SITES OF INJURY: NERVE: MANIFESTATION

NERVE HAND DEFORMITY SPECIFIC MUSCLE

DYSFUNCTION
Ulnar Claw hand deformity Dysfunction of lumbrical and
nerve interosseous muscles
Median "Ape hand" or "Hand of Dysfunction of thumb and finger
nerve Benediction" flexor muscles
Radial Wrist drop and weakness in Dysfunction of wrist and finger
nerve wrist/finger extension extensor muscles
Combined More complex deformity involving A combination of specific muscle
median + both nerves' respective muscle dysfunctions from both nerves'
ulnar innervations injuries

ARM
INJURY/FRACTURE NERVE(S) AT RISK
Medial epicondyle Ulnar nerve
fracture
Supracondylar Median nerve, radial nerve
humerus fracture
Radial head fracture Radial nerve
Midshaft humerus Radial nerve
fracture
Elbow dislocation Median nerve, ulnar nerve, radial
nerve
 TEMPOROMANDIBULAR JOINT

Cavities • Superior Cavity (discotemporal)

Translational movement.
• Inferior Cavity (discomandibular)
Rotational movement
Rotational • Elevation: Temporalis, Masseter and Medial
movements pterygoid muscles
• Depression: Lateral pterygoid, Digastric,
Geniohyoid and Mylohyoid muscles
Translational • Protrusion: Lateral pterygoid, Medial pterygoid
movements muscle, Masseter
• Retraction: Posterior fibres of Temporalis, deep
part of Masseter
• Lateral deviation (left or right):
Ipsilateral movement
Posterior fibres of Temporalis, Digastric,
Mylohyoid and Geniohyoid muscles.
Contralateral Movement
Lateral and Medial pterygoid muscles.
 BRAIN STEM SYNDROMES

Mid brain syndromes

BASE TEGMENTUM TECTUM DORSAL

MID-BRAIN
WEBER CLAUDE BENEDIKT NOTHNAGEL PERINAUD
SYNDROME SYNDROME
Cranial 3 3 3 U/L or B/L 3 None
Nerves
Tracts Corticospinal Red Nucleus 1. Red Nucleus Superior Periaqueductal
Tract 2. Corticospinal Cerebellar Gray matter
Tract peduncles nuclei for
upward gaze
(MLF)

Signs 3rd CN Palsy 3rd CN Palsy 3rd CN Palsy 3rd CN Palsy Upward gaze
Contralateral Contralateral Contralateral Gaze Palsy Palsy
Hemiplegia tremors Hemiplegia Ataxia Fixed pupils
Tremors
 Pontine syndromes

Millard Guber Syndrome Pontocerebellar Syndrome

(Basilar Artery) (AICA)
Region Medial inferior region of Lateral region of caudal Pons
Pons (Spares Medial
Lemniscus)
Cranial Nerves 6 and Some 7th Nerve fibres 7th and 8th
Tracts Corticospinal Spinal trigeminal
Spinothalamic tract
Signs/Symptom I/L Medial Squint I/L Facial Palsy(LMN)
s I/L Facial nerve palsy LMN Tinnitus/Deafness/Vertigo

C/L Hemiplegia I/L Loss of pain and temperature

I/L loss of pain/temp over face

Pontine Haemorrhage
Damage to branches of Basilar + AICA results in Extensive B/L Damage

Involvement Signs/Symptoms
1. Sympathetic fibres (B/L) Pin point pupils
2. Hypothalamus (Heat regulation) Hyperpyrexia
3. Reticular formation Deep Coma
4. Co and Facial Nerve nuclei B/L facial paralysis & Quadriplegia
 MEDULLARY SYNDROMES

MEDIAL MEDULLARY LATERAL MEDULLARY

SYNDROME SYNDROME
(DEJERINE (PICA Syndrome/WALLENBERG
SYNDROME) Syndrome)
Artery ASA (Ant. Spinal) PICA (Post. Inf. Cerebellar)
CN 1.12th CN 1. 9th , 10th , 11th
Tracts 2.Medial lemniscus 2. Sympathetic chain
3.Corticospinal Tract 3. Spinothalamic tract
4. Spinal Trigeminal
5. Vestibular nuclei
Signs/symptoms 1. I/L Tongue deviation 1. Dysphagia , hoarseness, decreased
2. C/L Loss Vibration & gag reflex
discriminative touch 2. I/L Horner's [miosis, ptosis,
3. C/L Hemiplegia anhidrosis]
3. C/L loss of pain & Temp sensations
over Body
4. I/L loss of pain & Temp over face
5. Nausea, diplopia, vertigo
MOVEMENTS AT THE SHOULDER JOINT AND MUSCLES PRODUCING THEM

Movements Main muscles (prime movers) Accessory muscles (synergists)

Flexion • Pectoralis major • Biceps brachii (short head)
(clavicular part) • Coracobrachialis
• Deltoid (anterior fibres) • Sternocostal head of
pectoralis major
Extension • Deltoid (posterior fibres) • Teres major
• Latissimus dorsi • Long head of triceps
Adduction • Pectoralis major • Teres major
(sternocostal part) • Coracobrachialis
• Latissimus dorsi • Short head of biceps
• Long head of triceps
Abduction • Deltoid (lateral fibres) • Serratus anterior
• Supraspinatus • Upper and lower fibres of
trapezius
Medial • Subscapularis • Pectoralis major
rotation • Latissimus dorsi
• Deltoid (anterior fibres)
• Teres major
Lateral • Deltoid (posterior fibres) • Infraspinatus
rotation • Teres minor
HEAD & NECK – IMPORTANT NERVE/ARTERIAL SUPPLY
 UMBILICAL CORD DERIVATIVES

UMBILICAL FOLDS RELATED TO THE BLADDER

NAME OF DERIVED FROM/ CLINICAL SIGNIFICANCE

DERIVATIVE CONTENT

Median Derived from Patent urachus, urachal cyst, urachal sinus,

Umbilical allantois; remnant - diverticulum; used as a landmark for laparoscopic
Ligament Urachus hernia repair

Medial Obliterated foetal Direct hernias are present in medial fossa which
Umbilical umbilical arteries lies between medial and lateral umbilical folds on
Ligament either side

Lateral Inferior Epigastric Reference site for hernia; laterally - lateral fossa
Umbilical Vessels (indirect hernia)
Ligament
Aortic Arch Derivatives
 Median Nerve/Carpel Tunnel Syndrome/Related Test

• The median nerve may be compressed at the level of the carpal tunnel. Carpal
Tunnel Syndrome arises due to anatomic compression or inflammation.

Clinical examination for the same involves:

1. Assessment of sensory loss:

The palmar cutaneous branch of the median nerve passes above the carpal tunnel and
supplies the skin of the thenar eminence. Thus, this area is typically spared, and
sensory loss over the thenar eminence would indicate a more proximal lesion.

2. Assessment of motor function:

The median nerve supplies five muscles including three muscles of the thenar
eminence - flexor pollicis brevis (FPB), opponens pollicis (OP) and abductor pollicis
brevis (APB), along with the first and second lumbricals. In severe or advanced CTS,
muscles of the thenar eminence may be affected leading to weakness of thumb
abduction (APB) and thumb opposition (OP.)

3. Provocative manoeuvres/ tests:

Phalen test: Patient brings the dorsal surfaces of the hands against each other to
provide hyperflexion of the wrist. If pain/ paresthesia in the distribution of the median
nerve is elicited the test is positive.
• Tinel test: Percussion performed over the course of the median nerve just proximal to
the carpal tunnel elicits pain/ paresthesias in the distribution of the median nerve.

• Durkan test or manual carpal compression: Pressure is applied over the transverse
carpal ligament for 30 seconds. Pain/ paresthesia indicates a positive result.

• Hand elevation test: The patient raises the hands above the head for one minute. If
the symptoms are reproduced, the test is positive.
BASAL GANGLIA & RELATED MOVEMENT DISORDERS

LESION EFFECT

1) SUBSTANTIA NIGRA PARKINSON’S

2) GLOBUS PALLIDUS ATHETOSIS

3) SUBTHALMIC NUCLEI BALLISMUS

4) LAUDATE & PUTAMEN CHOREA

 HISTOLOGY SPOTTERS

Cerebellar Histology
Outer molecular Stellate cells and basket cells
layer
Purkinje layer Purkinje cells
Granule cell Small granule cells, large Golgi type II cells, glomeruli
 Fourth ventricle

• Openings in 4th ventricle

o Central : Foramen of Magendie
o 2 lateral : Foramina of Luschka
o Central canal of medulla oblongata
o Cerebral aqueduct of midbrain
• Lateral boundaries of 4th ventricle:
o Superolaterally : superior cerebellar peduncle
o Inferolaterally : inferior cerebellar peduncle, supplemented by gracile
& cuneate tubercles.
• Angles of 4th ventricle
o Superior angle
o Inferior angle
o 2 lateral angles
• Recesses of 4th ventricle
o 2 lateral recesses
o A median dorsal recess
o 2 dorsal recesses
• Floor of the 4th ventricle (Most important)

Part of the floor Structures

• Abducent nucleus
Beneath the superior half of surrounded by internal
floor genu of facial nerve
• Vestibular nuclei

• Vestibular nuclei
Beneath inferior half of • Dorsal nucleus of vagus
floor • Nucleus intercalatus
• True vomiting centre
• Vital centres
 FED/FASTING STATE

Metabolic process Low insulin/glucagon state High insulin/glucagon

(Fasting/Diabetes Mellitus) ratio ( Fed state )
Gluconeogenesis Increased Decreased
Glycogenolysis Increased Decreased
Lipolysis Increased Decreased
Ketogenesis Increased Decreased
Glycogen storage Decreased Increased
 WATER SOLUBLE VITAMINS/ASSAYS

Water soluble vitamins

Vitamin Primary function Deficiency

B1 ( Thiamine ) Decarboxylation of Wet and dry beriberi

alpha keto acids Wernicke-Korsakoff Syndrome

B2 ( Riboflavin ) Mitochondrial electron Cheilosis

carrier for FAD and Magenta Tongue
FMN Corneal Vascularization

B3 ( Niacin ) Electron transfer Pellagra-3 Ds- Diarrhoea, dermatitis and

reactions in the form dementia
of NAD and NADP Peripheral neuropathy

B6 ( Pyridoxin ) Transamination of Cheilosis

amino acids required Stomatitis
for amino acid Glossitis
synthesis
B9 ( Folic Acid ) One carbon Megaloblastic Anemia
metabolism for purine Peripheral neuropathy
and pyrimidine Neural Tube defects
synthesis
B12 ( Cobalamin ) Isomerase and Megaloblastic Anemia
methyltransferase Peripheral neuropathy
cofactor

Vitamin Assay

Vitamin B1 Thiamine RBC transketolase

Vitamin B2 Riboflavin RBC glutathione reductase

Vitamin B6 Pyridoxin RBC transaminase

Vitamin B9 Folic Acid Histidine load test/FIGLU excretion

Vitamin B12 Cobalamin Serum methyl malonate level

 Vitamin B3

Vitamin B3 (Niacin)
Function
• Constituent of NAD/NADP+
• As a Constituent of NAD/NADP+, used in multiple redox
reactions/part of dehydrogenase
Synthesis
Can be synthesised from Tryptophan
Synthesis from Tryptophan requires Vitamin B2/B6(Pyridoxine)
Deficiency
Pellagra(3D’s)
1. Diarrhoea
2. Dementia (Hallucinations + too)
3. Dermatitis
(Broad Collar Rash called Casals Necklace)
4. Hypersensitivity (sun exposed regions).

Causes of Deficiency
1. Poor dietary intake
2. Hartnup Disease
• Autosomal Recessive.
• Defect in neutral amino acid transporters present in PCT(nephron)
and Enterocytes
• Causes neutral aminoaciduria/decreased absorption from intestine
• Decreased tryptophan à decreased conversion to niacin causing
pellagra
3. Maize rich diet (low in tryptophan à low niacin formation)
4. Isoniazid intake (Decreases Vitamin B6à Decreased tryptophan
to niacin conversion)
5. Carcinoid Syndrome (Excessive tryptophan use to form serotonin
à Decreased tryptophan conversion to Niacin)

Clinical Use
• Pellagra/deficiency symptoms
• Dyslipidaemia(Increases HDL/Decreases LDL)
 PEROXISOMAL DISORDERS

Due to mutations in PEX genes encoding PEROXINS

Defective import of 1
Or more protein to Peroxisome

Defective import of proteins PEX 7 defect

Containing PTS1 targeting signal

1.Zellweger (most severe)

2.Neonatal adrenoleukodystrophy RHIZOMELIC CHONDROPLASIA PUNCTATA
3.Infantile Refsum

Zellweger Syndrome

• Clinical features
1) Typical facies [Down's like ]
2) Hypotonia , Neonatal Seizures

• Lab findings :
a) Absent peroxisome
b) cytosol = Catalase enzyme positive
c) Decreased tissue plasmalogen
d) Defective oxidations age-dependent accumulation of phytanic acid/Very long Chain FA
 NADH:NAD RATIO IN CHRONIC ALCOHOLISM

Central to ethanol metabolism and its pathologies is the increased [NADH]/ [NAD+] redox
potential which is due to the oxidation of ethanol by alcohol dehydrogenase leading to
excess production of NADH.

Ethanol metabolism causes increased NADH/NAD+ ratio in the liver, causing:

1. Lactic acidosis due to increased pyruvate conversion to lactate.

2. Fasting hypoglycemia due to decreased gluconeogenesis due to more conversion of OAA
to malate
3. Ketoacidosis due to the diversion of acetyl-CoA into ketogenesis rather than the TCA
cycle
4. Lactate is known to increase renal urate reabsorption thereby decreasing its excretion
by the kidneys and causing hyperuricemia.

# Disulfiram inhibits Acetaldehyde dehydrogenase.

Contraindicated in active alcoholics.
 INBORN ERRORS OF METABOLISM VS URINE ODOURS

INBORN ERRORS OF URINE ODOURS TRICK TO

METABOLISM REMEMBER

MAPLE SYRUP URINE Burnt sugar /

DISEASE caramel/ maple syrup

HAWKINSINURIA Swimming Pool HAWK IN A

odour SWIMMING POOL

3 HYDROXY 3 Cat urine

METHYLGLUTARIC
ACIDURIA
ISOVALERIC ACIDEMIA; Sweaty Feet
GLUTARIC ACIDEMIA
TYROSINEMIA ; Boiled cabbage CAB TYRE BURNING
HYPERMETHIONINEMIA TO FUMES

MULTIPLE CARBOXYLASE Tomcat urine TOMCAT –

DEFICIENCY *MCA – Multiple
Carboxylase

PHENYLKETONURIA Mousy odour

TRIMETHYLAMINURIA Rotting fish

 ALKAPTONURIA

ALKAPTONURIA

• Congenial deficiency of Homogentisate oxidase enzyme leads to the accumulation

of pigment forming homogentisic acid which accumulates in the tissues.
• Autosomal Recessive condition
• Benign condition
• Bluish black colouration of connective tissue, ear cartilage, sclera, synovium
deposits(Ochronosis)
• Urine turns black on standing because of prolonged exposure to air
• Also causes debilitating arthralgias as homogentisic acid is toxic to cartilages.
• TREATMENT – Nitisinone ; Supplementation of vitamin C
 SIGNALLING PATHWAY OF ENDOCRINE HORMONES

Signalling pathway Hormones

cAMP FSH, LH, ACTH, TSH, CRH, hCG, ADH, MSH, PTH, Calcitonin,
Histamine, Glucagon, GHRH

cGMP BNP, ANP, EDRF

IP3 GnRH, Oxytocin, ADH, TRH, Histamine, Angiotensin II, Gastrin

Intracellular receptor Progesterone, Oestrogen, Testosterone, Cortisol, Aldosterone,

Thyroid hormone, Vitamin D

Receptor tyrosine IGF-1, FGF, PDGF, EGF, Insulin

kinase
(MAP kinase)
Non receptor tyrosine G-CSF, Erythropoietin, Thrombopoietin, Prolactin,
kinase Immunomodulators
(JAK/STAT pathway)
 GENETICS : DIAGNOSTIC MODALITIES

Method Type of mutation detected

Cytogenetic analysis Numerical or structural abnormalities

in chromosomes
Fluorescent in situ Numerical or structural abnormalities
hybridization (FISH) in chromosomes
Southern blot(DNA) Large deletion, insertion, rearrangement,
expansions of triplet repeat,
amplification
Polymerase chain reaction Expansion of triplet repeats, variable
(PCR) number of tandem repeats (VNTR),
gene rearrangements, translocations;
prepare DNA for other mutation
methods.
Reverse transcriptase PCR Analyze expressed mRNA (cDNA)
(RT–PCR) sequence; detect loss of expression
DNA sequencing Point mutations, small deletions and
insertions
Restriction fragment Point mutations, small deletions and
polymorphism (RFLP) insertions
Single–strand Point mutations, small deletions and
conformational insertions
polymorphism (SSCP)
Denaturing gradient gel Point mutations, small deletions and
electrophoresis (DGGE) insertions
RNAse cleavage Point mutations, small deletions and
insertions
Oligonucleotide specific Point mutations, small deletions and
hybridization (OSH) insertions
Microarrays Point mutations, small deletions and
insertions
Genotyping of SNPs.
Protein truncation test (PTT) Mutations leading to premature
truncations
Pyrosequencing Sequencing of whole genomes of
microorganisms, resequencing of
amplicons
Multiplex ligation–dependent Copy number variations
probe amplification (MLPA)
 BIOCHEMISTRY LAB TESTS

Name of the test/solution Compound detected

Rothera’s test Ketone Bodies, Branched chain
Ketoacids
Hay’s test Bile salt
Benedict’s solution Simple carbohydrate
Iodine solution Complex carbohydrate
Sudan Lipid
Biuret solution Protein
 GLYCOGEN STORAGE DISORDERS

TYPE NAME ENZYME CLINICAL FEATURES

I Von Gierke Voh Glucose 6 Hypoglycaemia,
phosphatase hyperuricemia,
hepatomegaly
II Pompe’s Phy Lysosomal Acid Cardiac dysfunction
Maltase Infant death
III Cori’s Chem Debranching Limit dextrinosis
(D after C) Cirrhosis
Hepatomegaly
Hypoglycaemia
IV Anderson Aur Branching Cirrhosis
(B after A) Hepatomegaly
Hypoglycemia
V McCardle Maths Muscle Exercise Intolerance
Phosphorylase(M) Myopathy
VI Hers Hoshiar Hepatic Hepatomegaly,
Phosphorylase(H) Hypoglycaemia
VII Tarui Tha PFK Haemolysis

Note: Type Ib has neutropenia in addition to other features of I

HB- OXYGEN DISSOCIATION CURVES
 Left shift (oxygen binding) Right shift (oxygen release)

• Decreased pCo2 • Increased pCo2

• Increased pH • Decreased pH
• Decreased temperature • Increased temperature
• Decreased 2,3 DPG • Increased 2,3 DPG

Oxygen content of blood

O2 content = (O2 bound to haemoglobin) + (O2 solubilized in plasma) =
(1.3XHbX SaO2) + (0.003X PaO2)

SaO2 = percent saturation of arterial blood with O2.

