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CLINICAL METHODS: PHYSICAL EXAMINATION AND CLINICAL HISTORY

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CLINICAL METHODS
(Physical Examination and Clinical History Taking)
for Health Science Students

(Lecture Note)
Prepared by
Abilo Tadesse, MD
Physical examination and Clinical history taking
Preface
Since text books in “Physical examination and Clinical history taking” for health science students are not
available as needed, this lecture note will alleviate the deficiency in ‘knowledge and skill’ transferred from text
books of “Clinical Methods”.
The lecture note comprises almost all of the course contents of ‘Clinical Methods’ provided to health science
students including Medical, Health Officer, Anesthesia and Physiotherapy students, so then it can be used as a
main learning material to these category of students.
I am grateful to internal and external reviewers who offered invaluable comments during write up of the lecture
note.
At last but not least, the quality of this lecture note will be kept up to date by continual comments made by users
of this lecture note.
Abilo Tadesse, MD
Associate Professor of Medicine
University of Gondar Hospital
February, 2023
1 Abilo Tadesse,MD
Acknowledgment
I would like to acknowledge my students, who were actively involved in the learning-teaching process during
“Clinical Bridging Course”, who gave me a good opportunity to improve my skills in clinical history taking and
physical examination.
2 Abilo Tadesse,MD
Contents
Page No.
Preface 01
Acknowledgment 02
Table of contents 03
Chapter One: Scheme of history taking and physical examination 04
Chapter Two: Vital signs in physical examination 19
Chapter Three: Physical appearance and HEENT 29
Chapter Four: Lymphoglandular system 49
Chapter Five: Respiratory system 64
Chapter Six: Cardiovascular system 91
Chapter Seven: Gastrointestinal system 125
Chapter Eight: Nervous system 162
Chapter Nine: Musculoskeletal system 228
Chapter Ten: Genitourinary system 259
Chapter eleven: Integumentary system 292
Medical case report 302
References 311
3 Abilo Tadesse,MD
CHAPTER ONE
Scheme of history taking and physical examination
Learning Objective
At the end of this lesson, the student should be able to:
1. Elaborate the duties and responsibilities of health professionals towards health care
2. List the classification scheme of clinical history taking
3. Mention the components of history of present illness (HPI)
4. List the scheme of physical examination
Physical examination and history taking are the essence of medical practice. The word ‘patient’ is derived from
the latin, patiens, meaning sufferance or forbearance. The overall purpose of medical practice is to relieve
suffering. In order to achieve this purpose, it is important to make a diagnosis, to know how to approach
treatment and to design an appropriate scheme of management for each patient.
Two major steps of making the diagnosis
a. To establish the clinical data by history taking and physical examination

b. To interpret the clinical data
Questions asked by the doctor can be open-ended questions, which invite questions for the patient to talk about
his general complaints, while closed-ended questions are specific questions of the doctor’s interest forwarded to
the patient. The doctor should use open-ended questions to encourage the patient to give a full and free account
of their illness. Encourage the patient to tell their own story without interruption, listen carefully and maintain
eye contact. An interview that uses lots of direct questions is often ‘disease-centered’ where as ‘patient-
centered’ interview will contain enough open-ended questions for the patient to talk through all their problems.
The doctor needs to grasp the difference between disease frame work (what is the diagnosis?) and illness frame
work (what are the patients’ experiences, ideas, expectations and feelings?). During any medical consultation,
the doctor should be concerned with all aspects of the patients’ health and not just the problem with which
patients have presented.
Clinical communication skills
Clinical communication skill is fundamental link between the doctor’s experiences in providing excellent
patient-centered care
1. Active listening
Hearing what is being said, and processing and interpreting the words that are spoken (and unspoken) to
understand the complete message
4 Abilo Tadesse,MD
Use ‘verbal tracking’ to show that you are paying attention
2. Empathy
When you place yourself in your patient’s situation, and respond based on either similar personal experience or
through vicarious understanding
3. Building rapport
Building good rapport allows the patient to feel comfortable with you, there by making the lines of
communication more open and honest
Improved rapport results in increase flow of conversation, disclosure of sensitive information, relaxed body
language, increased eye contact, and better listening and responding
4. Open and closed ended questions
Open-ended questions are invited questions for the patient to talk about his general complaints
Closed-ended questions are specific questions of the doctor’s interest forwarded to the patient
Open-ended question is the preferred technique to use during patient interview to obtain in-depth and insightful
responses
5. Silence
Silence after questioning the patient is able to reflect upon your questions and provide a more thoughtful and
accurateresponse
6. Leading questions
Leading question leads a patient to provide a response that the interviewer wants to hear
Avoid leading questions!
Eg. “You didn’t miss the morning medication dose, did you?”
7. ‘Why” questions
‘Why’ questions invite the patient from feeling to defend his choices and actions
Avoid ‘why’ questions!
Eg. “Why did you miss the morning medication dose?”
8. Non-verbal communication cues
Non-verbal communication is message exchange to or from the patient without the use of words. It includes
tone of voice, choice of language, facial expression, body gesture and postion, eye contact, appearances, and
5 Abilo Tadesse,MD
over allbehavior. A patient’s perception of non-verbal communication may be influenced by individual and
cultural differences.
Implement the ‘SOFTEN’ non-verbal communication cues during interviewing patients
. ‘Smile’ welcomes a patient and can put the patient at ease
. ‘Open posture’ facilitates being approachable and ready to interact
. ‘Forward lean’ slightly towards the patient indicates as attracted or interested
. ‘Touch’ like hand shake upon entering the room facilitates interaction with patients
. ‘Eye contact’ indicates paying attention to patients and not distracted by other activities
. ‘Nod’ encourages patients to continue with their story
Five-step patient-centered interviewing
Step-1: Set the stage for the interview (30-60 seconds)
. Welcome the patient
. Use the patient’s name
. Introduce youself and identify specific role
. Ensure patient readiness and privacy
. Remove communication barriers (have a seat).
. Establish patient comfort (ensure comfort and put the patient at ease)
Step-2: Elicit chief complaint and set an agenda for the visit (1-2 minutes)
. Indicate available time
. Obtain list of issues patient wants to discuss
. Summarize/finalize the agenda; prioritize items for current encounter and future encounter
Step-3: Open the history of present illness (non-focused) (30-60 seconds)
. Ask open-ended questions to elicit problems
. Use active listening (interest in the patient without judgment), empathy (emotional state of communication and
understanding), and concern (caring for the unique questions)
6 Abilo Tadesse,MD
Step-4: Continued the patient-centered history of present illness (3-10 minutes)
. Use focused, but open-ended questions to obtain description of symptoms
. Explore patient description of symptoms, emotional and social context of symptoms
Step-5: Transition to clinician-centered process (30-60 seconds)
. Summarize conversation and confirm accuracy of information
. Inform the patient that the style of questions will now change (eg. I am going to ask you specific medical
questions about your symptoms)
Duties of doctors (British General Medical Council)
. Make the care of your patient your first concern
. Treat every patient politely and considerately
. Respect patients’ dignity and privacy
. Listen to patients and respect their views
. Give patients information in a way they can understand
. Respect the right of patients to be fully involved in all decisions about their care
. Keep your professional knowledge and skills up-to-date
. Recognize the limits of your professional competency
. Be honest and trust worthy
. Respect and protect confidential information
. Make sure that your personal beliefs do not prejudice your patients care
. Avoid abusing your position as a doctor
. Act quickly to protect patients from risk if you have a good reason to believe that you may not be fit to practice
. Work with colleagues in the ways that best serve patient’s interest
. Never discriminate unfairly against your patients or colleagues
The Revised Declaration of Geneva: A Modern-Day Physician’s Pledge (October, 2017)
7 Abilo Tadesse,MD
As a member of the medical profession
I will solemnly pledge to dictate my life to the service of humanity
The health and well-being of my patient will be my first consideration
I will respect the autonomy and dignity of my patient
I will mainatain the utmost respect for human life
I will not permit considerations of age, disease or disability, creed, ethnic origin, gender, nationality, political
affiliation, race, sexual orientation, social standing, or any other factor to intervene between my duty and my
patient
I will respect the secrets that are confided in me, even after the patient has died
I will practice my profession with conscience and dignity and in accordance with good medical practice
I will foster the honour and noble traditions of the medical profession
I will give to my teachers, colleagues, and students the respect and gratitude that is their due
I will share my medical knowledge for the benefit of the patient and the advancement of health care
I will attend to my own health, wellbeing, and abilities in order to provide care of the highest standard
I will not use my medical knowledge to violate human rights and civil liberties, even under threat
I make these promises solemnly, freely, and upon my honour
8 Abilo Tadesse,MD
A. Scheme of clinical history taking
1. Identification of the patient
Full name, Age, Sex, Occupation, Address, Religion, name of admitted hospital, Hospital bed number, date of
admission
Eg, E.M., 40-year-old male, married, Orthodox Christian, daily laborer from Metema, North Gondar Zone,
admitted to University of Gondar hospital, medical ward D, bed number 24, on January 12, 2009 E.C
2. Previous admission
This is a list of previous hospitalization in the order they occurred
. Specify the date, name and location of the hospital, disease led to admission, treatment and outcome of illness
Egs,
1990 E.C, Gondar University Hospital, Gondar, Smear positive pulmonary tuberculosis, treated with anti-tbc
drugs, and discharged improved
2003 E.C, Black Lion Hospital, Addis Ababa, HIV-associated cerebral toxoplasmosis, treated with ARV drugs
and anti-toxoplasmosis drugs, and discharged improved
. If the previous admission is related to the current illness, details could be mentioned in appropriate place in the
history of present illness
. If details of previous admission required, it could be mentioned under past illness
3. Chief complaint
Chief complaint is symptom that prompts the patient to seek medical attention
It should be written in patient’s words and not necessarily in medical terminology
The duration of illness should be clearly written
If there is more than one main complaint, it should be listed in the order of occurrence
Eg: Cough of 3 weeks, and hemoptysis of 2 days duration
4. History of present illness (HPI)
This is part of the history where by detailed description of the chief complaint is indicated
9 Abilo Tadesse,MD
Chronological order of HPI
. Date of onset
. Mode of onset, course and duration
. Character and location (especially applicable for pain)
. Exacerbations and remissions
. Effect of treatment
. Negative-positive statements
. Changes in strength, weight and color
Date of onset
Start with ‘the patient was apparently healthy until…’ then write the complaint that led to medical attention
Mode of onset, course and duration
Mode of onset could be abrupt or gradual, and related precipitating cause could be mentioned if present
eg : “…. Sudden onset of back pain while lifting heavy object…”
The course of symptom (s) could be persistent, intermittent or relapsing, and increasing or decreasing in severity
Mention associated symptoms with chief complaint
eg. “...sudden onset of left sided pleuritic chest pain of 3 days duration associated with shortness of breath,
blood streaked sputum and low grade fever…”
Character and location
This is especially applicable for the description for pain
List of clarification for a complaint of pain (SOCRATES)
. Site/location: somatic pain is well localized while visceral pain is diffuse and ill-defined
. Onset: speed of onset (sudden, gradual)
. Character/type: dull/sharp, burning/tingling, boring/stabbing, etc…
. Radiation: referred pain eg. shoulder pain in diaphragmatic problem
10 Abilo Tadesse,MD
. Associated symptoms eg. visual aura (zigzag lines) accompanying migraine
. Timing: episodic or continuous. If episodic, duration and frequency of attacks; if continuous, any change in
severity
. Exacerbating and relieving factors: effects of specific postures or activities
. Severity: variation in day/month eg. relating to menstrual cycle
eg. ‘… sudden-onset, gradually worsening, throbbing, right sided frontal headache worsened by daily routine
activities and relieved by Cafergot/ Triptans ...’ favors migraine
Exacerbations and remissions
Usually mentioned while dealing with mode of onset, course and duration
Effect of treatment
Patients may have taken any medication prior to admission to the hospital.
. Mention any history of therapy prior to admission to the hospital which might have alleviated, worsened or no
effect on their illness.
. If drugs taken, mention the name, dose and duration of therapy
. If patients didn’t name the drug(s), mention the colour, texture and shape of the drug (s)
. Mention if there is history of taking local herbal medication
Positive – negative statements
Significant part of HPI where by supportive positive symptoms, risk factors and complications, and other
symptoms which rule out other diseases are mentioned
Color, strength and weight
How was the patient admitted to the hospital? Supported by relatives, on a stretcher, or walking by himself
Mention any apparent reduction in strength and weight which provides clues to the general condition of the
patient during admission.
5. Past illnesses
List any illnesses experienced in the past unrelated to the current illness including childhood illnesses
11 Abilo Tadesse,MD
A brief mention of each disease with an approximate date, severity, duration, complication and sequelae is
essential
6. Functional inquiry
Detailed account of symptoms referable to each system of the body
There is no need to repeat complaints already mentioned in the HPI
Functional inquiry should be recorded as follows:
HEENT (head, eye, ear, nose, throat)
Head: Headache, head injury
Eyes: Blurring of vision, pain in the eyes or orbit, eye itching, lacrimation, photophobia
Ears: Ear ache or pain, deafness, ear discharge, vertigo, tinnitus
Nose: Nose bleeds, discharge
Mouth and throat: Gum bleeding, dental hygiene, sore throat, sore tongue
Lymphoglandular system
Swellings in the neck, axillae and groin, breast lump, nipple discharge, goiter, testicular swelling or pain
Respiratory system
Cough, expectoration (sputum), hemoptysis, chest pain, shortness of breath, wheezing, stridor
Cardiovascular system
Dyspnea (exercise intolerance), palpitation, orthopnea (number of pillows required), paroxysmal nocturnal
dyspnea, swelling of legs, chest pain (angina), syncope, intermittent claudication, fatigue
Gastrointestinal system
Loss of appetite, nausea, vomiting, dysphagia, odynophagia, heart burn, abdominal pain, bowel habit change
(diarrhea, constipation), jaundice, tarry or clay-colored stool, hematemesis, hematochezia
Genitourinary system
Flank pain, suprapubic pain, urine color change (hematuria), oliguria, polyuria, frequency (in day-to-night ratio),
dysuria, urgency, hesitancy, dribbling, incontinence, menstrual history (age at menarche/interval between
periods/duration of flow/amount of flow), dysmenorrhea, menorrhagia, metrorrhagia, menometrorrhagia,
12 Abilo Tadesse,MD
dyspareunia, amenorrhea, urethral or vaginal discharge, postcoital bleeding, menopause, postmenopausal

bleeding
Integumentary system
Skin, hair and nail: Skin rashes, ulcers, urticaria, or nail changes
Locomotor system
Joint or bone deformities, joint pain or swelling, limping, loss of function of limbs or joints
Central nervous system
Amnesia (cognitive impairment), speech disturbance, seizures, diplopia, dysarthria, vertigo, weakness of
extremities, urinary incontinence or retention, fecal incontinence or stool impaction, disturbance in sensation
(anesthesia, hyperaesthesia), insomnia, nervous breakdown
7. Personal history
Early development: Place of birth, childhood development, health and activities
Education: School history, achievements and failures
Work record: Age begun, type of work, number of jobs (success or failure of each job), job hazards and
industrial exposures
Environment: Living condition of the patient
Habits: Alcohol, tobacco smoking, illicit drug use, herbs
Marital status: Health of wife/husband, adjustment (marital harmony), number of children and their health
8. Family history
Father and mother: Age, health, (if dead, mention date, age and cause of death)
Siblings: List with ages, health (if dead, mention date, age, cause of death)
Family disease: Diabetes mellitus, hypertension, migraine, asthma and other allergic diseases, other hereditary
diseases
13 Abilo Tadesse,MD
B. Scheme of physical examination
Vital sign
Blood pressure… mmhg (right or left arm, lying or supine)
Pulse rate… per minute (min)
Respiratory rate… per minute (min)
Temperature…0C (Axillary, oral, core)
Weight… Kg
Height… M
BMI … Kg/M2
General appearance
Acuteness of illness (acutely or chronically sick looking), physique, nutritional status, emotional state, color
change
HEENT
Head: Shape, size, masses, depression and tenderness of skull; amount, color, texture and distribution of hair;
scar and cleanliness of scalp
Ears: Tragus or mastoid tenderness, tophi, cerumen, light reflex, bulging, retraction and perforation of tympanic
membrane
Eye: Visual aid (spectacles), periorbital edema, xanthelasma, ptosis, lid lag; conjunctival pallor, injection,
hemorrhage and trachomatous changes; scleral colour (icterus), pterygium and granulation
Nose: Deformities, deviation and perforation of septum, polyps and unusual discharges
Mouth and throat: Breath odor; color, fissures and ulceration of lips; bleeding, ulceration, and leadline of gums;
tooth caries, extractions, dentures; tongue color, coating, fissure, papillae atrophy; color, ulceration, tumour,
monilial patches of bucal mucosa and soft palate; tonsillar inflammation and exudates; post-nasal drip
Lymph nodes: Site, size, consistency, tenderness, fixation, discrete or matted, regional or generalized
enlargement
Thyroid gland: Size, consistency, nodularity, tenderness, bruit
14 Abilo Tadesse,MD
Breasts: Lump, consistency, tenderness, fixation; skin retraction or ulceration, unusual nipple discharge
Respiratory system
Inspection: Cyanosis of lips and nails, clubbing of fingers, rate, depth and character of respiration, symmetry of
shape and expansion, use of accessory muscles, retractions
Palpation: Tenderness, subcutaneous crepitation, position of trachea, degree of chest expansion (in cm with tape
or hand grip), tactile fremitus
Percussion: percussion notes (resonance, hyper-resonance, dull, flat), diaphragmatic excursion
Auscultation: Character of breath sounds (vesicular, broncho-vesicular, bronchial, tracheal), crackles, wheezing,
friction rub, vocal resonance
Blood pressure: … in mmhg, right or left arm, sitting or lying
Arteries: pulse rate, rhythm, volume, character, radio-femoral delay, hardening (cording) of arteries
Carotid Brachial Radial Femoral Popliteal Dorsalis pedis Posterior tibialis
Right +++ ++ ++ +++ + ++ +
Left +++ ++ ++ +++ + ++ +
Veins: Internal Jugular vein (JVP) pressure measured fron sternal angle at an inclination of 45 0 and detect ‘a’
and ‘v’waves, kussmaul sign, hepato-jugular reflex
Precordium (Heart)
Inspection: Presence of precordial bulging, active or quiet precordium, location of apical impulse (interspace,
distance from left midclavicular line)
Palpation: Point of maximal impulse and its character, parasternal heave, thrill, shock
Percussion: cardiac outline (not frequently performed)
Auscultation: 1st and 2nd heart sounds, 3rd and 4th heart sounds, other added heart sounds (gallop, ejection click,
opening snap, pericardial ‘knock’), murmur, friction rub
Abdominal Examination
Inspection: Abdominal symmetry, shape (round, flat, scaphoid), movement with respiration, flank fullness,
everted or inverted umbilicus, dilated vessels, scars, visible peristalsis, presence of hernia at hernia sites
15 Abilo Tadesse,MD
Palpation: tenderness (superficial or deep, site), rebound tendeness, guarding and rigidity, enlarged liver (size in
cm below right costal margin along right midclavicular line, consistency, surface, edge, tenderness), enlarged
spleen (size in cm along splenic growth line below left costal margin, consistency, surface, edge, tendeness,
splenic (medial) notch), abdominal mass (size, consistency, surface, edge, tendeness, fixation, mobility with
respiration), and enlarged kidneys (size, consistency, surface,edge and tenderness by bimanual palpation)
Percussion: Total vertical liver span, liver and splenic dullness, shifting dullness, fluid thrill
Auscultation: Bowel sounds, bruit over the liver, friction rub over the liver and the spleen, renal bruit
PR (per digital rectal examination): Fissures, ulcers and hemorrhoid, and fistula in anal area; rectal ulcers or
tumor, sphincter tone, enlarged prostate (size, consistency, surface, tenderness, obliteration of medial sulcus)
Costovertebral angle and suprapubic tenderness. In male, scrotum (edema, hydrocele, hernia etc…), testes (size,
tumor, descent), vas deferens (nodules, tenderness), varicocele, urethral orifice (reddening, discharge, ulcer,
phimosis). In females, labia majora and minora (ulcers, nodules, tumors), bartholin’s duct, urethral orifice
(reddening, discharge), vaginal discharge, cystocele/rectocele, cervix (excitation tenderness, ulcers and
erosions), uterus (size, position, consistency), adnexal mass and tenderness
Integumentary system
Skin: Texture, rashes, ulcers, urticaria, pigmentation. Hair: texture, baldness or alopecia. Nails: color, shape
(clubbibg, spooning, etc…), texture, splinter hemorrhages, capillary refill time
Musculoskeetal system (Locomotor system)
Muscle: muscle tenderness, spasm. Spine: deformity (kyphosis, scoliosis, kyphoscoliosis), gibbus, tenderness on
percussion or pressure, limitation of movement. Joints: Swelling, tenderness, heat and redness, crepitus,
deformity, limitation of movement on active and passive motions. Bones: deformity, fracture, tenderness,
tumors
Nervous system
Mental status
Level of consciousness (GCS), orientation in time, place and person; memory (immediate, recent, and remote),
speech disturbance (dysphasia/aphasia), judgement, mood changes
Cranial nerves (CN)
CN I: Olfaction (each nostril)
CN II: Visual acuity, visual fields, color perception
16 Abilo Tadesse,MD
CN III, IV, and VI: Ocular movements; pupillary size and reaction to light (direct and consensual) and
accommodation, diplopia, nystagmus
CN V: Sensation over the face, contraction of temporalis and masseter muscles, corneal reflex
CNVII: Symmetry of face, presence of nasolabial fold, eyebrow frowning, cheeks puff, corneal reflex
CN VIII: Rinne’s and Weber’s test, Dix-Hallpike maneuver
CN IX and X: Position and symmetry of soft palate and uvula, gag reflex
CN XI: contraction of sternomastoid muscle on turning the head against resistance, contraction of trapezius
muscle on shrugging the shoulders against resistance
CN XII: Tongue protrusion, movement from side to side, deviation, atrophy, fasciculation and tremor
Motor system
Position, bulk, fasciculation (spontaneous or provoked), strength (power), tone, reflex (deep and superficial)
Deep tendon reflexes
Biceps Triceps supinators Patellar Ankle
Right +++ ++ ++ +++ +
Left +++ ++ ++ +++ +
Superficial reflexes
Corneal Abdominal Cremasteric Plantar
Right ++ ++ ++ ↓
Left ++ ++ ++ ↓
Sensory system
Superficial: Light touch, pain and temperature. Deep (proprioceptive): Vibration and position sense, Romberg’s
test
Cortical: Stereognosis, graphesthesia, two-point discrimination, double simultaneous stimulation
Cerebellar (Equilibrium and Balance) signs
Tandem walk, finger-to-nose test, heel-to-shin test, supination-to-pronation of forearm, rebound phenomenon
17 Abilo Tadesse,MD
Meningeal irritation signs
Nuchal rigidity, Kernig’s and Brudzinsky’s sign, Jolt accentuation of headache
18 Abilo Tadesse,MD
CHAPTER TWO
Vital signs in physical examination
Learning objective
1. Mention components of vital sign

2. List normal value of vital signs
3. Describe patterns of fever
4. Describe the parameters of nutritional assessment
Vital signs
Components of vital sign
. Temperature
. Pulse rate
. Respiratory rate
. Blood pressure
. Height
. Weight
. BMI (Body mass index)
Temperature
Normal body temperature is maintained, despite environmental variations, because the hypothalamic
thermoregulatory center balances heat production in the muscle and liver, and heat dissipation from the skin and
lungs
Fever is an elevation of body temperature that exceeds the normal daily variation, and occurs in conjunction
with an increase in the hypothalamic set point
Fever is mediated by endogenous pyrogen, which acts on hypothalamic thermoregulatory center
Mean oral temperature is 36.2 0c -37.2 0c with low levels at 6 AM and higher levels at 6 PM
19 Abilo Tadesse,MD
Normal daily temperature variation (diurnal variation) is typically 0.5 0c
Fever: AM oral T0 >37.2 0c or PM oral T0 >37.7 0c
Core T0 > Oral T0 >Axillary T0
Core T0 > 41.5 0c is referred as hyperpyrexia
Axillary T0 is lower than oral T0 by 0.5 0C, and the core T0 is higher than oral T0 by 0.50C.
Causes of fever include infection, trauma, surgery, malignancy, drug reactions and immune disorders.
Causes of hyperpyrexia include heat stroke, malignant hyperthermia, neuroleptic malignant syndrome, and
hypothalamic disease.
Average values for normal body temperature and fever
Characteristics Normal Fever
Oral T0 36.8 0c >37.2 0c
Axillary T0 36.4 0c >36.9 0c
Core T0 37.2 0c >37.7 0c
Grading of fever based on oral temperature (oral T0)
Low grade fever 37.2-37.8 0c
Moderate grade fever 37.8-39.4 0c
High grade fever 39.4-40.5 0c
Types of fever (based on duration)
Acute fever: fever that persists for ≤ 1 week. Eg. Common cold, tonsillitis, acute bronchitis
Prolonged fever: Fever that persists for ≥2 weeks. Eg. Viral (AIDS, Covid-19 infection), Bacterial (entric fever,
tuberculosis, infective endocarditis), protozoal (visceral leishmaniasis, amoebic liver abscess), autoimmune
diseases (SLE, RA, vasculitides), malignancies (leukemia/lymphoma, renal cell carcinoma, hepatocellular
carcinoma)
20 Abilo Tadesse,MD
Patterns of fever
1. Intermittent fever
Paroxysms of high grade fever lasting for only short periods of the day, and characterized by high peaks which
later subside to the normal level
Eg. Acute pyelonephritis, pneumonia
2. Remittent fever
The temperature remains above normal throughout the day, and the difference in maximum and minimum T0 > 1
0c in 24 hrs.
Most fevers are of this type
3. Continued fever
The temperature remains above normal throughout the day, and the difference in maximum and minimum T0 < 1
0c in 24 hrs.
Eg. Enteric fever, miliary tuberculosis, infective endocarditis
4. Relapsing fever
Periods of continued fever alternating with completely afebrile periods
Eg. Brucellosis, relapsing fever, malaria, Hodgkin’s lymphoma
© Jaypee. KV Krishna Das. Clinical Medicine 4the
Fig 2.1 Patterns of fever
Patten of rise in temperature
Rise of temperature may occur abruptly within hours as in pneumococcal pneumonia or influenza, or it may be
gradual and step-ladder type as in enteric fever and brucellosis.
21 Abilo Tadesse,MD
Fig 2.2 Pattern of rise of temperature 1) Abrupt rise 2) Step-laddern pattern
Pattern of defervescence (fall of temperature)
Crisis: This refers to an abrupt fall of temperature from a high level (40°C or above) to subnormal value within a
few hours. Crisis is accompanied by diaphoresis and diuresis. e.g. Pneumococcal pneumonia
Lysis: The temperature falls in steps day by day to reach normal over a few days. In many cases it falls to
subnormal level, after which the fever subsides, eg. Enteric fever
Fig 2.3 Patterns of defervescence: 1) Fall by crisis 2). Fall by lysis
Pulse fever types
The heart rate increases at the rate of 18 counts per minute for every 1°C rise of temperature.
Slow pulse fevers: Fevers in which the heart rate is not raised proportional to the temperature (relative
bradycardia or pulse-T0 deficit)
22 Abilo Tadesse,MD
eg. Relative bradycardia (pulse-T0 deficit) could be caused by enteric fever, Legionnaire’s disease, chlamydial
pneumonia and some viral infections (influenza)
Rapid pulse fevers: Fevers in which the pulse rate rises out of proportion to the rise in temperature
eg. Pneumococcal pneumonia, tuberculosis
Blood pressure (BP)
Normal BP level: Systolic BP = 90-120 mmhg; Diastolic BP = 60-80 mmhg
Hypertension is defined as systolic BP>130mmhg and/or diastolic BP>80mmhg
The cause of hypertension is unknown in majority of cases (>80-95%), named as primary or idiopathic
hypertension; the rest (5-20%) is secondary hypertension, and caused by renal diseases (renal parenchymal
disease or renovascular disease), endocrinopathies (primary aldosteronism, acromegaly, and Cushing’s
syndrome), drugs (corticosteroids), etc…
Clinical clues to secondary hypertension: Hypertension in younger or older age groups, Characteristic clinical
features, severe or drug resistant hypertension, recent onset of hypertension, disproportionate target organ
damage
Postural hypotension is defined as systolic BP drop by >20 mmhg while assuming from supine to standing
position. It corresponds to 10-15 % body fluid loss.
Hypotension is defined as drop in systolic BP <90 mmhg or mean BP <65mmhg, and corresponds to 20-25 %
body fluid loss.
The common cause of hypotension is body fluid loss including hemorrhage/bleeding, persistent vomiting,
diarrhea, and overzealous use of diuretics, etc…
Pulse rate (PR)
Normal value: 60-90 beats per minute (bpm)
Tachycardia: >90 beats per minute
Bradycardia: <60 beats perminute
Causes of Tachycardia
23 Abilo Tadesse,MD
a. Sinus tachycardia
. Physiological: exercise, anxiety/excitement
. Thyrotoxicosis
. Heart failure
. Pheochromocytoma
. Drugs: Sympathomimetics, vasodilators
b. Arrhythmic tachycardia
. Atrial fibrillation
. Supraventricular/ ventricular tachycardia
Causes of bradycardia
a. Sinus bradycardia
. Athletic heart
. Hypothyroidism
. Drugs, Eg. ß-blockers, digoxin
b. Arrhythmic bradycardia
. Sick sinus syndrome
. 2nd degree AV block
. 3rd degree AV block
Respiratory rate (RR)
Normal values: 14-16 breaths per min
Tachypnea: RR >20 breaths per minute
Bradypnea: RR <8 breaths per minute
24 Abilo Tadesse,MD
Causes of tachypnea
. Physiological, Eg. Strenuous exercise, anxiety
. Hypoxia due to pulmonary diseases
. Congestive heart failure
. Metabolic acidosis
. CNS lesions (central neurogenic hyperventilation)
. Hysterical hyperventilation
Causes of bradypnea
. Narcotic poisoning
. Hypothyroidism
. Hypothermia
. Uremia
. Increased ICP (intracranial hypertension)
Nutritional assessment
1. Body mass index (BMI)
BMI is weight in kg/ height in squared meter (Kg/M2)
Normal value: BMI of 18.5-24.9 Kg/M2
BMI is a major determinant of nutritiona status. Proper nutrition depends on optimal intake of carbohydrate,
protein, fat, viatmins, minerals and water.
Reduced macronutrient intake result in protein-calorie undernutrition, while reduced micronutrients intake result
in deficiencies of vitamins, minerals and trace elements
Protein-calorie undernutrition results in hypoalbuminemia and weight loss in adults
25 Abilo Tadesse,MD
Micronutrient deficiencies results in hypovitaminosis-A (night blindness, xerophthalmia), B1 (beriberi), B3

(dermatitis, diarrhea, dementia), B6 (peripheral neuropathy), B12 (megaloblastic anemia), C (scurvy), D
(osteomalacia), and K (hemorrhagic tendencies)
Mineral deficiences include iron deficiency anemia, hypocalcemia (tetany), hypomagnesemia (arrhythmia) and
iodine defieincy (goiter).
Obese individuals show excess deposition of fat over the trunks, abdomen, gluteal regions and limbs. They are
more likely to suffer from hypertension, diabetes, and dyslipidemia, collectively named as metabolic syndrome.
Those with metabolic syndrome are at risk of developing coronary artery disease, ischemic stroke and peripheral
arterial disease.
Table 2.1 Nutritional assessment based on BMI
Undernutrition
. Mild 17.5-18.5 Kg/M2
. Moderate 16-17.5 Kg/M2
. Severe <16 Kg/M2
Overweight 25-29.9 Kg/M2
Obesity ≥ 30 Kg/M2
. Moderately obese 30-34.9 Kg/M2
. Severely obese 35-39.9 Kg/M2
. Morbidely obese ≥ 40 Kg/M2
2. Mid upper arm circumference (MUAC)
If weight or height can’t be measured or obtained, nutritional assessment can be estimated using the MUAC
Mid arm is midpoint of shoulder and elbow
. Measure the circumference of the arm at the midpoint using tape measure
MUAC of 23.5-25 cm may indicate BMI of 18.5-20 Kg/M2
MUAC < 23.5 cm indicates undernutrition
26 Abilo Tadesse,MD
3. Waist circumference/ Waist-to-Hip ratio
Waist circumference: Midpoint between the costal margin and the iliac crest
Waist-to-hip ratio: Waist circumference (the midpoint between the costal margin and the iliac crest) divided by
that of the hip circumference (the widest part around the buttocks)
The waist circumference is a strong predictor of the degree of intra-abdominal (visceral) fat
Increased waist circumference can be a marker for increased cardiovascular risk even in persons with normal
weight
All adult patients should be screened for overweight and obesity by measuring BMI and waist circumference at
periodic health examination
Individuals with BMI ≥ 25 kg/m2, waist circumference > 80 cm (females) or > 94 cm (males), and waist -to-hip
ratio of >0.85 (females) and >0.90 (males), require evaluation for cardiovascular risk factors (dyslipidemia,
diabetes, and hypertension) and comorbidities (coronary heart disease, cerebrovascular disease, and peripheral
arterial disease).
Waist circumference and waist-to-hip ratio and risk of metabolic complications
Variables Increased risk of metabolic complications
1. Waist circumference
Males >102 cm (>94 cm)
Females >88 cm (>80 cm)
2. Waist-to-Hip ratio (WHR)
Males >0.90
Females >0.85
4. Skin fold thickness
Nutritional status using skin fold thickness can be measured at sites such as the biceps, triceps, infrascapular,
and supraclavicular regions using Harpenden calipers
Triceps skin fold (TSF): Mid way between shoulder and elbow is the most commonly used site
It is measured in the vertical plane with arm hanging relaxed by the side of the body
27 Abilo Tadesse,MD
Table 2.1 Triceps skin fold thickness measurement (mm)
28 Abilo Tadesse,MD
CHAPTER THREE
General observation and HEENT
Learning objective
1. Mention main symptoms in head, eye, ear, nose and throat problems
2. Interprete abnormal findings in eye,ear, nose and throat examination
3. List common causes of hearing loss and red eye
General observation
Physical examination requires a cooperative patient and quiet, warm and well lit room equipped with a coach or
chair. For a thorough examination, the patient should be asked to undress completely or at least to their under
clothes, and to lie or sit on the coach or bed partially covered with a bed sheet or dressing gown.
The general examination begins as soon as the patient enters the consulting room. Greet your patient in a
friendly, but professional manner. Facial expression and eye-to-eye contact are indicators of physical and
psychological well-being.
At the start of examination on coach or chair, analyze the patient’s facial expression, complexion, state of
clothing and personal hygiene, posture and gait, voice and speech, abnormal body odour, built or physique,
nutritional status, and emotional status; which constitute the individual’s observation.
1. Facial expression/appearance
A look of excitement and anxiety may be features of hyperthyroidism or hypomania; while a look of apathy and
poverty of facial expression may suggest hypothyroidism or Parkinsonism
2. Complexion
Complexion may become a remarkably sensitive index of disease; eg. carboxyhemoglobin in carbon monoxide
poisoning (pink), jaundice in liver disease (yellowish), uremia in chronic kidney disease (brownish tinge).
3. State of clothing and personal hygiene
Shabbily dressed and underwear soiled with fecal material occurs in demented patients. Excessive clothing in
patients with hypothyroidism gives clue to cold intolerance.
4. Posture, gait and abnormal body movement
Abnormal posture and gait are observed in rheumatological diseases, while abnormal body movement favors
neurological disorder.
29 Abilo Tadesse,MD
5. Voice and speech
Hoarseness of voice occurs due to laryngeal problem or recurrent laryngeal nerve damage. Low pitched, slow
speech suggests hypothyroidism. Dysphasia and dysarthria occur in neurological problem.
6. Abnormal body smell/odour
Halitosis (malodorous breath) is noticed in patients with poor dental hygiene, suppurative lung diseases, or
peptic gastoduodenal disease.
Pungent body smell occurs from poor personal hygiene, while malodorous body smell is noticed in demented
patients or physically disabled bed-ridden patients.
7. Built or physique
Short stature occurs in achondroplasia, chronic undernutrition or congenital heart disease; while increased
height suggests gigantism or marfan’s disease.
8. Nutritional status
BMI indicates nutritional status of an individual, and calculated as weight in Kg divided by height in squared
meter. Cachexia is observed in patients with malignancy, thyrotoxicosis and tuberculosis. Obesity is observed in
patients with metabolic syndrome or hypercortisolism (Cushing’s syndrome).
30 Abilo Tadesse,MD
Clinical history taking and physical examination of HEENT
Head
1. The hair: Notice its quantity, colour, distribution, texture, and loss of hair.
Hair distribution: Is it male or female type of hair distribution?
Recession of hair at forehead margins or temporal recession is in favor of male type hair distribution. Notice for
thin, sparse hair in hyperthyroidism, and coarse, brittle hair in hypothyroidism.
2. The scalp: Look for scaliness, lumps, nevi, warts
a. Itchy, scaling of scalp
. Pediculus capitis: Contact scratching with crusting and oozing scalp. Lice resemble grains of wild rice,
attached to scalp or loosely adherent to hair. Nits (ova of lice) appear along hair shaft as adherent white granules
b. Scaly, lumpy or inflamed scalp restricted to the scalp
. Fungal infection (Tinea capitis): Patches of thinned and broken scalp hair with crusted and scaly inflamed
scalp
. Bacterial infection: Crusted and oozy yellow patches scaterred on scalp with unpleasant odor and regional neck
lymphadenopathy
. Seborrheic dermatitis: Patchy or diffuse, yellowish greasy itching scale involving scalp
. Lichen simplex chronicus: Recurring, itchy, excoriated papules or patch
3. The skull: Notice for any deformities, depression, masses or tenderness
Eye
Main symptoms of eye disease
. Altered vision
. Eye pain
. Red eye
. Double vision (diplopia)
. Eye discharge
. Swollen eyes
31 Abilo Tadesse,MD
. Squint
Ask
1. Altered vision
. Have you had any blurring of vision?
. If yes, was it sudden or gradual onset?
Refractive errors most commonly causes gradual blurring of vision
Difficulty with close vision is names as hypermetropia (far-sightedness) or presbyopia (aging vision), while
difficulty with far vision is named as myopia (near-sightedness)
Sudden loss of vision suggests retinal detachment, vitrous hemorrhage or central retinal artery occlusion
. Is your visual blurring involved the whole visual field or part of it (central, peripheral, one-sided loss)? - refer
to cranial nerve II (CNS)
Slow central loss is noticed in nuclear cataract and macular degeneration
Peripheral loss is noticed in advanced open-angle glaucoma
One-seded loss (hemianopsia/quadrantanopsia) occurs in optic tract lesion
. Are there speckles (scotomas) in the vision? If yes, do they move around in the visual field or fixed with shifts
in gaze?
Moving scotomas are vitrous floaters, while fixed scotomas are retinal or visual pathway lesion
2. Eye pain
Onset-sudden or gradual, severity of pain, exacerbating factors, associated symptoms like red eye
Cornea is highly innervated structure of the eye. Keratitis (corneal injury) causes eye pain, sensation of foreign
body, reflex watering and photophobia. Other causes of painful eye include conjunctivitis, uveitis, scleritis,
glaucoma, optic neuritis, etc...
3. Red eye
Associated symptoms of red eye like painful/photophobic, visual blurring/loss, itchy, discharge,trauma, etc…
Cuuses of red eye includes conjunctivitis, uveitis, episcleritis/scleritis, corneal abrasion, subconjunctival
hemorrhage, etc…
. Is there red eye, eye pain, and excessive tearing? - refer to causes of‘red eye’ below
4. Double vision (diplopia)
32 Abilo Tadesse,MD
. Is there diplopia (double vision)? If yes, is it horizontal diplopia (the images are side by side) or vertical
diplopia (the images are on top of each other)?
Horizontal diplopia is noticed in cranial nerve III or VI lesion
Vertical diplopia is noticed in cranial nerve III or IV lesion
Causes of diplopia include CN III/IV/VI palsy, myasthenia gravis, internuclear ophthalmoplegia (INO), Graves’
disease, orbital cellulitis, etc…
5. Eye discharge
Ask: Eye discharge watery or opaque, itchiness, sensation of foreign body, eye redness, etc…
Causes of eye discharge: conjunctivitis, blephritis, trichiasis, blocked tear duct, foreign body, etc…
6. Swollen eyes
Is eye swelling unilateral or bilateral, acute or gradual, painful or not, itchness/irritation, diplopia, etc…
Causes of unilateral swollen eye: Orbital cellulitis, orbital tumors, orbital inflammatory diseases, etc…
Bilateral eye swelling is caused by Graves’ disease
7. Squint
Squint is deviation of eyes from their normal conjugate position. It results when the visual axes do not meet at the
point of fixation or there is failure of the normal co-ordination of the ocular axes.
It may be paralytic (weakness of one or more extraocular muscles) or non-paralytic (imbalance of ocular muscle
tone).
Examination of the eye
Visual acuity (Snellen chart test) - refer to cranial nerve II (refer to CNS)
The normal person can read the line 6 at 6 meters (6/6 vision)
The numerator records the distance of the subject from the test chart (usually 6 meters). The denominator
records the line read by the patient.
Visual field (confrontation test) - refer to cranial nerve II (refer to CNS)
Color vision (Ishihara plate test)
33 Abilo Tadesse,MD
It assesses the function of retinal cones and optic nerve.
Common causes of abnormalities in color vision: Genetic (red-green color blindness), age related macular
disease, and optic nerve disease
Eye lids
Notice for width of palpebral fissure, eye lid edema, and adequacy of eye lid closure
Blepharitis- inflammation of the eyelids along the lid margins, often with crusting or scales
Failure of eyelids to close occurs due to infranuclear facial nerve palsy, and leads to exposure keratitis
Lacrimal apparatus
Examine lacrimal gland by pulling up the outer part of upper eye lid while the patient looks downward and
inward
Inspect the lacrimal sac for swelling, look for excessive tearing or dryness of eyes
Excessive tearing is due to increased production (conjunctivitis, keratitis) or impaired drainage of tears
(ectropion, blocked tear duct)
Conjunctiva and Sclera
Look for conjunctival pallor, injection, hemorrhage and trachomatous changes, and for scleral jaundice and
pterygium
. Ask the patient to look up as you depress both lower eye lids with your thumbs, and inspect the lower
conjunctivae
Technique to view upper conjunctiva
. Instruct the patient to look down
. Grasp the upper eyelashes and pull them gently down and forward
. Place a stick or tongue depressor, 1cm above lid margin (upper border of tarsal plate)
. Pull down the stick as you raise the edge of the upper eye lid (everting/taking inside out)
. Inspect upper conjunctiva for trachomatous papules, other nodules or granuloma
34 Abilo Tadesse,MD
© Churchil Livingstone. Douglas G, Nicol F, Robertson C. Macleod’s ClinicalExamination 12the
Fig 3.1. Technique to view palpebral conjunctiva
Cornea and lens
Inspect the cornea of each eye for opacities with oblique lighting
Iris
Normal iris is flat and forms a relatively open angle with the cornea, and light shining directly from the temporal
side casts no shadow
Pupils
Inspect the size, shape and symmetry of pupils (large >5mm, small <3mm, or unequal)
Myosis is constriction of pupils, while mydriasis is dilation of pupils
Pupillary inequality < 0.5mm is named as physiological anisocoria, and observed in normal people
Causes of anisocoria
Dilated pupil: CN III palsy, Adie’s tonic pupil, mydriatic drugs (atropine, tropicamide), etc…
Constricted pupil: Horner’s syndrome, drugs (pilocarpine), synechiae due to iritis, etc…
. Perform direct and consensual light reflex, and test for convergence- refer to cranial nerve II (refer to CNS)
Extraocular movements
.Assess conjugate movements of the eyes in each direction- refer to cranial nerve III/IV/VI (refer to CNS)
. Does the patient have nystagmus?
35 Abilo Tadesse,MD
Nystagmus is fine rhythmic oscillation of the eyes. A few beats of nystagmus on extreme lateral gaze occurs in
normal eye. Biphasic or jerk nystagmus is the most common type.
Other eye problems
. Look for lid lag, lid retraction, proptosis, ptosis, xanthelasma, periorbital edema
Lid lag is upper eye lid lags behind the eyeball in a down ward gaze; lid retraction is evident by sclera visible
above limbus in wide-eyed staring expression. Lid lag and lig retraction occur in Graves’ disease
Proptosis is forward displacement of the eye ball. It is caused by Graves’ disease, orbital tumours and carotid
cavernous fistula
Ptosis is drooping of the upper eyelid, which occurs in oculomotor palsy, myasthenia gravis, myogenic
disorders, and Horner’s syndrome
Xanthelasma is subcutaneous lipid deposit at periorbital area; and signify presence of lipid disorder
(dyslipidemia)
Periorbital edema occurs in nephrotic syndrome, allergic eye diseases, Graves’ eye disease, and angio-oedema
Technique of performing lid lag:
. Position the examiner’s finger at patient’s primary gaze
. Instruct the patient to follow the examiner’s finger while the examiner moving his finger down ward
. “The upper eyelid lags behind the eyeball when the patient looks downward” indicates presence of lid lag
36 Abilo Tadesse,MD
© Lippincott. Bickley LS, Szilagyi PG. Bates’ Guide to Physical Examination and History Taking 12the
Table 3.1 Common causes of “Red eye”
Ear
Main symptoms of ear disease
. Otalgia – ear ache or pain
. Otorrhea – ear discharge
. Hearing loss
37 Abilo Tadesse,MD
. Tinnitus – Perception of sound in the absence of appropriate auditory stimulus
. Vertigo – Illusion of movement
. Nystagmus - Involuntary rhythmic oscillation of the eyes
1. Otalgia
Main causes of otalgia
a. Otological
. Suppurative otitis media (acute or chronic)
. Acute otitis externa
. Barotrauma
. Herpes zoster (Ramsay-Hunt syndrome- shingles of the facial nerve)
. Viral myringitis
. Malignant otitis externa (necrotizing otitis externa due to Pseudomonas aeroginosa)
b. Non-otological
. Tonsillitis/peritonsillar abscess
. Dental disease
. Temporomandibular arthritis
. Cervical spine disease
. Nasopharyngeal cancer
2. Otorrhea
Main causes of otorrhea
. Acute/chronic suppurative otitis media
. Acute/chronic otitis externa
. Cerebrospinal leak in basal skull fracture
38 Abilo Tadesse,MD
Profuse mucoid ear discharge with pulsation suggests acute otitis media with perforated tympanic membrane
3. Hearing loss
Conductive hearing loss is due to disease in the external ear canal, tympanic membrane or middle ear
Sensorineural hearing loss is due to pathologies in the chochlea and sensory neural connections
Causes of hearing loss
a. Conductive hearing loss
. Cerumen impaction in the external ear canal
. Chronic otitis media- ear drum perforation, ossicular erosion, cholesteatoma
. Otosclerosis
. Middle ear effusion
. Barotrauma to the eardrum or ossicular chain
b. Sensorineural hearing loss
. Degenerative (presbyacusis)
. Noise-induced hearing loss
. Meniere’s disease
. Drug-induced ototoxicity eg. Aminoglycosides, loop diuretics
. Infective- meningitis, syphilis, measles, mumps
. Acoustic neuroma
. Genetic (eg. Alport’s syndrome)
39 Abilo Tadesse,MD
© Lippincott. Bickley LS, Szilagyi PG. Bates’ Guide to Physical Examination and History Taking 12 the
Table 3.2 Types of hearing loss
4. Tinnitus
It is an awareness of a noise in the absence of an external stimulus. It is characterized by ringing, rushing or

