peptic ulcers.
- Malignancy.
Q: How can NSAIDs causes peptic ulceration?

A: - Topical irritant effect of these drugs on the epithelium.
- Impairment of the barrier properties of the mucosa.
- Suppression of gastric prostaglandin synthesis; (inhibition of Cyclooxygenase).
- Reduction of gastric mucosal blood flow.
- Interference with the repair of superficial injury.
49
◌ Management options:
- Omental patch repair, good peritoneal toilet, intraabdominal drain.
- In perforated gastric ulcers, we will take a biopsy to rule out malignancy.
◌ Post-operative medications:
- Long term PPIs.
◌ Mechanism of action of PPI:
- The PPIs binds irreversibly to a hydrogen/potassium ATPase enzyme (proton pump) on gastric parietal
cells and blocks the secretion of hydrogen ions, which combine with chloride ions in the stomach lumen
to form HCL.
◌ Actions of HCL:
- Activates pepsinogen to pepsin which help in proteolysis.
- Antimicrobial.
- Stimulates small intestinal mucosa to release CCK and secretin.
- Promotes absorption of calcium and iron in the small intestine.
◌ Phases of gastric secretions:
◌ Priority of the operation according to NCEPOD intervention classification:
50
EsOPHAGEAL VARIEcEs AND HEMATEMESIS
◌ Stem: Chronic alcoholic, 3 times of hematemesis, decreased blood pressure, increased HR.
◌ Differentials:
- Bleeding esophageal varieces due to pertal HTN caused by cirrhotic liver.
- Mallory-weiss tear.
- Boerhave's syndrome.
- Bleedding peptic ulcer.
Q: How does alcohol cause cirrhosis?

A: - Changes in lipid metabolism.
- Decreased export of lipoproteins.
- Cell injury caused by reactive oxygen species and cytokines.
Pathogenesis of portal HTN in chronic alcoholism

◌ Cirrhosis resulting from chronic liver disease and is characterized by liver cell damage, fibrosis and nodular
regeneration. The fibrosis obstructs portal venous return and portal hypertension develops.
◌ Arteriovenous shunts within the liver also contribute to the hypertension.
51
Mechanism of ascites
◌ Increased formation of hepatic and splanchnic lymph.
◌ Hypoalbuminaemia.
◌ Retention of salt and water due to increased aldosterone and antidiuretic hormone levels.
- cause of confusion: hepatic encephalopathy

- Blood findings in alcoholic patients :
low platlets due to toxic effect on bone marrow -
Q: Which varieces do usually bleed?

A: Varices in the submucosa of the lower oesophagus are the
common source of major bleeding.
Q: How will you manage this patient?

A:
◌ Active resuscitation:
- Group and cross-match blood
- Establish IV infusion line(s)
- Monitor pulse Blood pressure hourly urine output central venous pressure.
- Fresh blood transfusion, FFP and platelets.
◌ Assessment of coagulation status:
- Prothrombin time.
- Platelet count.
◌ Control of bleeding:
- Endoscopic banding or injection sclerotherapy.
- Tamponade (Minnesota tube) if bleeding uncontrolled.
- Pharmacological measures (e.g. vasopressin/octreotide).
◌ Urgent endoscopy:
- Endoscopic band ligation; not more than 6 bands per session.
52
Q: What are the cause of thrombocytopenia in this case?

A: - Hypersplenism.
- DIC.
Q: Patient with macrocytic anemia, what could be the cause?

A: Nutrition deficiency (vitamin B12 defeciency) with chronic alcoholism.
Q: How vitamin B12 deficiency causes macrocytic anemia?

A: Vitamin B12 is importnant in DNA synthesis. When DNA synthesis is impaired, the cell cycle
cannot progress from the G2 growth stage to the mitosis (M) stage. This leads to continuing cell
growth without division, which presents as macrocytosis.
sURGICAL TREATMENT OPTIONS

◌ Portosystemic shunts (splenorenal shunts; TIPSS which is a metal stent is inserted via the transjugular
route using a guidewire passed through the hepatic vein to the intrahepatic branches of the portal vein.)
◌ Stapled oesophageal transection: The gastric vein and short gastric veins are ligated, and the distal oe-
sophagus is transected and reanastomosed just above the cardia using a stapling gun.
◌ Orthotopic liver transplantation (OLT). It's the treatment of choice in patients with advanced liver disease.
53
Q: If the patient is to go for liver transplant, what will you tell his family?
A: - Counseling regarding patient condition, proposed treatment options, outcome of treatment,
lifestyle modifications.
- Abstinence from alcohol 6 months later.
- ABO matching.
- Immunosupression.
Sangstaken Blackemore tube

◌ Double ballon tamponade.
◌ Ports:
- Port for gastric ballon.
- Port for oesphageal ballon.
- Port for gastric suction.
◌ Modifiaction:
- Oesphageal suction port to help suction of oesphageal contents (Minnesota tube).
- If there is no modification, insert NG tube.
Indications of sangestaken tube placement :

• Acute life-threatening bleeding from esophageal or gastric varices that does not respond to medical
therapy (including endoscopic hemostasis and vasoconstrictor therapy)
• Acute life-threatening bleeding from esophageal or gastric varices when endoscopic hemostasis and
vasoconstrictor therapy are unavailable
◌ Technique:
- Position the patient and elevate the head of the bed to 45°.
- Anathesize the posterior pharynx and nostrils with topical anathetic.
- Coat the ballons with lubricating jelly.
- Pass the tube from the nostrils to at least 50 cm mark.
- Suction from the gastric and oesphageal ports.
- When the gastric ballon is correctly positioned in the stomach, infalte the ballon with 500 ml of air and
clamp, the port, pull the tube back until resistence is felt against diaphragm.
- Inflate the oesphageal ballon by the sphygnomanometer to 30-45 mmHg and clamp the port.
- When bleeding is controlled, reduce the oesphageal ballon by 5 mm.Hg every 3 hours until 25 mmHg is
reached without bleeding then keep the tube form 12-24 hours.
- Deflate the oesphageal ballon for 5 min. /6 hours to prevent oesphageal necrosis.
54
RENAL FAILURE WITH HYPERKALEMIA
◌ Stem: 78 yrs with dementia, renal impairment, history of recurrent UTI, baseline creat. 250, now devel-
opped UTI, nausea, vomiting.
◌ Blood: K+= 8 mmol, Na+ = 121 and Creat. = 700.
◌ Interpret: AKI (obstructive uropathy, pre-renal due to decreased oral fluid intake due to dementia).
◌ Pathophysiology: Due to recovery of the glomeruli first with no improvement in distal tubules which will
lead to increase in GFR (increased UOP with dehydration).
Q: This patient had urinary catheter inserted, drained 1500 ml, then 4 L/day, why?
A: This is the direutic phase of AKI, which occurs after correction of the cause.
55
Q: Why are uraemic patients anaemic?

A:
◌ Uraemic patients may develop a normocytic, normochromic anaemia for a number of reasons:
- Deficiency of erythropoietin (most important cause).
- Presence of circulating bone marrow toxins.
- Bone marrow fibrosis during osteitis fibrosa cystica.
- Increased red cell fragility caused by uraemic toxins.
Functions of potassium
◌ Potassium is essential for maintaining proper fluid balance, nerve impulse function, muscle function,
cardiac (heart muscle) functions.
◌ Homeostasis of k+:
- Gastrointestinal Diet:
○ The Western diet may contain 20–100 mmol of potassium daily.
- Endocrine:
○ Aldosterone: this mineralocorticoid, produced by the zona glomerulosa of the adrenal gland, stim-
ulates sodium reabsorption in the distal convoluted tubule and cortical collecting duct, through
an active exchange with potassium. It promotes its excretion.
○ Insulin: Stimulates potassium uptake into cells, reducing the serum level.
- Renal:
○ Acid–base balance: potassium and H+ are exchanged at the cell membrane, producing reciprocal
changes in concentration, e.g. acidosis leads to hyperkalaemia. Similarly, alkalosis can lead to hypoka-
laemia. Also, renal reabsorption of one causes excretion of the other.
○ Tubular fluid flow rate: increased flow promotes potassium secretion, one method by which diuretics
may cause hypokalaemia.
◌ Action of K+ on the cardiac muscle:
- Excess K+ causes the heart to be dilated, flaccid and decreases the heart rate and can block the conduc-
tion of cardiac impulse
- Mechanism: High K+ depolarizes the resting membrane potential causing it to be less negative which will
decrease the intensity of action potential making the contraction weaker.
Q: What use does knowledge of the cardiac effects of potassium have for surgical practice?
A: Potassium-rich cardioplegic solutions are used to arrest the heart in diastole to permit cardiac
surgery once cardiopulmonary bypass has been established..
Q: What are the manifestations of hypokalemia?
A: - Muscular weakness and cramps.
- Lethargy and confusion.
- Atrial and ventricular arrhythmias.
- Paralytic ileus.
Q: What are the manifestations of hyperkalemia?

A: - CVS: Wide QRS, Peaked T wave, dysrhythmia, hypotension, sudden death.
- MSK: Muscle cramps, muscle weakness, flaccid paralysis.
- GIT: Anorexia, nausea, vomiting, diarhea, hyperactive bowel sounds, abdominal, pain.
56
Q: What is the emergency management of hyperkalaemia?

A: - Immediate ABCDE assessment.
- Implement Continuous cardiac monitoring.
- Stop all potassium-containing intravenous fluids, including Hartmann's.
- Calcium gluconate (10 ml of 10%) is given IV over 10 min, which provides a short-term cardioprotec-
tive effect but does not decease the serum potassium.
- Give 5–10 U of insulin in 50 ml of 50% dextrose IV over 30 minutes, which increases cellular uptake
of potassium.
- Sodium bicarbonate (50 mmol IV over 5–10 min followed by IV infusion of 1.26% or 1.4% solution
at 100 ml/h).
- Haemodialysis might be needed if the potassium is persistently high or if there is severe acidosis
(pH <7.20).
- Salbutamol (5–10 g/min by intravenous infusion, or nebulised).
- Calcium resonium (15 g PO or 30 g PR) can be given to provide longer term potassium depletion.
Q: What are the ethical issues of dialysis of 77 year-old man with dementia?
A: - The patient will be unable to give a consent, so I will proceed for dialysis for the patient best
interest with two consultant signatures.
- Also I have to involve the staff of his residentiary house, special nurse.
BLOODY DIARRHEA
◌ Stem: 55 yrs old with abdominal pain, bloody diarrhea, hypotensive, tachycardiac, feverish, adimitted,
fluid resuscitation done, 10 episodes of bloody diarrhea, stopped after 6 hours.
◌ Labs:
- FBC: Hb: 8.7 g, platelets: 666000, WBCs: 12000.
- Hyponatremia, hypokalemia, increased CRP.
- Creat.: 109.
- urea: 9.
Q: What type of anemia?

A: Microcytic hypochromic anemia.
Q: Why platelets are elevated?

A: - Secondary to acute inflammation (acute phase reactants).
- Dehydration.
◌ Abdominal x-ray:
- Dilatation of the ascending and transverse colon, with narrowing of the descending colon with thumb-
printing sign (Thumbprinting is a radiographic sign of large bowel wall thickening, usually caused by
oedema, related to an infective or inflammatory process (colitis). The normal haustra become thickened
at regular intervals appearing like thumbprints projecting into the aerated lumen).
57
DD of bloody diarrhea
◌ Ulcerative colitis and Crohn’s disease (IBD).
◌ Ischaemic colitis.
◌ Amoebic colitis.
◌ Bacillary dysentery.
◌ Carcinoma colon.
◌ Infectious colitis by clostridium difficile, campylobacter jejuni.
Q: Why not to transfuse blood?

A: - State of sepsis.
- Not indicated as Hb is not below 7g.
Q: Why there is hyponatremia and hypokalemia?

A: Due to losses from diarrhea.
Q: How else would you investigate the patient?

A: - ESR, CRP.
- Stool analysis and culture.
- CEA.
- Antiobodies for UC, Crhon's.
- Colonoscopy (later stage).
Q: How will you monitor the patient response?

A: - Clinically: Fever settles, diarrhea stops.
- Lab.: Decrease CRP, decrease TLC.
Q: What are the indications of urgent surgical management?

A: - Toxic megacolon refractory to medical management.
- Fulminant attack refractory to medical management.
- Uncontrolled colonic bleeding.
- Perforation (free or walled off).
- Obstruction and stricture with suspicion for cancer.
◌ Surgical management:
- Pan-proctocolectomy with ileostomy.
58
POLYTRAUMA WITH PELVIC FRACTURE
◌ Stem: A 28 year-old motor-cyclist has fractured his femur and tibia treated along with ecchymosis in the
flanks, tenderness and pain in the lower abdomen with blood at the urethral meatus. The patient is
pale, hypotensive and tachycardic.
Q: What other injuries would you suspect and how will you manage the condition?
A: Since the patient has a RTA I will follow the ATLS protocol with ABCDE approach.
Q: What is the first thing you will do?
A: I will clear his airway and immobilize C-spine.
Q: Breathing is fine, what will you do in circulation?
A: - Assess pulse rate and character.
- Blood pressure.
- Capillary refill time.
- Pallor and peripheral temperature.
- ECG: this may initially just be rhythm lead.
59
- Gain IV access with 2 large bore cannulae into the antecubital fossas, taking blood for FBC, U&Es,
LFTs, glucose, ABG’s, lactate, coag and X-match for at least 4 units of bloods. Commence fluid resus-
citation with 2L of warmed crystalloid and move on to looking for any obvious source of bleeding in
the chest, abdomen, pelvis, long bones or floor (the 5 areas discussed in ATLS) and order FAST.
- If there was any question of a pelvic injury I would put on a pelvic binder and it would be appropri-
ate to ask for a trauma series of c-spine, chest and pelvic X-rays at this stage, as long as they don’t get
in the way of resuscitation.
Q: Describe the finding of the X-rays pelvis

A: This X-ray shows a pelvic fracture with an increased pubic diastasis distance along with a sacroiliac
joint disruption.
60
Q: What are the types of pelvic fracture?

A: The four patterns of force leading to pelvic fractures include (1) AP compression, (2) lateral com-
pression, (3) vertical shear, and (4) complex (combination) pattern.
Q: Given that the patient has hypovolaemic shock what % blood loss would you expect?
A: Due to his pelvic, femur and tibia fractures Grade 4 shock i.e. >40% as they have decreased BP
but they have a pulse >140 beats per minute.
61
Q: How would you manage the hypovolaemic shock?

A: Crystalloid and blood urgently, with urgent control of the bleeding e.g. pelvic binder/external
fixation for pelvic injuries, stabilisation of long bone fractures, laparotomy to control intraabdomi-
nal bleeding (if suspected).
Q: How will you monitor the response?

A: Heart rate, blood pressure, capillary refill time, urine output, mental status.
Q: What does blood on the urethral meatus signifie?
A: Urethral trauma (membranous urethra).
Q: What other urinary organ is most commonly injured in a pelvic fracture?

A: Urinary bladder.
Q: How will you confirm the diagnosis?
A: - Anterograde cystourethrogram.
- Retrograde urethrogram.
Q: What are the contraindications to foley’s catheterization?

A: - Pelvic fracture.
- Blood on the meatus (urethral trauma).
- Perineal hematoma.
- Bleeding tendency.
- Pre-existing infection around the glans or the meatus.
- High riding prostrate on DRE.
- Meatal stenosis.
Q: How will you manage and who will you involve?

A: Urologist for suprapubic catheterization..
Q: What other types of urinary catheters do you know?

A: - Condom catheter.
- Straight catheter.
- Coude tip catheter.
- Silicon catheter.
- 3-way catheter for continuous bladder irrigation.
- Suprapubic catheter.
- Nelaton’s catheter for irrigation of clots.
62
Q: How will you manage pelvic fracture?
POLYTRAUMA WITH CERVICAL sPINE INJURy
◌ Stem: A 26 year-old man, cyclist, involved in RTA with spine and chest trauma and hemorrhagic shock
secondary to hemothorax.
MANAGEMENT ACCORDING To ATLS PRoTocOL
◌ Airway and cervical spine control:

- Assessment:
○ Look:
- for the presence of accessory muscles of respiration (neck, shoulders, chest and abdomen) being used.
- presence of obvious foreign bodies in the airway,
- facial/airway injury and the ‘see-saw’ pattern of complete airway obstruction
- Note that: central cyanosis is a late sign.
63
○ Listen:
- for the presence of inspiratory stridor, as this indicates upper airways obstruction (laryngeal level and
above).
- also take note of grunting, gurgling (liquid or semi-solid foreign matter in the upper airways) and snor-
ing sounds (indicating the pharynx is partially occluded by the tongue or palate).
- expiratory wheeze suggests lower airways obstruction. Crowing indicates laryngeal spasm.
○ Feel:
- for chest wall movements and airflow at the nose and mouth (for 10 seconds).
○ Cervical spine control:
- semirigid neck collar, sandbag and tape plus spinal board immobilization.
- Managment of airway:
○ Simple measures:
- basic airway manoeuvres: these include chin lift and jaw thrust, which open up the airway and
permit the use of rigid suction devices (Yankauer sucker) to clear secretions and forceps (Magill) to
remove solid debris
- basic airway adjuncts: these include nasopharyngeal and oropharyngeal airways. If a patient toler-
ates an oropharyngeal, then it is prudent to request an anaesthetic review as the airway is at risk of
imminent collapse.
○ Complex measures:
- endotracheal intubation: this requires anaesthetic expertise and can be achieved through the mouth
(orotracheal) or the nose (nasotracheal) intubation
- Surgical airway : this requires a cut down through tissues (cricothyrodotomy, tracheostomy).
◌ Breathing and ventilation:
- Assessment:
○ Look: (evidence of respiratory distress)
- tachypnea.
- use of accessory muscles of respiration.
- abnormal/asymmetrical chest wall movement.
- cyanosis (late finding).
○ Listen : (signs of partial airway obstruction or compromis)
- asymmetrical or absent breath sounds.
- additional sounds (e.g., sounds indicative of hemothorax).
○ Feel: (air or fluid)
- hyperresonance to percussion.
- dullness to percussion.
- crepitance.
- Management:
○ Maintain a patient’s oxygenation, oxygenated inspired air is best provided via a tight-fitting oxygen
reservoir face mask with a flow rate of greater than 10 L/min. Other methods (e.g., nasal catheter,
nasal cannula, and non-rebreathing mask) can improve inspired oxygen concentration.
○ Tube thoracostomy in pneumothorax.
○ Needle or finger decompression followed by tube thoracostomy in tension pneumothorax.
○ 3 way occlusive dressing followed by tube thoracostomy in open pneumothorax.
Q: After inserting a chest tube, air column is not moving, why?

A: - Improper placement (not inside pleural cavity).
- Blockage (tissue or blood clots).
64
◌ Circulation:
- Assesment:
○ Level of Consciousness: When circulating blood volume is reduced, cerebral perfusion may be critically
impaired, resulting in an altered level of consciousness.
○ Skin Perfusion: This sign can be helpful in evaluating injured hypovolemic patients. A patient with pink
skin, especially in the face and extremities, rarely has critical hypovolemia after injury. Conversely, a
patient with hypovolemia may have ashen, gray facial skin and pale extremities.
○ Pulse: A rapid, thready pulse is typically a sign of hypovolemia. Assess a central pulse (e.g., femoral or
carotid artery) bilaterally for quality, rate, and regularity. Absent central pulses that cannot be attribut
ed to local factors signify the need for immediate resuscitative action.
- Management:
○ Definitive bleeding control: any source of external bleeding have to be controlled.
○ Appropriate replacement of intravascular volume:
- vascular access must be established; typically two large-bore peripheral venous catheters are placed
to administer fluid, blood, and plasma.
- blood samples for baseline hematologic studies are obtained including blood gases and/or lactate
level are obtained to asses the degree of shock.
- initiate IV fluid therapy with crystalloids: bolus of 1 L of an isotonic solution may be required to
achieve an appropriate response in an adult patient. If a patient is unresponsive to initial crystalloid
therapy, he or she should receive a blood transfusion.
○ Insert urinary catheter to measure UOP and monitor fluid response
○ Monitor the patient response to fluid therapy by the clinical parameters of blood pressure, pulse rate
and also urine output.
Q: What are classes of hemorrhagic shock?
65
◌ Define shock: A state of cellular and tissue hypoxia due to reduced oxygen delivery and/or increased
oxygen consumption or inadequate oxygen utilization.
◌ Classify shock:
- Distributive:
○ Septic shock.
○ systemic inflammatory response syndrome (SIRS).
○ neurogenic shock.
○ anaphylactic shock.
○ drug and toxin-induced shock.
○ endocrine shock.
- Cardiogenic:
○ cardiomyopathic.
○ arrhythmic.
○ mechanical.
- Hypovolemic:
○ hemorrhagic.
○ nonhemorrhagic.
- Obstructive:
○ pulmonary vascular.
○ mechanical.
- Combined.
◌ Difference between spinal shock and neurogenic shock:
Q: What are the agents given in neurogenic shock?

A: Phenylephrine hydrochloride, dopamine, or norepinephrine (vasopressors).
66
Disability
◌ As soon as the patient’s cardiopulmonary status is managed, perform a rapid, focused neurological exam-
ination. This consists primarily of determining the patient’s GCS score, pupillary light response, and focal
neurological deficit.
Exposure
◌ Logroll maneuver is performed to evaluate the patient’s spine and any postetior chest injuries.
◌ One person is assigned to restrict motion of the head and neck. Other individuals positioned on the same
side of the patient’s torso manually prevent segmental rotation, flexion, extension, lateral bending, or sag-
ging of the chest or abdomen while transferring the patient. Another person is responsible for moving the
patient’s legs, and a fourth person removes the spine board and examines the back.
Q: Identify the proplem in CT scan

A: C3 cervical spine fracture with cord compression.
67
Spinal cord syndromes

◌ Central cord syndrome:
- Characterized by a disproportionately greater loss of motor strength in the upper extremities than in the
lower extremities, with varying degrees of sensory loss.
- Occurs after a hyperextension injury in a patient with preexisting cervical canal stenosis.
- The prognosis for recovery in central cord injuries is somewhat better than with other incomplete injuries.
◌ Anterior cord syndrome:
- Characterized by paraplegia and a bilateral loss of pain and temperature sensation. However, sensation
from the intact dorsal column (i.e., position, vibration, and deep pressure sense) is preserved.
- Results from injury to the motor and sensory pathways in the anterior part of the cord mostly after cord
ischemia.
- This syndrome has the poorest prognosis in recovery of the incomplete injuries
◌ Brown sequard syndrome:
- Ipsilateral motor loss (corticospinal tract) and loss of position sense (dorsal column), associated with
contralateral loss of pain and temperature sensation beginning one to two levels below the level of inju-
ry (spino-thalamic tract).
- Results from hemisection of the cord, usually due to a penetrating trauma.
- Some recovery can be achieved.
Q: How to diagnose compartement syndrome in a patient with altered

sensorium or sensorimotor deficit?
A:
◌ This can be achieved by:
- Measurement of intracompartmental pressure, tissue pressures of greater than 30 mmHg suggest
decreased capillary blood flow, which can result in muscle and nerve damage from anoxia.
- Blood pressure: The lower the systemic pressure, the lower the compartment pressure that causes a
compartment syndrome.
68
NUTRITION 2
Patient with nasopharyngeal carcinoma had block neck dissection with resection
of half of mandible
“This is an AP chest radiograph of an adult

male/female. The chest x-ray view is
adequate and the NG tube cannot be seen
bisecting the carina and is above the midline
to the level of the diaphragm. The tip of the
nasogastric tube is also not visible below the
diaphragm. I can confirm that this tube is
not in a safe position to commence feeding”
“This is an AP chest radiograph

of an adult male/female. The
chest x-ray view is adequate and
the NG tube can be
seen bisecting the carina and
remaining in the midline to the
level of the diaphragm. The tip of
the nasogastric tube is visible
below the diaphragm and is at
least 10cm beyond the gastro-
oesophageal junction. I can
confirm that this tube is in a safe
position to commence feeding”
69
How to confirm correctly placed NG tube?
Follow NHS patient safety practice guide by:

1. Measuring the pH of aspirate using pH indicator strips/paper
2. Radiography (e.g. chest x-ray)
Methods which should be NOT be used for confirming NG tube position include:
1. Auscultation of air insufflated through the feeding tube (‘whoosh’ test)

2. Testing the acidity/alkalinity of aspirate using blue litmus paper
3. Interpreting the absence of respiratory distress as an indicator of correct positioning
4. Monitoring bubbling at the end of the tube
5. Observing the appearance of NG tube aspirate
Indications of Enteral nutrition:
Healthcare professionals should consider enteral tube feeding in people who are malnourished
or at risk of malnutrition and have:
1. Inadequate or unsafe oral intake, and

2. A functional, accessible gastrointestinal tract.
3. Surgical
1. Pancreatitis
2. Burns
3. Intensive care patients
4. Short bowel syndrome
5. Transition from parenteral nutrition
6. Orthopaedic trauma
7. Sepsis
8. Fistula
Complications of enteral feeding:
Related to intubation of gastrointestinal tract

–Fistulation
–Wound infection
–Peritonitis
–Displacement and catheter migration (including small bowel obstruction)
–Blockage of tube
Related to delivery of nutrient to gastrointestinal tract

–Aspiration and hospital-acquired pneumonia (especially if feed contaminated)
–Feed intolerance
–Diarrhoea
70
What should be monitored regularly during nutrition?

Fluid balance Monitor daily
Glucose tolerance Initially levels checked every 4-6 hours; daily when
stable
Weight 1. Daily weights can show fluid changes
2. Long term trends determine changes in
tissue mass
Venous access Venous access site regularly checked for signs of
infection, phlebitis
Routine biochemistry 1. Serum Na, K, urea and creatinine checked
daily initially
2. Ca, Mg and P checked at least twice a week
initially
3. Trace elements zinc, copper, selenium
checked monthly
4. Vitamins B12, Folate, Vitamin A, Vitamin E
checked monthly
Urinalysis Urinary levels of electrolytes useful when
determining clinical significance of plasma levels
General condition* Daily
To ensure that patient is tolerating feed and that

feeding and route continue to be appropriate
Temperature/blood pressure Daily initially, then as needed

Sign of infection/fluid balance
Abdominal girth Daily- ascites

BMI At the start of therapy
Mid-arm circumference Monthly
Triceps fold thickness Monthly
Why nasojujenal feed is preferred over nasogastric?

Nasojujenal feed is a postpyloric tube feed that goes beyond the pyloric sphincter in the jejunum
and is preferred over nasogastric tube in severe catabolic states as this:
1. Gives rest to the stomach and

2. Avoids the gastric phase of stimulation and
3. Does not stimulate pancreatic secretions and
4. The feed is directly delivered to the intestines thus maintaining mucosal integrity.
Types of Enteral Feed
Types of
Enteral Feed
Anatomical Content Route of access
oral
Pre-pyloric Blenderised
Post-pyloric Disease specific tube
Elemental feeds
Polymeric feeds 71
What is refeeding syndrome?

Refeeding syndrome is a constellation of metabolic and electrolyte changes resulting due to
potentially fatal shifts in fluids and electrolytes causing an in the imbalance of the above due to
aggressive reinstitution of nutrition (either enteral or parenteral) among malnourished patients in
a high catabolic state of critical illness or in a prolonged ebb phase of surgical trauma resulting
in detrimental clinical complications.6
Notable changes are:7
1. The hallmark biochemical feature of refeeding syndrome is hypophosphataemia
2. Abnormalities of glucose metabolism
3. Vitamin deficiency, e.g., vitamin B1 (thiamine)
4. Abnormalities of fluid balance
5. Hypo-magneseima
6. Hypo-kalaemia
6
.
7
72
Stem: 68 y old patient admitted with abdominal pain and distention
- How to manage this patient?

I will manage this patient according to the
protocol of CCRISP which includes :
1- immediate assesment and management :
A–AIRWAY:
• LOOK for the presence of central cyanosis,
obstructed‘see-saw’pattern of respiration or
abdominal breathing, use of accessory muscles
of respiration, tracheal tug, alteration of level of
consciousness and any obvious obstruction by
foreign body or vomitus
• LISTEN for abnormal sounds such as grunting,
snoring, gurgling, hoarseness or stridor •FEEL for air flow on inspiration and expiration
• TREAT–If objective signs of airway obstruction are present, the immediate goals are to
obtain and secure the airway to provide for adequate oxygenation and prevent hypoxic
brain damage. Administer high flow oxygen (12–15 l/min, preferably humidified, via a
reservoir bag).
B–BREATHING:
• LOOK for central cyanosis, use of accessory muscles of respiration, respiratory rate,
equality and depth of respiration, sweating, raised JVP, patency of any chest drains and
the presence of any paradoxical abdominal movement. Note the inspired oxygen
concentration (FiO2) and saturation if pulse oximetry is in use but remember that pulse
oximetry does not detect hypercarbia
• LISTEN for noisy breathing, clearance of secretions by coughing, ability of patient to talk
in complete sentences (evidence of confusion or decreased level of consciousness may
indicate hypoxia or hypercarbia, respectively), change in percussion note and auscultate
for abnormal breath sounds, heart sounds and rhythm
• FEEL for equality of chest movement, position of trachea, the presence of surgical
emphysema or crepitus, paradoxical respiration and tactile vocal fremitus if indicated.
Percuss the chest superiorly and laterally. Abdominal distension may limit diaphragmatic
movement and should be looked for as part of respiratory assessment
• TREAT–The precise resuscitative treatment will be determined by the cause of the
respiratory embarrassment if any.
73
C–CIRCULATION:
. Hypovolaemia should always be considered to be the primary cause of circulatory
dysfunction in the surgical patient until proven otherwise. Haemorrhage (overt or covert)
must be rapidly excluded. Furthermore, unless there are obvious signs of cardiogenic
shock (raised JVP particularly),i should regard any patient who is cool and tachycardic to
have hypovolaemic shock
Consider that his HR:100/min. Capillary refill 4ml/sec.
so i will establish and secure adequate venous access with at least one large (16G)
cannula, send blood off for cross-matching and other routine tests, and initiate
appropriate fluid replacement. Start with a rapid fluid challenge of 10 ml/kg of warmed
crystalloid in the normotensive patient or 20 ml/kg if the patient is hypotensive. I should
be more tentative in patients with known heart failure, starting with an initial bolus of 5 ml/
kg.
D-Disability:
In the initial assessment, a rapid determination of neurological status is performed by
examining the pupils and by using the AVPU system:
• A–Alert
• V–responds to Verbal stimulus
• P–responds only to Pain
• U–Unresponsive to any stimulus.
E- Exposure
2-full patient assessment :
*Chart review
*History and systematic examination
*Available results
-Where to manage this patient?
In HDU taking a consideration that he may require ITU admission if clinically detetiorated
- What are the investigations to do?

• Biochemistry profile –ABG’s –Glucose level
• Haematology –Blood count –Clotting –Cross-matched blood available
• Microbiology
. Occult blood in stools
• Radiology : CT abdomen and pelvis with I.V and oral contrast assuming renal functions
are within normal range
- His Hb is 9 with low MCV, what kind of anemia he has?

Microcytic hypochromic anemia
Mostly due to iron defeciency anemia
74
- Other investigations to know cause of

anemia? Ferritin and TIBC ( total iron binding
capacity)
- How o2 is transported in blood?

Only 1.5 percent of oxygen in the blood is dissolved directly into the blood itself. Most oxygen, 98.5
percent, is bound to a protein called hemoglobin and carried to the tissues.
- What is the structure of heamoglobin?

protein molecule found in red blood cells (erythrocytes) made of four subunits: two alpha
subunits and two beta subunits. Each subunit surrounds a central heme group that
contains iron and binds one oxygen molecule, allowing each hemoglobin molecule to bind
four oxygen molecules
75
History taking
Pre- operative confusion : (dementia)
- hello, i'm .... One of the surgical doctors , how are you today?
- Would you mind if I asked you some questions to test your memory?
Abbreviated mental test scoring:
*How old are you?
*What time is it to the nearest hour?
*Can you remember this address? 24 West St. I will ask you this at the end
*What year is it?
*What is the name of this place?
*What is my job? And what is the job of this person (e.g. a nurse)?
*What is your date of birth?
*When did WW2 end?
*Who is the current prime minister?
*Can you count backwards from 20-1?
*What was that address I asked you to remember?
AMTS:
Score < 6 suggests dementia or delerium
To complete my assesment of the patient i will do MMSE( mini mental state examination)
MMSE: A 30-point questionnaire that is used to measure cognitive impairment.
Discussion:
The patient has acute confusion with het AMTS SCORE of 2/10
Which suggests delirium or dementia
What is your differential diagnosis?
Page 1
Management:
Observations:
• Early Warning Scores can be useful
• BP / Pulse – ↓BP ↑Pulse may indicate sepsis / dehydration
• Temperature, respiratory rate and oxygen sats are all important diagnostic clues.
CT head:
• Ischaemic stroke
• Intracranial bleeds (from trauma or spontaneous)
• Space occupying lesions
Bloods:
• FBC – white cells for signs of infection, anaemia, increased MCV (macrocytic anaemia can
be caused by B12 or folate deficiency which can have a variety of origins: leukemias,
alcohol use, lack of intake, lack of absorption (i.e. post-gastrectomy), pernicious anaemia;
hypothyroidism, liver disease.)
• U&E – deranged electrolytes can cause confusion (consider sodium, but relative to what is
normal for the patient).
• LFTs – confusion can be caused by liver failure, malnutrition or be based on the
background of alcohol abuse.
• INR – can be useful to know if the patient is on Warfarin & you are concerned about
intracranial bleeding
• TFTs – confusion is more common in hypothyroid states.
• Calcium – Hypercalcaemia often causes confusion/delirium – Bones, moans, psychotic
groans
• B12 + folate/haematinics – macrocytic anaemias, and B12/folate deficiency can compound
confusion
• Glucose – hypoglycaemia is a common cause of confusion
CXR – As part of a sepsis screen to identify infection source – ?Pneumonia
Blood cultures if appropriate – as part of sepsis screen
Urine dipstick/culture – UTI is a very common cause of delirium in the elderly
History: take history from the patient ( as possible) , from the notes, from her relatives
Fitness for the operation?