0.003 = solubility constant of O2; PaO2 = partial pressure of O2 in arterial blood.
Normally 1g Hb can bind 1.34 mL O2; normal Hb amount in blood is 15 g/dL.
 TYPES OF HYPOXIA

TYPE OF
HYPOXIA CAUSES DESCRIPTION MANAGEMENT
Anemia, carbon Reduced oxygen- Address the underlying
ANAEMIC monoxide poisoning, carrying capacity of cause (e.g., blood
HYPOXIA hemoglobinopathies blood due to low transfusion for anaemia),
haemoglobin levels provide supplemental
or impaired oxygen, treat carbon
haemoglobin monoxide poisoning
function

Cyanide poisoning, Inability of tissues to Identify and remove the

HISTOTOXIC metabolic disorders, effectively utilize source of toxicity,
HYPOXIA certain drugs or toxins oxygen, despite administer antidotes if
adequate oxygen available, support vital
supply functions, enhance tissue
oxygenation

HYPOXIC High altitude, lung Inadequate oxygen Provide supplemental

HYPOXIA diseases (e.g., reaching tissues due oxygen, treat underlying
pneumonia, pulmonary to reduced partial lung disease or respiratory
edema), pressure of oxygen condition, adjust ventilation
hypoventilation, or impaired gas to improve oxygenation
impaired oxygen exchange in the
diffusion lungs

STAGNANT Heart failure, Reduced blood flow Treat the underlying

HYPOXIA circulatory shock, leading to circulatory problem,
peripheral vascular inadequate oxygen optimize cardiac function,
diseases, blood clot delivery to tissues improve blood flow to
formation, reduced tissues
blood flow to tissues
 CARDIAC ACTION POTENTIAL

Myocardial action potential Pacemaker action potential

Phase 0 – Depolarisation. Voltage Phase 0 – upstroke due to opening of

gated Na+ channels open. voltage gated K+ channels.

Phase 1 – initial repolarisation. Phase 3 – Repolarization. Inactivation

Voltage gated Na+ channels of Ca+ channels and rapid activation
inactivate, opening of K+ channels. of K+ channels

Phase 3 – Rapid repolarisation. Phase 4 – Slow spontaneous diastolic

Slow delayed rectifier K+ channels depolarisation due to If. The slope of
open and voltage gated Ca+ phase 4 determines the HR
channels close
Phase 4 – Resting potential. High
K+ permeability through K+
channels
 Nerve action potential

The following mechanisms are responsible for an action potential :-

• RESTING MEMBRANE POTENTIAL – Membrane is more permeable to K+ than

Na+ at rest. Voltage gated Na+ & K+ channels are closed.
• MEMBRANE DEPOLARISATION – Na+ flows INWARDS.
• MEMBRANE REPOLARISATION –Na+ inflow STOPS. K+ flows OUTWARDS
• MEMBRANE HYPERPOLARISATION -K+ gates are slow to close à Excess K+
EFFLUX occurs resulting in a period of HYPERPOLARISATION. Voltage gated
Na+ channels go back to resting state. Sodium potassium pump restores the
concentration of different ions.
 RENAL PHYSIOLOGY IN A NUTSHELL

Part of nephron Function

• Contains brush border
PCT • Reabsorbs glucose, amino acids, most
HCO3-,Na+,Cl-,PO4, K+, H20 & uric
acid.
• Generates NH3

• Passively reabsorbs H2O via medullary

Thin descending hypertonicity.
loop of Henle • Concentrating segment.
• Makes urine HYPERTONIC.

• Makes urine less concentrated

Thick ascending • Reabsorbs Na+,K+ & Cl-.
loop of Henle
• Paracellular reabsorption of Mg2+ and
Ca2+ through potential generated by K+
back leak.

• Makes urine fully dilute (hypotonic)

Early DCT • Reabsorbs Na,Cl

• Reabsorbs Na in exchange of K and H

Collecting duct (regulated by aldosterone)

DIURETIC AND NEPHRON PARTS IT ACTS UPON

DIURETIC PART
1) Carbonic anhydrase inhibitors PCT
Acetazolamide
2) Loop Diuretics - Furosemide Loop of Henle (Thick
Ascending limb)
3) Thiazide DCT
4) K+ sparing diuretics Collecting tubule
Spironolactone, Amiloride

Mannitol acts on both PCT and ascending loop of Henle

PROXIMAL CONVULATED TUBULE

THICK ASCENDING LIMB

DISTAL CONVULATED TUBULE

COLLECTING DUCT
 TRACTS/COLUMNS & FUNCTIONS

DESCENDING TRACT FUNCTIONS

Lateral corticospinal Controls conscious skilled movements of hands, fingers &
tracts(crossed) toes
Anterior corticospinal Same as that of lateral corticospinal tracts
(uncrossed)
Rubrospinal tract Unconscious coordination of movements
Vestibulospinal tract Unconscious maintenance of posture & balance
Tectospinal tract Controls movements of head, neck & arms in response to
visual stimuli
Lateral reticulospinal tract Mainly responsible for facilitatory influence on motor
neurons to skeletal muscles
Medial reticulospinal tract Mainly responsible for inhibitory influence on motor
neurons to skeletal muscles

ASCENDING TRACT FUNCTIONS

Lateral spinothalamic tract Carry pain & temperature from opposite side of body

Anterior spinothalamic tract Carry light touch, pressure, tickle & itch sensation from
opposite side of the body

Spinotectal tract Visuomotor reflexes, head & eye movements towards

source of stimulation

Spinocerebellar tract Unconscious kinaesthesia (proprioception)

Fasciculus gracilis & Joint sense, vibration sense, 2 point discrimination,

cuneatus stereognosis, conscious kinaesthesia.
 IRON ABSORPTION/METABOLISM

• Hepcidin is the primary Iron regulatory protein, it inhibits iron absorption by

inhibiting iron absorption by inhibiting Ferroportin at basolateral membrane.

• Ferritin is also an acute inflammatory reactant , its levels can be raised in

infections/HLH (>5000-10,000 is specific for HLH)

• Ferritin is low in IDA/ normal in Anemia of chronic disease

• Non-heme iron is absorbed in Fe2+ state.

• Ascorbic acid increases iron absorption while phytates/tannates decrease it.

 BLOOD PRESSURE REGULATION

Receptors:

• Aortic arch transmits via Vagus nerve to solitary nucleus of medulla (responds to
changes in BP).

• Carotid sinus (dilated region superior to bifurcation of carotid arteries) transmits via
glossopharyngeal nerve to solitary nucleus of medulla (responds to changes in BP).

Chemoreceptors:

• Peripheral – carotid and aortic bodies are stimulated by PCO2, pH of blood, and PO2
(<60 mm Hg.)

• Central – are stimulated by changes in pH and PCO2 of brain interstitial fluid, which
in turn are influenced by arterial CO2 as H+ cannot cross the blood-brain barrier. Do not
directly respond to Po2. Central chemoreceptors become less responsive with
chronically PCO2, (e.g., COPD) dependence on peripheral chemoreceptors to detect
O2 to drive respiration.

Baroreceptors:

• Hypotension - arterial pressure → ↓ stretch → ↓ afferent baroreceptor firing → ↑

efferent sympathetic firing and efferent parasympathetic stimulation →
vasoconstriction, contractility, BP. Important in the response to hypovolemic shock.

• Carotid massage - carotid sinus pressure → ↑ afferent baroreceptor firing → ↑ AV

node refractory period → ↓ HR → ↓ CO. Also leads to peripheral vasodilation. Can
cause presyncope/syncope. Exaggerated in underlying atherosclerosis, prior neck
surgery, older age.

• Component of Cushing reflex (triad of hypertension, bradycardia, and respiratory

depression) - intracranial pressure constricts arterioles → cerebral ischemia → ↑
pCO2 and pH → central reflex sympathetic in perfusion pressure (hypertension) → ↑
stretch → peripheral reflex baroreceptor-induced bradycardia.
SKELETAL MUSCLE CONTRACTION
 LUNG VOLUMES/CAPACITY

DESCRIPTION AVERAGE VALUE

Tidal Volume of air entering or leaving 500 ml
Volume lungs during a single breath
Inspiratory Extra volume of air that can be 3000 ml
Reserve maximally expired over and
Volume above the typical resting tidal
volume
Inspiratory Maximum volume of air that can 3500
Capacity be inspired at the end of a normal
quiet expiration (IC = IRV + TV)
Expiratory Extra volume of air that can 1000 ml
Reserve actively expired by maximal
Volume contraction
Residual Minimum volume of air 1200 ml
Volume remaining in the lungs even after
maximal expiration
 GI HORMONES

HORMONE SITE ACTION

Gastrin G cells (stomach antrum, Increased gastric
duodenum) acid secretion, gastric motility
& growth of gastric mucosa.
Somatostatin D cell (pancreatic islets, GI Decreases:
mucosa) 1.Gastric acid & pepsinogen
secretion
2.Pancreatic & small intestine
fluid secretion
3.GB contraction
4.Insulin & glucagon release
Cholecystokinin I cells (duodenum, jejunum) Increases:
1.Pancreatic secretion
2.GB contraction
3.Sphincter of oddi relaxation

Decreases:
Gastric emptying
Secretin S cells Increases:
(duodenum) 1.Pancreatic HCO3 secretion
2.Bile secretion

Decreases:
Gastric acid secretion
Glucose – dependent K cells Exocrine:
insulinotropic peptide (duodenum, jejunum) Decreases gastric acid secretion

Endocrine:
Increases insulin release
Motilin Small intestine Increasing gut motility
Vasoactive intestinal Parasympathetic ganglia in Increases :
polypeptide sphincters, GB and small 1. Intestinal water & electrolyte
intestine secretion
2. Relaxation of intestinal
smooth muscles &
sphincters
Nitric oxide Vagus Increased relaxation of smooth
muscles (LES)
Ghrelin Stomach Increases appetite
 AMINO ACIDS & ASSOCIATED HORMONES

Amino Acid Hormones Synthesized

Tryptophan Serotonin, Melatonin
Thyroid hormones (T3 and T4),
Tyrosine Dopamine, Epinephrine
Thyroid hormones (T3 and T4),
Phenylalanine Dopamine, Melanin
Bile acids, Taurine-conjugated bile
Taurine salts
Growth Hormone-releasing Hormone
Glutamine (GHRH)
 APOPTOSIS VS NECROSIS

APOPTOSIS NECROSIS
DEFINITION Programmed cell death Uncontrolled cell death due
characterized by controlled to injury or pathological
cellular dismantling processes
MORPHOLOGICAL Cell shrinkage Cell swelling
CHANGES Chromatin condensation Organelle damage
Formation of apoptotic Rupture of the plasma
bodies membrane, Release of
cellular contents
ENERGY ATP-dependent process ATP-independent process
REQUIREMENT
Involves caspase activation Not regulated by specific
SIGNALLING and regulated by pro- signalling pathways
PATHWAYS apoptotic and anti-apoptotic
factors

INFLAMMATORY Generally does not induce Often triggers an

RESPONSE an inflammatory response inflammatory response

PHYSIOLOGICAL Essential for development, Generally associated with

ROLE tissue homeostasis, and tissue injury and pathological
immune regulation conditions

Phagocytosis of apoptotic Inflammatory response may

REMOVAL OF bodies by neighbouring lead to clearance of cellular
CELL DEBRIS cells debris by immune cells

CONSEQUENCES No release of cellular Release of cellular contents

contents and minimal may cause inflammation and
damage to surrounding damage to surrounding tissue
tissue

Pro-apoptotic Factors Anti-Apoptotic Factors

BAX Bcl-2
PUMA Bcl-xL
BAK MCL-1
BAD XIAP
NOXA Survivin
 RENAL BIOPSY FINDINGS

Diseases Histopathological Findings

Minimal Change Disease Diffuse effacement of podocyte foot
processes
Focal Segmental Glomerulosclerosis Segmental sclerosis affecting some
glomeruli

Membranous Nephropathy Thickening of glomerular basement

membrane and spike-like subepithelial
deposits

IgA Nephropathy Mesangial proliferation and deposition of

IgA
Lupus Nephritis Immune complex deposition, including
subendothelial, mesangial, and
subepithelial deposits(Full house)

Acute Post-Streptococcal GN Glomerular hypercellularity, proliferation

of mesangial cells, and granular deposits
of immune complexes

Membranoproliferative GN Thickening of glomerular capillary walls

with mesangial cell proliferation
 LUNG CARCINOMA

SMALL CELL ADENOCARCINOMA SQUAMOUS LARGE CELL

CARCINOMA CELL CARCINOMA
(Oat cell carcinoma) CARCINOMA
Central in location Peripheral in location Central in Peripheral in
location location

Small dark blue cells present; Glandular pattern Keratin Pearls Pleomorphic giant
Salt/Pepper pattern Short plump microvilli (P40) cells with prominent
Neoplasm of neuroendocrine nucleoli present.
Kulchitsky cells
Highly anaplastic
Azzopardi effect undifferentiated
tumour
IHC Markers IHC Markers
Synaptophysin, TTF-1
Chromogranin A, Neuron Napsin A
specific enolase (NSE)
CD56
MYC amplification EGFR/KRAS/ALK/ROS CDK2NA lost

Smokers (Highest Commonly found in Commonly found Associated with

association) females, and in non- in smokers smoking
smokers
Paraneoplastic Syndromes • Associated with • Hilar mass • Poor prognosis
* Lambert Eaton syndrome Hypertrophic • Associated with • Diagnosis of
*Myasthenia gravis osteoarthropathy Cavitation and exclusion
*Carcinoid • Most Common hypercalcemia
*Cushing syndrome • Spreads aerogenously
*SIADH (satellite tumours)
 HEMOLYTIC ANEMIAS (CLASSIFICATION)

SITE OF HEMOLYSIS

Intravascular Extravascular Both( Intravascular &

Extravascular)
Mechanical injury: *Hereditary spherocytosis *G6PD deficiency
*Macroangiopathic
haemolytic anaemia *Sickle cell Anemia *AIHA
*Repetitive physical
trauma *Thalassemia
*Trauma by cardiac
valves
Antibody mediated
destruction
*HDN
*Drug induced
*Transfusion reactions

Infections
*Babesiosis/Malaria

Exogenous toxic factors

*Clostridial sepsis

TYPE OF DEFECT

Type of defect Intracorpuscular Extra-corpuscular

Congenital 1.Hemoglobinopathies Familial/Atypical HUS

2.Enzyme defects
3.Cytoskeletal defects
Acquired PNH (Paroxysmal 1.AIHA
nocturnal 2.Mechanical
haemoglobinuria) destruction (MAHA)
3.Toxins
4.Drugs
5.Infections
 COAGULATION DISORDERS

Coagulation Pathology Clinical Features Inheritance Laboratory

Disorder Findings
Haemophilia A Deficiency of Prolonged X-linked Prolonged PTT,
clotting bleeding, recessive normal BT,
factor VIII. spontaneous joint decreased factor
bleeding, easy VIII activity,
bruising. normal platelet
count.
Haemophilia B Deficiency or Prolonged X-linked Prolonged PTT,
dysfunction bleeding, joint recessive normal BT,
of clotting bleeding, mucosal decreased factor
factor IX. bleeding. IX activity, normal
platelet count.

Deficiency of Prolonged Autosomal Prolonged BT,

Willebrand bleeding, mucosal dominant or variable PTT,
von Willebrand factor. bleeding, heavy recessive, decreased von
Disease menstrual depending on Willebrand factor
bleeding. the subtype. antigen and
activity, normal or
decreased factor
VIII activity.