hissing sound in the absence of an appropriate auditory stimulus.
Ask
. Quality of tinnitus – high pitched, ringing, pulsatile, etc…
. Intermittent or constant in nature
. Unilateral or bilateral
. Associated ear disease symptoms eg hearing loss
5. Vertigo
40 Abilo Tadesse,MD
Illusion of movement; the patient feels the surrounding environment is moving around, or the patient is moving
in the surrounding environment
The vertigo may be peripheral (vestibular or labyrinthine dysfunction) and central (lesions of the brain stem or
cerebellum). Peripheral vertigo is sudden onset, severe in nature, usually unilateral, lasting few days, often
recurrent, and associated with tinnitus. Central vertigo is chronic, mild in nature, often bilateral, and associated
with other central abnormalities.
© Jaypee (P) Ltd. Chugh SN, Gupta E. Clinical Methods in Medicine: Clinical Skills and Practice 2nde
Table 3.3 Types of vertigo
6. Nystagmus
Nystagmus is an involuntary rhythmic oscillation of the eyes. Jerk nystagmus is the commonest form, and
consists of a slow drift in one direction with a corrective saccadic ‘jerk’ in the opposite direction.The direction
of the fast jerk is used to define the direction of nystagmus. Nystagmus is caused by disorders of the vestibular,
visual, brainstem or cerebellar pathways.
Table 3.4 Characteristics of nystagmus
41 Abilo Tadesse,MD
Examination of the ear
. Inspect the pinna for its size, shape and deformity. Notice for periauricular area swelling and erosions
Hot, tender postauricular swelling suggests mastoiditis
. Notice for tragus and mastoid tenderness
Tragus tenderness is tenderness while pulling the tragus, and suggests middle ear infection
Otoscopic examination
. Hold the otoscope like a pen between thumb and index finger with ulnar border of hand resting against the side
of patient’s head
. Gently retract the pinna backwards and upwards to straighten the external meatus into line with the bony canal
. Light is reflected from intact tympanic membrane at lower end down ward and forwards to its periphery
. Visualize for ear discharge, impacted wax, and membrane perforation
© Churchil Livingstone. Douglas G, Nicol F, Robertson C. Macleod’s ClinicalExamination 12 the
Fig 3.2 Examination of the ear using an otoscope
Nose
Main symptoms of nasal disease
. Nasal blockage (commonly due to allergic rhinitis with nasal polyposis)
. Rhinorrhea (nasal discharge)
42 Abilo Tadesse,MD
. Epistaxis (nose bleeds)
. Sneezing
. Disturbance of smell
1. Nasal discharge
Purulent discharge- infection in the nose/sinuses
Mucoid discharge- allergic rhinitis
Watery discharge- vasomotor rhinitis and cerebrospinal fluid (CSF) leak
2. Epistaxis
Unilateral- local cause in the nasal passage
Bilateral- systemic cause (thrombocytopenia, coagulopathy)
NB: The nasal septum has a very rich blood supply (Little’s area in anterior septum), which is a common site for
bleeding. Sinonasal malignancy should be considered in unilateral bleeding associated with nasal obstruction
and pain.
3. Sneezing: Sudden explosive effort to clear passages of irritants
It is common in viral upper respiratory tract infection and allergic rhinitis
4. Smell disturbance
Anosmia is complete loss of olfaction, and hyposmia is reduced sense of smell
Hyposmia or anosmia occurs in viral upper respiratory tract infection, allergic rhinitis with nasal polyposis
blocking nasal passage, and craniofacial trauma causing olfactory nerve damage
Cacosmia is unpleasant smell caused by chronic anaerobic infection of the nasal passages and sinuses (usually
unnoticed by the patient)
Important clues in smell disturbance: History of atopy, paranasal infection, maxillo-facial trauma, drug exposure
(NSAIDs, anticoagulants), ‘snorting’ cocaine, occupational inhalation of dusts and chemical particulates
43 Abilo Tadesse,MD
Examination of the nose
. Inspect the nose from the front, side and back in a good light
. Examine the nasal vestibule and intranasal contents by gently pushing the tip of the nose upwards with a
finger, preferably using reflected illumination from a hand mirror
. Inspect the anterior nasal cavity with nasal speculum or an otoscope
. Look for nasal blockage, granulation on the nasal septum, nasal polyps, and nasal septum deviation and
perforation
. Notice for the presence of sinus tenderness
Maxillary tendeness is elicited by firmly pressing at the maxillary area (bony cheeks just below zygomatic
bone), and frontal tenderness is elicited by pressing just below medial border of eye brow
Presence of sinus tenderness with headache and foul smelling nasal discharge suggests sinusitis
Mouth and throat
. Mouth odor: Notice mouth odor
Halitosis (unpleasant mouth odor) occurs in patients with poor dental hygiene, periodontal diseases, unclean
dentures, infective oral ulcers (herpetic ulcers), tonsillopharyngitis, chronic rhinosinusitis, suppurative lung
disease, peptic ulcer disease, smoking, alcohol consumption
Fetor hepaticus (fruity mouth odor) occurs in patients with hepatic encephalopathy
Uremic fetor (urine mouth odor) occurs in patients with uremia
Acetone breath occurs in patients with diabetic ketoacidosis
. Lip: Notice for lip ulcer, fissures and cracks
It could be caused by nutritional deficiency (iron), herpetic infections, oral candidiasis, etc…
. Gingiva: Notice for gum bleeding, lead line and ulcers
Gum bleeding is usually from thrombocytopenia of any cause, such as immune thrombocytopenia (ITP),
leukemia, autoimmune diseases (SLE), drugs, etc…
Lead line is a purple-blue line at the edge of the gums in chronic lead posoning
. Teeth: Notice for dental caries, extractions and dentures
44 Abilo Tadesse,MD
Dental caries results in dental decay. It is the result of complex interaction between acid producing tooth-
adherent bacteria and fermentable carbohydrates.The acid in the dental plaque demineralize the teeth, and
results in tooth decay. Risk factors for dental caries include high burden of cariogenic bacteria, high frequency
sugar consumption, inadequate salivary flow, insufficient fluoride exposure, and poor oral hygiene.
. Tongue: Notice for tongue coating, fissures, atrophy of papillae
Whitish tongue coating with erythematic base while scraping with spatula suggests oral candidiasis.
Tongue fissures with atrophic papillae could be caused by hematinic deficnecies such as iron, folate and vitamin
B12 deficiency.
. Buccal mucosa and palate: Notice for ulcers, patches, and masses in the bucal mucosa and palate
Oral ulcers could be caused by herpes virus, nutritional defiencies (iron/folate/Vitamin B12), autoimmune
diseases (SLE, Crohn’s disease), aphthous ulcer, etc…
Oropharyngeal patch is due to oral candidiasis, while oropharyngeal masses might indicate non-Hodgkin’s
lymphoma and Kaposi’s sarcoma in HIV infected patients.
. Nasopharynx: Notice for tonsillar exudates, ulcers, masses
. Notice for post-nasal drip
Post-nasal drip (PND) is ‘dripping down the throat’ and may be present with rhinorrhea, constant throat
clearing, and cough. PND occurs due to excessive mucus in the posterior nasal cavity. It is caused by allergic or
non-allergic rhinitis, sinusitis, gastroesophageal reflux disease (GERD), esophageal motility disorder, cold/flu,
medications, etc…
Main symptoms of throat disease
. Sore throat
. Stridor or stertorous (noisy) breathing
. Dysphonia
. Dysphagia
. Neck swelling
1. Sore throat
Common causes of sore throat
. Viral pharyngitis
45 Abilo Tadesse,MD
. Acute tonsillitis
. Acute follicular tonsillitis
. Glandular fever (EBV)
. Diphtheria
2. Stertor /stridor
Stertor is an inspiratory low-pitched snoring or gasping sound, which is caused by obstruction at the level of the
nasopharynx or oropharynx. It is commonly caused by adenotonsillar hypertrophy.
Stridor is a high-pitched noise produced by turbulent airflow through a narrowed laryngeal or tracheobronchial
tree. Inspiratory stridor suggests narrowing at the level of the vocal cords, biphasic stridor suggests subglottic or
tracheal obstruction, and stridor on expiration suggests tracheobronchial obstruction. Common causes of stridor
include infection/inflammation, foreign bodies and tumours of the epiglottis, larynx and tracheobronchial tree.
3. Dysphonia (hoarseness of voice)
If hoarseness has been present continuously for more than3 weeks, urgent laryngoscopy is indicated to exclude
laryngeal cancer.
Causes of dysphonia
. Acute and chronic laryngitis
. Laryngeal papillomatosis
. Recurrent laryngeal nerve damage (thyroid surgery, lung cancer)
. Vocal cord paralysis
. Gastro-esophageal reflux
. Psychogenic
4. Dysphagia (difficulty of swallowing)
Causes of dysphagia
. Neuromuscular- Stroke, motor neurone disease, myasthenia gravis
46 Abilo Tadesse,MD
. Intrinsic- acute tonsillitis, esophageal stricture, achalasia, esophageal cancer
. Extrinsic- goiter
. Systemic- scleroderma
. Psychosomatic- globus pharyngeus
5. Neck lump (swelling)
Causes of neck lump
Midline neck structures
. Goiter
. Thyroglossal cyst
. Submental lymph node swelling
. Dermoid cyst
. Laryngeal swelling
Lateral neck structures
. Pharyngeal pouch
. Branchial cyst
. Cervical lymph node swelling
. Cystic hygroma
. Carotid body tumour
. Carotid artery aneurysm
. parotid gland swelling
Throat examination
. Inspect the oral cavity, pharynx and larynx
. Depress the tongue with tongue depressor to visualize the tonsillar pillars, palatine tonsils, soft palate and
uvula
47 Abilo Tadesse,MD
Indirect laryngoscopic examination
. Have a good light source (head light)
. Remove if there are artificial dentures
. Gently hold the protruded tongue with the gloved left hand, and ask the patient to take deep slow breath
. Widely open mouth and gently introduce the laryngeal mirror
. Displace the soft palate upwards and backwards with the mirror, and instruct the patient to say ‘ah’ and the
larynx elevates towards the examining mirror
. Examine the vallecula, epiglottis, supraglottis, glottis and vocal folds
Fig 3.2 Indirect laryngoscope a) Position of mirror in relation to soft palate and larynx b) View of larynx and
vocal cord in mirror
48 Abilo Tadesse,MD
CHAPTER FOUR
Learning objective
1. List the peripheral accessible lymphnodes

2. Mention common causes of generalized lymphadenopathy
3. Show how to examine the thyroid gland and breast
4. Mention causes of goiter and breast lump
Lymph nodes
History taking of lymph nodes
Ask for swellings over the neck, axillae or groin
If there are swellings in lymph node areas- Ask for site and duration of swelling, painful or not, presence of B
symptoms (fever, sweating and weight loss), history of genital ulcer, cough and expectoration, risk factors and
clinical stigma of HIV infection (herpes zoster, oral thrush, chronic diarrhea), exposure to cats and pets (cat-
scratch disease), etc…
Examination of lymph nodes
Palpate the peripheral accessible lymphnodes: preauricular, postauricular, occipital, submental, submandibular,
anterior cervical, posterior cervical, supraclavicular, axillary, epitrochlear and inguinal lymphnodes
. Using the pad of your fingers, move the skin over the underlying tissues in lymph node areas
Note the size, shape, delimitation (discrete or matted together), mobility, consistency, tenderness, and
“fluctuation sign” in enlarged lymph nodes (lymphadenopathy)
NB: Small, mobile, discrete, non-tender lymph nodes are frequently found in normal person
Generalized lymphadenopathy: ≥ 2 significant (>1.5cm) extra inguinal lymphadenopathy
49 Abilo Tadesse,MD
© Jaypee (P) Ltd. Chugh SN, Gupta E. Clinical Methods in Medicine: Clinical Skills and Practice 2nd e
Table 4.1. Examination of a lymphnode mass or any swelling
© Elsevier. Glynn M, Drake WM. Hutchison’s Clinical Methods 23rde
Fig 4.1 Peripheral lymph nodes in head and neck regions
50 Abilo Tadesse,MD
Technique
Examination of the cervical lymphnodes
Examine the submental, submandibular, preauricular, and anterior cervical and supraclavicular lymphnodes
from behind of the patient
Examine the postauricular, occipital and posterior cervical lymphnodes from the front of the patient
A. Examination of lymphnodes from behind B. Examination of lymphnodes from the front
Fig 4.2 Examination of the anterior and posterior triangle of the neck, respectively
Examination of epitrochlear lymph nodes
. Epitrochlear lymphnodes are located at medial side of arm just proximal to medial epicondyle
. Support the patient’s right arm with your left hand, and palpate the right epitrochlear lymph node area with
fingers of right hand
. Support the patient’s left arm with your right hand, and palpate the left epitrochlear lymph node area with
fingers of left hand
51 Abilo Tadesse,MD
Fig 4.3 Examination of the left epitrochlear lymph node
Examination of axillary lymph nodes
. Axillary lymph nodes are located at the arm pits.
. Support the patient’s right arm with your right hand, and palpate the patient’s right axilla with your left hand
. Support the patient’s left arm with your left hand, and palpate the patient’s left axilla with your right hand
. Cup together the fingers of your hand and reach as higher you can toward the apex of axillae, and milk down
against the chest wall
Fig 4.4 Examination of the right axillary lymphnodes
52 Abilo Tadesse,MD
Common causes of generalized lymphadenopathy
. Infectious mononucleosis (EBV, CMV)
. Persistent generalized lymphadenopathy (HIV infection): ≥ 2 extra-inguinal significant (>1.5cm)

lymphadenopathy persisting for > 3 months
. Secondary syphilis (Treponema pallidum)
. Tuberculosis (Mycobacterium tuberculosis)
. Toxoplasmosis (Toxoplasma gondii)
. Hodgkin’s lymphoma
. Non-Hodgkin’s lymphoma
. Acute lymphoblastic leukemia
. Chronic lymphocytic leukemia
53 Abilo Tadesse,MD
Thyroid gland
The thyroid gland is located in the neck, anterior to the trachea, between the cricoid cartilage and the
suprasternal notch. The gland consists of right and left lobes connected by an isthmus. It is highly vascular and
soft in consistency. Enlarged thyroid gland is named as goiter.
History taking of thyroid gland
Ask about mode of onset and duration of anterior neck swelling? age at neck swelling?
Ask about hoarseness of voice? difficulty in swallowing?
Ask about associated symptoms of hot or cold intolerance, anxiousness or clumsiness, menstrual irregularities,
fatigue and weakness, dietary habits, residence in iodine-deficient area, family history of same illness, head and
neck irradiation, etc…
Examination of thyroid gland
Inspection
. Ask the patient to sit with neck muscles relaxed, and inspect the neck from the front
. Look for the thyroid gland while the patient swallows a sip of water, and describe contour and symmetry of the
gland
NB: The thyroid gland moves upwards on swallowing since it is enveloped in the pretracheal fascia which is
attached to the cricoid cartilage
Palpation
. Place the patient in sitting position on a chair/coach
. Palpate enlarged thyroid gland from behind (stand behind the patient)
. Extend the neck and head a bit backward
. Put fingers of both hands over the enlarged lobes of the gland
. Notice if the enlarged lobes move with swallowing. It suggests as goiter if it moves with swallowing
. Push the left lobe of the gland with fingers of left hand towards the opposite side. Feel for tenderness,
consistency, nodularity and surface of right lobe of the gland with your right hand fingers
. Push the right lobe of the gland with fingers of right hand to the opposite side. Feel for tenderness, consistency,
nodularity and surface of left lobe of the gland with your left hand fingers
54 Abilo Tadesse,MD
. Measure the length, width and depth of the goiter
. Palpate as well for enlarged cervical and supraclavicular lymph nodes
a) Anatomic structure of the thyroid gland
b) Palaption of the isthmus c) Palpation of thyroid lobes
© Elsevier. Glynn M, Drake WM. Hutchison’s Clinical Methods 23 rde
Fig 4.5 Technique of examining the thyroid gland: Examine the thyroid gland by standing behind the patient
Percussion
Percuss the anterior chest over the sternum for retrosternal extension of the goiter
NB: Dull to percussion over the sternum occurs in retrosternal goiter
Notice for ‘Pumberton’s sign’
Technique of eliciting ‘Pumberton’s sign’
. Ask the patient to lift the arms over the head and wait for one minute
. Note for development of facial plethora, cyanosis, inspiratory stridor and non-pulsatile elevation of the jugular
venous pressure due to compression of the superior venacava by retrosternal goiter at the thoracic inlet
55 Abilo Tadesse,MD
Auscultation
. Put your stethoscope over the upper 1/3 of goiter and listen for bruit
Bruit is present in diffuse goiter due to Graves’ disease
NB: Examination of thyroid gland is incomplete without palpating regional lymph nodes
Causes of goiter
a. Euthyroid goiter
. Thyroid nodule
. Nodular colloid goiter
. Thyroid carcinoma
b. Hypothyroid goiter
. Hashimoto’s thyroiditis
. Subacute throiditis (hypothyroid phase)
c. Hyperthyroid goiter
. Graves’ disease
. Toxic multinodular goiter
. Toxic adenoma
. Functioning thyroid carcinoma
. Subacute throiditis (hyperthyroid phase)
56 Abilo Tadesse,MD
______________________________________________________________________________________
_______________________________________________________________________________________
Table 4.2 Symptoms and signs of thyroid dysfunction
Thyroid cancer
Most common malignancy of the endocrine system
Presence of hard thyroid nodule fixed to adjacent structures with regional lymphadenopathy suggests thyroid
malignancy unless proved otherwise
Risk factors for thyroid cancer in a patient with thyroid nodule
. History of head and neck irradiation
. Age <20 yrs or >50 yrs
. New or rapidly enlarging neck mass
. Family history of thyroid cancer
. Vocal cord paralysis (hoarse voice)
. Nodule fixed to adjacent structure
. Suspected regional lymph node involvement
57 Abilo Tadesse,MD
Breast
The female breast lies between the 2nd and 6th rib, between the sternal edge and the midaxillary line
Components of breast tissue
. Glandular tissue- organizes into lobes that open into nipple
. Fibrous tissue- suspensory ligaments connected to skin and fascia underlying the breast
. Fat
Fig 4.6 Components of breast tissue
History taking of female breast
Ask presence of breast lump, swelling, skin ulceration and discharges from the nipple
Ask about age at menarche, marital status, parity, age at first child birth, history of lactation and breast-feeding,
age at menopause, family history of breast cancer in first degree relatives (mother, sisters), history and duration
of use of oral contraceptives and hormone replacement therapy (HRT)
58 Abilo Tadesse,MD
Indicators of risk for breast cancer
. Female gender
. Increasing age
. Family history of breast cancer
. Early menarche
. Nulliparity or late age of first child
. Late menopause
. Prolonged HRT use
. Radiation therapy to breast region
Examination of female breast
Tell the patient that you are going to examine the breasts
Use gentleness and a matter-of-fact approach during examination
Inspection
Place the patient in sitting or lying position with arms at her sides
. Look for size, symmetry and contour of the breasts
. Look for size and shape of nipples
. Look for skin retraction, ulceration and discharges
Ask the patient to sit and raise her arms over the head, or rest and press her hands against her hips
. Look for dimpling or retraction of the breasts, shift in the relative position of the nipples, or a fixed mass
distorting the breast
. Notice for any swelling in the axillae
NB: Unilateral visible veins, skin retraction and peau d'orange skin (oedematous skin pitted by the sweat glands)
suggests breast canncer
59 Abilo Tadesse,MD
Palpation
Place the patient in a sitting position with both arms by one’s side, leaning forward and then arms above the
head. Examination is repeated in a lying down position with arms above the head.
. Palpate upper outer quadrant followed by the lower outer, lower inner and upper inner quadrant in rotation, and
at last the nipple and subareolar region of both breasts with pulps of fingers for any discrete, hard lump. The arm
pits and the root of the neck above the clavicle are palpated for any nodular, hard swelling.
. Note for consistency, tenderness, breast dimpling and retraction, lump or mass
NB: Consistency of soft fat with firmer glandular tissue suggests a normal breast
If you detect breast lump
. Location by quadrant or clock with cm from the nipple
. Size in cm
. Shape (regular, irregular)
. Mobility in relation to skin and underlying muscle, and chest wall
. Tenderness
. Delimitation (well circumscribed or not)
. Skin changes (dimpling, erythema, peau d’ orange)
NB: Hard, irregular, poorly circumscribed breast lump, fixed to underlying tissue or chest wall strongly suggests
breast cancer
. Palpate each nipple, noting for elasticity
Thickening of the nipple and loss of elasticity suggests underlying breast cancer
. Compress the areola with your index finger placed in radial positions around the nipple
. Watch for discharge- describe for color, consistency and quantity of discharge
Blood- ductal papilloma, breast cancer
Serous/green/yellow-fibrocystic changes
Milky- lactation
Green fluid- mammary duct ectasia
Milky discharge in non-lactating patient suggests nonpuerperal galactorrhea
60 Abilo Tadesse,MD
Non-milky unilateral discharge suggests local breast disease, usually benign but may be malignant
Fig 4.7 Quadrants of right breast: Upper outer, lower outer, lower inner, upper inner
Fig 4.8 Direction of lymphatic drainage of the breast tissue
61 Abilo Tadesse,MD
A) Hands on side b) Hands on pelvis c) Hands over head d) Leaning forward
Fig 4.9 Position in breast examination: a) sitting position with both arms by one’s side, b) sitting position with
both arms pressing the pelvis , c) sitting position with arms raised above the head, d) sitting position with
leaning forward
A. B.
© Churchil Livingstone. Douglas G, Nicol F, Robertson C. Macleod’s ClinicalExamination 12 th e
Fig 4.10 A) Examination of the right breast in supine position B) Clinical examination of the left breast
62 Abilo Tadesse,MD
Table 4.3 Cause of breast lump/mass
63 Abilo Tadesse,MD
CHAPTER FIVE
Respiratory system
Learning objective
1. Mention symptoms of respiratory disease

