Documente Academic
Documente Profesional
Documente Cultură
MBBS (U.OF.K)
MRCP (Part1and 2)
Medical Registrar (SMSB)
بـســم هللا الرحـمـــن الرحــيــم
قال تعالى:
(وعلم آدم األسماء كلها ثم عرضهم على المالئكة فقال أنبئوني بأسماء هؤالء إن
كنتم صادقين* قالوا سبحانك ال علم لنا اإل ما علمتنا إنك أنت العليم الحكيم )
سورةالبقره32-31:
( ويسئلونك عن الروح قل الروح من أمر ربي وما أوتيتم من العلم إال قليالا )
سورة اإلسراء58 :
To my dearest mother...
And without her love, care and advice, it would have been virtually impossible for me to
continue my postgraduate studies.
Who taught me medicine from its principles and ethics to its practice …
Who helped me to defy the tough road of medicine and continued to do so till the day he left …
Who gave me a reason to work hard, a reason to struggle, a reason to succeed, a reason to
continue what he had begun and a reason to be distinguished as he was…
To my dear husband …
I would like to express great appreciation and gratitude for Professor. Mohamed Osman Mekki,
an eminent Professor of Medicine, for encouraging me to write this book and suggesting its
title, forrevising thoroughly and meticulously every chapter in this book and for his constructive
suggestions, comments and advices.
Without his encouragement, help and support it would have been virtually impossible for me to
prepare such a book.
Medicine is not only a science; it is an art. It does not consist of compounding pills and plasters;
it deals with the very processes of life, which must be understood before they may be guided.
To study the phenomena of disease without books is to sail an uncharted sea, while to study
books without patients is not to go to sea at all.
For one mistake made for not knowing, ten mistakes are made for not looking.
JA Lindsay
The best physician is the one who is able to differentiate the possible and the impossible.
Herophilusof Alexandria
Henry James
Title Page
History taking 1
The cardiovascular system 15
The respiratory system 25
The gastrointestinal system 39
The nervous system 59
References 90
First of all you must introduce yourself to the patient, offer a greeting and take permission for history
taking and clinical examination.
2- Weight:
Increased: Decreased: No change:
If decreased, how much? (Clothes, people noticed, previous weight records):
How quickly:
(Significant weight loss: > 3kg in 6 months).
4- Xerostomia(dry mouth):
11- Acid reflux (regurgitating gastric acid producing a sour taste in the mouth):
12- Dyspepsia (indigestion) : (epigastric pain, heartburn, distension, nausea or an acid feeling
occurring after eating or drinking)
14- Vomiting:
Frequency:
Volume:
Nature (recognizable food, digested food, clear acidic fluid, bile stained, blood stained or
faeculent):
Is it preceded by nausea or does it occur without warning?
Associated symptoms (dyspepsia or abdominal pain):
Is it related to meal times, early morning or late evening?
Is it projectile? (Gastric outlet obstruction, high small bowel obstruction or raised intracranial
pressure)
What medications has the patient been taking?
16- Melaena: (passage of black tarry stool with a characteristic odour, due to partially digested
blood)
20- Altered bowel habit: (normal bowel movement frequency ranges from 3 times/day to once
every 3 days)
a) Constipation:(Infrequent passage of hard stools; <3 times/week)
Frequency of defecation:
22- Jaundice:
Is it progressive or intermittent?
Is there skin itching?
What is the colour of urine?
What is the colour of stool?
Accompanying symptoms (abdominal pain, loss of appetite, fever, vomiting):
Is it associated with weight loss?
1- Chest Pain:
Site:
Time & mode of onset:
Severity:
Nature:
Progression:
End of pain:
Duration:
Aggravating factors:
Relieving factors:
Radiation:
Associated Symptoms:
2- Dyspnoea:
Mode of onset: (sudden/gradual)
Progression: (rapid/slow)
Duration:
Severity:
Exertional: (what exercise precipitates it? how many stairs? how far can he/she walk):
Does it occur at rest?
Is there orthopnoea? If yes, how many pillows needed at night?
Is there Paroxysmal Nocturnal Dyspnoea? (Wake up at night short of breath):
3- Exertional fatigue:
4- Palpitation:
Onset (abrupt/gradual):
Termination (abrupt/gradual, spontaneous or by medication):
1. Breathlessness:
Same as CVS, in addition to:
Is there variability in the symptom? (good days and bad days)
Is it worse during the day or at night?
1. Pain:
Site (loin, groin or suprapubic):
Time & mode of onset:
Severity:
Nature:
Progression:
End of pain:
Duration:
Radiation (iliac fossa, testicles, labia):
Aggravating factors:
Relieving factors:
Associated symptoms:
3. Dizziness and vertigo : (feeling of spinning of the patient or surroundings due to abnormal
perception of movement)
4. Disorders of movement:
a) Negative symptoms: (motor weakness, lack of co-ordination, lack of stability and body
stiffness).
Motor weakness: ask about:
Site: {a few muscles, a limb, both lower limbs (paraparesis), both limbs on
one side (hemiparesis) or all limbs (quadriparesis)}.
Onset (gradual/sudden):
What time of the day? What was he/she doing?
Progression (slow/rapid):
How did it occur? (In one limb then involved the others)?
After how long it reached the maximum?
5. Sensory Symptoms:
a/ Abnormal sensations (tingling, paraethesia ‘‘pins and needles’’, pain):
b/ Loss of normal sensations (touch, pain, temperature):
6. Headache:
Time and mode of onset:
Frequency & Periodicity:
Duration:
Time of the day(morning,night):
Precipitating Factors:
Aggravating & Relieving Factors:
Where does it start and how does it evolve:
Quality & severity:
what is the effect of posture, coughing and straining?
Symptoms preceding the headache (aura): {focal neurological symptoms e.g.: zigzag
(fortification spectra), spreading scintillating scotoma or senosory symptoms (tingling
sensation over part of the body)}.
Associated symptoms: (nausea, vomiting, photophobia, phonophopia, fever, rash, neck
stiffness)
Family History of Headache:
Other medical or neurological problems:
1. Joints:
Joint pain:
Swelling:
Stiffness:
*Time: (early morning or comes at rest and disappear with activity)
*Associated symptoms: (redness, warmth, tenderness, swelling, fever, and sweating)
Restriction of movement:
3. Bone:
Pain: History of injury:
Endocrine system:
1) Thyroid:
Weight loss: Weight gain:
Heat intolerance: Cold intolerance:
Muscle weakness:
Excessive sweating: Tremor: Palpitation:
Visual disturbances (diplopia, decreased acuity):
Loose stools: Constipation:
Dysphagia: S.O.B:
Neck pain: Neck swelling:
Oligo/amenorrhoea: Menorrhagia:
Dry/yellow skin:
Vitiligo:
Family history:
2) Pancreatic islets:
Polyuria: polydipsia:
Weight loss:
Impotence:
Family history:
Symptoms of hypoglycaemia (palpitation, sweating, tremor, decreased consciousness,
tinnitus):
3) Adrenal glands:
Weight loss: Weight gain:
Muscle weakness:
Postural unsteadiness:
Nausea: Vomiting:
Amenorrhoea:
Skin hyperpigmentation: Vitiligo:
Excess hair growth:
4) Hypothalamus/pituitary:
Polyuria: Polydipsia:
Impotence:Gynaecomastia:
Galactorrhoea: Amenorrhoea:
Visual field defects (type):
Delayed puberty (absence of secondary sexual characters):
Gynecological history:
Menarche:
Katamine:
Regularity:
Dysmenorrhoea:
Contraceptives:
Vaginal discharge:
Menopause:
(If positive: ask about: duration, medications, regular follow up, any complications)
Diabetes mellitus:
Hypertension:
Bronchial asthma:
Cardiac/renal diseases:
Others:
Hospitalization:
Surgical operations:
Jaundice:
Blood transfusion:
Family history:
Diabetes mellitus:
Hypertension:
Similar condition:
Cardiac/renal disease:
Others:
Drug history:
Summary:
Age:
Gender:
Past medical problems:
Presenting complaint:
Important positives and negatives:
Medications:
First of all you must introduce yourself to the patient, offer a greeting and take permission for history
taking and clinical examination.