Not fit for giving a consent , as she can not retain informations and she can not make an informed
decision
Should the operation go ahead?
No. The operation is non urgent, therefore it can be postponed until the cause of the confusion has
resolved. I would talk to my consultant and the anaesthetist in charge of the case to inform them of
the confusion and ask their advice before cancelling it.
If the cause of confusion was only senile dementia, how you will consent for the operation?
As the patient lack capacity, consent should be recorded using consent form 4 with 2 consultant
signatures
Page 2
Bleeding per rectum:
Scheme of history taking:

- identify your self
- Confirm the patient name and date of birth.
- Start by an open question: how can i help you today? Or what seems to be the proplem ?
- History of the presenting complaint( onset , duration, course, severity, ppt factors, releving
factors, associated features)
- Past medical and surgical history
- Drug history : doses, allergies
- Social history: occupation, home situation, mobility, smoking, alcohol
- Family history
- ICE: ideas, concerns, expectations
- Systems review
Discussion:
[History of the presenting complaint: ]
- onset: did this started suddenly or gradually?
- duration: when did you first noted this?
- course: does this bleeding comes and goes.? Does it get previously worse?
- Severity:what is the colour of the blood? , how much blood you notice every time?Streaks?
Teaspoon? More? Is that bleeding is painful when you pass stool?
- Releving factors: is there anything makes this bleeding stops
- Ppt factors: is there any thing makes that bleeding increases?
- Associated features: - do you have noticed any slime or discharge? Or pain in your tummy.?
- Do you have any disturbances regarding bowel habits?
- Abroad –Have you been abroad recently? If so , where?
- Tiredness –Have you been feeling more tired than normal recently? -
- - Swallowing/upper-GIT symptoms –Have you been nauseous or sick? ( If
so, ask about haematemesis. ) Any difficulties swallowing? Heartburn?
- Pain/pruritis ani
- Have you had any pain in your tummy? If so, SOCRATES. Have you
noticed any itching around the anus?
- Anorexia –How has your appetite been?
- Weight loss –Have you noticed any unintentional weight loss?
- Systemic features –Have you had any mouth ulcers? Fever? Painful red
eye? Joint or back pain?
[Past medical and surgical history: ]

Do you have any other medical conditions, see your GP for any thing, ever had surgeries?
[Drug history: ]
Do you take any medications? Dose? Do you have any allergy against any drug?
[Social history: ]
- What is your occupation?
- who is at home with you?
- do you have any difficulty with the stairs
- do you smoke ? How many packs/ day
- do you drink alcohol? How many units/ week
[Family history: ]
Is there any one else in the family has had a similar problem?
[Elicit ICE: ]
Page 3
Before i go any further, could i ask:

- what do you think the cause is?
- What are you the most concerned about?
- What are you hoping us to do for you?
[Systems review: ]
- resp., cvs: is there any chest pain,SOB, cough

- Malignancy: have you had any unintentional weight loss ,difficulty in swallowing, change in
bowel habits, night sweats
- Urinary: any proplems in passing urine?
- Rheumatic : any muscle or joint pain?
- Any thing i have missed?
Discussion:
What is your differential diagnosis?
The weight loss, change in bowel habit and PR bleeding are concerning. My main differential is
colorectal cancer, which would need thorough investigation. Other differentials for PR bleeding
include haemorrhoids, inflammatory bowel disease, angiodysplasia, diverticular disease, benign
polyp, and an anal fissure. It may also be secondary to medication or a hematological condition.
Page 4
What is the most important investigation to carry out?
As I am suspecting colorectal cancer, the most important investigation is a colonoscopy +/- biopsy
to examine the whole colon.
If immediately available in clinic, a rigid sigmoidoscopy may be carried out in the first instance
• Haematology: FBC (anaemia, leucocytosis of infective colitis, inflammatory bowel disease,

ischaemic colitis), low platelets (bleeding disorder), clotting screen, group and save / cross match
for transfusion.
• Biochemistry: U&Es, LFTs (hepatic failure with variceal bleed, malignancy)
• Arterial blood gases: Raised lactate (ischaemia), metabolic acidosis.
• ECG: Mesenteric ischaemia, atrial fibrillation (emboli).
• Endoscopy: OGD (to exclude upper gastrointestinal cause), sigmoidoscopy / proctoscopy
(haemorrhoids, anorectal lesion, distal colitis, rectal ulcer) and colonoscopy (malignancy,
diverticular disease, colitis, angiodysplasia).
• Mesenteric angiography (CT or invasive) / Technetium scan / Labelled red cell scan, if source not
identified by endoscopy (looking for angiodysplasia / Meckel’s diverticulum).
• Radiology: AXR (obstruction, toxic megacolon of inflammatory bowel disease) and US scan / CT
(if suspected malignancy, for liver metastases and staging).
• Microbiology: Stool cultures (infective colitis).
Dysphagia:
- Solids or liquids? –Do you have difficulty swallowing solids, fluids or both? Timing –Is it there all
the time or does it come and go?
- Onset –When did this start? Progression –Has it worsened over time?
Associated features:
- Stuck –Does the food get stuck in your throat when swallowing?
- Halitosis –Have you noticed having bad-smelling breath recently?
- Lump –Do you ever feel a lump in your throat?
- Gurgle –Do you ever notice gurgling or a wet voice after swallowing?
- Pain –Is there any pain when swallowing? Any chest pain?
- GORD/dyspepsia –Do you ever taste acid at the back of your mouth? Heartburn? Pain in your
tummy?
- Hematemesis –Have you vomited at all? If so, was there any blood?
- Bowels –Have you noticed any change in your bowels? How many times a day do you go to the
toilet? Has that changed at all? Have you noticed any blood in your stools? Is it darker or more
smelly than usual?
- Neuro –Have you noticed any weakness anywhere? Any problems walking?
- Autoimmune –Do you suffer with painfully cold hands? Dry eyes or mouth?
- Constitutional –Have you had any unintentional weight loss? If so , how much have you lost and
over how long?
Severity:
Do you experience this difficulty of swallowing to solid or to liquid foods or both?
History taking as previous
Page 5
Discussion:
Considering : difficulty in swallowing, weight loss, heavy smoking, alcohol drinking, hematemsis
my main diagnosis will be esophageal carcinoma causing mechanical obstruction of the
oesophagus
I also have to consider:
- lung cancer , pharyngeal pouch, retrosternal goiter ( compression from outside)
- Oesphageal web, plumer vinson sundrome
- Achalsia ( motility disorder)
- Myathenia gravis
Investigations:
- Full clinical examination checking for lymphadenopathy
- Bloods –FBC, U&Es, LFTs and clotting and bone profile
- Chest X-ray
- Oesophageal manometry: achalasia, GORD
- Barium swallow
- Endoscopy and biopsy
- Oesophageal endoluminal US, also for staging of carcinoma.
- Videofluoroscopy –assessing for aspiration
- Staging CT scan, depending on what the previous investigations reveal
Page 6
Treatment :
Operable cases: oesphagectomy + chemoradiotherapy
Non-operable cases: palliation: self expanding metallic stent, palliative chemotherapy and
radiotherapy , feeding jeujnosomy
Change in bowel habits (IBD)
- Open question –Can you tell me what has been going on?
- Specify –When you say constipation/diarrhoea, what do you mean exactly? Do you
mean you are going more/less often or the consistency has changed?
- Onset –When did you first notice this? Has this changed recently?
- Character/colour –What are the stools like? Are they watery, semi-solid or solid? Is
there any blood or mucus in the stools or on the tissue paper?
- What colour are your stools?
- Radiation (from upper GIT) –Do you get any dark, foul-smelling stools?
- Associated features :(BOWELS)
* Bloating –Do you tend to suffer from bloating and flatulence?
* Ouch! –Are you suffering from any abdominal pain? If so, SOCRATES
* Weight loss –Have you lost any weight recently? How is your appetite?
* Exhaustion –How have your energy levels been?
* Lasting urge –Do you feel like you always need to go to the toilet, even after you’ve just
been? Is this despite not passing very much stool? ( Tenesmus )
* Swallowing/upper-GIT symptoms –Any vomiting? ( If so, ask about haematemesis. )
Any difficulties swallowing? Heartburn?
* Extra-intestinal features IBD –Have you had any mouth ulcers? Fever? Painful red
eye? Joint or back pain?
* Foreign travel –Have you been abroad anywhere recently?
- Timing –How many times a day do you go to the toilet to pass faeces now? How often
do you normally go? What are your stools normally like? Have you ever suffered from
the opposite? (i.e. constipation/diarrhoea)
- Exacerbating/relieving factors –Does anything relieve the constipation/diarrhoea?
Does anything make it worse?
- Severity –How badly is this affecting your day-to-day life
Discussion:
Considering weight loss, diahrrhea, PR bleeding, mucous discharge, extra-intetinal
manifestations,my main diagnosis will be crhon's disease or ulcerative colitis
I will also consider:
- infective gastroenteritis
- Colrectal cancer
- Diverticular disease
Management:
Investigations:
-Abdominal examination including DRE
-Routine bloods – FBC, U&E, CRP, LFTs, calcium, magnesium, phophate, Coagulation screen, -
Group and Save. (Looking for raised inflammatory markers, dehydration, electrolyte disturbance
secondary to diarrhoea, albumin as a guide of nutritional status, coagulation defects.)
-Stool sample
Page 7
-Faecal occult blood test

-Abdominal Radiograph - assess for toxic megacolon
-+/-CT or MRI abdomen and pelvis if concerning features on examination and for pre-operative
planning if surgery is indicated
- colonscopy
Treatment:
Medical : mesalazine, prednisolone, immunomodualtors( infliximab)
Conservative: dietary control ( low residue diet)
Surgical : in toxic megacolon, IO, maignant transformation, fistulation, refractory cases
Thyroid status: (female with hyperthyroidism)

History taking as usual
Assiciated features:
Compressive symptoms:
1- changes in voice
2- difficulty in swallowing
3- do you breath well?
Toxic symptoms:
1- changes in vision or difference in eyes
2- diarrhea
3- menstruation ( do you menstruate regularly)
4- sleep disturbances
5- hot or cold intolerance
6- weight loss
7- mood or behavioral changes
8- appetite
Discussion:
Mr ... Is .... Y old , previously fit and well, presents with a lumb in her neck, the lumb has grown
over the past .... Years, in addition she has symptoms indicating hyperthyrodism such as .......
She has also compressive symptoms such as ..........
My main differentials will be:
- Toxic MNG
- simple MNG
- thyroid neoplasm
- Thyroiditis
Management:
Tripple assement:
. Full clinical examination
. Ultrasound imaging
. FNAC
Other investigations: radioisotope scan
Possible causes of sudden enlargement:

- hemorrhage inside a cyst.
- Malignant: papillary, follicular , medullary carcinoma
Treatment: thyroidectomy ( hemi, near total or total) with such compressive symptoms
Page 8
What possible complications of surgery do you advise this patient about?

- risk of RLN injury: hoarsness of voice, aphonia, stridor and possibility of tracheostomy
- Risk of hypocalcemia
- life long thyroxine replacement
Abdominal pain : ( IBS) female referred from her GP as

chronic calcular cholecystitis
O’SOCRATES
- Open question –I believe that you are suffering from pains in your tummy. Can you tell me a bit
more about your problem?
- Site –Where exactly do you get this pain? Can you point to it precisely? Where did the pain first
manifest? Has it moved?
- Onset –When did this pain start? Minutes, hours, days, weeks, months?
- Character –What does the pain feel like? You may need to provide examples, such as cramping,
aching, sharp, knife-like, dull, twisting, excruciating, like an electric shock, etc.
- Radiation –Does the pain move anywhere else? Can you show me? Does it go into your back/
around the side/groin/testicles? Do you get shoulder-tip pain?
- Associated features :
* Have you noticed any weight loss? How has your appetite been?
* Have you had any difficulty swallowing? Any heartburn? Any vomiting? If so , have you noticed
any blood in the vomitus?
* Any change in your bowel motions? Any blood or mucus in your stools?
- Timing –Is the pain there all the time or does it come and go? What is the periodicity if any
( length of time the pain is present and how long between bouts )? Is there any particular time
where you have noticed you get the pain ( day, night, mealtimes, menses )? Have you ever had
this pain before? If so, what happened?
- Exacerbating/relieving factors –What, if anything, brings the pain on? Does anything make it
worse? Does anything make it better? Have you taken anything to relieve the pain? Is it getting
better/worse with time? Does body position make a difference?
- Severity –If you had to rate the pain from 1 to 10, with 10 being the worst pain you can imagine,
how would you rate it?
Social history: social stress( her husband left his job with some financial problems)
Discussion:
Mrs ..... Is ..... Y old , presented by abdominal pain, the pain is colicky in nature, it is not related to
meals, she experience it in the middle of her abdomen, has no special timing, no aggrevating or
relieving factors, associated with disturbed bowel habits, she also has some social stress
My main diagnosis will br IBS, I will also consider IBD, colon cancer, chronic calcular cholecystitis.
Management:
Investigations: abdominal ultrasound, AXR, colonscope, stool analysis, FBC
Treatment: fiber diet, antispasmodics, antidepressants
Abdominal pain ( chronic pancreatitis) :

History summary:
40 y . Old divorced male with chronic epigastric pain radiating to the back for the past 1 year,with
steatorrhea, takes 5 glasses of beer/ day, previously admitted for acute pancreatitis. Takes 30 mg
of morphine / day to numb the pain, depressed
Page 9
SOCRATES approach as usual
Differentials:
- chronic pancreatitis ( in view of epigastric pain, steatorrhea, previous attack of acute
pancreatitis, being an alcohol drinker)
- Pancreatic pseudocyst
- PUD
What do you think about the history of taking 30 mg of morphine, what should be the normal dose?
15-30 mg /4hours as needed
Investigations :
- secretin stimulation test
- Serum amylase and lipase ( elevated)
- Serum trypsinogen
- CT scan ( pancreatic calcifications)
- MRCP : identify the presence of biliary obstruction and the state of the pancreatic duct
- Endoscopic ultrasound
Treatment:
Medical treatment of chronic pancreatitis:

1- Treat the addiction :■ Help the patient to stop alcohol consumption and tobacco smoking
■ Involve a dependency counsellor or a psychologist
2-Alleviate abdominal pain:
■ Eliminate obstructive factors (duodenum, bile duct, pancreatic duct) ■ Escalate
analgesia in a stepwise fashion
■ Refer to a pain management specialist
■ For intractable pain, consider CT/EUS-guided coeliac axis block
3- Nutritional and digestive measures:
■ Diet: low in fat and high in protein and carbohydrates
■ Pancreatic enzyme supplementation with meals
■ Correct malabsorption of the fat-soluble vitamins (A, D, E, K) and vitamin B12
■ Medium-chain triglycerides in patients with severe fat malabsorption (they are directly absorbed
by the small intestine without the need for digestion)
■ Reducing gastric secretions may help Treat diabetes mellitus
4- treat DM
The role of surgery is to overcome obstruction and remove mass lesions
Lower limb claudication:

Analysis of pain:
- Open question –Can you tell me about the pain?

- Site –Where do you get the pain? (buttock, thigh, calf)
- Onset –Did it come on suddenly or gradually?
- Character –What does it feel like? (cramping, tightening of muscles)
- Radiation –Does the pain go anywhere else?
- Associated factors –Do you get any pain at night? Have you noticed any ulcers in your legs or
feet? If so , are they painful? , do you have any numb in your legs or feet? Do you have any
back pain
- Timing –Do you get the pain when walking or at rest?
- Exacerbating & relieving factors –Is it relieved by rest? Is it made worse if you walk faster or up
a hill? Does cold weather affect it?
Page 10
- Severity –How badly does it affect you? How far can you walk before stopping?
Discussion :
My main diagnosis will br chronic lower limb ischemia causing vascular caludication
I will also consider : spinal canal stenosis, DVT, disc lesion causing spinal
claudications,osteoarthritis ,muskloskeletal injury
How to diff. Between spinal and vascular caludications:

Peripheral vascular disease :
- Claudication pain is a cramping pain in the calf, thigh or buttocks
- Brought on by exercise and relieved by rest (patients often pretend to ‘window-shop’ until the
pain disappears)
- Exacerbated by walking faster or up hills and also by cold weather
- Risk factors/associated factors for atherosclerosis: Diabetes Hypercholesterolaemia Stroke
- Rest pain may indicate critical limb ischaemia
Spinal claudication :
- Often relieved when walking up a hill
- Often has associated limb numbness
Sciatica :
- Shooting pain down the back of a leg to the feet
- History of lower-back pain
Management:.
Investigations:
- Full peripheral vascular, cardiovascular and neurological examination
- Assess gait and balance
- arterial duplex
- ct angiography ( if surgical intervention was needed)
- MR Angiography
Treatment:
- optimise blood sugar , cholesterol, blood pressure
- Antiplatlet agents: aspirin, clopidogrel
- Antilipemic agents: simvastatin
- Surgical treatment: endovascular stenting, surgical bypass, amputation
Anxious patient : ( SOB ) in pre-admission clinic

Lady planning for cholecystectomy, SOB for few minutes,
increasing in frequency 6 weeks after being scheduled for
operation
- Onset –How long has this been going on for?
- Frequency –Are you always breathless or only sometimes? What sets it off?
- Relieving factors –Does anything help you get your breath back? If you rest for a while, does it
improve? Do inhalers help?
- Exacerbating factors –Does anything make it worse? Is it worse lying flat? Sleeping upright –
How many pillows do you sleep with? Do you have to prop yourself up? Do you ever wake up
gasping for air?
- Severity –How far can you walk before the breathlessness stops you? Can you climb a flight of
stairs in one go? If not , how many can you manage?
- Associated features:
Page 11
- Cough –Have you noticed a cough? If so , for how long? Do you bring anything up?
Have you noticed any blood?
- Wheeze –Do you get wheezy? Is it worse at any time of the day?
- Fever –Have you recently had a cough or cold? Do you have a fever?
- Constitutional –Have you had any weight loss? How is your appetite?
- Chest pain –Do you suffer from chest pain? If so, SOCRATES
- Palpitations –Do you get palpitations with the breathlessness
- Anxiety –If relevant , do you only get breathless when you are anxious?
Discussion:
The SOB described does not fit with cardiac or pleuritic chest proplem , and the patient tells me
that she has been investigated and ruled out. My top differential would therefore be anxiety
related to her impending operation.
I will also consider: anginal pain, pneumonia, pleurisy.
Management:
- I should contact the GP to get hold of all the notes regarding investigation of the patient’s chest
pain.
- I would examine the patient and ensure that we repeat the patient’s bloods, ECG, CXR and get a
baseline ABG on room air.
- I would want to ensure she had a recent echo and angiogram and discuss these with a
cardiologist.
- I would reassure the patient that she is going to be well looked after, and ask her is there was
anything we could do to allay her fears.
- I would also suggest that we involve her close relatives or friends so that she has an adequate
support network in place before and after the operation
Can the operation go ahead:?

As long as we have no documented evidence that there is no cardiac or resp. Illness, the
operation should go ahead
- FEV1: Volume that has been exhaled at the end of the first second of forced expiration
- FVC: is the amount of air which can be forcibly exhaled from the lungs after taking the deepest
breath possible
- FEV1/FVC ratio: It represents the proportion of a person's vital capacity that they are able to
expire in the first second of forced expiration
In obstructive lung disease, the FEV1 is reduced due to an obstruction of air escaping from the
lungs. Thus, the FEV1/FVC ratio will be reduced
In restrictive lung disease, the FEV1 and FVC are equally reduced due to fibrosis or other lung
pathology (not obstructive pathology). Thus, the FEV1/FVC ratio should be approximately normal
Page 12
Knee pain: (OA)

Footballer, had right knee injury 30 years ago, had knee
operation that he has no idea about, developed worsening
right knee pain 4 months ago
Analysis of pain (SOCRATES)
-Site –Where is the pain?
-Onset –When did you first notice the pain? Was there any history of trauma?
-Character –What does the pain feel like?
-Radiation –Do you have pain anywhere else? (other joints)
*Did you notice any changes in the shape of your knee?( deformity)
- Did you experience locking of your knee?( menisci)
- Did you experience giving away when walking? ( ACL)
- Did you notice any numbness?( neurology)
- Stiffness –Have you noticed any stiffness in your joint(s) when you wake up in the
morning? How long does that last for?
- Swelling –Have you noticed any swelling, redness or heat in your knee
- Extra-articular features:
* Rashes –Have you noticed any rashes anywhere on your body?
* Enteropathy –Have you had any diarrhoea?
* Uveitis/iritis –Have you had painful or red eyes?
- Spondyloarthropathy –Have you had any back pain?
- Timing –When do you get the pain? Is it there all the time or does it come and go? Are the
symptoms worse at any particular time of the day?
- Exacerbating/relieving factors –Does anything make it better? Does anything make it worse? Is
it made better or worse by the cold? Is it made better or worse by exercise? Does resting the
joint help the symptoms at all? What painkillers have you tried so far? Do they help?
- Severity –If you had to rate the pain from 1 to 10, with 10 being the worst pain you can imagine,
how would you score your pain? How do your symptoms affect your day-to-day life? Is there
anything you find you cannot do now as a result of your symptoms?
Discussion:
Mr ......... a ....year old gentleman who has been referred with increasing pain from his right knee.
This started approximately .......years ago and has been increasing in severity over the past 4
months. He is experiencing a dull constant ache that is increased on exertion and at the end of the
day. However, the joint does not swell, lock or become unsteady on walking. The pain is limiting
his daily routine., the patient has a past history of knee trauma and surgery
My main differential will be:

- OA ( traumatic)
- RA
- Referred pain from hip or spine pathology
Managenent:
Invesigations:
- knee x- ray ( standing and weight bearing) : a-p , lateral views
Treatment:
Page 13
Conservative
• Maintain or achieve a healthy weight i.e. aim to decrease weight, and therefore force, going
through a joint
• Regular exercise, with particular attention to strengthening the muscles around the joint.
For example in OA of the knee, cycling is beneficial
• Analgesia: care to be taken with NSAID's with relation to gastric irritation
• Heat application to the joint may offer relief
• Physiotherapy
• Intra-articular steroids
Surgical:
. Arthroscopy and arthrocentesis
• Realignment osteotomy
• Total or partial knee replacement
Will the patient be likely to play soccer in 9 months? No
Headache: ( subarachnoid hemorrhage)

- Open question –Would you please tell me about your headaches?
- Site –ask about frontal, occipital, temporal, unilateral, all over
- Onset –Did it come on suddenly? Do you have any warnings prior to the headache?
- Character –Was it one episode or multiple? Describe the pain
- Radiation –Does the pain move anywhere else?
- Associated symptoms :
* Fever –Have you been feeling ill or had a fever?
* Trauma –Have you banged your head, had a fall recently?
* Sensorimotor changes –Have you had any arm or leg weakness? Any visual disturbances? Any
other sensory disturbance? Have you ever lost consciousness?
* Meningism –Are you sensitive to light? Do you have any neck stiffness? Have you noticed a rash
anywhere?
* Seizures/blackouts –Have you ever had seizures or blacked out?
* Vision –Any eye pain? Visual disturbances? Nausea or vomiting
- Timing –When can you remember this starting? Was it continuous or intermittent? How long do
they last? When was the last time you had a headache?
- Exacerbating or relieving factors –Does it get worse on coughing? Is it worse at night or in the
early morning? Any particular activities or movements? Does anything relieve the pain?
- Severity –How bad is the pain on a scale of 1–10, with 10 being the worst pain you can
imagine? Has it changed over time? How is it now? Is it painful to touch or press over?
Past medical history:

polycystic kidney ( relevant history)
Family history:
My aunt died suddenly of an aneurysm in the brain
Discussion :
My main differential is a subarachnoid haemorrhage, but I would also consider other causes of an
acute severe headache including :
meningitis, encephalitis, and a migraine, increased ICP due to brain tumour
Page 14
Management:
I would manage him in an ABC manner, ensuring that he is stable and arrange appropriate bloods
and a plain CT head.
Investigations:
- CT BRAIN
- CSF Tapping
Treatment:
- I would refer this patient to a neurosurgical unit.
- bed rest, 3L of IV fluids /24h.
- oral nimodipine 60mg every 4 hours, and laxatives
- attempt to coil the aneurysm is made
- Burr holes
- Craniotomy
- Discuss in neurovascular MDT
Seizures: ( brain tumor)

right arm seizures
- *Before:
- Open question –Can you talk me through what happened exactly? Where and when? What
were you doing at the time?
- Aura –How did you feel immediately before the episode? Any aura? Chest pain, anxious or
fearful? Did you have any warning that something was about to happen?
- Environmental –Did you trip over anything or slip?
- LOC –Did you lose consciousness? How long for?
- Witness –Did anyone witness the episode? How did they describe the episode?
- During Fall :
- How did you fall exactly? Did you hit your head?
- Seizure –Did you have a fit? Can you describe it? Did your whole body shake or only part of it?
-- Continence –Did you pass any urine or soil yourself?
- Tongue –Did you bite your tongue?
-After:
- Post-ictal state –How did you feel immediately after the fall/when you regained consciousness?
Were you confused? Drowsy? Aching muscles?
- Previous episodes –Has something like this ever happened before? If yes , can you describe
exactly what happened those times?
Past medical history:

- history of CNS infections ( meningitis,encephalitis)
- History of head injuries
- History of brain tumors
- History of cerebrovascular disease
Page 15
Discussion:
Management:
* Investigations : –
- Blood glucose
- CBCD
- Electrolytes, BUN, creatinine, calcium, magnesium, anion gap, lactate, prolactin (will be
elevated after seizure, sometimes used if not sure if event was a seizure)
- ABG, U/A, LP
- CT head if trauma, suspected intracranial hemorrhage, suspected structural lesion in first
time seizure, prolonged altered mental status, focal neurological deficit, anticoagulated
patient, HIV/Cancer patients
- If infection – may require full septic w/u (LP, cultures, etc)
- EEG – most likely to be done as an outpatient
- MRI – in consultation with neurology
Treatment
- If the patient is seizing
Move to safe place
Turn to side (recovery position) if possible
Observation for specific activity and progression and duration
Prepare to assess/monitor once seizure subsides (ABC’s)
Consider treatment if patient is in status
Postictal
Seizure precautions
ABC’s and monitors,O2
Benzodiazepines may be used to prevent further seizures
Consider anticonvulsant therapy
Phenytoin (Dilantin) 300-600mg PO tid
Phenobarbital 60-200mg PO daily
Valproic acid (Epival) 15-60mg/kg daily divided bid or tid
Carbamazepine (Tegretol) 400-1200mg daily divided tid/qid
Status epilepticus – 30+min of active seizing or no recovery/consciousness between
IV line, O2, monitors
Consider intubation
Benzodiazepines (diazepam 10-20mg IV, or lorazepam 4-8mg IV)
Phenytoin 18-20mg/kg IV @ 25mg/min
- streotactic biopsy and resection or debulking of brain tumors
Hematuria ( bladder cancer) :

CLOTS
- CLarify –When do you notice the blood? Is it only when you pass urine? Is there any chance it
could be coming from elsewhere? What colour is it? Have you recently eaten any beetroot?
- Onset –When did you first notice the blood?
- Timing –Is there always blood in your urine or does it come and go? Have you had this before?
Is the blood present at the start of urination, the end or throughout?
- Severity –Do you pass any clots?
- Associated symptoms:
Page 16
- Pain –Do you have any pain when you pass urine? Any pain in your tummy or back? If so,
SOCRATES
- Frequency –Any change in frequency? Any trouble with incontinence? Do you get sudden
irrepressible urges to pass water?
- Nocturia –How often do you get up at night to pass urine? Urinary stream –Do you have
difficulty getting the stream started? Is there prolonged dribbling at the end? Is your stream
powerful or weak?
- Constitutional –Have you been unwell recently, or had any fever or chills? How is your appetite?
Have you lost any weight?
- Trauma –Have you had any trauma to your stomach or groin recently?
Social history: occupation? Aniline dyes and beta-naphthylamine
Discussion:
Mr........ Is .......y old , presented by painless hematuria one month ago, with associated weight
loss over the last ........ , there is no any abdominal or loin pain, there is no proplems in urine
stream, he is concerned about the possibility of having cancer
DD:
- my main dd will be bladder cancer, renal cell carcinoma considering (his hemorrhage, weight
loss, occupation)
- Stone kidney, bladder, ureter
- Infection
- Trauma
- Bleeding tendency
Management:
- urine dipstick to confirm hematuria, assess infection, send a sample for cytology
- Bloods: FBC, U&E, clotting screen , PSA
- Cystoscopy And biopsy
- u/s, CT
Treatment:
Depends on the stage and the grade of the tumour
- surgical: TURBT, Radical cystectomy
- Non- surgical: chemotherapy and radiotherapy and immunotherapy
Urine retention: (BPH)

History taking as usual
- do you have any pain during urination?

- Any redness or blood in your urine?
- Any bone pains?
- do you have proplems in urination that awakes up from sleep
- Do you have any hesitancy in starting micturition?
- Do you have any senasation about incomplete evacuation
- Do you have any proplems with erections
Drug history:
Page 17
Patient takes nasal sprays containing phenylephrine ( which may cause additive effect to
tamsulosin espcially in decreasing blood pressure and postural hypotensions)
Discussion:
Mr ..... Is ..... Y old, presenting with difficulty in intiating urination, slow stream, hesitancy ,urgency
and incraesed frequency. He does not have dysuria, hematuria, bone pains, or weight loss
DD:
- begnin prostatic hyperplasia
- Overactive bladder
- Prostatic cancer
- Obstructive bladder pathology( malignancy or calculi)
Management:
Investigations:
- full clinicaL examination including DRE
- Bloods : PSA , Urine analysis, U&E
- imaging : abdominal u/s , transrectal u/s
-
- Treatment:
Medical:
- Tamsulin ( 1alpha adrenergic blocker)
- Finasteride ( 5 alpha reductase inhibitor)
Surgical:
TURP
Unilateral tonsillar enlargement: ( neoplastic)

- manifestations of malignancy:
* anorexia. Weight loss
* Rapid increase in size
* Change in voice
* New onset snoring
* Dysphagia
* Neck swelling
* Night fever
- manifestations of infection:
* fever
* Odynopahgia
* Abdominal swelling ( hepatosplenomegaly in glandular fever)
* Respiratory difficulties
Discussion:
Mr....... Is ...... year old previously fit and well gentleman, has presented with a 2 month history of
an enlarging left tonsil. He has lost approximately half a stone in weight and has increasing
discomfort on swallowing, with no other symptoms.
Page 18
Dd:
- neoplastic : lymphoma ( non-hodgkin’s) - SC

- infective:
* acute infection: peritonsillar abscess
* chronic infection: mycobactetia,fungi, actinomycosis, infection mononucleosis( glandular fever)
- asymmetric anatomical positions
Management:
Investigations :
- tonsillectomy for biopsy
- Biopsy with flowcytometry
- CT or PE -CT to rule out lymphoma
- Panendoscopy: examination of the upper aerodigestive tract (pharynx, larynx, upper trachea and
oesophagus).
-FBC: looking for raised WCC associated with infection
-U+E’s: looking for renal impairment if patient has had decreased oral intake
-LFT’s: derangement may indicate glandular fever or metastasis
-Monospot test (detecting glandular fever)
-
Treatment:
- Staging: MRI neck, CT neck, u/s liver
- Discuss in MDT
- Block neck dissection ( radical, modified radical, selective)
- Radiotherapy
Depression : ( reactive depression post operative on

discharging )
Opening the consultation:
-Introduce yourself – name/role
Developing a rapport:
-“How have you been feeling recently?”
Screening for core symptoms:

Screen for core symptoms of depression – feelings of depression, anhedonia and fatigue.
“In the past days during your hospital stay have you…”
Felt down, depressed or hopeless?

Found that you no longer enjoy, or find little pleasure in life?
Been feeling overly tired?
Assessing biological symptoms of depression:
Page 19
Screen for the presence, and assess extent of any biological symptoms
Biological symptoms
Sleep cycle:
“How has your sleep pattern been recently?”
“Have you had any difficulties in getting to sleep?”
“Do you find you wake up early, and find it difficult to get back to sleep?”
Mood:
“Are there any particular times of day that you notice your mood is worse?”
“Does your mood vary throughout the day?”
“Do you find that your mood gradually worsens throughout a day?”
Appetite:
“Have you noticed a change in your appetite?”

“What is your diet like at the moment?”
“What are you eating in a typical day?”
Libido:
“Have you noticed a change in your libido?”

“Since you have been feeling this way, have you noticed a difference in your sex drive?”
Past psychiatric History:
Previous episodes of depression or dysthymia:
“Have you ever felt like this before?”

“Have you ever had any other periods of feeling particularly low?”
“In the past, have you had any problems with your mental health?”
“Have you had any counselling for any issues before?”
“Have you ever been admitted to hospital because of your mental health?” If so, obtain details –
time, method of admission, result.
Management :
Mild :
- Regular exercise
- Advice on sleep hygiene (regular sleep times, appropriate environment)
- Psychosocial therapy –CBT
Moderate to severe:
- Regular exercise, advice on sleep hygiene,
- CBT
- Medication –SSRIs
- High-intensity psychosocial intervention (CBT or interpersonal therapy)
- Immediate and considerable high risk to themselves or others: Admit to psychiatric ward (use
Mental Health Act if necessary)
Page 20
Review of Systems
Impotence:
Erectile Dysfunction History

Introduction
Introduces self and checks patient’s identity (name and date of birth).
Explains consultation, obtains consent and offer a chaperone.
Presenting Complaint & History
When first noticed, Onset of Sx, Duration, Progression, Predisposing events (eg
trauma), Aggravating/ Relieving factors
Specific questions:
difficulty obtaining an erection?
is therection suitable for penetration?
can the penetration be maintained until partner has achieved orgasm?
does ejaculation occur & if yes, is it premature?
do both partners experience sexual satisfaction?
experience nocturnal/ morning erections?
is their associated pain/ discomfort - if yes, were, etc?
is penile curvature a problem?
Sexual History questions:

last sexual contact - when, who (gender & relationship), type, contraceptive
use?
Previous sexual contacts in 3mnths
Psychological history:
any episodes of ↓ mood, insomnia, lethargy, moodiness?
loss of libido
problems/ tension in sexual relationship?
any stress from work/ other sources?
Page 21
Any systemic features: SoB, ↑°c, night sweats, Kg ↓, loss of appetite?
Cardiovascular
chest pain, SoB, orthopnoea, palpitations, dizziness, ankle swelling
Respiratory
SoB, exercise tolerance, PND, wheeze, chest pain, cough, haemoptysis,
hoarseness
Gastrointestinal
change in appetite/ diet, Kg loss, dysphagia, odynophagia, change in bowels
Urogenital
abdominal pain, F of micturition, dysuria, urgency, polyuria, haematuria
CNS & PNS
fits, faints, headache, LoC, tremor, m. weakness, paralysis, sensory changes
MSK
muscle/ bone/ joint pain, deformity, swelling, stiffness, limb weakness
Metabolic system
change in BMI/ appetite, alteration in build/ appearance
Past Medical History
Any history of pelvic surgery/ trauma, previous prostate surgery, irradiation to prostate,
CV RFx?
Any past history of:
Thyroid dysfunction, Hypertension, Rheumatic, Epilepsy, Asthma, Diabetes,
Stroke, MI, Jaundice
Any investigations taken (eg CXR, ECG, exercise ECG etc)

Any current or past treatment?
Drug History
Specific: antihypertensives, anti ulcer (eg PPI), lipid lowering, 5a-reductase-i,

antidepressants, anti- ψ, testosterone anabolic steroids
General:
Any drug allergies?
Family History
Specific: CV RFx
General
Social History
Marital Status
Living accommodation
Occupation
Smoker?, alcohol?, recreational drugs?
Page 22
Psychological history:
. Explore stresses either related to home or employment.
• Any symptoms or signs of depression –insomnia, lethargy, low mood.
• Difficulties within a relationship.
• Family or social pressures. •
• Any changes to sexual desire.
• Any anxiety related to performance.
DD:
1- astherosclerotic vasucular disease ( being a smoker)
2- Drug induced ( antihypertensive drugs = Atenolol)
3- psychological
Investigations:
- Haematology: FBC, erythrocyte sedimentation rate, haematinics, clotting screen, group & save. -
- Glycated haemoglobin (cardiovascular risk assessment).
- • Biochemistry: U&Es, LFTs, CRP, lipid profile.
- • Prostate specific antigen (if relevant history).
- • Serum free testosterone.
- • Serum prolactin.
- • Serum FSH / LH.
Page 23
- • ACTH (synacthen) stimulation test.

- • Urinalysis: Microscopy to exclude a genitourinary cause.
- • Radiology: –Duplex ultrasonography to assess vascular function of the penis. –
Ultrasonography of the testes to exclude any abnormality.
- –Transrectal ultrasonography to exclude any pelvic or prostatic abnormality.
- Angiography: It can be useful for planning vascular procedures / reconstruction, particularly
following trauma.
- Injection of prostaglandin E1: This outpatient investigation includes the injection of prostaglandin
E1 directly into the corpora cavernosa and to assess rigidity after ten minutes. While it can help
to evaluate the vasculature, a positive result may still be found with mild vascular disease. It can
also be utilised to assess penile deformities to aid planning of surgical correction.
Treatment :
- Risk factor modification by controlling lipidaemia and diabetes, weight loss, smoking cessation,
increase exercise.
- Phosphodiesterase-5 inhibitor therapy (sildenafil)
- Intercavernous injection therapy (alprostadil)
- placement of a penile prosthesis which may take the form of either a semirigid or inflatable
implant.
Back pain: ( functional back pain ) / cauda equina

5 year history of back pain ,worse in the last 3 years, MRI 4 years ago showed mild degenerative
change , no neurological symptoms , no trauma, disabled husband, work commitment.
- Site –Where exactly do you feel the pain? Can you point to the area?
- Onset –When did you first notice the pain? Did it come on suddenly or gradually? Was there
any history of trauma? Have you had it before? If so , is it the same pain or different?
- Character –What is the pain like?
- Radiation –Does the pain go anywhere else? Does it travel down your legs? If so, how far? - --
* Cord compression / cauda equina: –Have you had any problems with your waterworks?
Bowels? Have your legs been feeling weaker than usual? Have you had any strange sensations
down your legs or buttocks? Have you had any difficulty in gaining an erection?
* Inflammatory –Is your back stiff in the morning? If so , how long does that last for? * * *
* Constitutional –Have you noticed any significant weight loss over the past few months? How is
your appetite? Have you been feeling feverish or ill recently? How has your mood been?
- Timing –Is the pain always there or does it come and go? Is it worse at any particular time of
the day?
- Exacerbating/relieving factors –Does anything make the pain better? Anything make it worse?
Is it made better or worse by movement? Is it made better or worse by rest? Is it worse when lying
down or standing? Is it tender when you press on it? Have you tried taking any painkillers for it? -
-- Severity –If you had to score the pain between 1 and 10, with 10 being the worst pain you can
imagine, how would you score your pain?
Social history:
Who is at home with you?
Her husband is bed ridden and she has to take care of him
Discussion:
My main differential diagnosis will be :

- functional back pain (Mechanical lower-back pain) :
.localised pain that worsens with movement and changes in posture
.history of heavy lifting
. history of previous similar episodes over a number of years
Page 24
. No features of systemic illness, nor neurological symptoms

- I have also to rule out organic pathology: Prolapsed intervertebral disc, spinal mets,
Seronegative spondyloarthropathy( ankylosing spondylitis),Spinal canal stenosis,Non-spinal
causes of back pain( AAA, fibromyalgia, pancreatitis, renal calculi)
Cauda equina:
- Urinary and faecal incontinence
- Sensory numbness of buttocks and backs of thighs and weakness of legs
Investigations:
- A full examination is required, particularly looking for perianal sensory loss and anal tone.
- I would carefully check for a reduction in power and decreased reflexes.
- Back examination and lower-limb neurological examination
- Bloods –FBC, LFTs, U&Es, CRP and ESR Chest X-ray and QuantiFERON-TB Gold if TB
suspected
- MRI (not needed if the history suggests uncomplicated mechanical back pain)
- Urgent MRI/CT scan if cord compression or cauda equina is suspected
- X-ray and a subsequent DEXA scan if a crush fracture is suspected
Management :
Simple back pain (including prolapsed intervertebral disc):
- Advise to stay active and avoid prolonged bed rest Physiotherapy, regular analgesia and
consider short-course muscle relaxants
- Serious pathology or red-flag symptoms: Cord compression –dexamethasone and urgent
surgery; radiotherapy in malignancy
- Cauda equina syndrome –urgent surgery
- refer to social worker
Chest pain : ( PE)

- Site –Where exactly is the pain? Can you point to where it is?
- Onset –When did it start? Did it come on suddenly or gradually? What were you doing at the
time?
- Character –How would you describe the pain?
- Radiation –Does the pain go anywhere?
- Associated factors :
* Breathlessness –Do you get breathless?