Disseminated Widespread Prolonged Secondary to

Intravascular activation of bleeding, various Prolonged PTT,
Coagulation coagulation thrombosis, organ underlying prolonged PT,
(DIC) system. dysfunction. conditions. decreased platelet
count, decreased
fibrinogen levels.
 RBC SHAPES AND CONDITIONS

Red Blood
Cell Shape Associated Conditions
Target cells Thalassemia, Liver disease, Iron deficiency
Tear-drop Myelofibrosis, Thalassemia, myelodysplastic
cells syndromes
Elliptocytes Hereditary elliptocytosis, Thalassemia
Hereditary spherocytosis, Autoimmune
Spherocytes hemolytic anemia
Microangiopathic hemolytic anemia, Severe
Helmet cells burns
Abetalipoproteinemia, Liver disease,
Acanthocytes Abetalipoproteinemia
Microangiopathic hemolytic anemia,
Schistocytes Disseminated intravascular coagulation (DIC)
Drepanocytes
(sickle cells) Sickle cell disease
 PNEUMOCONIOSIS

Type of Silicosis Asbestosis Coal Worker's Berylliosis

Pneumoconiosis Pneumoconiosis

Causative Agent Inhalation of Inhalation of Inhalation of Inhalation of

crystalline asbestos fibres coal dust beryllium particles
silica particles

Pathogenesis Fibrotic Fibrotic Fibrotic reaction Granulomatous

reaction to reaction to to coal dust reaction to
silica particles asbestos fibres particles beryllium particles
in the lung in the lung

Histopathological Silicotic Fibrosis with Coal dust-laden Non-caseating

Findings nodules with asbestos bodies macrophages granulomas
concentric and ferruginous and fibrosis
layers bodies
Radiological Multiple small Reticulonodular Small rounded Hilar
Findings nodules, opacities, opacities, lymphadenopathy,
eggshell pleural plaques progressive ground-glass
calcifications massive fibrosis opacities

Risk of Increased risk Increased risk Increased risk of Increased risk of

Malignancy of lung cancer of lung cancer, lung cancer lung cancer
and Mesothelioma
Tuberculosis
VACUTAINERS/USES
 ACUTE LEUKEMIAS

AML
( Granules/Auer rods in cytoplasm/nucleoli/abundant cytoplasm)

ALL
(No granules, minimal cytoplasm, high N/C ratio, 01- nucleoli)
 INVESTIGATION OF CHOICE IN LEUKEMIAS

ALL Flow cytometry of Bone Marrow aspirate

AML Flow cytometry of Bone Marrow aspirate
CLL Flow cytometry
CML RTPCR For BCR-ABL/FISH for t(9:22)

*Remember in case of Chlorma/Mediastinal mass in Emergency – next step is to do PS to

look for blasts, not BM.

ALL PROGNOSTIC FACTORS

GOOD POOR
1-10 years <1 , >10 years
Female Male
TLC<50,000 >50000
No HSM Hepatosplenomegaly +
B-ALL T-ALL
Good prednisolone Poor response
response
t(12:21) t(9:22) , t(4:11)
Hyper-diploidy Hypodiploidy
 IMMUNODEFICENCY DISORDERS

B CELL DEFECTS

DISEASE DEFECT TYPICAL FINDINGS

PRESENTATION
X-linked / Bruton · X-R Recurrent bacterial & · Absent B cells
agammaglobulinemia · No B-cell enteroviral infections · Decreased Ig,
maturation after 6 months all classes
· Defect in BTK · Absent/scanty
LN & tonsils

Selective IgA · MC 1° · Airway & GI · Decreased

deficiency immunodeficiency infections IgA
· Unknown cause · Autoimmune diseases · Increased
· Atopy susceptibility to
Giardiasis
Common variable · Defective B-cell · Usually diagnosed · Decreased
immunodeficiency differentiation after puberty plasma cells
· Unknown cause · Autoimmune disease · Decreased Ig
· Bronchiectasis
· Lymphoma
· Sinopulmonary
infections
 T CELL DEFECTS

DISEASE DEFECT TYPICAL FINDINGS

PRESENTATION

Thymic aplasia Failure of CATCH-22 • Decreased T cells

(DiGeorge syndrome) development of third Cardiac defects • Decreased PTH
& fourth pharyngeal Abnormal facies • Absent thymic
pouches. Thymic hypoplasia shadow on chest
Cleft palate Xray
Hypocalcemia
22q11 deletion

IL-12 receptor AR • Disseminated Decreased IFN-𝛾

deficiency Decreased Th1 mycobacterial & Increased
response fungal infections susceptibility to
• Present after BCG mycobacterial
administration infections

Autosomal dominant • STAT3 mutation Cold staphylococcal Increased Ig-E

hyper IgE syndrome • Impaired abscesses increased
(Job syndrome) recruitment of retained baby teeth eosinophils
neutrophils coarse facies
• Deficiency of Eczema
Th17 cells fractures with minor
trauma

Chronic • Defect in AIRE Persistent non-invasive Absent T-cell

mucocutaneous • Impaired cell- candidiasis response to candida
candidiasis mediated (in vitro)
immunity against Absent cutaneous
candida reaction to Candida
antigens
 COMBINED B and T CELL DEFECT

DISEASE DEFECT TYPICAL FINDINGS

PRESENTATION

Severe combined • Defective IL-2R (XR) • FTT • Decreased TREGs

immunodeficiency • ADA deficiency (AR) • Chronic diarrhea • Absent thymic
• RAG mutation (VDJ • Recurrent shadow
recombination defect) infections

Ataxia- • AR TRIAD • Raised AFP

telangiectasia (A) • Defect in ATM gene • Ataxia • Decreased IgA, IgG
• Failure to detect DNA • Spider & IgE
damage angiomas • Increased sensitivity
• IgA to radiation
deficiency

Increased risk
of leukaemia &
lymphoma

Hyper-IgM • XR • Severe pyogenic • Normal or increased

syndrome • Defective CD40L on Th infections (early IgM
cells life) • Decreased IgG, IgA
• Defective class witching • opportunistic & IgE
infections

Wiskott-Aldrich • XR • Thrombocytopenia • Normal to decreased

syndrome • WAS gene mutation • Eczema IgG, IgM
• Defective antigen • Recurrent • Increased IgE & IgA
presentation infections
• Increased risk of
malignancy
 PHAGOCYTE DISORDERS

DISEASE DEFECT TYPICAL FINDINGS

PRESENTATION

Leukocyte Adhesion • AR • Delayed • Neutrophilia

deficiency (type 1) • LFA-1 integrin separation of • Absence of
(CD18) on umbilical cord neutrophils at
phagocytes • Absent pus infection sites
• Impaired • Recurrent skin & • Impaired wound
migration & mucosal bacterial healing
chemotaxis infections

Chediak Hegashi • AR PLAIN • Giant granules in

syndrome • Defect in LYST Progressive platelets &
• Microtubule neurodegeneration granulocytes (B)
dysfunction Lymphohistiocytosis
• Defective Albinism
phagosome- Recurrent bacterial
lysosome fusion infections
Neuropathy • Pancytopenia
(peripheral) • Mild coagulation
defects

Chronic Granulomatous • X-linked more • Recurrent • Abnormal DHR test

disease common infections & • NBT reduction test
• Defective granulomas fails to turn blue
NADPH oxidase • Increased
• Defective susceptibility to
respiratory burst catalase +
in neutrophils organisms
 PEDIGREE ANALYSIS

MODE OF IMPORTANT POINTS

INHERITANCE
AUTOSOMAL ü No gender differences
DOMINANT ü All generations are affected
ü Example- Structural defects
AUTOSOMAL ü No gender differences
RECESSIVE ü Skip generations present
ü Example - Inborn errors of
metabolism (except Hunter disease,
Fabry disease – X linked Recessive)
X-LINKED ü Father transmits disease to daughters
DOMINANT ü Mother transmits disease to 50% of
the children
X- LINKED ü Males are affected
RECESSIVE ü Females are carriers
ü Skip generation present
MITOCHONDRIAL • Only FEMALE transmits the disease
to all other generations
 THROMBOELASTOGRAPHY

Throboelastography is a technique for evaluating the effectiveness of blood coagulation.

Surgery, anaesthesiology, emergency rooms, intensive care units, labour and delivery
departments are where TEG is most frequently employed. It evaluates fibrinolysis, clot
strength, and platelet function
ONCOGENIC VIRUSES
 ANTIDEPRESSANTS

Drug class MOA Toxicities

Tricyclic Block norepinephrine Alpha block, Muscarinic block,
antidepressants (NE) and 5-HT sedation, weight gain
Amitriptyline, transporters
clomipramine, Overdose
imipramine, etc Arrhythmias, seizures
Selective serotonin Block 5-HT Sexual dysfunction
reuptake inhibitors transporters
(SSRIs) Overdose
Citalopram, Serotonin syndrome
fluoxetine,
paroxetine,
sertraline, etc
Serotonin- Block NE and 5-HT Anticholinergic, sedation,
norepinephrine transporters Hypertension (venlafaxine)
reuptake inhibitors
(SNRIs)
Venlafaxine,
desvenlafaxine,
Duloxetine
5-HT2 antagonists Block 5-HT2 Sedation
Nefazodone, receptors Modest alpha and H1 blockade
trazodone (trazodone)
Trazodone - Priapism
Other Heterocyclics Mirtazapine blocks Lowers seizure threshold
Amoxapine, pre-synaptic α2 (amoxapine, bupropion)
bupropion, receptors Sedation and weight gain
maprotiline, (Mirtazapine)
mirtazapine Mechanism of action
of others uncertain
Monoamine oxidase Inhibit MAO-A and Hypotension, insomnia
inhibitors (MAOIs) MAO-B
Isocarboxazid, Selegiline more active
phenelzine, vs MAO-B
selegiline
 EXTRAPYRAMIDAL SIDE EFFECTS OF ANTIPSYCHOTIC MEDICATIONS

SIDE EFFECT ONSET CLINICAL SIGNS/SYMPTOMS MANAGEMENT

Acute Dystonia 1-5 days Muscular spasms involving Anticholinergics
Face/neck/back etc. (Benztropine
/Diphenhydramine)
Akathisia 5 to 50 days Restlessness/Agitation/inability to Propranolol/ BZD
stay still (Lorazepam)/
Anticholinergics
Parkinsonism 1 to 4 weeks Bradykinesia/tremors/rigidity Dose/Antiparkinsonian
drugs(anticholinergics)
Tardive Late(Months Involuntary repetitive body Deutetrabenazine (VMAT2
Dyskinesia to years) movements (M/C- Orofacial) inhibitor)
Neuroleptic Few Weeks Fever, Rigidity, Unstable BP Dantrolene
Malignant to Months
Syndrome
 ANTIPSYCHOTICS

DRUG CLASS MOA CLINICAL TOXICITIES

APPLICATIONS
Phenothiazines Block of D2 receptors >> 1.Schizophrenia, 1.Extensions of α- and M
Chlorpromazine 5-HT2 receptors 2.Bipolar disorder receptor-blocking actions
Fluphenazine (manic phase) 2.Extrapyramidal
Thioridazine 3.Antiemesis dysfunction
4.Pre-op sedation 3.Hyperprolactinemia

Thioxanthene
Thiothixene
Butyrophenone Block of D2 receptors >> 1.Schizophrenia Extrapyramidal
Haloperidol 5-HT2 receptors 2.Bipolar disorder dysfunction (major)
(manic phase)
3.Huntington’s
chorea
4.Tourette’s
syndrome
Atypicals Block of 5-HT2 receptors 1.Schizophrenia 1.Agranulocytosis
Aripiprazole( >> D2 receptors (positive and (clozapine)
Clozapine negative 2.Diabetes and weight
Olanzapine Aripiprazole is partialD2 symptoms) gain (clozapine,
Quetiapine Agonist 2.Bipolar disorder olanzapine)
Risperidone Risperidone has (olanzapine, 3.Hyperprolactinemia
Ziprasidone maximum D2 blockade risperidone) (risperidone)
3.Major 4.QT prolongation
depression (ziprasidone)
(aripiprazole)
4.Agitation in
Alzheimer’s and
Parkinson’s
Lithium Uncertain, sup Bipolar affective Tremor, edema,
presses IP3 and DAG disorder - prevents hypothyroidism, renal
signalling mood swings dysfunction, D pregnancy
(prophylaxis) category

Alternative Unclear actions in bipolar Valproic acid 1.Hepatotoxicity and

drugs for disorder competes with induction of drug
bipolar lithium as first metabolism
affective choice in bipolar (carbamazepine)
disorder disorder- acute 2.Rash (lamotrigine)
Carbamazepine phase. 3.Weight gain, and
Lamotrigine Others also used inhibition of drug
Valproic acid in acute phase and metabolism (valproic
for prophylaxis in acid)
depressive phase
 ANTICHOLINERGIC SIDE EFFECTS

Organ Effect Mechanism

CNS Sedation, anti-motion sickness Block of muscarinic

action, Antiparkinsonian action, receptors, several
amnesia, delirium subtypes

Eye Cycloplegia, mydriasis Block of M3 receptors

Bronchi Bronchodilation, especially if Block of M3 receptors

constricted

Gastrointestinal Relaxation, slowed peristalsis, Block of M1, M3

tract reduced salivation receptors

Genitourinary Relaxation of bladder wall, Block of M3 and

tract urinary retention possibly M1 receptors

Heart Initial bradycardia, especially at Tachycardia from

low doses, then tachycardia block of M2 receptors
in the sinoatrial node

Blood vessels Block of muscarinic vasodilation; Block of M3 receptors

not manifest unless a muscarinic on endothelium of
agonist is present vessels

Glands Marked reduction of salivation; Block of M1, M3

moderate reduction of receptors
lacrimation, sweating; less
reduction of gastric secretion
 TOXICITIES & ANTIDOTES

TOXIN TREATMENT
Acetaminophen N-acetylcysteine (replenishes glutathione)

AChE inhibitors, Atropine > pralidoxime

Organophosphates
Antimuscarinic, Physostigmine (crosses BBB), control Hyperthermia
Anticholinergic
agents
Arsenic Dimercaprol, Succimer
Benzodiazepines Flumazenil
β-blockers Atropine, glucagon, saline
Carbon monoxide 100% O2, hyperbaric O2
Copper Penicillamine, Trientene

Cyanide Hydroxocobalamin, nitrites + sodium thiosulfate

Dabigatran Idarucizumab
Direct factor Xa Andexanet alfa
inhibitors (eg,
apixaban)
Heparin Protamine sulfate
Iron (Fe) Deferoxamine, deferasirox, deferiprone
Lead Penicillamine, EDTA,
Dimercaprol, Succimer,
Mercury Dimercaprol, Succimer

Methotrexate Leucovorin
Methanol, Fomepizole > ethanol, dialysis
Ethylene glycol
Methaemoglobin Methylene blue, Vitamin C (reducing agent)
Opioids Naloxone
Salicylates NaHCO3 (alkalinize urine), dialysis
TCAs NaHCO3 (stabilizes cardiac cell membrane)
Warfarin Vitamin K (delayed effect), PCC (prothrombin
complex concentrate)/FFP (immediate effect)
 MONOCLONAL ANTIBODIES

Agent Target

Adalimumab, Soluble TNF-α

Certolizumab,
Golimumab,
Infliximab

Eculizumab Complement protein C5

Guselkumab IL-23
Ixekizumab, IL-17A
Secukinumab
Natalizumab α4-integrin
Ustekinumab IL-12/IL-23
Vedolizumab α4-integrin
Denosumab RANKL
Emicizumab Factor IXa and X
Omalizumab IgE
Palivizumab RSV F protein

Agent Target Use

Alemtuzumab CD52 Chronic lymphocytic leukaemia
(CLL), multiple sclerosis
Bevacizumab VEGF Colorectal cancer (CRC),
(inhibits renal cell carcinoma (RCC),
blood vessel non–small cell lung cancer
formation) (NSCLC), Angio-proliferative
retinopathy
Cetuximab, EGFR Metastatic CRC (wild-type
panitumumab RAS), head and neck cancer
Rituximab CD20 Non-Hodgkin lymphoma,
CLL, rheumatoid arthritis,
ITP, TTP, AIHA, multiple
sclerosis
Trastuzumab HER2 Breast cancer, gastric cancer
Pembrolizumab, PD-1 Various tumours (e.g., NSCLC,
Nivolumab, RCC, melanoma, urothelial
Cemiplimab carcinoma)
Atezolizumab, PD-L1 Various tumours (e.g., NSCLC,
Durvalumab, RCC, melanoma, urothelial
Avelumab carcinoma)
Ipilimumab CTLA-4 Various tumours (e.g., NSCLC,
RCC, melanoma, urothelial
carcinoma)
 ANTIRETROVIRAL THERAPY

DRUG MECHANISM OF ACTION SIDE EFFECTS

NRTIs Competitively inhibit Myelosuppression, nephrotoxicity.
Abacavir, nucleotide binding to reverse
Tenofovir, transcriptase and terminate the Abacavir contraindicated if patient has
Lamivudine, DNA chain. HLA-B*5701 mutation due to increased
Emtricitabine, risk of hypersensitivity.
Zidovudine.
NNRTIs Bind to reverse transcriptase at Rash and Hepatotoxicity are common to
Efavirenz, site different from NRTIs. all NNRTIs.
Nevirapine. Do not require phosphorylation Vivid dreams and CNS symptoms are
to be active or compete with common with efavirenz.
nucleotides.
Integrase Inhibit HIV genome integration Increased Creatine kinase, Weight gain.
inhibitors into host cell chromosome by
Bictergravir , reversibly inhibiting HIV
Dolutegravir integrase.
Protease Prevents maturation of new Hyperglycaemia, GI intolerance (nausea,
inhibitors virions by inhibiting protease diarrhea).
Ritonavir, that cleaves the polypeptide Rifampin (potent CYP/UGT inducer)
Lopinavir, products of HIV mRNA into decreases protease inhibitor
Atazanavir, their functional parts concentrations; use rifabutin instead.
Darunavir Ritonavir (cytochrome P-450 inhibitor) is
only used as a boosting agent.

Entry inhibitors
Enfuviritide Binds to gp41 inhibiting fusion. Skin reaction at injection site.

Maraviroc Binds CCR-5 on T cells,

inhibiting interaction with
gp120.
 THERAPEUTIC INDEX- LD50, ED50

• Measurement of drug safety.

• Therapeutic window—range of drug concentrations that can safely and effectively
treat disease

!"#$ 𝒎𝒆𝒅𝒊𝒂𝒏 𝒕𝒐𝒙𝒊𝒄 𝒅𝒐𝒔𝒆

%"#$
= 𝒎𝒆𝒅𝒊𝒂𝒏 𝒆𝒇𝒇𝒆𝒄𝒕𝒊𝒗𝒆 𝒅𝒐𝒔𝒆

DRUGS WITH NARROW THERAPEUTIC INDEX (REQUIRE TDM)

• Lithium
• Valproate
• Cyclosporine
• Tacrolimus
• Digoxin
• Theophylline
• Carbamazepine
• Phenytoin
• Methotrexate
• Warfarin
 DRUG AGONIST/ANTAGONIST

INTERACTION POTENCY EFFICACY COMMENTS

WITH AGONIST
Competitive Decrease No change Can be
Antagonist (A) overcome by
increasing
agonist
concentration
Non-competitive No change Decrease Cannot be
Antagonist (B) overcome by
increasing
agonist
concentration
Partial agonist (C) Independent Decrease Acts at same
site as agonist.