History:
Demographic Data:
Name, Age, Gender, Original home, Residence, Marital Status, Occupation, Date of Admission.
C/O:
(same words of the patient and duration in a chronological order:
e.g.: lower limb swelling / 5 days , shortness of breath / 3days and chest pain / 1 day)
(1- Full analysis of the complaint 2- The story 3- Similar condition 4- Complete the system)
e.g.:
Myocardial ischaemia (Angina): severe retrosternal chest pain, constricting/ gripping/ crushing
in nature (or just tightness or heaviness), radiates to arms/ throat/ jaw, provoked by exercise or
cold weather and relieved by rest or sublingual nitrates. Duration: 2 to 10 minutes.
Myocardial infarction: same as angina but the pain is more severe, more prolonged and not
relieved by rest or nitrates. It is associated with restlessness, shortness of breath, sweating,
nausea, vomiting and feeling of impending death (autonomic stimulation).
Aortic dissection: very severe tearing chest pain, of abrupt onset, radiates to the back between
the scapulae. May be associated with sweating and syncope.
3. Exertional fatigue:
a. Normal sinus rhythm: occurs in healthy people, precipitated by anxiety, physical stress,
excessive caffeine intake (tea, coffee, and cola) or nicotine. (rapid and regular).
b. Intermittent irregularities of heart beats (extrasystoles/ectopics): sensation of missed or
dropped beats followed by a strong beat, occurs at rest and abolished by exercise.
c. Sustained arrhythmias: starts suddenly, lasts for minutes or hours and not usually triggered
by anxiety or stress.
e.g.: Atrial fibrillation: (rapid, irregular, heart jumping or racing)
Supraventricular/ventricular tachycardia :( rapid, regular, heart racing/fluttering)
HTN, DM, dyslipidaemia (risk factors for coronary artery disease), rheumatic fever in childhood
(valvular heart disease), renal disease and thyrotoxicosis (AF).
*If infective endocarditis is suspected, ask about: recent dental work, skin infection, penetrating
trauma or IV drug abuse.
Family history:
HTN, DM, familial hypercholesterolaemia, IHD and HOCM (history of sudden unexpected death
at a young age).
Drug history:
Clinical examination:
1) Inspection of the patient:
a. General appearance: (Unwell? Breathless? Distressed? Cyanosed?)
Body built: Marfan's/ other syndromes:
b. Hand :
Finger clubbing:
Splinter haemorrhages: (multiple linear reddish-brown marks along the axis of finger/toe
nails due to circulating immune complexes)
c. Volume: (means the degree of pulsation and reflects the pulse pressure):
*large: (exercise, pregnancy, fever, thyrotoxicosis, anaemia, aortic regurgitation, hypertension
and Paget's disease of bone).
*small: (left ventricular failure, hypovolaemia and peripheral vascular disease)
e. Synchronicity:
f. Radiofemoral delay: (coarctation of aorta)
g. Peripheral pulses:
JVP is the vertical distance in centimetres between the top of the venous
pulsation and the sternal angle. Normally it is 3 - 4 cmH2 O. It reflects the
right atrial pressure which is equivalent to: JVP + 5
(5 cm is the distance between sternal angle and right atrium), so normal
right atrial pressure is 8 – 9 cmH2 O.
*Abnormalities of JVP:
6) Examination of precordium:
a. Inspection:
Chest deformities: (pectus excavatum, pectus carinatum): may displace the heart.
Scars: (midline sternotomy indicates coronary artery bypass surgery or aortic valve
replacement, left submammary indicates mitral valvotomy, infraclavicular indicates
pacemaker implantation).
Visible pulsations:
Prominent veins : (superior vena caval obstruction)
b. Palpation:
i. Apex beat: (is the lowermost outermost part of the precordium at which the cardiac
impulse can be distinctly felt).
*comment on location and character:
Normal apical impulse: is in the 5th left intercostal space at, or medial to, the
midclavicular line. It is localized.
Displaced apex (downwards and laterally): due to left ventricular dilatation (aortic
stenosis, severe hypertension and dilated cardiomyopathy), chest deformities and
mediastinal shift: (massive pleural effusion, tension pneumothorax).
Impalpable apex: (overweight/muscular people, patients with emphysema or asthma,
pericardial/pleural effusion and dextrocardia).
Tapping apex: is a palpable first heart sound, occurs in mitral stenosis (MS).
ii. Left parasternal heave: due to right ventricular hypertrophy (secondary to pulmonary
hypertension) or left atrial enlargement.
iii. Second heart sound (S2): pulmonary component (P2 ) palpable in pulmonary HTN. Aortic
component (A2 ) palpable in systemic HTN
c. Auscultation:
i. Heart sounds :
First heart sound (S1): is caused by closure of the mitral and tricuspid valves at the onset
of systole, best heard at the apex.
*comment on intensity : (normal, loud , soft)
Soft S1: (mitral regurgitation, low cardiac output and poor left ventricular function)
Loud S1: (mitral stenosis, increased cardiac output and atrial myxoma)
Variable intensity: (complete heart block and atrial fibrillation).
Second heart sound (S2): is caused by closure of the aortic and pulmonary valves at the end
of systole, best heard at left sternal edge.
*comment on intensity and splitting:
Soft S2: (calcific aortic stenosis, aortic regurgitation and low cardiac output)
Loud S2: systemic hypertension (aortic component) and pulmonary hypertension
(pulmonary component).
Splitting: (physiological, fixed, reverse)
o Physiological: occurs during inspiration and disappears during expiration
because the aortic valve closes before the pulmonary valve.
o Wide (enhanced physiological splitting): (wide in inspiration and
disappears during expiration), occurs in: RBBB, pulmonary HTN and
ventricular septal defect.
Third heart sound (S3): low- pitched early diastolic sound due to rapid ventricular filling.
It is either physiological (in children, young adults and during pregnancy) or pathological
(left ventricular failure and mitral regurgitation).
Fourth heart sound (S4): low-pitched, late diastolic sound due to atrial contraction
against a stiff ventricle (HOCM, HTN, AS). It is always pathological.
iii. Murmurs: (caused by turbulent blood flow across an abnormal valve, septal defect, outflow
obstruction or by increased flow through a normal valve)
Timing: (with carotid pulsation). Systolic (with carotid pulse), diastolic (alternates
with carotid pulse).
Character: (rough, rumbling, harsh, blowing)
Pitch: (low, high)
Intensity:
Grade I: audible with great difficulty in a quiet room
Grade II: easily audible but not loud
Grade III: loud without a thrill
Grade IV: loud with a thrill
Grade V: very loud, audible outside precordium
Grade VI: extremely loud, heard without stethoscope
Location: (position of maximum intensity)
Radiation: (towards left axilla: MR , towards neck: AS)
Effect of respiration: (murmurs in the right side of the heart increase in intensity
during inspiration while murmurs in the left side increase in intensity during
expiration).