2. Perform techniques of respiratory system examination
3. Interpret clinical findings of various respiratory pathologies and diseases
History taking of respiratory system
Patents with respiratory disease present with one or more of the following symptoms
. Cough
. Sputum
. Dyspnea (shortness of breath)
. Hemoptysis
. Wheeze
. Chest pain
. Stridor
Cough
Cough is an explosive expiration due to irritation of sensory receptors in the submucosa of the upper airways or
bronchi. It enables the tracheobronchial tree to be cleared of secretions and foreign bodies
Ask:
How long has the cough been present? Acute (< 3wks) or chronic (> 8wks) ?
Is the cough dry or productive (with expectoration of sputum)?
Is the cough worse at any time of the day or night?
Paroxysmal cough disrupting sleep due to nocturnal worsening suggests bronchial asthma
64 Abilo Tadesse,MD
Cough of a worker in cotton industry that lessens on weekends suggest occupational asthma
Is the cough aggravated by any thing? Such as cold air, pollen, house dust (increased reactivity of air ways in
brochial asthma)
What is the quality of cough? Barking cough occurs in epiglotitis; bovine cough indicates vocal cord paralysis;
brassy (metallic) cough occurs in tracheal compression; wheezy muffled cough occurs in chronic bronchitis
Most common causes of cough (duration)
a. Acute cough (< 3 weeks)
. Common cold
. Acute bronchitis
. Pneumonia
. Pulmonary embolism
b. Chronic cough (>8 weeks)
. Bronchiectasis
. Chronic obstructive pulmonary disease
. Interstitial lung disease
. Lung cancer
. Tuberculosis
Hemoptysis
Hemoptysis is blood coughed up from the respiratory tract (blood streaked sputum to frank blood)
Massive hemoptysis is defined as expectoration of coughed up blood > 600ml over 24 hrs. It is usually caused
by lung cancer eroding a pulmonary vessel, bronchiectasis, cavitary disease, pulmonary vasculitis and
pulmonary arteriovenous malformation.
NB: Never assume haemoptysis has a benign cause until serious pathology has been considered and excluded.
Ask: Is there any blood in the sputum? Quantify amount in ml per day, how often and for how long?
65 Abilo Tadesse,MD
Common causes of hemoptysis
a. Tracheobronchial tree
. Bronchiectasis
. Endobronchial tumor
b. Pulmonary parenchymal source
. Pneumonia
. Lung abscess
. Tuberculosis
. Lung cancer
c. Pulmonary vascular source
. Good pasture’s syndrome (pulmonary hemorrhage, glomerulonephritis)
. Granulomatosis with polyangitis (Wegener’s granulomatosis)
. Pulmonary embolism
d. Cardiac causes
. Mitral stenosis
. Acute left ventricular failure (pulmonary edema)
e. Hematological causes
. Bleeding diatheses (coagulopathy)
. Anticoagulants (over dosage)
Sputum (phlegm)
Ask:
. What is the color, odour, consistency, and amount (in teaspoonful or arabic coffee cup/day)?
Yellow or green sputum usually indicates bronchopulmonary infections
. Is it position-dependent or not?
Position-dependent expectoration occurs in bronchiectasis
66 Abilo Tadesse,MD
. Is it foul smelling or not?
Foul smelling, dark-colored, expectoration occurs in lung abscess caused by anaerobic organisms
Main types of sputum (color)
. Serous (watery/pink): pulmonary edema
. Mucoid (clear, grey): bronchial asthma, chronic bronchitis
. Purulent (yellow/green): bronchopulmonary infections: bronchiectasis, lung abscess
. Rusty (red): Pneumococcal pneumonia
Large volume (copious amount) of sputum is expectorated in bronchiectasis, and lung abscess and empyema
rupturing into bronchial tree
Chest pain
Chest pain originates from injured pleura, chest wall and mediastinal structures. The lungs are not a source of
pain for their exclusive autonomic innervation.
. Describe about the site/location, type, mode of onset, radiation, severity, relieving and aggravating factors of
chest pain (SOCRATES)
a. Pleuritic pain
Pleuritic chest pain is sharp and stabbing pain worsed by deep breathing and coughing
Pleural pain from upper six ribs causes localized pain
Pleural pain from lower six ribs and outer diaphragm referred to upper abdomen
Pleural pain from central diaphragm referred to shoulder or neck
Common causes of pleuritic chest pain are pneumonia, pulmonary embolism, pneumothorax and fractured ribs
b. Chest wall pain
Chest wall pain is usually musculoskeletal originated pain. It is characteristically tender to local palpation, and
can be reproduced by respiratory movements and/or movement of the spine or shoulder muscles. It occurs in rib
fracture, intercostal muscle injury, thoracic herpes zoster, and direct invasion of chest wall by lung cancer,
mesothelioma or malignant rib metastasis
67 Abilo Tadesse,MD
c. Mediastinal pain
Mediastinal pain is central, retrosternal and unrelated to respiration or cough. It occurs in irritation of
tracheobronchial tree, and injury to mediastinal structures
Dyspnea (shortness of breath)
Dyspnea is uncomfortable awareness of breathing that is inappropriate to the level of exertion
The patient often complains of ‘inability to get enough air into the chest’
. Describe about mode of onset, duration, severity and associated symptoms
Paroxysmal, variable in timing (from day to day) dyspnea associated with wheeze, which is worsened by
exposure to allergens or house dust mites favors diagnosis of bronchial asthma
Mode of onset of dyspnea
a. Minutes
Pulmonary embolism, pneumothorax, foreign body aspiration
b. Hours to days
Pneumonia, bronchial asthma, Exacerbation of COPD
c. Weeks to months
Pulmonary tuberculosis
COPD
Idiopathic pulmonary fibrosis
Pneumoconiosis
Pleural effusion
Wheeze and stridor
Wheeze is continous whistling noise during breathing. It is produced by air passing through narrowed small
airways. It occurs in bronchial asthma, chronic bronchitis and endobronchial obstruction by foreign body or
tumor
68 Abilo Tadesse,MD
Stridor is rasping or croaking noise loudest on inspiration. It indicates narrowing of the larynx, trachea or main
bronchus. It occurs in laryngitis, croup, tracheobronchial tumor, or foreign body occluding tracheobronchial tree
Social history
Smoking
. Ask: How many cigarettes per day, for how long?
How many pack-years? Pack-year is defined as number of packs of cigarettes smoked per day multiplied by
number of years smoked
Eg. One pack-year is equal to smoking one pack of cigarettes per day for one year, or two packs of cigarettes per
day for half a year
Almost all cases of lung cancer and chronic obstructive pulmonary disease (COPD) occur in those who have
smoked
Prolonged biomass fuel exposure (indoor cooking) is major risk factor for COPD in rural areas of developing
world
Alcohol
Drinking alcohol in binge can result in aspiration pneumonia, and alcoholics are more likely to develop
klebsiella pneumonia and lung abscess
Family history
Genetic susceptibility occurs in bronchial asthma, bronchiectasis (ciliary dyskinesia syndrome, cystic fibrosis),
emphysema (α-1 anti-trypsin deficiency), etc…
Occupational history
. Occupational asthma
. Malignant mesothelioma due to chronic asbestos exposure
. Pneumoconiosis due to chronic exposure to industrial fumes and gases
69 Abilo Tadesse,MD
Table 5.1 Common causes of cough and sputum
70 Abilo Tadesse,MD
Examination of the respiratory system
Anatomy
Anteriorly, the apex of each lung rises about 2-4 cm above the inner third of the clavicle, and the lower border
of the lung crosses the 6th rib at the mid-clavicular line, the 8th rib at the mid-axillary line and T-10 spinous
process posteriorly
The right lung has 3 lobes; upper, middle and lower lobes. The left lung has 2 lobes, upper and lower lobes
The right lung has 2 inter lobar fissures (major and minor interlobar fissures) while the left lung has one major
interlobar fissure
Surface lung markings of the interlobar fissures
A line from the 2nd thoracic spine to the 6th rib along the nipple corresponds to the upper border of the lower
lobe (major interlobar fissure) of the right lung. Horizontal line at 4th costal cartilage to meet the line of major
interlobar fissure marks the boundary between upper and middle lobes (minor inter lobar fissure)
The trachea bifurcates into main bronchi at the level of sternal angle anteriorly and the 4 th thoracic spinous
process posteriorly
71 Abilo Tadesse,MD
Fig 5.1 Surface anatomy of the lung: Right lung has three lobes and two fissures (major and minor interlobar
fissure), while the left lung has two lobes with single fissure (major interlobar fissure)
Technique of examination
Inspection
. Listen to the patient’s quality of voice while conversation
Clubbing
. Look for the presence of clubbing
Clubbing is selective bulbous enlargement of the distal segments of fingers and toes, probably caused by the
opening of anastomotic channels in the nailbed
Grading of clubbing
Grade 1: ‘Spongy feel’ at nail fold (nail bed fluctuation and softening)
Grade 2: Obliteration of the hyponychial angle (>1600).
Hyponychial angle (nail fold angle) is 160o in normal individuals
Grade 3: Drum stick appearance of distal phalanges of fingers/toes
Phalangeal depth ratio >1 (distal phalangeal depth/interphalangeal depth)
Grade 4: Hyperthrophic osteoarthropathy (HOA): Periosteal thickening of the long bones of forearm (radius and
ulna) and lower leg (tibia and fibula) with clubbing of fingers
72 Abilo Tadesse,MD
© Elsevier. Talley & O’Connor. Clinical Examination 5the
Fig 5.2 Nail clubbing: Obliteration of hyponychial angle (Nail fold angle > 1600) and Phalangeal depth ratio >1
(distal phalangeal depth (DPD) > interphalangeal depth (IPD))
Fig 5.3 Schamroth’s technique to identify clubbibg: Normal nail with hyponychial angle <1600 (top); and
Clubbed nail with obliteration of schamroth’s window sign (diamond-shaped space between the nail beds)
(bottom)
73 Abilo Tadesse,MD
Common causes of clubbing
. Hereditary (familial)
. Pulmonary diseases- primary and metastatic lung cancer, bronchiectasis, lung abscess, empyema, cystic
fibrosis, mesothelioma, tuberculosis
. Cardiac diseases- cyanotic congenital heart disease, infective endocarditis
. Gastrointestinal diseases- inflammatory bowel disease, hepatic cirrhosis
. Idiopathic
Cyanosis
. Look for the presence of cyanosis at lips and tongue
Cyanosis is bluish discoloration of the skin and mucus membrane resulting from an increased quantity of
deoxygenated hemoglobin (reduced oxygen saturation)
Cyanosis becomes evident when the absolute concentration of deoxygenated hemoglobin is ≥ 5gm/dl of
capillary blood
Cyanosis is usually obvious when the arterial oxygen saturation (Sa02) falls below 90% in a person with a
normal hemoglobin level
In patients with anemia, cyanosis doesn’t occur until greater levels of arterial desaturation is reached
Central cyanosis: bluish discoloration of lips and tongue due to arterial hypoxemia
Peripheral cyanosis (acrocyanosis): bluish discoloration of the distal parts of extremities due to vasoconstriction
Breathing pattern
. Look for rate, depth and pattern of breathing
Abnormal breathing pattern
. Rapid shallow breathing (Tachypnea: Respiratory rate (RR) >20 breaths per minute) occurs due to hypoxia in
respiratory diseases Eg. Severe pneumonia, pulmonary embolism, etc…
. Slow breathing (Bradypnea: RR <8 breaths per minute) occurs in drug-induced respiratory center depression
Eg. Barbiturate poisoning
74 Abilo Tadesse,MD
. Kussmaul’s breathing: Rapid, deep and labored breathing Eg. Metabolic acidosis
. Periodic (cheyne-stokes) breathing: Increasing rate and depth of breathing, followed by diminishing respiratory
effort and rate, ending in a period of apnoea or hypopnea. It is related to delayed sensitivity of the respiratory
centre to chemical control as in brain hemispheric damage, or delay in circulation time between the lung and
chemoreceptors as in advanced heart failure.
. Apneustic breathing: Post-inspiratory pause in breathing Eg. Pontine damage
. Ataxic (Biotic) breathing: Unpredictable, irregularity of respiration Eg. Medullary compression due to central
transtentorial herniation
. Paradoxical breathing: The abdomen sucks inwards with inspiration Eg. Diaphragmatic paralysis
Sign of respiratory distress
. Look for signs of respiratory distress
Signs of respiratory distress
. Tachypnea (RR >20 breaths per minute)
. Flaring of alae nasae
. Cyanosis
. Use of accessory muscles of respiration (sternomastoid, scalenes, platysma and strap muscles of the neck)
. Supraclavicular/intercostal/subcostal retraction
The accessory muscles of respiration causes elevation of the shoulders with inspiration and aid respiration by
increasing chest expansion
. Observe the shape of the chest
The normal chest is bilaterally symmetrical and elliptical in cross section
The thoracic ratio (Antero-posterior diameter to transverse diameter ratio) is 0.7-0.9
Chest shape
Types of abnormal chest shape
75 Abilo Tadesse,MD
. Kyphosis: Exaggerated forward curvature of the spine
. Scoliosis: Lateral curvature of the spine
. Kyphoscoliosis: Forward and lateral bending of the spine
Kyphoscoliosis is idiopathic (80%) in majority of patients. It reduces the ventilatory capacity and increases the
work of breathing
. Funnel chest (Pectus excavatum): Depression in the lower end of the sternum
. Pigeon chest (Pectus carinatum): Anteriorly displaced sternum with depressed costal cartilage
. Barrel chest: Increased antero-posterior diameter of the chest in comparison to transverse diameter of the chest.
The thoracic ratio (antero-posterior diameter to transverse diameter) > 0.9 declares barrel-chest deformity. It is
often seen in COPD, chronic asthma, and older aging.
. Harrison’s sulcus: Linear depression of the lower ribs just above the costal margins at the site of attachment of
the diaphragm, often seen in rickets and severe childhood asthma
. Observe symmetry of the chest during spontaneous breathing
. Observe presence of chest lag/delay, intercostal and subcostal retraction
Chest lag to affected lung occurs in pneumothorax, hydrothorax, lung collapse and fibrosed lung
. Look for the presence of paradoxical respiration (diaphragmatic paralysis?)
Fig 5.4 Chest deformity: Pigeon chest and funnel chest deformity
Palpation
76 Abilo Tadesse,MD
Assess for the presence of chest wall tenderness
Look at the face of the patient while palpating the anterior and posterior chest for chest wall tenderness
Assess for the presence of subcutaneous emphysema (crackling sensation felt on palpating over gas-containing
chest wall)
Assess for symmetry of chest expansion (lung excursion)
NB: Both sides of the chest should expand equally during tidal breathing and maximal inspiration
Technique for determining symmetry of chest wall expansion
Anterior chest
. Place the hands firmly on the lateral chest wall with your thumbs along each costal margin
. Slide your thumbs medially to raise skin folds
. Ask the patient to inhale deeply and watch for divergence of your thumbs as the thorax expands
. Observe for symmetry and degree of chest wall expansion
Posterior chest
. Grasp the lateral ribcage with your hands, and place your thumbs at the level of and parallel to the 10th rib
. Slide your thumbs medially in order to raise loose skin folds between your thumbs and the spine
. Ask the patient to inhale deeply
. Watch divergence of your thumbs during inhalation
. Observe for symmetry and degree of chest wall expansion
77 Abilo Tadesse,MD
Fig 5.5 Technique of examination for comparison of chest expansion (during expiration and inspiration)
Technique for determining degree of chest wall expansion
. Measure the total circumference of the chest along the nipple using tape measure during quiet and deep
respiration (the difference in chest expansion in deep and quiet breathing is about 4-6 cm)
Reduced chest wall movement on affected side may be due to localized lung fibrosis, lung collapse, pleural
effusion or pneumothorax
Symmetrically reduced chest wall expansion occurs in emphysema, interstitial lung disease and diffuse fibrotic
lung disease
Trachea position
. Assess position of the trachea
Technique
. Feel for the trachea by putting the index and ring fingers of right hand on each edge of sternal notch, and use
the middle finger to assess whether the trachea is central or deviated to one side
A slight deviation of the trachea to the right side may be found in healthy individuals
. Assess for the presence of tracheal tug
A tracheal tug is demonstrated when the finger resting on the trachea feels it move in inferiorly with each
inspiration. It is a sign of hyperinflation of the chest due to airway obstruction
Causes of tracheal displacement
Tracheal deviation towards the side of lung lesion
. Upper lobe fibrosis
. Pneumonectomy
. Upperl lung collapse
Tracheal deviation away from side of the lung lesion
. Massive pleural effusion
78 Abilo Tadesse,MD
. Tension pneumothorax
Mediastinal mass displaces the trachea away from the mass
. Retrosternal goiter
. Lymphoma
. Lung cancer
Tactile fremitus
Assess tactile fremitus (tactile resonance transmitted from the lung)
Tactile fremitus is palpable vibrations that is transmitted through the airways to the chest wall as the patient is
speaking
Technique
. Put your hand over the chest with the palm touching the chest wall
. Ask the patient to say ‘ninety-nine’ or ‘arba-arat’ repeatedly while the palm of hand over the chest wall
. Compare the tactile fremitus in symmetric fashion from the apices to the lung bases in both lung fields
anteriorly and posteriorly
Reduced tactile fremitus on affected lung occurs in lung collapse, pneumothorax, hydrothorax and fibrotic lung
disease
Increased tactile fremitus on affected lung occurs in lung consolidation due to pneumonia
Percussion
Percussion of the chest sets the chest wall and underlying tissues into motion, producing audible sounds
It helps to determine whether the underlying tissues are air-filled, fluid-filled or solid-filled
Technique of percussion
. Put the hyper-extended middle finger of the left hand (the pleximeter finger) on the chest wall with the distal
inter-phallangeal joint firmly on the surface to be percussed
79 Abilo Tadesse,MD
. Partially flex the right middle finger (the plexor), and strike the pleximeter finger at the distal inter-phallangeal
joint with the tip of the plexor finger at 90o with a quick, sharp and relaxed wrist motion.
. Percuss the anterior, lateral and posterior chest in symmetric fashion from the apices to the lung bases
Identify the level of diaphragmatic dullness
. Percuss the posterior chest in progressive steps down ward with the pleximeter finger held above and parallel
to the expected level of dullness
Dullness to percussion is noticed in consolidation, lung collapse, fibrosis, lung mass, and pleural thickening.
Hyperresonance to percussion occurs in pneumothorax.
‘Cracked pot sound’ is elicited by percussing over cavities which communicate with bronchus
Fig 5.6 Technique of percussion: Left middle pleximeter finger and right middle plexor finger
Diaphragmatic excursion
Change in diaphragmatic dullness at maximal expiratory and maximal inspiratory phases (normal range of
diaphragmatic excursion is 5-6 cm)
Technique of determining diaphragmatic excursion
80 Abilo Tadesse,MD
. Percuss posterior chest from apices to lung bases
. Determine the level of dullness at maximal expiration and then at maximal inspiration
. Determine the difference in cm
Reduced diaphragmatic excursion on affected side of lung occurs in hydrothorax, lung collapse and lung fibrosis
Fig 5.7 Sites of percussion on anterior and posterior chest wall
Table 5.2 Percussion notes and their characteristics
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Fig 5.8 Determining level of diaphragmatic excursion
Auscultation
Auscultation assesses airflow through the tracheobronchial tree
Breath sounds
Breath sounds probably originate from transmission of turbulent airflow in the large airways
Breath sounds are classified according to their intensity (loudness), pitch (quality) and duration of their
inspiratory and expiratory phases
Technique
. Listen to the breath sounds with the diaphragm of the stethoscope after instructing the patient to breathe deeply
through an open mouth
. Auscultate the anterior, lateral and posterior chest in symmetric fashion from top to bottom
. Note the intensity, pitch and duration of breath sounds in inspiratory and expiratory phase
NB: Avoid auscultation within 3cm of midline of chest, as these areas transmit sounds directly from trachea or
bronchi
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Table 5.3 Characteristics of breath sounds
Adventitious (added) sounds
. Listen for adventitious sounds
Crackles
Crackles are produced by sudden changes in gas pressure related to the sudden opening of previously collapsed
small airways
Crackles are intermittent and non-musical brief, high-pitched sounds
Wheezes
High pitched sounds with hissing or shrill quality
Wheeze is usually maximal during expiration and is accompanied by prolonged expiration
Rhonchi
Low-pitched sounds with snoring quality
83 Abilo Tadesse,MD
Table 5.4 Additional breath sounds
Pleural friction rub
It occurs in pleural inflammation with creaking or rubbing quality
Transmitted voice sounds
Commonly observed in lung consolidation (eg. pneumonia)
Consolidated lung conducts sounds better than air-containing lung, and vocal resonance is increased and the
sounds are louder and clearer
1. Bronchophony
. Ask the patient to say repeatedly ‘ninety-nine’; louder and clearer sounds are heard on the chest wall
2. Aegophony
. Ask the patient to say ‘ee-ee-ee’; ‘E-to-A’ change with nasal or bleating quality is heard
3. Whispering pectoriloquy
. Ask the patient to whisper ‘one-two-three’; louder and clearer whispered voices are heard
Physical findings of common lung problems
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Consolidation (lobar pneumonia)
Signs
Chest expansion- reduced on the affected side
Tactile fremitus- increased on the affected side
Percussion- dull to percussion
Breath sounds- bronchial
Additional sounds- medium, late or pan-inspiratory crackles
Vocal resonance- positive (aegophony, bronchophony and whispering pectoriloquy)
Pleural rub may be present
Lung collapse
Signs
Flattening of the chest wall on the affected side
Trachea- displaced towards the collapsed lung
Chest expansion- reduced on the affected side
Tactile fremitus- reduced on affected side
Percussion- dull over the collapsed lung
Breath sound- reduced +/- bronchial breath sound above the area of collapse
Cuauses of lung collapse
Intraluminal- mucus (post-operative, asthma/COPD, bronchiectasis, cystic fibrosis)
Mural- lung cancer
Extramural- peribronchial adenopathy
Pleural effusion: Collection of fluid in the pleural space
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Pleural collections consisting of blood (hemothorax), chyle (chylothorax) or pus (empyema) have similar
findings
Signs
Bulged chest wall on affected side
Trachea and apex beat- displaced away from a massive effusion
Chest expansion- reduced on affected side
Tactile fremitus: reduced on affected side
Percussion- stony dullness on affected side
Breath sounds- absent air entry; bronchial breath sound audible above the level of effusion
Causes of pleural effusion
1. Exudative pleural effusion: Fulfill one or more of the following (modified light’s criteria)
Pleural protein-to-serum protein ratio > 0.5, pleural LDH-to-serum LDH ratio >0.6, or pleural LDH (lactate
dehydrogenase) is above 2/3 of upper normal serum level
. Pneumonia with parapneumonic effusion
. Malignancies- lung cancer, metastatic cancer, mesothelioma, lymphoma
. Tuberculosis
. Pulmonary infarction
. Traumatic effusion
. Connective tissue diseases (rheumatoid arthritis, systemic lupus erythematosis)
. Acute pancreatitis
. Drugs (cytotoxins, hydralazine, etc…)
2. Transudative pleural effusion: doesn’t fulfill any of the above mentioned modified light’s criteria
. Hypoalbuminemia from protein-losing enteropathy
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. Nephrotic syndrome
. Hepatic cirrhosis
. Hypothyroidism
. Meig’s syndrome (ovarian fibroma causing pleural effusion and ascites)
Pneumothorax: leakage of air from the lung or chest wall punctures into the pleural space
Signs
Bulged chest wall on affected side
Chest expansion- reduced on affected side
Trachea is displaced away from affected side
Tactile fremitus- reduced on affected side
Percussion-hyperresonance on affected side
Breath sound- greatly reduced or absent
There may be associated subcutaneous emphysema (crackling sensation over gas-containing tissue)
Causes of pneumothorax
1. Spontaneous pneumothorax
. Subpleural bullae rupture (in tall and thin healthy individuals)
. Emphysema with rupture of bullae
. Pulmonary tuberculosis
. Bronchial asthma, lung abscess (rarely)
. Iatrogenic (following insertion of central venous catheter)
2. Traumatic
. Rib fracture
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. Penetrating chest wall injury
. Iatrogenic (during pleural or pericardial aspiration)
Tension pneumothorax: It occurs when there is a communication between the lung and the pleural space,
with a flap of tissue acting as a valve, allowing air to enter the pleural space during inspiration and preventing it
from leaving during expiration
It causes displacement of the mediastinum with obstruction and kinking of the thoracic great vessels
Signs
The patient is often cyanotic, tachypneic, and hypotensive
Trachea and apex beat- displaced away from the affected side
Chest expansion- reduced over affected side
Tactile fremitus- reduced over affected side
Percussion- hyperresonant over the affected side
Breath sound- absent over affected side
Causes of tension pneumothorax
. Penetrating chest wall injury
. Mechanical ventilation at high pressure
. Spontaneous
Emphysema
Signs
Barrel-shaped chest with thoracic ratio > 0.9
Pursed lip breathing
Use of accessory muscles of respiration
Positive Hoover’s sign: “drawing in” of the lower intercostal muscles with inspiration
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Palpation- reduced chest expansion of hyperinflated lung
Percussion- hyperresonant with decreased cardiac and liver dullness
Breathe sounds- decreased; early inspiratory crackles
Wheeze is often absent
Pulmonary fibrosis
Signs
General- dyspnea, cyanosis, and clubbing may be present
Palpation- reduced chest expansion and tactile fremitus on affected side
Percusssion- reduced on affected lung field
Auscultation- fine (Velcro-like) late inspiratory or pan-inspiratory crackles on affected side
Causes of lung fibrosis
1. Upper lobe: S2CHA2RT
. Silicosis
. Sarcoidosis
. Coal-worker’s pneumoconiosis
. Histoplasmosis
. Ankylosing spondylitis
. Allergic bronchopulmonary aspergillosis
. Radiation
. Tuberculosis
2. Lower lobe: RASCO
. Rheumatoid arthritis (RA)
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. Asbestosis
. Scleroderma
. Cryptogenic fibrosing alveolitis (IPF)
. Others: drugs-busulphan, bleomycin, methotrexate, hydralazine, amiodarone
Table 5.5 Chest signs in common respiratory problems
90 Abilo Tadesse,MD
CHAPTER SIX
Learning objective
1. Mention the main symptoms of cardiovascular disease

2. Describe characters of abnormal arterial pulse
3. Show techniques of precordial examination
4. characterize murmurs in various valvular lesions
History taking of the cardiovascular system
Patients with cardiovascular disease present with one or more of the following symptoms
. Dyspnea
. Orthopnea
. Paroxysmal nocturnal dyspnea
. Palpitation
. Angina
. Syncope
. Leg swelling
. Intermittent claudication
. Fatigue
Dyspnea (shortness of breath)
Dyspnea is uncomfortable awareness of breathing
Dyspnea in cardiac patients occur when ever the work of breathing is excessive due to elevated left atrial and
pulmonary capillary pressure causing transudation of fluid into the lung, requiring extra effort to ventilate the
stiff lung
Determine level of dyspnea by the type of exertion causing dyspnea
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Level of dyspnea (New York Heart Association Classification)
Grade I- Dyspnea occurring at heavy, but accustomed activities.
Eg. Short of breathe while farming
Grade II- Dyspnea occurring at moderate exertion. Slight limitation on ordinary activities
Eg. Short of breathe while walking uphills or climbing stairs
Grade III- Dyspnea occurring during mild exertion or doing daily routine activities. Marked limitation on
ordinary activities
Eg. Short of breathe while going to the toilet
Grade IV- Short of breathe at rest. Inabilityto carry on any activity without discomfort
Orthopnea
Dyspnea while assuming supine position due to gravitational pooling of fluid to the lungs
. Quantify the level of orthopnea by the number of pillows required to alleviate dyspnea (eg. three-pillow
orthopnea)
Causes of orthopnea
Common cause: Left ventricular failure (CHF)
Uncommon causes: Massive ascites, massive pleural effusion, bilateral diaphragmatic paralysis, severe
pneumonia, pregnancy
Paroxysmal nocturnal dyspnea (PND)
PND is sudden onset of severe dyspnea during sleep at night, which wakes the patient from sleep chocking or
gasping for air. Patients may sit on the edge of the bed and open windows in an attempt to relieve their distress.
Palpitation
Palpitation is unpleasant subjective awareness of one’s own heart beat
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Palpitation is caused by a change in the cardiac rhythm or rate, or by an increase in the force of cardiac
contraction
Patients commonly describe palpitation as ‘jumping’, ‘pounding’ ‘racing’ ‘skipping’ or ‘fluttering’ heart beats
Ask
. Speed of onset and offset (abrupt or gradual)
. Sustained or paroxysmal (frequency and duration of episodes if paroxysmal)
. Character of rhythm (ask the patient to replicate the rhythm by tapping it out on a table)
. Precipitating factors (eg. exercise, alcohol, drugs etc…)
. Associated symptoms (syncope, light-headedness, dizziness, dyspnea, etc…)
. Associated underlying cardiac disease (coronary artery disease, hypertensive heart disease, valvular heart
disease, cardiomyopathies, etc…)
NB: Rapid irregular palpitation is typical of atrial fibrillation. Transient skips and flip-flops signify extrasystole
(PVC).
Syncope
Syncope is a transient loss of consciousness due to inadequate cerebral blood flow causing cerebral anoxia
Syncope may represent a simple faint, and it is a symptom of cardiac or neurologic disease
Main causes of syncope
. Postural hypotension (drop in systolic blood pressure >20 mmhg on standing from supine position)
. Arrhythmias (brady- or tachy-arrhythmias)
. Left ventricular outflow obstruction (severe aortic stenosis, hypertrophic cardiomyopathy, severe pulmonary
hypertension, massive pulmonary embolism)
. Neurocardiogenic syncope (due to abnormal autonomic reflexes, i.e. painful or emotional stimuli)
Ask
. What is the circumstance during syncopal attack?
While standing for prolonged periods or standing up suddenly (postural syncope), or while passing urine
(micturition syncope), on coughing (tussive syncope) or with sudden emotional stress (vasovagal syncope)
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. Were there warning symptoms or not?
It may occur suddenly without warning or preceeded by symptoms of faintness or pre-syncope such as
lightheadedness, dizziness, feeling of warmth, diaphoresis, nausea and tunneling of vision
. How long does the episode last? Is it recurrent or not?
Syncope due to arrhythmia is often sudden onset regardless of the patient’s posture
Exertional syncope may occur with obstruction to left ventricular outflow by severe aortic stenosis (AS) or
hypertrophic cardiomyopathy
Inquire about use of anti-hypertensive or anti-anginal drugs in postural syncope
Angina
Angina is retrosternal chest pain with squeezing, heaviness, pressure or burning character, radiating to the left
shoulder, neck, jaw, teeth, and medial border of left arm, which is worsened by exertion and relieved by rest or
nitrates.
. Describe about the location, duration, quality of pain, radiation, aggravating and relieving factors
Types of angina
1. Stable angina
. Characteristic retrosternal chest discomfort persisting for 2-10 minutes, worsened by exertion and relieved by
rest or nitrates
2. Unstable angina
. Crescendo angina- increasing severity, frequency and duration of retrosternal chest discomfort
. New onset angina- Onset of angina in the last 2 months with at least slight limitation of ordinary activity
. Rest angina- Angina occurring at rest, lasted 20 minutes or more, and occurred in the last one week
3. Angina in acute myocardial infarction (AMI)
. Severe anginal discomfort or pain persisting for more than 30 minutes and not relieved by rest or nitroglycerin
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Table 6.1 Comparison of angina pectoris and myocardial infarction
Differential diagnosis of chest pain mimicking myocardial infarction
1. Pericarditis- Retrostenal or precordial sharp, stabbing, pleuritic chest pain radiating to left shoulder and
back. It is worsened by deep breathing or lying down, and relieved by sitting up and leaning forward.
Associated symptoms such as flu-like syndrome, fever and dyspnea may be present.
2. Acute aortic dissection- Abrupt onset of unrelenting, tearing, ripping, knife-like anterior chest pain radiating
to the back (between shoulder blades), and associated with symptoms of autonomic stimulation like pallor,
sweating, syncope, bradycardia or hypertension.
3. Massive pulmonary embolism- Abrupt onset of pleuritic chest pain, and associated with dyspnea, cyanosis,
syncope, and hypotension. Swollen, tender and warm leg may be present.
4. Spontaneous pneumothorax- Sudden onset of sharp or pleuritic pain localized to the chest with severe
dyspnea.
5. Esophageal spasm- Retrosternal burning, tightening or pressing pain, which persists for 2-30 minutes. It is
triggered by spicy foods, lying flat, and sometimes relieved by nitrates.
Fig 6.1 Site and radiation of angina (Levine’s sign is shown by clenched fist over the anterior chest)
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Intermittent claudication
Patients with caudication notice pain in one or both calves, thighs, or buttocks when they walk more than a
certain distance. The distance walked to cause calf pain is named as ‘claudication distance’.
History of claudication suggests peripheral arterial disease (PAD) with poor blood supply to the affected
muscles. Other vascular diseases like coronary artery disease are often present.
Ask:
. Have you ever had any pain or cramping in your legs on walking or exercise?
• How far can you walk without pain?
• Does the pain get better with rest?
• Ask also about coldness, numbness, pallor and loss of hair of feet
Leg swelling
Excess fluid in interistitial space causes tissue swelling (edema). Tissue swelling in heart failure is gravity
dependent and bilateral. Left sided heart failure is accompanied by pulmonary venous congestion and
pulmonary edema; whereas the right sided heart failure is accompanied by systemic venous congestion and
peripheral edema.
Ask
. Are there swelling over the legs in ambulating patient or pre-sacral area in bed-confined patient?
. Are the rings tight on your fingers?
Fatigue
Common symptom of cardiac disease, and may be associated with reduced cardiac output and poor blood supply
to the skeletal muscles
In longstanding left ventricular failure, as right ventricular failure develops, orthopnea and paroxysmal nocturnal
dyspnea decrease, while fatigue and weakness become more prominent.
Additional history
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. Ask about history of congenital heart disease: Was she/he not exerting equally with her/his friends during
childhood?
. Ask about previous history of acute rheumatic fever in patients with valvular heart disease (previous history of
migratory joint pain and swelling, chorea (abnormal body movement), and recurrent attacks of childhood
tonsillitis)
. Ask about major risk factors for coronary artery disease (CAD)
Hyperlipidemia (family history, on statin therapy or not)
Smoking (duration and amount of smoking in Pack-Years)
Hypertension (duration of hypertension, presence of target organ damage, on anti-hypertensive drugs or not)
Family history of premature CAD (1st degree relatives < 45 years in males, or < 55 years in females)
Diabetes mellitus (DM) (duration of DM, presence of chronic complications, on injectable insulin or oral
hypoglycemic drugs)
Chronic kidney disease (CKD) (how long? stage of CKD? etiology of CKD)
. Ask about habits like smoking, alcohol, and ellicit drug use (Pack-years of cigarrete smoking, binge alcohol
use, substance use)
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Examination of cardiovascular system
Blood pressure
Blood pressure is a measure of the force that the circulating blood exerts against the arterial wall
It is usually measured by means of sphygmomanometer
The length and width of inflatable bladder of the sphygmomanometer cuff should be about 80% and 40% of
upper arm circumference, respectively (usually 23-35cm in length and 12.5cm in width)
Technique of measuring blood pressure
. Patients should avoid smoking or ingestion of caffeine 30 minutes before, and rest in quiet, warm room for 5
minutes
. With the patient seated or lying down, position the arm so that brachial artery is at heart level
. Wrap the cuff securely over the upper arm of patient, with the centre of the bladder over the brachial artery,
and lower border of cuff to be 2.5 cm above the antecubital crease
. Place the bell of stethoscope lightly over the brachial artery
. Feel for radial artery with fingers of one hand and inflate the cuff until the radial pulse disappears and read the
pressure on the manometer and add 30 mmhg to it
. Deflate slowly at a rate of 2-3 mmhg per second, and notice at manometer where the sound appear, muffled
and disappear
Korotkoff sounds
Phase1- the 1st appearance of the sounds marking systolic pressure
Phase 2 and 3- increasing loud sounds
Phase 4- abrupt muffling of the sounds
Phase 5- disappearance of the sounds marking diastolic pressure
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Fig. 6.2 Measuring blood pressure and Auscultatory findings
Fig 6.3 Phases of Korotkoff sounds
When Korotkoff sounds remain audible despite complete deflation of the cuff, take phase 4 as diastolic pressure,
which usually noticed in aortic regurgitation, patent ductus arteriosus, arterio-venous fistula, pregnancy, etc…
Blood pressure (BP) should be taken in both arms at least once; a difference of ≤ 5 mmhg in both arms is
acceptable
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BP should be recorded in supine and sitting position to rule out postural hypotension
Postural hypotension: Drop in systolic BP >20mmhg while assuming from supine to sitting position
Causes of postural hypotension
. Hypovolemia (dehydration, acute blood loss)
. Drugs (eg. vasodilators, anti-depressants, diuretics)
. Addison’s disease
. Hypopituitarism
. Autonomic neuropathy (diabetes, amyloidosis)
. Idiopathic
Table 6.2 Classification of hypertension in adults
SBP (mmhg) DBP (mmhg)
Normal <120 <80
Prehypertension 120-129 <80
Stage 1 hypertension 130-139 80-89
Stage 2 hypertension ≥140 ≥90
Hypertension should be diagnosed only when a higher than normal level has been found on ≥ 2 visits after initial
screening
White coat hypertension: Blood pressure in the hypertensive range in medical settings, while mean ambulatory
readings in the normal range. It carries normal cardiovascular risk and it doesn’t require treatment.
Masked hypertension: Elevated blood pressure in ambulatory readings, while normal office blood pressure level
Nocturnal hypertension: A nocturnal fall (dipping) < 10% of day time blood pressure values
Masked and nocturnal hypertensions require intervention, as are associated with increased cardiovascular risk
Arterial pulse
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The palpable pulse in an artery reflects the pressure wave generated by the ejection of blood into the circulation
from the left ventricle.
The arterial pulses should be palpated for evaluation of rate, rhythm, character, volume, radio-femoral delay,
and condition of arterial wall (presence of arterial cording)
Feel for all peripheral arteries- radial, brachial, carotid, femoral, popliteal, posterior tibial and dorsalis pedis
arteries in both upper and lower extremities
1. Rate and rhythm
Radial artery is commonly used to assess number of pulses per minute and regularity of pulse
Normal pulse rate is 60 to 100 beats per minute
Bradycardia (slow pulse rate) is < 60 beats per minute
Tachycardia (fast pulse rate) is > 100 beats per minute
Technique
. Compress radial artery with pads of index and middle fingers and count pulse rate for one minute
. Determine the rhythm in radial artery; is the rhythm regular, regularly irregular or totally irregular?
Regularly irregular pulse rhythm is often due to ectopic beats, while total irregularity of the pulse is due to atrial
fibrillation
NB: Electrocardiography (ECG) is indicated to clearly characterize the rhythm of arterial pulse
Determine pulse deficit
Pulse deficit is difference in rate of heart beat and peripheral pulse. It is significant when the difference is >10
beats per minute. It is often observed in atrial fibrillation (due to failure in conducting all central beats to
peripheral pulse).

Table 6.3 Abnormalities in arterial rate and rhythm
Pulse character (amplitude and contour)
Pulse character is best assessed in the carotid artery, except in collapsing pulse of aortic regurgitation and pulsus
alternans of advanced heart failure where radial artery is preffered
Technique
. Place your left thumb, or left index and middle fingers on the right carotid artery on the lower third of the neck,
roughly at the level of cricoid cartilage
NB: Avoid pressing on the carotid sinus, which lies at the level of thyroid cartilage. Compression of the carotid
sinus results in reflex bradycardia or hypotension.
Never press both carotid arteries at the same time, which decreases blood flow to the brain and results in
syncope
. Characterize pulse amplitude and pulse wave contour
Amplitude of the pulse correlates reasonably with pulse pressure
. Characterize contour of the pulse wave – speed of upstroke, duration of summit and speed of down stroke
Normally, upstroke is smooth and rapid, the summit is smooth and rounded, and down stroke is less abrupt than
upstroke

. Notice for variation of amplitude from beat-to-beat and with respiration
Arterial pulse wave forms in altered cardiac hemodynamics
a. Hypokinetic pulse
It occurs in hypovolemia, left heart failure, constrictive pericarditis and mitral stenosis
b. Hyperkinetic pulse
Large, bounding pulse usually associated with increased left ventricular stroke volume, wide pulse pressure and
reduced peripheral vascular resistance
It occurs in anemia, patent ductus arteriosus, thyrotoxicosis and pregnancy
c. Anacrotic pulse
Slow-rising pulse with notched wave on upstroke and often seen in aortic stenosis
d. “water-hammer” (collapsing) pulse
Normal rising pulse wave, followed by abrupt decline due to rapid ‘run off’ of blood from arterial tree in
diastole, and usually occurs in aortic regurgitation
e. Bisferiense pulse
Rapidly and forcefully rising upstroke (percussion wave) followed by decline in pressure and then followed by
smaller and slowly rising pulse wave (tidal wave)
Two systolic peaks in bisferiense pulse, and characteristic of mixed aortic regurgitation and stenosis
f. Pulsus alternans
Alternating high and low systolic amplitude despite regular rhythm, which occurs in severely impaired left
ventricular contraction (advanced heart failure with reduced ejection fraction)
g. Pulsus paradoxus
Exaggerated decrease in arterial pulse amplitude during inspiration, which is observed in pericardial tamponade
2. Pulse volume

Pulse volume provides crude indications of stroke volume. It is small in advanced systolic heart failure, but
large in hyperkinetic heart disease
3. Radio-femoral delay
Press both radial and femoral artery at the same time, and notice for pulse delay at femoral artery in comparison
to radial artery. It is usually observed in coactation of the aorta.
4. Condition of the vessel wall
Thickening (cording) or tortuosity of vessel wall (arteriosclerosis) commonly detected in the arteries of elderly
individuals. It doesn’t indicate presence of luminal narrowing due to atherosclerosis.
Table 6.4 Surface markings of the arterial pulses

F) G) H)
Fig 6.4 Techniques of palpating arterial pulses
A) Radial pulse B) Feeling for collapsing radial pulse as in aortic regurgitation C) Brachial pulse medial to
biceps tendon D) Examining carotid pulse with thumb E) Femoral pulse midway between the anterior superior
iliac spine and the pubic tubercle. Notice for checking radio-femoral delay F) Feeling for popliteal pulse G)
Posterior tibial pulse H) Examining dorsalis pedis pulse
Jugular venous pressure (JVP)
The JVP is best assessed from pulsations in the right internal jugular vein, which is directly in line with the
superior venacava and right atrium. The dominant movement of the JVP is inward, coinciding with ‘X’ descent.
Technique:
. Position the patient
Elevate head of bed at 450 to maximize visibility of the jugular venous pulsation in the lower half of the neck
Turn patient’s head slightly away from the side you are inspecting
Use tangential (oblique) lighting and identify the pulsation of internal jugular vein
. Identify the highest point of pulsation of internal jugular vein

. Measure the vertical distance between the highest point of jugular pulsation and sternal angle with a metered
ruler, and then place tongue blade at an exact right angle to the ruler to show venous pulsation and read the
vertical distance on the ruler
The JVP reflects central venous or right atrial pressure and, indirectly, right ventricular function
The normal upper limit is 4 cm vertically above sternal angle. This is about 8-9 cm above right atrium,
corresponding to a JVP of 8-9 cm H20 (7 mmhg)
JVP > 4 cm vertically above sternal angle is considered as elevated JVP
NB: If the internal jugular vein pulsation is not visible, measure the vertical distance of the point above which
the external jugular veins appear to be collapsed from the sternal angle
. Observe the amplitude and timing of the jugular venous pulsation
JVP has 2 or 3 peaks (a, c, v waves) and 2 troughs (x, y waves)
Types of jugular venous waves
‘a’ wave- atrial contraction; ‘c’ wave-bulging of closed tricuspid valve towards the right atrium during right
ventricular systole; ‘x’ wave-atrial relaxation; ‘v’ wave-atrial filling, and ‘y’ wave-atrial emptying
‘a’ wave just precedes S1 and the carotid pulse, the ‘x’ descent seen at the systolic collapse, the ‘v’ wave almost
coincides with S2 and the ‘y’ descent follows early diastole
Hepatojugular reflex is elicted by applying firm continuous pressure over the liver for 15-30 secoonds while
observing the neck veins. Raised JVP in hepato-jugular reflex suggests heart failure.
Positive abdomino-jugular reflex test: An increase in JVP during firm, mid-abdominal compression for 10
seconds followed by a rapid drop in JVP of 4 cm on release of the compression. It suggests elevated left-sided
filling pressure.
Differences between jugular and carotid pulsation

Table 6.5 Differences between jugular and carotid pulsation
A) Inspecting JVP from the side B) Measuring the height of JVP
Fig 6.5 Technique of estimating height of JVP

Fig 6.6 Level of JVP in normal subject A) Supine: Jugular vein is distended, pulsation not visible B) Reclining
at 450: Point of transition between distended and collapsed vein can usually be seen to pulsate just above the
clavicle C) Upright: Upper part of vein collapsed and transition point obscured by sternum
Fig 6.7 Wave forms of JVP and their interpretation
‘a’ wave: atrial contraction, ‘C’ wave: atrial bulging of closed tricuspid valve, ‘V’ wave: atrial filling, ‘X’
descent: atrial relaxation, ‘y’ descent: atrial emptying (rapid ventricular filling)
Abnormal wave forms of JVP
Küssmaul's sign: a paradoxical rise in JVP on inspiration. It is seen in constrictive pericarditis, severe right
ventricular failure, right ventricular myocardial infarction, and restrictive cardiomyopathy
Giant 'a' wave: It occurs in obstruction to right chamber outflow as in tricuspid stenosis, or diminished right
ventricular compliance as in right ventricular hypertrophy or infarction
Cannon ‘a’ wave: It occurs when the right atrium contracts against the closed tricuspid valve. ‘Irregular cannon
‘a’ waves’ are seen in complete heart block and are due to atrioventricular dissociation. ‘Regular cannon ‘a’
waves’ occur during junctional tachycardia, and occasionally in ventricular and supraventricular tachycardias
Prominent 'v' wave: it is an increase venous wave visible on neck during ventricular systole, which is reliable
sign of tricuspid regurgitation, and associated with a pulsatile liver
Common causes of raised JVP
. Cor pulmonale
. Tricuspid valve disease
. Pericardial disease (tamponade/constriction)

. Restrictive cardiomyopathy
. Anterior wall myocardial infarction
. Superior venacaval obstruction
. Hypervolemia (fluid verload)
Precordial examination
The precordium is the area on the front of the chest which relates to the surface anatomy of the heart
Fig 6.8 Surface anatomy of the heart
Technique of precordial examination
Position the patient
. The patient should lie on bed at 450 with enough pillows
Inspection
Is there precordial bulging?
Presence of precordial bulging indicates chronicity of valvular heart disease
Is the precordium active or not?
Active precordium is defined as presence of 2 or more precordial impulses

Quiet precordium is noticed in thick chest wall, massive pericardial effusion or dilated cardiomyopathy
Is the apical impulse visible or not? If visible, determine the location in intercostal space in relation to left mid-
clavicular line (point out with a single finger!)
The apex beat is defined as the most lateral and inferior point at which the cardiac impulse can be palpated
Apical impulse is due to the recoil of heart as blood is ejected
The normal apical impulse is located in the 5th left inter costal space at or medial to left mid-clavicular line
(halfway between the suprasternal notch and left acromioclavicular joint).
Displaced apical impulse is encountered in left ventricular enlargement, chest wall deformity (scoliosis), or
mediastinal shift
Fig 6.9 Location of apical impulse in normal precordium
Palpation
. Localize apical impulse
Types of apical impulses
. ‘Hyperkinetic (forceful) apex beat’ occurs in increased stroke volume eg. Pregnancy, chronic anemia,
thyrotoxicosis, etc…
. ‘Sustained (heaving) apex beat’ occurs in increased pressure overload eg. Aortic stenosis, hypertension, etc…

. ‘Diffuse apex beat’ occurs in increased volume overload eg. Mitral regurgitation, aortic regurgitation, dialted
cardiomyopathy, etc…
. ‘Tapping apex beat’ classically occurs in mitral stenosis
. Localize and characterize point of maximal impulse (PMI) (location, diameter, amplitude, duration)
Character of PMI (point of maximal impulse)
. Location: It is usually located at site of apical impulse under normal circumstance
. Diameter: Discrete, ≤ 2.5 cm in diameter, occupies only 1 interspace
. Amplitude: It is brisk and tapping
. Duration: It occupies < 2/3 of systole
Technique
a. Apical impuse
. Localize the left 2nd intercostal space at lateral to sternal angle
. Count down the interspaces, and point out the most laterally and down ward located cardiac impulse
b. PMI
Technique
. Put the tip of index, middle and ring fingers over the site of PMI
Is it localized or diffuse?
Diffuse PMI occupies >2.5 cm in diameter or occupies more than one interspace
Is it sustained or not?
Sustained PMI occupies more than 2/3 of systole

a) Palpation of cardiac impulse b) localizing apex beat (left lateral position if required)
Fig 6.10 Localizing apical impulse
Heave/Lifts
Heave is a palpable impulse that lifts examiners hand noticeably, and usually noticed in ventricular enlargement
Technique
. Put ulnar border of the hand over left sternal area and look for lift (heave)
Left parasternal heave suggests right ventricular enlargment
Thrill
Tactile equivalent of a murmur, and feels similar to a vibrating mobile telephone
Technique
Palpate the apex, left sternal border, and the neck with palm of examining hand, and feel for thrill as “purring of
a cat”
Timing of the thrill is required (Is it systolic or diastolic?). If the thrill coincides with the carotid pulse, it is
systolic thrill.
Shock (palpable heart sound)
Feel for palpable heart sounds at apex and base of heart
Palpable S2 at pulmonic area occurs in pulmonary hypertension, while palpable S1 at mitral area occurs in mitral
stenosis