Formulas to remember
 POTENCY VS EFFICACY

EFFICACY POTENCY
Maximal effect a drug can produce. Amount of drug needed for a given effect
Represented by the y-value (Vmax). Represented by the x-value (EC50).
Increased y-value = increased Vmax = Left shifting =Decreased EC50 =
increased efficacy increased potency = less drug needed.
Unrelated to potency (ie, efficacious Unrelated to efficacy (ie, potent drugs
drugs can have high or low potency). can have high or low efficacy).
Partial agonists have less efficacy than
full agonists

DRUG A HAS HIGHER EFFICACY THAN DRUG B

DRUG A HAS HIGHER POTENCY THAN DRUG B

 CLINICAL TRIALS

Clinical Description Primary goal

Phase
Phase 1 Initial testing of a drug in a small group Safety, Determining safe dosage
of healthy volunteers to assess safety
and dosage levels.
Phase 2 Evaluating the drug's effectiveness and Test Effectiveness
side effects in a larger group of patients.
Phase 3 Large-scale testing in a diverse patient Confirm Effectiveness, Test
population to confirm efficacy, monitor against existing standard.
side effects.
Phase 4 Post-marketing surveillance to monitor Long term effects
long-term safety and effectiveness in
real-world use.
 ANTIDIABETIC DRUGS

Class Examples Mechanism of Action Common Side Effects

Biguanides Metformin Decreases glucose Nausea, diarrhoea, lactic
production in the liver acidosis
Sulfonylureas Glipizide, Stimulates insulin release Hypoglycemia, weight
Glyburide, from the pancreas gain
Glimepiride

Thiazolidinediones Rosiglitazone, Improves insulin sensitivity Weight gain, fluid

(TZDs) Pioglitazone in muscle and fat tissues retention, heart problems
Alpha-Glucosidase Acarbose, Delays absorption of Abdominal discomfort,
Inhibitors Miglitol carbohydrates in the gas, diarrhoea
intestines
Dipeptidyl Sitagliptin, Enhances the action of Nasopharyngitis, headache,
Peptidase-4 Saxagliptin, incretin hormones joint pain
Inhibitors (DPP-4 Linagliptin
Inhibitors)
Sodium-Glucose Canagliflozin, Promotes glucose excretion Genital yeast infections,
Cotransporter-2 Dapagliflozin, in the urine urinary tract infections
Inhibitors (SGLT2 Empagliflozin
Inhibitors)
Exenatide, Increases insulin secretion, Nausea, vomiting, weight
Glucagon-like Liraglutide, suppresses glucagon loss
Peptide-1 Dulaglutide release
Receptor Agonists
(GLP-1 Receptor
Agonists)
Insulin Regular insulin, Replaces or supplements Hypoglycaemia, weight
Insulin lispro, natural insulin production gain
Insulin glargine
 LITHIUM

Lithium
Pharmacokinetics
• Half Life: 20-24 hours
• Exclusively excreted by Kidney
• Concomitant THIAZIDE USE – increased Na+
absorption at PCT, Decreased clearance of
Lithium
Mechanism of Action
• Unknown
• Likely related to inhibition of Phospho-inositol
cascade
Uses
• Acute Mania/Bipolar disorder
• Suicide Prevention
Blood levels
• Narrow Therapeutic range
• Require TDM
• Therapeutic Range 0.8-1.2 mEq/L
• Toxicity > 1.5 mEq/L
• Prophylaxis/Maintenance 0.5-0.8 mEq/L
Contraindications
• Chronic Kidney disease
• Thiazide use
Adverse Effects
• M Movement disorders (coarse tremors, ataxia)
• N Nephrogenic DI(Diabetes Insipidus
• O HypOthyroidism
• P Pregnancy problems(Ebstein anomaly)
• Others- Acne/Weight gain/GI disturbances
 ASPIRIN TOXICITY

MANAGEMENT OF ASPIRIN TOXICITY:

• Activated charcoal is used in multiple doses of absorption of the ingested drug

• Metabolic acidosis is treated with 8.4% sodium bicarbonate
• IV NS is required to control severe dehydration (from sweating & vomiting). Fluids should
be given with caution to avoid precipitating pulmonary edema
• In severe poisoning, urinary alkalization is needed; one litre of 1.26% sodium bicarbonate
is infused over 3 hours, keeping urine pH around 7.5-8.5. alkaline urine facilitates aspirin
excretion
• Haemodialysis is very effective in removing salicylate, correcting acid base imbalance.
 IMPORTANT STAINS & CULTURE MEDIA

STAINS ORGANISMS
Gram stain First line lab test for bacterial identification:
- Gram Positive bacteria (thick peptidoglycan layer) :
Purple
- Gram Negative: Pink
Giemsa stain Chlamydia, Rickettsia, Trypanosome, Borrelia,
Helicobacter pylori, Plasmodium
Periodic acid Schiff Tropheryma whipplei
stain
Ziehl- Nelsen stain Acid-fact bacteria
India ink stain Cryptococcus neoformans
Silver stain Helicobacter pylori, Legionella, Bartonella henselae
Fluorescent Pneumocystis jirovecii, Giardia & Cryptosporidium
antibody stain
 RICKETTSIA AND OTHER ATYPICAL ORGANISMS

GENUS SPECIES DISEASE VECTOR

Rickettsia R. prowazekii Epidemic typhus Human body louse
R. typhi Endemic typhus Rat flea
R. rickettsia RMSF Ixodid ticks
R. conori Boutonneuse fever Ixodid ticks
R. australis Australian tick typhus Ixodid ticks
R. Siberia Siberian tick typhus Ixodid ticks
R. akari Rickettsial pox Mites
Orientia O. tsutsugamushi Scrub typhus Trombiculid mite
Coxiella C. burnetti Q fever Extra human: tick
Human:Nil
Ehrlichia E. chaffensis Human monocytic Tick
ehrlichiosis
E. ewingii Human monocytic Tick
ehrlichiosis like
Anaplasma A. phagocytophilum Human granulocytic Tick
Anaplasmosis
GRAM POSITIVE ORGANISMS IDENTIFICATION
GRAM NEGATIVE ORGANISMS IDENTIFICATION
SAMPLE COLLECTION FOR BLOOD CULTURE
 HANDWASHING

Hand hygiene is the single most important step to curb Hospital acquired infections
 MOTILITY PATTERNS

MOTILITY ORGANISM
Darting/vibratory Vibrio, campylobacter
Swarming Proteus, Bacillus cereus
Tumbling Listeria monocytogenes
motility
Spinning Fusobacterium gyrans
Stately Clostridia
Corkscrew Treponema pallidum
Falling leaf Giardia
Twitching Eikenella
Differential Yersinia enterocolitica & Listeria
motility monocytogenes
Jerky Trichomonas vaginalis
Gliding Mycoplasma, Entamoeba
Lashing Saprophytic spirochetes

MICRSCOPIC FEATURES OF FUNGI

Fungal Infection Microscopic Characteristics

Septate hyphae with acute-angle
Aspergillosis branching and conidial heads
(aspergillus conidiophores).
Candidiasis Oval or round budding yeast cells with
or without pseudohyphae.
Broad, irregular, non-septate hyphae
Mucormycosis with right-angle branching (ribbon-
like appearance).
Histoplasmosis Small, oval yeast cells within
macrophages (intracellular yeast cells).
Cryptococcosis Round yeast cells surrounded by a
clear capsule.

Blastomycosis Broad-based budding yeast cells

with single or multiple buds.
Coccidioidomycosis Spherules containing endospores.
Para
coccidioidomycosis Multiple budding yeast cells with a
"steering wheel" appearance.
 ROTAVIRUS

• Segmented dsRNA virus (reovirus)

• Most important cause of diarrhoea in children less than 5 years.
• Pathogenesis : villous destruction & atrophy leading to decreased absorption of Na+ and
K+ loss.(NSP4)

ORAL ROTAVIRUS VACCINES

Vaccine RotaVac RotaTeq RotaRix RotaSil
Type Indian Neonatal Human Bovine Human Bovine
(116E)/(G9P11) Pentavalent Monovalent Pentavalent;
Human Bovine (RV5) (RV1) Thermostable
Monovalent
Number Of 1 5 1 5
Strains
National 3 Doses Not Included Not Included Not Included
Immunisation 6, 10 & 14
Program Weeks
Iap 2021 3 Doses 3 Doses 2 Doses 3 Doses
6, 10 & 14 6, 10 & 14 6 & 10 6, 10 & 14
Weeks Weeks Weeks* Weeks
Or
10 & 14
Weeks
Dosage & 5 Drops 2 mL (Liquid) 1 mL 2.5 mL
Route Oral Oral (Lyophilized); Oral
1.5 ml
(Liquid),
Oral

CONTRAINDICATION : Intussusception, Immunodeficiency (since live)

Catchup allowed till 8 months
 TORCH

CMV RUBELLA HSV TOXOPLASMOSIS

Petechial Deafness, Skin Vesicles, Chorioretinitis,

Rashes, Cataract, Chorioretinitis, Hydrocephalus
Jaundice, Congenital Microcephaly
Chorioretinitis, Heart
HSM Disease,
PDA

Intracranial Salt And HSV Calcifications

Periventricular Pepper Encephalitis Throughout The
Calcifications Retinopathy Brain, Target Lesions

Important points to note

• CMV – Most common cause of non-syndromic SNHL, most cases are asymptomatic
at birth.
• Rubella – PDA – Most common congenital heart defect
• Toxoplasma – Spread via cat faeces.
• Congenital Syphilis – Triad of interstitial keratitis, malformed teeth (Hutchinson
incisors and mulberry molars), and eighth nerve deafness.
 ARSENIC TOXICITY

Arsenic
FATAL DOSE
120-200 mg
ACUTE POISONING/TOXICITY
• Garlicky odour
• Nausea, vomiting, burning pain in throat and
abdomen.
• Conjunctivitis
• Painful micturition.
• Diarrhoea (mimics cholera)
SUBACUTE/CHRONIC TOXICITY
• Anemia, leukopenia, Aplastic Anemia
• Sensory-Motor neuropathy
• Skin - Hyperpigmentation, hypopigmentation,
hyperkeratosis (Rain drop
type pigmentation)
• Other Skin changes
Blackfoot's disease
(peripheral vascular
disease resulting in gangrene)
Aldrich-Mees lines (transverse white lines in the
nails)
Milk rose (Brownish pigmentation)
• .Cancers – Basal Cell/Squamous

OTHER FEATURES
• Used in embalming and preserving bodies
• Cadaveric rigidity lasts longer than usual
• Antidote – Iron oxide/BAL
LEAD POISONING/TOXICITY
 METALLIC POISONING(SUMMARISED)

METALS FEATURES OTHER POINTS

COPPER • Blue Vitriol Antidote - KFeCN
• Hypersalivation
• Acute Haemolysis
• Inhalation Of Copper Sulphate Causes
Granulomatous Disease Called Vineyard
Sprayer Lung
• Clapton Lines Found In Gums
• Eye Findings – Chalcosis Lentis/KF Rings
ZINC • Metal Gume Fever
• Malaria Chills
CADMIUM Triad of
• Itai-itai disease / ouch-ouch disease
• PCT necrosis
• Golden hair
THALLIUM • Ideal homicidal poison
• Gastroenteritis
• Neuropathy
• Loss of eyebrows( pathognomonic)
LEAD • Seen with old house paint(painters colic) MNEMONIC
• also called Plumbism/Saturnism A- Anaemia
• Antidote – Calcium Disodium EDTA B-Basophilic Stippling,
Bartonian Lines
• Inhibit haem synthesis by inhibiting ALA
C-Colic Constipation
dehydratase & Ferro-chelatase D-Drops (Wrist/Foot)
• Blood levels>70 microgram/100 ml - toxic E-Encephalopathy
features appear. F-Perioral Pallor-
(Earliest Most Specific
Finding)
MERCURY • Erethism (Psychiatric Manifestations) - • Minamata Disease
Excessive Shyness • Danbury Tremors/
• PCT Necrosis Mad Hatter
• Gingivostomatitis Shake/Glass Blowers
• Mercuria Lentis - Affect The Anterior Shake ( Coarse
Capsule Of Lens Intentional Tremors)
• Pink Disease
(Acrodynia)
COBALT Cardiomegaly
MANGANESE Parkinson Disease
 DROWNING

FRESH VS SEAWATER

Freshwater drowning Seawater drowning

Mechanism of death Surfactant disruption Surfactant disruption
(surfactant denaturation) (surfactant dilution)
Fluid & electrolyte • Hypervolemia • Hypovolemia
changes • Hyponatremia • hypernatremia
• Hyperkalemia
Time to death Less (4-5 minutes) More (8-12 minutes)

ANTEMORTEM VS POST MORTEM

Feature Antemortem drowning Postmortem drowning

Frothing from + -
mouth
Cadaveric spasm + -
Lungs changes • Emphysema aquosum Passive collection of water in
• Edema aquosum lungs
(unconscious individual)
• Voluminous, bulky,
water-logged &
overinflated lungs.
• Paltauf haemorrhage
Foreign bodies Seen in bronchi & Passively trapped in upper
like fluid, debris, bronchioles respiratory tract
weeds etc.
Maybe seen in hand(tightly
clenced)
Diatoms Present in lungs, liver, brain, Present only in lungs
bone marrow etc.
Contents of • Water Water (less quantity as
stomach • Foreign bodies compared to antemortem
drowning)
 ASPHYXIAL METHODS

1. HANGING

2. STRANGULATION
• Ligature Strangulation
• Throttling (Manual By Hands)
• Bansdola (Between Bamboo Sticks)
• Garotting (Includes Spanish Windlass) – Rope From Behind
• Mugging (Compression Of Neck By Bend Of Elbow)

3. SUFFOCATION
• Smothering (mechanical occlusion of nose/mouth)
• Choking (mechanical occlusion of internal airway)
• Gagging(Filling a piece of cloth in the mouth)
• Traumatic asphyxia (Mechanical fixation of chest- Stampede/RTA etc. )
• Burking ((Sitting on chest and covering mouth/nose)
• Café Coronary (Food bolus obstructing larynx)
 UNCOMMON FORMS OF ASPHYXIA

Positional Asphyxia
Abnormal jack knife position of the victim's body compromises the process of
respiration.

Wedging
Child or infant falls in the small gap between the bed and the wall when asleep. It is a
type of traumatic asphyxia.
 IPC & CrPC sections

CrPC Relevant pointers

sections
2(c) COGNIZABLE OFFENCE
2(l) NON-COGNIZABLE OFFENCE
2(w) Summon case
2(x) Warrant case
53A Rape accused examination
164 A Rape victim examination
61-69 Deal with SUMMONS
174 Police Inquest
176 Magisterial Inquest
309 (l) Day to day trial of witnesses in Rape
trial
311 Power to recall witness
327 Camera trial
357(C) Hospital role for victims of sexual
assault & acid attack (free first aid)
If hospital refuses, punishable under
166 B IPC
416 Postponement of execution of death
sentence of a PREGNANT female by
high court.
IPC RELEVANT DESCRIPTION
SECTIONS
44 Injury definition
46 Death definition
82 No criminal responsibility <7yr child
84 McNaughten’s rule : legal test for insanity in India
85 Act under involuntary intoxication is not an offence
86 Act under voluntary intoxication is an offence
90 Consent for illegal act is invalid
92 No consent required for life saving procedures in good faith
94 Act compelled by threat is not an offence
191 Perjury definition
192 Fabricating false evidence
193 Punishment for perjury
197 Issuing false certificate is punishable(7 years)
201 Disappearance of evidence
228 A Disclosure of identity of rape victim is punishable
269 Negligent act to spread HIV/AIDS is punishable
270 Malignant act to spread HIV/AIDS is punishable
299 Culpable homicide definition
300 Murder definition
302 Punishment of murder
304 Punishment of culpable homicide not amounting to murder
304 A Rash/negligent act causing death(includes medical)
304 B Dowry death
305 Abetment of suicide of child/insane/intoxication
306 Abetment of suicide
307 Attempt to murder
308 Attempt to culpable homicide
309 Attempt to suicide (NOT as per Mental health Act 2017-
319 Decrimanlised
Defines Hurt suicide)
320 Defines Grievous Hurt
323 Punishment for voluntarily causing hurt
324 Punishment for voluntarily causing hurt by weapon
325 Punishment for voluntarily causing grievous hurt
334 Voluntarily causing hurt on provocation
335 Voluntarily causing grievous hurt on provocation
336 Rash/ negligent act to endanger life
337 Rash/ negligent act to cause hurt
338 Rash/ negligent act to cause Grievous hurt
351 Defines Assault
375 Rape(Definition)
376 Punishment for Rape
377 Unnatural sexual Offences
498A Punishment for cruelty by husband
509 Words/Gesture to attempt to outrage the modesty of woman
 BURNS

1ST DEGREE 2ND DEGREE 2ND DEGREE 3RD DEGREE 4TH DEGREE
BURNS (SUPERFICIAL (DEEP (FULL
PARTIAL PARTIAL THICKNESS)
THICKNESS) THICKNESS)
Only Epidermis Reticular dermis Deep dermis Subcutaneous Muscle and
is involved tissue bome
Painful Painful Less painful Painless Painless
Blisters - + - - -
Scars - May scar Scars + Contractures Loss of the
burned part
Heals within 1 Healing in 2-3 3-9 weeks to Excision with Excision with
week weeks heal skin grafting skin grafting
needed needed

PARKLAND FORMULA

• The Parkland formula is commonly used to calculate the fluid requirement for burn
resuscitation.
• According to the Parkland formula, the fluid requirement in the first 24 hours is
calculated as 4 mL × body weight (kg) × %TBSA (total body surface area burned).
• Administer half in 8 hours and rest in next 16 hours