Types of murmurs:
Mid diastolic:
a) Mitral stenosis: low-pitched, rumbling, best heard at the apex with the patient
rolled to the left side. It is accentuated by exercise.
b) Austin Flint murmur: accompanies aortic regurgitation, it is caused by the
regurgitant jet striking the anterior leaflet of the mitral valve, restricting inflow to
the left ventricle.
Continuous: (machinery- like) occurs in patent ductus arteriosus (PDA), best heard at
upper left sternal border and radiates towards left scapula.
First of all you must introduce yourself to the patient, offer a greeting and take permission for history
taking and clinical examination.
History:
Demographic Data:
Name: Age: Gender: Original home: Residence: Marital Status:
Occupation: Date of Admission:
1. Breathlessness:
Mode of onset: (sudden/gradual)
Progression: (rapid/slow)
Duration:
Sudden onset and rapid progression over minutes: respiratory (pulmonary embolism,
pneumothorax, asthma, inhaled foreign body) and cardiac (acute left ventricular failure).
Gradual onset and progression over hours to days: respiratory (pneumonia, asthma,
exacerbation of COPD).
Gradual onset and progression over weeks to months: respiratory (pleural effusion,
neuromuscular disorders) and anemia.
Gradual onset and progression over months to years: respiratory (COPD, pulmonary
fibrosis, pulmonary tuberculosis).
Severity:
Is it related to exertion?
What exercise precipitates it: heavy exertion, carrying loads, walking up stairs (how
many stairs?) Walking on the flat (how far can he/she walk?)
Does it occur at rest?
Orthopnoea (dyspnoea on lying flat): (how many pillows the patient uses to feel
comfortable?)
Paroxysmal Nocturnal Dyspnoea (PND): (patient wakes up at night with distressing
dyspnoea (gasping for air) and fear of imminent death, usually associated with cough and
frothy, blood stained sputum).
Associated symptoms:
*Wheeze and cough: Asthma, COPD.
*Pleuritic chest pain: Pneumonia, pneumothorax, pulmonary embolism, rib fracture.
*Central chest pain: Myocardial infarction with left ventricular failure, massive
pulmonary embolism/infarction.
*Without chest pain: Acute left ventricular failure/pulmonary edema,
hypovolaemia/shock, metabolic acidosis, pulmonary embolism, pneumothorax.
Causes of breathlessness:
Cardiac: left ventricular failure, mitral valve disease, cardiomyopathy, constrictive pericarditis,
pericardial effusion.
Respiratory:
Airways: Asthma, COPD, bronchiectasis, lung cancer, foreign body, laryngeal tumor, cystic
fibrosis, bronchiolitis.
Parenchyma: Pneumonia, pulmonary fibrosis, tuberculosis, sarcoidosis, alveolitis.
Pulmonary circulation: Pulmonary embolism, pulmonary vasculitis, pulmonary
hypertension.
2. Cough:
(is a forced expulsive maneuver against an initially closed glottis causing a characteristic sound)
For how long? (days or weeks)
Is it dry or productive?
Is it worse during the day or night?
Aggravating factors: (dust, fumes, pollen or cold air).
Types of cough:
Barking: harsh, painful, associated with hoarseness and inspiratory stridor (due to laryngeal
inflammation, infection or tumor).
Whooping: severe, persistent, dry and irritating bouts of coughing followed by a high-pitched
intake of breath that sounds like “whoop”. It is caused by Bordetella pertussis.
Moist: suggests secretions in the upper and larger airways (asthma, COPD and bronchiectasis).
*Persistent moist smoker’s cough first thing in the morning is typical of chronic bronchitis (COPD).
Timing/associated features:
Causes of cough:
Red flag symptoms: (if associated with cough, should prompt a chest X-ray)
Haemoptysis.
Breathlessness.
Fever.
Chest pain.
Weight loss.
3. Sputum:
Amount: how much is produced per day? Small amount (teaspoonful) or large (cupful)
*Large amount of purulent sputum (> a cupful) varying with posture: suggests bronchiectasis.
*Large amount of purulent sputum on a single occasion: suggests rupture of lung abscess or
empyema into the bronchial tree.
*Large volumes of watery sputum with a pink tinge: of acute onset suggests pulmonary oedema,
but occurring over weeks: suggests alveolar cell cancer.
Colour: (white, yellow, green)
Consistency:
Serous (clear, watery, frothy, pink): acute pulmonary oedema, alveolar cell cancer.
Mucoid (white-grey viscid mucus): bronchial asthma and chronic bronchitis/COPD.
Purulent: yellow; in acute broncho-pulmonary infection.
Green: in bronchiectasis, lung abscess, pneumonia and cystic fibrosis.
Mucopurulent: ( mucoid + purulent in chronic bronchitis with secondary infection).
Rusty (golden-yellow sputum due to degradation of haemoglobin): lobar pneumonia.
Very thick (or jelly-like difficult to cough up/mucus plug): in bronchial asthma.
Smell: offensive in bronchiectasis, lung abscess and empyema.
Causes of haemoptysis:
5. Chest pain:
Site:
Time & mode of onset:
Severity:
Nature:
Progression:
End of pain:
Duration:
Aggravating factors:
Relieving factors:
Radiation:
Associated Symptoms:
A. Non-central:
Pleural:
1) Infection: pneumonia, tuberculosis, bronchiectasis.
2) Malignancy: lung cancer, mesothelioma, metastatic.
3) Pneumothorax, pulmonary infarction.
4) Connective tissue disease: rheumatoid arthritis, SLE.
B. Central:
Cardiac: acute myocardial infarction/ischaemia, pericarditis, massive pulmonary
thromboembolism.
Great vessels: aortic dissection.
Tracheal: infection, irritant dusts.
Oesophageal: oesophagitis, rupture.
Mediastinal: lung cancer, thymoma, metastasis, mediastinitis.
Pleuritic pain: sharp, stabbing pain in the sides of the chest, aggravated by deep
breathing or coughing. It is caused by: pulmonary embolism, pneumonia,
pneumothorax, fractured ribs.
Malignant chest wall pain (due to local invasion by lung cancer, mesothelioma or rib
metastasis): dull, aching unrelated to respiration, progressively worsens and disturbs
sleep.
Intercostal nerve root compression, thoracic shingles (herpes zoster): cause chest pain
in a thoracic dermatomal distribution.
Sudden localized pain after vigorous coughing or direct trauma: suggests rib fracture or
intercostal muscle injury.
6. Wheezing:
(high-pitched whistling sound produced by air passing through narrowed small airways). It is limited
to expiration.
*Bronchial asthma: night wakening with wheeze, and on exercise.
*COPD: wheeze after wakening in the morning and on exercise.
**Do not mistake wheezing for stridor which is a high-pitched/harsh inspiratory sound
(aggravated by coughing) caused by partial occlusion of a large airway (larynx, trachea or main
bronchus) by tumour or foreign body.
Pulmonary tuberculosis or contact with a patient with pulmonary tuberculosis or chronic cough.
Bronchial asthma, eczema and hay fever.
Whooping cough, measles: recognized causes of bronchiectasis.
Connective tissue disorders e.g. rheumatoid arthritis: pulmonary fibrosis, effusion, bronchiectasis.
Previous malignancy: recurrence/metastasis.
Chemo/radiotherapy: pulmonary fibrosis.
Recent travel, immobility, cancer: pulmonary embolism.
Recent surgery, loss of consciousness: aspiration of foreign body/gastric contents,
pneumonia, lung abscess.