* Orthopnoea –Do you ever get breathless when lying flat? How many pillows do you sleep with at
night?
Page 25
* Paroxysmal nocturnal dyspnoea –Do you ever wake up gasping for breath?
* Cough –Have you noticed a cough? Do you bring anything up? Any blood?
* Constitutional –Have you noticed any weight loss? How is your appetite?
* Musculoskeletal –Is the pain worse on movement? Does it hurt to press on the area?
* Do you have any lower limb pain or swelling?
- Timing –Is the pain always there or does it come and go? What brings the pain on? Have you
ever had this pain before?
- Exacerbating/relieving factors –Does anything make the pain better or worse? Is it worse when
you walk? Does it go away with rest? Is there any relation to eating food? Is it better when you
are in any particular position, e.g. sitting up? Is it worse when taking deep breaths? Severity –
How bad is the pain on a scale of 1–10, with 10 being the worst pain you can imagine? How
would you score it at its worst?
Discussion:
Considering :pleuritic chest pain, acute onset of SOB,hemoptysis, my main diagnosis will be
pulmonary embolism , i will also consider:
- pneumonia
- Basal atelectasis
- MI
Manegement:
Investigations:
- CTPA
- V/Q scan
- CXR
- ECG
- ABG
Treatment:
- ABC PROTOCOL
- Non massive : heparin untill APTT 50-60 sec.
- Massive : thromolysis/ embolectomy
Inguinal hernia :
History taking as usual:
-How long have you noticed this symptom?

- What were you doing when you first noticed the bulge?
- Is the bulge always present or does it appear and disappear.
- When does it appear and when does it disappear or what do you do to make it disappear?
- Is there pain on the swelling?( uncomplicated hernia is classically painless)
- Is there change in the overlying skin?
- Is there wound or sore over the bulge?
- Is there discharge ( pain, change in overlying skin and discharge may suggest strangulation or
inflammation )
Ask for other GIT symptoms:
Abdominal pain, abdominal rumbling, abdominal distension, vomiting or constipation (can the
patient link these symptoms with the appearance of the bulge?)
- Is there straining at defecation

- Is there abdominal mass or distension
Page 26
Review of other systems:
All other systems must be reviewed starting from the nervous system. But the clinician should pay
attention to symptoms of chronic obstructive airway disease and obstructive uropathy such as
chronic cough and straining at micturition respectively
Special notes:
ICE:
How does a henia happen?
With straining like you do, there will be muscle tearing , and some gut will protrude through the
defect
Could it be better?
It usually needs a surgical operation for repair, the operation may be in open fashion or key hole
surgery
Where to get back to work?

Few weeks
History:
Stamina tonic : what are the components of it? Is it contains any steroids
Visit of the GUM clinic, foreign travel: did you make test for HIV, When you came back , did you
repeat it?
Groin swelling ( infected femoral pseudo aneurysm):

patient referred from his GP due to the presence of groin abscess
- onset: is that painful swelling in your groin started suddenly or gradually?

- Duration:since when you were experiencing this painful groin swelling?
- Course: during this period , did you notice that the swelling is increasing ,
decreasing or constant in size?
- Severity: how much pain do you feel in this swelling, can you rate your pain out
of 10?
- Associated features:
* fever: did you feel having fever in this period?
* discharge: did you notice having any pus discharging from the site of the
swelling
* Blood: did you notice any blood coming out from the swelling
* Injection: did you have any recent injection or trauma in your groin?
* Pulsatility: do you feel that this swelling is having pulses?
* Ischemic manifestations: do you feel any limb pain or coldness or colour
changes or limb swelling
* Neurologic manifestations: do you have any limb numbness
Rest of items as usual
Page 27
Discussion:
Differential diagnosis:
- infected femoral pseudo aneurysm
- Groin abscess
- Infected hematoma
- Inguinal lymphadenopathy
Investigations:
- duplex ultrasonography
- CT angiography
Treatment :
- ligation of the involved artery with delayed revascularization.
- Non operative treatment : Duplex ultrasound‐guided compression and percutaneous

thrombin injection
- Define pseudoaneurysm : is a collection of blood that forms between the two outer
layers of an artery, the tunica media and the tunica adventitia. It is usually caused by a
penetrating injury to the vessel, which then bleeds, but forms a space between the
above two layers, rather than exiting the vessel. It may be pulsatile and can resemble a
true aneurysm
- True aneurysm : involves all three layers of the blood vessel
Page 28
COMMUNICATION WITH A PATIENT OR A RELATIVE
Self discharge (DAMA) :
- Hello Mr....., I am..... One of the surgical doctors, i have been told that you
want to leave the hospital, can i ask you first why?
- ...................................
- Ok, i understand that staying in hospitals is frustrating and disappointing
but you have to know that people are only kept in hospitals when
absolutely necessary.
- ..................................
- First let me explain your case, you have what we call (splenic hematoma)
which means a collection of blood around the capsule of your spleen
( spleen is an organ which is present right here in the upper left side of
your tummy), this was due to fracture to your ribs. Your hemoglobin
dropped also by 1 gram which gives the possibility of continued bleeding
which may lead to serious deterioration and danger to your life.
- .................................
- I definitely understand your situation but you have to look also for your own
health. If something bad happened to you, your wife's condition will be
worse as no body will look after here. I can arrange with our social workers
to find a way to give help to your wife until your condition improves.
- .................................
- Ok Mr....., can you repeat for me what i have told you about your condition
so as to be able to know if you understand me right or not.
- .....................................
- Mr......, as i can not discharge you medically, you will have to sign a legal
document stating the exact details of your case and that the continued
admission was medically advised and that the potential sequences have
been explained and that you take the responsibility of any adverse
outcomes.
- .....................................
- Ok, if you felt that your state is deteriorating like feeling drowsy or having
non bearable tummy pain, i suggest that you should attend to the A&E
department immediately and ask them to contact me or the SHO in charge
directly.
- Mr....., you have decided to self discharge and you are going to sign the
appropriate documents, so i am going to sum up what we have been
through. You knew that you have a splenic hematoma and that the medical
advice is to keep you in hospital. You understood the risks of not being in
hospital which include becoming more unwell and possible even may lead
to a danger to your life. You have accepted the responsibility of those risks.
Page 1
Also we have discussed what signs to look for out and that you will return
to hospital if you were more unwell
If you have any other questions please ask me..
Thank you
Consent for OGD, dilatation and biopsy:
- Hello Mr......., i am....... One of the surgical doctors, i have been asked to
talk to you about an investigation we would like to arrange for you. Can i
ask you what do you know so far about this?
- ......................................
- Ok, this is what we call oesphageogastrodudonoscopy which can be
abbreviated to OGD. The camera is called the endoscope which will be
inserted through your mouth down to your food pipe then to your stomach
then along the first part of your small bowel. This camera will relay the
image to a TV screen so we can have a look inside. We shall also make a
widening of the narrow part of your food pipe which was discovered
previously on the barium image. We may also take some samples from
the lining of your food pipe which may help us in figuring out your case.This
will be typically under sedation which will make you slight drowsy and feel
no pain.
- ....................................
- No procedure is without risks. The possible risk may include:
. Damage to your teeth from the introduction of the scope
. Infection such as chest infection
. Bleeding from the sites of tissue samples
. The most serious risk is cutting through your food pipe wall which may need
a surgical operation for repair
-......................................
- listing those risks doesn't mean that they will essentially happen. My advice
is to accept doing this investigation as it is very crucial in determination of
your case. Also you have to know that only skilled and experienced
surgeons are the only allowed to perform such procedures.
- ....................................
- This is most probably due to the narrowing present inside your food pipe
which hinders your regular secretions to flow downwards smoothly
- ....................................
- Still early to confirm that, we will have to wait until the results of this
investigation appear and probably we may need to do further investigations
to figure it out
Page 2
- ...................................
- It usually appear within 2 weeks time frame, i can understand your
apprehension and will make sure to contact you once it is available
- (close the consultation and ask if any other questions)
Anxious mother ( 1) :
- Hi, i am..... One of the surgical doctors, i apologize that you have not been
contacted before. I will tell you everything about your child condition but let
me know first what so far did you know about what happened?
-.....................................
- Mrs.....,your child apparently felt off his climbing frame and probably
seriously himself. I apologize that you couldn't see him before taken to the
theater but the case was an emergency and we could not wait until you
arrive.
- ..........................,,,,,,,,
- Unfortunately, The scan we have made when he came in suggested that
he had a ruptured spleen ( which is an organ present inside his tummy in
the upper left side) and he is now being operated to fix that
- ..................................
- A ruptured spleen is definitely a serious condition, that's why he was taken
urgently to the theater. You have to know that he is now in very good and
experienced hands, however his condition remains serious to the extent
that may affect his life.
- ......................................
- .......................................
- His father told us that your child was playing at garden when he suddenly
called out in pain as he had fallen from a height. He noticed a big bruise on
the left side of his chest so he called an ambulance.
- ....................................................
- I will have to share this information. In any case like yours we have to
make extra precautions to ensure that your child is going to be safe. We
will take some standard procedures like finding out about your child
situation at home. Also we will need to involve a child protection consultant.
We routinely involve child protection services to make sure that anything
we do will be in your child best interest
- ..................................................
- The spleen has some functions in the body's defense mechanism, so if his
spleen is going to be removed, he will need to be vaccinated after that to
protect him against potential infections he may get. Also it will be
recommended to receive lifelong protective antibiotics.
Page 3
- ..............................................
- You have to make sure that our first priority is your chid medical care. We
will ensure that he will make a good recovery. We will not discharge him
until we have undertaken full clinical examination and make sure that his
GP is aware about any concerns.
Again if you need to ask me about anything, please let the nurses call me,
thank you
Anxious mother (2):
- Hello, i am dr....... One of the surgical doctors, i was told to speak with you
about your child condition. Can you first tell me what do you know so far?
- .....................................
- First, you don't have to feel guilty because this could happen anyway. Your
daughter was brought by your neighbor complaining of tummy pain. Our
initial investigation revealed the suspicion of acute appendicitis. She was
managed by our registrar and received some iv fluids and antibiotics. We
are now waiting for the consultant who will operate upon her
- .....................................
- We are suspecting acute appendicitis as this is common condition and also
her signs and symptoms denotes this. But we can not make sure by 100%
until we open and see
- ......................................
- In children specifically there is less fat inside the abdomen, so perforation
can be particularly dangerous. In such case your child may go to a higher
care area
- ..................................
- A small horizontal wound will leave a little scar, but we may need to expand
the wound and this may be disfiguring
- ....................................
- Yes probably, severe infection can block the reproductive tubes in young
girls, so future sub fertility may happen
-
- (close the consultation and thank the mother)
-
Page 4
Angry patient (1):
- Good morning Mr........., my name is Dr..........., i am the orthopedic trainee

covering for my consultant
- .....................
- I understand that you have come today for your knee operation
- ....................
- Mr.,........., i am very sorry to say that but unfortunately my consultant has
been called away for an emergency case and we will be unable to carry out
your case today
- ........................
- Again i do apologize. I can see that your knee has been really troubling
you. It have bern good to have been able to have it done today. I
understand your frustration as i see from your notes that you were
postponed once before. However surgical emergencies have to be
prioritized and this is why my consultant was called away. I am really sorry
for that.
- ...................................
- Sorry, as i told you he is busy now with that emergency case and he will be
unable to pickup my call
- ........................................
- Mr...., It is your right to choose your doctor but i am afraid that also will be
time consuming as the new consultant will study your case from the start
- ......................................
- I am sorry but i am not authorized to do such operations without
supervision
- ......................................
- I am sorry but i Can not give you the next available date just now. We will
call you once we put in a date. But i promise i will mention your
circumstances and emphasize the importance of having you listed the next
possible soonest session.
- .....................................
- I am sorry sir, but if such an emergency should rise again, it will need to be
prioritized
- .....................................
- I can write a letter to your employer explaining the medical reason of why
you will not be able to carryout your job as a post man for now and that you
will need more sick-leave as your procedure has been postponed. Even if
you want i can call him for you
- ..........................................
- Well, there will be some wearing and tearing. However, you should remain
active with non-weight bearing exercises such as swimming to keep the
Page 5
muscles around your knee strong. I can also refer you to a physiotherapist
who will recommend some good exercises to strengthen your knee
- ...........................................
- I can prescribe a different type of pain killer.you should stop diclophenac as
it increases the risks of stomach ulcers
Again accept my sincerest apologies
Counseling a patient before stopping warfarin:
- hello Mr. ......., i am dr. ....... one of the surgical doctors in this department,
i have been told that your are having some concerns regarding stopping
your warfarin pills, can you tell me more about your apprehension towards
this?
- ...............................................
- First let me explain what is warfarin and how it acts. Warfarin is a
medication that thins the blood by preventing the production of certain
chemicals. It is prescribed for patients to prevent or treat the formation of
clots in the blood. In your case you have been prescribed by warfarin to
prevent formation of clots over your artificial valve. As we are going to
operate upon you, we will have to stop this blood thinning effect of warfarin
for the fear that it might cause bleeding during or after the operation. The
problem here is that warfarin has a long duration of action, so to eliminate
its action we have to stop it 5 days before your surgery. But we can not
leave you without protection for this period, so to keep you safe from
formation in clots in the blood , you will be given another injectable drug
which is called (heparin) that will be equivalent in effect to warfarin but has
a shorter duration of action, so it can be stopped only for 12 hours before
surgery.
- ......................................
- Both of them are providing the same required blood thinning effect that will
protect you from formation of clots over your artificial valve, but the
difference is that warfarin has a long duration of action which means it will
be acting up to 5 days of its stoppage while the injectable heparin is having
only 12 hours of action. So as i told you it can be stopped shortly before
your surgery
- ...........................................
- After your surgery is finished and if we are satisfied that there will be no
more bleeding, we will continue giving you this injectable heparin together
with your warfarin tablets till we get sure through some blood investigations
Page 6
that the blood thinning effect of warfarin is regained. In this time we will
stop injectable heparin.
- .......................................
- Yes, during this period in which we are stopping warfarin and started
injectable heparin you will stay in hospital. This will be about 5 days prior to
your surgery.
- .......................................
- You should not stop your diazepam tablets till the morning of surgery but
only with a small sip of water
- ......................
- Summarize, ask the patient if there's still any issues that make any
apprehension., close the consultation, thank the patient
Angry patient (2):
- Hi,Mrs....., i am.......... One of the surgical doctors.i am very sorry that you
have been waiting for too long to see Mr. Mann.
- ......................................
- No, i am not, i am vey sorry he has been called for an emergency. I am
here to see what is wrong and talk to you about what i can do for you.
Definitely i will tell Mr. Mann that you were here and i can arrange another
appointment to meet him.
- .....................................
- I know that is a very tough situation. I knew that he came in couple of days
ago having some tummy swelling for 6 weeks and he was sent to do CT
scan. But unfortunately we have some problems in our CT machine.
- ..................................
- First, let me tell you why we request this investigation. We know that had a
tummy swelling due to accumulation of fluids inside. Some of these fluids
were taken for analysis which showed the presence of cancer cells. What
we need to know from this investigation is what is the kind of this cancer
and where it is coming from and how much it spreads
- ...................................
- As a temporary alternative, we can do an ultrasound scan ( like the jelly
scan of the pregnant women) which will give us an idea about his liver and
whether it contains any suspicious spots or not, also it will give us an idea
about the amount of fluids. Another alternative also is MRI scan which can
be equally helpful as CT, but we have to take Mr. Mann opinion in that. Our
last option is that we may transfer him to another hospital to do the scan.
- ................................
Page 7
- I am so sorry, i agree that we may be a small hospital and probably not

having over resources but we routinely do all the required investigations for
such patients within 2 weeks time frame. So, we will not leave him suffer if
we found that he needs to be moved to somewhere else.
- ....................................
- Well, to tell somebody that he is having cancer, i have to be ready to
answer questions like where it comes from, what is its stage, what are the
options of treatment. For your husband, the only thing that we have in hand
is the fluids analysis which tells that there is cancer.
- .....................................
- We do operations for cancers that we only think it may improve. In your
husband's case, the presence of tummy fluids gives an impression of an
advanced cancer. In cases like this, it will be unkind to put the patient in
suffer and pain with only little benefit.
- ....................................
- Yes, this is due to the presence of much fluids inside his tummy pushing
his lungs so he can not breath well. I will discuss with Mr. Mann if we can
withdraw some of the fluids from his tummy. Also, there are certain
medications which can help him to get rid of these much fluids.
- Summarize again, apologize at the end, ask for any other concerns, close
the consultation, thank the patient.
Page 8
Communication skills : phone call
Oliguria pod1:
( after right hemicolectomy for cecal tumour)
Hello, i'm ......... (SHO, ST1, CT2) working for mr. ..... . I am calling to speak to mr. .......to
ask him an advice about a patient who underwent right hemicolectomy for cecal tumour ,
he has been oliguric now. Could i check that i am speaking to ........
Who is the consultant of the case?
Mr. ........
Summarize your case?
Mr .... Is ....y old , he has been operated 24 h ago by right hemicolectomy for cecal tumour,
,his urine output in the last 8 hours is about (10-20 ml) ,i checked the urinary catheter
which was not blocked. He is tachycardiac , has low grade fever, with mild hypotension,
his abdomen is lax.
His bloods show his Hb dropped from 12-10 , urea is moderately raised, creatinine is
borderline high
What do you think the cause is ?
I think the patient is dehydrated, he received only 1100 ml of normal saline for pod1. Also
on checking the operative notes, there was a blood loss but he received 2 units of blood
Plans of action?
I will start fluid resucitation by giving 1 liter of normal saline over 1 hour and will continually
monitor the patient in the ward . I will repeat bloods tomorrow morning , if no response to
fluid challenge overnight , i will transfer the patient to HDU to insert a central line and
monitor. If bloods shows Hb more dropping, i will start blood transfusion
Do you think that the patient is bleeding?
May be, but i will monitor the vital signs continuously, i will do serial abdominal
examinations.if i found any signs of bleeding i will let you know
Do you think it is anastmotic leak?
For now , the patient is not toxic, his abdomen is lax , but i will do serial abdominal
examinations and prepare for abdominal ultrasound and will let you know if the patient
becomes peritonitic
If you need me to come back?
I will start fluid challenge , will update you subsequently
1
Bile leakage pod4 after lap. Interval cholecystectomy:
Hello, i am .........( SHO, ST1, CT2) working for MR. ...... In ...... Hospital . I am calling to
speak to MR. ......., the hepatobiliary consultant to ask him an advice about a patient , can i
check that i am speaking to Mr....
Summarize your case:
Mr. ..... Is .... Y old previously fit and well who underwent lap. Cholecystectomy 4 days ago.
He has been complaining of abdominal pain since . Today we noticed bile in his abdominal
drain.
Clinically, he is tachycardiac, pyrexic, slightly jaundiced, has generalised abdominal pain,
but his abdomen is lax. His bloods (taken 2 days ago )show elevated bilirubin, elevated
TLC and increased CRP. We have arranged for an abdominal ultrasound which showed
free intra-abdominal collection. We think that this patient has had a bile leakage and we
were hoping to transfer him to your specialist care for definitive treatment.
What are the possible sources of bile leakage?
May be due to:

- cystic duct stump leakage due to slipped clippage or retained CBD stone
- CBD injury
- Accessory cystic duct
- Leakage from the liver bed
What will be your management?
- I started fluid resuscitation and antibiotics

- I will order new set of bloods when i am off the phone
- We need to make an ERCP to delineate the source of leakage and probably to put a
stent ,but this is not available in our hospital now.
Is this urgent?
Yes, for the fear of developing biliary peritonitis
Do you need to arrange with anyone?
Yes, with the bed manager of both hospitals to discuss creating bed whether by facilitating
discharge or repartitioning of patients
2
Refer polytraumatized patient to a cardiothoracic consultant:
Hello, i am ......... (SHO, ST1, CT2) working for mr. ........ In ......... Hospital. I am calling to
speak to Mr. ....... The cardiothoracic consultant to ask him to accept a referral of a
polytraumatized patient with a widened mediastinum on the chest x ray. Could i check that
i am speaking to mr.....

A man aged ...... Came to us on motorcycle RTA , on examination, his GCS= 14 ,his pulse
rate was 120/ min, his BP= 100/80, he has a swollen left thigh.
We did a chest x ray which revealed a widened mediastinum with bilateral hemothorax, we
put a chest drain which drained 200 cc of fresh blood,we could not make CT as the
machine is being serviced for the next 3 hours.
His AXR showed absent psoas shadow , his x-ray on the femur showed fracture of the
shaft .
His bloods: Hb 8.9 , PH 7.32, with low HCO3 ,the patient is known to be diabetic.
We started fluid resuscitation by 4 litres of crystaloids and we cross matched 6 units of
blood but not yet transfused.
What will you do for the cervical spine?
I will support it using a hrad collar
What will you do for the leg?

I will use a Thomas splint
What will you do for the blood pressure?
We started fluid resuscitation and cross matched for blood , but we should not let the blood
pressure rises for the fear of increased hemorrhage
Why having metabolic acidosis?
Patient has a closed fracture of the femur, so compatement syndrome is a possible cause
The patient has a hemorrhagic shock
The patient may have diabetic ketoacidosis
What about the abdomen?
Absent psoas shadow denotes the presence of intra-abdominal collection , so he may

require exploratory laprotomy.
Who will accompany the case?
I will come with one of our anathesia colleagues or ITU colleagues
3
Call consultant to update him about a pod2 mastectomy

patient who her daughter wants to discharge her against
medical advice
78 y old lady , with a background of COPD , milld LVF , underwent mastectomy + axillary clearance
The daughter of the patient whose notes you have, has arrived at the hospital.
The patient was due to go home tomorrow but some complications have
arisen. Notwithstanding this the daughter wants to take her mother home this
afternoon to her house which is 60 miles away. She has persuaded her mother
that this would be the best course of action. You have spent the last 20 minutes
trying, unsuccessfully, to persuade the daughter that discharge today is not in
the patient’s best interest especially to a house 60miles away.
The patient was keen to go home to her own bungalow, however in view of her
complications she should stay in hospital until she is better
The daughter is very determined and wants to have her own way and does not
suffer fools gladly. She is convinced that her mother will be fine going home
with her today You have perceived that it would certainly be a lot more
convenient for the daughter because it will save her from coming to visit her
mother in hospital or at her bungalow She has convinced her mother that it will
be best for her to go home with her today, although the patient would almost
certainly prefer go to her own house when she is well enough to go home. The
daughter is a school teacher and is out at work all day, as is her husband.
They have two teenage daughters and a labrador so the house is busy and
noisy.
The patient has another daughter who lives near to the hospital, but she is a
paranoid schizophrenic.
Ring the on-call consultant surgeon, who is not the patient’s consultant, and
explain that this patient’s daughter wants to take her mother home.
for breast cancer, pod2 she developed axillary discomfort with axillary swelling with SOB
Her daughter wants to take her home .
Hello, i am ......... (SHO, ST1, CT2) working for mr. ........ In ......... Hospital. I am calling to
inform you about a pod2 patient who underwent mastectomy with axillary clearance
Summarize your case
Mrs Janice green 78 y old who had mastectomy with axillary clearance 2days ago for
breast cancer, now she has an axillary swelling and her wound suction drain has 90 ml of
fresh blood , also she experiences SOB. The patient has also a background of COPD and
mild LVF. Now her daughter wants to take her home which is 60 miles away. I spent 20
4
min. Trying unsuccessfully to persuade her daughter that discharge today will not in the
patient best interest
Has the PATIENT made her own decision or has she been bullied into making a decision to go
home today?
I think the daudhter has convinced her mother that it will be best for her to go home with her today,
although the patient would almost certainly prefer go to her own house when she is well enough to
go home.
Is the patient is suffeciently alert to make her own decision?

Yes, she has the competence to make an informed decision
What do you think has happened to this patient?

In view of the fresh blood in the vacuum drain and the swelling in the axilla , there is a
possiblity of a reactionary hemorrhage in the wound site
Also i have to consider the presence of DVT and pulmonary embolism in the view of SOB
What will be your plans of action in the event of these complications?

As for hemorrahge , i will order FBC to check Hb if there was continued bleeding
A wound hematoma may require evacuation later on. If i suspect DVT and PE , i would
arrange for a CTPA and i will manage accordingly
So, what will you do if they were insisting to go home?
I will inform the patient and her daughter about the possible complications which may
occur due to this premature discharge especially for a 60 miles away home. Also i will
inform that the patient will have to sign on a legal document stating that she has the full
responsibility of the discharge against medical advice.
Also i will inform the patient about the warning signs and symptoms that she has to be
alert for such as increasing wound discharge or being more unwell and increasing
shortness of breathing and that she has to seek advice immediately in a nearby hospital or
to come back here
Update the trauma head about a trauma case:

( RTA +open tibio fibular #+ pulsless foot+ abd. Collection)
Hello, i am ...... ( SHO, ST1, ..) , i am calling to speak to MR .....to update him
anout a trauma case ,could i check that i am speaking to MR .....
21 y old male came to A&E departement after RTA , his GCS is 15 at time of
examination, he is hemodynamically stable . He has an open tibiofibular fracture on
5
his left lower limb. Abdominal ultrasound shows free intra abdominal collection , on
examination of the left distal pulses, there was no felt pulses on the left foot
What is the most urgent?
The patient has an open fracture with an arterial damage on his left lower limb, so it
is urgent to interfer with him to avoid ischemia and compartement syndrome
Is the patient is wearing a c-collar?

( info. Is not given in the notes) , i will check for this
Is the patient id dehydrated?
info. Is not given in the notes) , i will check for this
Plans of action?
- I will inform the orthopedics consultant and the vascular consultant
- I will reduce and immobilize the fracture
- I will order Ct - abdomen and pelvis
- I will order CT- head and brain
Speak to ITU registrar to book a postoperative bed and ask

about pre-op. Advice:
( COPD + perforated viscus+ ARF+ metabolic acidosis)
- 73 y old lady brought by her daughter due to sudden abdominal pain and confusion after
she ate her breakfast
- Assesment revealed suspected perforated viscus
- Urgent laparotomy was required
- Call the ITU registrar
(Remember to write down his advice , he will ask you to repeat at the end)
Hello, my name is Mr ....... I am the surgical SHO working for Mr .......at ........ Hospital. I
am calling to speak to the ITU registrar to ask advice on an unwell patient who has been
today admitted and is going to require a laparotomy. I would also like to arrange an HDU
bed postoperatively. Could I check who I am speaking to, please?
Mr...... is a 73 year old with a background of COPD, presented with a perforated viscus
and has gone into acute renal failure, with hypokalemia. His bloods tests show an
potassium of... an creatinine of ...up from a baseline of ........
Her ABG shows a metabolic acidosis, with a high lactate and high negative base excess.
Please could I have some advice on optimisation before theatre and would it be possible
to arrange an HDU bed post_ operative?
Why do you think it is a perforated viscus?

On examination, there is signs of peritonisim, Hb dropped by 2 g, abdominal ultrasound
showed free intraabdominal collection .
What fluid resuscitation will you do?

6
I will start by crystalloids, rapid flush , then to colloids if poor response , i will cross match
for blood in view of rapid Hb drop
What are the pre-operative arrangements do you suggest?
- ECG: to look for arrythmias , AF, signs of hyopkakemia

- repeat CXR
- IDC insertion
- Antibiotics
- check if the patient is on steroids , to give I.v hydrocortisone
- I will keep the o2 saturation lower in the view of chronic COPD
- I will contact the anasthesist to review the patient pre-operative
What are the criteria of admission to ITU ?
- 2 organ systems impaired with acute reversible causes

- Impaired respiratory system requiring mechanical ventilation
- 1:1 nursing care
- 1 organ system chronically impaired with a possible 2nd system is being affected
- Type of o2 mask for COPD: venturi mask

- How much Fio2 suitable to be delivered to COPD patient : 24-28%
- How yo calculate potassium deficit :
Normal serum potassium is 3.5 to 5 mmol/L
reduction of serum potassium by 0.3 mmol/l suggests a total body deficit of 100 mmol. Based on
this formula, a patient with a serum potassium of 2.6 mmol/l needs at least 300 mmol of potassium
for the correction of the deficit
- How to replace potassium :

1. Serum Potassium < 3.0 mEq/L (total body deficit 200-300 meq)
• Give KCl 10 meq IV slowly every hour for 5 doses, then recheck level
2. Serum Potassium: 3.0 to 3.5 mEq/L (total body deficit 100-200 meq)
• Give KCl 10 meq IV slowly every hour for 3 doses, then recheck level
What if i only have 1 ITU bed left and there is asthmatic young lady coming first ?
I will continually monitor the patient in the recovery room untill a bed is available
7
Call a vascular consultant to refer a case of acute limb

ischemia:
- lady admitted for mild diverticulitis,symptoms improving with I.V Abs and I.V fluids,
- now complaining of sudden acute right lower limb pain
- ECG AF+ preventricular complex, sudden right acute limb ischemia,
- ABG metabolic acidosis, hypokalemia
- arterial duplex showing acute ischemia
Question asked:
- summarize your case?
- Is it urgent, can we send it tomorrow morning instead?
Yes , it is urgent, patient has a critical limb ischemia , so early intervention is
extremely needed for the fear of losing the limb
- Do you need cardiologist to review for PVC before transfer?

No, this can be assesed later on
- What do you think of her presumed diagnosis of diverticulitis?

Now , in view of acute limb ischemia and AF , i have to consider the presence of
mesentric ischmia as a cause of this patient abdominal pain
- Do you want to scan the abdomen first?

We will need to scan her abdomen , but i think after the transfer
- Could it be mesentric ischemia?
Yes, it could be , but for now the abdomen is soft and not tender, i will do serial
abdominal examination and if we need we may do CT Scan of the abdomen with
contrast if the renal functions were normal
- Management plan
* correction of hypokalmia
* Correction of AF
* Anticoagulation
* Correction of metabolic acidosis
- What will you tell her family?
I will tell them that the patient has devolpped acute reduction of ciruclation in her
lower limb which may need an urgent intervention and that is why we are going to
transfer her to a vascular consultant
- Ok you can send the patient over
8
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PERIPHERAL LOWER LIMB ARTERIAL EXAMINATION

◌lower limb chronic ischemia (intermittent claudication)
◌WIPER:
Wash your hands
Introduce yourself
Permission( explain the procedure)
Exposure
Reposition
A-INSPECTION: (with the patient lying on the couch)
◌General:
1. Inspect the hands looking for nicotine staining, tendon xanthomata, nail fold infarcts and
splinter hemorrhages and nail changes
2. Look at the skin and hair for changes suggestive of arterial disease, i.e., thin/shiny skin
and hair loss.
◌ Specific:
1- Look at the legs for Colour of the legs do they appear pale, cyanosed or red?
2- Scars suggestive of previous surgery (e.g., femoro-distal bypass) or amputated digits
3- Signs of venous insufficiency such as lipodermatosclerosis, venous eczema and atrophy
blanche
3- Venous guttering seen when veins collapse in limbs with peripheral vascular disease and
appear as shallow grooves
4- Ulceration comment on the location, shape depth and size of the ulcer
5- Gangrene
N.B.
Arterial ulcers typically have a “punched out” appearance and are generally found around
pressure areas, i.e., lateral and medial malleoli, tips of the toes, head of the 1st and 5th
metatarsals, the heel and the interdigital clefts –so remember to look between toes and under the
heel. (May often be confused with neuropathic ulceration; venous ulceration commonly occurs
around the gaiter region (medial side) of the leg)
B-PALPATION:
1- Compare the temperature on both legs using the dorsum of your hand. 2-
Check the capillary refill time in toes of both feet. ( NB: normal = <2 sec) 3-
Say you would like to perform BUERGERS TEST:
1
3
With the patient lying supine, ask if they have any pain or restriction in hip movements. Then lift
both legs slowly (ideally in about 10 degree increments and waiting for 10 seconds at each stage)
and evaluate the angle at which the leg becomes pale or white . This is known as Buerger’s angle
–in normal subjects it should be greater than 90 degrees (even if the limb is flexed further at the
hip, there should be no colour change in the limb). In patients with peripheral vascular disease, the
limb may go pale as it is lifted and reaches a certain angle. If the angle is less than 25-30 degrees,
it suggests severe ischemia.
Once you have established Buerger’s angle, sit the patient up and swing the legs over the side of
the couch. Watch for the foot to reperfuse –in normal subjects there should be no colour change
but in patients with peripheral vascular disease, you will observe the legs becoming a dusky
crimson/purple colour, which is caused by reactive hyperaemia. This represents a positive
Buerger’s test.
4-Palpate the pulses on both legs:

Femoral :felt in the mid-inguinal point , halfway between the pubic symphysis and ASIS.
Popliteal :felt deep in the midline of the popliteal fossa with the knee flexed to ~30 degrees
Posterior tibial: felt posterior to medial malleolus, 2/3rd of the way between the medial malleolus
and the inertion of the Achilles tendon
Dorsalis pedis felt in the 1st webspace, just lateral to the extensor hallucis longus tendon on the
dorsal surface of the foot (dorsiflexion of the hallux may aid palpation)
C- Auscultation : for iliacs and femoral bruits
D-ABPI: =Ankle Systolic Pressure/Brachial Systolic Pressure

The ABPI gives an indication of the severity of peripheral vascular disease where present
.A normal ABPI is >1.0
.If the ABPI is:
-0.7 –1 = mild disease (i.e., patient may present with intermittent claudication)
-0.5 –0.7 = moderate disease (i.e., likely to have rest pain)
-< 0.5 –0.3 (or absolute pressure <50mmHg) = severe disease (i.e., critical ischemia)
◌Complete the exam: Say you would like to:
-Perform a complete neurological examination of the lower limbs

-Perform a full cardiovascular examination
-Perform a vascular examination of the upper limbs
-Feel the abdomen for any evidence of an aortic aneurysm and auscultate for renal and aortic
bruits.
Discussion
A male/female patient who presents with leg pain on walking. He seemed generally stable, but I
noticed a toe amputation on the right. On closer examination he had difficult to palpate dorsalis
pedis and posterior tibial pulses on the right,ABPI was 0.9 on the left and 0.5 on the right,
consistent with claudication in the right leg. My main differential would be atherosclerotic or
diabetic peripheral vascular disease.
2
3
5
THYROID ( goiter)
◌Inspection:
- lumb
- 6s: site ,size, shape, symmetry, overlying skin, scars
- Neck veins.
- Swallow water .
- Protrude tongue.
◌Palpation:
Explain to the patient that you will examine him from behind
- feel the lumb: surface,edge,consistency,fixity,pulsatility
- Feel below the lumb:
- Trachea :
- Swallow water
- Protrude tongue
- Lymph nodes: submental, submandibular, preauricular, postauricular, occipital, post. Cervical,
ant. Cervical, pretracheal, supravlavicular.
◌Percussion:
Sternum
◌Auscultation :
Bruits
◌Thyroid status:
- 1- Hands:
- radial pulse
- tremors:
- Ask the patient to place their arms straight out in front of them
- Place a piece of paper across the backs of their hands
- Observe for a tremor (the paper will quiver)
- 2- Eyes:
- exophthalmos: examine from above
- lid lag:
◌Hold your finger high & ask the patient to follow it with their eyes (head still)
◌Move your finger downwards
◌Observe the upper eyelid as the patient follows your finger downwards
- eye movement:
◌Ask the patient to keep their head still & follow your finger with their eyes
◌ Move your finger through the various axis of eye movement (“H“ shape)
◌Observe for restriction of eye movements & ask the patient to report any double vision or pain
- 3- Leg:
- pretibial myxoedema
- ankle reflex
- proximal myopathy:
◌Ask patient to stand from a sitting position with arms crossed
◌An inability to do this suggests proximal muscle wasting
4
Discussion
◌Differential diagnosis
- Simple MNG
- thyroid neoplasm
Q: How would you manage this patient?