Percussion
Percussion adds little to inspection and palpation to demarcate cardiac size
Auscultation
Know your stethoscope!
High pitched sounds such as aortic diastolic murmur, all systolic murmurs, both the heart sounds (S1 and S2),
ejection and non-ejection systolic clicks, and opening snap are heard with the diaphragm firmly pressed against
the chest. Low-pitched sounds such as third (S3) and fourth (S4) heart sounds and mitral diastolic murmur are
heard with the bell loosely applied on the chest wall.
Location of heart valves (mitral, tricuspid, pulmonary and aortic valves)
. Cardiac apex-mitral area
. Left lower sternal border-Tricuspid area
. Left upper sternal border-pulmonic area
. Right upper sternal border-aortic area
Fig 6.11 Location of heart sounds: mitral, tricuspid, pulmonic and aortic area

Heart sounds: S1 (Lub) and S2 (Dub)
First heart sound (S1) corresponds to atrioventricular valves closure, and is best heard at the apex of heart
Second heart sound (S2) corresponds to outlet valves closure, and is best heard at base of heart
. Identifying systole and diastole
Palpate the right carotid artery in the lower third of the neck with your left index and middle fingers, and S 1 falls
just before tha carotid upstroke and S2 follows the carotid upstroke.
Use the diaphragm of stethoscope to listen 1st and 2nd heart sounds
NB: Opening of any normal valve is not audible
Pattern of auscultation
. Start auscultation of the heart starting at either the base or apex, listening first with the diaphragm, then with
the bell of stethoscope
. Notice intensity of heart sounds
Increased intensity of S1 at mitral area occurs in mitral stenosis, tachycardia and pregnancy, while reduced
intensity of S1 occurs in mitral regurgitation and mitral valve prolapse
Increased intensity of S2 at pulmonic area occurs in pulmonary hypertension
. Listen for physiologic splitting of S2 (A2__P2)
It occurs as left ventricle contracts earlier than right ventricle, and best heard at left sternal border (lub-d/dub)
Enhanced physiologic splitting of S2 (A2__P2) occurs in right bundle branch block, pulmonary hypertension,
etc…
Fixed splitting of S2 (A2__P2) occurs in atrial septal defect (ASD)
Reversed splitting of S2 (P2__A2) occurs in left bundle branch block, aortic stenosis, hypertensive heart disease,
hypertrophic cardiomyopathy, etc…
Added heart sounds (S3 and S4)
Third (S3) and fourth (S4) heart sounds are low-pitched sounds, which occur in ventricular diastole

Use the bell of stethoscope to listen 3rd and 4th heart sounds
S3 (lub-dub-dum) corresponds to an abrupt deceleration of inflow across the atriovetricular valve
S4 (da-lub-dub) is noticed in vigorous atrial contraction against increased ventricular stiffness
. Notice for the presence of added heart sound
Physiologic S3 occurs in young adults <40 yrs of age and pregnancy
Pathologic S3 often noticed in anemia, thyrotoxicosis, mitral regurgitation, etc…
S4 is usually pathological and occurs in stiff ventricle due to hypertensive heart disease, aortic stenosis or
hypertrophic cardiomyopathy
Fig 6.12 Heart sounds in relation to electrical activity of the heart
Heart murmurs
Heart murmurs are vibrations set up in the blood stream as a result of turbulent blood flow in the heart and great
vessels
Characterizing the heart murmur
. Location of maximal intensity
. Timing-systolic, diastolic or continuous
. Intensity/grading of the murmur
. Radiation
. Shape (configuration)
. Pitch and quality

Location of maximal intensity
Loudest heard murmur at specific location signify origin of a murmur
eg. Murmur of mitral stenosis is located with maximal intensity at mitral area
Timing
Identify whether the murmur is systolic, diastolic or continuous in comparison to carotid artery upstroke
Technique
. Slightly compress the right carotid artery with left index and middle fingers at the level of cricoid cartilage, and
time the murmur whether systolic or diastolic
Systolic murmurs coincide with carotid artery upstroke, while the diastolic murmurs do not
Systolic murmurs
. Mid-systolic murmur- begin after S1 and stops before S2 Eg. Murmur of aortic stenosis (AS)
. Pansystolic murmur- starts with S1 and stops at S2 Eg. Murmur of mitral regurgitation (MR)
. Late systolic murmur- starts in mid or late systole and persists up to S2 Eg. Murmur of mitral valve proplapse
(MVP)
Fig 6.13 Systolic murmurs: Midsystolic murmur of AS (upper), pansystolic murmur of MR (middle) and late
systolic murmur of mitral valve prolapse (lower)

Diastolic murmur
. Early diastolic murmur- starts after S2 and fades into silence before next S1 eg. Murmur of aortic regurgitation
(AR)
. Mid diastolic murmur- starts after S2 and fade away Eg. Murmur of mitral stenosis (MS)
. Late diastolic (presystolic) murmur- starts late in diastole and continuous up to S1 Eg. Murmur of mitral
stenosis in sinus rhythm
Fig 6.14 Diastolic murmurs: Early diastolic murmur of AR (upper), Mid-diastolic murmur of MS (middle), and
late diastolic or presystolic murmur of MS (lower)
Coninuous murmur
Begin in systole, peak at S2, and continue into all or part of diastole eg. Murmur of PDA (patent ductus
arteriosus)
© Lippincott. Bickley LS, Szilagyi PG. Bates’ Guide to Physical Examination and History Taking 12e
Fig 6.15 Continuous murmur of PDA
Grading of Intensity or loudness of a murmur

The loudness of a murmur reflects degree of turbulence (volume and velocity of flow) and not the severity of the
cardiac lesion
The Levine grading system
Grade I- Faint murmur, heard only with special efforts
Grade II- Quiet but heard murmur
Grade III- Easily heard murmur
Grade IV- Loud murmur, with a thrill
Grade V- Very loud, heard with a stethoscope partly off the chest
Grade VI- Extremely loud, heard with out a stethoscope
Shape (configuration)
Crescendo: Murmur grows louder Eg. Presystolic murmur of MS
Crescendo-decrescendo: Murmur that grows louder and then fall Eg. Mid systolic murmur of AS
Decrescendo: Murmur grows softer and slowly falls Eg. Early diastolic murmur of AR
Plateau: Murmur has same intensity through out Eg. Pansystolic murmur of MR

Fig 6.16 Shape (configuration) of the murmurs: Crescendo murmur (presystolic murmur of MS), decrescendo
(early diastolic murmur of AR), crescendo-decrescendo (midsystolic murmur of AS), plateau (pansystolic
murmur of MR) (from top to bottom)
Radiation
Signify direction of blood flow
Eg. Murmur of MR radiates to left axilla , murmur of AS radiates to neck, murmur of TR radiates to
epigastrium, etc…
Pitch
High, medium or low
Quality
Blowing, harsh, rumbling, musical, etc…

Fig 6.17 Location, timing and configuration of murmurs (CM-continuous murmur, MSM-mid systolic murmur,
EDM-early diastolic murmur, PSM-pansystolic murmur, LSM-late systolic murmur, MDM-mid diastolic
murmur, PSA-presystolic accentuated murmur)
Special techniques
Squatting and standing
Squatting position increases venous return, left ventricular volume and arterial blood pressure, while standing do
the opposite.
1. Squating
. It delays click and shortens murmur of mitral valve prolapse as it results in decreased mitral valve prolapse
. It decreases murmur intensity of hypertrophic cardiomyopathy as it reduces outflow obstruction
. It increases murmur intensity of aortic stenosis as it increases stroke volume
2. Standing
. Early click with longer murmur of mitral valve prolapse as it increases prolapse of mitral valve
. It increases intensity of systolic murmur of hypertrophic cardiomyopathy as it increases outflow obstruction
. It decreases murmur intensity of aortic stenosis as it reduces stroke volume
Isometric hand grip
Systolic murmur of mitral regurgitation, and diastolic murmurs of aortic regurgitation and mitral stenosis get
louder with hand grip exercise
Respiration
Intensity of left-sided murmurs increases with expiration, while intensity of right-sided murmurs increases with
inspiration
Other heart sounds

Pericardial friction rub
High-pitched scratching sound audible at any part of cardiac cycle; heard best at left lower sternal border in
maintained expiration and patient leaning forward. It is observed in acute pericarditis.
Pericardial knock
It is early diastolic sound caused by sudden halt in ventricular filling at diastole
It is observed in constrictive pericarditis
Opening snap
High-pitched, early diastolic, snapping sound best heard at the left sternal border, caused by forceful opening of
stenosed mitral valve by increased left atrial pressure
Ejection systolic clicks
High-pitched sound best heard at aortic or pulmonary area. It is caused by abrupt doming of the abnormal valve
early in systole in congenital aortic stenosis or pulmonary stenosis
Non-ejection systolic clicks
Early systolic high-pitched sound best heard at mitral area. It is caused by prolapse of redundant mitral valve
leaflets during systole in mitral valve prolapse
Venous hum
It is a continuous murmur heard both in systole and diastole, soft in character, heard above the medial third of
clavicle. It arises from the jugular vein commonly in children and young adults, hence, can be obliterated by
pressure on the jugular veins.
Mammary soufflé
Many women have a murmur heard both in systole and diastole during late pregnancy and lactation. These are
secondary to increased blood flow in their breasts. It is best heard in the 2nd and 3rd interspace on either side of
the sternum.

Characteristics of common cardiac valvular lesions
1. Mitral stenosis: Loud S1; early diastolic opening snap; low-pitched, rumbling, mid-diastolic murmur at
cardiac apex with presystolic accentuation in sinus rhythm, and increased intensity of murmur with
exercise and left lateral positioning
Fig 6.18 Murmur of mitral stenosis
2. Mitral regurgitation: laterally displaced apical impulse; muffled S1; S3 sound at apex; medium to high-
pitched, blowing pansystolic murmur at cardiac apex, which radiates to left axilla or base of heart
Fig 6.19 Murmur of mitral regurgitation

3. Aortic regurgitation: ‘Water-hammer’ pulse (Corrigan’s pulse), pistol-shot sounds at femoral artery,
laterally displaced apical impulse; S3 sound at apex; high-pitched, blowing early diastolic decrescendo
murmur at the 2nd left interspace (Erb’s point), which is accentuated by leaning forward and breath held at
expiration; Austin-Flint (mid-diastolic) murmur at the apex owing to preclosure of mitral valve by
regurgitant jet; and functional mid-systolic flow murmur at the A2 area
Fig 6.20 Murmur of aortic regurgitation
4. Aortic stenosis: Anacrotic arterial pulse, sustained apical impulse; faint A2 sound; reversed split (P2 _ A2);
S4 sound at apex; Ejection systolic click in pliable aortic valves; low-pitched, rasping, midsystolic,
crescendo-decrescedo murmur at A2 area, which radiates to the neck (carotid shudder)
Fig 6.21 Murmur of aortic stenosis

5. Tricuspid regurgitation: Prominent V wave (JVP); low to high-pitched, blowing, pansystolic murmur at the
left lower sternal border, which is accentuated by deep inspiration (positive caravello’s sign)
Leg edema
Interstitial tissue absorbs upto 5 litres of fluid (up to 10% weight gain) before pitting edema appears
Pedal and pretibial pitting edema occurs in congestive heart failure, varicose veins and DVT (deep vein
thrombosis)
Ankle edema of cardiac origin is usually symmetrical and worsens in the evening and improves early in the
morning
Technique:
. Gently compress behind the medial malleolus and dorsum of foot in ambulatory subjects, and over the sacrum
in bedridden patients for at least 15 seconds with the thumb. Edema of cardiac origin is symmetrically pitting
(the skin is indented and only slowly refills)
Grading of edema
a. Grading by body sites
Grade 1- pedal and pretibial edema
Grade 2- Edema involving the leg and thigh
Grade 3- Edema involving the abdominal wall and over the sacrum
Grade 4- Anasarca (generalized edema including serosal fluid accumulation)
b. Grading by time to refill the pitting edema
Grade 1- Refill time for pitting edema takes < 5 seconds
Grade 2- Refill time for pitting edema takes 5-10 seconds
Grade 3- Refill time for pitting edema takes 10-15 seconds
Grade 4- Refill time for pitting edema takes > 15-20 seconds

CHAPTER SEVEN
Gastrointestinal system
Learning objective
1. Mention main symptoms in gastrointestinal disease

2. List common causes of chronic diarrhea
3. Show techniques of abdominal examination
4. Perform examination of palpable abdominal swelling
History taking of the gastrointestinal system
Patients with gastrointestinal problem present with one or more of the following symptoms
Dysphagia
Odynophagia
Heart burn (dyspepsia)
Nausea and vomiting
Abdominal pain
Abdominal distension
Diarrhea
Constipation
Hematemesis
Melena
Weight loss
Jaundice
Inguinal swelling/lump
Dysphagia

Dysphagia is difficulty in swallowing
Ask:
. Does food or drink stick when you swallow (dysphagia)? If Yes, then
. How long? Recent or gradual in onset
. At what level does food stick?
. Is the dysphagia for solids or liquids or both?
. Is dysphagia intermittent or progressive?
. Any regurgitation or reflux of food or fluid?
. Any associated pain (odynophagia), heart burn or weight loss?
Difficulty in initiating swallowing with fluid regurgitation into the nose, or chocking on trying to swallow
indicates pharyngeal dysphagia due to neurologic disorders (motor neurone disease, myasthenia gravis, stroke,
etc…)
Food sticking in the lower retrosternal area indicates lower esophageal obstruction (stricture, cancer, etc…)
Swallowing difficulty more to liquids than solids suggest esophageal motor disorders (achalasia, diffuse
esophageal spasm)
Progressive dysphagia early to solids, and then to liquids indicates esophageal stricture or cancer. Longstanding
dysphagia with heartburn and no weight loss favors esophageal stricture. Recent onset dysphagia without reflux
symptoms and accompanied by weight losss favors esophageal cancer.
Intermittent dysphagia within the first few swallowing of food occurs in diffuse esophageal spasm
Causes of dysphagia
1. Mechanical
a. Extrinsic
. Retrosternal goiter
. Mediastinal masses
b. Intrinsic
. Esophageal stricture

. Esophageal cancer
. Esophageal web
2. Neuromuscular motility disorders
. Achalasia
. Diffuse esophageal spasm
. Scleroderma
. Neurologic diseases: Stroke, motor neuron disease (ALS), myasthenia gravis
Odynophagia
Odynophagia is pain during swallowing
Causes of odynophagia
. Infectious esophagitis- herpetic ulcers, cytomegalovirus ulcers, and esophageal candidiasis in HIV infected
patients
. Esophageal peptic ulceration
. Chemical esophagitis eg. caustic soda damage
. Drug allergies Eg. Sulfonamides, cytotoxic chemotherapeutics, etc…
. Immunologic dermatological diseases eg. pemphigus vulgaris, dermatitis herpetiformis, etc…
Dyspepsia (heart burn)
Substernal burning pain or indigestion
Classifying dyspepsia
. Reflux-like dyspepsia (heartburn-predominant dyspepsia)
. Ulcer-like dyspepsia (epigastric pain relieved with food or antacids)
. Dysmotility-like dyspepsia (belching, bloating and earily satiety)

“Alarm symptoms” in patients with dyspepsia require endoscopy to exclude esophageal and gastric cancer
. Difficulty of swallowing
. Intractable vomiting
. Evidence of GI bleeding (hematemesis or melena)
. Early satiety
. Weight loss
. Presence of anemia
. Palpable gastric mass
. Family history of gastric cancer
Nausea and vomiting
Nausea is involuntary effort to vomit
Vomiting is expulsion of gastric contents through the mouth
Describe about mode of onset, timing, content of vomitus, and projectile or not
. Mode of onset (acute or chronic)?
Acute onset occurs in food poisoning, raised ICP or bowel obstruction
Chronic onset occurs in pregnancy, medications (digoxin, dopamine agonists, chemotherapy), bowel motor
diseases (eg. gastroparesis in diabetics) or pyloric stenosis due to scarred peptic ulcer disease
. Timing of vomiting (related to meal time, early morning or late evening)?
Vomiting after hours of meal is typical of gastric outlet obstruction or gastroparesis.
Early morning vomiting before meal occurs in pregnancy or raised ICP
. Content of vomitus (bile-stained, blood-stained or faeculent)?
Vomiting of bile-stained material occurs in obstruction distal to pylorus.
Vomiting of blood suggests upper gastrointestinal bleeding such as bleeding peptic ulcer, variceal bleeding, or
erosive gastritis.
Vomiting of faeculent material with abdominal distension and colic suggests bowel obstruction

. Is the vomiting projectile or not?
Projectile vomiting of non-bilious, voluminous, old food suggests gastric outlet obstruction (GOO).
Abdominal pain
Patterns of abdominal pain
a. Visceral pain
It occurs when hollow abdominal organs such as intestine and biliary tree forcefully contract or distended or
stretched. It is poorly localized, and typically sited near the midline at levels varied from structure involved.
b. Parietal pain
It originates from inflamed parietal peritoneum. It is severe, steady, aching and localized over the structure
involved.
c. Referred pain
It is felt at distant sites of the structure involved, possibly explained by innervation at approximately same spinal
levels. It is usually localized, intense and seems radiated from the structure involved.
NB: Pain from foregut (stomach, pancreas, hepatobiliary structures) localizes to epigastric area, pain solely from
midgut (small bowel and proximal large colon) is felt periumbilical, and pain from hindgut (large bowel)
localizes to suprapubic area.
Characterize abdominal pain- Site/location, mode of Onset, Character/type of pain, areas of Radiation,
Associated symptoms, Timing, Exacerbating and relieving factors, and Severity (SOCRATES)
Common causes of abdominal pain
. Acute appendicitis . Acute cholecystitis . Acute pancreatitis
. Acute diverticulitis . Peptic ulcer disease . Intestinal obstruction
. Renal colic (calculi) . Acute intestinal ischemia

Fig 7.1 Abdominal pain and organ of origin
Table 7.1 Common causes of abdominal pain
Abdominal distension

Causes of abdominal distension
5 F’s: Flatus, faeces, fluid, fetus, fat, functional (bowel obstruction, ascites, pregnancy, obesity, irritable bowel
syndrome)
Causes of Ascites (excessive fluid in peritoneal cavity)
. Hepatic cirrhosis with portal hypertension
. Intra-abdominal malignancy with peritoneal seeding (peritoneal carcinomatosis)
. Bacterial peritonitis eg. S.pneumoniae, E.coli, M.tuberculosis
. Chemical peritonitis eg. Acute pancreatitis, biliary leak
. Hypoproteinemia eg. Nephrotic syndrome, protein-losing enteropathy
. Budd-Chiari syndrome (Hepatic vein occlusion)
. Constrictive pericarditis
Diarrhea
Passage of watery or loose stool > 3 times per day, or passage of large amount of stool >300 gram per day
Describe about mode of onset and duration, frequency of diarrhea/day, character (watery, loose stool, bloody,
mucoid), associated symptoms (thirst, oliguria)
Ask:
. Is the diarrhea acute, persistent or chronic?
. Is it watery, unformed or semiformed?
. Is the stool less frequent and voluminous as in small bowel disease?
. Is the stool of frequent and less in volume, and associated with tenesmus as in large bowel disease?
. Is there blood or mucus associated in stool?
. Is there past medical history of GI surgery, medical diseases?
. Is there family history of GI disorder? Eg. Gluten enteropathy, Crohn’s disease, etc…

. Are there symptoms of systemic disease? Eg. anorexia, weight loss, etc…
Classification of diarrhea based on duration
. Acute diarrhea (<2 weeks)
. Persistent diarrhea (2-4 weeks)
. Chronic diarrhea (> 4 weeks)
Acute diarrhea
Almost all cases of acute diarrhea are caused by infectious agents like E.coli, Salmonella spp, Shigella spp,
Campylobacter spp, Rotavirus, Norovirus, etc…
Traveller’s diarrhea: Travellers who toured to endemic area develop traveller’s diarrhea, most commonly caused
by Entrotoxigenic E.coli, Campylobacter spp., Shigella spp. and Salmonella spp.
Chronic diarrhea
It warrants evaluation to exclude serious underlying pathology
Most common causes of chronic diarrhea are non-infectious
Causes of chronic diarrhea
1. Secretory causes (voluminous diarrhea and persists with fasting)
. Hormone-producing tumors (colorectal villous adenoma, VIPoma)
. Exogenous and endogenous laxatives
2. Osmotic causes (voluminous diarrhea and disappears with fasting)
. Osmotic laxatives
. Disaccharidase deficiency Eg. Lactose intolerance
3. Steatorrheal causes
Steatorrhea is presence of >7 gm of fat in a 24-hr stool collection

Steatorrheal stool is characterized as fatty, pale colored, smelly voluminous stool that float in a toilet bowel and
more difficult to flush away
Sites of malabsorption includes
. Intra-luminal eg. Pancreatic exocrine deficiency, bacterial overgrowth syndrome, chronic liver disease
. Mucosal eg. Celiac disease, tropical sprue, etc…
. Post-mucosal eg. Primary and secondary lymphatic obstruction
4. Exudative causes (frequent, small volume of stool and may be associated with blood or mucus)
. Non-infectious causes-Inflammatory bowel disease (IBD), diverticulitis, colorectal cancer
. Infectious causes- Invasive viral, bacterial and parasitic infections, intestinal tuberculosis
Constipation
Normal frequency of bowel movement ranges from three times daily to once every three days.
Constipation is persistent, difficult, infrequent or seemingly incomplete defecation. It is defined as passage of

formed stool <3 times per week
Constipation is due to impaired colon motility, mechanical bowel obstruction, impaired rectal sensation with no
normal ‘call to stool’ or anorectal dysfunction impairing the process of evacuation (anismus)
Ask:
. Is it recent onset or chronic (life long)?
. How often the bowels empty each week?
. How much time is spent straining at stool?
. Is there associated abdominal pain, rectal bleeding, or anal pain on defecation?
. Has there been any change in drug therapy?
Causes of constipation
1. Recent onset
. Colonic obstruction- colonic cancer, colonic stricture, colonic diverticula
. Anal sphincter spasm- anal fissure, painful haemorrhoids

2. Chronic onset
. Inflammatory bowel disease
. Medications (codeine, antidepressants, aluminium or calcium antacids, iron salts)
. Endocrinopathies- hypothyroidism, hypercalcemia
. Neurologic diseases- Parkinsonism, spinal cord injury
. Psychiatric diseases-depression, eating disorders
Hematamesis
Hematemesis is vomiting of frank blood
It can be painless, fresh, and red as in variceal bleeding; or dark-brown resembling coffee ground matter with
abdominal pain as in bleeding peptic ulcer disease.
It usually results from bleeding in the gastrointestinal tract above the ligament of Treiz (duodenojejunal flexure)
Describe mode of onset; duration, frequency and severity of bleeding
Ask:
. Did the vomitus contain fresh blood or coffee-ground matter? Painless, voluminous, fresh blood loss favors
variceal bleeding, while vomiting of coffee ground matter associated with abdominal pain occurs in peptic ulcer
disease
. Is there history of aspirin/NSAIDs, alcohol or corticosteroid ingestion?, All are risk factors for peptic ulcer
disease?
. Was the hematemesis preceded by violent coughing or vomiting as in Mallory-Weiss tear?
. Is there preceding peptic ulcer disease or liver disease?
. Is there clinical ‘alarm symptoms’ signifying gastric cancer?
Major causes of hematemesis
. Peptic ulcer disease
. Esophageal varices
. Mallory Weiss tear

. Gastro-duodenal erosions
. Erosive esophagitis
. Gastric cancer
Melena
Tarry, foul smelling stool indicates bleeding above ileo-cecal valve
Melena results with as low as 60 ml of bleeding in the gastrointestinal tract
Hematochezia (rectal bleeding)
Passage of bright red or maroon blood from lower gastrointestinal bleeding
It uually occurs to bleeding from the sigmoid colon, rectum or anal canal
Common causes of rectal bleeding includes hemorrhoids, anal fissure, colorectal polyps, colorectal cancer,
inflammatory bowel disease, ischemic colitis, diverticular disease or vascular malformation
Weight loss
Quantify weight loss in kg, over how long?
Clinically significant weight loss is defined as ≥ 5% body weight loss over 6-12 months
Usual causes of weight loss
. Lack of food intake (with associated symptoms of anorexia, vomiting or dysphagia)
. Malabsorption syndrome
. Systemic effects due to cancer, tuberculosis, inflammatory bowel disease, etc…
Jaundice
Yellowish discoloration of the skin and mucus membrane resulting from the deposition of bilirubin
The presence of scleral icterus indicates a serum bilirubin level ≥ 2.5 mg/dl (normal serum bilirubin level < 1.0
mg/dl)

Causes of hyperbilirubinemia
a. Overproduction of bilirubin
b. Impaired uptake, conjugation or excretion of bilirubin
An increase in unconjugated bilirubin in serum results from either overproduction, impairment of uptake or
conjugation of bilirubin
An increase in conjugated bilirubin is due to decreased excretion into the bile ductules or back leakage of the
pigment
Causes of unconjugated (indirect) hyperbilirubinemia
. Hemolysis- hereditary or acquired hemolytic disorders
. Inherited disorders- Gilbert’s syndrome, Crigler-Najjar syndrome
Causes of conjugated (direct) hyperbilirubinemia
a. Hepatocellular Pattern
ALT/AST increase out of proportion to alkaline phosphatase
. Viral hepatitis
. Drug-induced hepatitis
. Autoimmune hepatitis
. Alcoholic hepatitis
b. Cholestatic pattern
Alkaline phosphatase increase out of proportion to ALT/AST
. Intrahepatic cholestasis eg. Primary biliary cirrhosis, cholestasis of pregnancy, vanishing bile duct
syndrome
. Extrahepatic cholestasis: Greenish-yellow discolored sclera, pruritis with excoriation marks and clay-
colored stool
Eg. Primary sclerosing cholangitis, choledocholithiasis, cholangiocarcinoma, biliary duct stricture, ampullary
stenosis, pancreatic head tumor

Fig 7.2 Metabolism of bilirubin: Uptake, conjugation and excretion of bilirubin: Increased haemolysis (1)
overwhelms the hepatocytes' ability to conjugate bilirubin leading to increased serum levels of unconjugated
bilirubin. Low levels of glucuronyl transferase (2) (e.g. Gilbert's disease) cause decreased conjugation.
Hepatocellular dysfunction (3) causes decreased uptake, conjugation and excretion with increases of
unconjugated bilirubin and conjugated bilirubin. Post-hepatic obstruction (4) from stones or tumor prevents
passage of bilirubin through the bile ducts into the bowel, leading to increased serum levels of conjugated
bilirubin
Groin swelling/lumps
Hernias are common causes of groin lumps and frequently present with dull, dragging discomfort (rather than
acute pain), which is often precipitated or exacerbated by straining due to chronic constipation, chronic cough,
micturition problem, or heavy manual labour.

Examination of the abdomen
. Good lighted room and coach is required
. Make the patient comfortable in the supine position
. The patient should keep the arms at the sides
. Exposure of the abdomen from the xiphoid process to the mid thigh; covering the genitalia is required
. The examiner should have warm hands, warm stethoscope and short finger nails
. Approach the patient slowly and avoid quick, unexpected movements
. If the patient is not at ease, distract her/him with conversation
. Monitor your examination by watching the patient’s face for any sign of discomfort
Fig 7.3 Nine regions of the abdomen: 1 and 3: right and left hypochondrium; 2: epigastrium; 4 and 6: right and
left lumbar; 5: umbilical; 7 and 9: right and left iliac; 8: hypogastrium or suprapubic

Fig 7.4The four quadrants of the abdomen
Inspection
. Proper positioning of the patient
Supine position of the patient on a coach with proper exposure of the abdomen
. Look for symmetry of the abdomen and flank fullness by standing at bed end, facing the patient
. Look for shape of the abdomen. Is it scaphoid, flat or distended?
. Look for contour of the umbilicus
Normally the umbilicus is slightly retracted, inverted with horizontal slit
. Look for abdominal movement with respiration
Normally there is gentle rise in the abdominal wall during inspiration and fall during expiration
Markedly diminished or absent abdominal movement (silent abdomen) signify generalized peritonitis
. Look for visible peristalsis
Vigorous peristalsis of the abdomen signify pyloric stenosis or bowel obstruction
. Look for scars and striae
Striae are wrinkled linear marks due to gross stretching of the skin
eg. Striae alba or atrophica in ascites, striae gravidarum in pregnancy, purple striae in Cushing’s syndrome or
prolonged steroid use

. Look for prominent superficial veins
Thin veins over the costal margin usually has no significance
If there are distended veins over the abdomen, determine direction of blood flow (towards or away from the
umbilicus)
Distended abdominal wall veins which are draining away from the umbilicus suggests presence of portal
hypertension
. Look for abdominal wall pigmentation eg. Linea nigra in pregnancy; erythema ab igne (due to application of
heat on the abdomen wall for chronic pain)
. Look for hernial sites
Support and lift patient’s head with the shoulder with your left arm and let him cough repeatedly while
observing sites of hernia (Notice for cough impulse for swelling at hernia sites)
Sites of hernia: Incisional hernia at surgical scar site, umbilical and periumbilical hernia at or around the
umbilicus, lumbar hernia in lumbar region, and inguinal and femoral hernia in groin region
Fig 7.5 Prominent veins of the abdominal wall: Thin veins over the costal margin occurs in normal individuals;
while caput medusae is suggestive of portal hypertension, and indicates anastomosis between portal and
systemic veins

a) Two fingers are placed firmly on the vein b) The second finger is moved along the vein to empty it of blood
and keep it occluded c) The second finger is removed but the vein doesn’t refill d) At repeat testing and
removing the first finger, refill occurs, indicating direction of venous flow
Fig 7.6 Determining direction of blood flow in distended abdominal wall veins
Palpation
Superficial palpation
Ask the patient if there is abdominal area which is tender? If there is tender abdominal area, start palpation far
away from the tender site and palpate the tender site at last. If there is no tenderness at any site, start at left lower
quadrant, and move quadrant-by-quadrant in clock-wise or anti-clockwise direction. Observe the patient’s face
for any sign of discomfort during palpation.
. Mould your relaxed and warm hand to the abdominal wall. Don’t hold it rigid and avoid sudden poking with
the finger tips
. Gently palpate the abdomen quadrant-by-quadrant for abdominal tenderness, palpable abdominal
masses/organs and abdominal resistance
Abdominal wall tenderness Vs deep visceral tenderness
. Raise the head and shoulder of the patient from supine position
. Persisting tenderness in abdominal wall origin, whereas tenderness in deeper visceral lesion decreases
Deep palpation

Performed to delineate abdominal mass or confirm presence of organomegaly (enlarged liver, spleen or kidney)
. Check for guarding, rigidity and rebound tenderness
Presence of guarding, rigidity and rebound tenderness indicate generalized peritonitis
Guarding is voluntary contraction of the abdominal wall
Rigidity is involuntary reflex board-like rigidity of abdominal wall muscle overlying an inflamed viscus
Rebound tenderness is eliciting pain while the examiner quickly withdraws his palpating hand
Ballottement
This is a maneuver performed to identify an organ or mass in the presence of massive ascites.
Technique
. Strighten and stiffen the fingers of your balloting hand
. Place the balloting hand on the distended abdomen, and make a brief jabbing movement towards the
anticipated structure
. The quick movement displaces the fluid, and the finger tips briefly touch the surface of the structure
Abdominal organ palpation
Spleen
The spleen has to be 2-3 times its normal size to be palpable. Enlargement of the spleen takes place in a superior
and posterior direction before it becomes palpable; once palapable, the direction of growth is towards the
umbilicus (along the splenic growth line)
. Start palpating from the right iliac fossa and move diagonally upward towards the left hypochondrium until
you reach the left costal margin
. Ask the patient to breathe in deeply and press in with the fingers of examining right hand beneath the costal
margin
If not palpable, turn the patient to the right side (with right leg extended and left leg flexed at hip and knee joint)
, and palpate for the spleen with right hand while supporting the left costal region with left hand

Characteristics of enlarged spleen (splenomegaly)
. Moves with respiration
. Direction of growth along the splenic growth line (towards the umbilicus)
. Palpable splenic (medial) notch
. Unable to go beneath the left costal margin
. Not bimanually palpable
If there is splenomegaly, characterize size (along splenic growth line), tenderness, consistency (soft, firm, hard),
surface (smooth, nodular) and edge (sharp, round)
Causes of massive splenomegaly
(7+ cm along splenic growth line)
. Hyperreactive malarial splenomegaly
. Hepatosplenic schistosomiasis
. Kala-azar (Visceral leishmaniasis)
. Chronic myeloid leukemia
. Non-Hodgkin’s lymphoma
. Thalassemia major
. Gaucher’s disease

Fig 7.7 Direction of splenic growth line
Liver
. Start palpating from right lower abdomen towards the right hypochondrium until you reach the costal margin
or feel the liver edge. The liver edge may be felt against the radial border of index finger
. Ask the patient to breath in deeply when you reach costal margin to feel for liver edge
. Repeat the maneuver from lateral to medial regions to trace the liver edge
The liver edge is often palpable in normal individuals
. Characterize the enlarged liver - size (below the right costal margin), tenderness, consistency, surface, edge
(Total vertical liver span is determined by palpation and percussion)
A) Palpation of the liver B)Palpation of the spleen
Fig 7.8 Technique of palpation of the liver and spleen
Kidney
Left kidney
. Place the left hand posteriorly in the left loin and right hand anteriorly in the left lumbar region
. Ask the patient to take deep breathe in, and press the left hand forwards and the right hand backwards, upwards
and inwards

The left kidney is often not palpable
Right kidney
. Place the right hand horizontally in the right lumbar region anteriorly with left hand placed posteriorly in the
right loin
. Ask the patient to take a deep breath in, and press the left hand forwards and the right hand backwards,
upwards and inwards
The lower pole of the right kidney is often palpable in healthy individuals
Enlarged kidney is bimanually palpable
A) Palpation of right kidney B) Palpation of left kidney
Fig 7.9 Technique of palpation of right kidney (A) and left kidney (B)
Gall bladder
The gall bladder is palpated the same as the liver
The normal gall bladder can’t be felt
When it is distended, it may be palpated as a firm, smooth or globular swelling with distinct border, just lateral
to the edge of rectus muscle near the tip of ninth costal cartilage
The upper border merges with the lower border of the right lobe of the liver or disappears beneath the right
costal margin
Murphy’s sign indicates acute cholecystitis
. Ask the patient to breathe in deeply, and palpate for the gall bladder in the normal way

. The breathing stops with a gasp at the end of inspiration as the inflamed distended gall bladder is felt with
palpating hand
Courvoisier’s law signify presence of jaundice with palpable gall bladder, which makes common bile duct
obstruction by gall stone as an unlikely cause
© Elsevier. Swash & Glynn. Hutchison’s Clinical Methods 22nde
Fig 7.10 Enlarged gall bladder: The fundus and part of body of enlarged gall bladder can be palpated
Urinary bladder
Normally, the urinary bladder is not palpable
Distended urinary bladder due to retention of urine is characterized by symmetric swelling in the supra pubic
region below the umbilicus and arising out of the pelvis
Supra pubic swelling is also caused by gravid uterus, uterine myoma and ovarian cyst

© Elsevier. Swash & Glynn. Hutchison’s Clinical Methods 22nde
Fig 7.11 Physical signs in retention of urine: Smooth, firm and regular swelling arising out of the pelvis which
one cannot 'get below', and dull in percussion note
Examination of palpable abdominal swelling
Palpable abdominal swelling is characterized by site/location, size/shape, surface (smooth or otherwise),

consistency (soft, firm or hard), tenderness (if so, severity), edge (sharp or rounded), mobility (capable of being
moved by palpation), movement with respiration (free or restricted), bimanual palpation (ballotable), and
pulsation (if present, expansile or transmitted).
Site/location
Is it abdominal wall swelling or intra-abdominal swelling?
. Feel the swelling while the patient lifts her/his head with shoulder to tense the abdominal wall
Prominent, protruded swelling indicates abdominal wall mass, while the swelling hides behind is intra-
abdominal mass
. Notice the regions occupied by the swelling
eg. Swelling in the right hypochondrium most probably arises from the liver, right kidney, hepatic flexure of
colon, and gall bladder
If the swelling occupies the upper abdomen, is it possible to ‘get above it’?
If one can’t ‘get above it’ hepatic, splenic or gastric origin should be suspected

If the swelling occupies the lower abdomen, is it possible to ‘get below it’?
If one can’t ‘get below it’ the swelling probably arises from the urinary bladder, uterus, ovary or upper rectum
Size and shape
Determine length, width and depth of the abdominal swelling
Characterize the surface, edge and consistency of the abdominal swelling
. Hard, nodular, irregular in outline mass is more likely to be malignancy
. Solid, tender, ill-defined mass is more likely to be inflammatory
. Regular round, smooth, tense swelling is more likely to be cystic
Mobility
Swelling arising from the liver, spleen, gall bladder and stomach moves down ward during inspiration
Swelling arising from the bowel, mesentery and omentum are not usually influenced by respiratory movement
Side-to-side movable lower abdominal swelling favors swelling of uterine origin (gravid uterus, uterine myoma)
Attachment
Fixed swelling usually signify mass of retroperitoneal origin or abdominal tumor with extensive spread to
abdominal wall
Pulsatility
Does the pulsation come from the swelling or is it transmitted?
Pulsatile and expansile abdominal swelling favors abdominal aortic aneurysm

Fig 7.12 Abdomen showing palpable abnormalities
Percussion
Technique
Put the left pleximeter finger of the examiner on the abdomen in horizontal position and percuss with the right
plexor finger from upper to lower abdomen and sideways of the abdomen
The normal abdomen is tympanitic in percussion note
Percuss if there is enlarged organ or any swelling in the abdomen
Liver
Total liver span (TLS) is usually mapped out by percussion
Percussion will detect the upper border of normal liver at about the 5th intercostal space along right mid-
clavicular line, and the dullness extends down to the lower border at the right subcostal margin. TLS under
normal condition is 10 ± 2 cm.
Spleen

Dullness of normal spleen extends from the left lower ribs into the left subcostal margin
Percussion for splenic dullness
Techniques
Nixon’s method
. Ask the patient to turn to the right side
. Begin percussing at the lower level of pulmonary resonance along the left posterior axillary line and proceed
diagonally along a perpendicular line towards the lower mid anterior costal margin
The upper border of dullness is normally 6-8 cm above the left costal margin
Dullness > 8cm suggests splenomegaly
Castell’s method
. Ask the patient to be on supine position
. Percuss the left intercostal space at 8th or 9th interspace along left anterior axillary line during full inspiration
and expiration
Dullness on full inspiration suggests splenomegaly
Traube’s method
. Ask the patient to be on supine position with the left arm slightly abducted
. Locate borders of Traube’s space: Superiorly 6th rib, laterally left mid axillary line, inferiorly left costal margin
. Percuss from medial to lateral margins in normal breathing. It usually produces normal resonant sound at
traube’s space
Dullness to percussion at Traube’s space suggests splenomegaly
Detection of ascites
Shifting dullness
The cardinal sign created by ascites
Technique
. Position the patient in supine

. Place your fingers in the longitudinal axis on the midline near the umbilicus
. Percuss from midline out to the flanks
. Note any change from tympanitic to dullness
. Keep your finger on the site of dullness in the flanks and ask the patient to turn onto his opposite side
. Pause for at least 10 seconds to allow for any peritoneal fluid to gravitate, then percuss again
. Shifting dullness is present if the area of dullness note is changed to tympanitic note
Peritoneal fluid of 1500ml usually elicits shifting dullness
Fig 7.13 Shifting dullness in ascites
Fluid thrill
Technique
. Position the patient in supine
. Place the palm of your left hand flat against the left side of the abdomen
. Ask an assistant to place the ulnar border of their hand on the midline of the abdomen
. Flick a finger of your right hand against the right side of the abdomen
. Fluid thrill is present if you feel for a ripple (wave) against your left hand

Fig 7.14 Technique of eliciting fluid thrill
Puddle sign
Puddle sign is elicited to detect the presence of mild ascites around 250 ml.
Technique
. Place the patient in knee-elbow position
. Percuss the abdomen around umbilical area
. Dullness to percussion around the umbilical area is evidence of ascites.
Clinical features of markedly distended abdomen
Gross ascites
. Flank fullness and dullness in flanks
. Umbilicus everted
. Shifting dullness and fluid thrill present
Large ovarian cyst
. Resonant in flanks

. Umbilicus vertical and drawn up
. Swelling arising out of the pelvis which one can’t get below
Intestinal obstruction
. Tympanitic to percussion
. Increased and noisy bowel sound
Fig 7.15 Cause of markedlydistended abdomen
Auscultation
Auscultation of the abdomen is for detecting bowel sounds, succession splash, vascular bruits and friction rub
Bowel sounds
Bowel sounds heard with unaided ear are called borborygmi.
Technique
. Place the stethoscope just to the right of the umbilicus, and listen to low-to-medium pitched gurgles interposed
by high pitched noise or tinkle.
. Note the bowel sounds frequency and character
Normal sounds consist of clicks and gurgles with a frequency of 5-30 per minute

Listen for up to 2 minutes before concluding that the bowel sounds are absent
Increased frequency of bowel sounds occur in diarrhea, gastrointestinal bleeding, and mechanical intestinal
obstruction
Reduced or absent bowel sounds occur in paralytic ileus and generalized peritonitis
Succession splash
Tachnique
. Place the patient in supine position
. Place the diaphragm of the stethoscope over the epigastrium (help may be needed!)
. Place your hands on the lumbar region of the abdomen, and roll the patient briskly from side to side
. Splashing sound is heard if the stomach is distended with fluid
. Positive test is confirmed if there is splashing sound after ‘4 hours’ of meal intake
Positive succession splash indicates gastric outlet obstruction or paralytic ileus
Vascular bruits and friction rub
Technique
. Place the stethoscope above and right/left of umbilicus for renal bruits (renal artery stenosis), over the enlarged
liver for bruits (hepatocellular cancer/acute alcoholic hepatitis), and over the abdominal mass (malignancy,
aneurysm).
. Place your stethoscope over the enlarged spleen for friction rub (perisplenitis/splenic infarction 20 to chronic
myeloid leukemia, sickle cell anemia, infective endocarditis, or after splenic puncture), and over the liver for
friction rub (hepatocellular carcinoma, sickle cell anemia, liver abscess, or after liver pucture for biopsy)

Table 7.2 Common Causes of ‘Acute Abdomen’

Patient who presented with swelling (lump) in the groin
Technique
In supine position
. Place the patient in supine position
. Lift the patient’s head with the shoulder and ask him to give loud cough
. Feel with hand for any impulse at groin area
Inguinal swelling with positive cough impulse suggests hernia
In standing position
. Ask the patient to stand in front of you
. Look at the groin lump and note if it extends into the scrotum
. Feel for an impulse of the lump after the patient gives loud cough
Inguinal swelling with positive cough impulse suggests hernia
. Is the groin lump inguinal or femoral hernia?
. Determine relationship of hernia sac to the pubic tubercle (bony prominence 2 cm from midline on suprapubic
crest)
. Gently push upwards from beneath the neck of scrotum with the index finger to reach for pubic tubercle
In inguinal hernia, hernia sac passes medial to and above the index finger placed on the pubic tubercle
In femoral hernia, the hernia sac is lateral to and below the index finger placed on the pubic tubercle
. Notice for content of hernial sac
. If omentum, if feels firm and doughy in consistency
. If bowel, it tends to gurgle, compressible and soft in consistency
. Is the hernia reducible or non-reducible?