Family history:
Social history:
Occupational history:
(Record any exposure to recognized hazards and length of exposure)
Occupational Asthma:
Byssinosis:
Due to exposure to Cotton dust: (symptoms are worse at the beginning of the working week, unlike
occupational asthma which is worse at the end of the working week)
Exposure to Coal dust particles (coal miners): leads to coal worker’s pneumoconiosis (pulmonary
fibrosis).
Exposure to Silica particles (metal mining, stone quarrying, ceramic manufacture): causes silicosis
(progressive dyspnoea, increased incidence of tuberculosis, pulmonary fibrosis).
Exposure to Asbestos (shipyard, construction workers, plumbers): may cause asbestosis
(progressive dyspnoea, pulmonary fibrosis) and mesothelioma (carcinoma of the pleura) 20 to 30
years later.
Exposure to Beryllium (nuclear, aerospace industries): leads to berylliosis (pulmonary fibrosis).
Exposure to Fungal spores (Micropolyspora faeni) in mouldy hay: causes Farmer’s lung.
Exposure to Fungal spores (Thermophilic actinomycetes): Mushroom worker’s lung.
Exposure to Aspergillus clavatus: Malt worker’s lung.
Exposure to Avian proteins (droppings/excreta): Bird fancier’s and Pigeon fancier’s lung.
Drug history:
2. Hands:
o Finger clubbing:
Grade 1: loss of the normal angle between the nail and the nail bed.
Grade 2: Increased nail bed fluctuation.
Grade 3: Increased nail curvature.
Grade 4: Increased bulk of the soft tissues over the terminal phalanges (drumstick
appearance).
Causes of clubbing:
1) Familial.
2) Respiratory disease: lung cancer, mesothelioma, suppurative lung disease (bronchiectrasis,
empyema, lung abscess), cystic fibrosis, idiopathic pulmonary fibrosis, asbestosis.
3) Cardiovascular disease: bacterial endocarditis, cyanotic congenital heart disease, atrial myxoma.
4) Gastrointestinal/liver: liver cirrhosis, coeliac disease, Crohn’s disease, ulcerative colitis.
o Peripheral cyanosis:
o Tobacco staining:
o Tremor:
*Fine: due to hypoxia or excessive use of beta- agonists or theophylline.
*Flapping ‘‘asterixis’’: intermittent failure of parietal mechanisms required to maintain posture.
Causes:
Respiratory: failure/acidosis (CO2 retention).
Liver: failure, Wilson’s disease (hepato-lenticular degeneration).
Renal failure.
Electrolyte disturbances: hypokalaemia, hypomagnesaemia, hypoglycaemia.
Drugs: barbiturates, alcohol, sodium valproate, phenytoin, carbamazepine,
metoclopramide, gabapentin, opioids.
Nervous system: haemorrhage (intracerebral, subdural, subarachnoid), cerebral
ischaemia.
o Pulse: tachycardia (pneumonia, COPD, respiratory failure), pulsus paradoxus (severe asthma).
3. Face:
Horner’s syndrome (due to apical lung tumour ‘‘Pancoast’s tumour’’ compressing the
sympathetic nerves in the neck).
Central cyanosis (lips and tongue)
Pursed lips (severe COPD).
4. Neck:
o JVP: raised in:
Cor pulmonale (right-sided heart failure secondary to lung disease e.g. COPD)
Raised intrathoracic pressure (tension pneumothorax, acute severe asthma).
Massive pulomonary embolism.
Superior vena caval obstruction secondary to lung cancer or upper mediastinal tumours:
(lymphoma, thymoma).
o Lymph nodes: cervical, supraclavicular and scalene (in the angle between sternocleidomastoid
and clavicle).
b) Palpation:
I. Position of the trachea:
Well centralized or deviated to one side (upper mediastinal shift)
Causes of tracheal deviation:
Towards the side of the lung lesion:
*Upper lope collapse.
*Upper lobe fibrosis.
*Pneumonectomy.
Away from the side of the lung lesion:
*Massive pleural effusion.
*Tension pneumothorax.
Upper mediastinal mass:
*Retrosternal goitre,
*Lung cancer.
*Lymphoma.
Distance between the suprasternal notch and the thyroid cartilage: is normally 3-4
finger breadths, if decreased it suggests lung hyperinflation.
II. Position of the apex beat: (displacement indicates lower mediastinal shift).
*Displaced cardiac impulse without deviation of the trachea: left
ventricular enlargement, kyphoscoliosis, severe pectus excavatum.
Liver dullness (by tidal percussion): the upper border of the liver is in the 5th intercostal
space in the right mid-clavicular line. If the chest is resonant below this level, it is a sign of
hyperinflation (COPD or severe asthma).
Cardiac dullness: over the left anterior chest. It may be decreased in COPD/severe asthma.
d) Auscultation:
I. Breath sounds:
Intensity: normal, increased (very thin individuals) or diminished (obesity, pleural
effusion, marked pleural thickening, pneumothorax, hyperinflation due to COPD,
over an area of collapse with occlusion of major bronchus).
Quality:
*Vesicular (normal): louder and longer on inspiration than on expiration (fades
rapidly) and there is no gap between the two phases.
*Bronchial breathing: high- pitched sound with a blowing quality similar to
that heard over the trachea and larynx. (The breath sounds are of similar length
and intensity in inspiration and expiration with a characteristic pause between
the two phases). It is heard in:
1. **Lung consolidation (pneumonia).
2. **At the top of a pleural effusion.
3. **Collapsed lung with a patent major bronchus.
First of all you must introduce yourself to the patient, offer a greeting and take permission for history
taking and clinical examination.
History:
Demographic Data: Name: Age: Gender: Original home: Residence:
Marital Status: Occupation: Date of Admission:
24- Weight:
Increased: Decreased: No change:
If decreased, how much? (Clothes, People Noticed, previous weight records):
How quickly: (Significant weight loss: > 3kg in 6 months).
Causes of weight loss:
- Reduced energy intake: starvation/dieting, loss of appetite, malabsorption and anorexia
nervosa.
- Increased energy expenditure (catabolism): hyperthyroidism, uncontrolled diabetes mellitus,
malignancy, infections ‘‘tuberculosis and HIV’’, liver diseases, adoption of a more energetic
lifestyle.
27- Halitosis (bad breath): due to gingivitis (Vincent’s angina), dental caries, pharyngeal infection,
bronchiectasis and lung abscess.
29- Odynophagia (pain on swallowing): due to local infection in the oesophagus (candida, herpes
simplex). Common in AIDS patients.
31- Dysphagia: (difficulty in swallowing and sensation of something sticking in the throat or chest)
Is it Painful or painless?
Intermittent or progressive
Duration
Is it for solids, liquids or both?
Level at which food sticks:
Is there complete obstruction and regurgitation?
Previous history of dysphagia or heartburn:
Causes:
1. Oral: painful mouth ulcers, tonsillitis, glandular fever, pharyngitis, peritonsillar abscess.
2. Neurological: (cerebrovascular accident, bulbar or pseudobulbar palsies): worse for liquids
than for solids, may be accompanied by chocking and regurgitating fluid from the nose.
3. Neuromuscular: (achalasia, myasthenia gravis and oesophageal dysmotility): worse for
solids.
4. Mechanical: usually presents with initial difficulty in swallowing solids then progresses to
difficulty in swallowing liquids.
*Benign (peptic) stricture: longstanding dysphagia without weight loss but
accompanied by heartburn.
*Malignant oesophageal stricture: short history, weight loss, no reflux symptoms.
*Extrinsic compression: by lung cancer or goiter.
*Systemic sclerosis.