AS PER ATLS

• Fluid resuscitation in burns has been adjusted to mirror the changes in trauma fluid
resuscitation. Adult patients with deep-partial and full-thickness burns involving more
than 20% total body surface area (TBSA) should receive initial fluid resuscitation of 2
ml/kg/%TBSA.
• In paediatric burns 3 ml/kg/%TBSA should be used, and 4 ml/kg/%TBSA used for
electrical burns.
• The first half of the fluid should be given over the course of eight hours, and the
remaining half is provided over a span of 16 hours.
 SNAKE BITE

Clinical Features

Feature Cobra Common Russell’s Saw Hump-

krait viper scaled nosed
viper viper
Local pain/tissue Yes No Yes Yes Yes
damage
Neurotoxicity Yes Yes Yes No No
Response to Yes No No No No
neostigmine
Hematotoxicity No No Yes Yes Yes
Renal No No Yes No Yes
complications
Response to ASV Yes Yes Yes Yes No

First Aid Protocol : “Do It RIGHT”

R: Reassure 70% snakebites nonvenomous; 50% of

venomous snakebites are dry bites
I: Immobilize the As you would do for a fractured limb
limb
GH: Go to Hospital Get to Hospital immediately for early
ASV administration
T: Tell the doctor of For early identification of envenomation
systemic symptoms & early ASV administration
DON’Ts
1. Tie a tight tourniquet – can cause gangrene
2. Cut the bite area & suck out blood – harmful
3. Use herbs, ice packs & snake stones – useless & delays ASV

ASV:
• Polyvalent
• Contains Equine Immunoglobulin to 4 common snake venoms : Russell’s
viper, saw-scaled viper, common cobra & common krait
 FIREARM INJURIES

RANGE FEATURES
CONTACT • Cruciate / stellate shaped wound
WOUND • Burning, Blackening, Tattooing Inside the entry
wound
CLOSE RANGE • Burning, Blackening, Tattooing seen outside
• Grease collar seen
• Abrasion collar seen
NEAR/ • Only Tattooing seen
INTERMEDIATE • No Burning, Blackening seen
RANGE • Grease Collar seen
• Abrasion Collar seen
DISTANT • Only single entry wound seen
SHOTS • No Burning, Blackening, Tattooing seen
• No Grease collar seen
• Abrasion collar seen
 POSTMORTEM CHANGES

Immediate Early Late (decomposition)

• Loss of • Pallor & loss of skin elasticity • Putrefaction
voluntary • Eye changes (tache noire) • Adipocere formation
power • Primary flaccidity • Mummification
• Cessation of • Rigor mortis
respiration & • Hypostasis
circulation • Cooling of body

DESCRIPTION OF POSTMORTEM CHANGES

Changes Description
Tache noire

Rigor mortis

Cadaveric
spasm

Hypostasis
Changes Description
Putrefaction

Adipocere
formation

Maceration

Mummification
CONTRAINDICATIONS OF LIVE ATTENUATED VACCINES

CONTRAINDICATIONS OF LIVE ATTENUATED VACCINES

1. Immunocompromised state (e.g. SCID etc)
2. Haematolymphoid Malignancy (Leukaemia/Lymphoma)
3. On chronic steroid use(e.g. Nephrotic syndrome)
4. Antimetabolite/Alkylating agent therapy /On Radiotherapy
5. Organ Transplantation
6. Pregnancy
7. Anaphylaxis

INCUBATION PERIODS OF VARIOUS DISEASES

DISEASE INCUBATION PERIOD

Chicken pox 10-20 days
Measles 7-21 days
Mumps 14-21 days
Rubella 14 – 21 days
Diphtheria 2-6 days
Pertussis 7-14 days
Polio 4-30 days
Typhoid 10-14 days
Influenza 18- 72 days
Hepatitis A 15-20 days
Syphilis 90 days
Hepatitis B 50-150 days
Cholera 5 hrs – 5 days
Dengue 5 days
Rabies 30 -90 days
 BIOTERRORISM

CATEGORY FEATURES EXAMPLES

A • High priority agents 1. Bacillus Anthracis
• Easily disseminated 2. Botulism
• Easily transmitted 3. Yersinia pestis
• High mortality rates 4. Ebola
• Cause social disruption
B • Moderate priority 1. Coxiella Burnetti ( Q Fever)
agents 2. Burkholderia mallei
• Moderate 3. Burkholderia pseudomallei
dissemination 4. Ricin Toxin
5. Salmonella
6. Brucellosis
C • Low priority agents Emergent Virus Like Hanta, Nipah
• Potentially high
morbidity and mortality
 LEVELS OF PREVENTION

Primordial Primary Secondary Tertiary

Underlying Risk factors or Disease present Morbidity due to disease
socioeconomic or specific causal present
environmental factors present
conditions present
Progression Health promotion Diagnosis and Disability limitation and
prevented by Health and specific treatment rehabilitation
education protection
E.g. Adaption of E.g. giving E.g. screening for E.g. prescribing
healthy lifestyle benzathine cancer spectacles for refractive
from childhood penicillin G to a error
child suffering
from strep throat

Immunisation
 ODDS RATIO/RELATIVE RISK

All the terms are described using 2X2 or contingency table

Disease/outcome
+ -

Exposure/ + a b
intervention
- c d

TERM DEFINITION INTERPRETATION FORMULA

Odds Ratio Represents odds of OR=1 : Odds of 𝑎/𝑐
𝑂𝑅 =
(Used In Case- exposure amongst exposure equal in 𝑏/𝑑
Control cases (a/c) to odds cases & control Or
Studies) of exposure among OR>1 : odds of 𝑎𝑑
controls (b/d) exposure more in 𝑂𝑅 =
𝑏𝑐
cases
OR<1 : odds of
exposure more in
controls
Relative Risk Risk of developing RR=1 : no association 𝑎/(𝑎 + 𝑏)
𝑅𝑅 =
(Used In disease in the between exposure & 𝑐/(𝑐 + 𝑑)
Cohort Studies) exposed group disease
[a/(a+b)] divided RR>1 : exposure
by risk in associated with
unexposed group increased disease
[c/(c+d)] occurrence
RR<1 : exposure
associated with
decreased disease
occurrence
Attributable Difference in risk More the difference,
Risk between exposed more the contribution 𝐴𝑅
[a/(a+b)] & of exposure to 𝑎 𝑐
= −
unexposed groups disease. 𝑎+𝑏 𝑐+𝑑
[c/(c+d)]
𝐴𝑅%
𝑅𝑅 − 1
= 𝑋 100
𝑅𝑅
 STANDARD DEVIATION AND VARIANCE

• VARIANCE

Variance is a measure of how much a data point differs from the mean. It is a
measure of how far a set of data are from the mean value. Variance means to find the
expected difference of deviation from actual value.

• COEFFICIENT OF VARIATION

The coefficient of variation is defined as the ratio of the standard deviation to the
mean. The coefficient of variation should be computed only for data measured on
scales that have a meaningful zero and helps in relative comparison of two
measurements.
FORMULA = σ/μ

• STANDARD ERROR OF MEAN – It is the standard deviation of the means.

FORMULA = s/Ön

• STANDARD DEVIATION – It is the most frequently used measure of deviation.

SD = ( x-x )2ɳ [ Sample size > 30]

SD = ( x-x )2ɳ-1 [ Sample size < 30]

 NORMAL DISTRIBUTION CURVE

Normal distribution of data is described by Bell Curve. The data are normally distributed
around zero.

The below image describes a STANDARD NORMAL DISTRIBUTION CURVE

POINT 0 – It is the measure of Central Tendency.

MEAN = MEDIAN= MODE = 0
 DEVELOPMENT/FERTILITY INDICATORS

Human Development Physical Quality of

Index (HDI) Life Index (PQLI)
Range 0 to +1 0 to 100

Longevity (Life expectancy

at birth)
Life expectancy at 1
A decent standard of living year of age
(Real GNI per capita in PPP
Components
US$) Infant Mortality rate

Knowledge (mean years of Literacy rate

schooling and expected
years of schooling)

• HDI = 1/3(Life Expectancy)+1/3(Education)+1/3(Per-Capita Income) (use of

Geometric mean too)

• PQLI = (Life expectancy x Literacy rate x (1 - Infant mortality rate/1000))/1000.

FERTILITY INDICATOR FORMULA

Number of live births per 1000 women
General fertility rate (GFR)
of reproductive age (15-49 years)
Average number of children that would
be born to a woman if she were to live
Total fertility rate (TFR) to the end of her childbearing years and
bear children at the current age-specific
fertility rates
Number of daughters that a hypothetical
cohort of 1000 women would bear if
Net reproduction rate
they were subject to the current age-
(NRR)
specific fertility and mortality rates
throughout their reproductive lifespan
 Metric Definition Parameters
Perinatal Rate of stillbirths and Late fetal deaths or stillbirths
Mortality early neonatal deaths >1000 g (correlates to 28 weeks
Rate (PMR) during a particular of gestation), Early neonatal
time period deaths, Live births >1000 g

Neonatal Rate of deaths within Early neonatal deaths, Late

Mortality the first 28 days of neonatal deaths (after 7th day
Rate (NMR) life but before 28th completed day
of life)
 MALARIA

ACT
• Artesunate 4mg/kg orally OD for 3 days + Sulfadoxime + pyrimethamine (ASP) (S
25mg/kg & P 1.25 mg/kg) on day 1
• Artemether 20 mg + Lumefantrine 120 mg (AL) BD for 3 days (6doses)

Antimalarials for severe malaria

Drug Dosage
Artesunate • 2.4mg/kg IV stat, at 12 hours & 24 hours & then
once daily
• Once the patient is able to swallow, complete the
course of 7 days by*:
- Artesunate plus sulfadoxime- pyrimethamine in
all states except NE
- Artemether + lumefantrine in NE

Artemether 2mg/kg (loading dose) followed by 1.6mg/kg daily once

the patient is able to swallow, complete the course of 7
days
Quinine Loading dose: 20mg salt/kg by infusion over 4 hours
salt Maintenance dose: 10 mg/kg every 8 hours for 7 days.
Add Doxycycline/Clindamycin if able to swallow.
 DOG BITE MANAGEMENT

Immunisation Schedule

• Essen –0.5 ml IM on Day 0,3,7,14,28 (1-1-1-1-1)

• Zagreb- 2 doses 0.5 ml IM on Day 0 followed by 1 dose on day 7, 21 (2-0-1-0-1)
Rabies Immunoglobulin

HRIG = 20IU/kg , Equine = 40IU/kg needs to begiven and infiltrated near the wound and rest
IM in category III bites within 7 days (ideally within 24 hours)

Local treatment

• Wash the wound with soap and water

• Inj TT 0.5mL
• Oral antibiotics like Amoxiclav if at risk(Immunocompromised etc.)
 METHODS OF WASTE DISPOSAL/DISINFECTION

Method Use
Landfill Placenta at PHC
Inertization Pharmaceutical waste
Incineration ashes
Heat Sharps and plastic wastes
disinfection
Hot air oven Glassware
Powders
Oils
Autoclave Surgical instruments
Plastic sharps containers
Glassware
Solutions
Gamma Reusable medical equipment and clothing
irradiation
Incineration Human anatomical waste
Soiled waste
Expired/discarded medicines and vaccines
Bedding and linens/Chemical waste
 FOOD ADULTERATION DISEASES

Lathyrism

• Khesari dal is the most feared contaminant of red gram (arhar dal)
• Long term consumption leads to:
o Neurolathyrism in humans
o Osteolatyrism in animals
• Responsible toxin : BOAA (Beta Oxalyl amino alanine)
• Signs/Symptoms: Spastic paralysis of lower limbs/Gluteal atrophy
• Endemic states for lathyrism:
o Madhya Pradesh
o Uttar pradesh
o Bihar
o Odisha

Epidemic Dropsy

• Non inflammatory B/L swelling of legs/ protein loss/cardiac failure/edema

• Toxin: Sanguinarine
• Adulterant – Argemone Mexicana oil with mustard oil
 CATARACTS

CONGENITAL CATARACT

Punctate Blue-dot cataract, most common congenital cataract

cataract

Zonular/Lamella Most common congenital cataract with diminished

r cataract vision; Spokes of a wheel appearance (Rider’s
Cataract) A, B, and C

Fusiform/corallif Anteroposterior spindle shaped appearance.

orm cataract

Nuclear cataract Most common type of cataract seen in congenital

rubella syndrome

Coronary Appears as a corona of club-shaped opacities near the

cataract periphery of the lens.

Anterior polar May arise either due to delayed development of

cataract anterior chamber or due to corneal perforation

Posterior polar Progressive form of posterior polar cataract, which

cataract typically shows an "onion whorl appearance"

Disease Type of Cataract

Myotonic Christmas tree cataract
dystrophy
Wilson's disease Sunflower cataract
Penetrating Sunflower cataract
trauma
Diabetes Snowflake/Snowstorm
mellitus, Down’s cataract
syndrome
Congenital Nuclear cataract
rubella
Galactosemia Oil drop cataract
 CORNEAL ULCERS

Bacterial corneal ulcer Fungal corneal ulcer

• More pronounced symptoms • Less pronounced symptoms

• Well defined ulcer margins • Feathery ulcer margins
• Clean ulcer base • Necrotic base of ulcer
• No satellite ulcer • Satellite ucers +
• Mobile, flat & sterile hypopyon • Fixed, dome shaped & nonsterile ulcer
• No immune ring • Immune ring +
• Staining : • Diagnosis/staining:
o Gram stain o KOH mount
• Blood agar : isolating organism o Sabouraud’s dextrose agar
• Treatment: • Treatment :
o Fortified antibiotic drops o Antifungal drops
o Cefazoline drops o DOC- Natamycin
o Tobramycin eye drops o Amphoterin B for non-filamentous

Complications Image
Corneal thinning

Desmatocele
formation

Corneal
perforation

Keratitis Important points

Viral keratitis • Geographical ulcer

• Punctate epithelial keratopathy
HSV keratitis • Dendritic ulcer
• Geographical ulcer
Herpes zoster • Pseudo-dendritic keratitis
keratitis
 KF RINGS

KAYSER-FLEISCHER RING (KF RINGS)

Pathophysiology
• Brownish yellow discoloration in limbic zone
of cornea
• Copper deposition in
Descemet’s membrane
• Do not interfere with vision
• Can be seen with naked eye
• Definitive – Slit lamp
Conditions having KF Rings
• Wilson’s disease(not pathognomic)
• Primary biliary Cirrhosis
• Intrahepatic cholestatic syndromes
• Autoimmune hepatitis
Association with Wilson
• All patients with Neurological/Psychiatric
symptoms(99%)
• 30-50% of patients with hepatic disease.
• Absence of KF rings doesn’t exclude
diagnosis of Wilson

DIRECT VS INDIRECT OPTHALMOSCOPY

DIRECT INDIRECT
OPHTHALMOSCOPY OPHTHALMOSCOPY

Viewing Direct viewing through Viewing through a

Method an ophthalmoscope held condensing lens held at a
close to the eye. distance from the eye.
Magnification Low magnification High magnification
(typically 15x) (typically 2x-5x)
Field of View Narrow field of view Wide field of view (larger
(smaller area observed) area observed)
Image Provides an upright, non- Provides an inverted,
Orientation inverted image. reversed image.
Applicability Useful for a quick Particularly useful for
examination and detailed examination,
screening of the fundus. diagnosis, and treatment of
various eye conditions.
 EXTRAOCULAR MUSCLES

MUSCLE ACTION INNERVATION

Oculomotor Nerve
Superior Rectus Elevation, Intorsion, Adduction
(III)
Oculomotor Nerve
Inferior Rectus Depression, Extorsion, Adduction
(III)
Oculomotor Nerve
Medial Rectus Adduction
(III)
Abducens Nerve
Lateral Rectus Abduction
(VI)
Trochlear Nerve
Superior Oblique Intorsion, Depression, Abduction
(IV)
Oculomotor Nerve
Inferior Oblique Extorsion, Elevation, Abduction
(III)
Levator Palpebrae Oculomotor Nerve
Elevation Of The Upper Eyelid
Superioris (III)
 GLAUCOMA

• Optic neuropathy leading to progressive vision loss (peripheral to central), Not always
accompanied by raised IOP.
• Aetiology:
• Primary (most common)
• Secondary (as seen in Uveitis, glucocorticoids)
• Fundus changes:
• Optic disc cupping
• Thinning neuroretinal rim
• Lamellar dot sign
• Bayonetting of blood vessels / double bending of blood vessel or Z bending

Drug Mechanism Ocular adverse effects

β blockers Decrease aqueous humor Burning , redness
Timolol synthesis
α agonists • Decrease synthesis • Mydriasis (not to be used in
Epinephrine, • Increase outflow angle closure glaucoma)
brimonidine • Blurry vison, allergic
reactions
Diuretics Decrease synthesis Stinging, irritation, red eyes
Acetazolamide
Prostaglandins Increase outflow via • Increased iris pigmentation
Bimatoprost, decreased resistance • Growth of eyelashes
Latanoprost through uveoscleral
pathway
Cholinergic Increase outflow via • Miosis
drugs opening of trabecular • Cyclospasm
Direct : meshwork
Pilocarpine,
carbachol
Indirect :
Physostigmine,
Echotihophate
 RETINOBLASTOMA

• Most common intraocular malignancy in children

• Mutation : RB1 tumour suppressor gene on chromosome 13q14
• Can be Sporadic or Familial (Autosomal dominant)
• 2 hit hypothesis by Knudson
• Presentation: Leukocoria, strabismus, nystagmus.
• Other causes of Leucocoria – Toxoplasma/ PPHV/Congenital cataract/Coats/ROP
• Osteosarcoma 2nd most common malignancy after RB in RB mutations.
 COMMON RESPIRATORY ILLNESS

DISEASE CLINICAL CAUSE(M/C) XRAY TREATMENT

FEATURES SIGNS
Croup Barking Parainfluenza Steeple Single dose
(Laryngo- Cough/Seal Dexamethasone
tracheobronchitis) like Cough Racemic Epinephrine
in severe cases only
Epiglottitis Tripod H. Influenzae Thumb Print IV Ceftriaxone
Position Sign
Drooling of
saliva
Sick looking
Bronchiolitis Wheezing RSV Hyperinflation Hydration
Oxygen
Ribavirin in
immunocompromised
 HEARING TESTS

Test Normal hearing Conductive HL

SNHL Total HL
Rinne AC>BC AC>BC AC>BC BC+ (heard from
(positive Rinne) (Negative Rinne)
But both good ear)
decrease AC-
(pathological (false negative
positive Rinne)
Rinne)
Weber Sound heard at Sound better in Sound heard Sound heard in
midline Bad ear better in good ear.
good ear
 RHINOSPORIDIOSIS VS RHINOSLEROMA

• Rhinosporidiosis is a chronic granulomatous disease caused by

Rhinosporidium seeberi.
• It is more common in the southern states of India in people with a history
of taking bath in ponds frequented by animals.
• Presentation: In the nose, the disease presents as a leafy polypoidal mass,
pink to purple in color and attached to nasal septum or lateral wall.
• The mass is very vascular and bleeds easily on touch.