A: I would perform a triple assessment, taking a history as well as my examination, arrange an
ultrasound and a fine needle aspiration or a biopsy. Also i have to check thyroid functions.
Q: If the patient come back with pain on swallowing, difficulty in breathing few months later,
does it change your management?
A: Yes, these are obstrucive symptoms requiring thyroidectomy
Q: Her FNA comes back showing a follicular cell tumour. The report says “unable to differentiate
carcinoma from adenoma”. Why is this?
A: Follicular carcinomas are differentiated from follicular adenomas as they invade the tumour
capsule or surrounding vessels. Therefore histology rather that simply cytology is needed.
Q: What is the next step in the patient’s management following this histological result?
A: This lady needs to be discussed in the MDT and worked up for a total or hemithyroidectomy
5year survival rate of follicular carcinoma: more than 90%.
5
6
7
6
PAROTID
◌Inspection:
-6s
-The contralateral side
-Facial nerve: raise your eyebrow, shut your eyes aganist resistence, blow out your cheek, show your
teeth, tense your neck muscles.
-Oral cavity: inspect the stensen’s duct ( at the level of the upper 2nd molar tooth)
◌Palpation:
Explain to the patient that you will examine him from behind.
-palpate the lumb: ( ask the patient to clench his teeth) surface, consistency, fixity, edges, pulsatility.
-Lymph nodes( as above).
-Palpate the stensen’s duct.
-Bimanual examination.
-Palpate the contralateral side.
Discussion
Diffrential diagnosis of parotid lump:
-Infective: parotitis
-Inflammatory: sjögren syndrome, mikulicz’s syndrome
-Bengin neoplasm: pleomorphic adenoma, warthin’s tumour
-Malignant neoplasm: mucoepidermoid carcinoma, adenoid cystic carinoma, adenocarcinoma, lymphoma
◌Investigations:
-CT , MRI to assess the extent of local, bony, or perineural invasion.
-Us.
-FNAC.
TREATMENT
Superficial parotidectomy.
8
7
SUBMANDIBULAR GLAND
◌Inspection :
-6s.
-The contralateral side.
-The oral cavity : wharton duct on either side of the lingual frenulum.
-Marginal mandibular nerve: show your teeth.
-Hypoglossal nerve: take out your tongue ( deviation to the affected side).
◌Palpation:
Explain to the patient that you will examine him from behind
-palpate the lump: surface, edges, consustency, fixity, pulsatility
-Wharton duct
-Bimanual
-Lymph nodes
-Lingual nerve: touch sensations to ant. 2/3 of the tongue
-Palpate the contralateral side
Discussion
Examination revealed a diffusely enlarged left / right submandibular gland, approximately 4cm in
diameter. There was no associated cervical lymphadenopathy and there was normal flow of clear
saliva into the oral cavity. The neck examination was otherwise normal.
Q: What is your differential diagnosis?
A:
-Submandibular sialolithiasis
-Submandibular neoplasm
Q: How would you investigate this patient?

A:
-ultrasound
-Sialogram if a salivary stone is suspected
-X- ray
-Ct scan
-FNA if a neoplasm is suspected
Q: What are the treatment options?

1. Conservative management: Analgesia, oral antibiotics,
good hydration and gland massage 2.Sialogram can
occasionally be therapeutic, as the injection of contrast can
‘wash out’ the gland 3.If the stone is within the duct then the
duct can be laid open and the stone retrieved. The duct is
then left open as suturing would result in a stricture
4.Sialendoscopy: stone retrieval via endoscopic techniques
5.Submandibular gland excision
9
8
CARDIOVASCULAR EXAMINATION
[mitral reguarge , aortic stenosis, valve replacement, pacemaker] Patient going for elective hernia repair
◌Inspestion+palpation:
-General: walking aids, o2, medications, observation charts, ECG, midline sternotomy scar
-Hands: . Signs of IE( splinter Hges, janeway lesions)
-Tar staining
-Capillary refill
-Palpate the radial pulse ( rate , rhythm, radioradial delay, collapsing pulse)
-Clubbing
-Blood pressure measurement
-Neck: JVP assesment, palpate the carotid pulse
-Eye: mucous membranes, corneal arcus, xanthelasma
-Mouth: oral hygiene, central cyanosis
-Face: malar flush
-Chest : scars( sternotomy, thoracotomy, infraclavicular) Visible apex pulsations Palpate for: apex beat
(5 ICS midclavicular line)
Heaves(ventricular hypertroph
Thrills (palpable murmurs)
◌Auscultation:
(Put your left hand on the carotid pulse to time systole and diastole)
-Mitral area: 5th ICS midclavicular line Pan systolic murmur radiating to the axilla
-Tricuspid area: 4th ICS left parasternal edge
-Pulmonary area: 2nd ICS left parasternal edge
-Aortic area: 2nd ICS right parasternal edge Ejection systolic murmurs radiating to the carotids
-Accentuation maneuvers:
◌These maneuvers cause particular murmurs to become louder DURING expiration:
-Roll onto left side & listen to mitral area with bell during expiration – mitral murmurs (stenosis &
regurgitation)
-Lean forward & listen over aortic area during expiration – aortic murmurs are louder (stenosis &
regurgitation)
-Metallic heart sounds:
One metalic click corresponding to S1= mitral valve replacement Two
metalic clicks corresponding to s2 = aortic valve replacement
- Carotid bruits
- Lung bases
◌Check lower limb for :

-Edema
-Vein graft harvest scars
Discussion
Q: What investigations would you order preoperatively?
A: This patient appears well, but would require a baseline ECG and echo preoperatively. In addition
he would require bloods including an INR as he is on warfarin.
10
Q: How would you manage this patient’s anticoagulation?

A: Here are some general guidelines for stopping anticoagulation. you should always check local policy
and ask the advice of a haematologist.
◌Low thromboembolic risk:
-stop wafarin 5 days pre-op;
-restart wafarin post-op as soon as oral fluids are tolerated.
◌High thrombembolic risk:
-stop wafarin 4 days pre-op and start low molecular weight.
-Heparin (LMWH) at therapeutic.
-Stop the (LMWH) 12-18h pre-op;
-Restart (LMWH) 6hours post-op (assuming haemostasis achieved);
-Restart Wafarin when oral fluids are tolerated;
-Stop (LMWH) when INR is in range again.
◌The patient presents with fever 5 days postoperatively:

Might have infective endocarditis
◌Causes of valve lesions:
11
10
◌Note the pacemaker spikes, no p- waves

◌Indications of pacemaker:
-Permanent Pacemaker Indication:
-Symptomatic Sinus Bradycardia.
-S A Node Disease.
-Symptomatic A V Node Disease.
-Hypertrophic Obstructive Cardiomyopathy (HOCM).
-Dilated Cardiomyopathy (DCM)
-Long Q T Syndrome.
Q: Who would you inform about the pacemaker?
A: An anaesthetist, ideally the consultant who will be doing the case. I would ensure it is clearly
documented in the notes.
Q: What precautions would you take?
A: I would arrange a pacemaker check pre- and postoperatively and contact their pacemaker follow-
up clinic to inform them of the operation and ask for advice.
◌During the operation I would avoid monopolar completely, or limit its use to short bursts only.
The return electrode should be placed so that the pathway between the diathermy electrode and
return electrode is as far away from the pacemaker and leads as possible
I’d ensure that appropriate resuscitation equipment was available.
12
13
11
RESPIRATORY EXAMINATION
◌Inspection+ palpation:
-General: o2 , medications, SOB, ask to take a deep breath and cough
-Hand: tar satining, clubbing, radial pulse, repsp. Rate
-Mouth: central cyanosis
-Lymph nodes: cervical
-Trachea: central or not
-Chest:
◌Scars for thoracotomy: can you put your hand on your hips and bend your elbows forward for me
please.
◌Chest expansion:
-Place your hands on the patient’s chest, inferior to the nipple
-Wrap your fingers around either side of the chest
-Bring your thumbs together in the midline, so that they touch
-Ask patient to take a deep breath
-Observe movement of your thumbs, they should move apart equally
-If one of your thumbs moves less, this suggests reduced expansion on that side Reduced expansion
can be caused by lung collapse / pneumonia.
◌Percussion :
-1st : supraclavicular
-2nd: medial 1/3 of the clavicle
◌Auscultation:
-from the same levels of percussion:
Ask patient to take deep breaths in and out through their mouth.
-Assess quality – Vesicular (normal) / Bronchial (harsh sounding) – consolidation
-Assess volume – quiet breath sounds suggest reduced air entry – consolidation / collapse / Fluid.
◌Added sounds:
- Wheeze – asthma / COPD
- Coarse crackles – pneumonia / fluid
- Fine crackles – pulmonary fibrosis
◌Vocal resonance:
Ask patient to say “99” repeatedly & auscultate the chest again
Increased volume over an area suggests increased tissue density – consolidation/fluid/tumour
◌Back of the chest:

repeat :
-chest expansion
-Percussion and auscultation
-Vocal resonance
14
Discussion
A: Main diagnosis is COPD in a smoker of this age; however asthma is also a possibility
Q: Who would you inform about this?

A: I would inform an anaesthetist, ideally the consultant who will be doing the case, otherwise the
coordinating anaesthetic consultant and the operating surgeon.
Q: What further investigations would you arrange?

A: A chest X-ray to rule out a preop pneumonia or underlying malignancy
Spirometry and respiratory function tests
A baseline ABG to identify preoperative paO2 and PaCO2
Q: How could you try to reduce the risks in a patient with COPD about to undergo an operation?
A:-I would ask the GP to optimise medication before the operation and refer to a respiratory medic if
necessary.
-Any infection should be treated before the operation.
-The patient should be encouraged to stop smoking
-I would arrange chest physio before and after surgery to encourage excretion of excess mucus
-In addition I would inform HDU in case more intensive care is required post operatively
-Use open surgery , not laparoscopic because of co2 pneumoperitoneum
-Use regional anathesisa instead of grneral anathesia
C
◌olfactory nerve:
With eyes closed, ask patient to identify various scents – e.g. coffee,vinegar
- optic nerve: (5)
◌Visual acuity:
1. Stand the patient at 6 metres from the Snellen chart.
2. If patient normally uses distance glasses, ensure they wear them for the assessment.
3. Ask the patient to cover one eye & read to the lowest line they can manage.
4. Visual acuity is recorded as chart distance (numerator) over number of lowest line read
(denominator).
5. Record the lowest line the patient was able to read (e.g. 6/6 which is equivalent to 20/20)
15
16
12
CARNIAL NERVE EXAMINATION

(bitemporal hemianopia, conductive hearing loss -anterior cranial fossa tumour)
◌-olfactory nerve:
With eyes closed, ask patient to identify various scents – e.g. coffee,vinegar
◌ optic nerve: (5)
Colour vision :( not done)
Pupils:
- Direct reflex– shine torch into eye – look for pupillary constriction in that eye
- Consensual reflex – shine torch into eye – look for pupillary constriction in opposite eye
Visual acuity:
1. Stand the patient at 6 metres from the Snellen chart.

2. If patient normally uses distance glasses, ensure they wear them for the assessment.
3. Ask the patient to cover one eye & read to the lowest line they can manage.
4. Visual acuity is recorded as chart distance (numerator) over number of lowest line read
(denominator).
5. Record the lowest line the patient was able to read (e.g. 6/6 which is equivalent to 20/20)
Accommodation reflex:
1. Ask patient to focus on a distant point (clock on a wall / light switch).
2. Place your finger/object approximately 15cm in front of the eyes.
3. Ask the patient to switch from looking at the distant object to the nearby finger / object.
4. Observe the pupils, you should see constriction & convergence bilaterally.
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13
Confrontation:
1. Ask the patient to cover their left eye with their left hand.
2. You should cover your left eye and be staring directly at the patient (mirror the patient).
3. Ask patient to focus on your face & not move their head or eyes during the assessment.
4. Ask the patient to tell you when they can see your fingertip wiggling.
5. Outstretch your arms, ensuring they are situated at equal distance between yourself & the patient.
6. Position your fingertip at the outer border of one of the quadrants of your visual field.
7. Slowly bring your fingertip inwards, towards the centre of your visual field until the patient sees it.
8. Repeat this process for each quadrant – at 10 o’clock /2 o’clock / 4 o’clock / 8 o’clock.
9. If you are able to see your fingertip but the patient cannot, this would suggest a reduced visual field.
10. Map out any visual field defects you detect.
11. Repeat the same assessment process on the other eye.
Fundoscopy:
-Assess for red reflex
1. Position yourself at a distance of around 30cm from the patient’s eyes.
2. Looking through the ophthalmoscope observe for a reddish / orange reflection in the pupil.
-An absent red reflex may indicate the presence of cataract, or in rare circumstances
neuroblastoma.
◌Move in closer & examine the eye with the fundoscope
- Begin medially & assess the optic disc – colour / contour / cupping
- Assess the retinal vessels – cotton wool spots / AV nipping / neovascularization
- Finally assess the macula – ask to look directly into the light – drusen noted in macular degeneration
◌occulomotor + trochlear+ abducent:( eye movement)

- Eye movements:
1. Ask the patient to keep their head still & follow your finger with their eyes.
2. Move your finger through the various axis of eye movement (“H” shape).
3. Ask the patient to report any double vision.
4. Observe for restriction of eye movement
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◌Trigeminal Nerve:
-Sensory: close your eyes, use a cotton wool
-Ophthalmic : forehead , corneal reflex ( not done)
-Maxillary: cheek bones
-Mandibular: jaw angles
-Motor: muscles of mastication
-Close and open your jaw against resistance
-Clench your teeth and feel temporalis and masseter
-Reflexes: corneal reglex , jaw jerk ( not done)
◌ facial nerve:
-Temporal ( raise your eye brows)
-Zygomatic ( close your eyes against resistance)
-Buccal ( blow your cheeks)
-Marginal mandibular( show your teeth)
-Cervical ( tense and flare your neck muscles)
-Chorda tympani( is there any proplems in taste sensations)
◌vestibulochoclear nerve:
-Whisper no. And repeat
◌Rinne test :
1. Tap a 512HZ tuning fork & place at the external auditory meatus & ask the patient if they are able to
hear it (air conduction)
2. Now move the tuning fork (whilst still vibrating), placing its base onto the mastoid process
(bone conduction)
3. Ask the patient if the sound is louder in front of the ear (EAM) or behind it (mastoid process)
Normal = Air conduction > Bone conduction (Rinne’s positive)

Neural deafness = Air conduction > Bone conduction (both air & bone conduction reduced equally)
Conductive deafness = Bone conduction > Air conduction (Rinne’s negative)
◌Weber test:
1. Tap a 512HZ tuning fork & place in the midline of the forehead.
2. Ask the patient where they can hear the sound:
Normal = sound is heard equally in both ears
Neural deafness = sound is heard louder on the side of the intact ear Conductive
deafness = sound is heard louder on the side of the affected ear
◌Vestibular testing :
Ask patient to march on the spot with arms outstretched and eyes closed:
• Normal – patient remains in the same position
• Vestibular lesion – patient will turn towards the side of the lesion
◌glossopharyngeal+ vagus:
-Open your mouth and say AAH ( look for any deviation of uvula and soft palate)
-Ask the patient to cough( asses adduction of both vocal cords by vagus nerve)
-Gag reflex( not done)
◌spinal accessory:
-Trapezius( shrug shoulder against resistance)
-Sternomastoid ( turn head against resistance)
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◌hypoglssal nerve:
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Discussion
[Bitemporal hemianopia]
Q: Where might the lesion be to cause this symptoms?
A: A bitemporal hemianopia is suggestive of a lesion affecting the optic chiasm, where the more
medial fibres cross over to the contralateral eye. This may be either a lesion of the optic chiasm itself or
a mass pressing on it (e.g. a pituitary tumour, craniopharyngioma, meningioma, anterior coomunicating
artery aneurysm)
Q: What else might you expect if a pituitary tumour were the cause of this lady’s bitemporal
hemianopia?
A: The other signs and symptoms of a pituitary tumour can be general or specfic to hormone
production:
◌General - raised intracranial pressure may cause papilloedema (as seen on fundoscopy) or headaches.
◌Specific - hyperpituitarism: this depends on the type of hormone secreted. The most common are
growth hormone and prolactin from pituitary adenomas. The former causes acromegaly and the
latter hyperprolactinaemia.
◌Signs of acromegaly - prognathism, prominent brow, macroglossia, thickening of the skin,
enlargement of hands and feet, hyperhidrosis, carpal tunnel syndrome.
◌Signs of hyperprolactinaemia - increased lactation, loss of libido, erectile dysfunction in males,
amenorrhoea and infertility (anovulatory) in females.
Management
Invesigations:
-hormone assays
-MRI
-CT (disadvantages: poor soft tissue visualization, need for contrast)
Treatment
-antiprolactin ( bromocryptine)
-Surgery( trans-sphenoidal, trans-frontal)
Hemotympanium
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Q: Cause of conductive hearing loss in this patient?

A: Hemotympanum secondary to skull base fracture
Q: What cranial nerves to examine together?

A: Vestibulochoclear+ facial ( they exit together from IAM)
Q: How to fit otoscope?
A: 1. Pull the pinna upwards & backwards – to straighten the external auditory meatus
2. Position otoscope at the external auditory meatus:
-Otoscope should be held in your right hand for the patient’s right ear and vice versa
-Hold the otoscope like a pencil and rest your hand against the patient’s cheek for stability
3. Advance the otoscope under direct vision
4. Look for any wax, swelling, erythema, discharge or foreign bodies
5. Examine the tympanic membrane:
-Colour – pearly grey & translucent (normal) / erythematous (inflammation)
-Erythema or bulging of the membrane? – inspect for a fluid level e.g. otitis media
-Perforation of the membrane? – note the size of the perforation
-Light reflex present? – absence / distortion may indicate ↑ inner ear pressure e.g. otitis media
-Scarring of the membrane? – tympanosclerosis – can result in significant hearing loss
6. Withdraw the otoscope carefully
Management
Ct brain ,audiometry , ENT review
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[anterior cranial fossa tumor]:
-Do AMTS:
◌Abbreviated mental test scoring:
-How old are you?
-What time is it to the nearest hour?
-Can you remember this address? 24 West St. I will ask you this at the end
-What year is it?
-What is the name of this place?
-What is my job? And what is the job of this person (e.g. a nurse)?
-What is your date of birth?
-When did WW2 end?
-Who is the current prime minister?
-Can you count backwards from 20-1?
-What was that address I asked you to remember?
-Score less then 6/10 suggests dementia / delerium
Q: What do you want to look for in fundoscopy?

A: Ophthalmoscopy serves to identify:
- Papilloedema suggestive of sustained raised intracranial pressure (e.g. caused by a tumour or
hydrocephalus). This may be absent in the context of acutely raised intracranial pressure, or there
may be atrophic changes in longstanding chronic disease.
- Haemorrhage into the vitreous humour (Terson’s syndrome) or other intraocular haemorrhage
secondary to a subarachnoid haemorrhage.
Q: Differential diagnosis of anterior cranial fossa tumour

A: Meningioma, olfactory neuroblastoma, sinonasal malignancies
Management
-CT scan
-MRI with gadolinium
-Streotactic biopsy
-Involve neuro-oncology MDT
-treatment is by surgical resection and proton beam radiotherapy
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KNEE EXAMINATION
[LCL + meniscus injury] or [OA]
Look
Look for:
-Swelling: pre-patellar / infra-patellar Scars Muscle wasting Erythema
-Deformities (valgus and varus)
-Asymmetry
-Baker’s Cyst in Popliteal Fossa
-Accessories , e.g., walking stick / crutches
-Observe gait :Ask the patient whether he/she uses any walking aids, then ask him/her to walk across the
room.
Feel
Ask the patient if there are any areas of localized pain
- assess temp.
- Palapte joint lines:
Palpate the following with the knee flexed at 90°:
Patella – palpate the borders for tenderness / effusion
Tibial tuberosity
Head of the fibula – irregularities / tenderness
Tibial & Femoral joint lines – irregularities / tenderness
Collateral ligaments – both the medial and lateral
Popliteal fossa – feel for any obvious collection of fluid (e.g. a Baker’s cyst)
- Measure quadriceps circumference and compare( 10 cm above patella)
- Effusion: patella tab test( large effusuions) :
1. Empty the suprapatellar pouch by sliding your left hand down the thigh to the patella.
2. Keep your left hand in position and use your right hand to press downwards on the patella with
your fingertips.
3. If fluid is present you will feel a distinct tap as the patella bumps against the femur.
Bulge test ( small effusions);
1. Empty the suprapatellar pouch with one hand whilst also emptying the medial side of the joint
using an upwards wiping motion.
2. Now release your hands and do a similar wiping motion downwards on the lateral side of the joint.
3. Watch for a bulge or ripple on the medial side of the joint.
4. The appearance of a bulge or ripple on the medial side of the joint suggests the presence of an effusion.
Move
-ROM: test active and passive flexion and extension + feel crepitus
◌Special tests:
- Ant. Drawer and post. Drawer test:
1. Flex the patient’s knee to 90º.
2. Inspect for evidence of posterior sag as this can give a false positive anterior drawer sign.
3. Wrap your hands around the proximal tibia with your fingers around the back of the knee.
4. Rest your forearm down the patient’s lower leg to fix its position.
5. Position your thumbs over the tibial tuberosity.
6. Ask the patient to keep their legs as relaxed as possible (tense hamstrings can mask pathology).
7. Pull the tibia anteriorly – significant movement suggests anterior cruciate laxity /rupture 26
8. Push the tibia posteriorly – significant movement suggests posterior cruciate laxity /rupture
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- Lachman’s test( ant. Cruciate);

The knee is flexed at 20–30 degrees with the patient supine.
The examiner should place one hand behind the tibia and the other grasping the patient’s thigh.
It is important that the examiner’s thumb be on the tibial tuberosity.
The tibia is pulled forward to assess the amount of anterior motion of the tibia in comparison to the femur
-Valgus stress test: (MCL)

1. Extend the patient’s knee fully.
2. Hold the patient’s ankle between your elbow and side.
3. Place your right hand along the lateral aspect of the knee.
4. Place your left hand on the lower limb (e.g. calf or ankle).
5. Push steadily inward with your right hand whilst supplying an opposite force with the left.
6. If the MCL is damaged your hand should detect the medial aspect of the joint opening up.
-Varus stress test: (LCL)

1. Extend the patient’s knee fully.
2. Hold the patient’s ankle between your elbow and side.
3. Place your right hand along the medial aspect of the knee.
4. Place your left hand on the lower limb (e.g. calf or ankle).
5. Push steadily outward with your right hand whilst supplying an opposite force with the left.
6. If the LCL is damaged your hand should detect the lateral aspect of the joint opening up.
◌If after this assessment the knee appears stable you can further assess the collateral ligaments by repeating
this test with the knee flexed at 30°. At this position the cruciate ligament are not taught so minor collateral
ligament laxity can be more easily detected.
-Mcmurray’s test ( medial and latetal menisci)

◌To test the medial meniscus, the examiner palpates the postero-medial aspect of the knee while extending
the knee and externally rotating the tibia.
◌To test the lateral meniscus, the examiner palpates the postero-lateral joint line while extending
the knee and internally rotating the tibia.
If pain is felt by the subject or if a ‘click’ is felt by the subject or examiner, the test is considered
positive.
Discussion

A: Medial collateral ligament tear
Cruciate injuries
Combination injuries
Bony injuries
Q: What investigations would you perform?

A: Initially I would arrange a weight bearing X-ray of the knee; however the most important investigation
would be a knee MRI.
Q: What to look for in MRI?

A: -increased internal signal intensity in the meniscus.
-abnormal meniscus shape
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Management
◌Nonoperative treatments:
Rest (with weight bearing as tolerated or with crutches)
Ice
Compression bandaging
Elevation of the affected limb to minimise acute swelling and inflammation.
◌Operative:
-Repair or partial menisectomy
◌X ray of OA:
There are four main radiographic signs in osteoarthritis:
1-Narrowing of the joint space
2-Subchondral sclerosis
3-Cyst formation
4-Osetophyte formation
Q: How is osteoarthritis of the knee managed?

A: Conservative
-Maintain or achieve a healthy weight i.e. aim to decrease weight, and therefore force, going through a
joint.
-Regular exercise, with particular attention to strengthening the muscles around the joint. For example in
OA of the knee, cycling is beneficial.
-Analgesia: care to be taken with NSAID’s with relation to gastric irritation.
-Heat application to the joint may offer relief.
-Physiotherapy.
-Intra-articular steroids.
◌Surgical:
-Arthroscopy and arthrocentesis
-Realignment osteotomy
-Total or partial knee replacement
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HIP EXAMINATION
[hip ostearthritis]
Look
-front ,sides,post.
-gait( antalgic gait, telendenberg’s gait)
-Walking aids
-Scars, pelvic tilt, quadriceps wasting, gluteal wasting, lumbar lordosis
Do telendenberg’s test:
1.Place hands on the iliac crests on either side of the pelvis.
2.Ask the patient to stand on one leg for 30 seconds.
3. Observe your hands to see which moves up or down.
4. Normally the iliac crest on the side with the foot off the ground should rise up.
5.Repeat the test on the opposite side.
The test is deemed positive (abnormal) if the pelvis falls on the side with the foot off the ground.
This abnormal result suggests weak hip abductors on the contralateral side of the pelvis
Feel
- palpate the joint( tenedrness or warmth)
- Palpate the greater trochanter
- Measure ( apparent leg length:umbilicus to the tip of medial malleolus)
( true leg length: ASIS to the tip of medial malleolus)
◌Do Thomas test:

1. Place hand under patient’s spine.
2. Passively flex both legs (hips/knees) as far as you are able to.
3. Your hand should detect that the lumbar lordosis is now flattened.
4. Ask patient to fully extend the hip you are assessing:
Incomplete extension suggests a fixed flexion deformity at the hip joint.
5. Repeat the test to assess the contralateral hip joint
Move
-ROM ( active+ passive ) , crepitus:
-Flexion( bring your knee towards your chest)
-Adduction
-Abduction
-Internal rotation(passive only)
-External rotation( passive only)
-Extension( prone or lateral, passive)- ( don’t perform if Thomas +ve)
◌To complete my examination I would assess the neurovascular status of the lower limbs and
examine the joint above and below - knee and spine.
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Discussion Www.Medicalstudyzone.com

A: My top differential for this patient with hip pain and reduced range of movement is osteoarthritis.
Other arthritides should be considered. These include rheumatoid arthritis, pseudogout, gout,
inflammatory or infective arthritis and a reactive arthritis.
Q: How would you investigate and manage this patient?

A: I would take routine bloods, paying particular attention to raised inflammatory markers, which
would alert me to possible infection, and order hip and knee X-rays. If required an MRI of the
affected joint could also be ordered but may be unnecessary.
◌ If this patient had osteoarthritis then management is aimed at alleviating pain and improving the patient’s functional
status. Non-operative measures include weight loss, exercise, physical and occupational therapy. Simple analgesia such
as regular paracetamol and prn NSAID can be prescribed. More invasive measures such as a corticosteroid injection can
be considered, but ultimately the patient may need surgery in the form of an arthroplasty.
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SPINE &LL PERIPHERAL NEUROLOGICAL EXAMINATION

[disc prolapse+ sciatica]
Look
-general: walking aids- gait
-Behind: scars, muscle wasting, scoliosis, abnormal hair growth
-Side: cervical lordosis, thoracic kyphosis, lumbar lordosis
-Front: posture of the head and neck, symmetry of shoulders
Feel
◌Palpate:
-spinous processes and sacroiliac joints
-Paraspinal muscles
Move
◌Assess active movements
-Cervical spine: flexion, extension, lateral flexion, rotation
-Lumbar spine: flexion , extension, lateral felexion
-Thoracic spine: rotation
◌Special tests:
- straight leg raise: +ve in sciatic nerve root impingement due to prolapsed disc
1. Position the patient supine on the bed.
2. Holding the ankle, raise the leg (passively flexing the hip) – keeping the knee straight
3. Normal ROM is approximately 80-90º of passive hip flexion.
4. Once the hip is flexed as far as the patient is able, dorsiflex the foot.
5. The test is positive if the patient experiences pain in the posterior thigh / buttock.
If this causes pain in lower back /thigh/ buttocks, it suggests sciatic nerve root impingement.
-Femoral nerve stretch: +ve in femoral nerve root compression

1. Position patient prone
2. Flex knee
3. Extend hip
4. Plantar-flex foot
◌Positive test = pain felt in thigh/ inguinal region.
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-Schobber’s test: ankylosing spondyolitis

1. Identify position of the posterior superior iliac spine (PSIS) – “dimples of Venus”p
2. Mark the skin in the midline 5cm below PSIS
3. Mark the skin in the midline 10cm above PSIS
4. Ask the patient to touch their toes – full lumbar flexion
5. Measure the distance between the two lines (started at 15cm)
Normally the distance between the two marks should increase to >20cm.
Reduced range of motion can indicate conditions such as ankylosing spondylitis.
◌Peripheral neurological examination:

-TOPCARS
◌Tone:
1. leg roll:roll the patient’s leg & watch the foot – it should flop independently of the leg
2. Leg lift – briskly lift leg off the bed at the knee joint – the heel should remain in contact with the bed
3.Ankle clonus:
Position the patient’s leg so that the knee & ankle are 90º flexed
Rapidly dorsiflex & partially evert the foot
Keep the foot in this position
Clonus is felt as rhythmical beats of dorsiflexion/plantarflexion (>5 is abnormal)
◌Power:
Hip:
- flexion ( L2,L3):raise your leg off the bed & stop me from pushing it down
- Extension ( L4,L5):stop me from lifting your leg off the bed”
Knee:
- extension ( L3,L4) :
- Flexion ( L5, S1):bend your knee & stop me from straightening it”
Ankle:
- dorsiflexion ( L4,L5):point your foot towards your head & don’t let me push it down”
- Plantar flexion (S1,S2):press against my hand with the sole of your foot
Big toe:
- halux extension( L 5):don’t let me push your big toe down”
◌Co-ordination:
-Heel to shin test:
run your heel down the other leg from the knee & repeat in a smooth motion”
◌Reflexex:
-knee jerk : ( L3, L4)
-Ankle jerk: ( L5,S1)
◌Sensations:
-light touch ( dorsal column)
-Pin - prick ( spinothalamic tract)
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Discussion
I examined the peripheral neurology of the lower limbs of this patient with back pain. His gait was
normal, he had a positive Lasegue’s sign on the right, with normal tone, power, co-ordination and
reflexes throughout both lower limbs. He had impaired sensation over the L5 dermatome on the
right leg, to both light touch and pin prick.
Diffrentials
-Disc herniation between L4-5 impinging on the L5 spinal nerve.
-spinal canal stenosis
-Diabetes Mellitus (peripheral neuropathy)
-Vitamin B12 deficiency(subacute combined degeneration of the cord)
-Drug therapy (e.g. anti-retrovirals, thalidomide, phenytoin)
-Heavy metal/chemical exposure (lead, arsenic, mercury)
-Carcinoma (most likely spinal metastases)
-Tabes dorsalis (syphilitics myelopathy).
Management
◌Imaging :
-x ray on lumbosacral spine
-MRI of lumbosacral spine
◌Treatment:
- conservative
- Surgical : discecctomy , laminectomy
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ANKLE EXAMINATION
Simulated patient, played soccer, sprained ankle
Look
(Gait)
Is the patient demonstrating a normal heel strike / toe off gait?
Is each step of normal height? – increased stepping height is noted in foot drop
Is the gait smooth & symmetrical?
Swelling / erythema of the foot or ankle – may suggest injury / inflammatory arthritis / infection
Scars – suggestive of previous injury / surgery
Feel
Ask the patient to lay on a bed.
Assess temperature & compare between legs – ↑ temperature may indicate inflammatory pathology
Assess pulses in both feet – posterior tibial & dorsalis pedis
Palpate the achilles tendon – assess for thickening or swelling
Palpate the joints / bones
Work distal to proximal – assess for tenderness / swelling / irregularity
Squeeze MTP joints – observe patient’s face for discomfort
Tarsal joint
Ankle joint
Medial / lateral malleoli
Proximal fibula
Move
Assess each of the following movements actively & passively (feeling for crepitus).
-Foot plantarflexion – “push your feet downwards, like pushing a car pedal” – 30-40 º
-Foot dorsiflexion – “point your feet towards your head” – 12-18 º
-Foot inversion – grasp ankle with one hand & heel with the other – turn sole towards midline – passive
assessment only
Foot eversion – grasp ankle with one hand & heel with the other – turn sole away from midline – passive
assessment only
◌Special tests:
Simmonds’ test
used to assess for rupture of the achilles tendon
1. Ask patient to kneel on a chair with their feet hanging off the edge.
2. Squeeze each calve in turn.
3. Normally the foot should plantarflex.
4. If the achilles tendon is ruptured there will be no movement of the foot.
The anterior drawer test of the ankle

assesses the integrity of the anterior talofibular ligament (ATFL).
-Technique : With the patient sitting and 10° of plantarflexion, stabilise the tibia, with one hand and
cup the heel with the other, apply an anterior force to the foot.
-Positive test : As with the anterior drawer test in the knee, asymmetrical anterior movement of the
hindfoot in relation to the tibia confirms an ATFL injury.
-.
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The talar tilt test Www.Medicalstudyzone.com
this is a lateral ligament stress test and helps identify a deltoid or calcaneofibular ligament injury.
-Technique : With the patient sitting with the knee flexed to 90°, a valgus or varus force is applied across
the ankle joint, with one hand cupping the heel and the other the tibia.
◌Positive test :
- Asymmetrical opening up in valgus stress indicates a deltoid or medial ligament injury.
-Asymmetrical opening up in varus stress indicates calcaneofibular ligament injury
Diffrentials
-Ankle ligament sprain ( calceneofibular ligament)
-Fracture lateral maleolus, base of fifth metatarsal, cuboid, cuneforms
Management
◌x-ray on ankle joint
◌Xray showed undisplaced fracture of fibula with swelling of the ankle? Management
-Backslab and analgesia
-Rest , ice , elevation to reduce edema
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INGUINOsCRoTAL ExAMINATION
(inguinal hernia, hydrocele)
◌Expose the patient from umblicus to feet

- inspect the lumb , ask the patient to cough
- Palpate the other side
- Palpate the lumb: ask the patient to cough
- Id ASIS, Pubic tubercle: show the position of the lumb in relation to the inguinal ligament
- Ask the patient to reduce the hernia
- Perform DIR test
- Auscultate the lumb
- Examine the scrotum : scrotal neck, transillumination, testis seprable or not
Discussion
Q: What are the differentials for a scrotal swelling?
A: Common differentials include a hernia e.g. a inguinal or femoral hernia, lymph nodes, varicocoele
or a swelling related to the testes, such as a hydrocoele, epididymal cyst, lipoma of the cord or
testicular tumor. Other differentials include infection such as orchitis or epididymitis, testicular
torsion, and a spermatocoele
Management
-Inguinal hernia: mesh repair
Lichtenstein repair: Once the hernia sac has been

removed and any medial defect closed, a piece of mesh, measuring 8 × 15 cm, is placed over the posterior
wall, behind the spermatic cord, and is split to wrap around the spermatic cord at the deep inguinal ring.
Loose sutures hold the mesh to the inguinal ligament and conjoint tendon
Modified Bassini`s Herniorrhaphy: Conjoined tendon and inguinal ligament are approximated using
interrupted non- absorbable monofilament sutures (polypropylene)
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-Hydrocele : surgical procedures
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ABDOMINAL ExAMINATION
Acute cases
all will be presented with observational charts, lab. Data + ECG
-pod6 (post left hemicolectomy anastmotic leakage)- CCRISP APPROACH.