33- Acid reflux: (regurgitating gastric acid producing a sour taste in the mouth)
36- Vomiting:
Frequency:
Volume:
Nature (recognizable food, digested food, clear acidic fluid, bile stained, blood stained or
faeculent):
Is it preceded by nausea or does it occur without warning?
Associated symptoms (dyspepsia or abdominal pain):
Is it related to meal times, early morning or late evening?
Is it projectile? (Gastric outlet obstruction, high small bowel obstruction or raised intracranial
pressure)
What medications has the patient been taking?
Causes:
A. Gastrointestinal: gastroenteritis, cholecystitis, pancreatitis, hepatitis, gastric outlet
obstruction (projectile, large volume of vomitus, not bile stained) and small bowel
obstruction (bile stained vomitus, associated with abdominal distension and intestinal
colic). Vomiting is precede by nausea and accompanied by abdominal pain/discomfort.
B. Neurological: raised intracranial pressure (meningitis, brain tumour: vomiting not
preceded by nausea), labrynthitis, Meniere’s disease, migraine, vasovagal syncope, shock,
fear and severe pain (renal colic, biliary colic, myocardial infarction).
C. Metabolic/endocrine: pregnancy, diabetic ketoacidosis, renal failure, hepatic failure,
hypercalcaemia and Addison’s disease.
D. Alcohol and drugs: opioids, digoxin, theophylline, cytotoxic agents, antidepressants and
others.
E. Psychological: anorexia nervosa and bulimia.
38- Melaena: (passage of black tarry stool with a characteristic odour, due to partially digested
blood).
* It indicates upper GI bleeding but can result from bleeding anywhere proximal to the
transverse colon.
* Melaena must be distinguished from the matt black stools associated with oral iron or bismuth
therapy.
Epigastrium:
Stomach: peptic ulcer disease (gastric/duodenal), gastritis, gastric cancer.
Pancreatitis.
Oesophageal disease: GORD, inflammation, spasm, rupture.
Gall bladder disease.
Vascular: ruptured aortic aneurysm.
Cardiac: myocardial infarction, pericarditis.
Peri-umbilical:
Early appendicitis.
Intestinal obstruction.
Vascular: mesenteric ischaemia (superior mesenteric artery occlusion:
thrombosis, embolism), ruptured aortic aneurysm.
Others: (may affect any quadrant, more than one quadrant or may cause generalized
abdominal pain)
Gastroenteritis, enteric fever, malaria.
Peritonitis (generalized or localized).
Abdominal wall: mesenteric traction, rectus sheath haematoma
(anticoagulants), trauma, myositis.
Metabolic: diabetic ketoacidosis, uraemia, hyperlipidaemia,
hyperparathyroidism, porphyria, acute adrenal insufficiency, familial
Mediterranean fever, C1 esterase deficiency (angioneurotic oedema).
Neurologic/psychiatric: herpes zoster, tabes dorsalis, acute vertebral
collapse, nerve root compression, irritable bowel syndrome, psychiatric
disorders.
Toxic: lead poisoning, snake bite.
Causes:
1. Portal hypertension related: (high serum-ascites albumin gradient: > 1.1 g/dL)
Sinusoidal: liver cirrhosis, spontaneous bacterial peritonitis, acute hepatitis, extensive
malignancy (hepatocellular carcinoma or metastatic tumours).
Pre- sinusoidal: portal vein thrombosis, splenic vein thrombosis, Schistsomiasis.
Post- sinusoidal: Budd- Chiari syndrome, hepatic veno-occlusive disease, congestive or right-
sided heart failure, tricuspid regurgitation, constrictive pericarditis.
2. Non- portal hypertension related: (low serum-ascites albumin gradient: < 1.1 g/dL)
Peritoneal carcinomatosis.
Peritonitis: tuberculosis, ruptured viscus.
Pancreatitis.
Hypo-albuminaemia: nephrotic syndrome, protein loosing enteropathy.
Meig’s syndrome.
Bowel obstruction/infarction.
Lymphatic leak (obstruction of main lymphatic duct): chylous ascites.
Vasculitis.
42- Altered bowel habit: (normal bowel movement frequency ranges from 3 times/day to once
every 3 days)
a) Constipation: (Infrequent passage of hard stools ; < 3 times/week)
Frequency of defecation:
Consistency of stools:
Causes of constipation:
Common causes: low fibre diet, immobility (stroke, Parkinson’s disease), irritable bowel
syndrome, hospital environment, old age.
Anorectal disease: anal fissure, anal stricture, rectal prolapse.
Intestinal obstruction: colorectal carcinoma, Crohn’s disease (stricture).
Metabolic/endocrine: hypothyroidism, hypercalcaemia, hypokalaemia, porphyria.
Drugs: opiate analgesics (morphine, codeine), anticholinergics, iron.
Neuromuscular: spinal or pelvic nerve injury.
Causes:
(anorexia, weight loss, anaemia or nocturnal diarrhoea suggest an organic cause)
Mucus with diarrhoea: occurs in irritable bowel syndrome, colonic adenocarcinoma, colonic polyps.
Small bowel diarrhoea: large volume (>1 litre/day), watery or steatorrhoea, may be associated with
periumbilical or RIF pain not relieved by defecation. (e.g.: malabsorption, osmotic, secretory, Crohn’s
disease, infections “E.coli, cholera, Rota/Norovirus, Giardia, cryptosporidia, cyclospora” and food
poisoning).
44- Jaundice:
Is it progressive (carcinoma of the head of pancreas)?
or intermittent (peri-ampullary carcinoma or gallstones)?
Is there skin itching?
What is the colour of urine?
What is the colour of stool?
Accompanying symptoms (abdominal pain, loss of appetite, fever, vomiting): (indicate
acute hepatitis or gallstones)
Is it associated with weight loss? (malignancy)
Past history of blood transfusion, surgical operations, intravenous drug abuse or tattooing
(hepatitis B, C)
Sexual and contact history: (hepatitis B, C)
Drug history: (see below)
Alcohol intake: how many units/day? For how long?
History of travel and immunizations (hepatitis A)
Past history of jaundice: When? How long did it last?
Past history of hepatitis:
Family history of jaundice: (hereditary spherocytosis, haemochromatosis, Wilson’s
disease, Gilbert’s syndrome)
Chronic GI bleeding.
Progressive dysphagia.
Progressive unintentional weight loss.
Persistent vomiting.
Iron deficiency anaemia.
Epigastric mass.
Suspicious barium meal.
A: Anaemia.
L: Loss of weight.
A: Anorexia.
R: Recent onset of progressive symptoms.
M: Melaena/haematemesis.
S: Swallowing difficulty.
Family history:
- IBD, colorectal cancer, haemochromatosis, Wilson’s disease, Gilbert’s syndrome.
- DM, hypertension and other chronic illnesses.
Social history:
*Dietary history: allergy or food intolerance (lactose, gluten).
*Alcohol consumption: ( type: quantity: (in units) duration: )
*Smoking: (quantity: duration: )
(smoking increases the risk of oesophageal/gastric and colorectal cancer,
crohn’s disease and peptic ulcer disease).
*Travel history: (diarrhoeal illnesses).
*Risk factors for viral hepatitis: (see above)
*Stress/emotional ill health: (irritable bowel syndrome and dyspepsia)
Drug history:
*Aspirin/ NSAIDs: dyspepsia, gastric erosions/ulcers (GI bleeding).
*Opioid analgesics: nausea, vomiting, constipation.
*Antibiotics, proton pump inhibitors: diarrhoea
*Oral corticosteroids: weight gain.