. Place the patient in supine position and ask the patient to reduce the hernia himself (to confirm for you!)
. Is it direct or indirect inguinal hernia?
. Direct hernia tends to bulge straight out through the posterior wall of the inguinal canal
. The lump with an impulse travelling obliquely down along the inguinal canal is indirect inguinal hernia, and it
is controlled by placing one finger over the deep inguinal ring (over the mid inguinal point)
Fig 7.16 Sites of inguinal and femoral canal

Fig 7.17 Technique of examining inguinal hernia
Fig 7.18 Direct and indirect inguinal hernias
Differential diagnosis of inguinal hernia
. Femoral hernia
. Hydrocele (able to ‘get above’ the swelling)
. Epididymal cyst
. Undescended or ectopic testis (empty scrotum on the affected side)
. Inguinal lymphadenopathy (LAP)
Differential diagnosis of femoral hernia
. Inguinal hernia
. Lipoma in femoral triangle
. Aneurysm of the femoral artery (expansible pulsation positive)
. Sapheno-varix
. Psoas abscess
. Inguinal lymphadenopathy

Digital rectal examination
Abdominal examination without per digital rectal examination is incomplete!
Technique
. Explain what you are going to do and ask for permission to proceed (be gentle during PR examination!)
. Position the patient to lie on left lateral side with buttocks at the edge of the coach, knees drawn up to the chest
. Put on gloves and spread the buttocks apart
. Inspect for perianal areas for excoriations, inflammation, ulcers and lumps
. Lubricate your gloved index finger, and gently insert your index finger tip into the anal canal in a direction
pointing toward the umbilicus
Notice for sphincter tone of the anus, tenderness, induration, irregularities or nodules
. Insert your finger into the rectum as far as possible
. Rotate your finger to palpate the rectal surface for nodules, irregularities or induration
. Identify the uterine cervix in women and prostate in men
. Examine the prostate gland to identify its lateral lobes and the medial sulcus
. Characterize the size, shape, tenderness and consistency of the prostate (normal prostate is rubbery and non
tender)
. Gently withdraw your finger and wipe the patient’s anus
. Look for blood staining of fecal matter on the glove

Table 7.3 Indications for digital rectal examinations (PR examination)
A) Left lateral position for digital rectal examination B) Correct method of inserting index finger
Fig 7.19 Technique of digital rectal examination

Fig 7.20 Examination of the rectum. Insertion of the finger (A and B); Examining the rectum, and identify the
cervix in females (C); Examining the rectum, and identify the prostate in males (D)

CHAPTER EIGHT
Nervous system
Learning objective
1. Mention main symptoms in nervous system disorders

2. Assess level and content of consciousness
3. Show techniques of cranial nerves and motor system examination
4. Identify the location of lesion in a patient presenting with neurologic deficit
5. Identify clinical features of upper motor neuron lesions from lower motor neuron lesions
History taking of the nervous system
Major symptoms in nervous system
. Headache
. Cognitive disturbance
. Difficulty of speech (dysphasia/aphasia)
. Loss of consciousness
. Difficulty in vision, hearing, swallowing
. Weakness of extremity
. Abnormal body movement
. Bladder or bowel dysfunction (urinary retention or incontinence/ fecal impaction or incontinence)
. Abnormal sensory symptoms
Headache
Causative factors for headache
. Spasm, inflammation or trauma to cranial or cervical muscles
. Meningeal irritation and increased intracranial pressure

. Distension, traction, or dilation of intracranial or extracranial arteries
. Traction or displacement of large intracranial veins or their dural envelope
. Activation of brain stem structures (dorsal raphe of the midbrain)
Important clues regarding history of headache
. Location and type of headache
. Mode (sudden vs insidious) and course (intermittent or persistent) of onset
. Frequency, intensity, duration of headache episodes
. Precipitating and relieving factors
. Associated systemic symptoms
. Presence of aura or prodrome
. Relation with food, alcohol, drugs (oral contraceptive pills), menses, etc…
. Response to analgesics
. Family history of headache
. Age at onset
Primary headache syndromes
1. Tension-type headache
Episodic or chronic bilateral, pressure-like headache of mild to moderate intensity, lasting for several days,
which is triggered by stress or sleep deprivation, and responds to NSAIDs or acetaminophen.
2. Cluster headache
Unilateral retro-orbital, excruciating/explosive, headache associated with autonomic symptoms like red and
tearing eye, myosis, ptosis, and rhinorrhea. The headache is characterized by circadian attacks, and each attack
lasts for 15 minutes to 3 hours, and responds to high-flow oxygen.
3. Migraine
Unilateral, throbbing type of headache, lasting for 4-72 hours, and moderate to severe in intensity. It is
aggravated by routine activities, and associated with nausea, vomiting, photophobia, and phonophobia. It may

be heralded by aura such as visual changes (zig-zag lines/flashing lights) or sensory symptoms (paresthesias,
numbness), or speech disturbance. It is triggered by foods (cheese, chocolate), stress, fatigue, menses, and
responds to therapy with triptans and cafergot.
Headache features that suggest serious underlying disorder
. ‘Worst’ headache ever
. Subacute worsening headache over days to weeks
. Vomiting which precedes headache
. Headache, which disturbes sleep or presents immediately upon awakening
. Headache with fever or unexplained systemic symptoms
. Headache induced or worsened by bending, coughing or straining
. Headache with known systemic illness (systemic cancer/HIV infection)
. Headache with abnormal neurologic deficit
. Headache onset > 55 yrs of age, or < 5 yrs of age
Serious underlying causes of headache
Subarachnoid hemorrhage: The first ‘worst’ headache ever, neck stiffness and altered mentation
Infective meningitis: Headache with fever, neck stiffness, and altered mentation
Brain tumor: Subacutely worsening headache with nausea and vomiting, disturbs sleep, worsen during
awakening, aggravated by bending, coughing or straining
Temporal arteritis: Elderely individual with pounding, temporal headache and visual changes
Glaucoma: Severe, protracted headache, red eye with eye pain
Cognitive impairment (amnestic state)
. Age at onset (senile or presenile dementia)
Cognitive disturbance under 60 years of age is presenile dementia, and usually pathological in nature

. Ask for history of head injury, chronic alcoholism, stroke, brain tumor, CNS infections, etc…
Types of amnesia
. Anterograde amnesia: Inability to recall or recognize events, facts or concepts following the illness or injury
. Retrograde amnesia: Inability to access or recall experiences prior to the insult or illness occurred
Causes of dementia
a. Most common causes of dementia
. Alzheimer’s disease
. Vascular dementia (multi-cerebral infarction, diffuse white matter disease)
. Alcoholism
. Parkinson’s disease
. Drug/medication toxicity
b. Less common causes of dementia
. Vitamin deficiency
Vitamin B1 (Wernicke’s encephalopathy), vitamin B12 (pernicious anemia), and nicotinic acid deficiency
(pellagra)
. Endocrine failure- Hypothyroidism, Addison’s disease and Cushing’s syndrome
. Chronic infections- HIV/AIDS, neurosyphilis
. Head injury- chronic subdural hematoma, dementia pugilistica
. Normal-pressure hydrocephalus (clinical triads of dementia, ataxia and urinary incontinence)
. Neoplastic – primary brain tumors, metastatic brain tumors, paraneoplastic limbic encephalitis
. Toxic disorders- heavy metal intoxication, organic toxins
. Degenerative disorders- Dementia with Lewy bodies, Pick’s disease, Huntington’s disease, fronto-temporal
dementia, etc…
Abnormal body movement

Seizures
Seizure is paroxysmal event due to abnormal, excessive, hypersynchronous discharges from an aggregate of
central nervous system neurons
Epilepsy is recurrent seizures due to chronic, underlying process in the brain cortex
Generally, seizure disorder is broadly divided into partial (focal) and generalized seizures
Partial (focal) seizure: seizure activity in discrete areas of the cerebral cortex. It may be associated with
preserved consciousness (focal seizures with intact awareness), or impaired consciousness (focal seizures with
impaired awareness)
Generalized seizure: seizure activity involving diffuse regions of the brain and usually associated with loss of
consciousness
. Ask
Was it a seizure or not? Take clinical history from an attendant if a seizure activity is associated with
impaired/loss of consciousness
If Yes, was it associated with impaired/loss of consciousness? Impaired or loss of consciousness during ictal-
phase of seizure occurs in complex partial and generalized seizure disorders, respectively
Was there prodromal phase?, which begins hours to days before the seizure, and manifests with irritability,
headache, insomnia, bad temper, depression or manic behavior
. Was there preceding aura?
Presence of preceding aura signals focal onset of the seizure, and presents with extreme fear, strange epigastric
sensations, dream-like experiences, unpleasant smells, etc…
. Was there post-ictal syndrome?, which may be brief or last for several hours, and manifests with headache,
irritability, confusion, drowsiness, muscle ache/soreness, paralysis (Todd’s paralysis), altered speech/aphasia,
altered behaviors or emotional outbursts
. Age at onset, frequency and duration of the attack (fit), the time of day that the seizure occurs, altered
behaviors during the attack, history of anti-seizure drug use (what drug/s, how long in use, effect of
medication)
. Were there underlying endogenous, epileptogenic and precipitating factors?
Endogenous factors
. Family history of epilepsy, genetic susceptibility for epilepsy
Epileptogenic factors

History of head injury, stroke, brain tumor, CNS infections, degenerative CNS diseases, etc…
Precipitating factors
. Flashing lights (reflex epilepsy) . Poor or excesive sleep . Physical or mental stress
. Special smells or sounds . Excessive alcohol intake . Hormonal changes eg. Catamenial (menses)
. Fever . Hyperventilation
Positive likelyhood of a seizure to be recurrent
. Initial seizure presenting as status epilepticus
. Seizure associated with post-ictal Todd’s paralysis
. Family history of epilepsy
. Seizure associated with abnormal neurologic deficit
. Seizure associated with abnormal electroencephalography (EEG)
Common causes of seizure in adults
. Head injury
. Alcoholism (Binge alcohol intake or alcohol withdrawal)
. Brain tumor
. Cerebrovascular disease
. Metabolic disorders such as uremia, hepatic failure, etc…
. Degenerative central nervous system (CNS) diseases such as Alzheimer’s disease
. CNS infections such as meningitis, encephalitis
. Idiopathic

_____________________________________________________________________________________
Table 8.1.1 Classification and Clinical manifestations of seizure disorders

______________________________________________________________________________________
Table 8.1.2 Classification and Clinical manifestations of seizure disorders
Movement disorders
Common terminologies in movement disorders
Akithesia Motor restlessness; constant semi-purposeful movements of the arms and legs
Asterixis Sudden loss of muscle tone during sustained contraction of an outstretched limb
Athetosis Writhing, slow movements of hands and wrists
Chorea Irregular, jerky and brief rapid extremity movements. Chorea and athetosis often occur combined,
and named choreoathetosis
Dyskinesia Purposeless and continuous facial and mouth movements
Dystonia Sustained contractions of agonist and antagonist muscles, which results in bizarre postures (twisting)

in flexion or extension
Ballismus Violent flinging movement of extremity
Myoclonus Brief muscle contraction which causes a sudden purposeless jerking of a limb
Myokymia Repeated contraction of a small muscle group involving orbicularis oculi muscles
Tic Repetitive, irresistible, stereotyped movement
Tremor Rhythmical alternating movement
Weakness of extremities
Weakness is reduced strength or power of one or more muscles
Was there weakness of any part of the body (paralysis)? Which body parts were involved? Was it distal or
proximal weakness? Date and mode of onset, temporal course, co-morbidities
Proximal weakness is due to muscle disease (myopathy), and manifests with difficulty in standing from sitting
position, or difficulty in combing hair
Distal weakness is due to peripheral neuropathy, and manifests with slapping of feet while walking, or
difficulty in opening a jar or using hand tools (scissors/screw driver)
Hemiparesis: Weakness of ipsilateral upper and lower extremities
Causes of hemiparesis
a. Acute hemiparesis (onset in minutes to hours)
. Head trauma
. Stroke
. Bleeding into brain tumor
b. Subacute hemiparesis (onset in days to weeks)
. Subdural hematoma
. Brain abscess
. Cerebral toxoplasmosis/primary CNS lymphoma (AIDS patients)
c. Chronic hemiparesis (onset in months)
. Tuberculoma

. Neurocysticercosis
. Brain tumor
. Chronic subdural hematoma
. Degenerative CNS diseases
Paraparesis: Weakness of both lower extremities
Causes of paraparesis
Usually caused by spinal cord disorders
a. Acute paraparesis (onset in hours)
. Acute transverse myelopathy, eg. transverse myelitis
. Spinal cord injury (spinal shock)
. Spinal cord infarction
b. Subacute or chronic paraparesis (onset in weeks to months)
. Disc prolapse or herniation
. Pott’s disease (tuberculous spondylitis)
. Compressive myelopathy eg. epidural abscess, vertebral osteomyelitis, and secondary tumor deposits
. Degenerative spondylosis: Disk-osteophyte complex
Monoparesis (brachial or crural): Weakness of one upper (brachial) or lower (crural) extremity
Causes of monoparesis
a. Acute monoparesis (onset in hours to days)
. Ischemic stroke
. Poliomyelitis
. Cerebral vasculitides
b. Subacute or chronic monoparesis (onset in weeks to months)

. Brachial or lumbosacral plexopathy
. Cauda-equina syndrome
. Peripheral nerve entrapment
Abnormal sensory symptoms
What type of abnormal sensory symptoms felt (pins-and-needles or numbness)? Date and mode of onset,
temporal course, co-morbidities (eg. diabetes, chronic kidney disease, etc…), exposure to drugs and toxins
(herbicides, pesticides and industrial chemical solvents), etc…
1. Positive sensory symptoms
. Paresthesia- Pins and needles sensation
. Dysesthesia- abnormal sensation whether a stimuli is evident or not
Positive sensory phenomena usually results from ectopic impulses generated at a site or sites of lowered
threshold or heightened excitability along a sensory pathway
2. Negative sensory symptoms
It represents loss of sensory function and is characterized by diminished or absent feeling, often experienced as
numbness
In contrast to positive phenomenon, negative phenomenon is accompanied by abnormal findings on sensory

examination
At least half of afferent axons of innervating a given site are lost to demonstrate sensory deficit
Sensory signs are always a measure of negative sensory phenomenon

Examination of the nervous system
Mental state examination (MSE)
. Appearance and behavior (level of consciousness; posture and motor behavior; dress, grooming and personal
hygiene; facial expression)
. Mood and affect
. Thought and perception
. Insight and judgment
. Cognitive function (memory, intelligence, abstraction)
. Speech and language (speech, language (aphasia), dysarthria, apraxia)
1. Appearance and behavior
a. Level of consciousness
Note for any disturbance in consciousness such as lethargy, obtundation, stupor or coma
Level of consciousness primarily reflects the patient’s capacity for arousal or wakefulness.
Level of consciousness is assessed by Glasgow Coma Scale (GCS), numerical value to the patient’s responses to
defined stimuli
Score of ≤ 8/15 indicates coma, unarousable to any external noxious stimuli
Reduced level of consciousness results from acute cerebral dysfunction from cerebral hypoperfusion, metabolic
diseases, CNS infections, and brain stem reticular activating system (RAS) lesions
Assessment variables and scores of GCS
1. Eye opening
Spontaneous (4); to speech (3); to pain (2); none (1)
2. Best verbal response
Oriented (5); confused (4); inappropriate speech (3); incomprehensible sound (2); none (1)
3. Best motor response

Obeys command (6); localizes pain (5); withdrawal (4); abnormal flexion (3); abnormal extension (2); none (1)
Total score out of 15______________________
Table 8.2 Conventional method of assessing level of consciousness
b.Posture and motor behavior
Look for any unusual features in the behaviour, eg. tense posture and restlessness of anxiety, slowed movement
of depression, and singing and dancing movements of a manic episode.
c.Dress, grooming, and personal hygiene
Compare the dress, grooming and personal hygiene of the patient with other people of comparable age, lifestyle,
culture, occupation and social class
Deteriorated personal hygiene (body odour, lack of shaving and dirty clothes) is usually noticed in patients with
depression, schizophrenia or dementia

d. Facial expression
Observe the patient at rest and while interacting with others. Does a patient maintain good eye contact?, Is a
patient anxious or apathetic?
2. Mood and affect
Mood is the patient’s pervasive emotional state, while affect is the observable expression of their emotions.
Think of mood as the emotional climate, and affect as the weather.
Mood is described by quality (subjectively or objectively), stability (over a period of time), reactivity (variation
with stimuli), and persistence (length of time it lasts)
Affect is described by quality, range (emotional changes over time), depth or intensity (normal, increased,
blunted), and appropriateness (congruence in relation to thought and circumstances)
Eg. Quality of mood/affect: Does the patient appear elated or euphoric (mania), filled with despair or dismay
(depression), or incongruent or blunted affect (schizophrenia)?
3. Thought and perceptions
Thought form and content abnormalities
Thought assesses the logic, relevance, and coherence of patient’s thought process during the interview.
. Give attention to thought flow and thought content
Thought flow is a patient’s thoughts rate, flow, sequencing, and abstraction in a logical way.
. Assess for circumstanciality (speech not to the point), tangentiality (loosening of associations), blocking
(sudden speech interruption due to losing the thought), flight of ideas (Shifting from one to the other subject),
neologism (use of invented and distorted words), incoherence (illogical and incomprehensive speech),
confabulation (fabrication of facts and or events in response to questions), perseveration (persistent repetition of
words or ideas), or echolalia (repetition of the words and phrases of others)
Thought content is the main theme and subjects occupying the patient’s mind. These are preoccupation (belief
that dominates patient’s thinking), obsession (recurrent persistent thoughts), compulsion (repetitive behavioral
response to obsession), phobias (persistent irrational fears), rumination (repetitive, senseless thoughts), over-

valued ideas (belief of great personal significance), and abnormal beliefs (delusions: thought control, thought
insertion, thought withdrawal, thought broadcasting)
Disorders of thought form and content are common in psychotic disorders.
Delusions
Delusions are false, fixed beliefs which can’t be shared by others.
There are primary (true delusions) and secondary (delusion-like ideas) delusions
Primary delusions are delusional perceptions to which the patient attaches delusional significance
Secondary delusions are delusional peceptions to abnormal mood state or hallucinatory experience
Ask for delusion of persecution, grandieur, jealous, love, reference, hypochondriachal symptoms, nihilism, guilt, self-
blame, poverty, etc…
It generally occurs in schizophrenia or severe depression
Perception abnormalities (hallucination, depersonalization, derealization, illusion)
Hallucination is false subjective sensory perceptions in the absence of relevant external stimuli
Hallucinations may be auditory, visual, olfactory, gustatory, or tactile/somatic.
Hallucinations are features of psychotic disorders, delirium, epileptic seizures, substance use (formication), extreme
fatigue, grief reaction, etc…
Depersonalisation (subjective experience of feeling unreal) and derealisation (subjective experience that the
surrounding environment is unreal) are experienced in extreme fatigue, intense anxiety or psychotic disorders.
Illusion is false perception of understandable misinterpretation of a real stimulus. It is noticed in patients with
delirium or dementia.
4. Insight and judgement
Insight is awareness of one’s own mental health.
Ask the patient ‘what brings you to the hospital’, ‘what do you think was wrong’?
Patients with psychotic disorders often lack insight into their illness.
Judgment is the ability to make right decisions in specific situations.
It is assessed by social judgement and test judgement.

. Social judgement: Noting the patient’s response to family situations, jobs or interpersonal conflicts
. Test judgement: Asking the patient what he would do to a certain test situation eg. ‘a house in fire’, ‘a sealed,
stamped envelope found on the street’
Poor judgement is seen in dementia, delirium, mental retardation and psychotic states.
5. Cognitive function
It encompases orientation (time, place, and person), attention and concentration (digit span, serial 7s, spelling
words backward like WORLD), memory (immediate recall, short term, recent, remote), calculating ability,
abstract thinking, and constructional ability
Impaired orientation occurs in patients with delirium; impaired attention is noticed in patients with delirium,
dementia, intellectual disability and anxiety; impaired memory and calculating ability is seen in patients with
dementia (amnestic disorders); impaired abstract thinking is seen in patients with organic frontal lobe disease.
Cognitive impairment assessment
Mini-mental state examination (MMSE) evaluates severity of cognitive impairment
Assessment variables and scoring system for cognitive impairment (MMSE)
1. Orientation (time and place)
Time- Ask day, date, month, season and year (score 1 for each correct answer)
Place- Ask ward, hospital, town, capital city, country (score 1 for each correct answer)
2. Registration
Name three common objects, and tell and rehearse with the patient to remember them (score 1 for each correct
registration), remind him that he will be asked to name them after 5 minutes
3. Attention and calculation
Ask him to subtract 7 from 100, or 3 from 30 for a total of 5 times (score 1 for each correct subtraction)
4. Recall
Ask the patient to name the three objects registered in question number 2 (score 1 for each correct recall)
5. Language
a. Show him 2 objects (eg. pen, watch) and assess if named correctly (score 1 for each correct naming)

b. Assess correct repetition of “no ifs, and, buts” (score 1 for correct repetition)
c.Assess if the three-stage command correctly obeyed eg. “Take this piece of paper in your left hand, fold it in
half, and place it on the table” (score 1 for each correct answer)
d. Assess response to written command such as “Raise your left hand” (score 1 for correct answer)
e. Ask the patient to write any sentence; and assess if it is meaningful, and has subject and verb (score 1 for a
sentence which is meaningful, has subject and verb)
f.Test for patient’s ability to copy complex diagram of 2 intersecting pentagons (score 1 for correct coping)
Total score out of 30_______________
MMSE numerical value < 21/30 indicates presence of impaired cognition (dementia)
Memory
Disturbance in memory is named as amnesia
Assess type of cognitive impairment (Is it immediate, short-term or longer-term (recent or remote) memory
loss?)
Major types of memory loss
1. Long-term memory loss
A.Remote memory loss
Ask about autobiographical events from the distance past or national historical events
When did you get married? What is the name of Ethiopian leader in the 1940’s E.C?
B.Recent memory loss
Ask about recent events in the past few hours or days
Ask a recent social affairs on TV (political dialogue on Election Day), circumstance of admission to the hospital
2. Short-term memory loss
Tell him repeatedlyto register new information and ask him what he was told after 2-3 minutes
Failed to register new information (3 or more mistakes) at 5 minutes suggests impaired short term memory
3. Immediate memeory loss

Can be tested by ‘digit span’ (repeating a series of digits immediately after the interviewer has said)
. In digit forward test, the patient is asked to repeat 3 digits and build up the number until the patient makes
mistakes
. In digit backward test, the digit given by the examiner has to be repeated in the reverse order (eg. 2549 as
9452)
7 forwards and 5 backwards constitute normal ability. Impaired recall is defined when repeat ≤ 5 forward.
It can be assessed by reading out a sentence, and ask the patient to repeat it immediately
Interlligence
It is the ability to think logically, act rationally, and deal effectively with the environment.
. Enquire about educational and occupational history
. Assess a general knowledge like reading and writing, and solving simple mathematical problems as in
shopping activities
Abstraction
Helpful in assessing concept formation problems in organic frontal lobe disease
It is assessed by
. Proverb testing: Ask the patient the meaning of a well known proverb (at least 3) eg. ‘Too many cooks spoil
the broth’ or ‘People in glass houses shouldn’t throw stones’ (answer is concrete/abstract)
Concretisation of response or inappropriate answer occurs in schizophrenia.
. Similarities (and differences) between familiar objects eg. table and chair, banana and orange, etc…
6. Speech and language
Assess patient’s speech: Quantity (talkative/poverty of speech), rate (fast/slow), volume (louder/soft),
articulation (are words clear and distinct?), and fluency (rate, flow, and melody of speech, and the content and
use of words)
Accelerated and louder speech suggests mania, while poverty of speech is noticed in depression or
schizophrenia
Language abnormalities can be assessed by word comprehension, fluency, repetition, naming, reading
comprehension, and writing.

Dysphasia (aphasia): Difficulty in understanding and producing language
Major types of aphasia
a. Wernicke’s aphasia
. Impaired comprehension of spoken and written language
. Fluent speech devoid of meaning (jargon aphasia)
. Inappropriately uttered phrases of fluent speech (paraphasia)
. Patient is unaware of his speech deficit, and shows paranoid behavior
b. Broca’s aphasia
. Impaired fluency with poverty of speech
. Intact comprehension of spoken or written language
. Patient is aware of the speech deficit and feels depressed
c. Global aphasia
. Impaired comprehension and poverty of speech (Wernicke’s and Broca’s aphasia)
. Generally, the patient is in mute state

Table 8.3 Disorders of speech: Dysphonia, dysarthria and dysphasia
Dysarthria: Difficulty in speech articulation
Types of dysarthria
. Spastic (cortical) dysarthria: strangled and spastic speech eg. Pseudobulbar palsy
. Hypokinetic dysarthria eg. Parkinsonism
. Cerebellar (staccato) dysarthria: ‘scanning’ and robotic speech with syllables pronounced individually and
slowly eg. Cerebellar lesions
. Flaccid (bulbar) dysarthria: difficulty in pronunciation of consonants eg. Bulbar palsy
Apraxia: Impairment in executive complex motor tasks, and usually observed in parietal lobe diseases
Types of apraxia

. Dressing apraxia: Inability to dress when asked to put on clothes
. Constructional apraxia: Inability to copying designs or figures
. Ideomotor apraxia: Inability to perform movements on command although the patient performs those
movements automatically
. Gait apraxia: Inability to walk, though patient has normal leg movements while in bed

Cranial nerves
Location of cranial nerves
Cranial nerves I and II are central nervous tissue
Cranial nerves III and IV --- Mid brain
Cranial nerves V-VIII --- Pons
Cranial nerves IX-XII --- Medulla oblongata
Types of cranial nerves
Sensory cranial nerves --- Cranial nerves I/II/VIII
Motor cranial nerves --- Cranial nerves III/IV/VI/XI/XII
Mixed (sensory and motor) cranial nerves --- Cranial nerves V/VII/IX/X
Cranial nerves never cross, except trochlear nerve, and clinical findings are always on the same side of affected
cranial nerves
Cranial nerve I: Olfactory nerve
Sensory cells in olfactory epithelium pass through cribriform plate to olfactory bulb, then to olfactory centers in
the uncus and parahippocampal gyrus
Technique
. Evaluate the patency of the nasal passages bilaterally by asking the patient to breathe in through their nose
Procedure
. Place non-irritating powder of coffee or solution of alcohol near the patent nostril
. Ask the patient to smell the object and report what it is, while the patient has closed her/his eyes
. Switch nostril and repeat the test
Ask the patient to compare the strength of the smell in each nostril

Anosmia (loss of sense of smell) results from damage to olfactory filaments after head trauma or invasive basal
skull tumor
Parosmia (pleasant odor perceived as unpleasant) results from head trauma, sinus infection or drugs side effect
Cranial nerve II: Optic nerve
Fibers of optic nerve from the retina project to optic chiasm, and then to optic tract to end at occipital lobe via
optic radiation
1. Test Visual Acuity
Technique
Allow the patient to use his glass or contact lens if available
. Position the patient 6 meter in front of the Snellen eye chart
. Have the patient cover one eye at a time with a card
. Ask the patient to read progressively smaller letters until they can go no further
. Record the smallest line the patient read successfully (6/6, 6/10, etc…)
. Repeat with the other eye
If patient can not see the top letter at 1meter, check whether patient can count fingers, see hand movements, or
just see light
2. Test for Visual Fields by Confrontation
Technique-1
. Stand one meter in front of the patient and have him look into your eyes
. Hold your hands about half meter away from the patient's ears, and wiggle a finger on one hand
. Ask the patient to indicate which side they see the finger move
. Repeat two or three times to test both temporal fields
. If an abnormality is suspected, test the four quadrants of each eye while asking the patient to cover the opposite
eye with a card

Technique-2
. Sit or stand in front of the patient at a distance of one meter
. The patient covers the right eye and the examiner cover the left eye, and the patient fixes her/his gaze on the
examiner’s opposite eye
. Keep the wiggling finger of the examiner mid way and out of view for the examiner and the patient
. Bring the wiggling finger slowly into view from out of view
. Tell the patient to tell you ‘yes’ when she/he see the examiner’s wiggling finger come into view
. Each of the upper temporal, lower temporal, upper nasal and lower nasal quadrants is tested separately
. Repeat the test in the other eye
Fig 8.1 Technique of testing visual fields
Testing of visual fields: A. Testing the temporal field in each eye separately; B. Testing both simultaneously for
inattention hemianopsia

Fig 8.2 Visual field defects in optic pathway abnormalities
A lesion at 1 produces blindness in the right eye with loss of the direct light reflex. A lesion at 2 produces
bitemporal hemianopia. Lesions at 3a and 3b produce binasal hemianopia (a rare disorder). A lesion at 4
produces right homonymous hemianopia with macular involvement. A lesion at 5 produces right homonymous
hemianopia with sparing of the macular field. A lesion at 6 produces right homonymous central (macular)
hemiscotoma. A lesion at 7 produces altitudinal hemianopia (upper half of contralateral visual field is lost)
Visual field abnormalities
Homonymous hemianopia is loss of vision on half of the visual field in both eyes. When the extent of visual loss
in the homonymous fields of the two eyes is similar (congruous hemianopia) the lesion is likely to be
postgeniculate (in optic radiation). Incongruous hemianopia is more likely to be pregeniculate (in optic tract or
lateral geniculate nucleus).
Homonymous quadrantanopia is loss of vision limited to one quadrant of a visual field in both eyes.

Contralateral homonymous superior quadrantanopia occurs in temporal lobe lesion, while contralateral
homonymous inferior quadrantanopia occurs in parietal lobe lesion.
Bitemporal hemianopia: Loss of vision in the temporal (outer) halves of both fields is due to a lesion of the optic
chiasm, often caused by compressive pituitary tumors.
Altitudinal hemianopia: The upper or lower half of the contralateral visual field is lost in altitudinal hemianopia.
3. Test for color vision
Color perception, especially red, is affected in optic nerve disease before changes in visual acuity can be
detected
Technique
. Show the patient a red target one eye at a time
. Ask the patient if there is a difference between the eyes
. Red appears ‘washed out’ (desaturated) in the affected eye
The Ishihara test assesses both congenital color anomalies (color blindness) and acquired visual disorders
Most inherited color blindness occurs in males (sex-linked recessive inheritance), and it ranges from total color
blindness (monochromatopsia) to confusion between colors, typically between red and green
Cranial nerve III – Oculomotor nerve
Function: The 3rd cranial nerve controls adduction with adducted and abducted eye (medial rectus muscle);
elevation of abducted eye, and elevation and intorsion (internal rotation) of adducted eye (superior rectus
muscle); depression of abducted eye, and depression and extorsion (external rotation) of adducted eye (inferior
rectus muscle); elevation of adducted eye, and elevation and extorsion of abducted eye (inferior oblique
muscle); elevation of eyelid (levator palpebrae superioris); and pupillary size (parasympathetic to the pupil)
The extraocular movements are controlled by the paired oculomotor, trochlear and abducens nerves. They are
interconnected by the medial longitudinal fasciculus (MLF). MLF carries fibers from 6th nerve nucleus to
contralateral 3rd nerve nucleus to integrate horizontal gaze.
Light reflex loop

Afferent fiber of light reflex arises from optic nerve to relay at Edinger-Westphal nucleus in brain stem, and
efferent fiber arises from the nucleus and project into the oculomotor nerve, and then to ciliary ganglion and
finally to ciliary muscle and iris (constrictor pupillae muscle)
Fig 8.3 Light reflex pathway
Test Pupillary Reactions to Light
. Dim the room lights as necessary
. Ask the patient to look into the distance
. Shine a bright light obliquely into each pupil in turn
. Look for both the direct (same eye) and consensual (other eye) reactions
. Assess pupil size in mm and any asymmetry or irregularity
. If abnormal, proceed with the test for accommodation
Test Pupillary Reactions to Accommodation
. Hold your finger about 10cm from the patient's nose
. Ask them to alternate looking into the distance and at your finger
. Observe the pupillary response in each eye

Light reflex and accommodation abnormalities
Third nerve lesion: Dilation of ipsilateral pupil owing to pupilloconstrictor nerve lesion, and failure of
consensual light reflex due to disrupted efferent arc of light reflex
Marcus-Gunn pupil: Relative afferent pupillary defect due to partial defect of afferent pathway of light reflex
Argyll Robertson pupil: Bilateral small and irregular pupil, which reacts to accommodation, but not to direct and
consensual light reflex due to a lesion at pretectum (brain stem)
Holms-Adie pupil: Unilateral tonically dilated pupil with delayed constriction to light, but responds to
accommodation
Extraocular cranial nerve lesions cause diplopia, worse in the direction of action of the weak extraocular muscle
Fig 8.4 Pupillary defects A) Right Horner’s syndrome (ptosis and myosis) B) Right Holmes-Adie pupil C)
Argyll Robertson pupil (bilateral ptosis and small, irregular pupils) D) Right oculomotor palsy (ptosis, dilated
pupil, and down and outward looking right eye)
Cranial nerve IV – Trochlear nerve
Function: Trochlear nerve controls depression of adducted eye, and depression and intorsion (internal rotation)
of abducted eye (Superior oblique muscle)
Test extraocular movements: Depression of adducted eye, and depression and intorsion (internal rotation) of
abducted eye

Cranial nerve VI – Abducens nerve
Function: Abducens nerve controls abduction with adducted or abducted eye (lateral rectus muscle)
Test extraocular movements- Lateral movement
© Jaypee. SN Chugh, E Gupta. Clinical Methods in Medicine 2nde
Fig 8.5 A and B: Functions of external ocular muscles (left eye).
The superior rectus and inferior rectus act as elevator and depressor, respectively, when eye is in abduction; and
inferior oblique and superior oblique act in as elevator and depressor, respectively, when the eye is in adduction
(SR, superior rectus muscle; IR, inferior rectus muscle; IO, inferior oblique muscle; SO, superior oblique
muscle; MR, medial rectus muscle; LR, lateral rectus muscle)
Technique
Test extraocular movements
. Check for ptosis
. Stand or sit 1-2 meter in front of the patient
. Ask the patient to follow your finger with their eyes without moving their head
. Check gaze in the six cardinal directions using a cross or "H" pattern
. Pause during upward and lateral gaze to check for nystagmus
. Check convergence by moving your finger toward the bridge of the patient's nose

Cranial nerve V – Trigeminal nerve
Function: Trigeminal nerve supplies sensation over the face, muscles of mastication, and mediates jaw jerk and
corneal reflex
Technique:
Test Temporal and Masseter Muscle Strength
. Ask patient to both open his mouth and clench his teeth
. Palpate the temporal and massetter muscles as he does this
NB: Ipsilateral trigeminal nerve lesion results in jaw deviates towards the side of the lesion as
the mouth opened
Test the Three Divisions for Pain Sensation
. Explain what you intend to do
. Use a suitable pointed object to test the forehead, cheeks, and jaw on both sides
. Substitute with a blunt object and ask the patient to report "sharp" or "dull."
. If you find an abnormality, then
. Test the three divisions for temperature sensation with a tuning fork heated or cooled by water
. Test the three divisions for sensation to light touch using a wisp of cotton
Jaw jerk: Refer to deep tendon reflex (DTR)
Test the Corneal Reflex (afferent loop of corneal reflex is mediated by Trigeminal nerve)
. Ask the patient to look up and away
. From the other side, touch the cornea lightly with a fine wisp of cotton
. Look for the normal blink reaction of both eyes
. Repeat on the other side
NB: Use of contact lens may decrease this response