-Acute diverticulitis
-Acute cholecystitis
-Acute appendicitis
Chronic cases
-paraumblical hernia
-Incisional hernia
POD6 ANASTMOTIC LEAKAGE

(after left hemicolectomy)
Stem : patient is presented with shotness of breathing, left shoulder tip pain,abdominal lower
midline covered scar with dressing)
- WIPER
- Note that the patient will simulate SOB , Note the nearby O2 mask
- Ask the patient if he is having any pain at the moment, the patient will point to his abdomen
- Tell the patient that you will examine his tummy and that you will be gentle, and take verbal permission
- Start by light palpation of the RIF , Note : the patient will jump in pain simulating acute abdomen
- Tell the examiner that the patient is experiencing severe abdominal pain , so further abdominal
examination can not be continued, and that you are going to start assessing the patient using the CCRISP
◌AIRWAY : the patient was talking so his airway is patent
◌BRAETHING :
-look for any central cyanosis
-Look for chest wall movements , equal or not
-Palpate for chest expansion
-Percuss the anterior and lateral chest wall only
-Auscultate anterior and lateral chest walls
◌CIRCULATION:
-look for the neck veins
-Look for signs of dehydration (dry tongue, sunken eyes)
Auscultate the heart
◌DISABILITY : ( consciousness level)
-the patient is alert
◌EXPOSURE:
-Offer to remove the dressing to expose the laparotomy wound
-Look and squeeze for the calfs to rule out DVT and PE
◌CHARTS: EWS charts( rising temp., risinig pr, incresing o2 requirements) FBC ( leucocytosis) , ECG ( AF)
Discussion
I examined this patient presented by SOB , Left shoulder tip pain. On general inspection, the patient
looks obviously having SOB and generalized abdominal pain. I started by doing light palpation on his
RIF , which showed that the patient was having severe abdominal tenderness,so
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this patient looked critically ill and therefore i started assessing the patient according to the CCRISP .
- his airway is patent
- breathing: no central cyanosis, equal chest wall movements, percussion note was normal, equal
air entry with no added sounds
- Circulation: no congested neck veins, no signs of dehydration,normal heart sounds
- The patient was alert
- There was no any swelling or pain in his calves
- His charts showed: rising temp., rising pr, increasing o2 requirements
- FBC ( leucocytosis) ,
- ECG ( AF)
So, my main diagnosis for that case is generalized peritonitis secondary to anastomotic leakage
which caused the patient to have sepsis.shoulder tip pain in such case may be due to the presence
of intrabdominal collection causing irritation of the diaphragm
Management
-NBM
-Urinary carheter to monitor output
-NG tube for suction and bowel rest
-May refer the patient to HDU to insert a central
line and monitor
-Fluid resuscitation by crystalloids
-I.V antibiotics
-Bloods: ABG, U&E
-Chest x-ray to rule out any respiratory problem
-CTPA to rule out PE
-Abdominal ultrasound to detect any abdominal
collections
-CT with gastrograffin enema to identify the
leaking anastomosis
This patient will need urgent laparotomy :

Harman’s procedure plus good peritoneal toilet
plus drainage
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ACUTE DIVERTICULITIS
-Perform classic abdominal examination --- > tenderness on LIF, otherwise normal findings
-Note: do not do deep palpation on LIF
-Read the patient charts after completing examination ---- > fever, mild tachycardia
-Stem: severe left side abdominal pain in patient with a long standing history of constipation
GENERAL EXAMINATION
◌ from the end of the bed
-Does the patient look comfortable?
-How is the general appearance and nutritional status?
-Is there any obvious pallor or jaundice?
THE HANDS
Nails, Anaemia, Clubbing (Crohn’s disease, Ulcerative colitis, Cirrhosis)
Leuconychia (Caused by hypoproteinaemia associated with liver disease), Koilonychia (Spoon
shaped nails seen in iron deficiency anaemia) ! Asterixis( liver flap), seen in decompensated
liver disease.
THE FACE
Eyes Anaemia (pale conjunctiva) , Jaundice, Mouth Dentition- Ulcers (Inflammatory
bowel disease, herpes simplex) , Tongue Dehydration- red, beefy (B12 deficiency) - Angular
stomatitis Caused by iron, folate and vitamin B/ C deficiency Also seen in herpes simplex and
oral candidiasis- Hepatic Foetor.
THE ARMS & TRUNK

Spider Naevi are found along the distribution of the Superior Vena Cava
(i.e., above the nipple line) and are associated with oestrogen excess , Purpura, petechiae Can
be caused by low platelets or raised prothrombin time, Gynaecomastia , Signs of pruritus –
scratch marks.
SUPRACLAVICULAR LYMPH NODES

Virchow’s Node in the left supraclavicular fossa can be enlarged in gastric cancer.
LOCAL EXAMINATION
◌Inspection:
- Scratch marks
- Swelling,
- distension
- Caput medusae
- Skin changes (bruising, signs of weight loss)
- Scars Striae
- Any visible pulsations
- Ask the patient to cough or lift his/ her head off the bed to reveal any herniae or signs of peritonism
(the patient will exprience pain in LIF)
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◌Palpation:
Tips:
-Kneel down at the patient’s right side.
-Ask the patient if there is any generalized pain or localized pain.
-Palpate all nine distinct areas of the abdomen starting furthest from you, unless the patient indicates an
area of pain, in which case palpate this area last.
-Look at patient’s face for signs of pain while palpating.
-Palpate the abdomen with flattened fingers.
-start by superficial palpation of the 9 quadrants then by deep palpation and feel the presence of any
masses.
-Liver: Start in the right iliac fossa, asking the patient to take deep breaths in and out. Move your hand
upwards towards the costal margin during inspiration until you feel a liver edge on expiration.
◌If the liver is palpable check the:
-Size (record enlargement in cm below costal margin).
-Texture (soft / firm / hard / nodular) .
-Edge (smooth / irregular) An irregular liver edge suggests metastases.
-Murphy’s test: With your hand in the position of the gallbladder, fingers pointing up, ask the patient to
take a deep breath in and out. Pain on expiration as the gallbladder comes to rest against your fingertips
is a positive Murphy’s test.
-Spleen: Start palpating in the right iliac fossa, using the same breathing technique as for liver palpation.
However, this time move gradually towards the left upper quadrant . Note the size, texture and edge of the
-Kidneys: ‘Ballot’ the kidneys using both hands
-Abdominal aorta: Palpate in the region of the lower epigastrium/ upper umbilical area, slightly towards
the left of the mid-line, deeply for a pulsatile mass. Note the approximate diameter by using both hands to
feel the lateral edges of the mass.
◌Percussion:
-Upper liver border
-Spleen
-Bladder
-Ascites: Start by percussing in the midline towards either flank and note any change in pitch from reso-
nant to dull, indicating fluid . If there is dullness, keep your finger on this area and ask the patient to roll
onto his/ her side so that the dull area is now superior.Percuss again and note any change in pitch back to
resonance . If present, this is shifting dullness.
◌Auscultation:
-Over the left iliac fossa for bowel sounds
-Over the liver for a bruit
-Over the aorta, iliac vessels and the renal arteries for bruits
◌Say you would like to :

-Feel the hernial orifices
-Examine external genitalia (e.g., for testicular atrophy in chronic liver disease)
-Perform a rectal examination
-Examine the lower limbs for peripheral oedema
Questions
◌Differential diagnosis of LIF pain :

-diverticulitis - rectal carcinoma
-constipation - ulcerative colitis 49
-irritable bowel syndrome -ectopic pregnancy
Q: If CT shows only sigmoid wall thickening with one locule of gas seen, what will be your
management?
A:
-antibiotics: co-amoxiclav, garamycin, clindamycin
-Bowel rest
-DVT prophylaxis
Q: If no response to antibiotics , what will you do?

A:
-percutaneous drainage
-Hartman’s procedure
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ACUTE CHOLECYsTITIs
-Stem: right hypochondrial pain since 4 days
-Perform classic abdominal examination ---- > positive murphy sign, otherwise normal examination
-Note: do not do percussions on the liver
-Read the patient charts ------ > fever, undetectable urobilinogen in urine, increased liver enzymes
Differentials
-Acute cholecystitis
-Ascending cholangitis
-PUD
-Lower lobe pneumonia
-Acute pancreatitis
-Renal pathology
Investigations
-liver function tests
-Urea and electrolytes
-Full blood count
-Crp
-Abdominal ultrasound may show dilated CBD and IHBR or my show CBD stone
-MRCP
Treatment
-conservative treatment: (nil by mouth, intravenous fluids, antibiotics /3rd generation cephalsporins +
metronidazole, nasogastric suction if appropriate)
-Surgical treatment: cholecystectomy in 5 days if conservative treatment fails
ACUTE APPENDIcITIs
Stem : RIF pain in simulated young lady
Perform classic abdominal examination ------ > RIF pain , positive rebound, Rovsing , obturator, psoas signs
Examine the patient charts : fever, mild tachycardia, leucocytosis
Special signs
-Rovsing’s sign: Pressure in the LIF causes pain in the RIF with appendicitis
-Obturator sign: Ipsilateral hip and knee are flexed; internal rotation of the hip (heel moves
outwards) stretches obturator internus, which causes pain if in contact with an inflamed appendix.
-Psoas sign : Inflammatory processes in the retroperitoneum irritate the psoas muscle, causing ipsilateral
hip flexion, Straightening the leg causes further pain.
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Differentials
-acute appendicitis
-leaking duodenal ulcer
-pelvic inflammatory disease
-salpingitis
-ureteric colic
-inflamed Meckel’s diverticulum
-ectopic pregnancy
-Crohn’s disease
-Complicated ovarian cyst
Investigations
-urine analysis
-Urea and electrolytes
-Full blood count
-Abdominal ultrasound
-Ct abdomen and pelvis
Treatment
Appendectomy ( open - laparoscopic )
Q:What will you do if you encountered blood in the peritoneal cavity while doing
appendectomy?
A:
-i will call for an obstetric surgeon ( may be ruptured ectopic pregnancy)
-I will order group and save
-I will have to perform appendectomy eventually
PARAUMBLICAL HERNIA
◌Perform classic abdominal examination
-Notes:
◌Inspection:
-Describe any scars and look for other scars, stomas etc
-Ask the patient to lift their head off the bed and look for bulging of the hernia or the scar
◌Palpation:
-Enquire about tenderness and palpate the hernia, commenting on any defect you can feel
-Ask the patient to cough and demonstrate weakness in the scar or abdominal wall, feeling for
bulging of abdominal contents against your hand
-Try to determine the size of the defect
-If there is a midline longitudinal abdominal bulging with no scar, consider divarication of the recti.
◌Auscultation:
Listen for bowel sounds
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Questions
Treatment
open or laparoscopic mesh repair is possible. At open surgery, the mesh can be inserted as an
onlay, inlay, sublay or intraperitoneal position.
c
.
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CHEST PAIN (PULMONARY EMBOLISM)

STEM: chest pain POD 8 after hip replacement or abdominal surgery
This is a potentially unwell patient, therefore you should approach him in an ABC manner
A-you know his airway is patent as he is talking to you
B-inspect chest for respiratory movement, is it equal? Look for central cyanosis, use of accessory muscles,
Feel for chest expansion, tracheal position
-Percuss the chest for dullness / hyper-resonance, test vocal fremitus
-Listen for bilateral air entry, crackles of consolidation or pulmonary oedema
C-Inspect for cyanosis, and look at the JVP
Feel the pulse, making note of any rhythm abnormalities and tachycardia, and peripheries (cold and poorly
perfused v hot and septic).
Auscultate the heart – muffled heart sounds could indicate tamponade, a murmur could suggest a significant
valve lesion
D-GCS / AVPU
E-make a point of checking the calves for a DVT
Then check patient charts
Discussion
This patient presented with acute pleuritic chest pain and shortness of breath 8 days after a hip
operation. I note from their drug chart that they have missed two dose of their subcutaneous heparin.
He is haemodynamically stable, but had saturations of 88% on 2L. This improved with high flow oxygen.
They also had a swollen left calf. Otherwise examination showed a clear chest with good bilateral air entry
and a normal percussion note making a pneumonia and pneumothorax unlikely.
An MI is possible but less likely due to the nature of the pain, however I am awaiting an ECG and troponin.
My top differential is a pulmonary embolus.
Q: What investigation would you arrange now?

A:
-Assuming renal function was within acceptable limits I would arrange a CTPA to exclude a PE
-Chest x-ray
-D- dimer
-ABG : respiratory alkalosis
-ECG:
◌Right ventricular strain pattern – T wave inversions in the right precordial leads (V1-4) ± the inferi- or leads (II, III,
aVF).
◌Right axis deviation
◌SI QIII TIII pattern – deep S wave in lead I, Q wave in III, inverted T wave in III
Q: What is the management of a pulmonary embolism?
A:
Management follows the usual ALS sequence of securing the airway before moving on to breathing where high flow
oxygen is essential and then circulation. Assuming this was all done, the management can be spilt into massive PE and
non-massive PE. Massive PE is characterised by haemodynamic compromise and may require thrombolysis. I would put
out a crash call if the patient presented in this way to get urgent help.
-If the patient is stable, treatment initially with a therapeutic dose of subcutaneous heparin, followed by warfarin is warranted. I
would involve the appropriate medical team to follow this patient up.
Q: If you were scrubbed in a the theatre and have been updated with the patient condition, what
will you do? 56
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VARIcoSE VEINS
◌Inspection:
-Inspect with the patient standing up
-Ensure that the patient is adequately exposed whilst dignity maintained.
-Inspect from all sides -easiest done by kneeling in front of the patient then asking the patient to turn-
around.
◌Look for:
-Varicosities
-Skin changes and ulceration from chronic varicosities and their complications especially the medial
“gaiter” area
-Lipodermatosclerosis
-Venous eczema
-Haemosiderin staining
-“Atrophie blanche” –white patches found in areas of healed ulceration
-Oedema
-Scars from previous surgery, including avulsion scars
-sapheno varix in the groin
- Palpate for saphina varix
◌Palpate :
-Feel at the sapheno-femoral junction (~4cm below and lateral to the pubic tubercle) for a sapheno varix. If
a swelling is present check for a palpable thrill and a cough impulse which
indicates an incompetent valve between the superficial and deep systems
-Feel down the leg over the course of the long saphenous and then short saphenous veins for tenderness
along the veins which may indicate perforator incompetence.
◌Special tests:
◌Telendenberg’s test:
-With the patient lying supine, lift his/her leg to about 45 degrees and gently empty the veins (this may be
aided by “milking” the veins)
-Occlude the sapheno-femoral junction and ask the patient to stand up ensuring that the finger or thumb is
firmly over the junction
-If the superficial veins do not fill and the varicosities are controlled at the level of the sapheno-femoral
junction by occluding it, it strongly suggests sapheno-femoral incompetence. This can be confirmed by
releasing the pressure from the sapheno-femoral junction that will cause the blood to return from the
femoral vein into the saphenous vein (through the incompetent sapheno-femoral junction), resulting in the
varicosities becoming prominent.
-As the patient stands, if the veins fill from below with the sapheno-femoral junction occluded,
incompetent perforators are the most likely cause for the varicosities.
◌Touniquet test:
-The tourniquet test follows the same principle but is easier to perform than Trendelenberg’s test as it uses
a tourniquet to control the sapheno-femoral junction rather than the examiner’s fingers.
It also has the added advantage that if varicosities are due to perforator incompetence, it can be performed
further down the leg to identify the level of the incompetence
-Once the superficial venous system has been controlled with the tourniquet you can perform Perthe’s test
to assess the patency of the deep venous system, particularly important if considering varicose vein surgery
.
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◌Perthe’s test:
With the patient standing and with the tourniquet still around the thigh ask the patient to go up and down on
his/her tiptoes or ask him/her to walk, thus exercising the calf muscles. If the deep venous system is intact,
the calf pumps encourage venous return. However, if the deep venous system is occluded or valves
incompetent, when the patient performs this action venous return is restricted and blood is forced into the
superficial system from the deep system, causing engorgement of the superficial veins associated with a
bursting pain
-hand held doppler assesment:
hold the Doppler probe at a 45 degree angle to the skin at the level of the sapheno-femoral junction and
the squeeze the patient’s calf. In a patient with a competent sapheno-femoral junction you will hear a
short “swoosh” as you squeeze, but this ceases as soon as you let go of the calf. If
however, the sapheno-femoral junction is incompetent, there is a more prolonged “swooooosh” of blood
as it regurgitates back down though the incompetent valve.
-to complete my examination i would examine the arterial system and the abdomen.
Discussion
-On closer inspection of the legs, she has obvious varicosities bilaterally. There were no ulcers,
but I noted venous eczema, lipodermatosclerosis and haemosiderin deposition reflecting chronic venous
insufficiency. Doppler assessment demonstrated incompetence at the saphenofemoral junction.
Q: What further investigations would you arrange?

A:Venous duplex: Duplex ultrasound scan to determine the site of valvular incompetence, ensure patency
of the deep venous system.
Q: What are her management options?

A:
Depends on symptoms and effect on quality of life.
-Conservative: Graduated compression stockings, leg elevation, exercise and avoidance of prolonged
sitting or standing.
-Invasive, non-operative: Foam sclerotherapy, radiofrequency or photocoagulation (Laser) ablation
(under local anaesthesia).
-Invasive, operative (under general anaesthesia): Varicose vein surgery is reserved for symptomatic
patients with skin complications. It can involve ligation of the vein (long or short saphenous) near the site
of incompetence and excision (for the long saphenous) by stripping through small skin incisions to reduce
the risk of recurrence.Varicose veins can be avulsed through small stab incisions (phlebectomies), fol-
lowed by compression bandaging.
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suPERFIcIAL LUMB
◌Inspection :
-Site
-Size
-Shape - hemispherical
-Surface – smooth, irregular
-Skin – any overlying skin changes
-Scars
◌Palpation:
-Tenderness
Temperature
-Surface
-Margins
-Consistency
-Surrounding area
-Pulsatility
-Compressibility
-Reducability
-Fluctuation
Assess regional lymph nodes
Discussion
A:
Lipoma
Sebaceous cyst
Abscess
Soft tissue tumour
Bone tumour
Vascular malformation
Management
◌Investigations:
-Ultarsound
-Tru- cut biopsy
◌Treatment:
-Exicision
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cEREBELLAR ExAMINATION
◌Gait:
1. Stance – a broad based gait is noted in cerebellar disease
2. Stability – can be staggering and often slow & unsteady – can appear similar to a drunk person walking
3. Tandem (‘Heel to toe’) walking – Ask patient to walk in a straight line with their heels to their toes
This is a very sensitive test and will exaggerate any unsteadiness.
4. Romberg’s test – ask patient to put their feet together, keep their hands by their side and close their eyes
(be ready to support them in case they are unsteady!)
This is a test of proprioception – a positive Romberg’s test indicates that the unsteadiness is due t a sensory
ataxia (damage to dorsal columns of spinal cord) rather than a cerebellar ataxia.
◌Head:
- speech ( stacatto): say british constitution
- Nystagmus : follow my fingers by your eyes
◌Arms:
-Pronator drift:
1. Ask patient to close eyes & place arms outstretched forwards with palms facing up
2. Observe the hands / arm for signs of pronation / movement
A slow upward drift in one arm is suggestive of a lesion in the ipsilateral cerebellum.
◌Rebound phenomenon:
Whilst the patient’s arms are still outstretched and their eyes are closed:
1.Ask the patient to keep their arms in that position as you press down on their arm.
2.Release your hand.
Positive test = Their arm shoots up above the position it originally was (this is suggestive of cerebellar
disease).
◌Tone:
1. Support the patient’s arm by holding their hand & elbow.
2. Ask the patient to relax and allow you to fully control their arm.
3.Move the arm’s muscle groups through their full range of movements .
4.Is the motion smooth or is there some resistance?
◌Reflexes:
Assess the patient’s upper limb reflexes, comparing left to right.
1.Biceps(c5, c6)
2.Triceps (c7)
3.Supinator (c6)
In cerebellar disease, there is often mild hyporeflexia.
◌Co-ordination
-Finger to nose test
1.Ask patient to touch their nose with the tip of their index finger, then touch your finger tip.
2.Position your finger so that the patient has to fully outstretch their arm to reach it.
3. Ask them to continue to do this finger to nose motion as fast as they can manage.
4. Move your finger, just before the patient is about to leave their nose, to create a moving target
(↑sensitivity).
An inability to perform this test accurately (past pointing/dysmetria) may suggest cerebellar pathology.
◌Intentional tremors
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◌Dysdiadokinesia
1.Demonstrate patting the palm of your hand with the back/palm of your other hand to the patient.
38
3.Then have the patient repeat this movement on their other hand.
An inability to perform this rapidly alternating movement (very slow/irregular) suggests cerebellar ataxia.
◌Legs:
-tone: leg roll, leg lift
-Reflexes: ( knee, ankle)
-Co-ordination ( heel to shin)
◌To complete my examination , i would do:

◌full neurological examination including:
-Cranial nerves
-Upper and lower limbs
Discussion
Patient has (DANISH) : dysdiadokinesia, ataxic gait, nystagmus, intention tremors, stacatto
speech, hypotonia
My main diagnosis will be cerebellar ataxia due to posterior fossa tumour, other diffrentials include:
- cerebellar metastases due to lung or breast cancer
- Head trauma
- cerebrovascular stroke
- TIA
- MS
Posterior fossa tumors:

-cerebellar astrocytoma
-Primary neuroectodermal tumors
-Medulloblastoma
-Ependymoma and ependymoblastoma
-Choroid plexus papilloma and carcinoma
-Dermoid tumors
-Hemangioblastoma
-Metastatic tumors
-Brainstem gliomas
Management
◌investigations:
-Plain x-ray skull: It may show calcification.
-MRI brain ( enhanced) with gadolinum
-CT brain : CT scan of the posterior fossa is inferior to MRI in diagnostic value because of the artifact
produced from the surrounding thick bone. However, CT scan is helpful for postoperative
follow-up.
-CT ( whole body) to detect primary tumours
-guided biopsy
◌Treatment :
Excision
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HAND ExAMINATION
carpal tunnel syndrome
Wash hands
Introduce yourself
Confirm patient details – name / DOB
Explain examination
Gain consent
Expose patient’s hands, wrists and elbows
Position patient with hands on a pillow
Ask if the patient currently has any pain
Look
◌Dorsum :
-Inspect hand posture – asymmetry / abnormalities
-Scars or swellings
◌Skin colour:
-Erythema – e.g. cellulitis (erythema) / palmar erythema
-Pallor – e.g. peripheral vascular disease / anaemia
◌Deformities:
-Bouchard’s nodes (PIP) / Heberden’s nodes (DIP) – OA
-Swan neck deformity – distal interphalangeal (DIP) joint hyperflexion with proximal interphalangeal (PIP)
joint hyperextension – RA
-Z-thumb – hyperextension of the interphalangeal joint, in addition to fixed flexion and subluxation of the
metacarpophalangeal (MCP) joint – RA
-Boutonnières deformity – PIP flexion with DIP hyperextension – RA
◌Nail changes:
-Nailfold vasculitis – small areas of infarction
-Pitting and onycholysis – associated with psoriasis
◌Palms:
-Inspect hand posture – asymmetry / abnormalities (e.g. clawed hand)
-Scars – e.g. carpal tunnel release surgery
-Swellings
◌Skin colour:
-Erythema – e.g. cellulitis (erythema) / palmar erythema
-Pallor – e.g. peripheral vascular disease / anaemia
- Deformity – Dupuytren’s contracture
- Thenar/ hypothenar wasting – isolated wasting of the thenar eminence is suggestive of carpal tunnel
syndrome.
◌Elbows – psoriatic plaques or rheumatoid nodules.
Feel
◌Dorsum
◌Assess radial nerve sensation by touching:
-First dorsal webspace- radial nerve
◌Assess and compare temperature using the back of your hand:

-Forearm
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-Wrist
-MCP joints
40
- Gently squeeze across the metacarpophalangeal (MCP) joints – observe for non-verbal signs of discomfort
– tenderness may indicate inflammatory arthropathy
- Bimanually palpate the joints of the hand (MCP / PIP / DIP / CMC) – assess and compare for tenderness /
irregularities / warmth
-Metatarsophalangeal (MCP) joint
-Proximal interphalangeal (PIP) joint
-Distal interphalangeal (DIP) joint
-Carpometacarpal (CMC) joint of the thumb (squaring of the joint is associated with OA)
- Palpate the anatomical snuffbox – tenderness may suggest scaphoid fracture

- Bimanually palpate the patient’s wrists Elbows
Palpate the patient’s arm along the ulnar border to the elbow:
-Note any rheumatoid nodules or psoriatic plaques (extensor surface)
Move
- Assess each of the following movements actively first (patient does the movements
independently). Then assess movements passively, feeling for crepitus and noting any pain.
. Finger extension – “open your fist and splay your fingers”
. Finger flexion – “make a fist”
. Wrist extension – “put palms of your hands together and extend wrists fully”
. Wrist flexion – “put backs of your hands together and flex wrists fully”
- Test separately for both sets of flexor tendons:

. Flexor digitorum profundus: stabilise the PIPJ and ask the patient to flex at the DIPJ
. Flexor digitorum superficialis ,: isolate the finger being examined by holding the other fingers in extension,
then ask the patient to flex at the PIPJ
- Assess all movements of the thumb –flexion, extension, abduction, adduction and opposition
NB: To simply check for extension of the thumb, ask the patient to place his/her hand palm down
on the table and see if he/she are able to raise his/her thumb off the table. Feel for integrity of
the Extensor Pollicis Longus tendon.
Function
-Power grip – “squeeze my fingers with your hands”
-Pincer grip – “place your thumb and index finger together and don’t let me separate them”
-Pick up small object or undo a shirt button – “can you pick up this small coin out of my hand?”
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Neurlogical examination
◌Motor:
-Median Nerve:
Test the function of abductor pollicis brevis; with patient’s palm facing up, stabilise the rest of
patient’s hand on the table and ask them to point with the thumb to the ceiling.
-Ulnar Nerve:
Palmar interossei –adduct the fingers
Dorsal interossei –abduct the fingers
Froment’s sign: ask the patient to grasp a piece of paper between the index finger and the thumb.
You then try to pull the paper away. If there is an ulnar nerve lesion, the distal phalanx of the thumb
flexes (due to action of the unaffected flexor pollicis longus) to compensate for the weak muscle
(adductor pollicis) that is supplied by the ulnar nerve. This is a positive Froment’s sign
◌radial nerve:
ask the patient to extend the fingers and wrist against resistance.
◌Sensory:
-Volar aspect of index finger (median n. and C6)
-Volar tip of middle finger (C7).
-Volar tip of little finger (ulnar n. and C8).
-First dorsal web space (radial n).
Special tests
◌Tinel’s test
Tinel’s test is used to identify nerve irritation and is therefore can be useful in the diagnosis of carpal tunnel
syndrome.
◌The test involves the following:
-Tap over the carpal tunnel
-If the patient develops tingling in the thumb and radial two and a half fingers this is suggestive of median
nerve irritation and compression.
◌Phalen’s test
If the h examination findings are suggestive of carpal tunnel syndrome this test may be used to further
support the diagnosis:
-Ask the patient to hold their wrist in complete and forced flexion (pushing the dorsal surfaces of both hands
together) for 60 seconds
-If the patient’s symptoms of carpal tunnel synd
rome are reproduced then the test is positive (e.g burning, tingling or numb sensation over the thumb)
◌To complete my examination , :
-Perform a full neurovascular examination of the upper limbs

-Examine the elbow joint.
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Discussion
-Sensory deficit present on the palmar aspect of the first three digits and radial one half of the fourth digit.
-Motor examination: Wasting and weakness of the median-innervated hand muscles (LOAF muscles) can
be detectable.
-Positive phalen’s and tinel’s tests
◌Differential diagnosis:
-cervical disc disease
-Diabetic neuropathy
The following have been associated with higher risk of CTS.
-Increasing age.
-Female sex.
-Increased body mass index (BMI).
-Square-shaped wrist, short stature, dominant hand.
-Race (white).
-Strong family susceptibility.
-Wrist fracture (Colles).
-Acute, severe flexion / extension injury of wrist.
-Space-occupying lesions within the carpal tunnel (eg, flexor tenosynovitis, ganglions, haemorrhage,
aneurysms, anomalous muscles, various tumours, oedema).
-Diabetes.
-Thyroid disorders (usually myxoedema).
-Rheumatoid arthritis and other inflammatory arthritides of the wrist.
-Recent menopause (including post-oophorectomy).
-Renal dialysis.
-Acromegaly.
-Amyloidosis.
-Repeated activity involving severe force and extreme posture of the wrist / vibrating activity.
Investigations
-Electrophysiologic studies including electromyography (EMG) and nerve conductions studies (NCS) are the
first-line investigations in suggested CTS.
-MRI scan can exclude underlying causes in the carpal tunnel.
-laboratory: blood glucose, thyroid functions
Treatment
-Treatment of underlying disease, if any.
-Conservative management of mild to moderate disease (EMG and NCS) includes: –Splinting the
wrist at night time for a minimum of three weeks –Steroid injection into the carpal tunnel –Non-steroidal
anti-inflammatory drugs (NSAIDs) and / or diuretics
-Surgical treatment is indicated for severe disease, or when conservative management fails and includes
carpal tunnel release.
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REAsT ExAMINATION
Gynecomastia
◌Position :
-Ask the patient to sit upright, ideally on the side of the bed.
-Ask the patient to uncover the breasts at this point.
◌Inspection:
◌Arms by side:
-Position the patient with their hands on their thighs relaxed.
-Scars – small scars (lumpectomy) / large diagonal scars (mastectomy)
-Asymmetry – healthy breasts are often asymmetrical
-Masses – note the size and position- look for overlying skin changes
Skin changes:
-Erythema – infection / superficial malignancy
-Puckering – may indicate an underlying malignant mass
-Peau d’orange – cutaneous oedema – inflammatory breast cancer
Nipple changes:
-Retraction – congenital / underlying tumour / ductal ectasia
-Discharge – may indicate infection or malignancyp
*Scale – may indicate Eczema or Paget’s disease
◌Hands on hips:
Ask patient to place hands on their hips and push inwards (to tense pectoralis major).
-Repeat inspection.
-Observe for any masses once again:
-If a mass is noted, observe to see if the mass moves with the pectoralis muscle
-This is known as tethering and suggests invasive malignancy
◌Arms above head:

Ask patient to place both hands behind their head.
◌Inspect the breast tissue for any evidence of:
-Masses
-Asymmetry
-Dimpling / puckering
Ask the patient to now lean forwards, keeping their hands behind their head.
◌Repeat inspection of the breast tissue as above.
This position will exacerbate any skin dimpling / puckering which may relate to an underlying mass.
◌Palpation:
-Breast:
-Examine the “normal” asymptomatic breast first. Ensure to warm your hands before touching the patient.
-Position the patient laid on the bed at a 45 degree angle.
-Ask the patient to place their hand on the side being examined behind their head.
-Use the flat of your fingers to compress the breast tissue against the chest wall, feeling for any masses.
-Use a systematic approach to ensure all areas of the breast are examined:
-Clock face method – examine each “hour” of the breast
-Spiral method – start at the nipple and work outwards in a concentric circular motion
Axillary tail:
Palpate the axillary tail of breast tissue
Nipple:
ask the patient to squeeze the nipple to demonstrate the presence of discharge
-Yellow / green discharge – suggestive of infection 68
-Bloody discharge – more suspicious of malignancy – e.g. papilloma
44
Axilla:
1. Have the patient sit on the edge of the bed facing you.
2. Support the patient’s arm on the side being examined with your forearm.
3. If you’re examining the right axilla, use your right arm to support the patient’s (vice versa for left).
4. Palpate the axilla with your free hand, ensuring to cover all areas of the axilla:
-Medial / lateral / anterior / posterior walls
-Apex of the axilla
5. Note any lymphadenopathy – malignancy / infection
Other lymph nodes:
Finally perform a general lymph node examination of the following areas:
-Cervical
-Supraclavicular
-Infraclavicular
-Parasternal
◌To complete my examination :

-complete abdominal examination to detect liver enlargement (liver cirrhosis)
-Testicular examination to rule out testicular enlargement( tumor) , or atrophy
-External genitalia examination to rule out hypogonadism
-Check thyroid status to rule out hyperthyroidism
-Check signs of liver failure
-Check signs of renal failure
-Visual field examination to rule out prolactinoma
-Chest examination to rule out bronchial carcinoma
Discussion
◌Bilateral gynecomastia which may be due to:
-liver cirrhosis due to alcoholism ( the main probable cause in this patient) as a result of failure of the liver
to metabolise oestrogens
-Bronchial carcinoma
-Pituitary tumours ( prolactinoma)
-Hyperthyroidism
-Testicular tumours
-Renal failure
-Hypognadism
-Drug related
-Senililty
◌Workup:
Laboratory studies:
-A serum chemistry panel may be helpful in evaluating for renal or liver disease.
-Free or total testosterone, luteinizing hormone (LH), estradiol, and dehydroepiandrosterone sulfate levels
are used to evaluate a patient with possible feminization syndrome.
-thyroid-stimulating hormone (TSH) and free thyroxine levels if hyperthyroidism is suspected.
-Serum prolactin levels , if pituitary tumours were suspected
-Testiclar tumour markers
◌Imaging studies:
-mammogram if 1 or more features of breast cancer are apparent upon clinical examination.
-This can be followed by fine-needle aspiration or breast biopsy, as the case merits.
-Testicular ultrasonogram if the serum estradiol level is elevated and the clinical examination findings
suggest the possibility of a testicular neoplasm.
-Abdominal ultrasound to detect liver cirrhosis 69
-Chest x ray to rule out chest malignancies
70
45
Treatment
- treatment of the underlying cause
◌Surgical :
-Reduction mammoplasty
-mastectomy with preservation of the areola and nipple can be performed
ARTERIo-VENOUS fIsTULa
brachiocephalic fistula with distal ischemia
◌Stem: patient known to be chronic kidney disease and had AV fistula for renal dialysis , the patient had blue
discoluration of his hand and upper limb over night. Examine his upper limb
◌Position: Put the patient’s hands and place his

palms upward on a
white pillow if available
◌Exposure: Expose hand, forearm, shoulder and
chest
Inspection:
◌Fistula:
- site: anterior aspect of forearm
( antecubital fossa)
-size: 3*1 cm
-Shape: oval
-Skin overlying: brown
pigmentation- Erythema
-Surface: regular
-Scars: there is an overlying scar , any aneurysmal dialtations
(localized bulging zone)
◌Extremity:
-arm elevation test:
If the arm is elevated to a level above
that of the heart, the normal AV fistula
will collapse. Even if the patient has a
large “mega-fistula,” it will at least become flaccid. However, if a venous stenosis is present, that portion of
the AV fistula distal to the lesion will remain distended while the proximal portion collapses. If the entire
fistula collapses when the patient’s arm is elevated, one can conclude that the outflow of the fistula is
normal.
-pallor or bluish discoluration ( evidence of ischemia)
-Edema
-venous collateralization over the chest or shoulder that might suggest central venous outflow ostruction.
71
46
◌Palpation:
-Tenderness: not tender
-Temprature: warm
-Pulsatility: The pulse in the fistula may be best appreciated using the fingers (not the palm or thumb) and
should be evaluated along the length of the fistula from the arteriovenous anastomosis through the venous
outflow. very little pulse
should be detected with palpation of the fistula.
-All upper limb pulses have to be evaluated, if any not palpable use handheld doppler
-Augmentation test: When the normal fistula is occluded a short distance from the arteriovenous anasto-
mosis, the arterial pulse at the wrist should be increased or augmented.
-Thrill:
best evaluated using the palm of the hand, rather than the fingers. The normal
hemodialysis arteriovenous fistula is characterized by a soft, continuous, diffuse
thrill that is palpable over the course of the fistula and most prominent over the
arteriovenous anastomosis. It should have both a systolic and diastolic component.
-Direction of flow :
The direction of flow can be easily determined by occluding the fistula with the tip of the finger and
palpating on each side of the occlusion point for a pulse. The side without a pulse is the downstream
(ie, in the direction of flow) side.
◌Auscultation:
The bruit over a well-functioning fistula has a low-pitched, soft, machinery-
like rumbling sound and, like the thrill, has both a systolic and diastolic
component. The bruit is also more accentuated at the arterial anastomosis.
◌Examination to detect extremity ischemia:

Two clinical variants of ischemia are recognized, both with characteristic findings on physical examination
1-Dialysis ischemic steal syndrome :
-hands appear pale or cyanotic and feels cool to the touch
-The radial pulse is generally diminished or absent
-Compression of the fistula augments the distal pulse and may temporarily relieve painful symptom
-Using a Doppler to listen to the bruit over the distal artery frequently aids in this examination. The sound is
significantly augmented when the fistula is occluded.
-With chronic ischemia, ulceration and gangrene at the fingertips may be present
2-Ischemic monomelic neuropathy :
characterized by ischemic changes that are confined to the nerves of the hand and spare other tissues
-paresthesias; and numbness in the hand
-diffuse motor weakness or paralysis:
poor wrist extension (radial nerve), poor function of the intrinsic hand musculature (ulnar nerve), and poor
thumb opposition (median nerve) are typically present.
-the hand is warm, and often a palpable radial pulse or audible Doppler signal is present.
Discussion
Dialysis ischemic steal syndrome( DASS)
Investigations
Arterial duplex study
72
47
Treatment options
1- Restriction of fistula flow through banding, or modulation through surgical revision.
2- ligation of the fistula and creation of a more proximal fistula in the same or the contralateral limb
fooT DRoP : cOMMON PERONEAL NERVE INJURY