• Rhinoscleroma is caused by Klebsiella rhinoscleromatis.

• It presents as atrophied rhinitis in the initial stages and can present as hard/
woody nose in later stages.
• Biopsy shows macrophages with bacteria phagocytosed in the cytoplasm,
known as MIKULICZ CELLS. Plasma cells with inclusion bodies can also
be seen, known as RUSSEL BODIES.
 VENTILATOR SETTING

VENTILATOR DESCRIPTION
SETTING
Mode The specific ventilation mode used, such as volume
control, pressure control, or pressure support.

Tidal Volume (VT) The volume of air delivered with each breath.

Respiratory Rate The number of breaths delivered per minute.

(RR)
Fraction of Inspired The concentration of oxygen in the delivered air.
Oxygen (FiO2)

Positive End- A baseline pressure maintained in the airways at the

Expiratory Pressure end of expiration to improve oxygenation.
(PEEP)

Preferred Setting In ARDS

• Tidal volume = 6ml/kg

• High PEEP
• FiO2 to maintain SaO2 >90%
• RR to allow Permissive hypercapnia(pCO2 between 45-50) (Higher RR results in low
pCO2)
• Plateau pressure at < 30cm H2O
• Prone ventilation

MALLAMPATTI GRADING

MALLAMPATI DIRECT DIFFICULTY

CLASS VISUALIZATION OF
INTUBATION

I Soft palate, fauces, Easy

uvula, pillars

II Soft palate, fauces, Moderate

uvula

III Soft palate, uvula base Difficult

IV Hard palate only Very Difficult
 RESUSCITATION (IMPORTANT POINTS)

CPR is said to be of high quality if it meets the following criteria :

• Depth of compression = 5-6 cm

• Frequency of compressions = 100-120 minutes
• Allow for complete chest recoil.
• Minimise interruptions in compressions to <10 seconds.
• Avoid excessive ventilation.
• Rotate compressor every 2 minutes or earlier if fatigued.
• If no advanced airway, 30:2 compression-ventilation ratio should be followed.

AIRWAY
MANOEUVRES DESCRIPTION
CHIN LIFT Technique used to open the airway by
placing fingers under the mandible and
lifting the chin upwards.
IN-LINE Technique used to maintain neutral
MANUAL alignment of the head and neck during
STABILIZATION airway management, usually performed
by an assistant to prevent movement
during intubation or other procedures.

JAW THRUST Maneuver used to open the airway by

placing fingers behind the angle of the
mandible and lifting the jaw forward,
without head extension.
HEAD Technique used to extend the head
EXTENSION backward to help open the airway by
positioning the head in a neutral
alignment or slightly extended position.
 CAPNOGRAPHY

Condition Capnograph curve

Bronchospasm

Curare Cleft

Endobronchial
Intubation

Hypoventilation

Hyperventilation

Oesophageal
intubation

*ETCO2 is the best measure of adequacy of CPR and for return of spontaneous circulation
 SKIN ANATOMY

1 Stratum Stratum corneum is the outermost

corneum layer consisting of cells called
corneocytes. It has a dense network
of keratin filaments.
2 Stratum Stratum lucidum is found only in
lucidum palmoplantar skin. It is electron-
lucent.
3 Stratum Stratum granulosum contains
granulosum intracellular granules of
keratohyalin
4 Stratum Stratum spinosum or prickle cell
spinosum layer is formed by the enlargement
of epibasal keratinocytes
5 Stratum Stratum basale is a continuous
basale layer that is generally only one cell
thick but may be thicker in
glabrous skin or in the
hyperproliferative epidermis.
 PEMPHIGUS VULGARIS VS BULLOUS PEMPHIGOID

Pemphigus vulgaris Bullous pemphigoid

Pathogenesis Autoimmune skin disorder IgG antibody against
with IgG antibody against hemidesmosomes
Desmoglein 1 and 3

Clinical features Flaccid blisters, denuded skin, Large tense blisters on flexor
Oro-mucosal lesions surfaces and trunk

Histology Acantholytic blister formed Subepidermal blister

in supra-basal layer of with eosinophil-rich infiltrate
epidermis
Oral mucosa Involved Spared
Nikolsky sign Positive Negative
Immunofluorescence Fishnet pattern Linear deposition of IgG/C3

PEMPHIGUS

BULLOUS PEMPHIGOID
 SKIN LINES

Kraissl’s lines Langer’s lines Blashko’s lines

Lines of Defined in terms Lines of normal
maximum skin of collagen skin development
tension orientation
Measured in Seen in cadavers they can become
living apparent as whorls,
individuals patches, streaks or
lines in a linear or
segmental
distribution over
the skin.
 WOODLAMP’S COLOR

Disease Wood Lamp Colour

Tinea Capitis Microsporum – Blue Green
Trichophyton schoenleinii – Dull
Green
Other Trichophyton
Non Fluorescent
Erythrasma Coral Red

Pityriasis Versicolor Yellow

(Spaghetti & Meat
Balls )
Pseudomonas Green
Scabies Fluorescence
Vitiligo Ivory White
Porphyria Pink Fluorescence (Urine)
 LEPROSY

Age Drugs used

group 12 months for multibacillary leprosy
6 months for paucibacillary leprosy
Children Rifampicin 10 mg/kg once a month
<10 years Clofazimine 100mg once a month, 50mg twice
(or <40 kg) weekly
Dapsone 2 mg/kg daily
Children Rifampicin 450 mg once a month
10 – 14 Clofazimine 150 mg once a month and 50
years mg alternate days.
Dapsone 50 mg daily
Adults Rifampicin 600 mg once a month
Clofazimine 300 mg once a month and 50 mg
daily
Dapsone 100 mg daily
 MOOD DISORDERS

Mood disorder Description

Unipolar Recurrent episodes lasting ≥ 2 weeks characterized by ≥ 5 of 9
Depression diagnostic symptoms including
Major depressed mood or anhedonia (or irritability in children). SIG:
depressive E CAPS:
disorder • Sleep disturbances
• Decreased interest in pleasurable activities
(anhedonia)
• Guilt or feelings of worthlessness
• Decreased energy
• Decreased concentration
• Appetite/weight changes
• Psychomotor retardation or agitation
• Suicidal ideation
Bipolar type I Requires 1 or more manic episode +/- hypomanic or
depressive episode (separated by any length of time)
Bipolar type II Requires a Hypomanic & a depressive episode (no past manic
episodes )
Dysthymia • Continuous low mood >2 years in adults & >1 year in
children & adolescents.
• Not crossing the threshold for depression
Double • Continuous low mood >2 years in adults & >1 year in
depression children & adolescents.
• With depressive episodes in between lasting for atleast
2 weeks.
Cyclothymia • Mild form of Bipolar disorder
• Fluctuating between mild depressive & hypomanic
episodes.
• Duration : should last for 2 or more years with
symptoms persisting for at least half of time, with
remission lasting for less than 2 months.
 MANAGEMENT OF OPIOID DEPENDENCE

OPIOIDS TYPES USE

METHADONE Long acting opioid Heroin detoxification, Long term
maintenance therapy
BUPRENORPHINE Partial opioid agonist Used to suppress withdrawal and
for maintenance therapy
NALOXONE Short acting opioid antagonist; Acute opioid overdose
Given IM/IV or as nasal spray (particularly used to reverse CNS
and respiratory depression.)
NALTREXONE Long acting opioid antagonist, Used after detoxification to
oral drug prevent relapse. Also used in
alcohol and nicotine cessation

ALCOHOL WITHDRAWAL SYNDROME

MANIFESTATIONS FEATURES TIMELINE

MILD Tremors, diaphoresis, Earliest
WITHDRAWAL palpitations manifestation
6-24 hrs
ALCOHOLIC Hallucinations can be 12-24 hrs
HALLUCINOSIS visual, auditory or tactile.
INTACT ORIENTATION
SEIZURES Generalised tonic-clonic 24-48 hrs
seizures
DELIRIUM Commonly seen in After 48 hrs or
TREMENS hospital setting. from 3RD DAY
Confusion, agitation,
hallucinations,
diaphoresis, autonomic
hyperactivity.
ORIENTATION NOT
INTACT.
Treatment-
Benzodiazepines
 SUBSTANCE ABUSE

SUBSTANCE INTOXICATION WITHDRAWAL OTHER IMP POINTS

HEROIN Miosis, CNS depression, Yawning, piloerection Most common cause of death
(BROWN SUGAR, Resp. depression, (cold turkey), due to drug overdose.
DOPE, Euphoria mydriasis,
SMACK) lacrimation, Routes of taking heroin
hyperactive bowel 1. Mainlining – Directly
Treatment of drug sounds, diarrhea, and injecting into IV
overdose flu like symptoms 2. Skin popping –subcutaneous
Naloxone injection
Treatment of drug 3. Snorting
withdrawal –
Methadone
AMPHETAMINE, Violent Behavior, Depression, ‘crash’ Amphetamine aka Ice, crystal
MDMA Tachycardia, Meth
Hypertension, MDMA aka Ecstacy
Psychosis
Choreiform Movement,
Tooth Decay

Treatment -
Benzodiazepines
COCAINE Chest Pain, Agitation, Restless, Depression Common causes of brain
Euphoria, Tachycardia, (Not significant hemorrhage in adults include –
Hypertension, Angina findings to be asked in Trauma > AV malformation >
Sudden Cardiac Death, exams) Cocaine
Seizures, Mydriasis
Tactile Hallucinations –
Magnan Bugs
Paranoid Psychosis
Perforated Nasal Septum
Bruxism
Black Discoloration of
Teeth
Brain Hemorrhage
NICOTINE Restless (No Significant Increased appetite,
Findings) irritability, inability to
sleep bradycardia
Treatment.
1. Nicotine
replacement therapy
patch gum lozenges
2. Drugs which can be
used - Bupropion,
Varenicline.
 SUBSTANCE ABUSE

SUBSTANCES INTOXICATION OTHER IMP POINTS

LSD Visual Hallucinations, Bad Trips /Hallucinations
Euphoria, Dysphoria, Panic,
Tachycardia, Hypertension
Synesthesia (Anomalous
Blending of Senses.
Stimulation Of One Modality
Produces Sensation in A
Different Modality)

CANNABIS Increased appetite, euphoria, Most common drug of abuse in India

dysphoria, conjunctival Amotivational Syndrome
injection Run amok (run to homicide/suicide)
Smell of burnt rope
PHENCYCLIDINE Nystagmus, Violent Also known as Angel dust
Behavior, Hallucinations,
Amnesia, Dissociation

DELUSION VS HALLUCINATION

TERM DESCRIPTION
Illusion Illusions are unique perceptual experiences in which information
derived from “real” external stimuli results in a false perception
of the thing or thing that is being stimulated.
Hallucination A hallucination is a false perception of objects or events involving
your senses: sight, sound, smell, touch and taste in the absence of
an external stimulus.
Delusion Delusion is a disorder of content of thought.
It’s a misguided opinion/False Belief that is maintained in the
face of overwhelming evidence to the contrary.
Depersonalization When you have the sensation that you are looking at yourself
Disorder from outside of your body, that things around you aren’t real, or
both, you have depersonalization-derealization disorder.
 ECG CHANGES IN ELECTROLYTE ABNORMALITIES

ELECTROLYTE ECG CHANGES

IMBALANCE
HYPERKALEMIA - Peaked T waves
- Prolonged PR interval
- Widened QRS complex
- Loss of P waves
- ST segment depression
- Sine wave pattern (severe cases)
HYPOKALEMIA - Flattened T waves
- U waves
- ST segment depression
- Prominent U waves (severe cases)
- Prolonged QT interval
HYPERCALCEMIA - Shortened QT interval
- Shortened ST segment
- T wave inversion
- Prominent U waves (rare)
HYPOCALCEMIA - Prolonged QT interval
- Prolonged ST segment
- T wave inversion
HYPERNATREMIA - Non-specific ECG changes
- Severe cases may exhibit T wave
flattening/inversion
- ST segment elevation

Tumor Lysis Syndrome

Tumour Lysis Syndrome

Tumour lysis syndrome refers to the constellation of metabolic
disturbances that may follow the initiation of cancer treatment due
to lysis of tumour cells and release of intracellular contents.
Common Malignancies
• Burkitt’s Lymphoma
• ALL
Electrolyte Abnormalities in Tumour Lysis Syndrome
(Cairo Bishop Criteria- presence of 2 or more)
• Hyperkalaemia. >6mEq/L
• Hyperphosphatemia >6.5mg/dL
• Hypocalcaemia <7mg/dL
• Hyperuricemia >8mg/dL
Management
• Hyperhydration (Fluids at 3L/m2/day)
• Anti-hyperuricemia drugs: Allopurinol/Rasburicase
• Dialysis
 STROKE THROMBOLYSIS

Indications for Thrombolysis in Acute Ischemic Stroke

1. Time Window: Within the approved time window for
treatment
2. Age: No upper age limit, eligibility based on individual
assessment
3. Clinical Presentation: Significant neurological deficits
4. Imaging Confirmation:
- Absence of intracranial hemorrhage on brain imaging
- Involvement of one-third or less of MCA territory
5. Exclusion of Other Contraindications:
- No absolute contraindications present. Preferably no relative
contraindications

Absolute Relative Contraindications

Contraindications
1. Previous intracranial 1. Severe stroke with significant mass
haemorrhage or structural effect
cerebral lesion
2. Known or suspected non- 2. Severe uncontrolled hypertension
traumatic subarachnoid (systolic BP >185 mm Hg or diastolic
haemorrhage BP >110 mm Hg)
3. Active internal bleeding 3. Recent major surgery or trauma
(excluding menses) (within the previous 3 months)
4. Known bleeding diathesis 4. Recent gastrointestinal or urinary
or significant coagulopathy tract bleeding (within the previous 21
days)
5. Use of oral anticoagulants 5. Arterial puncture at non-compressible
with INR >1.7 or PT >15 site within the previous 7 days
seconds
6. Lumbar puncture or 6. Known history of intracranial
major surgery within the neoplasm
previous 2 weeks
7. Rapidly improving or 7. Intracranial or intraspinal surgery,
minor stroke symptoms at head trauma, or stroke within the
evaluation previous 3 months
8. Pregnancy (including suspected or
confirmed)
9. Active infective endocarditis
10. Symptomatic severe aortic arch
disease
 SODIUM

Condition Primary Urine Serum Thirst Volume

Defect Output Sodium Response Status
Diabetes Insufficient Increased Normal or Increased Dehydrated
Insipidus (DI) production (polyuria) Hypernatremia (polydipsia) (hypovolemia)
or action of
ADH
Syndrome of Excessive Decreased Hyponatremia Impaired Euvolemic or
Inappropriate production (oliguria) Hypervolemic
ADH or release
(SIADH) of ADH
Cerebral Salt Increased Increased Hyponatremia Variable Hypovolemic
Wasting renal (polyuria)
(CSW) sodium
loss

Cause Sodium Extracellular Urine Plasma

(Na+) Fluid Osmolality Osmolality
HYPONATREMIA Decreased Volume
Varies Increased Varies

- Hypovolemic (Diarrhoea) Decreased

- Euvolemic (SIADH) Normal

- Hypervolemic (Dilutional) Increased

HYPONATREMIA WITH Decreased Normal or Increased Increased

HYPERGLYCEMIA Increased

PSEUDOHYPONATREMIA Decreased* N/A N/A Normal

*Pseudohyponatremia refers to a laboratory artifact where the measured sodium level appears low due to an
abnormal distribution of plasma water, typically caused by high lipid or protein content in the blood. Plasma
osmolality stays normal.
 ACID BASE DISORDER

Disorder pH Pco2 HCO3 Compensatory response

Metabolic Hyperventilation (immediate)
acidosis
Metabolic Hypoventilation (immediate)
alkalosis
Respiratory Increased renal HCO3 reabsorption
acidosis
Respiratory Decreased renal HCO3 reabsorption
alkalosis
 JVP WAVES

1. A wave (Atrial contraction): This is the first positive wave seen in the JVP
waveform. It corresponds to atrial contraction, which occurs just before ventricular
systole (contraction). The A wave reflects the increased pressure caused by blood
flowing into the right atrium during atrial contraction.

2. X descent (Atrial relaxation): After the A wave, there is a downward descent known
as the X descent. This descent is caused by the relaxation of the right atrium, which
results in decreased pressure in the jugular vein.

3. C wave (Isovolumic ventricular contraction): The C wave is a small upward

deflection that occurs shortly after the A wave. It represents a slight increase in
pressure in the right atrium caused by the bulging of the tricuspid valve into the
atrium during isovolumic ventricular contraction.

4. X' descent (Ventricular ejection): Following the C wave, there is a rapid descent
known as the X' descent. It is caused by the downward movement of the tricuspid
valve as the right ventricle contracts and ejects blood into the pulmonary artery.