Cranial nerve VII – Facial nerve
Function: Facial nerve control muscles of facial expression, somatic sensation from external ear canal, gustatory
sensation (taste) from anterior 2/3 of tongue, and autonomic innervation to salivary and lacrimal glands
Upper motor neuron (UMN) facial weakness
Unilateral UMN lesion causes contralateral weakness of cheek, mouth and platysma but not upper face
Face deviates towards the side of the lesion
Lower motor neuron (LMN) facial weakness
Nuclear and infranuclear lesions cause ipsilateral flaccid paralysis of upper and lower face
Face deviates away from the side of the lesion
© Lippincott. Bates, Bickley & Hoekelman. A Guide to Physical Examination and History Taking 12the
Fig 8.6 Central CN VII lesions: Cortico-pontine tract lesion causes contralateral paralysis of lower face only

Fig 8.7 Peripheral CN VII lesions: Peripheral facial nerve lesion causes ipsilateral paralysis of upper and lower
face
Technique:
. Observe for any facial droop or asymmetry
. Ask patient to do the following (note any lag, weakness, or asymmetry)
. Raise eyebrows, Close both eyes to resistance, Smile, Frown, Show teeth, and Puff out cheeks
Test the Corneal Reflex (efferent loop of corneal reflex is mediated by cranial nerve VII)
Cranial nerve VIII – Vestibulochochlear nerve (Auditory vestibular nerve)
Vestibulo-cochlear nerve controls hearing (acoustic division) and balance (vestibular division)
Normally, air conduction is better than bone conduction in Rinne test, and does not lateralize in weber’s test
Techniques:
Whispered voice test

. Stand behind the patient
. Whisper about 60 cm (arm length) from the ear you are testing
. Mask hearing in the other ear by rubbing the fingers
. Ask the patient to repeat your words
If a patient can hear a whispered voice at 60 cm, his hearing is better than 30 dB i.e. normal
If abnormal, proceed with the Weber and Rinne tests
Test for lateralization (Weber test)
Use a 512 Hz or 1024 Hz tuning fork
. Start the fork vibrating by tapping it on your opposite hand
. Place the base of the tuning fork firmly on top of the patient's head or in the middle of forehead
. Ask the patient where the sound appears to be coming from (normally in the midline)
Lateralizes to normal ear in sensorineural hearing loss
Lateralizes to affected ear in conductive hearing loss
Fig 8.8 Weber test
Test for Comparison of air and bone conduction (Rinne test)

Use a 512 Hz or 1024 Hz tuning fork
. Start the fork vibrating by tapping it on your opposite hand
. Place the base of the tuning fork against the mastoid bone behind the ear
. When the patient no longer hears the sound, hold the end of the fork near the patient's ear (air conduction is
normally greater than bone conduction)
Sensorineural hearing loss: Air conduction > Bone conduction
Conductive hearing loss: Bone conduction > Air conduction
Fig 8.9 Rinne test
Dix-Hallpike maneuver
Commonly used in patients with benign positional vertigo (vestibular function)
Dix-Hallpike maneuver assesses the effect of positional change
Technique:
. Ask the patient to sit upright on the examining coach
. Turn the patient’s head 450 to one side
. Lie back rapidly with her/his head extended over the end of the bed (keep eyes open)
. Watch eyes for nystagmus. Repeat the test, turning the head to other side

. Presence of positional vertigo is suggested by torsional nystagmus beating to the lower ear with feeling of
vertigo persisting for 5-30 minutes
. Positional vertigo is thought to be caused by misplaced calcium debris (otoconia or ear rocks) in the posterior
semicircular canal
Fig 8.10 Dix-Hallpike’s maneuver: Technique for positional nystagmus
Cranial nerves IX and X – Glossopharyngeal and Vagus nerves
Function: Glossopharyngeal and vagus nerves control swallowing and phonation. Both nerves receive somatic
sensation from the oral cavity and throat. Cranial nerve IX receives gustatory sensation from posterior 1/3 of
tongue. In addition, vagus nerve supplies autonomic innervation to thoracic and abdominal viscera.
Lesions of IX and X nerves cause dysphagia, dysphonia, and diminished or absent gag reflex.
A.Cranial nerve IX lesion
Unilateral IX lesion results in
. Unilateral loss of palatal, tonsillar or pharyngeal sensation
. Absent or depressed gag reflex (afferent limb of the reflex)
. Unilateral loss of taste in posterior one-third of tongue
B.Cranial nerve X lesion
Unilateral X lesion results in
. Failure of elevation of the uvula on the affected side
. Absent or diminished gag reflex (efferent loop of the reflex)

Bilateral X nerve lesion
. Dysphagia with nasal regurgitation of fluids
. The voice may sound hoarse or may have nasal quality (palatal dysarthria)
. Dysphonia, bovine cough, and stridor with respiratory obstruction due to vocal cord paralysis
Technique:
. Listen to the patient's voice, is it hoarse or nasal?
. Ask the patient to cough; assess strength of cough
. Ask patient to say "Ahh", and watch the movements of the palate and Uvula.
Unilateral damage to the IX or X nerve leads to deviation of the uvula to normal side when the soft palate is
elevated saying 'Ahh'.
. Ask the patient to puff out the cheeks with the lips tightly closed. Air escapes audibly via the nose in palatal
weakness
Water swallow test (for conscious patient)
. Adminster 30 ml of water with teaspoon
. Observe for swallow, cough, choking, and voice quality change after each teaspoon of water
. Watch the patient while the patient swallows a glass of water if no problem with above procedure
Coughing, choking or voice quality change while water swallowing indicates swallowing test abnormality
Testing the ‘Gag reflex’ (Unconscious/Uncooperative patient)
. Stimulate the back of the throat on each side
. It is normal to gag after each stimulus
Cranial nerve XI – Accessory nerve
Accessory nerve innervates trapezius and sternomastoid muscle and coordinates head movement at the neck
Technique:

. Look for atrophy or asymmetry of the trapezius muscles from behind
. Ask patient to shrug shoulders against resistance
. Ask patient to turn their head against resistance, and watch and palpate the sternomastoid muscle on the
opposite side
Normally, the patient is able to shrug shoulders and contraction of the sternomastoid muscle against resistance
Fig 8.11 Testing the trapezius and left sternomastoid muscles
Cranial nerve XII – Hypoglossal nerve
Function: Hypoglossal nerve controls taste in posterior 1/3 of tongue, and tongue movement
Technique:
. Listen to the articulation of the patient's words
. Observe the tongue as it lies in the mouth for atrophy and fasciculation
. Ask patient to protrude tongue, move tongue from side to side
. Test strength by asking the patient to press the tongue against the inside of each cheek while you press from
the outside with your finger
Tongue deviates to the affected side in ipsilateral hypoglossal nerve lesion

Motor system
Upper motor neurons lie in the motor strip of the cerebral cortex and their axons synapse with motor nuclei in
the brainstem (for corticobulbar tracts) and in the spinal cord (for corticospinal tracts). Lower motor neurons
extend from cell bodies in the brainstem nuclei or anterior horn cells of spinal cord and terminate as cranial
nerves or peripheral nerves, respectively.
The corticospinal tracts mediate voluntary movement, and integrate skilled, complicated or delicate movements.
Fig 8.29 Motor pathways: Corticospinal tracts
Weakness is reduction in muscle strength, and occurs in lower and upper motor neuron lesion. Generally,
weakness in lower motor neuron lesion causes flaccid paralysis while weakness in upper motor neuron lesion
causes spastic paralysis. The arm extensors and leg flexors are more affected in upper motor neurone lesions.
Distal weakness favors neuropathic lesions, while proximal weakness favors myopathic disorders.

Technique:
Inspection
. Look position of the extremities after repositioning by the examiner
. Compare left to right extremities, and proximal to distal extremities
. Look for muscle Symmetry
. Look for presence of muscle bulk atrophy and fasciculation (Pay attention to the hands, shoulders, and thighs)
Palpation
. Determine for the presence of muscle atrophy on upper or lower extremities
. Test for muscle strength (power)
. Assess for tone at joint sites
. Assess for deep tendon reflexes, and check for clonus in hyperreflexia
. Assess for superficial reflexes (Notice for plantar response and abdominal reflex)
Technique for determining muscle bulk
. Measure the circumference of both biceps bulk on upper limbs equal distance from the elbow
. Measure the circumference of both mid thighs of lower limbs equal distance from the tibial tuberosity
. Measure the circumference of both calf muscles of lower limbs equal distance from the tibial tuberosity
. Compare bulk symmetry in both upper and lower limbs, and deremine for the presence of muscle atrophy
Muscle Strength (power)
Muscle strength indicates the capacity of muscle to exert force
Test strength by having the patient move against your resistance
Always compare one side to the other
Muscle weakness causes loss of speed or agility of movement and a decrease in the range or amplitude of
movement

Table 8.4 Grading of strength on a scale from 0 to 5 "out of five":
Grading Motor Strength
Grade Description
0/5 No muscle movement
Visible flicker muscle movement, but no movement

1/5
at the joint
2/5 Movement at the joint, but not against gravity
Movement against gravity, but not against added

3/5
resistance
4/5 Movement against resistance, but less than normal
5/5 Normal strength
Test the following:
Flexion at the elbow (C5, C6, biceps)
Extension at the elbow (C6, C7, C8, triceps)
Extension at the wrist (C6, C7, C8, radial nerve)
Squeeze two of your fingers as hard as possible ("grip" C7, C8, T1)
Finger abduction (C8, T1, ulnar nerve)
Oppostion of the thumb (C8, T1, median nerve)
Flexion at the hip (L2, L3, L4, iliopsoas)
Adduction at the hips (L2, L3, L4, adductors)
Abduction at the hips (L4, L5, S1, gluteus medius and minimus)
Extension at the hips (S1, gluteus maximus)
Extension at the knee (L2, L3, L4, quadriceps)

Flexion at the knee (L4, L5, S1, S2, hamstrings)
Dorsiflexion at the ankle (L4, L5)
Plantar flexion (S1)
Fig 8.12 Flexion and extension at the elbow (Biceps and triceps)
Fig 8.13 Testing (a) flexor digitorum superficialis; (b) flexor digitorum profundus I and II; (c) flexor digitorum
longus; (d) flexor pollicis longus

Fig 8.14 Testing adductors of the hip
Fig 8.15 Testing the hip abductors (gluteus medius and minimus)
Fig 8.16 Testing the quadriceps femoris

Fig 8.17 Testing (a) Dorsiflexion of foot; (b) Eversion of foot; (c) Plantar flexion of foot
Muscle Tone
Muscle tone is resistance of a muscle to passive stretch
There is normally a small, continuous resistance to passive movement
Technique
. Ask the patient to relax and ‘go floppy”
. Passively move each joint both slowly and quickly
Upper limb
. Hold the patient’s hand as if shaking hands, other hand supporting his elbow
. Rotate the forearm, and flex and extend the wrist, elbow and shoulder
Lower limb

. Roll and rotate the leg from side-to-side
. Flex and extend patient's ankle and knee
. Observe for decreased (flaccid) or increased (spastic) tone
Types of muscle tone
1. Hypotonia
Uniformly reduced resistance to passive movement, Eg. Peripheral neuropathy, cerebellar disorders, myopathy,
drugs (muscle relaxants, anaesthetics), neuronal shock (stroke, transverse myelitis), electrolyte imbalance
(hypokalemia, hypercalcemia)
2. Hypertonia
a.Spasticity (clasp-knife spasticity)
Velocity-dependent spasticity with sudden release after reaching a maximum resistance, commonly seen in
pyramidal tract lesions (stroke, spinal cord injury, spondylytic myelopathy, multiple sclerosis)
b. Rigidity
. Plastic type (lead-pipe) rigidity: Uniformly encountered resisitance to all phases of the passive movement eg.
Extrapyramidal lesion (Parkinsonism), tetanus, strychnine poisoning
. Cogwheel rigidity: Intermittent jerks (tremor) are encountered during passive movement against resistance,
commonly seen in extrapyramidal (basal ganglia) lesions.
. Paratonic rigidity (Gegenhalten phenomenon): Active resistance by the patient while attempting to move
her/his limb. It is observed in catatonic state, dementia, drug-induced (phenothiazines)
. Hysterical rigidity: Voluntarily increased rigidity by the patient to passive movement eg. Convesion reaction
Reflexes
Deep Tendon Reflexes
A tendon reflex is the involuntary contraction of a muscle in response to stretch.

The patient must be relaxed and positioned properly before starting.
Reflex response depends on the force of your stimulus. Use no more force than you need to provoke a definite
response

Reflexes can be reinforced by having the patient perform isometric contraction of other muscles (clenched teeth
for upper limb reflexes, and hooking up fingers of both hands for lower limb reflexes), and named as
Jendrassik’s maneuver . Use reinforcement whenever a reflex appears to be absent.
Table 8.5 Grading scale of deep tendon reflex
Deep Tendon Reflex Grading Scale
Grade Description
0 Absent (with Jendrasik maneuver)
1+ Hypoactive (less brisk)
2+ "Normal" (brisk)
Hyperactive without clonus

3+
(very brisk)
4+ Hyperactive with clonus
Technique:
Biceps reflex (C5, C6)
The patient's arm should be partially flexed at the elbow with the palm down
Place your thumb firmly on the biceps tendon
Strike your thumb with the reflex hammer
You should feel the response even if you can't see it
Triceps reflex (C6, C7)
Flex the patient's arm at the elbow and hold it close to the chest
Strike the triceps tendon above the elbow with the broad side of the hammer
Observe for contraction of triceps

Brachioradialis/ Supinator reflex (C5, C6)
Have the patient rest the forearm on the abdomen or lap
Strike the radius about 1-2 inches above the wrist
Watch for flexion and supination of the forearm
Finger Jerk
Place your middle and index fingers across the palmar surface of the patient's proximal phalanges
Tap your own fingers with the hammer
Observe for flexion of the patient's fingers
Hoffman’s sign (reflex)
. Place your right index finger under the distal interphalangeal joint of the patient's middle finger
. Using your right thumb, flick the patient's middle finger downwards
. Look for any reflex flexion of the patient's thumb in UMN lesions
Rossolimo’s sign (reflex)
. Place your right index finger under the distal interphalangeal joint of the patient's middle toe
. Using your right thumb, flick the patient's middle toe downwards
. Look for any reflex flexion of all the five toes of foot in UMN lesions
Knee/ Patellar reflex (L2, L3, L4)
Have the patient sit or lie down with the knee flexed
In supine positioned patient with the knee in partial flexion:
Place your left pronated arm below the patient’s right knee and left hand over the patient’s left knee, and strike
the right patellar tendon just below the patella
Place your left supinated arm below the patient’s right and left knees, and strike the left patellar tendon just
below the patella
Note contraction of the quadriceps and extension of the knee
Ankle (S1, S2)
Dorsiflex the foot at the ankle

Strike the Achilles tendon
Watch for contraction of gastrocnemius muscle and plantar flexion at the ankle
Jaw Jerk (Trigeminal nerve)
. Partially open the mouth and put your index finger on the jaw
. Gently strike the index finger on jaw with the hammer
. Watch for closure of the mouth due to reflex contraction of both masseters
Clonus
Clonus is a rhythmic series of contractions evoked by a sudden stretch of the muscle and tendon.
Test for ankle clonus
If the reflexes seem hyperactive, test for ankle clonus
Support the knee and ankle in a partly flexed position
Quickly dorsiflex and partially evert the foot
Observe for sustained rhythmic oscillations (≥ 3 rhythmic oscillations)
Test for knee clonus
Partially flex the knee
Hold the patella with thumb and forefinger, and quickly push downwards
Observe for sustained rhythmic oscillations

Fig 8.18 Technique of eliciting deep tendon reflexes: Biceps reflex, triceps reflex, brachioradialis (supinator)
reflex, finger reflex (look for eliciting Hoffman sign), knee reflex, and ankle reflex
Fig 8.19 Technique of eliciting Jaw jerk

a) Jendrassik’s maneuver b) Eliciting clonus
Fig 8.20 Technique of reinforcement (Jendrassik’s maneuver) while eliciting knee jerk, and eliciting the knee
and ankle clonus
Superficial reflexes
Plantar response (L5/S1)
Stroke the lateral aspect of the sole of each foot with the end of a reflex hammer or key
Note movement of the toes, normally flexion (withdrawal)
Extension of the big toe with fanning of the other toes is abnormal. This is referred to as a positive Babinski’s
sign, which indicates upper motor neuron lesion.
Alternative methods of eliciting Babinski’s sign: Extension of big toe with fanning of other toes is also obtained
by pressing heavily along the medial border of the tibia (Oppenheim’s sign), squeezing the calf or achilles
tendon (Gordon’s sign), stroking the lateral border of foot (Chadok’s sign), passive abduction of the 5th digit
(Stansky’s sign), and pressing the dorsum of big toe (Bing sign)
No response to plantar reflex indicates lower motor neuron lesion

Fig 8.21 Technique of eliciting plantar response (Positive Babinski’s sign as shown)
Abdominal reflex (T8, T9, T10, T11, T12)
Use a blunt object such as a key or tongue blade
Stroke the abdomen lightly on each side in an upward and downward direction above (T8, T9, T10) and below
the umbilicus respectively (T10, T11, T12)
Note the contraction of the abdominal muscles and deviation of the umbilicus towards the stimulus
Fig 8.22 Technique of eliciting abdominal reflex
Cremasteric reflex (L1 and 2)
. Stroke the upper medial thigh; look for upward movement of testicle
Anal reflex (S3 and 4)
. Stroke or scratch the skin near the anus, notice for contraction of anal sphincter
Bulbocavernosus reflex (S3 and 4)
. Gently pinch the dorsum of glans penis, Look for contraction of bulbocavernosus muscle
Scapular reflex (C5-T1)
. Stroke the skin in interscapular region; look for contraction of scapular muscles
Corneal reflex (5th and 7th cranial nerves): refer to cranial nerves

Table 8.6 Comparison of lower (LMN) and upper motor neuron (UMN) lesion
Characteristics LMN lesion UMN lesion

Fasciculation Present Absent
Atrophy Present None/mild
Tone Hypotonia Hypertonia
Reflex Hyporeflexia Hyperreflexia
Plantar reflex No response Up-going/Babinski +ve
Arm Drift
1. Pronator Drift
Ask the patient to stand for 20-30 seconds with both arms straight forward, palms up, and eyes closed
Instruct the patient to keep the arms still for a while
Unable to maintain extension and supination of arm, and "drift into pronation” indicate ‘upper motor neuron’
lesion
2. Cerebellar drift
Ask the patient to stand for 20-30 seconds with both arms straight forward and palms up
Instruct the patient to keep the arms still while you tap them briskly downward
Excessive upward rebound movements of arms indicate cerebellar lesion
3. Parietal drift
Ask the patient to stand for 20-30 seconds with both arms straight forward and palms up
Displace the ulnar border of the supinated hand
Lateral drift of the arm indicates parietal lesion
Coordination and Gait
Coordination and gait is maintained by cerebellum. Cerebellar function is tested by rapid alternating
movements, point-to-point movements, gait abnormalities and presence of nystagmus
Technique:

Rapid Alternating Movements
Ask the patient to repeatedly tap the palm of one hand with the palm and back of the opposite hand as quickly
and regularly as possible
Ask the patient to repeatedly strike one hand on the thigh, raise the hand, turn it over, and then strike it back as
fast as possible
Ask the patient to repeategly tap the distal thumb with the tip of the index finger as fast as possible
Ask the patient to tap the examiner’s hand with the ball of each foot as fast as possible
Point-to-Point Movements
Ask the patient to repeatedly touch examiner’s index finger and her nose alternately. Move the examiner’s
finger about as the patient performs this task (Finger-to- Nose test)
Ask the patient to move her arm and return to your finger with her eyes closed
Ask the patient to place one heel on the opposite knee and run it down the shin to the big toe (Heel-to-Shin test).
Repeat with the patient's eyes closed
Fig 8.23 Performing Finger-to-Nose test A) Patient touches the tip of her nose then the examiner’s finger B) The
examiner moves her finger from side-to-side or towards-or-away from the patient as the patient touches
examiner’s finger

Fig 8.24 Performing Heel-to-Shin test
Gait
Difficulty in maintaining an upright posture while standing or walking indicates gait disorder
Technique:
Ask the patient to:
. Walk across the room, turn and come back
. Walk heel-to-toe in a straight line (tandem walk)
. Walk on their toes in a straight line
. Walk on their heels in a straight line
. Hop in place on each foot
. Do shallow knee bend
. Rise from a sitting position
Romberg’s test
Be prepared to catch the patient if they are unstable
Ask the patient to stand with the feet together and eyes closed for 5-10 seconds without support
The test is said to be positive if the patient becomes unstable, which indicates a proprioceptive problems

Fig 8.25 Cerebellar signs: Difficulty in coordination and balance
Common types of gait
Natural gait
The patient should be able to walk with a smooth, coordinated gait with normal associated movement of the
upper extremities
Hemiplegic gait

The arm is held in adduction and internal rotation with flexion at the elbow, wrist and fingers; and the leg is in
extension at the hip, knee and ankle. Therefore, the patient has to circumduct or swing the leg around to step
forward. This type of gait is seen with a pyramidal tract lesion.
Festinating (shuffling) gait
Stooped posture and walking in short, rapid steps in shuffling manner as if trying to catch the centre of gravity.
Increase axial tone and patient turns around stiffly “all in one piece”. Postural instability is evident on
anteropulsion/retropulsion. This type of gait is seen in Parkinsonism.
Cerebellar ataxic Gait
Wide-based with truncal instability and irregular lurching steps which results in lateral veering and falling. ii
This type of gait is seen in cerebellar lesion.
Sensory ataxic Gait
Wide-based, maintained balance during standing with eyes open and rapid loss of balance and fall with loss of
visual input (positive Romberg sign). This type of gait is seen in large-fiber peripheral neuropathy.
Steppage gait
Foot is lifted high and slapped on to the floor and unable to walk on the heels, which is caused by foot drop
owing to lower motor neurone lesion.
Waddling gait
The body is tilted backwards with an increase in lumbar lordosis. The body sways from side to side with each
step. This type of gait is seen in myopathic diseases.
Hysterical gait
Bizzare or irregular gait which doesn’t fit to any of the above. It is seen in conversion disorder.
Nystagmus
Nystagmus is an involuntary rhythmic oscillation of the eyes. It is noticed in visual, auditory, brainstem and
cerebellar lesions.
Types of nystagmus
1. Peripheral vestibular nystagmus

It occurs in lesions of the labyrinthine or vestibular nerve. Nystagmus is directed away from the affected side.
2. Gaze-evoked nystagmus (Nystagmus while looking away from the primary position)
It is caused by drugs (benzodiazepines, antiepileptic drugs, alcohol), cerebellar hemispheric lesions

(nystagmus towards the affected side), and brainstem lesions
Upbeat nystagmus occurs in brainstem or cerebellar vermis lesions. Downbeat nystagmus is noticed in
chiasmal herniation at cervicomedullary junction or cerebellar degeneration
3. Congenital nystagmus
It is horizontal nystagmus in which left beating on left gaze and right beating on right gaze
4. Pendullar nystagmus
It is a complication of poor vision (congenital or acquired) or pontine lesion (eg. multipl sclerosis)

Sensory system
The sensory receptors relay impulses from skin, tendons, muscles, and viscera that travel through sensory nerves
into the posterior root ganglia, which direct impulses centrally into the spinal cord. Sensory impulses then travel
to the sensory cortex of the brain via the spinothalamic tract and the posterior columns.
The peripheral component of the spinothalamic tract arises in free nerve endings in the skin that register pain,
temperature, and crude touch.
The peripheral fiber projections of the posterior column transmit the sensations of vibration, position, and fine
touch from skin, muscle spindle and joint position receptors.
Fig 8.30 Sensory pathways: A) Spinothalamic tract and B) Layering of spinothalamic tract in the cervical region

Abnormal sensory signs
1. Positive sensory signs
. Hyperesthesia- pain in response to touch
. Allodynia- non painful stimuli is perceived as painful
. Hyperalgesia- severe pain in response to a mildly noxious stimulus
. Hyperpathia- encompasses all the phenomena described by hyperesthesia, allodynia and hyperalgesia
2. Negative sensory signs
Impaired or absent primary sensory modalities (to touch, pain, and temperature)
. Hypoesthesia- reduction of cutaneous sensation to a specific type of testing (pressure, light touch, warm or
cold stimuli)
. Hypalgesia- reduced pain perception (nociception) like pricking quality of a pin
. Anesthesia- complete absence of skin sensation to pin prick
Primary sensory tests
General
Explain each test before you do it
Unless otherwise specified, the patient's eyes should be closed during the actual testing
Compare symmetrical areas on the two sides of the body, and also compare distal and proximal areas of the
extremities
When you detect an area of sensory loss, map out its boundaries in detail
Vibration
Use a low pitched tuning fork (128Hz)
Test with a non-vibrating tuning fork first to ensure that the patient is responding to the correct stimulus
Place the distal end of the fork over the distal interphalangeal joint of the patient's index fingers and big toes
Ask the patient to tell you if they feel the vibration

If vibration sense is impaired proceed proximally:
Wrists → Elbows → Medial malleoli → Patellas → Anterior superior iliac spines → Spinous processes
→Clavicles
Position Sense
Grasp the patient's big toe at the sides
Show the patient "up" and "down" of big toe
Ask the patient to identify the direction you move the big toe with the patient's eyes closed
If position sense is impaired move proximally to test the ankle joint.
Test the fingers in a similar fashion.
If indicated move proximally to the metacarpophalangeal joints, wrists, and elbows
Pain
Use a suitable sharp object to test "sharp" or "dull" sensation.
Test the following areas:
Shoulders (C4)
Inner and outer aspects of the forearms (T1 and C6)
Thumbs and little fingers (C6 and C8)
Front of both thighs (L2)
Medial and lateral aspect of both calves (L4 and L5)
Little toes (S1)
Temperature
Often omitted if pain sensation is normal
Use a test tube filled with warm or cold water, and ask the patient to identify "hot" or "cold" respectively

Shoulders (C4)
Inner and outer aspects of the forearms (C6 and T1)
Little toes (S1)
Light Touch
Use a fine wisp of cotton or your fingers to touch the skin lightly
Ask the patient to respond when ever a touch is felt
Shoulders (C4)
Inner and outer aspects of the forearms (C6 and T1)
Little toes (S1)
Dermatomal Testing
You need to check primary sensory modalities (touch and pain) following a dermatome.

Fig 8.26 Testing vibration sensation on big toe and medial malleolus, and position sense in the big toe
Fig 8.27 Segmental and peripheral nerve innervations: anterior and posterior view

Cortical sensory tests
Since these tests are dependent on touch and position sense, they can not be performed when the tests above are
clearly abnormal
Cortical sensory loss indicates damage to sensory cortex (parietal lobe) and includes the following:
Astereognosis: failure to identify common objects placed in the hand while the eyes are closed
Agraphesthesia: failure to identify a number written on the palm of hand
Impaired two-point discrimination: failure to recognize two-point separation of 2-4 mm on the lips and finger
pads, 8-15 mm on the palms, and 3-4 cm on the shins
Extinction or simultanagnosia: Perceiving only one of the stimuli on double stimulation of symmetric sides of
the body
Technique:
Graphesthesia
With the blunt end of a pen or pencil, draw a large number in the patient's palm
Ask the patient to identify the number
Stereognosis
Place a familiar object in the patient's hand (coin, paper clip, pencil, etc.)
Ask the patient to tell you what it is
Two Point Discrimination
Use an opened paper clip to touch the patient's finger pads in two places simultaneously
Alternate irregularly with one point touch
Ask the patient to identify "one" or "two."
Find the minimal distance at which the patient can discriminate
Double simultaneous stimulation (DSS)
. Touch both sides of the body with a wisp of cotton at the same time

. Ask the patient whether both stimuli are perceived
NB: Impaired two-point discrimination, astreognosis, agraphesthesia and extinction are noticed in cerebral
cortical (parietal lobe) lesion
Primitive reflexes
Observed in frontal lobe disease
. Snout reflex: Touching the lips causes pouting lip movements
. Sucking reflex: Rubbing the chin causes suckling lip movements
. Palmo-mental reflex: Scratching the palm produces ipsiilateral puckering of the chin
. Grasp reflex: The patient tends to grasp objects when placed on the hand, and continually grasp as you try to
remove from his hand
. Glabellar reflex: Repeategly tap between his eye brows with the tip of your index finger. Blink response
persists after 3-4 taps

Signs of meningeal irritation
Kernig's sign
Place patient supine with hip flexed at 900
Attempt to extend the leg at the knee >1350
The test is positive when there is pain in the lower back or resistance to extension
Brudzinski's sign
Place patient in the supine position
Passively flex the head towards the chest
The test is positive when there is flexion of the knees and hips while passively flexing the head
Neck stiffness
The examiner passively flexes patient’s neck towards the chest
The test is positive when the there is pain and resistance to neck flexion
Jolt sign
The examiner rotates patient’s head horizontally two to three times per second
The test is positive if the patient reports exacerbation of his headache
Fig 8.28 Testing meningeal irritation: A) Neck stiffness and B) Kernig’s sign

Summary of localization by sensory abnormalities
Nerve and root lesions
Nerve lesion
Polyneuropathy: simultaneous involvement of many nerve trunks
Polyneuropathy is nerve-length dependent, “stocking-glove” type, and generally graded, distal and symmetric in
distribution of sensory deficit
Small fiber polyneuropathy- burning, painful dysesthesias with reduced pin prick and thermal sensation
Proprioception, and motor function with deep tendon reflexes are spared (sensory dissociation)
Large fiber polyneuropathy- position sense deficit, imbalance, absent tendon jerks and variable motor
dysfunction with preserved most cutaneous sensation
Root lesion
Deep, aching radicular pain along the course of a related nerve trunk occurs. Dermatomal pattern of sensory loss
may occur.
Spinal cord lesion
Sensory level (all primary sensory madalities lost below the level of cord lesion)
Brain stem lesion
Impaired touch and pain sensations (numbness) on the ipsilateral face and contralateral body
Hemisphere (thalamic) lesion
Lesions in the cerebral hemisphere or thalamus produce loss of all forms of sensations on opposite side of the
body (hemisensory loss) due to involvement of both spinothalamic and posterior columns involvement. Cortical
sensory loss (impaired two point discrimination, sensory extinction, astreognosis, agraphaesthesia) is noticed in
parietal lobe lesion.

Table 8.7 Summary of neurological lesions
© Jaypee. SN Chugh, E Gupta. Clinical Methods in Medicine 2nde

CHAPTER NINE
Musculoskeletal (Locomotor) system
Learning objective

1. Mention main symptoms in musculoskeletal problem
2. Apply GALS (Gait/Arm/Leg/Spine) screening tests to detect musculoskeletal disorder
3. Mention common causes of joint disorders
4. perform technique of eliciting stretch test for back pain
History taking of the locomotor system
Major symptoms in locomotor system problem include

. Pain
. Swelling
. Morning stiffness
. Loss of function
. Deformity
. Instability
. Associated systemic symptoms
Joint pain
Describe about location of joint pain (s), mode of onset and course, pattern of spread, effect of exercise and rest,
morning stiffness, other symptoms in affected joint, and associated systemic symptoms
Have you had any pain in joint (s)?

Has the pain involved one joint or its adjacent tissues? Or have several joints been involved?
Involvement of one joint implies a monoarthritis; 2-4 joints, oligoarthritis; and 5 or more, polyarthritis.
Mode of onset and course

Did the pain develop rapidly over few days (acute arthritis < 6 weeks) or insidiously over weeks or months
(chronic arthritis > 12 weeks)?
Have there been periods of improvement or worsening? How long does the pain last?
Pattern of joint involvement

If more than one joint is involved, determine pattern of spread
Migratory- involving new joint while the initial involved joint improved, eg. arthritis in acute rheumatic fever

and gonococcal arthritis

Progressive or additive- progressed to involve new joint while the initial involved joint persisted, eg. rheumatoid
arthritis
Assess symmetry of involvement in polyarthritis eg. Symmetrical involvement of joints is observed in
rheumatoid arthritis
Effect of rest and exercise
Inflammatory arthritides produce pain at rest and on movement, and often worse in the morning.
Non-inflammatory arthritides tend to become more painful with activity and ease with rest.
Morning stiffness
Stiffness (gelling): Perception of tightness or resistance to movement, and often associated with discomfort
(muscle soreness) or pain
Stiffness in inflammatory arthritides often lasts ≥ 30 minutes
Associated symptoms with joint pain

Other symptoms in the involved joint (s) such as swelling, tenderness, warmth. or erythema; stiffness; limitation
of motion
Problems in tissues around the joint include inflammation of bursae (bursitis), tendons (tendonitis), tendon
sheaths (tenosynovitis), or stretching or tearing of ligaments (sprains)
Associated systemic symptoms such as fever, fatigue, anorexia, weight loss, and generalized weakness
Fever and chills with acute monoarthritis suggests infectious cause
Presence of systemic symptoms with chronic polyarthritis suggests connective tissue diseases like rheumatoid
arthritis, lupus arthritis, etc…
Other system symptoms giving important clues to the nature of the problem such as butter fly rash over the
cheeks (SLE); scaly rash and pitting nails (psoriatic arthritis); dry eyes and mouth (Sjogren’s syndrome); penile
erosions and scales, and red itchy eyes (Reiter’s arthritis)
Deformity
Notice for degree of deformity and functional impairment
Presence of joint deformity with functional impairment indicates advanced disease
Instability
The patient usually say “Giving way” or “Coming out” of the joint, and may be due to true dislocation, or
alternatively to muscle weakness or ligamentous problem

Raynaud’s phenomenon
Abnormal response of the fingers and toes to cold (white-blue-red response of the fingers after exposure to
cold). Patients with Raynaud’s disease have Raynaud’s phenomenon without an obvious underlying cause
(familial, more in females); or occurs seconday to connective tissue diseases (eg. scleroderma) with digital
ulcers.
Family history
Some diseases with chronic arthritis run in families including rheumatoid arthritis, crystal-induced arthropathy,
primary osteoarthritis, seronegative spondyloarthropathy, inflammatory bowel disease, etc…
Musculoskeletal terminologies
Crepitus
A palpable (less commonly audible) vibratory or crackling sensation elicited with joint motion. Coarse joint
crepitus indicates advanced cartilaginous and degenerative changes (as in osteoarthritis)
Subluxation
Alteration of joint alignment such that articulating surfaces incompletely approximate each other
Dislocation
Abnormal displacement of articulating surfaces such that the surfaces are not in contact
Contracture
Loss of full movement resulting from a fixed resistance caused either by tonic spasm of muscle (reversible) or
to fibrosis of periarticular structures (permanent)
Deformity
Abnormal shape or size of a structure. It may result from bony hypertrophy, malalignment of articulating
structures, or damage to periarticular supportive structures
Enthesitis
Inflammation of the entheses (tendinous or ligamentous insertions on bone)

Examination of the locomotor system
The gait, arms, legs and spine (GALS) screen is a rapid and sensitive screening method for detecting
musculoskeletal disorders
Gait
Watch the patient walking and turning back.
Describe the gait. Look for smoothness and symmetry of the gait. Note a limp or use of cane or crutches. The
normal gait is divided into the phases of stance (60%) and swing (40%). The stance phase is from foot-strike to
toe-off, when the foot is on the ground and load-bearing. The swing phase is from toe-off to foot-strike, when
the foot clears the ground. When both feet are on the ground, it is double stance.
Clinically important gaits include
a. Antalgic gait is a short stance phase on the painful side
b. Short-leg gait is pelvic obliquity and flexion deformity of the opposite knee
c. Coxalgic gait is an antalgic gait with a lurch toward the painful hip
d. Metatarsalgic gait is avoiding weight bearing on the forefoot
Arms
Ask the patient to put his hands behind his head, with his elbows back; observe shoulder and elbow function
Have patient bend and straight elbows
Have patient turn palms up (supination) and down (pronation) with arms at sides
Ask patient to extend and spread fingers of both hands
Ask patient to make a fist with thumbs across knuckles
Ask patient to flex, extend, ulnar and radial deviate the wrists
Legs
With tihe patient in standing position:
Examine the lower limbs for swelling, deformities or limb shortening
With the patient lying on a coach:
Flex each hip and knee with a hand on the knee to feel for crepitus
Flex leg to ninety degree at the hip and knee, and then swing the leg medially for external rotation and laterally
for internal rotation (internal rotation restriction is indicative of hip joint disease)
Flex knee upwards and pull firmly against abdomen
Abduct the hips- spread the extended legs apart
Palpate each knee for warmth and swelling, and press on the patella feeling for an effusion
Palpate the anterior surface of ankle joint for swelling and tenderness
Dorsiflex and plantar flex the foot at the ankle
Stabilize the ankle with one hand and invert/evert foot at the subtalar joint
Stabilize heel with one hand and invert/evert the forefoot at transverse tarsal joint

Squeeze gently across the metatarsals for tenderness

Flex toes on metatarsophallangeal joint
Inspect the soles of the feet for calluses and ulcers
Spine
Inspect the standing patient:
From behind- look for abnormal spinal and paraspinal anatomy and look at the legs
From the side- look for abnormal spinal posture, then ask the patient to bend down and try to touch their toes
From the front- ask the patient to try and put his ear on his left and right shoulder’, ‘touch chin to chest’, ‘touch
chin to each shoulder’, and ‘put head back’
Gently press the midpoint of each supraspinatus muscle, spinous process and paravertebral muscles with a
thumb to elicit tenderness
In sitting position on a coach: Lateral bending while stabilizing the pelvis, backward bending (extension of
spine), and twisting shoulders (rotation of spine)

Fig 9.1 Screening tests for locomotor system (GALS)
Fig 9(1).1: Inspect patient from behind and side, observing for normal spinal curves (cervical and lumbar
lordosis, and thoracic spinal kyphosis), and then ask the patient to bend forwards to try and touch his toes
Fig 9(1).2: From the front, ask the patient to place his ear on his right and then his left shoulder
Fig 9(1).3: Gently press the midpoint of each supraspinatus to elicit tenderness
Fig 9(1).4: Ask patient to put his hands behind his head. Observe for pain or restricted movement
Fig 9(1).5: Ask patient to put his hands out palms up and then turn his hands over
Fig 9(1).6: Ask patient to make a fist with both hands
Fig 9(1).7: Gently squeeze across the metacarpophalangeal (MCP) joints to elicit tenderness

Fig 9(1).8: Gently flex the hips and knees, and look for pain and restriction of movement. Look for knee
effusion
Fig 9(1).9: Squeeze across metatarsophalangeal (MTP) joints and inspect the soles of the feet
Fig 9.2 Cervical spine movement: Rotation, flexion and extension, and lateral bending

Fig 9.3 Lumbar and dorsal Spine movements: Flexion, extension, lateral bending and rotation
Fig 9.4 Spinal deformities

Fig 9.5 Shoulder movement: Flexion-extension, rotation, adduction-abduction and elevation
Fig 9.6 Movement of arm: Arm flexion and hyperextension
Fig 9.7 Movement at the wrist: Forearm supination and pronation

Fig 9.8 Finger movement: Extension and opposition of thumb
Fig 9.9 Movement at the hip joint: Flexion, rotation in extension, abduction -adduction, rotation in flexion

Fig 9.10 Movement at the knee joint: Flexion and extension
Fig 9.11 Feet movement: Foot inversion-eversion (1), forefoot adduction-abduction (2), forefoot flextion-
extension (3)

Rheumatological (Joint) disease
Combination of joint pain, swelling, stiffness (gelling) and loss of function are the classic features of joint
disease
Describe range of movement, distribution of joint involvement, signs of inflammation (warmth, tenderness,
redness, and swelling), crepitus, deformities, and associated clinical conditions
Articular structures include synovium, synovial fluid, articular cartilage, intra-articular ligament, joint capsule,
juxtaarticular bone
Non-articular (periarticular) structures include extraarticular ligament, tendon, bursae, muscle, fascia, and
overlying skin
Articular disorders are characterized by deep seated or diffuse pain, pain on active or passive movements,
swelling (due to synovial proliferation, effusion or bony enlargement), crepitus, instability, locking or deformity
Non-articular disorders tend to have pain on active but not passive movement, range of motion, and point
tenderness in regions adjacent to articular structures. Swelling, crepitus, instability or deformity seldom
demonstrated.
Fig 9.12 Structure of joint and surrounding structures
Features of mechanical joint disease