◌Stem: patient had radio-frequency ablation for right lower limb varicose veins and now
complaining of numbness
◌Inspection :
- while standing
◌Look for :
-scars ( Stab avulsions scars will be demonstrated over the leg)
-swelling and erythema, which may be present after trauma and may suggest compartment syndrome
-Muscle wasting ( anterior and lateral compartments )
-Fasciculations ( may suggest motor neuron lesion)
-Gait ( The actor will demonstrate high stepping gait on the affected side : The foot hangs with the toes
pointing down, causing the toes to drag on the ground while walking, requiring the patient to lift the leg
higher than normal when walking)
-Ask the patient to walk on the heels ( difficulty on the affected side)
◌Palpation:
-Palpate the course of the common peroneal nerve for local tenderness
-Tinel’s sign (lightly tap over the nerve at the fibular head; tingling or “pins and needles” in the nerve distri-
bution indicates a lesion here)
-Check the popliteal space for masses
◌Peripheral lower limb neurological

examination:
◌Tone : ( normal tone , no clonus)
Ask the patient to keep their legs fully relaxed and “floppy” throughout your assessment.
1. Leg roll – roll the patient’s leg and watch the foot – it should flop independently of the leg
2. Leg lift – briskly lift leg off the bed at the knee joint – the heel should remain in contact with the bed
3. Ankle clonus:
-Position the patient’s leg so that the knee and ankle are slightly flexed, supporting the leg with your hand
under their knee, so they can relax.
-Rapidly dorsiflex and partially evert the foot
-Keep the foot in this position
-Clonus is felt as rhythmical beats of dorsiflexion/plantarflexion (>5 is abnormal)
◌Power: ( weak ankle dorsiflexion, weak eversion)
Assess one side at a time and compare like for like.
Remember to stabilise the joint whilst testing power.
◌Hip:
Flexion (L1/2) – “raise your leg off the bed and stop me from pushing it down”
Extension (L5/S1) – “stop me from lifting your leg off the bed”
ABduction (L4/5) – “push your legs out”
ADduction (L2/3) – “squeeze your legs in”
◌Knee:
Flexion (S1) – “bend your knee and stop me from straightening it”
Extension (L3/4) – “kick out your leg” 73
48
◌Ankle
Dorsiflexion (L4) – “keep your legs flat on the bed…cock your foot up towards your face…don’t let me push
it down
Plantarflexion (S1/2) – “push down like on a pedal”
Inversion (L4) – “push your foot in against my hand”
Eversion (L5/S1) – “push your foot out against my hand”
◌Big toe
Extension (L5) – “don’t let me push your big toe down”
Co-ordination: ( normal)
Heel to shin test –“put your heel on your knee, run it down your shin, lift it up and repeat”
Reflexes: ( decreased ankle reflex with negative babinski sign )

1.Knee jerk (L3/4)
2.Ankle jerk (L5/S1)
3.Plantar reflex (S1):
-Run a blunt object along the lateral edge of the sole of the foot, moving towards the little toe, then medially
under the toes
-Observe the great toe
-Normal result = Flexion of the great toe and flexion of the other toes
-Abnormal (Babinski sign) = Extension of the great toe and spread of the other toes – upper motor neuron
lesion
Sensations: ( dmininished sensations over the dorsum of the foot and the anterolateral aspect of
the lower leg)
Light touch sensation
Assesses dorsal/posterior columns
1. The patient’s eyes should be closed for this assessment
2. Touch the patient’s sternum with the cotton wool wisp to confirm they can feel it
3. Ask the patient to say “yes” when they are touched
4. Using a wisp of cotton wool, gently touch the skin (don’t stroke)
5. Assess each of the dermatomes of the lower limbs
6. Compare left to right, by asking the patient if it feels the same on both sides
Pin-prick sensation
Assesses spinothalamic tracts.
Repeat the previous assessment steps, but this time using the sharp end of a neurotip.
To complete the examination:
- spine examination
- Hip and knee examination
Discussion
Foot drop causes:
1- Common peroneal nerve injury: ( in this case my be due to radio-frequency ablation,
fracture head, neck of fibula, prolonged tight plaster cast, fracture dislocation of the knee)
-weakness of foot dorsiflexion (tibialis anterior muscle),
-Weakness in toe extension (extensor digitorum longus muscle and extensor hallucis longus muscle),
-Weakness in foot eversion (peroneus longus and brevis muscles),
-sensory loss in dorsum of foot.
-sensory loss of the anterolateral aspect of the lower leg
2- Sciatic nerve injury involving common peroneal division ( fracture dislocation of the hip, fracture femur,
hip surgery) 74
49
3- L4 , L5 disc herniation with L5 nerve root compression

( weak hip abduction)
4- Central causes ( motor neuron disease, multiple sclerosis, stroke, brain tumour,Parkinsonism)
- positive babinski sign, hyperactive tendon reflexes
5- Other causes :DM, vit. B12 deficiency, alcohol misuse
investigations
1- Electrodiagnostic studies (EMG/NCS)
2- MRI lumbar spine
3- Blood analysis for a possible metabolic cause like diabetes or alcoholism
Treatment
1- consider an ankle foot orthosis to support the foot while walking and to reduce risk of falling.
2- Consider physiotherapy for specific muscle training if weakness is severe.
3- Surgical treatment:
-exploration , decompression or repair
-Tendon transfer
75
LL peripheral arterial examination : (one limb affected, examine two)
Position : Lying down
Discussion
I examined this pt presented by (Rt or Lt) LL claudicating pain
On inspection: The pt had
Skin changes Skin trophic changes of LL chronic ischemia, in the form of pale
skin especially Lt LL, thin shiny skin, hair loss,
Scars No Scars of previous surgery
Venous There is venous guttering of LL
guttering
Ulcers No Arterial ulcers were noted
Gangrene No tissue loss or previous amputation scars seen
On palpation : There is
Temperature Slight decrease in temperature of LL

Capillary refill Delayed capillary refill
Buerger’s angle Buerger’s angle in LL was 40, with +ve Buerger’s test
& test
Pulses All pulses of both LL were palpable except for (dorsalis pedis &
posterior tibial arteries)
+/- Doppler I used the hand-held doppler for dorsalis pedis & posterior tibial
arteries pulse which revealed dampened monophasic sound
On auscultation : there was no audible bruits over femoral & iliac arteries
ABPI: I started to do ABPI measuring for Lt LL but I couldn’t finish due to time
To complete my examination I would like to examine:
-LL Neuro
-U.L vascular
-CVS
-Abdomen for aortic aneurysm and any bruit over aortic or iliac bruits
My main DD is Lt LL peripheral vascular disease due to DM or atherosclerosis
1
Varicose veins : (Pt has bilateral, stem asks for one side ex)
Position : Standing : except when evacuating veins (milking)
Discussion
I examined this pt presented by (Rt or Lt) VV
On inspection
Varicosities & There are varicosities along the distribution of (LSV or SSV),
perforators and also there are multiple incompetent perforators above &
below knee
Venous There are some signs of chronic venous insufficiency over LL
insufficiency in the form of lipodermatosclerosis, venous eczema, (atrophie
signs blanche, hemosiderin deposition, venous ulcers)
Scars There is no scars of previous operations
Edema No LL edema
On palpation
Saphena varix There is no palpable Saphena varix

Tenderness There is no tenderness over sites of varicosities & incompetent
perforators
By doing
Trendlenberg Trendlenberg test was +ve indicating SFJ incompetence

test
Tourniquet test I did tourniquet test above & below the knee which revealed
presence of multiple incompetent perforators above & below
knee
Perthe’s test Perthe’s test couldn’t be done as complete occlusion of
superficial system of veins couldn’t be achieved due to
presence of multiple incompetent perforators
SFJ Doppler By assessing SFJ by doppler it was incompetent
To complete my examination I would like to examine:
- Arterial system and abdomen
My main DD is 1ry varicose veins with incompetent saphenofemoral junction and

above and below knee multiple incompetent perforators
2
Thyroid : (examine this patient presented by neck swelling)
Position: sitting
Discussion
I examined this pt presented by front neck swelling
On inspection: the swelling turned to be
Site Front of neck in midline

Size About 3x4cm in size
Shape Oval in shape
Surface With irregular surface
Scar No scars of previous operations
Skin Overlying skin doesn’t show any signs of inflammation
Neck veins Neck veins aren’t distended on both sides
Swallowing The swelling is mobile with swallowing
Tongue And not mobile with tongue protrusion
protrusion
On palpation: the swelling has
Surface Nodular surface

Edge Well defined edges
Consistency Firm in consistency
Temperature Skin overlying has normal temperature
Tenderness The swelling is not tender
Trachea Trachea was central
Lymph nodes There are no palpable lymph nodes
Pulsatility The swelling is not pulsatile
Fixity The swelling in mobile and not attached to overlying or
underlying structures(partially overlapped by sternomastoid
muscle)
Get below I could get below the swelling
Pulse And carotid pulses were equally felt bilateral
Do but not say Swallowing & tongue protrusion
On percussion:
The upper end of sternum is resonant denoting no retrosternal extension of the

swelling
On auscultation:
There are no audible bruits heard over the swelling
On examination of thyroid status:
Patient is in euthyroid status
My main DD are SMNG and Thyroid neoplasm
3
Parotid :
Position: sitting
Discussion
I examined this pt presented by neck swelling which revealed that
On inspection
Site The swelling at the area of Rt parotid gland

Size 3x4 cm in size
Shape Oval in shape
Surface With irregular surface
Scars No scars of previous surgeries
Skin And skin has no signs of inflammation
Duct By inspecting the oral cavity for stenson’s duct opening, it has no
“stenson” signs of surrounding inflammation with clear salivary secretions
Other side The contralateral side is free (not swollen, no scars)
Facial N Assessment of facial nerve branches bilaterally was normal
On palpation
Surface The swelling has nodular surface

Consistency Firm consistency
Temperature With normal skin temperature
Tenderness The swelling was not tender
Pulsatility The swelling was not pulsatile
Fixity And not fixed to overlying structures or skin
Duct “stenson” On palpating the duct, there is no palpable stones
Other side The contralateral side is free on palpation
Bimanual On bimanual examination, the deep lobe couldn’t be felt
Lymph nodes There were no palpable lymph nodes
My main DD is Parotid gland neoplasm either benign which is most probably

pleomorphic adenoma or whartin’s tumour or less probable malignant tumour like
mucoepidermoid, adenoid cystic, adenocarcinoma, acinic cell tumour or SCC
4
Submandibular gland:
Position : sitting
Discussion
I examined this pt presented by neck swelling which revealed that
On inspection
Site The swelling is in the anterior triangle of neck, Submandibular

region
Size 2x1 cm in size
Shape Oval in shape
Surface Irregular surface
Scar No scars of previous operation
Skin Skin overlying shows no signs of inflammation
Duct Inspection of oral cavity for wharton’s duct revealed no
“wharton” surrounding inflammation and clear saliva
Other side The contralateral side is free
Nerve Assessment of marginal Mandibular and hypoglossal nerves was
“Marginal normal
Mandibular &
Hypoglossal”
On palpation
Surface The swelling has nodular surface

Consistency Firm consistency
Temperature Normal skin temperature
Tenderness The swelling is not tender
Pulsatility And not pulsatile
Fixity The swelling is fixed to surrounding structures but not to skin
Duct On palpation of wharton’s duct, there is no stones felt
“Wharton”
Other side Other side palpation is free
Bimanual ex On bimanual examination of the floor of mouth, the swelling is
bimanually felt
Lymph nodes There are no palpable cervical lymph nodes
Nerve “lingual” Assessment of lingual nerve is normal on both sides
My main DD are Submandibular neoplasm or Submandibular Sialolithiasis
5
Inguinal hernia : (Main features: anatomical site, reducibility, cough impulse)
Position: standing (lying down during reduction)
Discussion
I examined this pt presented by Rt groin swelling,
On inspection
Site The swelling turned to be in right groin region occupying right

inguinal (Inguinoscrotal) compartment
Scars There is (+/-no) scar of previous operation
Skin The skin shows no signs of inflammation
Cough The swelling shows visible impulse on cough
Other side Inspection of other side is free
On palpation
Other side By palpation, the other side was free

Cough Showing palpable impulse on cough
Temperature On palpation the skin has normal temperature
Tenderness The swelling was non-tender
Relation to It lies above & lateral to pubic tubercle
pubic
tubercle
Reducibility The swelling was reducible (unless the pt couldn’t reduce the
swelling or it was painful to reduce)
DIR test +ve (or I couldn’t be elicited)
On examining the scrotum : the scrotal neck was empty
Scrotal neck The scrotal neck was full (inguinoscrotal) or empty

(bubonocele)
Testis The swelling is separable from testis
Transillumination The swelling is not transilluminating
On auscultation:
- There were some (no) gurgling sounds indicating presence (absence) of

bowel
My main DD is Rt indirect (oblique) inguinal hernia
6
Hydrocele:
Position: standing
Discussion
On inspection:
Site The swelling is completely scrotal with no visible swelling in Rt

groin region
Size It is 3x4cm in size
Shape Oval in shape
Surface Regular surface
Scars There is no scars of previous operation
Skin The skin shows no signs of inflammation
Cough There is no visible impulse on cough
Other side Inspection of other side is free
On palpation
Groin Rt groin region is free

Scrotum The swelling is purely scrotal
Surface With smooth surface
Tenderness The swelling is non-tender
Consistency And soft consistency
On examining the scrotum :
Scrotal neck The scrotal neck is empty

Separation And isn’t separable from testis
Transillumination The swelling shows transillumination
7
AV-fistula:
Position: hand on pillow
Exposure: full U L with shoulder and pectoral region
Discussion
I examined this pt presented by forearm swelling
On inspection
Site The swelling is in anterior aspect of forearm in antecubital fossa,

most probably brachio-cephalic AV fistula
Size It is 3x4cm in size
Shape Oval in shape
Surface Irregular surface
Scars There is overlying scar
Skin The skin overlying has brown pigmentation, no erythema
(+/- aneurysmal dilatation, if +ve thin, shiny, ulcer, ??impending
rupture)
Arm elevation +ve arm elevation test
Ischemia Pale skin distally, without ulcer or gangrene
Edema No edema
Venous No venous collateralization over the chest or shoulder
collateralization
On palpation
Temperature On palpation the skin has normal temperature

Tenderness The swelling was non-tender
Thrill With normal thrill
Pulse Radial pulse is absent and not heard by handheld doppler
Pulsatilty The swelling was not pulsatile (pulsatile if there is outflow
obstruction)
Pulse With +ve pulse augmentation test
augmentation
Compression Radial pulse is augmented with fistula compression (check with
doppler)
On auscultation:
There are audible soft, machinery, low-pitched bruits with systolic and diastolic
components heard over the swelling
There are no murmurs heard over the heart
Extras: Peripheral U L neurovascular examination
8
Gynecomastia:
Position: sitting upright on side of bed
Exposure: both breasts
Discussion
I examined this pt presented by bilateral breast enlargement
On inspection (arm by side, on hips, above head)
Skin There is no erythema

Asymmetry Both breasts are symmetrical
Mass No visible masses
Scars There is no overlying scar
Nipple No nipple retraction or discharge
On palpation (semi-sitting 45 deg, hand on side & behind head)
Mass There are no palpable masses over the breast or axillary tail
Nipple No nipple discharge
Axilla Axillary walls are free
Axillary LN No palpable LNs
Lymphadenopathy No other lymphadenopathy
To complete my examination I would like to :

Examine Visual field to rule out hyperprolactinemia
Check thyroid status to rule out Hypothyroidism,
Do Chest examination to rule out Bronchial carcinoma,
Do abdominal examination to detect liver enlargement (Liver Cirrhosis)
Check sign of Renal failure,
Examine external genitalia to rule out Hypogonadism,
Examine both testes to rule out Testicular tumours
9
Foot drop:
Position: standing, then lying on bed
Exposure: hip to foot
Discussion
I examined this pt presented by foot drop
On inspection (walking & standing)
Gait High steppage gait with difficulty in heel walking

Scar There is stab avulsion scar over the leg
Muscle No muscle wasting or fasciculations
Swelling No swelling
On palpation (lying on bed)
Tenderness There is no tenderness over the course of common peroneal

nerve
Swelling in No swelling in popliteal fossa
popliteal fossa
Tinel sign Tinel sign is negative
Peripheral L L neurological examination
Power All are normal except weak ankle dorsiflexion & eversion
Sensory Decreased sensations over anterolateral part of leg and dorsum
of foot for both light touch and pin prick sensations
Reflexes Normal reflexes with -ve babinski sign
Tone Normal tone, no clonus
Co-ordination Normal co-ordination

Perform spine, hip and knee examination
10
Cerebellar examination:
Position: variable
Discussion
I examined this pt presented by posterior cranial fossa tumour
On examination of:
Gait Broad based gait with ataxia, and inability to perform tandem
gait
-ve Romberg sign
Head Staccato speech
No nystagmus
Upper Limbs
Pronator drift +ve Pronator drift sign

Rebound +ve Rebound phenomenon
phenomenon
Tone Hypotonia
Reflexes Bilateral normal reflexes
Co-ordination Inco-ordination (past pointing)
Dysdiadokinesia With dysdiadokinesia
Intentinal And intentional tremors
tremors
Lower Limbs
Tone Normal tone

Reflexes Bilateral normal reflexes
Co-ordination Inco-ordination (heel to shin)

Perform complete upper & lower limb neurological examination
Examine lower 4 cranial nerves
11
Cardiovascular examination:
Position: semi-sitting
Exposure: chest & abdomen
Discussion
I examined this pt presented by
By Inspection & Palpation
General
Walking aid No walking aids

O2 cylinder or No oxygen cylinder or mask
mask
Drugs No drugs (or Warfarin in Valve replacement)
Face No malar rash

Eye No mucous membrane pallor, no xanthelasma, no corneal
arcus
Mouth Proper oral hygiene
No central cyanosis
Neck Neck veins are not congested
Carotid pulses are equal bilaterally with no palpable thrill (+ve
thrill in AS)
Upper Limb
Nails Average capillary refill time

No clubbing
Tar staining No tar staining
IE signs No signs of IE
Radial pulse Radial pulse is ~, regular rhythm, no R-R delay, no collapsing
pulse
BP ABP is ~
Chest
Scars No scars (or midline sternotomy scar in VR, or Lt infra-clavicular

scar in pace maker)
Apex beats Apex beats are felt in 5th I C space MCL (or displaced in AS)
Heaves No heaves (or LV heaves in AS)
Thrill No thrill (or thrill at 2nd I C space Rt parasternal in AS, thrill at
apex in MR)
12
By Auscultation
Mitral regurge Audible pansystolic murmur over the apex, propagated to axilla
& accentuated in Lt lateral position
Aortic stenosis Audible ejection systolic murmur over 2nd I C space Rt
parasternal, propagated to carotid & accentuated on leaning
forward
Valve Audible metallic click of prosthetic valve
replacement
Valve Audible metallic click of valve replacement with pansystolic
replacement + murmur over the apex, propagated to axilla & accentuated in Lt
MR lateral position
Carotid bruits No carotid bruits
Basal No basal crepitations
crepitations
Lower Limbs examination
Scars No scars of graft harvest

Edema No edema
13
Respiratory examination:
Position: semi-sitting
Exposure: chest & abdomen
Discussion
I examined this pt presented by
By Inspection & Palpation
General
SOB No SOB
O2 cylinder or No oxygen cylinder or mask
mask
Drugs No drugs (may be inhaler)
Mouth There is central cyanosis

Neck Trachea is central
No palpable LNs
Upper Limb
Nails Clubbing
Tar staining Tar staining
Radial pulse Radial pulse is ~, regular rhythm
Chest
Scars No chest wall scars

Shape Barrel-shaped chest
Chest wall Equal expansion on both sides
movement
Respiratory Respiratory rate is ~
rate
By Percussion
- Hyperresonance on both sides
By Auscultation
- Equal air entry on both sides

- Harsh bronchial breathing with expiratory wheezes
- Normal vocal resonance on both sides
14
Spine and peripheral LL neurological examination:
Position: standing (look, feel, move), then lying on bed
Exposure: back and lower limbs
Discussion
I examined this pt presented low back pain
Look
Gait Normal gait, +/- walking aid

Spine No shoulder asymmetry,
inspection No abnormal curvatures,
No scars, deformities, muscle wasting or abnormal hair
Feel
Tenderness There is lower back tenderness

No tender paraspinal muscles or sacroiliac joints
Move
Range of motion No limitaton of movement in flexion, extension or lateral

flexion
Schobber test No limitation in forward flexion
Special tests
Straight leg Positive on affected side

raising and
Lasegue test
Femoral stretch Negative bilaterally
test
Peripheral L L neurological examination
Power All are normal except weak big toe extension

Sensory Decreased sensations over anterolateral part of leg and dorsum
of foot for both light touch and pin prick sensations
Reflexes Normal reflexes with -ve babinski sign
Tone Normal tone, no clonus
Co-ordination Normal co-ordination
15
Hip examination :
Position: standing (look) then lying on bed (feel, move)
Exposure: lower limbs
Discussion
I examined this pt presented with hip pain
Look
Gait Trendlenberg gait, +/- walking aid

Skin No erythema, (+ scar on lateral side for previous operation)
Muscle No muscle wasting
Asymmetry No pelvic tilt
Deformity No visible deformity
Trendlenberg Positive trendlenberg test (sagging of non-operated side)
test
Feel

Tenderness No tenderness (+/- tender anterior part of OA side)
Effusion No effusion
Leg length Equal bilateral leg length
discrepancy
Thomas test Positive on non-operated side (fixed flexion deformity)
Move
Range of motion No limitaton of movement (extension in OA side not done due

to fixed flexion deformity)
16
Knee examination:
Exposure: hip to ankle
Discussion
I examined this pt presented knee pain
Look
Gait +/- walking aid & antalgic gait

Skin No scars or erythema
Swelling No swelling, effusion, bursae or baker cyst
(including back)
Asymmetry No asymmetry
Feel

Tenderness Tender lateral aspect of joint (LCL, meniscus)
Effusion No effusion
Quadriceps Equal quadriceps circumference bilaterally
circumference
Move
Range of motion No limitaton of movement (+/- limited flexion and crepitus in

OA), (+/- limited extension “locking” in meniscus)
Hyperextension No hyperextension
Special tests
Cruciate Intact anterior and posterior cruciate ligaments

ligaments
Collateral Intact bilaterally (+ve varus stress test in LCL)
ligaments
Menisci No meniscal injury (+ve McMurray test in meniscal injury)
17
Ankle examination:
Exposure: knee to ankle
Discussion
I examined this pt presented ankle pain
Look
Gait antalgic gait & +/- walking aid

Swelling No swelling, effusion
Feel

Tenderness Tender lateral malleolas or LCL
Pulse Intact pulse
Move
Range of motion Limited ROM in active and passive movements
Special tests
Simmond’s test Intact achilles tendon

Anterior drawer Intact ATFL
test
Talar tilt test Intact deltoid ligament, possible injury to calcaneofibular
ligament
18
Hand examination:
Position: hands on pillow
Exposure: elbow to hand
Discussion
I examined this pt presented hand pain and parasthesia
Look

Nails No abnormality
Elbow No visible nodules
Feel

Tenderness No tenderness
Elbow No palpable nodules
Move
Range of motion No limitaton of movement
Function
Functions Intact power & pincer grip

Intact fine functions
Neurological examination of upper limb
Motor Intact motor functions

Sensory Parasthesia over radial three and half fingers
Special tests
Tinel test Positive tinel sign

Phalen test Positive phalen test
19
Cranial nerves examination:
Position: sitting
Discussion
Olfactory Stem 3 Bilateral anosmia

Optic Stem 3 Visual acuity: bil decreased acuity to 20/50 on
Snellen chart
Stem 1 Field: Defective temporal field on both sides
(bitemporal hemianopia)
Stem 1 & Pupils: normal direct, consensual &
3 accomodation reflexes
Not Colour vision
done
Stem 3 Fundoscopy: offer only to do and possibilities will
be discussed (optic disc cupping)
Oculomotor, Stem 1 Free in all directions
Trochlear, Stem 3 Defective lateral gaze (abducent)
Abducent
Trigeminal Stem 1 & Normal findings
3
Not Pin prick sensation, jaw jerk & corneal reflexes
done
Facial Stem 1,2 Normal findings
&3
Vestibulocochlear Stem 1 & Normal findings
3
Stem 2 Unilateral conductive hearing loss
Glossopharyngeal, Stem 1 & Normal findings
Vagus 3
Not Gag reflex
done
Accessory Stem 1 & Normal findings
3
Hypoglossal Stem 1 & Normal findings
3
AMTS Stem 3 Score < 6/10 suggesting dementia
20
Abdomen examinations:
Exposure: chest, abdomen, groins
Discussion
Diverticulitis Cholecystitis Appendicitis Paraumbilical &

Incisional hernia
General - No jaundice or pallor
- No signs of dehydration
- No enlarged cervical lymph nodes
- No skin changes over the trunk
- No asterixis, no clubbing or nail changes
Local - No swelling - There is a swelling in
1. the peri-umbilical
Inspection region (elsewhere over
the abdomen in
incisional hernia)
- Increasing in size on
coughing
- No scars - Scar of previous
operation (in incisional
hernia)
- No abdominal distention
- No scratch marks
- No skin changes
- No visible pulsations
Light - No palpable masses - There is a palpable
palpation Tender LIF Tender Rt Tender RIF mass in the peri-
hypochondrium umbilical region (supra,
Deep - No palpable masses infra, Rt, Lt) to the
palpation Don’t do LIF Don’t do Rt Elicit umbilicus (or over the
hypochondrium Rebound scar of previous
tenderness operation in incisional
hernia)
- The swelling is not
tender, shows
expansile impulse on
cough, doughy in
consistency, reducible
- Defect size is ~ cm
Palpation & - Liver is not enlarged
Percussion - Spleen is not enlarged
- Kidneys show not tender renal angle
- No palpable pulsatile masses
- No abdominal collection by percussion
Special - Murphy sign - Rebound
signs tenderness
- Rovsing
- Obturator
- Psoas
Auscultation - Normal bowel sounds
- No audible bruits over aorta, renal, iliac arteries
21
Acute cases:
Position: lying down
Exposure: chest, abdomen
Discussion
POD6 Anastomotic leak Chest pain

Light abdominal Very tender (start from RIF) Not tender (in abdominal
palpation surgery scenario)
Scar Lower abdominal midline Lower abdominal midline
incision or hip scar
Airway - Patent
Breathing - No central cyanosis
- Trachea is central
- Equal chest wall movement bilaterally
- Normal percussion note bilaterally
- Equal air entry bilaterally with no added sounds
Anterior & Lateral walls Anterior, Lateral &
Posterior walls
Circulation - No signs of dehydration
- No congested neck veins
- Normal heart sounds
Disability - Patient is alert
Exposure - Wearing TEDS - Not wearing TEDS
- No swelling on tenderness - Tender (right or left) calf
on both calves
Chart review - rising temp. - Tachycardia
- rising pule rate - increasing o2 reqirements
- decreasing blood pressure
- increasing o2 requirements
- leukocytosis in FBC
- AF in ECG
22
ORDERING A THEATRE LIST
1) strangulated inguinal hernia ( COPD+Pacemaker).

2) Diverticular abscess ( allergic to penicillin and iodine).
3) BKA( IDDM+ MRSA+AF).
General principles:
◌Patients with diabetes go early in the list. : This prevents complications of hypoglycaemia and allows
early return to normal glycaemic control. Peri and post-operative normoglycaemia is essential in order to
reduce rates of surgical site infections.
◌Patients with latex allergies should be considered to be first in the list.: Natural rubber allergies require a
clean theatre and time must be given for previous latex “dust” to settle before starting the case. All latex
products must be removed form theatre or clearly labelled.
◌Children should be operated on early. This minimises distress to the child and the parents.
◌Procedure under local anaesthesia (minor point) : Some surgeons would put local anaesthetic cases
first or last as a professional courtesy to their anaesthetic colleagues. However, it is also practical to place
small local anaesthetic cases between major cases to allow the anaesthetist to recover the last patient
and anaesthetise the next to optimise theatre time.
◌Major procedures should be considered to be early in the list.: Major procedures and patients for cancer
resection should not be cancelled due to time constraints. It is often best to put these cases first or early
on the list.
◌Patients with infection go last in the list. MRSA and C. difficile must go last on a list to prevent cross con-
tamination between patients. If possible, order a list according to USA NRCS guidelines (Clean, Clean-con-
taminated,Contaminated,Dirty).
◌Clinical Priority: . It is important to appreciate the difference in operative priority between emergency
and elective procedures. Life-or limb-threatening conditions must go first on an emergency list.
National Confidential Enquiry into Patient Outcome and Death (NCEPOD)

Criteria for emergency surgery
◌1a. Immediate.:
- Life or limb threatening.
- Simultaneous haemodynamic resuscitation and intervention.
-Ruptured AAA, Ruptured spleen and
-Haemodynamically unstable pelvic trauma.
◌1b. < 6 hours. :

-Life threatening but not immediate.
-Intervention following resuscitation.
- Ischaemic bowel, large bowel obstruction.
◌2. <24 hours.:
-Deterioration of condition that may threaten life.
-Appendicitis (not perforated).
◌3. < 7 days.:
-Deterioration of elective condition.
-Acute cholecystectomy.
◌4. Scheduled. Elective procedure with no threat to life or limb.
Q: What are the current guidelines for perioperative glycaemic control in the
diabetic patient?
◌Patients with diabetes must be prioritised in the operating list.
◌Routine overnight admission is not necessary.
◌Starvation time should be no more than one missed meal.
◌Analgesia and anti-emetics should be used to enable early return to diet and usual
insulin regime.
◌Insulin infusions should only be used if a patient is expected to miss
more than one meal.
◌0.45% sodium chloride with 5% glucose and 0.15% or 0.3% KCl is the
recommended IV fluid.
◌Capillary blood glucose should be measure hourly during and after the any
surgical procedure.
◌The target blood glucose should be 6-10 mmol/L (acceptable range 4-12 mmol/L).
Q: What precautions should be taken in a patient with a pacemaker?

◌Preoperatively:
- the patient should undergo a pacemaker check where a “passport” containing information on the device
model, date of implant, and reason for implant should be available.
- They should have had a recent review by their pacemaker follow up clinic with information regarding
degree of pacing dependency, extent of any heart failure and any particular safety advice communicated
to the anaesthetic and surgical team.
◌Intraoperatively :
- the use of monoplolar should be strictly limited, and not used near the pacemaker device. Where its
use is unavoidable, it should be limited to short bursts. The return electrode should be placed so that the
current pathway is as far away from the pacemaker as possible.
- The theatre should have cardio-pulmonary resuscitation and temporary pacing equipment available.
- The patient’s ECG should be monitored throughout from before induction
Q: What is the difference between bipolar and monopolar diathermy?

A:In monopolar diathermy current passes from the active electrode through the tissues being operated
on to an electrode plate on the patient. The current is disseminated thought a larger surface area of at
least 70 cm2 than it originated in, therefore preventing a heating effect at the plate electrode.
In bipolar diathermy, current passes between the two tips of the active electrodes, therefore only passing
though tissue that lies between the tips. There is no plate electrode
4 Www.Medicalstudyzone.com
Q: What complications are patients with COPD at particular risk from?
A:Patients with COPD have a several fold increase (2.7-4.7x) in postoperative complications including
atelectasis, pneumonia, and respiratory failure.
Q: How can you reduce these?
A:◌The risk of pulmonary complications can be reduced though smoking cessation at least 4-8 weeks
before surgery and early mobilization following surgery.
◌Pre- and postoperative respiratory physiotherapy to provide deep breathing exercises, intermittent
positive pressure breathing, and incentive spirometry can help reduce complications.
◌Postoperatively, adequate pain relief and an upright position in bed should aim to ensure the
patient is able to cough and that the diaphragm is not splinted.
Q: How would you manage warfarin?

A:It depends on her current risk. If the patient has recently been started on warfarin for AF and the AF
is the source of an emboli that has led to vascular problems in the leg to be operated on, then I would
place him in the high risk thromboembolic category. I would take advice from a consultant haematologist.
They might advise that he stop warfarin 4 days before surgery, and commence subcutaneous low mo-
lecular weight heparin. This would be withheld the evening before surgery, and then restarted from 6h
after surgery once haemostasis had been achieved. I would ensure the INR had fallen to below 1.4 before
operating.
Q: What to use in case of iodine allergy?

A:Chlorhexidine based antiseptic instead.
Q: What prophylactic antibiotic in patient with penicillin allergy?

A: vancomycin.
Colostomy preparation:
- Stoma site marking should be done prior to surgery
- stoma has to be made within the rectus abdominis muscle, below the belt line, on a flat surface, and
easily visualized by the patient ( in this case will be on LIF) , avoid skin creases, bony
prominences, scars, drain site
- Involve a stoma nurse and stoma specialist
Q.Type of anesthesia for each case of the list?

Inguinal hernia:(spinal)-regional as being COPD
the other cases : GA
Q.Which antiseptic of the following will be used in patient with MRSA ?

( chlorhexidine)
CANNULATION OF ATLS PATIENT
Preparations:
◌Tell the examiner that you would wash your hands prior to setting up your equipment.
◌Choose an appropriate sized cannula as indicated by the clinical situation :
◌Prepare 10mL of 0.9% normal saline flush in a 10mL syringe.
◌Introduce yourself and include your full name and grade.
◌Ask to check the patient’s identity, “Can I just check you are….. and what is your date of birth?”
◌Explain what you are about to do, why and what the complications are.
◌The patient must give verbal or implied consent for the procedure.
◌Position yourself and the patient, and select an appropriate vein. It can often be helpful to allow the
patient’s arm to hang over the side of the bed in order to distend the veins or offer to warm the patient’s
hands.
◌In general, the veins on the dorsum of the hand should be used and the antecubital fossa should be re-
served for trauma or emergency situations.
Procedure:
1- Apply the tourniquet and offer to don two pairs of gloves for high risk patients.
2- Sterilise the skin with an alcohol wipe and allow it to dry.
3- Do not re-palpate.
4- Check the cannula, apply skin traction and insert cannula until flashback is seen.
5- Flatten off the angle of your approach and advance while removing the needle.
6- Place the needle in the sharps bin.
7- If a blood sample is required, it can be taken from the cannula at this point using a syringe or vacutainer.
8- Release the tourniquet and occlude the vein above the level of cannulation
9- Position the hub on the end of the cannula. Flush with 10ml normal saline ensuring that no resistance is
felt.
10- Apply the appropriate cannula dressing with the time and date of insertion written on it.
11- Dispose off all equipment into a yellow bag.
12- Wash your hands.
13- Offer to document date, time and site of insertion in the patient notes.
Q: What the fluid regimen will you administer?
A:1 liter of crystalloids over 15 min

.
KNOT TYING
◌Tie a braided non- absorbable simple reef-knot:
- The reef knot consists of two throws: the coming down and going up throw.
- To start with, the coming down throw: Pick up the end furthest away from you (the shortest end or the
white end in this example) with your left thumb and ring finger. Then lay the suture over your index and
middle fingers ).
-Using your right hand pick up the other (red) end and lay it up over the left middle and index fingers .
-Bend (flex) the left middle finger under the white end and straighten again so that the white end is behind
the middle finger under tension.
-Keep the red end under tension with your right hand. Now release the white end and draw it through the
loop with fingers of your left hand.
-Lay the knot using some tension.
◌Tie an absorbable braided knot at depth:
- Though the throws are the same for a reef knot, your hands have to move in the vertical plane to tie at
depth.
- This can be tricky when operating and the difficulty is replicated by using a narrow cup on the hand
tying jig in the exam.
- Pass a suture around the hook and tie the first throw of a reef knot.
- Lay the knot by pushing down with the index finger of your left hand and lifting.
the suture vertically with your right hand .
- Tie your second throw of a reef knot
- Lay the knot using your index finger again to put the knot under tension.
◌Perform a hemostatic suture for bleeding tissue using an non- absorbable monofilament suture:
- You will need to use instruments for this part of station and demonstrate safe handling of the sharp
needle.
- Angle the needle perpendicular to the tissue, to one side of the bleeding area.
- Pass the suture through the tissue and re-mount the needle.
- Aim to put the next suture on the other side of the bleeding tissue, through the tissue in the same
direction as the first pass.
- Tie the two ends of the suture under some tension.
Q:What other knots do you know?

A:Surgeon's knot - Granny knot.
Q:What is vicryl is made up from?
A:Polygalactin.
Q:When vicryl is absorped?

A:Within 56–70 days.
Q:how long it holds a tensile strength?

A:For two to three weeks.
Q:Advantages of braided sutures?