5. V wave (Venous filling): The V wave is a large positive wave that occurs after the X'
descent. It represents the filling of blood into the right atrium from the peripheral
veins during systole. The V wave is often prominent in conditions such as tricuspid
regurgitation or right-sided heart failure.

6. Y descent (Rapid ventricular filling): The Y descent is a downward slope that

follows the V wave. It represents the rapid ventricular filling phase, during which the
tricuspid valve opens and blood flows from the right atrium to the right ventricle.
 ANEMIA LAB APPROACH

MICROCYTIC ANEMIA COMPARISON

IDA Anemia of Thalassemia Sideroblastic

Chronic Minor Anemia
Disease
Ferritin Low Normal/High Normal High
S. Iron Low Low Normal High
TIBC High Low Normal Normal
Transferrin Low Low Normal High
Saturation
DKA MANAGEMENT
 Hepatitis B

Serum Acute Window Chronic Chronic Recovery Vaccinated/

marker HBV period HBV (high HBV (low Immunized
infectivity) infectivity)

HBsAg + + +
Anti + +
HbS

HBeAg + +
HBeAb + + +
Anti- IgM IgM IgG IgG IgG IgG
HBcAb
HBV +++ + +++ + + or -
DNA

Resolved HBsAg Negative

infection (most Anti-HBc Positive
common) OR Anti-HBs Negative
Low-level
chronic
infection OR
Resolving acute
infection.
Chronic HBsAg Positive
hepatitis Anti-HBc Positive
IgM anti-HBc Negative
Anti-HBs Negative
Acute hepatitis HBsAg Positive
Anti-HBc Positive
IgM anti-HBc Positive
Anti-HBs Negative
Vaccinated for HBsAg Negative
hepatitis B Anti-HBc Negative
Anti-HBs Positive
Recovered HBsAg Negative
(immune) Anti-HBc Positive
Anti-HBs Positive
Prone or HBsAg Negative
susceptible to Anti-HBc Negative
hepatitis B Anti-HBs Negative
 Serum marker Notes

HBsAg Antigen found on surface of HBV. Indicates hepatitis B infection.

Continued presence indicates a carrier state.
Anti-HBs Antibody to HBsAg. Indicates immunity to hepatitis B (vaccination or
Antibody recovery).

HBeAg Indicates active viral replication and high transmissibility

HBeAb Antibody to HBeAg. Indicates low transmissibility
HBcAg Antigen associated with core of HBV.
Anti-HBc Antibody to HBcAg. IgM
Antibody anti-HBc + indicates infection during window period. IgG HBcAb +
indicates prior or current infection.
HBV DNA Quantitative marker of replicative phase

Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E

Family Picornaviridae Hepadnaviridae Flaviviridae Kolmioviridae Hepeviridae
(Deltavirus
genus)
Genetic RNA, non- DNA, enveloped RNA, RNA, RNA, quasi-
material, enveloped enveloped enveloped enveloped
envelope (from HBV)
Transmission Fecal-oral Parenteral, sexual, Blood Parenteral, Faecal-oral
perinatal sexual, (water)
perinatal
Carrier state Absent Present Present Superinfection Absent
on hepatitis B
infection
Most • Acute • Viral hepatitis • Acute • Highest • Acute
common hepatitis overall. Viral risk of viral
viral cause of in • Viral hepatitis hepatitis fulminant hepatitis in
children in pregnancy. leading to hepatitis. adults.
• Hepatocellular Chronic • Acute
carcinoma. hepatitis. viral
• Chronic • Maximum Hepatitis
hepatitis. risk of in
• Carrier State chronic Pregnancy.
hepatitis. • Viral
• Highest Fulminant
potential hepatitis
of
chronicity
• Cirrhosis.
 Cardiac Failure

Definition Clinical syndrome of cardiac pump

dysfunction leading to congestion & low
perfusion.

Left heart failure Right heart failure

• Orthopnea • Congestive hepatomegaly
• Paroxysmal nocturnal dyspnea • Increased JVP
• Pulmonary edema • Peripheral edema

Systolic dysfunction Diastolic dysfunction

• Reduced ejection fraction • Preserved ejection fraction

(HFrEF) • Decreased compliance
• Decreased contractility (increased EDP)
• Often secondary to • Often secondary to myocardial
ischemia/MI or dilated hypertrophy.
cardiomyopathy

Treatment modalities in heart failure:

Treatment Effect
ACE inhibitors Decreasing remodelling
ARBs Decreasing remodelling
Neprilysin inhibitors Not used in acute decompensated HF
Beta blockers Decreasing remodelling/Decreased
demand
Aldosterone receptor blockers Decreases mortality in HFrEF
Loop & thiazide diuretics Symptomatic relief
Hydralazine with nitrate therapy Improves both symptoms & mortality in
selected patients
 CYSTIC FIBROSIS

Genetic defect Autosomal recessive

More prevalent in Europeans
• Chromosome 7
• CFTR gene
• Most common mutation : ∆F508
Pathophysiology CFTR encodes for chloride channel that:
• Secretes Cl in lungs (thinning secretions)
• Reabsorbs Cl in sweat glands.
Defective CFTR:
• Thick mucus
• Salty sweat
Diagnosis 1) Typical clinical features
2) History of CF in sibling
3) Laboratory tests (confirmatory) : Any 1+
• Increased sweat chloride >60mEq/L on 2
separate occasions
• 2 CF mutations
• Single abnormal value (<-40mV) of
transepithelial nasal potential difference .
Treatment 1) Respiratory signs/symptoms:
• Physiotherapy
• Mucolytics (3% NS, Recombinant DNase –
Dornase alfa)
• Prophylaxis for pseudomonas:
o Inhaled Tobramycin/ Aztreonam OR
o Oral Azithromycin 3 times/week.
• Antibiotic for pneumonia :
Co-amoxiclav
2) Dietary measures:
• Increased fat, protein & calorie in diet
• Pancreatic enzymes
• Vitamin A,D,E & K
3) CFTR modulators:
• Ivacaftor (Increase Chloride conductance)
• Lumacaftor (Protein folding chaperone)
• Tezacaftor
• Elexacaftor
DEVELOPMENT
 GROWTH

PARAMETER GROWTH PATTERN

WEIGHT • Average birth weight of an Indian child = 3kgQ
• Physiological weight loss (10%) in the first 7 days due to loss of ECF.

GA % weight Regained
loss by
Term 10% D10
Preterm 15% D14

• Ready reckoner for weight gain, if birth wt. is x :

5 2x
mo
1 yr 3x
2 yr 4x
3 yr 5x
5 yr 6x
7 yr 7x
10 10x
yr

Height / • Devices:
length <2 year Length Infantometer
>2 year Height Stadiometer

length @ birth = 50 cm

1 yr = 75 cm

2yr = 85-90 cm

Puberty

Boys = 10cm/yr Girls = 8cm/yr

• Weech’s formula for height :
𝐸𝑥𝑝𝑒𝑐𝑡𝑒𝑑 ℎ𝑒𝑖𝑔ℎ𝑡 (2 − 12 𝑦𝑒𝑎𝑟𝑠) = 6(𝑎𝑔𝑒 𝑖𝑛 𝑦𝑒𝑎𝑟𝑠) + 77𝑐𝑚
US: LS ratio • Useful in evaluation of short stature.
• Appropriate ratio for age = Proportionate SS
• Inappropriate ratio for age = Disproportionate SS

Birth 1.7 : 1
3 years 1.3 : 1
6 years 1.1 : 1
10 years 1:1
Adults 0.9

Arm span • Evaluation of tall stature

At birth AS<height by 2.5

cm
11 years AS=height
>11 years AS>height by <1cm

Head • HC at birth = 33-35 cm (average=34cm)

circumference first 3
3-6 months
6-12
Birth 34 cm months : months:
: 1cm/mo
2cm/mo 0.5cm/mo

• Ready reckoner for HC

Birth 34 cm
3 months 40 cm
6 months 43 cm
1 yr 46-47 cm
2 yr 48 cm
12 yr 52 cm
•
HC : CC
relationship
Birth HC>CC
(3cm)
1 year HC=CC
>1 year HC<CC
 CONGENITALHEART DISEASE AND ASSOCIATIONS

ASSOCIATION DEFECT
PRENATAL ALCOHOL EXPOSURE VSD,PDA,ASD,TOF
(FETAL ALCOHOL SYNDROME)
CONGENITAL RUBELLA PDA
DOWN SYNDROME Endocardial cushion defects
INFANT OF DIABETIC MOTHER TGA
MARFAN SYNDROME Mitral valve prolapse
PRENATAL LITHIUM EXPOSURE Ebstein anomaly
TURNER SYNDROME Bicuspid aortic valve, coarctation of
aorta
WILLIAM SYNDROME Supravalvular aortic stenosis
22Q11 SYNDROME/DIGEORGE Conotruncal defects
SYNDROME
EDWARD SYNDROME VSD
PATAU SYNDROME VSD
NOONAN SYNDROME Pulmonary stenosis
SLE WITH ANTI RO/LA Congenital heart blocks

RADIOLOGICAL APPEARANCE OF CHD

Egg in cup heart Constrictive pericarditis

Triangular shaped heart Constrictive pericarditis
Box shaped heart Ebstein’s anomaly/Tricuspid atresia
Tubular heart Emphysema
Pentagon shaped heart Mitral incompetence
Sitting duck heart Persistent truncus arteriosus
Jug handle appearance Primary pulmonary hypertension
Cor-triatriatum Pulmonary venous obstruction
Snowman’s heart/figure of 8 heart Supra cardiac TAPVC
Egg on side Transposition of great vessels
Boot shaped Tetralogy of Fallot
 FEVER WITH RASH(PEDIATRIC VIRAL EXANTHEMS)

Rash Name Causative Clinical Features

Agent

Measles Measles virus High fever, cough, coryza, conjunctivitis, Koplik spots,
(Rubeola) maculopapular rash starting from the face and spreading
downward

Rubella Rubella virus Mild fever, lymphadenopathy, rash starting on the face and
(German spreading to the trunk and extremities, pinkish-red
Measles) maculopapular rash

Chickenpox Varicella- Fever, malaise, pruritic rash with vesicles that progress to
zoster virus pustules and then crusts

Erythema Parvovirus Slapped cheek appearance, followed by a lacy, reticular

Infectiosum B19 rash on the trunk and limbs

Roseola Human High fever for several days followed by a rash appearing
Infantum herpesvirus 6 as pink, discrete, flat or slightly raised macules and papules
(HHV-6)

Scarlet Group A Fever, sore throat, "strawberry tongue," sandpaper-like

Fever Streptococcus rash starting on the trunk and spreading to the extremities

Hand, Foot, Enteroviruses Fever, painful oral ulcers, rash on the hands, feet, and
and Mouth (e.g., buttocks consisting of small vesicles or ulcers
Disease Coxsackievirus
A16)
 RICKETS

• Rickets is a disorder of growing skeleton.

• Deficiency of normal mineralization seen in rickets is most evident at metaphyseal
zones of provisional calcification.
• There is an excess of non-mineralized osteoid resulting in growth plate widening and
abnormal configuration of the metaphysis.
• Fraying: indistinct margins of the metaphysis
• Splaying: widening of metaphyseal ends
• Cupping: concavity of metaphysis
• Findings of rickets are most prominent at the bones where growth is greatest:
Knee: distal femur, proximal tibia Wrist: ulna
Anterior rib ends: rachitic rosary

Other findings:

• Outward bowing of legs with variable deformity of the hips (both coxa vara and coxa
valga seen)
• Genu valga and vara
• Protrusio acetabuli
• Inward drawing of lower ribs due to inferior attachment of the diaphragm-Harrison's
sulcus
• Codfish vertebra
 SCURVY

• Vitamin C deficiency
• Defective hydroxylation of proline & lysine (important for collagen maturation)
• Effect on connective tissues
• Clinical features :
1. Gum bleeds
2. Subperiosteal bleeds: pain : pseudoparalysis
3. Corkscrew hair & perifollicular bleeds
4. Scorbitic rosary (painful, angulated)
• X ray findings :
1. Subperiosteal bleeds
2. White line of Frenkel
3. Scorbutic zone/trummerfeld zone
4. Ring epiphysis
5. Pelkan spur
6. Pencil thin cortex
 NRP

• The most important & effective action in neonatal resuscitation is ventilation of the
baby’s lungs. Rise in HR is best sign of effective ventilation

• Ventilation corrective steps:

M Mask adjustment
R Reposition airway
S Suction mouth & nose
O Open mouth
P Pressure increase
A Alternate airway

• Medications used during/following resuscitation of a newborn

Medication Dosage & route Concentration Precautions

Epinephrine • IV (UVC • 1:10,000 Give rapidly
preferred Repeat every 3-5
route) : 0.1- minutes if HR<60
0.3ml/kg with chest
• Endotracheal : • 1:1000 compressions.
0.5-1 ml/kg

Volume 10 mL/kg (UVC) Indicated for

expanders shock.
• Isotonic Give over 5 -10
crystalloid minutes.
(NS) Reassess after each
• Blood bolus.

• Immediate cord clamping is done if baby is not crying/limp at birth

• Stimulation done by rubbing back or flicking of feet, never slap the baby!
• M before N (Mouth suctioning prior to nose)
• PPV needs to be started within 60 seconds of birth if initial steps of resuscitation do not
result in crying/normal tone along with SpO2 and ECG monitoring
• Chest compressions are started after 30 seconds of PPV which moves the chest and HR is
less than 60
• CPAP for laboured breathing only if HR>100.
 Antenatal counselling, Team briefing & equipment failure

Birth

Rooming in with mother,

Term? Tone? Warm & maintain
Breathing or temperature, position
crying? airway, clear secretions if
needed, dry, ongoing
evaluation

Warm & maintain normal temperature, position

1 minute airway, clear secretions if needed, dry, stimulate.

Apnea, gasping
, or HR <100
bpm

PPV, SpO2
monitoring; ECG Labored breathing or
monitor persistent cyanosis?

HR <100 Position & clear airway, SpO2 monitor, consider

bpm? CPAP
No

Post resuscitation care, Team

Check chest movements, Ventilation debriefing

corrective steps; ETT/LMA if needed.

HR <60
bpm?

Intubate if not already done. Chest compressions,

cordinate with PPV. 100% O2. ECG monitor

HR <60
bpm?

IV epinephrine

If HR persistentlt Pre-ductal SpO2

below 60 bpm Target:
1 min 60-65%
2 min 65-70%
Consider Consider 3 min 70-75%
hypovolemia pneumothorax 4 min 75-80%
5 min 80-85%
10 min 85-95%
Needle thoracotomy
Volume expansion
 HEAD TRAUMA

EDH SDH
Origin of bleed Middle meningeal artery Bridging cortical veins
Laterality Unilateral Unilateral/bilateral
Clinical features Lucid interval followed by Gradually increasing
unconsciousness headache and altered
sensorium
Fracture Present Absent
association
Limited by Cranial sutures. Not limited by Dural Dural folds/venous sinuses.
folds/venous sinuses Not limited by cranial
sutures
Shape Biconvex/Lentiform Concavo-convex/crescentic
shaped

SUBARACHNOID HEMORRHAGE (SAH)

Definition Bleeding into the subarachnoid space of the brain
Common Cause Ruptured intracranial aneurysm
Clinical Features Sudden severe headache (often described as
"thunderclap headache")
Neck stiffness
Altered level of consciousness
Nausea and vomiting
Focal neurological deficits
Diagnosis Non-contrast CT scan of the head
Lumbar puncture (if CT scan is negative)
Complications SAH Vasospasm
Rebleeding
Hydrocephalus
Seizures
Cerebral edema
Ischemic stroke
Management Supportive care (e.g., analgesics, antipyretics,
antiemetics)
Secure the ruptured aneurysm (surgical clipping or
endovascular coiling)
Prevent complications (e.g., nimodipine for
vasospasm, antiepileptic drugs for seizures) -
Rehabilitation
SUBDURAL HEMMORHAGE
Subdural haemorrhage is characterized by accumulation of blood between dura and arachnoid
matter which appears as concavo-convex hyperdensity on NCCT scan.

SUBARACHNOID HEMMORHAGE
Subarachnoid haemorrhage appears as collected hyperdensity in sulcal spaces or basal
cisterns, usually secondary to traumatic brain injury or rupture aneurysm.