*Hepatotoxic drugs: (see above)
Clinical examination:
1. General assessment:
Degree of illness: does the patient look well, mildly ill or severely ill?
Physical attitude:
Is the patient lying comfortably at bed? Lying still (peritonintis)? Restless or
roll about (colic)? Is he/she in pain?
Is he/she breathless? Lying propped up at bed or sitting up and bending forward?
The neck:
For lymph node enlargement: (submental, submandibular, pre-auricular, post-auricular,
anterior/ posterior cervical, occipital and supraclavicular).
*Examine for other groups of lymph nodes: axillary, epitrochlear and inguinal.
Signs of decompensated liver disease: Flapping tremor (asterixis), jaundice, ascites and hepatic
encephalopathy (drowsiness, hyperventilation).
2. The Abdomen:
I. Inspection:
Shape: (normal contour, distended or sunken)
Generalized distension: fat, fluid, flatus, faeces, fetus or functional.
Localized distension: enlarged organ (liver, spleen or ovary) or superficial
swelling.
Scaphoid abdomen: indicates rapid weight loss (starvation/malignancy).
Umbilicus:
Inverted, flat or everted.
(In obesity: umbilicus is sunken, in ascites: flat or everted).
Movements of the abdominal wall:
Normally the abdomen moves with respiration
In peritonitis the movement is absent or diminished (still abdomen).
Visible peristalsis: (obstruction at the pylorus, congenital pyloric stenosis or distal
small bowel obstruction).
Visible pulsation: of the abdominal aorta in epigastrium (thin individuals).
Stomas: ileostomy/colostomy.
Prominent veins: (in inferior vena caval obstruction or portal hypertension) Note direction
of blood flow (from below upwards in IVC obstruction), or away from the umbilicus (caput
medusa) in portal hypertension.
II. Palpation:
a) Superficial:
1. Tenderness:
*Generalized: due to generalized peritonitis.
*Epigastric: suggests peptic ulcer.
*Right hypochondrial: cholecystitis.
*Right iliac fossa: appendicitis/Crohn’s ileitis.
5. Temperature:
b) Deep:
1. Tenderness:
2. Rebound tenderness: the abdominal wall is compressed slowly then released
rapidly and a sudden stab of pain results. (strongly suggests peritonitis).
3. Masses:
Causes of hepatomegaly:
5) Haematological disorders:
Lymphoma.
Leukaemia.
Myeloproliferative disorders.
2. Gall bladder: (just lateral to rectus abdominis near tip of 9th costal cartilage)
Firm, smooth, globular swelling, moves with respiration (carcinoma of the head of
pancreas or mucocele of the gallbladder).
3. Spleen:
Not normally palpable, has to be enlarged to 2-3 times its usual size before it becomes
palpable. (to palpate a small spleen turn the patient to his/her right side)
Its characteristics are:
1) Firm swelling appearing beneath the left subcostal margin.
2) Dull to percussion.
3) Moves downwards on inspiration.
4) Not bimanually palpable.
5) Its upper border cannot be felt (i.e. one cannot get above it)
6) Has a notch in the lower medial border
*If palpable measure its size below the costal margin.
*Auscultation for a splenic rub
Causes of splenomegaly:
1. Portal hypertension.
2. Haematological disorders:
Lymphoma/leukaemia.
Myeloproliferative disorders.
Haemolytic anaemias.
3. Infections:
Glandular fever.
Malaria.
Visceral leishmaniasis.
Bacterial endocarditis.
Brucellosis, tuberculosis, salmonellosis.
4. Rheumatological conditions:
Rheumatoid arthritis (Felty’s syndrome).
SLE.
5. Others: (sarcoidosis, amyloidosis, glycogen storage disease)
a. With hepatomegaly:
o Early cirrhosis with portal hypertension.
o Lymphomas/leukaemias.
o Myeloproliferative disorders.
5. Urinary bladder:
If distended can be palpated as a rounded swelling in the hypogastrium.
IV. Auscultation:
A. Bowel sounds:
Normal (intermittent low or medium pitched gurgles).
Increased (borborygmi: frequent loud gurgles): in mechanical intestinal obstruction.
Absent: in paralytic ileus
B. Vascular bruits:
Aortic: (above and to the left of the umbilicus)
Renal: (on either side of the midline in the mid abdomen)
Femoral:
C. Succussion splash:
Heard in pyloric stenosis, advanced intestinal obstruction and paralytic ileus.
First of all you must introduce yourself to the patient, offer a greeting and take permission for history
taking and clinical examination.
History:
Demographic Data:
Name: Age: Gender: Original home: Residence: Marital Status:
Occupation: Date of Admission:
iii. Cardiac:
Occurs suddenly without prodromal symptoms.
Due to: complete heart block, supraventricular/ventricular tachycardia,
HOCM and aortic stenosis (AS).
Syncope occurring during exercise suggests HOCM or AS.
Recovery is rapid.
b) Seizures:
Defined as: any abnormal clinical event caused by an electrical discharge in the brain.
Major seizures cause loss of consciousness due to sudden dysfunction of the electrical
mechanisms of the brain.
Epilepsy is defined as tendency to have recurrent seizures.
III. Partial:
a. Partial motor:
Epileptic activity arising in the motor cortex causes partial motor
seizures in the form of rhythmical jerking or sustained spasm of the
contralateral face, arm, trunk or leg.
May remain localized to one part or may spread to involve the whole
side (Jacksonian seizures).
Prolonged episodes may cause paralysis of the involved limb lasting for
several hours after the seizures (Todd’s paralysis).
b. Partial sensory:
Seizures arising in the sensory cortex causes unpleasant tingling or
electric sensations in the contralateral face or limbs.
May spread over the body (Jacksonian).
What are the triggering factors? (sleep deprivation, alcohol withdrawal, recreational
drug misuse, physical and mental exhaustion, flickering lights: TV/computer screens and
intercurrent infections)
Ictal: (tongue biting, frothing, upward rolling of eyeballs, cyanosis and loss of
sphincteric control)
3- Dizziness and vertigo : (feeling of spinning of the patient or surroundings due to abnormal
perception of movement)
Causes of vertigo are:
A. Peripheral: {labrynthitis (vestibular neuronitis), benign paroxysmal positional
vertigo and Meniere’s disease (vertigo, tinnitus, sensorineural deafness and
sense of fullness in the ear)}.
B. Central: (brainstem ischaemia/infarction, acoustic neuroma).
4- Disorders of movement:
a) Negative symptoms: (motor weakness, lack of co-ordination, lack of stability and body
stiffness).
5- Sensory Symptoms:
a/ Abnormal sensations: {tingling, paraethesia (pins and needles) and pain}
b/ Loss of normal sensations: (touch, pin-prick, temperature, vibration and joint position)
6- Headache:
a) Time and mode of onset: (very sudden onset: subarachnoid haemorrhage or migraine)
b) Frequency & Periodicity:
c) Duration:
d) Time of the day(morning, night):
e) Precipitating Factors:
f) Aggravating & Relieving Factors:
g) where does it start and how does it evolve (progression):
h) Quality & severity:
What is the effect of posture, coughing and straining?
i) Symptoms preceding the headache (aura): {focal neurological symptoms e.g.: zigzag
(fortification spectra), spreading scintillating scotoma or senosory symptoms (tingling
sensation over part of the body)}.
j) Associated symptoms: (nausea, vomiting, photophobia, phonophopia, fever, rash, neck
stiffness)
k) Family History of Headache:
l) Other medical or neurological problems:
Chronic: tension headache (bilateral, constant, described as pressure over the head),
analgesic overuse headache, cervical spondylosis and depression.