Eg. degenerative joint disease or meniscal tear
. Brief stiffness after rest (usually lasting less than 30 minutes), which disappears with activity
. Pain in the affected joint on activity, usually improving with rest
. Clicking sensation and locking of a joint
. Symptoms are confined to affected joint

Features of inflammatory joint disease

. Early morning joint stiffness that persists for more than 30 minutes , and precipitated by prolonged rest
and improve with activity
. Pain in affected joint worsens with inactivity/rest in inflammatory arthritis
Ask about redness (rubor), warmth (calor), tenderness (dolor) and swelling (tumour)
Other systemic symptoms may be present, such as fever, sweating, malaise, weight loss, etc…
Distribution of joint disease
1 .Monoarticular (single joint involvement) and oligo- or pauci- articular(2-4 joint involvement)
usually occur in septic arthritis, crystal-induced arthritis and seronegative spondyloarthropathies
2. Polyarticular (≥ 5 joint involvement) occurs in immune-mediated arthritis, such as rheumatoid arthritis,

SLE and acute rheumatic fever
Causes of monoarthritis
1. Acute monoarthritis: A single warm, tender and swollen joint

. Septic arthritis: Haematogenous (e.g. Staphylococcal )/Secondary to penetrating injury
. Traumatic
. Crystal-induced arthropathy (eg. Gout, pseudogout, or hydroxyapatite arthropathy)
. Hemarthrosis(e.g. hemophilia)
. Seronegative spondyloarthritis (occasionally)
2. Chronic monoarthritis: A single chronic inflamed joint

. Chronic infections e.g. tuberculosis
. Seronegative spondyloarthritis
Causes of polyarthritis
1 .Acute polyarthritis
. Infection-viral, bacterial(gonococcal)
. Onset of chronic polyarthritis
2 .Chronic polyarthritis

. Rheumatoid arthritis
. Seronegative spondyloarthritis
. Primary osteoarthritis
. Crystal-induced arthropathy (occasionally)
. Connective tissue disease, e.g. systemic lupus erythematosus
. Infection, e.g. Lyme arthritis, spirochaetal infection (rare)
Fig 9.13 Pattern of involved joints in polyarthritis
(A) Rheumatoid arthritis (symmetrical, small and large joints, upper and lower limbs)
(B) Psoriatic arthritis (asymmetrical, large > small joints, associated periarticular inflammation, giving
dactylitis)
(C) Seronegative inflammatory spondylitis (axial involvement, large > small joints, asymmetrical)
(D) Osteoarthritis (symmetrical, small and large joints)

Approach to regional rheumatologic complaints
1. Hand pain
Unilateral hand pain results from trauma, overuse, infections or crystal-induced arthritis
Bilateral hand complaints commonly suggest degenerative (osteoarthritis), systemic or immune inflammatory
causes (rheumatoid arthritis)
Osteoarthritis causes distal interphalangeal (DIP) and proximal interphalangeal (PIP) joint pain with bony
hypertrophy, and pain at base of thumb.
Rheumatoid arthritis (RA) causes DIP, PIP, metacarpophalangeal (MCP), intercarpal and carpometacarpal
(CMC) joint pain and deformity.
Psoriatic arthritis causes DIP and PIP joint pain and swelling, nail pitting and onycholysis.
Carpal tunnel syndrome is hand pain along the distribution of median nerve, and occurs in trauma, osteoarthritis
and inflammatory arthritis (RA).
Tinel’s and Phalen’s sign are usually positive in carpal tunnel syndrome: Paresthesia in a median nerve
distribution is reproduced by “thumping” the volar aspect of the wrist (Tinel’s sign) or pressing the extensor
surfaces of both flexed wrists against each other (Phalen’s sign)
Fig 9.14 Technique of eliciting Phalen’s sign (reproducing paresthesia with the above maneuver)
Hand examination
Look

Colour change: Erythema suggests acute inflammation caused by soft tissue infection, septic arthritis or crystal-
induced disease (gout and pseudogout)
Swelling: swelling at the MCP or IP joints suggests synovitis
Deformity: Boutonnière (button-hole) deformity is a flexion deformity at the PIP joint with hyperextension at
the DIP joint, and 'Swan neck' deformity is hyperextension at the PIP joint with flexion at the DIP joint. Both
are hand deformities seen in patients with rheumatoid arthritis.
Dupuytren's contracture affects the palmar fascia, resulting fixed flexion deformity at MCP and PIP joints of the
little and ring fingers
Feel
Soft swellings suggest synovitis, while hard swellings suggest bony outgrowths
Heberden’s and Bouchard’s nodes at DIP and PIP joint bony growths of fingers suggest osteoarthritis
. Detect synovitis in the IP joints by gently squeezing with your thumb and index finger above and below the
joint to detect sponginess
. Test the MCP joints by examining for sponginess by squeezing gently across the metacarpal joints
. Palpate the flexor tendon sheaths in the hand and fingers to detect local swellings or tenderness
Move
Range of motion of hand: Ask the patient to make a fist with each MCP and IP joint flexed to 900; and ask the
patient to squeeze two of your fingers to test grip
a. Rheumatoid arthritis b. Osteoarthritis
Fig 9.15 Joint deformities in rheumatoid arthritis (Swan neck and Boutonniere derormities); and bony out
growths in osteoarthritis (Heberden and Bouchard nodes)

2. Shoulder pain
It results from trauma, fibromyalgia, infections, inflammatory diseases, occupational hazards or cervical disease
It may be referred pain from intrathoracic lesions (pancoast tumor), gall bladder, hepatic, or diaphragmatic
diseases
Shoulder pain occurs in subacromial bursitis, bicipital tendonitis, osteoarthritis, rheumatoid arthritis, and rotator
cuff tear or tendonitis
Rotator cuff tendonitis is the common cause of shoulder pain. It is characterized by pain on active abduction,
night pain, and impingement sign
Shoulder Examination
Look
Examine the whole shoulder girdle from front and back side
Look for deformities in joint dislocation
Look for any swelling, deformity or muscle atrophy
Feel
Palpate the acromioclavicular joint, glenohumeral joint, subacromial space, bicipital groove and the scapula
Tenderness in shoulder is due to synovitis, rotator cuff impingement, or bicipital tendonitis
Move
Range of motion of shoulder: Forward flexion (180°), extension (45°), abduction (150°), external rotation (90°),
internal rotation (90°), and horizontal adduction (130°)
. Limitation of external rotation is a good sign of true glenohumeral disease as in erosive damage by
inflammatory arthritis or adhesive capsulitis (frozen shoulder)
Rotator cuff tendonitis

It is caused by repetitive overhead activities such as throwing, raking, washing, etc…
It presents with shoulder pain and limitation of shoulder activities
Ask the patient to abduct the arm from the side of the body. If abduction is painful from 600 to 1200, it
suggests rotator cuff tendonitis

Rotator cuff impingement

Shoulder impingement syndrome occurs when the tendons of the rotator cuff and the subacromial
bursa are pinched in the narrow space beneath the acromion. The pinching is worse when the arm is
raised away from the side of the body. It results from minor injuries and repetitive motions.
Impingement sign
1. Neer’s sign - extreme forward flexion with the forearm pronated
2. Hawkin’s sign - 90° forward flexion of the shoulder with the elbow flexed to 90° then internal and
external rotation movements of the shoulder
3. Crossover sign - extreme horizontal adduction across the chest
Pain with these maneuvers suggests rotator cuff impingement in the subacromial space
Adhesive capsulitis (Frozen shoulder)
It is characterized by stiffness and pain at the shoulder joint. Immune, inflammatory and fibrotic
changes appear to be involved in the pathophysiology of frozen shoulder. It is caused by trauma,
surgery, inflammatory disease, diabetes, and shoulder maladies. Initially, it causes shoulder pain with
limited range of motion, followed by stiffer joint with subsiding pain, and at last improvement in range
of motion.
Fig 9.16 Painful arc (shoulder pain from 600 to 1200 during abduction) indicates rotator cuff tendonitis

3. Knee pain
Knee pain and swelling result from synovial effusions due to inflammatory arthritis (RA, gout, pseudogout or
reactive arthritis), hemarthrosis (coagulopathy and torn cruciate ligament), or bony enlargement in degenerative
arthritis (osteoarthritis)
Knee locking is block to full extension, which is caused by a loose body or meniscal tear
Knee instability (‘giving way’) occurs in ruptured or loose ligament from injury or degenerative disease
respectively
Knee joint examination
Look
. Observe the patient walking and standing
. Look for posture and deformities; Genu varum (bow legs) and genu valgum (knock knee)
. Look for muscle wasting; measure the thigh girth in both legs 20 cm above the tibial tuberosity
. Measure leg length discrepancy
. Notice for enlarged prepatellar bursa (housemaid's knee), effusion of the knee joint, and Baker's cyst (bursa
enlargement in the popliteal fossa)
Feel
Knee joint effusions give positive ‘bulge sign’ and ‘balloon sign’
a. The bulge sign (for minor effusion)
With the knee extended, place the left hand above the knee and apply pressure on the suprapatellar pouch,
displacing or “milking” fluid downward. Stroke the medial aspect of the knee and apply pressure to force fluid
into the lateral area. Tap the knee just behind the lateral margin of the patella with the right hand. Bulge on the
medial side between the patella and the femur is positive test for knee effusion.

Fig 9.17 Testing technique for bulge sign
(A) Empty the suprapatellar pouch (B) Stroke the medial side of the joint to displace excess fluid to the lateral
side of the joint. (C) Stroke the lateral side while watching the medial side closely for a bulge
b. The balloon sign (for large effusion)
With the knee extended, place the thumb and index finger of your right hand on each side of the
patella.Compress the suprapatellar pouch against the femur with the left hand. Palpate for fluid ejected or
“ballooning” into the spaces next to the patella under your right thumb and index finger. A palpable fluid wave
is positive test for knee effusion.
Fig 9.18 Testing technique for balloon sign
Move
Range of motion of knee: Ask him to flex the knee up to the chest and then extend the leg back down (normal
range 0-140°)
A restriction to full extension occurs with meniscal tears, osteoarthritis or inflammatory arthritis.
Knee meniscal cartilage (medial and lateral) damage
Suspect meniscal cartilage damage when a patient complains of locking, clicking or ‘giving way’ of the joint,
usually occurs in trauma or athletic activity
Positive McMurray test indicates meniscal tear

. Flex the knee at 90o, and then extend the legs while the lower extremity is simultaneously torqued medially or
laterally
. Painful click during inward rotation or outward rotation indicates lateral and medial meniscal tear respectively
Knee collateral ligament damage
. Hold the ankle between your elbow and side with patient’s knee extended
. Use both hands to apply a valgus and then varus force to the knee
. Use your thumbs to feel the joint line and assess the degree to which the joint space opens
Major opening of the joint indicates collateral injury
Knee cruciate ligament damage
It occurs in traumatic injury to knee
Drawer sign: Positive drawar sign indicates cruciate ligament damage
. While the patient in recumbent position, partially flex the knee and the foot stabilized on the examining surface
. Manually attempt to displace the tibia anteriorly or posteriorly with respect to the femur
. Excessive anterior or posterior ‘glide’ or ‘draw’ may indicate respective anterior and posterior cruciate
ligament laxity or instability
Fig 9.19 Testing A) Collateral and B) Cruciate ligaments of the knee

4. Hip pain
True hip joint pain tends to be located anteriorly over the inguinal ligament and may radiate medially to the
groin or along the anteromedial thigh
Anterior hip pain is due to true hip pain, iliopsoas bursitis, enthesitis or meralgia paresthetica
Posterior hip pain is due to sacroiliac pain, buttock pain in sciatica, trochanteric bursitis, ischiogluteal bursitis,
or gluteal and trochanteric pain due to fibromyalgia
Hip joint Examination
Look
. Look the two phases of gait
Stance-when the foot is on the ground and bears weight (60% of the walking)
Swing-when the foot moves forward and doesn’t bear weight (40% of the walking)
. Observe for pelvic tilt and deformities of hip
Feel
Palpate for tenderness over anterior hip joint, anterior superior or inferior iliac spine, posterior superior iliac
spine, sacroiliac joint, ischial tuberosity and gluteus muscles
Move
Range of motion of hip
Internal rotation (30°) - Stabilize knee at 90° flexion with patient supine, move the leg away from midline
External rotation (60°) - Stabilize knee at 90° flexion with patient supine, move the leg toward midline
Flexion (120°) - with patient supine, grasp bent knee and pull to chest (stop when back flattens)
Extension (15°) - while prone, lift the leg off table
Abduction (45°) - with patient supine, pull the leg away from midline
Adduction (30°) - with patient supine, pull the leg toward midline (until pelvis tilts)
Special tests for hip joint

1. Measurement of 'true' and 'apparent' shortening of the leg
. Measure the length of the two legs from the anterior superior iliac spine to the medial malleolus. Any difference
is termed ‘true' shortening’; and results from disease of the hip joint on the shorter side
. Measure the lengths of the two legs from the umbilicus to medial malleolus. ‘Apparent' shortening’ is due to
tilting of the pelvis by adduction deformity of the hip
Fig 9.20 Measuring ‘apparent’ and ‘true’ length of lower limb
2. Test for flexion deformity (Thomas’s test)
. Position the patient supine on hard surface
. Flex both the patient's legs (hips and knees) as far as possible to the point of abolishing the lumbar lordosis
. Keep the non-test hip maximally flexed, and ask the patient to extend the test hip
. Incomplete extension of the test hip indicates fixed flexion deformity

Fig 9.21 Thomas’s test: Testing flexion of hip
3.Trendelenburg’s test
. Observe the patient from behind , and ask the patient to stand on one leg
. Normally, the pelvis tilts upwards on the side with the leg off the ground
. When the weight bearing hip is abnormal, the pelvis sags upward due to weakness of the gluteal muscles on the
same side
Fig 9.22 Trendelenburg’s test for abnormal hip abductors: Weakness of the right gluteal muscles results in
upward pelvic tilt when standing on the right leg

Tests for inflamed hip joint
. Patrick sign: Hip pain is reproduced by internal or external rotation at the hip with the knee and hip in flexion

5. Back pain
Types of back pain
. Local pain- Caused by stretching of pain-sensitive structures that compress or infiltrate sensory nerve endings
. Pain referred to the back – arises from abdominal or pelvic viscera
. Pain of spine origin (sclerotomal pain) – located in the back or referred to the buttock or legs
. Radicular pain – sharp pain radiating from the spine to the legs within the territory of a nerve root
. Pain associated with muscle spasm- dull spinal pain accompanied by abnormal posture
Common causes of back pain
. Congenital – spondylosis and spondylolisthesis, tethered spinal cord
. Fracture
. Traumatic- fall accident, motor vehicle accident
. Non-traumatic- osteoporosis, metastatic neoplasm deposits, prolonged steroid therapy
. Intervertebral disc prolapse
. Arthritis- spondyloarthropathies
. Degenerative – Disk-osteophyte complex, internal disk disruption, spinal stenosis with neurogenic claudication
. Infection – vertebral osteomyelitis, spinal epidural abscess, septic disk
. Neoplasm – metastatic solid tumors, multiple myeloma, primary bone tumor
. Others – referred from visceral disease, postural, psychiatric, chronic pain syndrome
‘Warning features’ of back pain for underlying systemic disease
. Age < 20 years or >50 years
. Unexplained fever or weight loss
. Pain at night or present at rest
. Back pain lasting more than 1 month, or not responding to treatment
. Associated neurologic symptoms, or progressive neurologic deficits
. Presence of immunosuppression or HIV infection

. History of cancer
. Long term steroid therapy
Examination of the back
Look
The normal spine has cervical and lumbar lordosis and thoracic kyphosis
Look for hyperkyphosis (lame back) of the thoracic spine, or hyperlordosis (sway back) of the lumbar spine
Inspect the lateral curvature of the spine (scoliosis)
Feel
Palpate and percuss the spine: back pain of bony spine origin is often reproduced by palpation or percussion
over the spinous process of the affected vertebrae
Move
Range of motion of the spine
Forward flexion (normally 80 to 90°) can measure distance of fingertips from floor and is thus more likely to
increase disc pain
Extension (20 to 30°) loads the facets and thus is more likely to increase facet pain
Lateral bending (20 to 30° in each direction) stretches muscle and is more likely to aggravate pain from muscle
strain
Twisting (30 to 40° in each direction) stretches muscle and increases pain from muscle strain

Fig 9.23 Anatomic structure of the lower back
Tests for back pain due to disc prolapse
Straight leg-raising (lasegue’s) sign
Back pain is reproduced on passive flexion of the extended leg at the hip (straight leg-raising) while the patient
lying supine is a feature of prolapsed intervertebral disc, which causes irritation or compression of one of the
roots of the sciatic nerve. If in doubt, dorsiflex the foot once the limit of straight leg-raising has been reached,
which further stretches the sciatic nerve
Crossed straight leg-raising sign (crossed SLR sign)
More specific but less sensitive to disc prolapse than straight leg-raising sign
Flexion of one leg at the hip reproduces the pain in the opposite leg or buttock while the patient lying in supine
position
The femoral stretch test (reverse SLR test)
It is a useful confirmatory test for prolapsed disc
Back pain is reproduced by flexion at the knee while the patient lying prone

1. Sciatic nerve 2. Femoral nerve
Fig 9.24 Stretch test
1) Left side (Sciatic nerve)
A) Straight leg raising limited by tension of root over prolapsed disc B) Tension increased by dorsiflexion of
foot (Bragard's test) C) Root tension relieved by flexion at the knee D) Pressure over centre of popliteal fossa
bears on posterior tibial nerve which is 'bowstringing' across the fossa, causing pain locally and radiation into
the back
2) Right side (Femoral nerve)
A) Pain may be triggered by knee flexion alone B) Pain may be triggered by knee flexion in combination with
hip extension
Special test in back pain
Modified Schober's test
The extent of lumbar flexion can be assessed more accurately by marking a vertical 10 cm line on the skin
overlying the lumbar spinous processes and the sacral dimples and measuring the increase in the line length on
flexion (normally ≥5 cm)

. Mark the spine at lumbosacral junction parallel to posterior iliac spine, then 10cm above and 5cm below the
point.
. Flattening out of lumbar lordosis and 5cm or more increase between the two upper marks during flexion of the
spine is observed in normal individuals. (The distance between the lower two marks should be unchanged)
NB: Persistence of lumbar lordosis with reduced (≤4cm) lumbar flexion length suggests ankylosing spondylitis
Fig 9.25 Modified Schober’s test: Measuring extent of flexion of the spine

_______________________________________________________________________________________
Table 9.1 Causes of lower back pain

CHAPTER TEN
The urinary tract
Learning objective
1. Mention main symptoms in urinary tract problem

2. Show techniques of examining the kidneys
3. List and interpret major urinary syndromes
4. List causes of oliguria
History taking of urinary system
Major symptoms in urinary tract problem include
. Flank pain
. Oliguria or anuria
. Hematuria
. Polyuria
. Urinary incontinence
. Lower urinary tract symptoms: Dysuria (pain during urination), frequency of micturition, urgency, hesitancy,
dribbling, reduced caliber and force of urinary stream, and straining to void
Flank pain
. Flank pain is visceral pain typically dull, aching, and steady pain due to sudden distension of renal capsule in
acute pyelonephritis or acute glomerulonephritis
. Renal colic is colicky pain in the loin that radiate to the medial thigh or groin, which results from sudden
distension of ureter or renal pelvis by renal stone, sloughed papillae or blood clots
Oliguria or anuria

Oliguria is urine volume < 400ml per day
Anuria is urine volume < 100ml per day
Causes of oliguria
Intrinsic renal causes
. Acute tubular necrosis (ATN) secondary to ischemic or nephrotoxic injury to the kidney
Ischemic: Hypovolemia due to GI loss (severe diarrhea or intractable vomiting), blood loss (variceal
hemorrhage)
Nephrotoxic: Aminoglycosides, radiocontrasts, rhabdomyolysis
. Acute glomerulonephritis/ vasculitis: Post-infectious glomerulonephritis, anti-neutrophil cytoplasmic antibody

(ANCA)-positive glomerulonephritis
. Acute renal vascular obstruction: Hemolytic uremic syndrome (HUS) /thrombotic thrombocytopenic purpura
(TTP), accelerated hypertension, toxemia of pregnancy
. Acute interstitial nephritis: Allergens (antibiotics, Non-steroidal anti-inflammatory drugs), infections (viral,
bacterial, fungal)
. Intratubular deposition and obstruction: Multiple myeloma, uric acid nephropathy
Pre-renal causes
. Hypovolemia due to hemorrhage, burns, dehydration, gastrointestinal fluid loss (persistent vomiting or
diarrhea)
. Low cardiac output- congestive heart failure
. Systemic vasodilatation- sepsis, anaphylaxis, hepatic cirrhosis
Post-renal causes
. Bilateral ureteric obstruction- calculi, blood clot, sloughed papillae, cancer
. Bladder neck obstruction- Benign prostatic hyperplasia (BPH), prostatic cancer, neurogenic bladder
. Urethral obstruction- stricture, phimosis

Hematuria
Hematuria is reddish discoloration of urine due to blood in the urine
It could be gross or microscopic hematuria
Gross hematuria is reddish discolored urine visible with naked eye, while microscopic hematuria is microscopy
or dipstick proven presence of red cells in the urine
Significant hematuria is defined as >3 RBCs/high power field (hpf) on 3 urinalyses, >100 RBCs/hpf on single
urinalysis, or gross hematuria
Types of hematuria
. Initial hematuria- hematuria at the beginning of urination, and indicates bleeding from urethra
. Terminal hematuria- hematuria at the end of urination, and indicates bleeding from the urinary bladder
. Hematuria throughout urination indicates bleeding from the kidney
Common causes of isolated hematuria
. Calculi
. Neoplasms
. Trauma
. Renal tuberculosis
. Prostatitis
The most common causes of isolated glomerular hematuria (hematuria with dysmorphic RBCs, RBC casts and
proteinuria >500mg/day)
. IgA nephropathy
. Hereditary nephropathy
. Thin basement membrane disease
Hematuria of renal parenchymal disease is usually painless, continuous, microscopic, while hematuria of renal
tumor is likely to be painful, continuous, and macroscopic

Polyuria
Polyuria is urine volume >3 liters in 24-hours
It must be differentiated from urinary frequency, abnormally frequent voiding. Urinary frequency is often
associated with relatively small volumes at each passage while polyuria is associated with high volumes of urine
with each voiding
Causes of polyuria
. Neurogenic polydipsia (hypothalamic-pituitary abnormality)
. Nephrogenic polydipsia (antidiuretic hormone (ADH)-insensitive kidney)
. Diabetes mellitus
. Primary polydipsia (psychogenic- excessive water intake)
. Solute diuresis (diuretics, mannitol infusion, saline infusion)
. Electrolyte abnormalities- hypercalcemic or hypokalemic nephropathy
Urinary incontinence
Urinary incontinence refers to an involuntary loss of urine
Types of urinary incontinence
. Urge incontinence: Spastic bladder due to strong detrussor muscle contraction
It occurs in diminished cortical control (stroke, Alzeimer’s disease), hyperexcitability of sensory pathways
(cystitis), or deconditioning of voiding reflex (frequent voiding at low bladder volume)
. Stress incontinence-weakened urethral sphincter resulting in reduced urethral resistance
It results from weakened pelvic floor from repeated child birth, surgery or urethral infection
. Overflow incontinence: Flaccid bladder
It results from weakness of detrussor muscle due to peripheral neuropathy (pudendal nerve damage), or
impaired bladder sensation (diabetic neuropathy)
. Functional incontinence- functional inability to go to the toilet in time due to impaired health or inconvenient
environmental conditions

Symptoms of lower urinary tract abnormalities include the following:
. Frequency of micturition-passing urine more often than usual
. Urgency-unusually intense and immediate desire to void
. Hesitancy-difficulty or delay in initiating urine flow
. Straining to void
. Reduced caliber and force of the urinary stream
. Dribbling after micturition
. Dysuria- pain (burning sensation) on urination, indicates inflammation of the bladder or urethra
Females perceive dysuria as internal urethral discomfort in cystitis and urethritis, or as external burning
sensation in vulvovaginitis
Hesitancy, straining, reduced force and caliber of urinary stream and dribbling after micturition occur in bladder
outlet obstruction (BOO) due to benign prostatic hyperplasia (BPH) or urethral stricture
If straining increases force and caliber of urinary stream, it favors urethral stricture, but not BPH
Lower urinary tract infection (cystitis or urethritis) frequently presents with suprapubic pain, dysuria, frequency
of urination, urgency and hesitancy
Upper urinary tract infection (pyelonephritis) frequently presents with fever, chills, rigors, vomiting, flank pain,
hematuria, with or without local urinary tract irritative symptoms

Examinations of the kidneys and urinary bladder- refer to abdominal examination
. Notice for costo-vertebral angle tenderness (CVA tenderness)
Technique:
. Locate the costovertebral angle at the back
. Place the ball of left hand in the costovertebral angle and strike it with the ulnar border of the fisted right hand
Pain with fist percussion at the costovertebral angle suggests pyelonephritis
Fig 10.1 The surface anatomy of the kidneys from the back
Fig 10.2 Eliciting costo-vertebral angle (CVA) tenderness to left kidney

Major urinary syndromes
1. Acute kidney injury (AKI)
Abrupt onset of declining in renal function occurring over a period of hours or days
Clues to diagnosis- oliguria, recent decline in glomerular filtration rate (recently raised serum creatinine)
Common findings- hypertension, edema, hematuria, proteinuria, casts
2. Acute nephritic syndrome
Brisk onset of reduction in renal function with retention of nitrogenous wastes, and salt and water
Clues to diagnosis- Azotemia (↑ serum Cr), hematuria, red cell cast, proteinuria
Common findings-oliguria, hypertension, and edema
3. Chronic kidney disease (CKD)
Clues to diagnosis- azotemia (↑ serum Cr) > 3 months, bilateral shrunken kidney, broad casts in urinary
sediment
Common findings- anemia, nocturia, hypertension
4. Nephrotic syndrome
Clues to diagnosis- Heavy proteinuria > 3.5gm/1.73m2/day, hypoalbuminemia, hypercholesterolemia and edema
5. Asymptomatic urinary abnormalities
Clues to diagnosis- hematuria, sub-nephrotic range proteinuria
6. Urinary tract infection
Clues to diagnosis- Presence of a significant number of infecting bacteria in the urine (bacteria ≥105 colony
forming units (cfus)/ml in mid stream urine), pyuria, leukocyte casts
Common findings- fever, flank pain, flank tenderness, +/- lower urinary tract irritative symptoms (suprapubic
pain, frequency of urination, dysuria, urgency, etc…)
7. Renal tubule defects
Clues to diagnosis- polyuria, nocturia, renal calcification, large kidneys, renal transport defects
Common findings- ‘tubular’ proteinuria (<1gm/day), hematuria, enuresis
8. Hypertension

Renal parenchymal and vascular diseases account for 90% of secondary hypertension. Renal parenchymal
hypertension is caused by glomerulonephritis, renal tubulointeristial disease, renal obstruction, and renal stone
disease.
Secondary hypertension is suspected when blood pressure is refactory to 3 or more anti-hypertensive

medications, recently recognized highly elevated blood pressure in young individuals (age < 35 years) or older
adults (age > 55 years), or presence of clinical and imaging clues to secondary hypertension.
Clues to diagnosis- Blood pressure ≥ 130/80 mmhg
Common findings- proteinuria, casts, azotemia
9. Nephrolithiasis
Nephrolithiasis is the presence of one or more stones in any part of the urinary tract.
Presentation: asymptomatic, asymptomatic urinary abnormality, or symptomatic (renal pain or ureteric colic)
Clues to diagnosis- renal colic, history of stone passage, history of stone seen by KUB X-ray
Common findings- hematuria, pyuria
10. Urinary tract obstruction
Lower urinary tract obstruction is urinary retention (residual urine) in the bladder after micturition associated
with frequency, nocturia, poor stream, hesitancy, and terminal dribbling as consequence of a low functional
bladder capacity, inability to empty the bladder completely and impairment of the urinary flow rate. Eg. Prostatic
hypertrophy or carcinoma
Upper urinary tract obstruction is demonstrated by dilated renal collecting system (renal pelvis and/or calyces), often
seen to be proximal to a specific ureteral obstructing lesion. Eg. Ureteric stone, clot, or neoplasia
Clues to diagnosis- oliguria, retention of urine, azotemia, large prostate, dilated renal pelvis and/or calyces
Common findings- hematuria, pyuria, enuresis

Female Genitalia
Learning objective
1. Mention symptoms in gynecologic problem

2. Describe vaginal discharge and genital ulcer syndromes
3. Perform pelvic examination of gynecologic patient
4. Describe types of abnormal menstrual bleeding
Gynecologic history taking and pelvic examination
Gynecologic history taking
Female patients with gynecologic problem present with one or more of the following symptoms
. Vaginal bleeding (abnormal uterine bleeding)
. Menstrual irregularities
. Amenorrhea (10, 20)
. Vaginal discharge
. Genital ulcer with/without inguinal swelling
. Lower abdominal or pelvic pain
. Pre-menstrual symptoms
. Pre-menopausal symptoms
. Dyspareunia
. Premature menopause
Menstrual history
Age at menarche (age of starting menses), how often do the menstrual periods come? how regular or irregular
are menstrual periods? how heavy is the menstrual flow? (number of pads or tampoons used daily)
What color is the menstrual flow? Under normal circumstance, it is dark red menstrual flow. Bright red with
clot indicates excessive menstrual flow

Pelvic discomfort or pain before or during menstrual periods (express type of pain, how long does it last?)
History of abnormal menstrual bleeding
History of abnormal menstrual bleeding may have organic causes or may be dysfunctional uterine bleeding
(DUB)
Menorrhagia- Excessive menstrual flow
Metrorrhagia- Irregular menstrual flow (intermenstrual bleeding)
Metromenorrhagia- Irregular, prolonged and excessive menstrual flow
Oligomenorrhea- Infrequent menstrual periods
It occurs at intervals longer than 35 days. It frequently occurs during the 1st 2yrs after menarche or before
menopause in normal women.
Polymenorrhea-Abnormally frequent menstrual periods (less than 21-day intervals between menses)
Dysmenorrhea- Crampy or aching lower abdominal or pelvic pain prior to or during menstrual period
Post-coital bleeding- indicates cervical disease such as cervical polyp or cancer
Post-menopausal bleeding- vaginal bleeding more than 1 year after the final menstrual period. Investigate to
exclude cancer of genital tract. Eg. Endometrial cancer
History of premenstrual syndrome
A cluster of emotional, behavioral and physical symptoms, which occurs five days before each menses for three
consecutive cycles
It is characterized by the presence of nervousness, irritability, depression and mood swings, abdominal bloating,
headache, and tenderness and edema of the breast
Amenorrhea: Absence of menstrual periods
Primary amenorrhea- failure to initiate menstrual periods by age of 16 years
Secondary amenorrhea- cessation of periods for more than 3 months after menstrual periods have been
established
Physiologic causes of secondary amenorrhea includes pregnancy, lactation and menopause

Vaginal discharge with/ without lower abdominal or pelvic pain
. Notice for color, amount, odor and consistency of vaginal discharge
Mucopurulent cervicits and vaginitis present with abnormal vaginal discharge
All cases of cervicitis are sexually transmitted infections, however most cases of vaginitis are reproductive tract
infections
Genital ulcer with/without inguinal swelling
Characterize the genital ulcer: Site, single or multiple, painful/tender or not, clean based or dirty ragged ulcer,
associated inguinal swelling (painful/tender or not, unilateral or bilateral inguinal lymph node involvement)
Dyspareunia
Discomfort or pain during sexual intercourse
Superficial pelvic pain (vaginismus) may be due to inadequate lubrication, vulvovaginitis or atrophic vaginitis
Deep pelvic pain suggests pelvic inflammatory diseases like cervicitis, endometritis or adnexitis
Menopause
Cessation of menstrual periods, usually occurs at age of 45-52 yrs
Age at menopause and menopausal symptoms (hot flushes)
Post menopausal bleeding- bleeding that occurs after 6 months of established menopause, usually raises the
question of endometrial cancer

Fig 10.3 Female external genitalia
Fig 10.4 Female pelvic organs (coronal section)

Table 10.1 Tips for the successful pelvic examination
Pelvic Examination
. Explain what you are going to do so that she can better understand your gynecologic procedure
. Explain in advance each step of the examination
. Ask the patient to empty her bladder before the examination
. Position the patient and drape her appropriately
. Wear gloves throughout the examination
Indications for pelvic examination
. Menstrual abnormalities
. Unexplained lower abdominal pain
. Vaginal discharge
. Contraceptive prescription
. Bacteriological and cytological studies
. Rape cases
. Patient’s desire for assessment
Patient positioning
. Place the patient in lithotomy position with her arms at her sides or folded across her chest, and assist her to
place her legs on the straps of examining coach
. The drape should cover her thighs and knees
. Ask her to move toward the end of examining coach
. Her thighs should be flexed, abducted, and externally rotated at the hips

Fig 10.5 Position for pelvic examination
Inspection/Palpation
. Note for distribution of pubic hair (assessment of sexual maturity in adolescents)
. Inspect the external geneitalia (labia majora and minora, clitoris, urethral meatus, vaginal opening, introitus,
bartholin’s gland and Skene’s gland) for inflammation, ulceration, discharge, swelling or nodules/warts
Bartholin’s cyst
. Look for Bartholin’s cyst in labial swelling
. Palpate between your index finger (inside) and thumb (outside) for swelling due to bartholin’s cyst, and notice
for discharge and tenderness near the posterior end of the introitus

Fig 10.6 Technique of palpating the Bartholin’s cyst
Paraurethral (Skene’s) cyst
. Insert your index finger into the vagina and milk the urethra from inside to outward, and note for discharge
Fig 10.7 Milking the urethra (Skene’s cyst)

Vaginal wall and Cervix
. Locate the cervix
Lubricate your index finger with water and insert into the vagina and identify the firm, rounded surface of cervix
It helps to choose the size of speculum and to accurately angle the speculum
. Assess vaginal walls
Separate the labia with your middle and index finger and ask her to strain down and note for any bulging of
vaginal walls (cystocele or rectocele)
. Insert the speculum
Select speculum of appropriate size and shape, and lubricate with warm water
Hold the speculum with your left hand, and insert and slide the speculum inward along the posterior wall of the
vagina
Rotate the speculum in horizontal position, and insert it to its full length
. Inspect the cervix
Open the speculum and adjust until it cups the cervix
Maintain speculum position by tightening the thumb screw
Note the cervical color, position, ulceration, nodules, masses, bleeding or discharge
Obtain specimens for cervical cytology (papanicolaou smear) by endocervical swab, cervical scrape or cervical
brush
Release the thumb screw and withdraw the speculum slowly while observing the vagina
Inspect the vaginal mucosa for any inflammation, discharge, ulceration, or masses during speculum withdrawal
Close the speculum as it emerges from the introitus

Fig 10.8 Technique of inserting the speculum
Bimanual examination
Perform bimanual examination to appreciate any abnormalities of the cervix, uterus and adnexa (ovary and
adjacent structures)
. Lubricate and insert index and middle fingers into the vagina with your ring and little finger flexed into your
palm and press inward on the perineum with your flexed fingers
. Palpate the cervix and note for any nodularity, shape, consistency, regularity, mobility and tenderness
. Feel for fornices around the cervix
NB: Presence of cervical motion (excitation) tenderness suggests cervicitis
Palpate the uterus
. Place the left hand on the lower abdomen midway between umbilicus and synphysis pubis
. Elevate the cervix and uterus with your pelvic hand, and place and press your abdominal hand in and down to
grasp the uterus between your hands
. Note for uterine size, shape, consistency, mobility, masses and tenderness
Palpate the ovary
. Place your abdominal hand on the right lower quadrant or left lower quadrant of the abdomen, and your pelvic
hand in the lateral fornices

. Press your abdominal hand in and down to push the adnexal structures toward your pelvic hand
. Identify the ovaries and adjacent adnexal masses
. Note for ovary size, shape, consistency, mobility and tenderness
NB: Adnexal tenderness suggests pelvic inflammatory disease (PID)
Assess the strength of pelvic muscles as you withdraw the pelvic fingers
. Ask the patient to squeeze her pelvic muscles around your fingers as hard and as long as possible
Full strength is noticed by snugly compressing the fingers, and moving them upward and inward lasting for ≥ 3
seconds
. Withdrew your pelvic fingers
Fig 10.9 Technique of bimanual examination of the uterus

Fig 10.9 Technique of bimanual examination of the adnexa (Ovary and adjacent structures)
Rectovaginal examination
. Reintroduce your index finger into the vagina and your middle finger into the rectum
. Repeat the maneuver of bimanual examination
. Wipe off the external genitalia and anus after withdrawing the fingers
Rectovaginal examination is especially valuable in assessing retroverted uterus
Vaginal discharge syndrome
Vaginitis and cervicitis
Disease Etiology
Bacterial vaginosis Gardnerella vaginalis, Mycoplasma hominis
Vulvovaginal candidiasis Candida albicans
Trichomonal vaginosis Trichomonas vaginalis
Mucopurulent Cervicitis Neisseria gonorrhea, Chlamydia trachomatis

Vaginitis
Majority of cases of vaginitis are not sexually transmitted infections, and caused by endogenous normal flora of
the vagina
1. Bacterial vaginitis
Etiology: Gardnerella vaginalis
It causes endogenous reproductive tract infection with fishy odor homogenous vaginal discharge
Presence of Clue cells (distorted vaginal epithelial cells coated heavily with gram-negatve coccobacilli) in wet
mount smear of the vaginal discharge is characteristic of Gardnerella vaginalis infection
Predisposing factors: Use of antiseptic/ antibiotic vaginal preparations, or absent/reduced vaginal douching
2. Vulvo-vaginal candidiasis
Etiology: Candida albicans
Non-offensive whitish curd-like vaginal discharge with vulval itching and soreness, and erythematic vulva with
excoriations from scratching and vulval edema on examination
Predisposing factors: Use of antiseptic/ antibiotic vaginal preparations, or absent/reduced vaginal douching
3. Trichomonas vaginitis
Etiology: Trichomonas vaginalis
Sexually transmitted infection which is characterized by offensive profuse foaming greenish-yellow vaginal
discharge and vulval itching
Cervicitis
All cases of muco-purulent cervicitis are caused by sexually transmitted bacteria
Etiology: Neisseria gonorrhea, Chlamydia trachomatis
Both bacteria cause cervicitis, and major cause of sexually transmitted infection, which present with
mucopurulent vaginal discharge with pelvic pain and cervical motion tenderness
Redness, contact bleeding, spotting and endocervical discharge in speculum examination
Positive cervical motion/excitation tenderness on vaginal digital examination

Genital ulcer syndrome
All genital ulcers are sexually transmitted infection
Causative organism Disease
Treponema pallidum Syphilis
Haemophilus ducreyii Chancroid
Chlamydia trachomatis LGV (lymphogranulomavenereum)
Herpes simplex virus-type 2 Genital herpes
Table 10.3 Causes of genital ulcer
___________________________________________________________________________
Disease Genital ulcer Inguinal Lymphadenopathy

___________________________________________________________________________
Syphilis Non-tender, indurated clean based ulcer Non-tender, non-suppurating rubbery
bilateral LAP
Chancroid Tender, non-indurated shallow ragged ulcer Suppurative, tender lymphadentis
LGV Small, painless papules may be seen Non-tender, suppurative lymphadenitis
with multiple draining sinus tracts
Genital herpes Tender, multiple vesicles coalescing Non-suppurative, tender, bilateral LAP
to form an ulcer
__________________________________________________________________________________________