EXTRADURAL HEMMORHAGE
Hyperdense lentiform shaped bleed along left frontal convexity.
History of unconsciousness-brief period of alertness-again unconsciousness which is
suggestive of lucid interval is diagnostic of extradural hemorrhage.
VARICOSE VEINS
 GCS

EYE OPENING Verbal response Motor response

•Spontaneous :4 •Oriented :5 •obeys command : 6

•To voice :3 •confused :4 •localises pain :5
•To pain :2 •inappropriated words :3 •withdrawl to pain : 4
•None :1 •incomprehensible words :2 •abnormal flexion : 3 *
•silent :1 •abnormal extension :2 **
•no movement :1
 BREAST CARCINOMA

BI-RADS (Breast Imaging-Reporting and Data System):

• Risk assessment and quality assurance tool developed by American College of

Radiology.
• Provides a widely accepted lexicon and reporting schema for imaging of the breast.
• Applicable to mammography, ultrasound and MRI.
 HISTOPATH FEATURES OF BREAST CONDITIONS

BREAST HISTOPATHOLOGICAL
CONDITION FEATURES
Benign Breast Tightly arranged ductal epithelial cells
Tumour with dyscohesive bare nuclei
Invasive Ductal Polymorphism with single or arranged
Carcinoma (IDC) ductal epithelial cells
Phyllodes Tumour Stromal predominance with spindle cell
hyperplasia
Ductal Carcinoma Dyscohesive ductal epithelial cells
In Situ (DCIS) without cellular fragments
Invasive Lobular Loss of E-cadherin expression, single-file
Carcinoma (ILC) arrangement of tumour cells

Fibroadenoma Stroma-rich, well-circumscribed tumour

with glandular and stromal components

VAN NUYS SCORING

Parameters Score 1 Score 2 Score 3

40-60
Age >60 years <40 years
years
Size ≤15 mm 16-40 mm ≥41 mm
Margin ≥10 mm 1 – 9 mm <1 mm
Grade 1 or Grade 1 or Grade 3 with
Class 2 without 2 with or without
necrosis necrosis necrosis
 THYROID MALIGNANCY

MOST COMMON ASSOCIATIONS

Most common primary thyroid malignancy
Most common thyroid malignancy associated with radiation
PAPILLARY Most common malignancy of thyroid associated with lymphatic
CARCINOMA spread
Most common thyroid malignancy in iodine sufficient areas

Most common thyroid malignancy associated with blood and bone

FOLLICULAR metastasis
CARCINOMA Most common thyroid malignancy in iodine deficient areas
Most common thyroid malignancy associated with Multi Nodular
Goiter
ANAPLASTIC
CARCINOMA Most aggressive thyroid malignancy with worst prognosis

THYROID
CARCINOMA TYPE LYMPH NODE INVOLVEMENT

PAPILLARY Lymphatic spread, commonly involving central (level VI)

CARCINOMA and lateral neck lymph nodes (levels II, III, IV, and V)

MEDULLARY Moderate lymph node involvement, including central and

CARCINOMA lateral neck lymph nodes

FOLLICULAR Bloodborne metastasis, lymph node involvement is

CARCINOMA uncommon

ANAPLASTIC Anaplastic carcinoma of the thyroid is one of the most

CARCINOMA aggressive malignancies. It has rapid growth with visceral
invasion and distant metastases.
 COLON CANCER

RIGHT-SIDED LEFT-SIDED COLON

COLON CANCER CANCER
Cecum, ascending Splenic flexure, descending
ANATOMICAL colon, and hepatic colon, sigmoid colon, and
LOCATION flexure rectum
Vague abdominal Change in bowel habits,
pain, iron deficiency hematochezia (blood in
CLINICAL anemia, palpable stool), left-sided abdominal
PRESENTATION mass on the right pain
side.

Generally associated
PROGNOSIS with a better Generally associated with a
prognosis poorer prognosis
Less commonly
associated with More commonly associated
microsatellite with microsatellite instability
GENETIC instability (MSI) and (MSI), BRAF mutations, and
MUTATIONS BRAF mutations KRAS mutations
 PNEUMOTHORAX

SIMPLE
PNEUMOTHORAX TENSION PNEUMOTHORAX
ETIOLOGY Spontaneous, Traumatic, iatrogenic, rarely
traumatic, iatrogenic spontaneous
CLINICAL Chest pain, dyspnea, Severe respiratory distress,
FEATURES decreased breath cyanosis, tracheal deviation to
sounds on affected contralateral side, absent breath
side sounds on affected side
HEMODYNAMIC Hemodynamically
STATUS stable Hemodynamically unstable
MANAGEMENT Observation, Initial management with needle
supplemental oxygen, thoracostomy (Insert the wide-
possible aspiration or bore needle in the 5th intercostal
chest tube insertion space in the midaxillary line),
if symptoms worsen followed by definitive chest tube
or pneumothorax is insertion
large
URINE MICROSCOPY
 FOURNIER'S GANGRENE

It is a polymicrobial infection involving the subcutaneous tissue leading to obliterative

arteritis and gangrene.

Management is emergency surgical debridement.

Testis are usually spared in Fournier's gangrene due to dual blood supply.

qSOFA

qSOFA includes:

1. Hypotension- systolic BP < 100 mmHg

2. Altered mental status
3. Tachypnoea- RR > 22/ minute

A score of more than or equal to 2 criteria suggests a greater risk of a poor outcome
 MUSCLE FLAPS

MUSCLE FLAP DESCRIPTION USED IN IMAGE

TRANSVERSELY
ORIENTED Transverse Breast
RECTUS orientation, well- reconstruction,
ABDOMINIS vascularized lower
MUSCLE FLAP tissue extremity
defects

VERTICALLY Vertical Chest wall

ORIENTED orientation, reconstruction,
RECTUS versatile tissue abdominal
ABDOMINIS defects
MUSCLE FLAP

PECTORALIS Muscle and skin Head and neck

MAJOR flap, head and reconstruction,
MYOCUTANEOUS neck oral cancer
FLAP reconstruction

SERRATUS Chest wall Chest wall

ANTERIOR reconstruction, reconstruction
MUSCLE FLAP reliable tissue after
oncological
resections
 NERVE INJURY CLASSFICATION

SEDDON SUNDERLAND INJURY TREATMENT PROGNOSIS

NEUROPRAXIA I Local myelin Spontaneous Excellent
(COMPRESSION) damage
Nerve still
intact
AXONOTMESIS II Continuity of Full recovery
(CRUSH) Axon is lost possible without
Endo-, Epi-, surgery
Perineurium
intact
III Same as Regeneration
above with 1mm/day
endoneural
injury
1V Same as Surgical
above with reconstruction
endo and Scar build-up
perineural prevents
injury regeneration
NEUROTMESIS V Complete Surgical Worst
(TRANSECTION) transection
 TRANDELENBURG SIGN

• In Superior Gluteal nerve injury, paralysis of gluteus medius & gluteus minimus
muscles is seen.
• When the leg on one side is lifted off the ground, the gluteus medius &
minimus muscles, on opposite supported side, exert traction on hip bone by acting
from femur.
• This action results in the slight raising of pelvis on unsupported side, which helps
maintain the trunk in upright position
• When the gluteus medius & minimus are paralyzed, the pelvis sinks down on
unsupported (normal) side when pt. tries to stand on affected Limb.
 SPLINTS

SPLINT USE
LOWER LIMBS
Thomas Femur fracture
Bohler-Braun
Toe-raising Foot drop
Dennis Brown splint CTEV
UPPER LIMBS
Cock up splint Radial nerve injury
Volkmann’s turn buckle Volkmann’s ischemic contracture
Knuckle bender splint Claw hand (ulnar nerve)
Aeroplane splint Brachial plexus injury
SPINE
Milwaukee brace scoliosis
Boston brace
SOMI brace Cervical spine injury
ASHE (anterior spinal hyperextension) Dorso-Lumbar spinal injury
brace
 UPPER LIMB FRACTURES

COLLE’S FRACTURE Extra-articular # distal radius with dorsal

angulation of distal bone fragment

GALEAZZI FRACTURE # lower third of radius & subluxation of

DISLOCATION distal radio-ulnar joint

MONTEGGIA FRACTURE # shaft ulna with dislocation of proximal

DISLOCATION Radioulnar joint

BARTON’S FRACTURE Intra-articular # distal radius

ROLANDO FRACTURE Intra articular communated # of base of 1st

metacarpal with T or Y configuration
CHAUFFEUR’S FRACTURE/ # radial styloid
HUTCHINSON’S FRACTURE

SMITH’S FRACTURE Reverse colle’s #

ESSEX-LOPRESTI LESION # radial head with disruption of interosseous

membrane & distal radio-ulnar joint
ligaments

NIGHT STICK FRACTURE Isolated # ulna

 LOWER LIMB FRACTURES

Hoffa fracture Coronal fracture of femoral condyles

Tillaux fracture Avulsion fracture of tibia by the anterior tibiofibular ligament
Runner’s fracture Fracture of distal shaft of fibula
Pott’s fracture Bimalleolar ankle #
Aviator’s fracture Neck of talus #
Chopart’s fracture # between talonavicular & calcaneocuboid joints
Lisfranc’s fracture- Fracture of metatarsal bases with associated tarsometatarsal
dislocation dislocation
March fracture Fracture of neck of 2nd or 3rd metatarsal
Jone’s fracture Extra-articular fracture at the base of 5th metatarsal
Dancer’s fracture Fracture of distal shaft of 5th metatarsal

VERTEBRAL FRACTURES

Burst fracture Vertebral compression injury

Cance fracture Horizontal fracture of vertebral body
Clay-shoveller’s fracture Spinous process fracture of C6, C7 or T1
Dens fracture Odontoid process fracture
Hangman’s fracture Fracture of both pedicles of C2
Holdsworth fracture Unstable spinal fracture- dislocation at the
thoracolumbar junction
Jefferson’s fracture Fracture of 1st cervical vertebra
Motorcyclist’s fracture Transverse fracture across base of skull
Whiplash’s injury Hyperextension followed by flexion
Undertaker’s fracture Post-mortem fracture of the lower cervical
spine with C6-C7 disc disruption
 SEXUAL DIFFERENTIATION SYNDROME

ENZYME CORTISOL ALDOSTERONE TESTOSTERONE CLINICAL

DEFICIENCY FEATURES
21- hydroxylase Low Low High Salt wasting,
Hypotension,
Precocious
puberty and
virilisation
11-beta Low High High Hypertension,
hydroxylase Precocious
puberty,
Virilisation
17-alpha Low High Low Hypertension
hydroxylase but no
virilisation
3-beta Low Low Asymptomatic
hydroxylase or precocious
puberty,
Hirsutism and
Primary
amenorrhea.
 PCOS

• DIAGNOSTIC CRITERIA (Rotterdam criteria) : Any 2/3 required for diagnosis:

o Ovulatory dysfunction (Oligomenorrhea/amenorrhea)
o Clinical or biochemical evidence of hyperandrogenism
§ Clinical: hirsutism, acne, alopecia
§ Biochemical: s. testosterone 70-150 ng/dl (>200ng/dl indicates
testosterone secreting tumour)
o Polycystic ovarian morphology on USG scan :
§ Presence of 12 or more cysts (2-9mm) in any one/both ovaries aalong
with,
§ Enlarged ovaries (>10ml)

• Hormonal changes in PCOS

Increased Decreased
• Androgens • FSH
• LH • Progesterone (due to anovulation)
• Estrogen • SHBG
• Insulin (due to resistance) • HDL & Apoprotein A1
• Prolactin
• LDL/cholesterol & triglycerides

• Management of PCOD :

Issues Management
Irregular Menses OCPs
Obesity Life style modifications
Insulin Resistance Metformin
Hirsutism/ Acne OCPs with cyproterone acetate
Infertility • Reversible & treatable
(Due To • Advise weight loss (resumption of ovulation in 5-10% cases
Anovulation) by weight loss)
• Ovulation inducing drugs :
o First line : SERMs
§ Clomiphene citrate (DOC)
§ Tamoxifen (unable to tolerate clomiphene)
o Second line :
§ Gonadotrophins
§ LH/FSH injection
o Third line : GnRH agonist:
§ Leuprolide
§ Gusareline (pulsatile manner)
§ Nafarelin
 ABNORMAL UTERINE BLEEDING

Any uterine bleeding beyond normal volume, regularity or frequency is considered as

abnormal uterine bleeding.

NORMAL MENSTRUATION:
Cycle duration 28 days (21-35 days)
Menstrual flow 4-5 days
Amount of blood loss 35ml (20-80 ml)

ETIOPATHOLOGY:
AUB classification (FIGO)

Structural cause (PALM) Non- structural cause (COEIN)

§ Polyp § Coagulopathy
§ Adenomyosis § Ovulatory dysfunction
§ Leiomyoma § Endometrial
o Submucosal § Iatrogenic
myoma § Not yet identified
o Other myoma
§ Malignancy & hyperplasia

Management of AUB :

Condition Management
Age >45 years Endometrial biopsy
§ D/C
§ Hysteroscopy
Adolescent female Needs exclusion of bleeding disorders
 HPV

• E6 inhibits p53, E7 inihibts RB

• WHO recommends: A one or two-dose schedule for girls aged 9-14 years. A one or
two-dose schedule for girls and women aged 15-20 years. Two doses with a 6-month
interval for women older than 21 years.

SIGNS OF PREGNANCY

• Chadwick's sign
- Bluish-purple coloration of the vaginal mucosa and cervix

• Goodell's sign
- Softening of the cervix

• Hegar's sign
- Softening of the lower uterine segment or isthmus
 ANEMIA IN PREGNANCY / ANEMIA MUKT BHARAT GUIDELINES

Who will screen Health service provider at any ANC

contact

Periodicity of screening At every ANC contact

Anemia in Mild Moderate Severe

pregnancy (10-10.9 g/dl) (7-9.9 g/dl) (5-6.9 g/dl)
First level § 2 tabs IFA § 2 tabs IFA daily § IV Iron
treatment daily § Parenteral IV (IV sucrose or IV
§ Parenteral IV sucrose or FCM) if FCM
(IV sucrose or detected late/non- § If detected in
FCM) if compliance is 3rd trimester :
detected suspected. Immediate
late/non- hospitalization
compliance is in the centre
suspected. with round the
clock
specialist care.

Follow up § Every 2 § Every 2 months for § Monthly after

months for compliance. first level
compliance. § Monthly Hb treatment.
§ If Hb reaches estimation § Or as
normal level, § If Hb reaches prescribed by
discontinue normal level, medical
treatment & discontinue officer
switch to treatment & switch
prophylactic to prophylactic
doses. doses.
Treatment Refer to FRU/DH Refer to FRU/DH by As prescribed by
protocol if no by health care health care provider MO.
improvement provider
(<1g/dl increase
after 1 month of
treatment)
Special note if Referral to higher Referral to higher If Hb <5g/dl,
any centre for centre for investigations immediate
investigations & & IV iron hospitalisation
IV iron irrespective of
POG.

NOTE : Protocol mentioned for severe anaemia is C/I in patients with Thalassemia & SCA. In such cases,
treatment by FA is recommended.
 STI SYNDROMIC MANAGEMENT

KIT
SYNDROME COLOR CONTENTS
NO.
UD (Urethral discharge),
Kit 1 ARD (Anorectal Grey Tab, Azithromycin 1 g (1) and Tab. cefixime 400 mg (1)
discharge), Cervicitis
Tab. Secindazole 2 g (1) and Tab. Fluconazole 150 mg
Kit 2 Vaginitis Green
(1)
Inj. Benzathine penicillin 2.4 MU (1) and Tab.
GUD (Genital ulcer
Kit 3 White Azithromycin 1 g (1) and Disposable syringe 10 ml with
disease) Nonherpetic
21 gauge needle (1) and Sterile water 10 ml (1)
GUD (Genital ulcer Tab. Doxycycline 100 mg (30) & Tab. Azithromycin 1g
Kit 4 Blue
disease Nonherpetic) (1)

GUD (Genital ulcer

Kit 5 Red Tab. Acyclovir 400 mg (21)
disease Nonherpetic)

LAP (Lower abdominal Tab. Cefixime 400 mg (1) and Tab. Metronidazole 400
Kit 6 Yellow
pain) mg (28) and Cap. Doxycycline 100 mg (28)
Tab. Doxycycline 100 mg (42) and Tab. Azithromycin 1
Kit 7 IB (Inguinal bubo) Black
g (1)
 Turner syndrome

Genotype : 45 XO
Streak gonads

Suboptimal estrogen levels

Short stature
Primary amenorrhea Absent/underdeveloped
secondary sexual
characterstics

• Most common : Monosomy X (45 XO)

• Occurs due to non-disjunction of chromosome during meiosis
• Retained X chromosome is Maternal in origin.
• Other causes : Mosaics 45XO/46XX or 45XO/46XY

CONTRACEPTIVE METHODS
Pearl index: It indicates the effecDveness of a contracepDve or is an index of contracepDon
failure.

WHO CATEGORY OF CONTRACEPTION :

NOTE :Least failure rate is with perfect use. If nothing is mentioned in the question
assume Typical use.

WHO Category 1 (user independent)

Contraception Perfect use rate Typical use

Implants 0.5% 0.05%
Sterilization
• Male 0.1% 0.15%
• female 0.5% 0.5%
IUCD 0.2% 0.2%
Cu T 0.6% 0.8%

Methods of contraception

Permanent Temporary

Tubectomy (females) barrier method

Vasectomy (Males) natural contraception

OCPs

Injectables

Implants

IUDs
 WHO Category 2 (user dependent)

Contraception Perfect use rate Typical use

OCP 0.3% 8.7%

Vaginal ring 0.3% 8%

Transdermal patch 0.3% 8%

DMPA 0.3% 8%

Condom
• Male 2% 16%
• female 5% 21%

Diaphragm 20% 20%

Sponge
• Nulliparous 9% 16%
• Multiparous 26% 21%

LABOUR
 Differentiating True & false labour pains

Features True Labour pains False Labour pains

Frequency & duration of Regular & increases Irregular
contractions gradually
Cervical changes + -
Pain Lower abdomen & back Lower abdomen only
Radiating to thigh
Bag of water Formed Absent
Show + -
Relief with enema/sedation No Yes

• Level of cervical dilatation with phase of labour:

• 8 cardinal movements of head during normal labour:

Mnemonic : Every Decent Female I Choose to Employ Rises Extremely.
o Engagement
o Descent
o Flexion
o Internal rotation
o Crowning
o Extension
o Restitution
o External rotation

FHR MONITORING / CTG/ PARTOGRAM

Late Deceleration suggestive of utero placental insufficiency leading to foetal distress

Remember all the types and causes of decelerations . Frequently repeated question

• The most common procedure done in a labour room is the Nonstress Test.
 • This test looks at the foetal heart rate acceleration in response to foetal
movement as a measure of foetal health.
• It involves the use of Doppler to detect the foetal heart rate accelerating
when the mother perceives foetal movement.

The given graph represents the modified WHO partograph of a patient in labor which is a
graphical representation of the progress of labor in which cervical dilatation and descent of
fetal head is plotted against the time, as well as maternal and fetal vital parameters.

Summary of the partograph findings, as seen in this patient are summarized below:
1. This a multiparous female (G2) with the foetus showing signs of foetal
distress(bradycardia and meconium-stained liquor).
2. 3+ molding i.e., fixed overlapping of bones is present.
3. Slow progression of labour (overall the rate of dilation has been 6 cm in 8 hours) which
is less than 1 cm/ hr.
4. The contractions are seen to be adequate.