A:Greater tensile strength. - Better flexibility.
Q:How to protect tissues while tying at depth?
A:- obtain more light in the field.
- Retraction of tissues outside.
- Making the knot loose then securing it by pushing it down by finger.
DEBRIDMENT OF A CONTAMINATED WOUND

◌Firstly, dirt and debris must be gently removed to expose any underlying tissue damage. It is important to
use a swab on an artery forcep to keep your fingers away from the tissue, as there may be sharp materials
concealed in the wound.
◌Use a systematic approach, starting at the centre of the wound and working out to the periphery. Gently
sweeping the debris away shows that there is a lot of dirt in this wound. After an initial washout, forceps
may be used to inspect the wound.
◌Any foreign bodies should be removed using the forceps; this should prevent any ongoing infection.
◌Deep within this wound, there is a damaged tendon which will need to be repaired at a later stage. Work-
ing systematically around the wound, in an anticlockwise fashion, any devitalised tissue should be identi-
fied and removed.
◌The next step is to irrigate the wound with saline. It is the pulsed pressure of the fluid that is important
for clearing the tissues.
◌A swab is then used to gently mop out and clear the wound. Any deeper areas of damage should also be
irrigated to ensure that the wound is clear.
Q:When is tetanus toxoid / tetanus immunoglobulin indicated?

A:-There are specific guidelines on tetanus prophylaxis for each hospital but in general wound are
considered high risk if they:
- are contaminated with farmyard material such as soil or manure.
- involve the axilla or Feet.
- penetrate into the deep tissues. are animal or human bites.
- have large amounts of devitalised tissue.
◌Areas of devitalised tissue must be removed. In general, it is better to remove too much tissue that too
little.
◌Once the wound is clear, it is important to insert a pack In this case, a saline wick is gently inserted to
hold the wound open and the tail is trimmed to allow easy removal.
FNAC
◌For this technique we will use a 10ml syringe with a green needle and a vial of heparinized saline.
1- The first step is to draw up a little heparinized saline into the syringe. This is then drawn up and down the
syringe as shown.
2- The saline is then expelled, leaving the needle and syringe flushed with heparinized saline.
3- In this specimen, there is a palpable lesion simulating cystic swelling . It is not common practice to use lo-
cal anaesthetic for this procedure, but this may be required if the patient is particularly anxious. It is neces-
sary to obtain some cells for cytology.
4- After cleaning the overlying skin, the needle is passed directly into the lesion.
5- Once the tip of the needle is inside the lesion, the plunger is pulled back with the thumb whilst keeping
the syringe and needle in place with the other fingers.
6- Multiple passes are needed through the lesion to collect an adequate sample.
7- The needle is then removed and you should have a small sample of aspirate in the green portion of the
needle.
8- Using a pair of slides, pre-marked with the patients details, pass a small amount of aspirate onto one
slide as shown. The other slide is then passed across the first to form two smears.
9- One slide will then be air dried and the other sprayed with a fixing agent.
10- The rest of the aspirate can be placed in a pot with some saline, to be spun down for further analysis.
(cytospin container).
SUTURING OF A WOUND
◌You should also ask about the patient's tetanus status, whether they have any allergy and state that you
would like to arrange an X-Ray of the limb to check for foreign bodies.
◌Equipment: Due to time constraints, the correct equipment is usually provided for you and the patient is
already prepared and draped. However, be prepared to clean and drape the wound if asked.
◌Equipment that you may require includes: Sterile gloves and gown. Skin preparation solution (Iodine or
Chlorhexidine in alcohol). Sterile drapes. 10ml syringe. Needles (1 x 21 & 1 x 25 gauge needle). Local anaes-
thetic (1% Lignocaine). Toothed forceps. Skin suture. Suture scissors. Adherent dressing. Gauze swabs.
◌Preparation: If the equipment is not already laid out for you and the patient is not prepared and draped,
firstly open up a wound care pack, pour some antiseptic solution into the receptacle and open the relevant
remaining equipment onto the sterile field. At this point state the need to wash your hands before donning
a pair of sterile gloves.
◌Local anaesthetic: Firstly state that you would like to check the local anaesthetic and its expiry date. Then
attach the 21G needle to the syringe and draw up the desired amount of anaesthetic. Discard this needle
into a sharps bin and mount the 25G needle onto the filled syringe. At this point, if not already done for
you, clean the wound using the antiseptic solution and use the drapes to create a surgical field. Administer
the local anaesthetic appropriately around the wound, remembering to warn the patient before introduc-
ing the needle. Introduce the needle in a smooth motion, pull back on the plunger to ensure you that are
not injecting into a vessel, and then slowly administer the local anaesthetic whilst withdrawing the needle.
Repeat this step until the surgical field is anaesthetised adequately. Discard the needle into a sharps bin
and state that you would now leave the anaesthetic to work for at least 5 minutes. Before starting to suture
the wound, always check that the local anaesthetic has taken effect, either using a needle or pinching with
toothed forceps.
◌Closure: It is most likely that the wound will be a clean, straight incision. If it is not, then state that you
would like to debride the unhealthy wound edges to turn a ‘traumatic wound’ into a ‘clean, surgical wound’
before closing. In this scenario, when suturing a traumatic wound, it is advisable to use interrupted sutures
to close rather than a continuous suture. This is because if the wound became infected, then not only could
the wound discharge between the interrupted sutures, but individual sutures could be removed to allow
drainage, without opening up the whole wound. A suitable suture in this scenario would be a non-absorb-
able, monofilament suture material such as 4.0 Nylon. Start at one end, and place a simple interrupted
suture.
◌Ensure your needle enters the skin at 90 o and use the curve of the needle by fully pronating and supinat-
ing supinating your wrist to ensure the wound edges are everted. Bring the needle out into
the wound, grasp the needle again and repeat the same action for the other side of the wound. Take equal
bites (roughly 0.5cm) either side of the wound, and ensure that they are of the same depth to avoid steps
in the wound edges. Place sutures roughly 1cm apart along the remainder of the wound, until it is closed
adequately. Finish by applying a simple adherent dressing to the wound.
◌Post-operative instructions & follow up Once you have finished the procedure, the first thing you should
do is discard your sharps into a sharps bin, which will be provided in the station. At this point the patient
may ask you a few questions regarding post-op instructions, but you will appear far more professional if
you offer this information without being prompted. Explain that the patient will go home with some sim-
ple analgesia, and that they must seek medical attention if they are concerned about any of the following
signs/symptoms:
- Increased pain.
- Redness.
- Discharge/blood through the dressing.
- Malodour.
- Systemic symptoms (fever/nausea/malaise).
- Give the patient the appropriate follow-up information with regards to when and where the sutures must
be removed.
◌Xylocaine dose: ( lidocaine 1%)

-3mg/kg ( up to 20 ml of 1% concentration)
◌Lidocaine+ adrenaline:
-7 mg/kg.
◌Mechanism of action: Blocks Na channels thus preventing depolarization.
Q:If allergic to xylocaine, what to give?

A:Bupivacaine.
Q:Dose of bupivacaine?
2mg/kg
In this scenario, the patient would need at least a single dose of antibiotic. If there was a delay in presen-
tation, two further doses would be required post closure. For the type of antibiotic prescribed, you should
follow hospital/ department guidelines where available. In this clinical scenario a broad-spectrum
antibiotic such as Co-amoxiclav is appropriate.
EXCISION OF A NEVUS
◌The best way to excise the lesion is using an ellipti-
cal incision. The incision site should be measured to
allow enough clearance on either side of the lesion.
◌The two points indicate ideal 2mm clearance mar-
gins. This distance is then multiplied by three to indi-
cate the length of the long axis of the elliptical
incision.
◌To create this incision, it is most effective to hold the blade in a pencil grip. Whilst holding the skin taught
with your other hand, start the incision using the belly of the blade. Move the blade along perpendicular to
the skin, smoothly along the line of the ellipse.
◌At the edge, it is important to make sure that it forms a smooth V shape to allow excision of the lesion.
Make sure that you have cut through all of the skin and then proceed to remove the lesion, dissecting
through the subcuticular plane.
Take care to dissect along the line of the ellipse and not cut into the skin edge.
◌Complete the excision with a smooth V shape, keeping the blade perpendicular at all times. The le-
sion is then removed.
◌It is now necessary to close this ellipse.
◌Sometimes you may find that there is a lot of tension in the mid portion of the
ellipse. In these circumstances, it is helpful to undermine the subcutaneous
tissue away from the skin edges
◌To close this ellipse, the best method is to place the first sutures at the distal edges, then gradually work
towards the centre. If you try to start the closure at the widest part of the wound, you may find it difficult
to bring the edges together.
◌Post-operative instructions & follow up Once you have finished the procedure, the first thing you should
do is discard your sharps into a sharps bin, which will be provided in the station. At this point, the patient
may ask you a few questions regarding post-op instructions, but you will appear far more professional if
you offer this information without being prompted. Explain that the patient will go home with some simple
analgesia, and that they must seek medical attention if there are any worrying signs/ symptoms (increased
pain,redness, discharge/ blood through dressing etc). Give the patient the appropriate follow-up informa-
tion with regards to when and where the sutures must be removed, and that a further clinic appointment
will be posted to them once the results are available from histology.( within 2 weeks).
Langer’s lines:
They correspond to the natural orientation of collagen fibers in the dermis, and are generally parallel to
the orientation of the underlying muscle fibers.
MALE CATHETRIZATION
◌Consent: It is not necessary to obtain written consent for catheterisation. Talk through the procedure in
layman’s terms. Indication for procedure. Risks, if not performed. Alternatives. What the procedure entiles.
Complications. Failure (need for alternatives). False passage. Haematuria. Pain (bladder spasm).
Occasional need for monitoring urine output post catheterisation (diuresis).
◌Equipment: A second examiner may act as an assistant and offer to get a trolley ready for you.
-Basic catheter pack .-Kidney dish, gallipot, gauze and sterile drape.
-Skin preparation solution (sterile water is acceptable). - * 10ml syringe + 10ml water (not saline) if
not supplied with catheter.
*Instillagel (anaesthetic, antiseptic lubricant) –minimum 10ml.
-10ml syringe + 10ml water (not saline) if not supplied with catheter.
-Instillagel (anaesthetic, antiseptic lubricant) –minimum 10ml.
-Appropriate catheter bag (large ‘night’ bag or a urometer).
-Positioning: Patient should be as flat as possible to perform the procedure.
Procedure:
1- Confirm patient’s identity and ask if they have previously had a catheter and, if so, whether any problem
or complications were encountered.
2- Ask for allergies (iodine/ n /lignocaine/latex) before positioning the patient supine and covering them.
3- Wash your hands and prepare your equipment.
4- Ask the assistant to obtain adequate exposure.
5- Cleanse hands with an alcohol-based agent and don non-sterile gloves.
6- Use one hand to retract the foreskin with gauze and clean the foreskin, glans and meatus (separate
swabs for each). Change to sterile gloves and apply a sterile drape.
7- Place the kidney dish or collecting dish between the patient’s legs.
8- Instil at least 10ml of gel into the urethra, hold the urethra at the base of the glans and wait for 3-5 min.
9- Advance the catheter with the penis held pointing to the ceiling with gentle traction.
10- Pass the catheter all the way to the hilt and wait for urine to drain.
11- After urine has started to drain, inflate the balloon with the appropriate amount of sterile water (usu-
ally 10mL, but some such as 3-way catheters require 30mL) and withdraw the catheter gently.
12- Replace the foreskin if present.
13- Dry and cover the patient before asking them to redress.
14- Dispose off the equipment in the appropriate bin.
15- Measure the amount of urine draining after an adequate period of time (5-10 minutes) and obtain a
CSU for microscopy, culture and sensitivity.
16- Document the procedure in the notes.
Q:What would you do if no urine drains after catheterisation?
1. Reevaluate presence of urine in bladder by percussing the suprapubic region if you haven't done this
already.
2. Apply suprapubic pressure. 3. Aspirate with a syringe.
4. Flush with a 50ml catheter syringe and sterile water.
◌You insert the catheter; it drains no urine and you therefore remove it. You then examine this patient’s
abdomen and there is a supra-pubic mass. What is your differential diagnosis?
-A bladder that was not catheterised appropriately.
-Colonic carcinoma.
-Large iliac aneurysm.
CHEST DRAIN INSERTION

◌Equipment:
- Sterile gloves and gown.
- Skin preparation solution (iodine or chlorhexidine in alcohol). - Sterile drapes.
- 10ml Syringe. Needles (21–25 gauge).
- Gauze swabs. Local anaesthetic (1% or 2% lignocaine). - Scalpel and No. 11 blade.
- Suture material (1 silk).
- Large haemostat or Spencer-Wells Clamp for blunt dissection. - Large bore chest tube (24 to 30 French).
- Connecting tubing. - Closed drainage system(underwater seal).
- Occlusive dressing (sleek tape).
◌Positioning :
- Patients should be supine with 30 o of head up if possible and the bed slightly rotated towards the side of
insertion.
- The patient’s arm should be placed behind their head to expose the axillary area. It is essential that the
patient undergoes regular haemodynamic observations and pulse oximetry during the procedure.
◌Insertion Site: Although variations have been suggested, the ‘safe triangle’ for insertion of a chest drain
has the following borders.
-Anterior Margin Lateral border of Pectoralis Major.
- Inferior margin 5 th intercostal space (above 6 th rib).
- Apex –Below the axilla.
◌Ideal placement should be just anterior to the midaxillary line within this triangle to avoid damage to the
long thoracic nerve of Bell. Blunt dissection should be over the superior aspect of the inferior rib in order to
avoid damage to the intercostal neurovascular bundle.
◌Anaesthesia: Lignocaine or similar is infiltrated to the skin and periosteum of the superior margin of the
inferior rib. There is no evidence that local anaesthetic with adrenaline reduces the risk of iatrogenic hae-
mothorax. The skin is tested before any incision is made. Despite local anaesthetic the procedure is poorly
tolerated by patients and concomitant anxiolytics or opiates are recommended by the BTS.
◌Insertion: Make a skin incision parallel and just above the rib below, slightly longer than the tube diame-
ter (1French is 1/3mm). Use a large haemostat or clamp to blunt dissect through the parietal pleura before
doing a finger sweep.
-A small clamp can be attached to the end of the tube through one of the holes to guide placement. Aim
the tube apically for pneumathoraces and basally for haemathoraces. Watch for tube fogging to confirm
appropriate placement.
-Suture the drain in place with a stay suture and pass a horizontal mattress closing suture but leave this un-
tied. The end of the closing suture can be covered in sleek or a transparent adhesive dressing with the drain
to stop it coming loose.
◌Drainage: A unidirectional closed drainage system such as the underwater seal drain is most commonly
used. Connection tubing is used between the chest tube and underwater drain. Before the procedure is
completed it is essential to ensure that the fluid within the tube is moving with respiration (“swinging” or
bubbling). Post Procedure It is essential to obtain a chest X-ray to ensure appropriate tube placement.
Q:What are the Indications for contacting thoracic surgeons ?

A:- A persistent pneumothorax despite drainage may suggest a bronchial tear.
-Haemothorax .
- More than 1,500 mL of blood immediately evacuated by tube thoracostomy.
-Persistent bleeding 150 mL/h to 200 mL/h for 2 hours to 4 hours.
- Persistent blood transfusion is required to maintain hemodynamic stability.
TAKING BLOOD CULTURE FROM HIGH RISK PATIENT

◌Procedure:
.Although you are talking to an arm, you should treat it as a patient.
.Wash your hands, introduce yourself and gain permission to take blood.
.Prepare your equipment You will need.
-Gloves.
-2% chlorhexidine 70% isopropyl alcohol wipe Tourniquet.
-Winged Vacuette blood collecting set or a needle and syringe.
-Sterile gauze.
-An aerobic and an anaerobic culture bottle.
-A microbiology request form
.Wash your hands again.
.Wear an apron, eye protection and gloves.
-Once you have chosen vein, make sure you clean thoroughly with the chlohexidine wipe, and then
do not touch the area again before venepuncture. Allow the skin to dry.
-Flip the tops off the two culture bottles and clean with a fresh chlorhexidine wipe. Allow to dry.
-Insert the bottles into the collection port, or the needle and syringe into the bottle depending on what
equipment is available,
-inoculate the aerobic bottle first, then the anaerobic bottle, and rotate 180o to ensure the blood mixes
evenly.
-Label the bottles with the demographics, time and date,
-complete the request form. Send for microscopy, sensitivity and culture.
-Thank the patient and wash your hands.
Q:What is the rate of HIV transmission from a needle stick injury?

A:It is around 0.3% following a needle stick injury from an HIV positive patient.
Q:How does this compare to hepatitis B and C transmission?

A:Before vaccination the risk of transmission following a needlestick injury from a patient with hepatitis
B was around 30%, but has been reduced significantly by the hepatitis vaccination, obligatory for at risk
health care workers, which is 90- 95% effective. The risk of hepatitis C transmission is around 1.8%.
Q:What should you do if you get a needle stick injury?
A:Clean the wound with soap and water. Report the incident to your occupational health department
or A&E out of hours. Another doctor should approach the patient and ask permission to take some blood
to test it for HIV, and viral load, hepatitis B and C. They should also take a sample of blood from you for
testing. Retest again at 6 weeks and 3 months for HIV, HBC and HCV antibodies, and for elevated liver
enzymes, which could indicate hepatitis.
SCRUBBING
◌Pre scrub:
1. Mention you would be in scrubs with appropriate footwear and a scrub cap.
2. Remove any watches or rings (make sure you are not wearing nail varnish!)
3. Expose hands and forearms to elbows 4. Put out a gown and appropriate sized gloves.
5. Put on a face mask.
6. Put a nailbrush on the sink.
◌Scrub:
1. Scrub time - 5 mins for first scrub of the day and 3 mins for each subsequent scrub (look at a clock!).
2. Hold hands at a higher level than elbows at all times.
3. Initial pre-scrub – apply surgical detergent, work up a lather then wash hands and forearms to elbow
and rinse from finger-tip to elbow.
4. Then apply more scrub solution to hands.
5. Clean each nail under running water with nail stick.
6. Scrub each nail against palm of opposite hand.
7. Scrub each finger on all 4 sides - 5 strokes/side.
8. Scrub back of hand and palm from base of fingers to wrist.
9. Small overlapping circles are used to scrub from wrist to 2 inches above elbow 10. Rinse hands and
forearms from fingertip to elbow.
◌Drying:
1-Lift one of the drying towels up and away from the sterile field.
2. Dry fingers and hand then dry remainder of the forearm.
3. Drop towel into bin.
4. Lift the other towel and dry the other hand and forearm.
◌Gowning and gloving:
1.With one hand, pick up the gown and hold by the neck and allow to unfold with arm holes facing.
2.Slide arms into sleeves and your assistant will secure at the back.
3. “Gloving” is performed by the closed or open method (practice this before the exam so you look slick).
4. Hand your assistant the belt tie and turn around to then secure waist belt.
ABCESS DRAINAGE
◌The first step is to make a generous incision at this point. This will result in an immediate release of pus,
which should be cleared away using swabs.
◌We are left with a cavity which still contains pus and an overlying linear skin incision.
◌It is vital to ensure that the skin incision cannot close over. This can be achieved firstly by making
a generous skin incision. Usually, an elliptical incision should be made.
◌At this point, a swab is taken, placed in a container and sent for culture and sensitivity tests at the
bacteriology lab.
◌The next stage is to express the remaining pus using two handed pressure and plentiful swabs to
clear away the exudate. We are now left with a cavity and an overlying cruciate incision. It is sometimes
necessary to excise the edges of necrotic skin tissue further.
◌A finger is then inserted into the cavity to break down any loculi, leaving one continuous space. If
necessary, the cavity can be irrigated with saline using either a bladder tipped or standard syringe.
On occasion, 3% hydrogen peroxide can be used to help clean out the cavity.
◌A pack must the be inserted into the cavity to keep the osteum open and to absorb any further exudate.
Either a saline wick or an alginate dressing can be used. The pack is loosely inserted and the wick trimmed,
leaving a small tail to aid subsequent removal.
◌The wick will remain in place for about 24 hours and will then be replaced by an alginate dressing.
◌When removing the pack, make sure that it is moist, as pulling out a dry dressing will disturb the
granulation tissue forming at the base of the cavity.
◌If an alginate dressing is used from the outset, it is important to trim this to match the size of the cavity, as
a larger dressing may cause maceration of the surrounding normal tissue.
AIRWAY MANAGEMENT IN ATLS PATIENTS

Q:How is the airway assessed clinically?
Assessment is based on the principle of: Look, Listen and Feel.
Look: for the presence of accessory muscles of respiration (neck, shoulders, chest and abdomen) being
used, presence of obvious foreign bodies in the airway, facial/airway injury ( le forte fractures) and the ‘see-
saw’ pattern of complete airway obstruction (NB. central cyanosis is a late sign).
Listen: for the presence of inspiratory stridor, as this indicates upper airways obstruction (laryngeal level
and above). Also take note of grunting, gurgling (liquid or semi-solid foreign matter in the upper airways)
and snoring sounds (indicating the pharynx is partially occluded by the tongue or palate). Expiratory
wheeze suggests lower airways obstruction. Crowing indicates laryngeal spasm.
Feel: for chest wall movements and airflow at the nose and mouth (for 10 seconds).
Q:What techniques of airway management will you do?

Simple measures:
- Basic airway manoeuvres: these include a[ chin lift and jaw thrust].
- Basic airway adjuncts: this include oropharyngeal airway.
Chin lift: the fingers of one hand are placed under the mandible in the mid-line and then lifted upwards to
bring the chin forward.
Jaw thrust: the angles of the mandible are identified on both sides, the index and middle fingers are
placed behind it and a steady upwards and forwards pulling pressure is applied to lift the mandible (this is
painful, and if a patient tolerates it, consider an anaesthetic review). Finally, the thumbs are used to slight-
ly open the mouth by downward displacement of the chin.
Oropharyngeal airway: open the mouth employing basic airway manoeuvres. Suction out debris and in-
sert it upside down (curved side pointing to the palate).
Rotate it 180° between the hard and soft palate and seat the flattened section between the gums and
teeth.OPA should be measured so that it stretches from the corner of the mouth to the angle of the
mandible.
Cervical spine control: Neck collar,sandbag and tape.
- With the patient in neutral alignment, use your fingers to measure the distance from the top of the
shoulder to the bottom of the chin.
- Find the SIZING LINE on the collar and match the collar size to the patient.
- Adjust and lock both sides of the adjustable collar by pressing the two lock tabs.
- Apply the collar while manually maintaining neutral head alignment; ensuring the chin support is well
under the chin.
- Head immobilization with adhesive tape and lateral head support ( sand bag).
-Ventilations are delivered at 8 to10 per minute (1 ventilation every 6-8 seconds).
Complex measures:
◌Endotracheal intubation: this requires anaesthetic expertise and can be achieved through the mouth
(orotracheal) or the nose (nasotracheal) intubation.
◌Surgical airway: this requires a cut down through tissues in the neck and can be achieved in three ways.
◌There are three types of surgical airway :
- Needle cricothyroidotomy (and jet insufflations of oxygen).
- Cricothyroidotomy.
- Tracheostomy, which may be performed in the emergency or elective setting.
Q:What are the indications for a surgical airway?
A:- Failed intubation, e.g. due to oedema.

- Traumatic fracture of the larynx.
Q:In which anatomic location are the surgical airways sited?
A:Both types of cricothyroidotomy are performed through the median cricothyroid ligament. This is the
thickened anterior portion of the cricothyroid membrane that runs between the cricoid and thyroid
cartilages.
A tracheostomy may be placed from the 2nd to 5th tracheal rings.
1. Thyroid gland (Blood supply, Lymphatic Drainage)

2. Embryology of thyroid + (abnormalities)
3. Strap muscles (names & N S)
4. Vertebral level of thyroid cartilage
5. Why thyroid moves up with deglutition:
6. Commonly injured nerves during thyroidectomy
7. Cell origin of medullary carcinoma
8. Late complications of thyroidectomy
9. Larynx (NS, attachments of vocal cords)
10. Parathyroid (location, hormone, embryology, blood supply)
11. Skull (Age cranial sutures ossify, mastoid age to ossify, diploic veins)
12. Pterion
13. Skull foramina (carotid canal, lacerum, rotundum, ovale, spinosum, optic
canal, SOF, stylomastoid foramen, foramen magnum, jugular foramen, IAM)
14. MCF boundaries & contents
15. PCF boundaries & contents, benign tumors
16. Clivus (juvenile structure forming it, CN tracking on it, type of growth plate)
17. TMJ (articulating surfaces, type, movement, muscles of opening)
18. Cavernous sinus (site, tributaries, drain to, contents, thrombosis syndrome)
19. Blood supply temporalis muscle, scalp over temporalis
20. Dural venous sinuses
21. Tongue (muscles, NS “motor + sensory”)
22. Facial nerve (course, branches, muscle affected in the ear, why pt with
acoustic neuroma hear voice louder)
23. Spinal accessory nerve (surface anatomy, muscles)
24. Great auricular nerve (root value, supply)
25. Parotid gland (surface anatomy, blood supply, structures passing, type of
secretion, DD of parotid lump, Frey syndrome)
26. Triangles of neck boundaries
27. External carotid artery (course, nerve ant. to it, branches, carotid body, carotid
sinus)
28. Muscles of mastication
29. Regions drained by pre-auricular LN
30. Facial artery palpation
1
31. Submandibular duct opening

32. Submandibular gland secretion type
33. Nerves at risk of injury on submandibular gland excision
34. Circle of Willis
35. What branch gives off before ACA, MCA?
36. Berry aneurysm rupture
37. Signs of MCA infarct
38. Vertebral artery course (what are areas supplied by vertebrobasilar system)
39. Roof of the middle ear
40. How middle ear infections cross the skull (where else it can spread to)
41. CP of meningism
42. Which vein drain the dangerous area of the face:
43. Difference between UMNL and LMNL facial palsy
44. Relations of the middle ear
45. MRI brain sagittal cut
46. CSF circulation
47. Subarachnoid cisterns
48. Arnold chiari malformations
49. CN carrying parasympathetic fibers
50. Meningioma & GBM in MRI
51. Identify (tentorium cerebelli, ant. attachment, optic nerve, ICA, optic chiasm,
occulomotor nerve, abducent nerve)
52. Muscles supplied by occulomotor nerve (effect of paralysis)
53. What is the exact structure on which the occulomotor nerve is pressed against?
54. Blood vessel supplying the inner table of temporal bone
55. If there is a tumour in the precentral gyrus , what is the bone to penetrate?
56. What is the aggressive form of glioma
57.
58. Identify (abdominal aorta, IVC, celiac trunk, IMA)
59. Aorta (branches with levels and aspects), IV contrast
60. CT with infrarenal AAA
61. Saccular aneurysm (define, pathogenesis, causes)
62. Dissecting aneurysm (pathogenesis, complications)
63. IVC tributaries
2
64. Renal veins (anterior relations)

65. Spleen (blood supply, ribs, structure to wary about during splenectomy, course
of splenic artery)
66. Pancreas (parts, cell groups, blood supply, ducts, vessels encountered in
whipple, ligaments connecting with spleen, embryological development)
67. Liver (stab in epigastrium, separation of right & left lobes, arterial & venous
drainage, porta hepatis, ligaments supporting)
68. Gall Bladder (surface marking, cause of shoulder pain)
69. Urinary Bladder (arterial & venous supply, NS of detrusor, cancer types & CP
& risk factors, ureteric orifice, peritoneal covering, layers encountered in
suprapubic catheterization, posterior relations in males & females)
70. Esophagus (beginning, each part arterial & venous supply, LD, cells lining,
barret’s, achalasia definition & character & microscopy, indentation,
complication of perforation)
71. Stomach (parts, arterial & venous supply)
72. Appendix (common positions, arterial & venous supply, cause of pain referral
to umbilicus)
73. Diaphragm (openings, attachments)
74. Duodenum (peritoneal covering, relations of parts, major duodenal papilla)
75. External oblique & Internal oblique (attachments, NS, direction of fibers)
76. Inguinal canal (boundaries)
77. How many cusps have the pulmonary valve?
78. Vertebral level of the pulmonary valve
79. Where to auscultate pulmonary valve:
80. Identify (images P 16)
81. Azygous vein tributaries
82. Ascending aorta branches
83. Sympathetic nerves (origin, connection to spinal nerve, how to leave chain)
84. Lung (identify mediastinal surface, pulmonary ligament, surface anatomy,
number of bronchopulmonary segments, nerves ant & post to hilum)
85. Course of clot from calf to pulmonary artery
86. Intercostal muscles NS
87. Aortic arch branches
88. Subclavian steal syndrome
3
89. Thoracic outlet syndrome

90. Site of location of chest tube
91. Cause of bradycardia after chest tube insertion
92. Posterior mediastinum (boundaries, contents)
93.
94. CS (X-ray transoral with odontoid)
95. Ligaments attached to odontoid process
96. Type of atlanto-axial joint
97. Ligaments between C1 & C2
98. 1st spinous process to be felt
99. Why we can not feel the upper spinous processes
100. Atypical cervical vertebrae and the atypical features
101. How many vertebrae & spinal nerves make the spinal column
102. Lumbar vertebra structures
103. Intervertebral foramen: structures passing
104. Level of the lumbar puncture (layers to pass through)
105. IV disc anatomy, type of joint
106. Movement on lumbar vertebrae
107. Level of the spinal cord in newborn and adult
108. Contents of the spinal canal below L2
109. Location of the paravertebral venous plexus
110. Contents of epidural space
111. How does spinal mets happen
112. Tumours metastatising to the spine
113. Demonstrate the hyoid bone (C3) and the cricoid cartilage (C6) on a
subject
114. Structures found at C6
115. Brachial plexus (surface anatomy, parts location, nerves)
116. Erb’s palsy (pathology, CP)
117. Klumpke’s paralysis (pathology, CP)
118. Elbow joint (articulating bones)
119. Muscles flexing the elbow joint
120. Structures passing in spiral groove
121. Radial N injury in spiral groove
4
122. Supracondylar fracture humerus associated injuries

123. Median, Ulnar & Radial N sensory distribution of hand
124. Median N supply in hand
125. Median N injury at elbow CP
126. Ulnar N injury at wrist CP
127. Ulnar paradox
128. Superficial palmar arch
129. Carpal bones
130. Scaphoid blood supply
131. Flexor retinaculum (attachment, structures passing through)
132. Thumb movements by muscle & NS
133. FDP & FDS (test & insertion)
134. How to test ulnar artery
135. Tendon attached to pisiform
136. 1st dorsal interosseous muscle (attachment, action, NS)
137. Role of radial nerve in power of grip
138. Why handgrip is more powerful in extension than flextion
139. What attaches extensor tendon to phalanges
140. Functions of intertendinuous connections
141. Anatomical snuff box (boundaries)
142. Surface marking of coracoid process
143. Structures attached to the coracoid process
144. Rotator cuff muscles (attachment & NS)
145. Muscles inserted in bicepital groove
146. Shoulder joint abduction
147. Factors decreasing the stability of the shoulder joint
148. The main stabilizer of the shoulder joint
149. Quadrangular space
150. Axillary nerve
151. Pectoralis major
152. Axillary artery
153. Cubital fossa (boundaries, contents)
154. Upper limb reflexes (biceps, triceps, supinator)
155. Upper limb dermatomes
5
156. Biceps muscle (attachments, action, NS, tendon relations)

157. Triceps muscle (attachments, action, NS)
158. Trapezius muscle (attachments, action, NS)
159. Serratus anterior (attachments, action, NS)
160. Foot bones
161. Arches of the foot (bones, ligaments, muscles)
162. Deltoid ligament attachment
163. Subtalar joint (movements, muscles acting)
164. What is the type of the subtalar joint
165. What are the bones forming ankle joint
166. Movements at the ankle joint
167. Ankle joint is most stable in dorsiflexion why
168. What is the type of inferior talofibular joint
169. Where to palpate dorsalis pedis and post. Tibial aa
170. Structures passing behind the medial malleolus
171. Demonstrate the foot pulses on this actor
172. Course of dorsalis pedis artery, medial & lateral plantar arteries
173. What makes Achilles tendon
174. Identify tendons at dorsum of foot
175. What nerve supplies the muscles in the posterior compartment of the
leg?
176. Where would you test sensation of S1, L4, Deep peroneal N,
Superficial N, Sural N
177. What movements do extensor hallucis longus perform
178. What vessels & nerves would you find deep to extensor hallucis longus
179. Knee and ankle reflexes (demonstrate on subject) & root values
180. What movement is ankle dorsiflexion & what joint & muscles
181. What nerve supplies the anterior compartment of the leg
182. How would you demonstrate ankle plantarflexion & muscles
183. What action did by tibialis anterior and posterior contract together &
what joint on
184. What muscles are responsible for ankle eversion & their NS
185. Damage to the superficial peroneal nerve (motor & sensory effect)
6
186. How many compartments are there in the leg and what structures are in
each compartment
187. How would you recognise compartment syndrome in the lower leg
188. Blood supply of the head of femur (their origin)
189. What muscles attach to the lesser trochanter of the femur
190. Psoas major (origin, action)
191. Iliotibial tract (attachment, muscles inserted, clinical significance)
192. Gluteus maximus (attachment, action, NS)
193. Tensor fascia lata (NS)
194. Gluteus medius (attachment, action, NS)
195. Clinical sign noted is weakness of gluteus medius & minimus
196. Sciatic N (surface anatomy, variation)
197. Greater sciatic foramen (nerve & vessels exiting)
198. Lower limb dermatomes
199. Quadriceps (attachment)
200. Quadratus femoris (attachment, NS & action)
201. Popliteal fossa (boundaries, contents, DD of swelling)
202. ASIS related nerve, Meralgia parasthetica
203. Hamstrings (attachments & NS)
204. Femoral triangle (boundaries & contents)
205. Hunter’s canal (definition, surface marking, boundaries, contents)
206. Femoral artery surface marking
207. Vascular lacuna (lacuna vasorum & lacuna muscolorum)
7
Pathology
11.Temporal arteritis:
60 y old female with headache and skull tenderness on mastication, transient
loss of vision
1. *Biopsy from the temporal artery ----->
2. *Describe the pathological changes in microscopic picture: MORPHOLOGY
3. *One simple blood test to prove:
4. *Why blindness:
5. *Treatment----->
6. *One year later developed fracture NOF why?
7. *Why osteoprosis in this patient:
8. *Pathological changes in osteoporosis:
9. *Mechanism by which corticosteroids cause osteoporosis:
10. *Other causes of pathological fracture:
11. *Multiple myeloma :
12. *Diagnosis:
13. *Bence Jones protein:
14. *Concerns if going to surgery:
15. *How to prevent:
16. *The patient went for THR , died in POD1 suddenly------->
1
17.Sickle cell disease + brain tumour:

(Stem: a lady known to have sickle cell didease, had head injury, CT done and
a temporal mass of 3.8 cm accidentally discovered)
1. *What is sickle cell disease:
2. *Complications:
3. *Mechanism of autosplenectomy;
4. *What are the surgical relevance of sickle cell disease?
5. *Why the patient is immunocompromised:
6. *Most common brain tumour in elderly:
7. *Manifestations of brain tumours:
8. *What if the tumour left untreated, ----->
9. *Biopsy showed squamous cells:
10. *Possible primary sources:
11. *Post biopsy had wound infection: Common organisms:
12. *Wound discharge showed glucose:
2
18.Polytrauma+ transfusion:
Stem: HCV patient -> trauma-> blood loss/-> splenectomy+transfusion-> DIC
1. *Define DIC:
2. *Characterized by:
3. *Functions of the platelets:
4. *How platlets are formed from bone marrow?
5. *Why this patient has bleeding tendency:
6. *Very late manifestations of HCV:
7. *What activates intrinsic and extrinsic pathways:
8. *……. tests for intrinsic pathway

9. *……. tests for extrinsic pathway and the common pathway
10. *Hypersenstivity reactions:
11. *Which blood product will you give?
12. *Percentage of white blood cells in packed RBC's?
13. *Life span of RBC's:
14. *What tests to do before blood transfusion:
15. *What is GXM:
16. *Antigen in cross matching:
17. *Stages of bone healing:
18. *Effects of prolonged immobility on bone:
19. *Infected implant, why you should remove?
20. *What the 1st test to do?
21. *What is PVL staph aureus?
22. *What is the effect of this cytotoxin?
3
Pathology
1. Infective endocarditis:
1. *Def.:
2. *Why rheumatic heart and valve replacement patients are more susceptible
to IE:
3. Diagnosis:
4. Major criteria:
5. Minor criteria:
6. *Common organisms:
7. *Signs in hand:
8. *Treatment:
9. *Matching before heart transplantaion:
10. *If not matched:
11. *How to prevent graft rejections:
12. *Side effects of long term steroid:
13. *After valve replacement why on warfarin:
14. *Mechanism of action of warfarin:
15. *How to monitor: INR
16. *Reversal:
17. *Right sided vegetations
1
12. Gangrene + mesothelioma:

[ worker,smoker, toe gangrene, ]
1. *Define gangrene:
2. *Define necrosis:
3. *Types of cell death:
4. *Pathogenesis of necrosis:
5. *Define atherosclerosis:
6. *Risk factors: smoking, HTN, DM, family history, increased LDL
7. *Patient developed cough--> one bedside test to do :
8. *Xray --> pleural plaque
9. *Pleural plaques,
10. *Significance:
11. *Give one classification of lung cancer:
12. *Now the patient is presented with Mets, poorly differentiated, how to
tell its epithelial origin?
13. *If the tumour was epidermal growth factor positive, what will be the
chemotherapeutic agent?
2
14. Aortic stenosis:

1. *Causes:
2. *How stenosis occur ?
3. *Cause of sudden death in AS?
4. *Aortic valve endocarditis, after a while weakness in Arm ?
5. *Which coagulation system will not be affected by warfarin?
6. *Define thrombus:
7. *If metallic valve replacement was done and the patient developed IE,
why the valve should be removed?
8. *If we found microscopic branching hyphae on a removed metallic valve:
3
Pathology
19. MEN I syndrome:
Man with parathyroidectomy, pancreatic mass
1. *Define hyperplasia:
2. *How many parathyroid glands mostly affected? The 4 glands
3. *Microscopic picture of hyperplasia?
4. *The patient developed stupor, confusion and hypoglycemia (1.2 mmol/l),

5. What do you think ?
6. *What cell derived from?
7. *What other causes of unresponsive hypoglycemia do you know?
8. *CP of insulinoma:
9. *Biochemical diagnosis:
10. *What do you suspect as another pathology in this patient?
11. *What are the 3 gene mutations in insulinoma?
12. *What is double hit hypothesis?
13. *What is telomere?
14. *What is apoptosis?
1
27. MEN II syndrome:

Stem: female with thyroid nodule, elevated calcitonin levels
1. *Single best test to diagnose?
2. *Pathology report:
- FNAC showed malignant cell features, amyloid deposits,
- Immunohistochemistry stains +ve for calcitonin, stains -ve for
thyroxine
3. *What type of cancer?
4. *Why medullary?
5. *Cell source?
6. *What is IHC in simple words?
7. *How it works?
8. *Type of Ag-Ab reaction in IHC?
9. *Another pathology report showing size, No. of Positive lymph nodes (2-
6)?
10. *If the patient developed hypertension, what do you think she
might have?
11. *How can you diagnose pheochromocytoma?
12. *If this condition was familial, what other condition you suspect?
13. *Types of MEN syndromes? Oncogene mutations? Modes of

inheritance?
14. *Treatment of medullary thyroid cancer.?
2
Pathology
2. Inflammatory bowel disease:
[STEM: lady known to have ulcerative colitis and on surveilliance colonoscopy
found to have a lesion less than 1cm in sigmoid colon.]
1. *What is ulcerative colitis:
2. *Pathogenesis:
3. Colonoscopy done with biopsy showing tubular dysplasia in one part,

adenocarcinoma in other part - showing a picture of a tumour eroding
through the muscularis layer + 1/4 positive node
4. *What will you offer this lady?