B. Dysarthria: difficulty in speech articulation due to local lesions of the tongue, lips, ill-fitting
dentures or any disruption of the neuromuscular pathway such as:
1) Pseudobulbar (spastic) dysarthria:
Due to bilateral upper motor neuron lesion of the corticobulbar tract. It is characterized by
spastic contracted tongue, jerky speech, emotional lability and brisk jaw jerk.
2) Bulbar palsy:
Due to lower motor neuron lesion of 9,10,11,12 cranial nerves (weakness of tongue and
palatal muscles leading to nasal quality of speech).
3) Extrapyramidal dysarthria:
Monotonous speech as in Parkinson's disease.
4) Cerebellar dysarthria:
Slow slurred speech (similar to the speech of a drunken person).
5) Myasthenia gravis:
Fatiguing speech.
C. Dysphonia: failure of the vocal cords to generate sounds properly (hoarse voice or whispered
speech) due to vocal cords pathology (laryngitis) or paralysis (recurrent laryngeal nerve
damage).
Clinical examination:
1. Higher mental function:
a) Assessment of the level of consciousness: by the Glasgow Coma Scale (GCS):
Eye opening:
Spontaneous: 4
To speech: 3
To pain: 2
No response: 1
Motor response:
Obeys commands: 6
Localizes to pain: 5
Withdrawal: 4
Abnormal flexion: 3
Abnormal extension: 2
No response: 1
*maximum GCS is 15, minimum is 3, 8 or less indicates coma.
Abnormal findings:
Unilateral lesion of the optic nerve: leads to total loss of vision.
Compression of the optic chiasm: leads to bitemporal hemianopia.
Lesion of the optic tract: leads to homonymous hemianopia.
Lesion of the lower fibres of optic radiation (in temporal lobe): leads to superior
quadrantanopia.
Lesion of the upper fibres of optic radiation (in parietal lobe): leads to inferior
quadrantanopia.
Lesion of the occipital lobe (primary visual area): leads to homonymous
hemianopia with sparing of the macula.
Lesion of secondary visual areas: leads to visual agnosia (inability to recognize
visual stimuli) and visual hallucinations.
Bilateral occipital lobe lesion: leads to cortical blindness.
Examination sequence:
1. Inspection: for
A. Eyelids:
*Ptosis (drooping of the upper eyelid) is due to :
i. Neurogenic causes: 3rd nerve palsy and Horner's syndrome
ii. Neuromuscular junction: myasthenia gravis
iii. Myogenic: myotonic dystrophy
iv. Local causes: chronic orbital inflammation, tumours, degenerative
disease or trauma.
v. Congenital (bilateral ptosis is due to: myotonic dystrophy, myasthenia
gravis, syphilis or congenital)
*Lid retraction: sclera is visible above the iris due to thyroid eye disease (do lid
lag test)
B. proptosis: forward bulging of the eyeball due to: thyroid eye disease, carotico-
cavernous fistula, local causes (orbital cellulitis, haematoma, tumour) or Wegner's
granulomatosis.
2. Visual acuity: by Snellen chart 6 meters from the patient or by finger counting, hand
movement or just light.
4. Examination of the pupil: for shape, symmetry, light and accommodation reflexes.
Light reflex (direct and consensual): when light is shown on one eye both pupils
constrict due to the dual innervation of the pupils.
Afferent limb of the reflex: optic nerve, chiasm, optic tract terminating in Edinger-
Westphal nucleus.
Efferent limb: occulomotor nerve passing through the ciliary ganglion to constrictor
pupillae muscle.
Accommodation reflex: ask the patient to look at a far object then suddenly bring the
object near to the eyes, the pupils constrict. Afferent and efferent limbs are the same
as light reflex.
Abnormal findings:
Marcus Gunn pupil: due to optic nerve damage leading to relative afferent pupillary
defect (RAPD): (loss of direct and consensual light reflex when light is shown on the
affected eye with normal direct and consensual reflex when light is shown on the
normal eye).
Essential anisocoria: (common normal variant, one pupil is larger than the other but
they both behave normally).
Abnormal findings:
Oculomotor nerve palsy: ptosis, dilated pupil and the eye is deviated
downwards and laterally.
It is caused by:
Diabetes mellitus
Vasculitis: temporal arteritis, SLE
Posterior communicating artery aneurysm (headache or periorbital pain + 3rd
nerve palsy).
Cavernous sinus thrombosis (3rd,4th and 6th nerves palsies, hyperesthesia of
the upper face and eye pain due to trigeminal nerve involvement (ophthalmic
division), grossly oedematous eyelids and chemosis).
Weber's syndrome: ipsilateral 3rd nerve palsy + contralateral hemiplegia (due
to midbrain stroke).
False localizing sign: due to uncal herniation throught tentorium if raised ICP.
Others: amyloidosis, MS.
a) Ocular alignment: look for squint which is either congenital (non-paralytic, not associated with
diplopia) or acquired (due to paresis of one of the ocular muscles and it is associated with diplopia).
b) Ocular movement: ask the patient to follow your finger and note the following:
* If the patient develops diplopia determine whether it is horizontal or vertical.
* Nystagmus: involuntary oscillations of the eye, classified according to direction into: (horizontal,
vertical and multidirectional) and according to type into: jerk (which has fast and slow phases) and
pendular (equal oscillations about a central point).
Jerk: is the most common type of nystagmus, it is due to:
- Peripheral vestibular disease: (vestibular neuronitis and Meniere's disease), the direction of the
jerk is either horizontal or vertical, usually associated with vertigo.
- Central vestibular disease: (multiple sclerosis and cerebrovascular disease involving the central
vestibular connections), not associated with vertigo.
Pendular: results from cerebellar or brainstem disease (multiple sclerosis, spinocerebellar
degeneration and brainstem ischaemia).
Vertical: further subdivided into:
Upbeat: due to upper brainstem lesions (MS, infarction, Wernicke's
encephalopathy) and cerebellar vermis lesions.
Downbeat: due to lesions around foramen magnum (Arnold- Chiari malformation
or demyelination) or drugs (phenytoin and lithium intoxication).
*Internuclear ophthalmoplegia: is due to demyelination of the medial longitudinal bundle
within the brainstem (which co-ordinates the lateral rectus of one eye with the medial rectus of
the other). It is manifested as ataxic nystagmus in the abducted eye with failure to adduct the
other eye.
- The cell bodies of the sensory fibres are located in the trigeminal ganglion then pass to the pons.
- The sensory division has 3 branches:
*Ophthalmic (V1): provides sensation to the skin of upper eyelid, forehead, scalp and eye (cornea and
conjunctiva).
*Maxillary (V2): supplies mucous membranes of the upper mouth, roof of pharynx, (gums, teeth and
palate) of the upper jaw and sinuses.
*Mandibular (V3): supplies the floor of the mouth, common sensation to the anterior two thirds of the
tongue, gums and teeth of the lower jaw, mucosa of the check, skin of lower lips and jaw except the
angle of the jaw (supplied by C2).
The motor division: runs in the mandibular branch and supplies muscles of mastication (temporalis,
masseter, lateral and medial pterygoids).
Examination sequence:
Abnormal findings:
a) Unilateral lower motor neuron facial palsy (weakness of both upper and lower
facial muscles) is due to:
Lesions in the pons: (infarcts, tumours, demyelinating diseases (MS)
Ipsilateral 6th and 7th nerve palsies with contralteral hemiplegia (crossed
hemiplegia).