Pregnant woman
Learning objective
1. List main symptoms in obstetric history taking

2. Perform and interpret modified Leopold’s maneuvers
3. Describe systemic changes during pregnancy
Obstetric history taking and examination
Obstetric history taking
Current parity and gravidity
Physiologic amenorrhea (duration), GA (gestational age) by date, EDC (expected date of confinement)
Expected weeks of gestation by date, if last menstrual period (LMP) is known
. Count in weeks from the first day of the LMP (menstrual age) OR the day of conception (conception age)
Menstrual age is used most frequently to express the weeks of gestation calculated by dates
The 1st day of the LMP is used to calculate the expected date of confinement (EDC)
The EDC can be determined by adding 7 days to the 1st day of the LMP, subtracting 3 months and adding 1 year
(Naegele’s rule)
Early symptoms of current pregnancy: tenderness and increased size of breasts, urinary frequency, nausea and
vomiting (emesis gravidarum), easy fatigability, GA by week of quickening (mother’s feeling of fetal
movement, usually occurs at 20 wks of gestation)
Current history of antepartal bleeding (R/o threatened abortion, abruptio placenta or placenta previa) Prior mode
of delivery (instrumental delivery, caesarian section)
Current history of hypertension (pre-eclampsia) and diabetes in pregnancy (gestational diabetes)
Prior history of miscarriages, still births, preterm and post term deliveries
History of exposure to teratogenic drugs, and level of stress
History of smoking, use of alcohol or illicit drugs
Current history of vaginal discharge (note for color, amount, odor and consistency) and vulval itching
Past history of sexually transmitted infections (STIs) such as gonorrhea, syphilis or herpes genitalis

Assess risk factors and clinical stigma of HIV infection (previous or current STIs, herpes zoster, etc…)
Personal and family history of hypertension, diabetes, cardiac disease
Sociodemographic history- age, income, address, woman’s attitude toward her pregnancy
Obstetric Examination
Blood pressure (BP)
Record the blood pressure in every scheduled visit
In early and mid pregnancy, BP is normally lower than the baseline BP
High BP prior to 20 weeks of gestation indicates chronic hypertension
High BP after 20 weeks of gestation indicates pregnancy-induced hypertension (pre-eclampsia). It can present as
late as 6 weeks post partum. Pre-eclampsia is clinically defined as hypertension and proteinuria, with or without
pathological edema.
Weight
Weigh the woman in every antenatal visit
Weight loss may occur in 1st trimester due to emesis gravidarum
HEENT
Mask of pregnancy (chloasma) is normal in pregnancy
Chloasma is referred as hyperpigmented patches around the cheeks and across the bridge of the nose
Conjunctival pallor: Anemia in pregnancy may occur normally due to hemodilution resulting from
disproportionate increase in plasma volume
Nasal congestion with nose bleeds, and gingival hypertrophy with epulis are noticed during pregnancy
LGS
Mild symmetric thyroid gland enlargement is expected in pregnancy
Breast
Inspect the breasts and nipples
Tender and nodular enlarged breast is noticed in pregnancy

Palpate the breast for breast mass/lump
Compress each nipple between your index finger and thumb, and express colostrum from the nipple
Bloody and purulent discharges from the nipple are pathological
Lungs
Shortness of breath with tachypnea occurs late in pregnancy
Heart
Upward and laterally displaced PMI (point of maximal intensity) is noticed in pregnancy
S3 sound and systolic murmur at apex occurs in pregnancy due to increased blood volume
Abdomen
Semi-sitting position with her knees flexed
Inspect for surgical scars, striae, shape and contour of the abdomen
Purplish striae and linea nigra are normal in pregnancy
Scars of ‘Pfannenstiel’s incision’ at suprapubic area indicates previous caesarean section
Palpate the abdomen for abdominal masses and organs, fundal height, fetal movements and uterine contraction
Quickening is noticed by the mother at 18-20 weeks of gestation, and felt by the examiner after 24 weeks of
gestation
Braxton-Hick’s contraction is noticed late in pregnancy
Modified Leopold’s maneuver
Adjunct to palpation of the pregnant woman from 28 weeks on wards
Determine lie (longitudinal, transverse, oblique), presentation (cephalic, breech), attitude, descent and estimated
weight
1st maneuver (Upper pole)
Stand at the woman’s side facing her head
Gently palpate with the finger tips of both examining hands to determine upper pole of the uterine fundus

Most commonly, fetal buttocks are at the upper pole in longitudinal lie
Measure for fundal height: Measure from the top of symphysis pubis to the top of uterine fundus along the
midline of the abdomen using tape measure
2nd maneuver (sides of maternal abdomen)
Place each hand on each side of the woman’s abdomen, and palpate the fetal parts
The hand on the fetal arms and legs feels irregular bumps while the hand on the fetal back feels regular and
smooth
Fig 10.11 Leopold’s maneuver to determine fetal lie and location of the back
3rd maneuver (lower pole of fetal parts)
Stand at the woman’s side facing her feet
Palpate the fetal part occupying the lower pole above the symphysis pubis with palmar surface of fingers of both
hands
Note whether the hands diverge with downward pressure or stay together
The fingers feel a smooth, firm rounded surface on both sides in cephalic presentation
If hands diverge, the presenting part descended into pelvic inlet

Fig 10.12 Leopold’s maneuver to determine presenting part
4th maneuver (confirmation of the presenting part)
Pawlick’s grip
Grasp the lower pole of the fetal part with your dominant hand and the upper pole of fetal part with your non-
dominant hand
Distinguish between the head and the buttock: fatal head feels smooth, firm and rounded and the buttock feels
firm and irregular
Fetal heart beat (FHB)
Auscultate the fetal heart using fetoscope or doptone
Note for FHB location and rhythm
FHB is audible after 18 weeks of gestation
Normal FHB is usually in the 160s during early pregnancy, and then slows to between 120s and 140s near term
Location of FHB
Midline of the lower abdomen from 12-18 weeks of gestation
FHB is best heard at fetal back or chest after 18 weeks of gestation

Rhythm of FHB
Beat-to-beat variation of 10-15 bpm over 1-2 minutes is expected
Lack of beat-to-beat variance of FHB late in pregnancy indicates fetal compromise
Fig 10.13 Listening to fetal heart using ‘Pinard stethoscope’ (fetoscope)
Genitalia
. Inspect external genitalia for warts, ulcers, abnormal vaginal discharge, and Bartholin’s and Skene’s gland
swellings
Enlargement of labias and clitoris are normal in pregnancy
Look for episiotomy (perineal incision to facilitate delivery of an infant) scars
Palapate Bartholin’s and Skene’s glands for tenderness
Check for cystocele and rectocele
Speculum examination to visualize vaginal wall and cervix
Inspect the vaginal wall for color, discharge, rugae and relaxation
Bluish color, deep rugae and milky vaginal discharge (leukorrhea) are normal in pregnancy
Inspect the vagina for color, shape, and healed lacerations

Fig 10.14 Fundal height and GA by week of pregnancy
Bimanual examination
Technique:
. Insert lubricated index and middle fingers into the introitus, palmar side down with slight pressure downward
on the perineum
. Slide the fingers into the posterior vaginal vault
. Gently turn the fingers palmar side up while maintaining downward pressure
. Gently place your fingers in the cervical os, and then sweep around the surface of the cervix
Nulliparous woman has closed cervical os, while multiparous woman cervical os admits a finger tip
Inner cervical os (narrow passage between endocervical canal and uterine cavity) is closed in nulliparous and
multiparous women
. Estimate the length of cervix by palpating the lateral surface from the cervical tip to the lateral fornix
Effacement of cervix prior to 32 weeks indicate preterm labor
. Palpate the uterus for size, shape, consistency and position
Early softening of isthmus (Hegar’s sign) is characteristic of pregnancy
Globular uterus by 10-12 weeks of gestation
. Place pelvic fingers at either side of the cervix, and gently lift the uterus to the abdominal hand and estimate
uterine size

. Palpate the adnexas to rule out tubal pregnancy
. Palpate the pelvic muscle strength while withdrawing examining fingers
Extremities
Inspect hands and legs for edema: physiologic edema occurs in pregnancy
Significant edema in pregnancy may be due to pregnancy-induced hypertension (preeclampsia) or chronic

kidney disease

Male Genitalia
Learning objective
1. List common causes of scrotal swelling

2. Mention causes of genital ulcer and urethral discharge
3. Show techniques of examining the testes
History taking in male genitalia
. History of urethral discharge (note for color, amount, odor and consistency)
Common causes of urethral discharge in male are Neisseria gonorrhea and Chlamydia trachomatis (STIs)
. History of penile sores, ulcers or growths/warts, scrotal swelling or pain
Common causes of penile sores/ulcers are genital herpes, syphilis and chancroid
. Past history of STI such as gonorrhea, syphilis or genital herpes
. History of lack of desire for sex (It could be due to medications, medical illnesses or psychogenic)
. History of erectile dysfunction (can’t attain and maintain penile erection that is adequate to complete the sexual
activity)
Erectile dysfunction may be caused by organic (endocrine, neurologic and vascular causes), medications and
psychogenic
. History of premature ejaculation (too soon and out of control)
Lack of orgasm with ejaculation is usually psychogenic
. Risk factors and clinical stigma of HIV infection (history of unprotected sexual intercourse, previous or current
STIs, chronic diarrhea, or herpes zoster)
Examination in male genitalia
The penis
. Note appearance and size of penis, presence or absence of prepuce, position of external urethral orifice
. Examine the penile shaft for warts, ulcers, scabies and rashes

. Examine the scrotal skin for swelling, erythema and ulceration
Phimosis is narrowing of the preputial orifice which prevents retraction of foreskin
It predisposes to recurrent infections of the glans penis (balanitis), prepuce (prosthisis) or both (balanoprosthisis)
Hypospadias is external urethral orifice at the ventral surface in the midline, anywhere from the glans to the
shaft of penis
Epispadias is external urethral orifice on the dorsal surface of penis
The testis
Palpate both testes and note for size, tenderness, consistency and nodularity of the testis
Technique of examination of the testis
. Patient in supine position, and the examiner stands on the right side of the patient
. Place both hands on the scrotum with right hand being inferior and palpate the testes
. Support the posterior testis by middle, ring and little fingers of each hand, leaving the index finger and thumb
free to palpate the anterior and lateral part of testis
. Feel for upper pole of testis between approximated index finger and thumb of left hand
. Feel for lower pole of testis between approximated index finger and thumb of right hand
Normal testes are equal in size (length 3.5-4 cm) and firm in consistency
. Palpate the epididymis on posterior aspect of upper pole of testis
. Palpate the spermatic cord
. Notice for varicocele (dilated tortuous veins), hydrocele of the tunica vaginalis (perform transillumination test
to check for hydrocele), spermatic cord cyst
NB: Unilateral hard enlarged testis in an adult is considered to be malignant, unless proved other wise

Fig 10.14 Palpation of the testis
Fig 10.16 Scrotum and its contents

Fig 10.17 Cause of scrotal swelling

Chapter Eleven
Integumentary system (Skin, Nail, Hair)
1. Understand how to ask symptoms of skin lesions
2. Identify primary and secondary morphologic skin lesions
3. List clinical syndromes of skin lesions
The skin
The skin is the largest organ of human body. It covers an area of ̴ 2 m2 and weighs ̴ 4kg.
Functions of human skin
. Protection: Physical, chemical and infection
. Physiology: Homeostasis of water and electrolytes
. Thermoregulation
. Sensation: Specialized nerve endings
. Immunity: Langerhan’s cells and lymphocytes
. Vitamin D synthesis

Fig. 11.1 Structure of the skin
Skin has three layers. These are epidermis, dermis and subcutis.
The epidermis is stratified squamous epithelium. It has four layes (basal, prickle, granular and horny),
representing stages of keratin maturation. Hair and nails are specialized epidermal structures.
The dermis is connective tissue containing specialized structures like sebaceous gland, sweat gland and hair
follicle.
The subcutis is loose layer of connective tissue and fat.
History taking
Symptoms of skin lesions: Skin eruption (rash), itch (pruritis), growth (lump), disfigurement, etc…
Questions to ask in patients with skin lesions
How long has the lesions been present? (Duration)
How did it look when it first appeared, and how is it now different? (Morphology)
Where did it first appear? Where is it now? (Distribution)
What associated symptoms present? Eg. Itch, pain, etc…
Was it related to sun exposure, sexual exposure?

Were constitutional symptoms present? Eg. Fever, malaise, weight loss, etc…
Was systemic disease present? Eg. Diabetes, connective tissue diseases, inflammatory bowel disease
Are any other family members affected?
Was there recent travel history?
What does the patient think caused the skin lesions? (Drugs, personal care products, occupational or recreational
exposure)
What treatment has been used?
Physical examination
The skin should be fully exposed, preferably in natural light.
1. Color and pigmentation
Pallor is abnormal whitening of skin and buccal mucosa. Persistent pallor is due to anemia of any cause.
Conjunctival and mucosal pallor is a better indicator of anemia than the skin color.
Pigmentation is abnormal coloration with or deposition of pigment.
Dark-brown pigmentation: Abnormal depositition of hemosiderin (eg. hemochromatosis)
Jaundice: Yellow pigmented skin
Depigmentation: Absence of melanin with in the skin
. Albinism-absence of skin pigment
. Vitiligo-loss of pigment in affected skin
2. Skin lesions and eruptions (rash)
Characterize morphology, distribution and configuration of skin lesions using inspection and palpation
technique (put on gloves if the skin is broken).
Observe for size, shape, color and border changes. Palpate the lesions with your finger tips, noting consistency,
tenderness, temperature, depth and mobility.

a. Morphology of skin lesions
1. Primary skin lesions: macule, papule, nodule, tumor, patch, plaque, vesicle, bulla, pustule, wheal,
telangiectasia, petechiae, purpura, ecchymosis, erythema, burrow, cyst, comedo, papilloma, and freckle
a. Macule: Localized area of color and texture change of the skin
b. Papule: Solid elevation of skin < 5mm in diameter
c. Nodule: Solid elevation of skin > 5 mm in diameter
d. Tumor: > 5 mm solid elevation on the skin and extending deeper to dermis
e. Patches: Macular skin lesions >5 mm in diameter
f. Plaque: palpable elevation of skin >2 cm diameter and <5 mm in height
g. Vesicle: clear, fluid-filled blister <5 mm in diameter
h. Bulla: fluid-filled blister >5 mm in diameter
i. Pustule: visible collection of pus in a blister
j. Wheal: compressible, red papule or plaque of dermal oedema
k. Telangiectasia: Dilated dermal blood vessels resulting in a visible lesion
l. Petechiae: haemorrhagic punctate spot 1-2 mm in diameter
m. Purpura: Extravasation of blood resulting in redness of skin or mucous membranes
n. Ecchymosis: > 2 mm sized macular red or purple haemorrhage in skin or mucous membrane
o. Erythema: Redness of the skin due to vascular dilatation
p. Burrow: tunnel in epidermis caused by ectoparasite
q. Cyst: nodule consisting of an epithelial-lined cavity filled with fluid or semisolid material
r. Comedo: plug of sebum and keratin wedged in a dilated pilosebaceous orifice on the face
s. Papilloma: nipple-like projection from the surface of the skin
t. Freckle: macular area showing increased pigment formation by melanocytes
2. Secondary skin lesions (evolving from primary skin eruption): Scale, crust, excoriation, lichenification,
fissure, erosion, ulcer, scar, atrophy, abscess, striae, and callus

a. Scale: Accumulation of easily detached fragments of thickened keratin
b. Crust: Dried exudate of serum, blood or pus on the skin surface
c. Excoriation: superficial, often linear, abrasion due to scratching
d. lichenification: Chronic thickening of skin with increased skin markings, from rubbing or scratching
e. fissure: Linear split in epidermis, often just extending into dermis
f. Erosion: superficial break in the epidermis, not extending into dermis, heals without scarring
g. Ulcer: circumscribed area of skin loss extending into the dermis
h. Scar: Replacement of normal tissue by fibrous connective tissue at the site of an injury
i. Atrophy: Loss of epidermis, dermis or both, with thin, translucent and wrinkled skin, and visible blood vessels
j. Abscess: Localized collection of pus
k. Striae: Atrophic linear band in skin from connective tissue changes
l. Callus: Local hyperplasia of horny layer on palm or sole due to pressure
b. Distribution of skin lesions
Is it symmetrical (generalized) or asymmetrical (localized)? Symmetry often implies an internal causation

whereas asymmetry may imply external factors.
Is the skin eruption centripetal or centrifugal? Eg. Chicken pox and pityriasis rosea are centripetal while
erythema multiforme and erythema nodosum are centrifugal.
Is there flexor or extensor bias in body distribution? Eg. Eczema is flexor while psoriasis is extensor in body
distribution
Are only exposed body areas affected?
Are the genitalia involved?
c. Configuration (arrangement) of each skin lesion
. Nummular/discoid (round or coin-like)
. Annular (ring-like)
. Circinate (circular)
. Arcuate (curved)

. Gyrate/serpiginous (Wave –like)
. Linear (in a line)
. Grouped (clustered)
. Reticulate (net-like)
Correlation of physical signs and skin diseases
a. Erythrosquamous eruptions: Red and scaly, asymptomatic or itchy, well demarcated or diffuse bordered skin
eruptons
. Psoriasis (bright pink plaques with silvery scale)
. Atrophic eczema (diffuse erythema with fine scales)
. Pityriasis rosea (paler pink, scaly, macular lesions)
. Nummular eczema (round patches)
. Contact dermatitis (irritant or allergic)
. Dermatophytosis (ring worm)
. Lichen planus (violet colored polygonal papules)
. Secondary syphilis (flat, red, hyperkeratotic lesions)
b. Blistering eruptions (blisters and vesicles)
. Traumatic burns and blisters
. Bullous impetigo
. Viral blisters (herpes simplex, varicella)
. Bullous erythema multiforme
. Bullous pemphigoid
. Dermatitis herpetiformis
. Pemphigus
. Porphyria

. Epidermolysis bullosa
. Dermatophyte infections
. Acute contact dermatitis
c. Erythroderma: Inflammatory, erythematous and exfoliative full thickness skin lesions with involved muscle
mass loss and edema. It may present as a dermatological emergency.
. Eczema
. Psoriasis
. Drugs Eg. phenytoin, allopurinol, etc…
. Pityriasis rubra pilaris
. Lichen planus
. Pemphigus foliaceus
. Dermatophytosis
. Mycosis fungoides (sezary syndrome), leukemia, lymphoma
. Hereditary disorders
d. Pustular and crusted lesions: Primarily infectious process or inflammatory skin lesions
. Acne vulgaris
. Impetigo
. Folliculitis
. Acne rosacea
. Viral lesions
. Pustular psoriasis
. Drug eruptions
. Dermatophyte infections

e. Dermal plaques: Localized thickening of skin, caused by chronic inflammatory process or scarring sclerotic
process
. Granuloma annulare
. Necrobiosis lipoidica
. Sarcoidosis
. Erythema nodosum
. Lupus erythematosus
. Morphea and scleroderma
. Tuberculosis
. Leprosy
3. Lump (tumor)
Approach to diagnosis of a lump
. Determine site, size, shape, consistency and tenderness
. Note signs of inflammation (rednes, swelling, heat and tenderness)
. Is a lump fluctuant? Perform ‘transillumination test’ if fluctuant
. Evaluate site of tissue layer attachment of a lump
Lump in the skin moves when the skin is moved; lump in subcutis moves the skin over the lump; lump in
muscle moves with muscle contraction; and lump in nerve elicits pins and needles in the distribution of the
nerve upon pressing
Lump in bone is immobile
. Palpate regional lymph node site if inflammatory or neoplastic lump is suspected
a. Benign skin tumors
. Warts
. Molluscum contagiosum

. Seborrhoeic keratosis
. Dermatofibroma
. Neurofibroma
. Angioma
. Xanthoma
b. Malignant skin tumors
. Basal cell carcinoma
. Squamous cell carcinoma
. Malignant melanoma
. Bowen’s disease (squamous cell carcinoma confined to epithelial layer of skin-carcinoma in situ)
. Secondary deposits
The hair
Hair color and texture are genetically determined racial characteristics. Mongols have black and straight hair,
Negroid people have black, curly hair, and Caucasians have brown or black silky hair.
Excess hair growth
Hirsutism: Excess male-pattern terminal hair growth in females.
Hypertrichosis: Excess terminal hair growth in a non-androgenic distribution in males and females.
Hair loss
Baldness in men is genetically determined.
Alopecia (scalp hair loss): Localized or diffuse types
Localized hair loss is caused by ring worm infection (tinea capitis), 20syphilis (moth-eaten alopecia), traction
alopecia in psychologically disturbed person, autoimmune (alopecia areata).

Diffuse hair loss is caused by hypothyroidism, severe IDA, anti-mitotic chemotherapeutic drugs, autoimmune
(alopecia totalis).
The nail
The nail consists of keratinous nail plate over the dorsal surface of the end of each digit.
Nail changes in systemic diseases
Anonychia (absence of the nail plate): Congenital, trauma, frostbite, vascular disease, drugs, etc…
Koilonychia (spoon-shaped depression of nail plate): IDA, hemochromatosis, hypothyroidism, SLE, Raynaud’s
disease, lichen planus, detergent exposure, etc…
Paronychia (inflammation of the nail folds): ingrown toe nails, trauma to nail bed or cuticle, irritation from
chemicals, cuts, etc…
Onycholysis (nail separation from nail plate): Psoriasis, thyrotoxicosis, tetracycline (photo-onycholysis),
trauma, etc…
Onychauxis (abnormal thickening of the nail): congenital, trauma, acromegaly, psoriasis, diabetes, etc…
Onychomycosis: Fungal infection of the nail
Pitting nail: Psoriasis, reactive arthritis, alopecia areata, chronic eczema, pemphigus vulgaris, etc…
Splinter hemorrhages (longitudinal red streaks in nail plate): Infective endocarditis, collagen vascular disease,
psoriasis, trauma, etc…
Clubbing (loss of the normal angle between nail fold and nail plate): Infective endocarditis, congenital heart
disease, bronchiectasis, lung abscess, lung cancer, inflammatory bowel disease , hepatic cirrhosis, etc…

MEDICAL CASE REPORT
Identification
This is E.M., 40-year-old male, married, Orthodox Christian, daily laborer from Tach-Armachiho, North Gondar
Zone, admitted to University of Gondar hospital, medical ward D, bed number 24, on January 12, 2009 E.C.
Previous admission
August, 2007 E.C., University of Gondar hospital, Gondar, acute subdural hematoma 20 to traumatic head
injury, burr hole done to evacuate hematoma, and discharged improved.
Chief complaint
Fever of 1 month duration
History of present illness
The patient was last relatively healthy one month back at which time he started to experience a gradual onset of
high grade intermittent fever, which got worse at night and associated with chills, rigors, drenching night sweat
to the extent it soaked his clothes. Two weeks after the onset of fever, he began to notice swelling over the left
upper quadrant of his abdomen associated with aching abdominal pain, dragging sensation and early satiety. The
pain was non-radiating localized to upper abdomen with no specific aggravating or relieving factor. He visited a
local drug store near by, and bought and took Coartum, 4 tabs twice daily for three days thinking it was malaria,
but no avail. Two week before admission, he began to develop blurring of vision, tinnitus, light headedness; and
easy fatiguability which prohibited him from doing his routine daily activities. He had repeated episodes of
bilateral nasal bleeding, which stopped with nasal pack. He had unquantified weight loss to the extent his
clothes become loose. He had shortness of breath while engaged in routine activities like loading and unloading
objects from lorry. He lives in kala azar and malaria endemic area. He had repeated attacks of malaria, last
attack being 3 months back. He had episodes of vomiting of ingested matter, anorexia and nausea, but no bowel
habit change. He gave history of consuming under cooked meat or raw milk, and close contact with domestic
animals; but has no contact with animal abortus material. He had history of unprotected sexual activity, but was
not screened for retroviral infection, and had no recurrent oral ulcers, herpes zoster scar, or chronic diarrhea. He
had no petechial rash, gum bleeding, hematuria or stool color change. He had no swelling over the neck, axillae
or groin area, and no bone pain. He had no jaundice, close contact with jaundiced person, blood transfusion,
blood letting, ear piercing or tattooing. He had no joint pain or swelling, malar rash, photosensitivity or oral
ulcers. .He had no cough with expectoration, contact with chronic cougher, or previous treatment for
tuberculosis. He had no history of exposure to herbal or modern medications. He had no history of exposure to
herbicides, pesticides, organic solvents or ionizing radiation. There was no similar illness in any of family
members. He visited this hospital for better care as treatment in local health institution didn’t help him. Then, he
was admitted to the medical ward of the hospital supported by family members with significant weight loss, and
ashen gray skin color change noticed by relatives.

Past illness
He had history of mumps, and chicken pox, but no other childhood illness.
Functional enquiry
HEENT
No head trauma
No eye pain, discharge or excessive lacrimation.
No ear pain, discharge or decreased hearing.
No nasal discharge.
Lymphoglandular system: Mentioned in HPI
Respiratory system: Mentioned in HPI
Cardiovascular system: Mentioned in HPI
Gastointestinal system: Mentioned in HPI
Genitourinary system: No flank pain, uegency, frequency of micturition, or supropubic pain
Musculoskeletal system: Mentioned in HPI
Integumentry system: Mentioned in HPI
Central nervous system: No loss of consciousness, abnormal body movement or weakness of extremities;
others mentioned in HPI
Personal history
He was born in a small village 5 km away from Tach-Armachiho, North Gondar zone, in 1969 E.C. He was
breast fed and spent a healthy childhood. He grew up with his family as a shepherd.He attend formal education
upto grade 6, and then engaged in labor work. He drinks on casual days but no history of smoking or chewing
khat. He is married and has two kids. All are alive and healthy.
Family history
Mother is alive and healthy. Father died at age of 65 years due to unknown cause. He had one brother and two
sisters. All are alive and healthy. He is the third child for his family.No family history of diabetes, hypertension
or asthma.

Physical Examination
Genaral appearance
Conscious and cooperative; chronically sick looking, looks undernourished.
Vital sign
BP=110/70 mmhg, right arm, supine position
PR= 80 bpm
RR=20 breathes per minute
T0=36.6 0c, right axilla at 10:00 AM
Anthropometric measurement
Weight-50kg
Height-1.65 meters
BMI=18 kg/m2, undernourished
HEENT
Head: There is clearly visible scalp surgical scar and depressed skull at left temporal area.
Eye: Pale conjunctivae, no icteric sclerae, no eye discharge or periorbital swelling
Ear: Normal contour of pinna, clear external ear canal; no ear discharge, no mastoid or tragus tenderness
Nose: Central nasal septum, no active nasal bleeding or discharge
Mouth and throat: Pale toungue and buccal mucosa; no gum bleeding, ulcers or fissures on lips, or tooth caries
Lymphoglandular: No palpable lymphadenopathy in accessible sites, no anterior neck swelling, or no breast

lump
Respiratory system
Inspection: No cyanosis of palm of hands or clubbing of fingers; no cyanosis of lips or tongue; regular and
shallow breathing pattern; no subcostal or intercostal retractions; no use of accessory muscles of respiration; no
chest wall deformity, chest wall moves symmetrically with respiration
Palpation: Trachea is centrally located; no chest wall tenderness or subcutaneous crepitation; normally
comparable tactile fremitus; symmetric chest expansion, and measures 6 cm along mid chest.
Percussion: resonant all over the chest; diaphragmatic chest expansion is 4 cm.

Auscultation: Vesicular breath sound heard all over the chest
Arterial system: All accessible peripheral arteries are palpable; full in volume and regular in rhythm; no radio-
femoral delay; no arterial cording.
Venous system: No superficial visible distended veins on the neck. JVP is not raised.
Precordial examination:
Inspection: No precordial bulge; active precordium; apical impulse is visible at 5th intercostal space medial to
left midclavicular line.
Palaption: PMI is at apical impulse. PMI is diffuse and tapping. No palpable heart sound; no heave or thrill.
Auscultation: S1 and S2 are well heard. There is grade-3, mid-systolic, high pitched, harsh murmur at erb’s area,
which radiates to the neck. No gallop.
Abdominal examination
Inspection: Symmetric abdomen that moves with respiration; no flank fullness; flat umbilicus with transverse
slit; no visible peristalsis, no pulsation or distended veins; no scar or pigmentation; hernia sites are free.
Palpation: Superficial and deep palpation
Superfical palpation: No tenderness, guarding or rigidity. There is superficially palpable mass on left side of the
abdomen.
Deep palpation: There is a non-tender mass on the right upper quadrant of the abdomen, which is 4 cm below
the right costal margin along right midclavicular line; the mass is smooth surface, round edge, firm in
consistency, moves with respiration. Not bimanually palpable.
There is non-tender mass on the left upper quadrant of the abdomen which is 10 cm below the left costal margin
along the splenic growthline, moves with respiration; difficult to enter fingers through left costal margin; medial
notch is palpable. The mass is smooth surface, round edge, firm in consistency. Not bimanually palpable. It is
massive splenomegaly.
Percussion: Tympanitic all over the abdomen, except at masses which is flat to percussion. No shifting dullness
or fluid thrill. Total vertical liver span is 16 cm.
Auscultation: Normoactive bowel sound at a rate of 10 per minutes. There is no friction rub or bruit over the
enlarged spleen or liver.
Per digital rectal examination: No rectal mass or ulceration or nodules. Anal sphincter tone is intact. No perianal
nodules, ulcers or discharges.

Genitourinary system: No costovertebral angle tenderness or suprapubic tenderness
Musculoskeletal system
Look: No deformity, no scar or pigmentation. Symmetrically atrophied muscle bulk on upper and lower
extremities
Feel: No tenderness or swelling on extremities
Move: Full active range of movement of extremities
Measure: Comparable circumference and length of extremities
Integumentary system: The skin is dry and warm. The palms of hands and sole of feet were pale. No
petechial rash. No clubbing or deformity of nails.
Neurologic examination
Mental status examination: Oriented in time, place and person
Glasgow comma scale (GCS): Eye opening; spontaneous =4/4; best verbal response; oriented=5/5; best motor
response; obeys command=6/6; Total=15/15
Cranial nerve examination
CN-I: Can identify the odor of lemon in each nostril
CN-II: Has comparable visual field with the examining physician. Direct and consensual light reflexes are
intact.
CN-III, IV and VI: Can move his eye in all cardinal direction.
CN-V: Sensation to light touch and pain is intact over his face. The muscle of mastication contract while
clenching his teeth. Corneal reflex is intact.
CN-VII: He can smile, frown his forehead, and puff out his cheeks. He can close his eyes against resistance.
Corneal reflex is intact.
CN-VIII: He can hear finger rub in both ears. Weber’s test and Rinne’s test are intact.
CN-IXand X: Uvula is centrally located; soft palate rise in the mid line when he says‘Ah’. Intact gag reflex.
CN-XI: He can shruggle his shoulder and turn his head against resistance.
CN-XII: He can protrude and move his tongue in both directions.

Motor examination
Inspection: Comparable muscle bulk in both upper and lower extremities. No spontaneous or provoked
fasciculation.
Palpation: Normal tone while moving extremities along the joints; he can lift his extremities against full
resistance (power=5/5),
Deep tendon reflex is normal
Biceps Triceps Supinator Knee Ankle
Right ++ ++ + ++ +
Left ++ ++ + ++ +
Superfical reflex is normal: Flexor plantar response; intact abdominal and corneal reflexes
Sensory examination: Light touch, pain, temperature, vibration and position sensation are intact.
Coordination: Tandem walk, finger-to-nose and heel-to-shin movements are intact.
Meningeal irritation signs: No neck stiffness; Kernig’s and Brudzinsky’s signs are negative.
Subjective summary
A 40-year-old male patient from Tach-Armachiho, North Gondar Zone, presented with a high grade intermittent
fever of 1 month duration associated with chills, rigors and profuse sweating. He also has loss of appetite and
weight. He noticed abdominal swelling with dragging sensation. He also has blurring of vision, tinnitus, light
headedness, easy fatiguability and epistaxis. He lives in Kala azar endemic area, and had repeated attacks of
malaria.
Objective summary
He is chronically sick looking patient, consclious and cooperative. Looks undernourished.
Vital sign: BP=110/70 mmhg, PR=80bpm, RR=20 breaths per minute, T0=36.6 0c, All are with in normal
limits.
BMI=18 kg/m2, mildly under-nourished. MUAC=20 cm, under-nourished.
He has pale conjunctivae, tongue and buccal mucosa, palm of hands and sole of feet. There is midsystolic
murmur at erb’s area in CVS exam. Abdomina examination reveals huge splenomegaly and hepatomegaly.

Diagnosis: Visceral leishmaniasis (kala azar)
Required investigation
Complete blood count (Hgb, Hct, WBC with differential, platelets, ESR)
Blood film
Peripheral morphology
Blood culture
Serologic tests (rK-39, DAT test, ELISA)
Brucella serologic test, Hepatic viral markers (HBsAG, Anti-HBc-antibody, Anti-HCV-antibody)
HIV serologic tests; CD4 count and viral load, if positive HIV serology
Tissue aspirate from spleen or liver (FNAc)
Bone marrow aspirate and biopsy: morphology, flow cytometry, cytogenetics
Organ function tests (LFT, RFT), electrolytes
Coagulation profile (PT, aPTT)
Abdominal U/S, CXR
Differential diagnosis (most likely to least likely)
1. Visceral leishmaniasis (kala azar)

2. Chronic myeloid leukemia
3. Non-Hodgkin’s lymphoma
4. Hyper-reactive malarial splenomegaly (HMS)
Discussion of differential diagnosis (least likely to most likely)
1. Hyper-reactive malarial splenomegaly (HMS)
HMS is an abnormal immune response to recurrent malarial attack, which is caused by Plasmodia species.
It is more common in malaria endemic area, most of tropical regions of the world; commonly seen in older
children and young adults. Repeated malarial infections cause uninhibited B-cell production of

immunoglobulin and immune complex formation, and stimulate reticuloendothelial tissue hyperplasia
characterized by massive splenomegaly. Clinical features include massive splenomegaly +/- perisplenitis,
hepatomegaly, hypergammaglobulinemia, anemia +/- pancytopenia, infection of skin, respiratory system or
sepsis. Diagnostic criteria for HMS include residence in malaria endemic area ≥ 10 years with recurrent
attacks, massive splenomegaly, perisinusoidal lymphocytosis, increased serum titer of IgM and malarial
antibodies, pancytopenia and smear negative for malaria. In conclusion, residence in malaria endemic area
with repeated malarial attack, and massive splenomegaly favors HMS, but prolonged fever with systemic
symptoms is unlikely in HMS, and HMS is a diagnosis of exclusion.
2. Non-Hodgkin’s lymphoma (NHL)
NHL represents clonal proliferation of lymphoid cells (B-cell-75%, T-cell-25%) in reticuloendothelial

tissue. Cause is unknown in most cases, but etiological factors include pesticide or herbicide exposure, viral
and bacterial infections, and inherited or acquired immunodefiency state. It occurs in middle aged adults.
Clinical features include lymphadenopathy +/- organomegaly and systemic symptoms (fever, sweating, and
weight loss). Bone pain and symptoms of cytopenia including fever, fatigue and bleeding occurs in
advanced disease. In conclusion, systemic symptoms, organomegaly, and clinical features of cytopenia
favors advanced extranodal NHL. Excisional biopsy of nodal and extranodal sites is required for
morphological, immunophenotying and cytogenetic study to settle the diagnosis.
3. Chronic myeloid leukemia (CML)
It is a myeloproliferative disease characterized by clonal proliferation of myeloid cells in bone marrow.No

clear etiologic factor is known, except ionizing radiation exposure. It is a disease of older adults in
westerns data. Ethiopian literatures mention median age of patients with CML is 40ys. Philadelphia
chromosome is identified in 90-95% of patients with CML. CML has three phases, named as chronic phase,
accelerated phase and blast phase. This patient fits to accelerated/blast phase of CML, due to presence of
prominent systemic symptoms, massive splenomegaly and clinical features of cytopenia, like fever, fatigue
and bleeding. Presence of all cells of myeloid series in bone marrow aspirate or peripheral smear suggests
CML. Cytogenetic study for Ph’ chromosome is required to confirm diagnosis of CML.
4. Visceral leishmanisis (Kala azar)
Kala azar means black fever in Hindu. It is an anthroponotic or zoonotic systemic disease caused by an
obligate intracellular protozoan, named as Leishmania donovani complex. The vector for transmission of
leishmania spp. is named as sandfly (phlebotomus). The disease is prevalent in North West (Mettema,
Humera, Wolkait, LIbo/Fogera), North East (Ethio-Djibouti border, Awash valley), and South West (Segen,
Genale, Woito, Konso, Omo, Gambela, Ethio-South Sudan border) regions of Ethiopia. Population
migration is main risk factor to acquire the infection. It is transmitted to healthy person by the bite of
infected sandfly. Clinical features include fever ≥2 weeks, weight loss, splenomegaly, anemia +/-
pancytopenia. In conclusion, patient residence in kalazar endemic area, prolonged fever, weight loss and
massive splenomegaly, and clinical features of cytopenia including fever, fatigue and bleeding favors kala

azar. Positive leishmanial serologic tests (rK-39/ DAT test) or isolation of leishmanial LD-bodies in tissue
aspirate from spleen confirm diagnosis of kala azar.

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CLINICAL METHODS: PHYSICAL EXAMINATION AND CLINICAL HISTORY

Book · January 2016

The user has requested enhancement of the downloaded file.

for Health Science Students

Associate Professor of Medicine

University of Gondar Hospital

Chapter One: Scheme of history taking and physical examination 04

Chapter Two: Vital signs in physical examination 19

Chapter Three: Physical appearance and HEENT 29

Chapter Four: Lymphoglandular system 49

Chapter Five: Respiratory system 64

Chapter Six: Cardiovascular system 91

Chapter Seven: Gastrointestinal system 125

Chapter Eight: Nervous system 162

Chapter Nine: Musculoskeletal system 228

Chapter Ten: Genitourinary system 259

Chapter eleven: Integumentary system 292

Medical case report 302

Scheme of history taking and physical examination

At the end of this lesson, the student should be able to:

Two major steps of making the diagnosis

a. To establish the clinical data by history taking and physical examination

Clinical communication skills

Use ‘verbal tracking’ to show that you are paying attention

4. Open and closed ended questions

Avoid leading questions!

Avoid ‘why’ questions!

Eg. “Why did you miss the morning medication dose?”

8. Non-verbal communication cues

Implement the ‘SOFTEN’ non-verbal communication cues during interviewing patients

. ‘Smile’ welcomes a patient and can put the patient at ease

. ‘Open posture’ facilitates being approachable and ready to interact

. ‘Forward lean’ slightly towards the patient indicates as attracted or interested

. ‘Nod’ encourages patients to continue with their story

Five-step patient-centered interviewing

Step-1: Set the stage for the interview (30-60 seconds)

. Welcome the patient

. Use the patient’s name

. Introduce youself and identify specific role

. Ensure patient readiness and privacy

. Remove communication barriers (have a seat).

. Indicate available time

. Obtain list of issues patient wants to discuss

Step-3: Open the history of present illness (non-focused) (30-60 seconds)

. Ask open-ended questions to elicit problems

Step-4: Continued the patient-centered history of present illness (3-10 minutes)

. Use focused, but open-ended questions to obtain description of symptoms

. Explore patient description of symptoms, emotional and social context of symptoms

Step-5: Transition to clinician-centered process (30-60 seconds)

. Summarize conversation and confirm accuracy of information

Duties of doctors (British General Medical Council)

. Make the care of your patient your first concern

. Treat every patient politely and considerately

. Respect patients’ dignity and privacy

. Listen to patients and respect their views

. Give patients information in a way they can understand

. Keep your professional knowledge and skills up-to-date

. Recognize the limits of your professional competency

. Be honest and trust worthy