5. *Why?
6. *If there is liver Mets, how will this affect TNM staging?
7. *Microscopic features of Crohn's :
8. *Microscopic features of ulcerative colitis:
9. *Complications :
10. *Why patient having diarrhea:
11. *Why you need endoscopic surveillance:
12. *Renal stone formation in Crohn's :
13. *Describe adenoma carcinoma sequence:
14. *How proto-oncogenes and tumour supressor genes act?
15. *Function of KRAS:
16. *Function of P53:
17. *Function of APC:
18. *Had resection of terminal ileum but diarrhea continued----->
19. *Stoma-----> ischemia---->
20. *Type of vit. Defeciency:
21. *Other investigations:
1
3.Familial adenomatous polyposis FAP:

STEM: a young lady with endometriosis concerned that her father fied of a cancer
at an early stage, she had a colonoscopy just now
1. *ID a picture of FAP:
2. *Def.:
3. *Function of APC tumour suppressor gene:
4. *Classification of polyps:
5. *Malignant potential of adenomas depend on:
6. *Extracolonic manifestations: in the related gardener syndrome
7. *Management:
8. *If the patient is having a child 2y, what is your advice:
9. *Define endometriosis:
10. *Definitions:
- Dysplasia:
- Severe dysplasia
11. *Abscess:
12. *Pus:
13. *Ulcer:
14. *Secondary intention:
15. *Life style modifications to reduce risk of cancer colon :
2
5. GB cancer + pseudomembranous colitis:

[ cholecystectomy+ surgical site infection]
1. *Causes:
2. *Spread:
3. *Pathology:
4. *Surgical site infection in POD3 with yellowish discharge------>
5. *What is the most common organism causing surgical site infection?
6. *Organisms causing necrotising fascititis:
7. *DIAGNOSIS:
8. *Pathology:
9. *Management:
10. *Who to involve in care:
11. *Post-operative bloody diarrhea:
12. *Pathogenesis of PMC:
3
9. Peptic ulcer disease+ hyperparathyroidism:

[gastric ulcer -> hematemesis -> OGD -> peptic ulcer, biopsied] + hypercalcemia
1. *Def. ulcer:
2. *Risk factors of PUD:
3. *H- pylori:
4. *CLO test: ( campylobacter like organism) :
5. *How H-Pylori can survive in acidic medium?
6. *Mechanism by which H-pylori can colonize the stomach?
7. *Type of gastric cancer that can be caused by H-Pylori? Adenocarcinoma
8. *Eradication of H-pylori:
9. *Other causes of hematemesis in this patient:
10. *Common causes of hypercalcemia:
11. *Cause of UTI in this patient:
12. *How to localize parathyroid glands:
13. *What is frozen section:
14. *How the specimen is fixed:
15. *Why we cannot use paraffin based histopathology intraoperatively?
16. *How many platelets present in packed RBC’s?
17. *Histopathology report:

- 1 gland 0.2g chief cells
- 3 glands ranging from 0.08 to 0.09g oxiphilic cells and fat cells
18. *Interpret:
19. *Histology of parathyroid adenoma:
20. *Where to find parathyroid gland if you do not see them in the normal
position?
21. *Treatment of parathyroid adenoma:
22. *Types of hyperparathyroidism:
23. *Treatment of hypercalcemia:
4
13. Diverticulitis + endometriosis:

Stem: (LIF pain + peritonism -------> ruptured diverticulitis -------> Hartman's
procedure -------> histopath --------> diverticulitis + endometriosis)
1. *Pathophysiology of diverticulosis
2. *Cause of diverticulitis in diverticular disease?
3. *How neutrophils migrate to the site of infection?
4. *How did endometriosis got the colon
5. *Is endometriosis can increase the risk of cancer?
6. *Why endometriosis causes pain?
7. *Few days later developped LIF collection, why?
8. *What antibiotics to give?
16. Gastric carcinoma:

(Gastrectomy with splenectomy, pathology report)
Stem: surgery done -------> histopath ------> signet ring carcinoma
1. *2 major risk factors for gastric cancer:
2. *Discuss pathology report with the family in 4 simple lines:
3. *7-10 days later the patient had axillary vein thrombosis, what predisposes to
that?
4. *6 months later came with ascites, deranged liver functions, hepatic mets/
mention 2 pathological tests to do?
5. *Treatment of this patient:
5
26. Cancer esophagus:

Stem: patient with dysphagia, smoker, GERD, with 20 pounds loss of weight
1. *What is the normal oesophagus lining?
2. *Most probable diagnosis?
3. *What the etiological factors of cancer esophagus in this patient?
4. *What is the effect of prolonged GERD?
5. *Which test to do for this patient?
6. *What are the obtained cells will tell you?
7. *What is the stain used in immunohistochemistry?
8. *Pathology report showed Barrett’s esophagus?
9. *Define:
10. *Type of lining:
11. *Type of cancer:
12. *Staging: TM
13. *If pleural effusion : Causes:
14. *Pathological test to do:
15. *How to treat:
16. *Developped enlargement of a supraclavicular lymph node ?

a. Investigation:
b. Features under the microscope:
17. *Investigations of MI:
18. *What is troponin:
19. *Where it is found :
6
28.Carcinoid tumor:
Stem: Middle aged man with RIF pain, surgery was done, revealed dilated
appendix (looks like mass), histopathology revealed appendicular abscess plus
6mm appendicular mass involving the mucosa and the muscularis layers
1. *Define abscess:
2. *Structure of the abscess:
3. *H ow neutrophils migrate to the site of inflammation:
4. *Blood tests to identify the inflammation:
5. *What is carcinoid tumor?
6. *Where it is most commonly found?
7. *Cells arising from?
8. *What does it release?
9. *Clinical presentation :
10. *How does it spread?
11. *Most common metastatic site?
12. *Why a person with heavy mets in liver has symptoms than with
primary tumour?
13. *Diagnosis of carcinoid syndrome :
7
30.Cancer colon + hemorrhoids + myocardial infarction

Stem: PR bleeding diagnosed as hemorrhoids, colonoscopy done revealed
adenocarcinoma with melanosis coli, biopsied, histopathology revealed lesion in to
muscularis layer
1. *Dukes staging :
2. *What are hemorrhoids?
3. *Pathogenesis of hemorrhoids?
4. *Pathogenesis of thrombosed hemorrhoids?
5. *Why coronary arteries get thrombosed?
6. *How coronary arteries get atherosclerosis?
7. *Risk factors of atherosclerosis?
8. *What is the function of thrombus?
9. *How it is formed?
10. *Mechanism of myocardial infarction :
8
Pathology
23. Osteomyelitis:
Stem: patient with leg operation with an implant for 3 years and got infected
1. *Common organisms:
2. *Pathogenesis of osteomyelitis:
3. *Why pus may burst through the bone?
4. *Why the fixing plate should be removed?
5. *SCC developed in the sinus, why?
6. *Treatment:
24. Pathological fractures:

Stem: young female was cycling developed pain in her thigh soon as she put her
foot on the ground. X-ray showed fracture shaft femur with hypodense shadow
1. *What is pathological fracture?
2. *Causes of bone lesions:
3. *Possible primary sites for metastasis:
4. *Fixation was done, how to check malignancy? Bone biopsy
5. *Pathology report: typical bland appearance (follicular cells) Where is the

primary may be?
6. *We have done FNAC of the thyroid but unable to differentiate cancer, why?
7. *What investigations to do to confirm thyroid Mets?
8. *Which thyroid cancer will show no response to iodine uptake?
9. *If a patient is O +ve, what test to do prior to blood transfusion?
10. *If the patient is telling you his group, you will still do cross matching
and why?
11. *Complications of incompatible blood transfusion:
Page 1
Pathology
10. Testicular teratoma:
[35 y man with left groin mass+single palpable testis]
1. *On ultrasound, Lt groin mass turned to be undescended testis with solid

and cystic components --> tissue diagnosis ---> pathology report --->
comment:
2. *Define cryptorchidism:
3. *How does undescended testis contribute to increased risk of testicular

cancer?
4. *What will be your management:
5. *Discuss pathology report with family in 3 simple lines:
6. *Where teratoma spread to first?
7. *Classification of Germ Cell Tumours
8. *Where does it spread to next :
9. *Serological markers:
 Value of serum markers is fourfold:
10. *Post-operative developed hematoma, mention stages of hematoma

resolution?
11. *After few months developed small pneumothorax----->
12. *Define metastasis:
13. *1year later the patient came with para-aortic lymph node compressing
renal artery and vein + SOB + PE , Why PE in this patient?
14. *Which part of Virchow's triad doesn't contribute ?
15. *What is choriocarcinoma and what is its tumour marker?
16. *What is the common tumour in this age group?
17. *Non–Hodgkin lymphoma is the most common testicular tumor in

men>60
18. *What is the cell origin of seminoma?
19. *Histopath showed papillary thyroid tissue and GIT adenocarcinoma,

why?
1
16. Polycystic kidney disease:

Stem: ADPK going for bilateral nephrectomy due to intractable abdominal pain
1. *Describe gross pathology:
2. *Mode of inheritance:
3. *Pathogenesis of cyst formation:
4. *Other organs in the abdomen causing cyst formation?
5. *Complications:
6. *Associated lesion in the brain:
7. *Type of matching before transplant:
8. *Types of graft rejections:
9. *What types of malignancy occuring with immunosupression:
2
20. PROSTATE CANCER:

Stem : A man with BPH, Poor urine stream, low back pain
1. *How to take a prostate biopsy?
2. *Why multiple biopsies?
3. *How to differntiate between rectum and prostate cells in a needle biopsy?
4. *What are the gene mutations involved in pathogenesis of prostate cancer?
5. *Patient went to radical prostatectomy, PSA is 7 after 3 months
6. *How can you judge the scuccess of radical prostatectomy ?
7. *High PSA after prostatectomy----->
8. *Why PSA is not reliable?
9. *What is the grading system ?
10. *One test to exclude bony Mets?
11. *What kind of metastases?
12. *Why?
13. *Post operative, patient developed fever, dusky red urine, Why?
14. *Which of the blood components will rise?
15. *Most common organisms?
16. *What is the rational in treating prostste cancer by bilateral

orchidectomy?
17. *What are the cells producing testosterone?
3
Pathology
4. T.B
[ A young indian lady came back from a foreign travel with cervical
lymphadenopathy, loss of weight, night sweating]
1. *DD:
2. *Which labs you will send her sputum to:
3. *What are the tests of TB?
4. *How to label the sputum specimens:
5. *Where to put:
6. *Organism of T.B:
7. *Other mycobacteria:
8. *What are the culture media for mycobacteria:
9. *How long to culture:
10. *What type of protein deposition:
11. *Given the FNAC result: necrotic tissue, Histiocytes, giant cells ----->
12. *What is giant cells:
13. *Public health concern/ community concerns
14. *Contact tracing:
15. *What is your advice to contacts:
16. *Granuloma:
17. *Other Causes of granuloma:
1
29. Nasopharyngeal carcinoma:

1. *Define carcinoma:
2. *What are the differences between Benign and malignant cells?
3. *What is the mechanism of radiotherapy?
4. *What is the SI units of radiotherapy?
5. *Risk factors for nasopharyngeal carcinoma :
6. *Patient had an oral lesion, swab showing hyphae?
7. *What are the risk factors for that patient for oral candidiasis?
8. *What are the routes of spread of nasopharyngeal carcinoma?
9. *Where to spread locally?
10. *What are the common lymph node tumors?
11. *How will you investigate for mets in lymph nodes?
2
Pathology
6. MALIGNANT MELANOMA METS:

Stem: a patient known to have hypothyroidism with a hard swelling in her right
inguinal region, her GP sent her for biopsy
1. *DD:
2. *Infections associated with inguinal lymph nodes are as follows:
3. *Malignancies associated with inguinal lymph nodes are as follows:
4. *Results of histopathology revealed malignant melanoma:
5. *What are types of malignant melanoma?
6. *Where would you examine this lady?
7. *How to treat this lady?
8. *How can you know the phenotype of the tumor?
9. *Post operative the wound is red and swollen, culture was done revealed
diplococci?
- Examples of gram-negative diplococci are
- Examples of gram-positive diplococci are
10. *Next the patient got toxemia with rapidly spreading infection? What do
you think?
11. *What is SIRS
12. *What happens to lung in SIRS?
13. *Define ARDS?
1
7. Malignant melanoma:
Stem [Pathology report]
1. *Definition:
2. *Skin conditions associated with melanoma?
3. *Other risk factors of malignant melanoma:
4. *Comment on the pathology report:
5. *How to differentiate MM from SCC?
6. *Poor prognostic factors:
7. *Genes responsible for familial MM?
8. *Lesion excised Breslow thickness 1.5 mm, margins 0.5 mm , what to do?
9. *Management?
10. *What to do to ensure adequate margins?
11. *Post excision the patient developed regional lymphadenopathy,

Management?
12. *Post excision the patient developed painful swelling of the arm +
dyspnea?
13. *Risk factors for thrombosis?
14. *Management:
2
21. BASAL CELL CARCINOMA:

1. *Describe the lesion?
2. *Why the surrounding skin is red?
3. *Most probable diagnosis?
4. *Natural hx of BCC?
5. *What is your concern in pathology report?
 How would you manage a pt with deep margin involvement?
6. *Treatment options for basal cell carcinoma?
7. *How to prevent recurrence of deep margin involvement during re-operation.
8. *Skin graft placed for pt and subsequently had graft failure?

- Cause for graft failure:
9. *Common organism?
10. *Wound C&S grew MRSA, What is MRSA?
11. *How would you manage this pt with MRSA wound infection.
12. *Infection control of MRSA:

- Measures apply to all patients, regardless of MRSA status:
- The following additional precautions should be used for all
MRSA positive patients
13. *After excision, the patient developed regional lymphadenopathy?
14. *FNAC done revealed (lymphocytes, PMNL, Histiocytes, cells with an

bilobed nuclei)
15. Interpret:
16. *Mechanism of lymphatic spread:
3
Pathology
8. Breast cancer:
[mammogram+ pathology report]
1. *What can you recognize in mammogram:
2. *What other tests to do?
3. *Most common type of breast cancer?
4. *Excision----> pathology report----> what to look for:
5. *One microscopic test to do before LD flap? Culture and Sensitivity of MRSA
6. *HER2:
7. *Herceptin (trastazumab):
8. *What else in management?
9. *Hormonal therapy:
1
22. Parotid tumours:

1. *What is the most common parotid benign swelling?
2. *What is the meaning of pleomorphic?
3. *Describe pleomorphic adenoma appearance?
4. *Clinical signs of malignancy?
5. *Types of parotid tumours?
6. *Features of malignant cells?
7. *Anaplastic Features:
8. *Single best test to differentiate between benign and malignant cells? FNAC
9. *Difference between cytology and histology?
10. *How to rule out malignancy intra-operative?
11. *In FNAC,

- If you find: lymphocytes, langerhan's giant cells ----->
- If you find: lymphoid cells with pleomorphism ------- >
- If you find: epithelioid cells with brown cytoplasm --->
12. *High sensitivity test (true positive rate)
13. *High specificity test (true negative rate)
2
25. Abscess:
Stem: forearm abscess
1. *Def.:
2. *What is present inside abscess?
3. *Organisms causing abscess?
4. *One simple test to detect the cause of abscess?
5. *What is the cause of fever in abscess?
6. *Define cellulitis:
7. *What is the difference between abscess and cellulitis?
8. *When to give Antibiotic in abscess?
9. *What are giant cells?
10. *Most common cause of granuloma formation?
11. *Causative agent:
12. *Type of stain:
13. *What changes you see in lymph node affected with inflammation?
3
ASSCC
3. Epidural:
[ lobectomy using thoracic epidural ]---> hypotensive, bradychardia, desaturation,
upper limb parasthsia
1. Differentials:
2. Why patient having bradycharia:
3. Management plan :
4. Factors affecting epidural efficency:
5. Why epidural:
6. How to test the level of the block:
7. Why we use temp. Sensation ?
8. How to differntiate high epidural block from hypovolemic shock :
1
8. Ruptured AAA (hypothermia):

Perioperative hypothermia: Under anaesthesia hypothermia is defined as a core
temperature less than 36°C.
1. How to measure core temp.?
2. Risk factors:
3. Aetiological factors for perioperative hypothermia include:
4. Ways of heat loss:
5. Complications:
6. How to prevent these complications: NICE GUIDELINES:
7. DIC:
8. Def.:
9. Characterised by:
10. Cause of DIC in this patient:
11. Treatment of DIC:
12. Who to involve in care:
13. Indications of platelet transfusion:
14. Shelf life : 5 days
15. Stages of hemostasis:
16. Massive blood transfusion:
17. Complications:
18. Measures to reduce blood loss intra-operative :
19. Early post operative complications of AAA repair:
2
13. Pain management:

Stem: post operative pain, drug chart ----> had only panadol and arcoxia (selective
COX2 inhibitor)
1. How will you manage this patient after this drug chart:
2. IMMEDIATE MANAGEMENT:
3. FULL PATIENT ASSESSMENT:
4. Side effects of opioids:

5. What is the pain pathway?
6. Patient controlled analgesia: (PCA)
7. Problems :
8. Complications of pain:
3
21. Inotropes and vasopressors:

Inotrope: drug increases cardiac contractility
Vasopressor: drug increases vasoconstriction, MAP
both are acting through autonomic nervous system
1. Receptors acting on :
2. Indications:
3. SHOCK:
4. Def. :
5. SIRS:
6. Sepsis:
7. Septic shock:
8. Which inotrope to be used in septic shock:
9. How would you monitor :
10. MAP:
11. Preload:
12. Starling law of the heart:
13. Control of blood pressure:
14. When blood pressure increases:
15. When blood pressure decreases:
16. ITU admission criteria:
4
ASSCC
5. Atrial fibrillation+ rupture viscous:
[ CXR+ ECG]
1. Items to be commented on a chest x-ray:
2. Identify the pathology in CXR----->

3. Identify the pathology in ECG ----->
4. Count the heart rate in ECG------>
5. Why it is different from recorded by the automatic machine:
6. What is the cause of AF in this patient :
7. Management of AF:
8. Differentials of perforated viscous:

9. How to consent in such case :
1
6. Preoperative aortic stenosis:

[elective TURBT]
1. Pathophysiology of aortic stenosis:
2. Coronary perfusion pressure =
3. Clinical picture of aortic stenosis:
4. ID (ECG)
5. How to calculate HR based on this ECG :
6. What are the complications of aortic stenosis?
7. Investigations:
8. What to do :
9. If this patient had a bladder cancer , will you proceed to bladder surgery
or valve surgery first?
10. If the operation was cancelled, what are you worried about?
11. If you will proceed to surgery:
2
ASSCC
11. Steroids:
Stem:RA patient on steroids / immunomodulators
1. Layers of adrenal cortex: GFR
2. Actions of aldosterone : ( mineralocorticoid)
3. Actions of cortisol:
4. Hypothalamic pit. Adrenal axis:
5. Advice to patients starting steroids:
6. Addisonian crisis:
7. Def:
8. Primary:
9. Secondary:
10. Cardinal features:
11. Management:
12. -Prevention:
1
12. Calcium homeostasis:

Stem: post thyroidectomy hypocalcemia, calcium 1.8 ----> pod4 0.7
1. Causes of post-thyroidectomy hypocalcemia:
2. How calcium is transported in the blood:
3. Physiologic role of calcium in the body:
4. Hormones involved in ca+2 homeostasis:
5. How vitamin D3 is
formed:
6. Signs of hypocalcemia:
7. Which muscle are you worried about in tetany?
8. How to treat hypocalcemic tetany?
2
14. Hypothyroidism:
Stem: a lady with a neck swelling, lethargy, malaise
Labs show: low T3 and low T4 with high TSH , anemia
1. Hypothalamic pit. Thyroid axis:
2. Difference between T3 and T4:
3. Synthesis of T3 and T4:
4. Type of anemia in this case:
5. Causes of hypothyroidism:
6. Signs of hypothyroidism:
7. Patient with hypothyroidism not compliant to medications comes for an

emergency surgery, what are the risks:
8. Involve endocrionolgist in care, anesthesia consultant
9. How to increase patient compliance with the treatment:
3
ASSCC
4. Gastric outlet obstruction:

1. Causes:
2. ABG: metabolic alkalosis
3. Biochemical abnormalities: Hypocholeremic, hypokalemic, metabolic

alkalosis Hypochloremia:
4. Hypokalemia:
5. Why bicarbonate is increased:
6. Why paradoxical acuduria:

7. Why hyponatremia:
8. Management:
9. CP of hyponatremia:
10. Causes of hyponatremia:
1
7. Respiratory acidosis:
[morphine overdose]
1. How CO2 is transported in the blood:
2. Chloride shift: chloride diffuses into the red cell to maintain cellular
balance
3. Why still no metabolic compensation:
4. What type of respiratory failure is that?
5. How morphine act:
6. Why pao2 is in normal range:
7. Management: (ITU)
8. ITU admission is indicated for multi-organ mechanical support:
2
9. Burns + ARDS:
1. Calculate the surface area of the burn
2. Management: ABC
3. Why not to give colloids in burn :
4. How do you assess the adequacy of fluid therapy?
5. ARDS:
6. Def.:
7. Characterised by:
8. Pathophysiology of ARDS:
9. Management:
3
23. TURP syndrome:

[ post TURP confused , hypoxic, hypotensive]
1. Possible causes:
2. Def:
3. CP:
4. Causes of confusion:
5. Cause of hypoxia?
6. Management:
7. Will you give hypertonic Saline?
8. Other system can be affected by TURP? Cardiac system
9. Action of furesmide:
10. Other direutics :
4
24. Crush injury:

[compartement syndrome + rhabdomyolysis]
Stem: leg crushed for few hours in 28 y old male, left unobserved on ortho ward
Bloods: AKI, Urine dipstick: blood
1. Labs of rhabdomyolysis:
2. CP of compartment syndrome:
3. Normal compartment pressures
4. Indication of fasciotomy
5. Treatment:
6. Acute renal failure: (why)?
7. Myoglobin :
8. Rhabdomyolysis:
9. Def. :
10. Causes:
11. Management:
5
25. Fluid management post operative:

Stem: 48 year old lady presented by persistent hypotension and tachycardia post
operative THR/Hartman’s procedure, transferred to the ward at 3 PM, hypotensive
and tachycardiac 70/30 at 2 AM
1. Fluid chart: 2X250 ml bolus with small improvement initially
2. Explain the fluid chart:
3. Is that adequate:
4. How would you manage this case:
5. Formula of fluid challenge:
6. The patient is on every 2 hours monitoring, is that adequate?
7. Who to notify ,when?
8. How blood pressure is calculated?
9. How to increase blood pressure?
10. Hormonal response to surgery and trauma:
11. What are the mechanisms by which the kidneys increase osmolarity in
the renal medulla ?
12. Mechanism of action of ADH :
13. Actions of renin angiotensin aldosterone system (R A A S):
6
28. RENAL FAILURE WITH HYPERKALEMIA:

Stem: 78 y, dementia, renal impairment, history of recurrent UTI,
baseline creat. 250, now developped UTI, nausea, vomiting
Bloods:
- K+= 8 mmol Na+ = 121 Creat. = 700
1. Interpret:
2. This patient had urinary catheter inserted, drained 1500 ml, then 4 L/day ,
why?
3. Pathophysiology:
4. Why are uremic patients anaemic?
5. Functions of potassium:
6. Homeostasis of K+:
7. Action of K on the cardiac muscle:
8. What use does knowledge of the cardiac effects of potassium have for surgical
practice?
9. Manifestations of hypokalemia?
10. Manifestations of hyperkalemia?
11. What is the emergency management of hyperkalaemia?
12. Ethical issues of dialysis of 77 y old man with dementia:
7
ASSCC
1. Acute pancreatitis:
Stem: 45 y old male diagnosed and managed for acute pancreatitis 2 weeks later,
now having tachycardia,tachypnea, SOB
1. Differentials:
2. The patient is tachypnic why?
3. Scoring systems:
4. Pathophysiology of hypocalcemia:
5. Pathophysiology of hyperglycemia:
6. CT findings in acute pancreatitis:
7. Management of nutrition:
8. Complications of pancreatitis:
9. Functions of the pancreas:
10. Cause of normal amylase in pancreatitis: ( too early , too late )
11. Causes of acute pancreatitis:
12. Pseudocyst:
13. Def:
14. When
15. Symptoms:
16. Complications of pseudocyst
17. Management of pain:
18. Management of pancreatitis:
19. Management of pseudocyst:
1
2. Surgical feeding options:

Stem: lady with crohn's ------> ileocecal resection------> POD4 anastmotic leakage -
-----> defunctioning ileostomy
1. What does AXR show ?
2. What may be the cause in this patient:

3. Feeding options:
4. Types of non-parentral feeding:
5. Nasojeujenal tube : advantage vs disadvantage
6. Complications of enteral feeding:
7. Complications of parentral feeding :
8. TPN: Indications:
9. Routes of TPN administration:
10. Types of electrolytes in TPN:
11. Complications:
12. How it is given:
13. Components:
14. From which sources may the energy requirements be satisfied?

How much energy does each of these provide?
15. What are the disadvantages of using glucose as the main

energy source?
2
16. Diverticular abscess + septic shock

Stem: old lady ,critically ill, with LIF pain and tendeness
1. DD:
2. Interpret ABG, FBC:

Metabolic acidosis with partial compensation
Increased total lecocytic count
3. Define shock:
4. What kind of shock this patient having? Septic shock
5. Define septic shock:
6. Basic principles of management of septic shock?
7. Antimicrobials:
8. CT confirmed the presence of diverticular abscess, what are the management

options, with advantages and disadvantages?
3
17. Pregnant lady undergoing open chole :

Stem: 34 weeks undergoing open chole for necrotising cholecystitis, BP is
decreasing, HR is decreasing, reversed telendenberg position, combined GA,
epidural, the operation is taking longer duration than expected)
1. Benefits and risks of this patient undergoing this operation:
2. Who to involve in care:
3. Where to mange this case postoperative?
4. Why blood pressure is decreasing?
5. Pre-load:
6. Shock:
7. What will be the body response to decreased blood pressure?

8. Baroreceptors?
9. Factors affecting venous return?
10. Can you name some devices used in mechanical DVT prophylaxis may
be used to improve circulatory parameters in this patient?
11. What can be done to improve the preload of this patient:
12. Actions of inotropes:
4
19. Obstructive jaundice:

[epigastric pain, nausea,vomiting ,diarrhea, increases ALT, AST, ALP,
GGT, urobilinogen undetectable in urine ]
1. Normal bilirubin level:

2. Apparent jaundice --->
3. Why clotting derranged:
4. Alkaline phosphatase :
5. Function of bile:
6. Constituents of bile:
7. How does bile salts help in emulsification of fat?
8. What is bilirubin conjugated to ?
9. Bilirubin metabolism :
10. What is urobilinogen ? How it is formed?
11. Enterohepatic circulation :
12. How to correct clotting abnormality:
13. Other investigation you want to do ?
14. If you find a CBD stone?
15. If the patient had fever, pain, chills?
16. Causes of jaundice:
5
22. Enterocutaneous fistula:

Def.: abnormal communication lined by granulation tissue between the skin and
gastrointestinal tract
1. Predisposing factors:
2. Complications of ECF
3. Management:
4. Factors preventing spontaneous healing:
5. Imaging:
6. Fluid management: High output fistula:
6
26. PERFORATED GASTRIC ULCER:

Stem: middle aged man, OA, NSAID's, peritonism
1. Comment on CXR:
2. The most likely diagnosis:
3. Risk factors of perforation:
4. How can NSAID's causes peptic ulceration?
5. Management options:
6. Post- operative medications:
7. Mechanism of action of PPI:
8. Actions of HCL:
9. Phases of gastric secretions:
10. Priority of operation according to NCEPOD :
7
27. Esophageal varieces and hematemesis:

Stem : chronic alcoholic, 3 times of hematemesis, decreased blood pressure,
increased HR
1. Differentials:
2. How alcohol causes cirrhosis?
3. Pathogenesis of portal HTN in chronic alcoholism:
4. Mechanism of ascites:
5. Sites of portosystemic anastomosis
6. Which Varices are usually bleeding?
7. How will you manage this patient ?
8. Cause of thrombocytopenia in this case?
9. Patient with macrocytic anemia, what could be the cause?
10. How vit. B12 def. causes macrocytic anemia:
11. Surgical treatment options:
12. If the patient is to go for liver transplant , what will you tell his family?
13. Sangstaken Blackemore tube:
14. Ports:
15. Modifiaction:
16. Technique:
8
29. Bloody diarrhea:

55 y old abdominal pain, bloody diarrhea, hypotensive, tachycardiac, feverish,
adimitted , fluid resuscitation done, 10 episodes of bloody diarrhea, stopped after 6
hours
Labs:
FBC : Hb: 8.7 g , platlets: 666000 , wbc's: 12000
Hyponatremia, hypokalemia, increased CRP
Creat. : 109 , urea: 9'
1. What type of anemia ?
2. Why platlets are elevated?
3. Abdominal x-ray :
Dilatation of the ascending and transverse colon , with narrowing of the
descending colon With thumbprinting sign ( Thumbprinting is a
radiographic sign of large bowel wall thickening, usually caused by
oedema, related to an infective or inflammatory process (colitis). The
normal haustra become thickened at regular intervals appearing like
thumbprints projecting into the aerated lumen.)
4. DD of bloody diarrhea:
5. Why not to transfuse blood?
6. Why there is hyponatremia and hypokalemia?
7. How else would you investigate the patient?
8. How will monitor the patient response?
9. Indications of urgent surgical management ?
10. Surgical management :
9
ASSCC
15. Extradural hematoma:

Stem: RTA---> GCS 15----> 2 episodes of vomiting----> amnesic events---> GCS 8
1. Comment on CT: EDH
2. When to consider CT brain for trauma:
3. Normal value of ICP:
4. Ways to measure:
5. Pathophysiology of increased ICP: (Monoro - Kellie hypothesis)
6. Lucid interval :
7. CPP= MAP - ICP
8. MAP auto-regulation range
9. CP of increased ICP:
10. Management:
1
2
3
ASSCC
10. Pneumothorax + CV line insertion:

1. System for reading CXR:
2. Types of pneumothorax:
3. Difference between tension and simple pnemothorax:
4. Safe triangle of insertion of chest tube:
5. Indications of central line insertion:
6. Complications of central venous line insertion:
7. NICE guidlines for insertion:
8. Technique for insertion of central venous line: ( IJV)
9. Removal technique:
10. Sites for inserting a central venous line:
11. Organism causing infection:
12. How to prevent line infection:
1
18. Polytrauma:
Stem: RTA
1. Management of airway and breathing according to ATLS protocol:

(primary survey)
2. Comment on this CXR:
3. How will you manage this?
4. Now, patient is shocked, how will you manage the circulation?
5. Management:
6. How will you monitor the response?
7. Comment on this CT: There is a liver tear
8. Grades of liver tear:
9. Management of liver tear:
10. Is CT was a good investigation of this patient?
11. The four classic areas that are examined for free fluid are :
2
20. Pulmonary edema (fluid overload):
Stem: [post-operative pt., fluid chart + vitals chart : taken crystalloids plus colloids
about 7 litres, 4 litres of them are normal saline, now he is tachycardic,
hypertensive, desaturated, oliguric]
1. What are your expected physical findings?
2. Management:
3. Chest x ray findings in pulmonary edema:
4. Why this patient is on high risk of MI?
5. What is the minimal UOP?
6. Can you explain why the patient is oliguric?
7. Explain what are the fluids given to this patient:
8. Amount of Na in 0.9 % saline:
9. Amount of Na in Hartman's solution:
10. Daily requirement of Na and K:
11. Prevention:

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MRCS OSCE REVISION GUIDE 3rd EDITITION 1 1

◌Ligaments attached to the odontoid process:

◌Ligaments between C1 and C2:

◌Atypical cervical vertebrae and the atypical features:

◌IV disc anatomy:

◌Movement on lumbar vertebrae: Flexion, extension, lateral

◌Level of the spinal cord in newborn and adult: L3 ( at birth) ,

◌Location of the paravertebral venous plexus:

Tumours metastatising to the spine:

◌Structures found at c6:

Where are parts of brachial plexus found:

Erb’s paralysis Klumbek's paralysis

BONES OF THE UPPER LIMB

◌Articulate humerus, radius and ulna:

Scaphoid bone blood supply:

MEDIAN AND ULNAR NERVES

◌Median nerve sensory distribution in the

C/p of ulnar nerve injury at wrist: ( complete claw hand)

◌Why ulnar paradox: In proximal ulnar nerve

Attachments of flexor retinaculum:

◌Proximal: pisiform+ tubercle of scaphoid

◌Structrues passing through carpal tunnel:

MOVEMENTS OF THE THUMB

Q:Where are tendons of FDS and FDP insert?

Q:How to test FDP?

Q:How to test FDS?

Q:How to test ulnar artery( allen' s test)?

Q:Why hand grip is powerful in extension than flexion?

1: Extensor digitorum tendon. 2: Extensor indicies tendon.

◌Tendon attached to pisiform : flexor carpi ulnaris.

◌1st dorsal interosseus :

Q:What makes extensor tendons attached to the phalanges?

ANATOMICAL SNUFF BOX

Insertion of EPL: dorsum of the base of the terminal phalanx of

◌Strucutres passing in spiral groove:

◌C/p of radial nerve injury at the spiral groove:

Median nerve injury at elbow:

◌Supracondylar fracture humerus:

ROTATOR CUFF MUSCLES

◌Shoulder joint abduction:

Factors decreasing the stability of the shoulder joint:

◌sup.: teres minor.

Motor : deltoid + teres minor.

◌Muscles inserted in bicepital groove : ( lady bw 2

UPPER LIMB RELEXES

◌Surface marking of coracoid

◌Structures attached to the coracoid process:

◌Origin: ext.occipital protuberance,superior nuchal

SERRATUS ANTERIOR MUSCLE

◌Origin: 9-10 slips from the 1st to 8 th ribs.

ARCHES OF THE FOOT

Q:What are the components of the Medial Longitudinal arch?

◌ID ligaments on the medial and lateral aspects of the ankle:

Q:What movements occur at the subtalar joint?

A:Inversion and eversion of the foot occur at the subtalar joint.

Q:What are the bones forming ankle joint: ( synovial-hinge)?