Paralysis of facial muscles (salivation, lacrimation and taste are NOT affected).
Lesions at the cerebello-pontine angle: (Acoustic neuroma)
*Ipsilateral 5th, 6th, 7th and 8th nerves palsies.
*Ipsilateral cerebellar signs.
*Paralysis of facial muscles and diminished salivation, lacrimation
and taste in the anterior two thirds of the tongue.
Lesions in the facial canal (geniculate ganglion): (Bell's palsy, Ramsay hunt
syndrome)
* Paralysis of facial muscles, diminished (salivation, lacrimation and taste in the
anterior two thirds of the tongue) and hyperacusis.
Bell's palsy: idiopathic condition presenting with acute lower motor
neuron facial palsy, often preceded by post-auricular pain, may be
associated with loss of taste in the anterior tongue (hypogeusia
/ageusia), hyperacusis (high-pithched sounds are heard unpleasantly
louder than normal) and dry eyes.
c) Upper motor neuron facial palsy: weakness is marked in the lower facial muscles
with relative sparing of the upper face (because of the bilateral cortical innervation
of the upper face), is due to supranuclear lesions (stroke above the level of the
pons).
8) The Vestibulochoclear nerve: sensory nerve
Arises from the pons, has 2 components:
*Vestibular: concerned with balance and equilibrium (connected with the
cerebellum)
*Cochlear: concerned with hearing.
Examination sequence:
a) Testing hearing: properly by audiometry, at the bedside by:
1. Whispered voice test
2. Rinne's test: normally air conduction is better than bone conduction (AC
> BC), this is a positive Rinne's test.
If BC > AC, negative Rinne's test, indicates conductive deafness.
3. Weber's test: normally the sound is heard equally in both ears.
- Weber's lateralizes to the affected ear in conductive deafness (the sound is
better heard in the affected ear).
- Weber's lateralizes to the unaffected ear in sensorineural deafness (the
sound is better heard in the unaffected ear).
b) Vestibular function:
*Inspect for nystagmus
*Dix- Hallpike positional test: if the patient has peripheral vestibular
disease he/she develops vertigo and nystagmus which fatigues on repetition
of the test (adaptation).
If the patient has central pathology he/she develops nystagmus which
persists on repetition (no adaptation).
Tone: is the resistance felt by the examiner when moving a joint passively through its range
of movement.
Abnormal findings:
1. Hypotonia (flaccidity): occurs in lower motor neuron lesions, cerebellar
disease and in the early phases of cerebral or spinal schock.
2. Hypertonia:
has 2 principal types:
*Spasticity: velocity- dependent resistance to passive movement (i.e. it is
detected with quick movements). Occurs in upper motor neuron lesions.
- In mild forms it is detected as a 'catch' at the beginning of passive
movement (clasp- knife spasticity).
- In more severe cases it limits the range of movement and may be
associated with contracture.
Power:
Grades of muscle power:
Grade 0: no muscle contraction visible
Grade 1: flicker of contraction but no movement
Grade 2: joint movement when effect of gravity is eliminated
c) Muscles of the trunk: (the patient is asked to lift his/her head up from the
pillow against resistence). If the muscles of the lower abdomen are
paralyzed the umbilicus moves upwards, if muscles of the upper abdomen
are paralyzed the umbilicus moves downwards (Beevor's sign).
Upper motor neuron lesion: muscle weakness, no wasting, hypertonia (spasticity), hyper-
reflexia, extensor plantar response and depressed abdominal reflexes.
Common causes: cerebrovascular disease (hemiplegia), spinal injury/disease (paraplegia) and
multiple sclerosis.
- Hemiplegia: is paralysis of one side of the body involving the arm, leg and usually the face,
due to a lesion in the corticospinal pathway.
- Uncrossed hemiplegia: cranial nerve involvement and hemiplegia are on the same side,
(cortical lesion).
- Crossed hemiplegial/paresis: is weakness in an ipsilateral cranial muscle group with a
contralateral paralysis, (brainstem lesion).
*Features of hemiparesis: (see above), in addition to slow, dragging, rolling gait on the affected side
(circumduction).
Lower motor neuron lesion: muscle weakness, hypotonia (flaccidity), hypo/areflexia, muscle
wasting and fasciculations.
Common causes: anterior horn cell damage (motor neuron disease or
poliomyelitis), root lesion (radiculopathies) or peripheral nerve lesion
(peripheral neuropathies).
Lesion in the muscles (myopathies): muscle weakness and wasting (usually proximal),
hypotonaia, muscle tenderness (myositis), pseudohypertrophy (muscular dystrophies).
Common causes: hereditary conditions (Duchenne, Becker's, myotonic
and fascioscapulohumeral muscular dystrophies), polymyositis,
alcohol and other toxins.
Reflexes:
a) Deep tendon reflexes: involuntary contraction of a muscle in response to stretch
(monosynaptic reflex), e.g.:
Knee jerk: L3, 4
Ankle jerk: S1, 2
Triceps jerk: C6, 7
Biceps jerk: C5, 6
Brachioradialis jerk: C5, 6
Abnormal findings:
Hyper-reflexia: occurs in UMNL, thyrotoxicosis and tetanus.
Examination sequence:
Upper limb:
a) Finger- nose test: (past pointing, intension tremor and slow clumsy movement).
b) Rapid alternating movements: (dysdiadochokinesis: slowness, disorganization and
irregularity of movements).
Lower limb:
Heel- shin test: (irregular movement)
1. Rebound phenomenon
2. Nystagmus
3. Dysarthria (scanning speech)
4. Hypotonia
5. Pendular knee jerk
6. Gait: ataxic (drunken, wide base) on tandem walking: unsteadiness and patient deviates
towards the side of the lesion.
Sensory ataxia: is due to sensory neuropathies or posterior column lesion (tabes dorsalis). The position
sense is impaired in the legs and this sensory defect is compensated for by vision, so the unsteadiness
becomes apparent only when eyes are closed or in the dark.
Romberg's sign: is a test for sensory ataxia (ask the patient to stand with feet close together, then to
continue in this posture with the eyes closed: patient becomes unsteady and sway about or may even
fall). *In cerebellar disease the ataxia is equally severe whether the eyes are open or closed.
Upper limb:
C5: lateral aspect of the shoulder, C6: thumb, C7: middle finger,
C8: little finger, T1: medial aspect of the forearm, T2: medial aspect of the arm.
Examination sequence:
10. Gait:
Spastic (hemiplegic): patient has difficulty in bending the knees and drags the feet
(circumduction).
Scissoring/stiff: in para/quadriparesis.
High- stepping: in common peroneal nerve palsy (L5/S1); weakness of the extensor muscles
of the feet (foot drop).
Ataxic/drunken/wide- base: ataxia is equally severe whether the eyes are open or closed.
Stamping/sensory ataxia: patient raises the foot very suddenly and abnormally high then
jerks it forward and brings it again to the ground with a stamp (heel first).
*Patient walks steadily when eyes are open but develops severe ataxia when eyes are closed
or when walking in the dark.
Festinant: is characteristic of Parkinson's disease.
The patient is bent forwards and advances with rapid, short, shuffling steps without
swinging of the arms.
Waddling: sways from side to side as each step is taken.
It is a feature of proximal pelvic girdle muscular weakness (myopathies, dystrophies) and
diseases of the hip joint.
*Trendelenburg's sign: weakness of gluteus medius muscle causes hip to drop when the
affected leg is held off the ground in erect posture.
Loss of cortical sensations on the opposite side of the body: (localization, two point
discrimination, stereognosis and graphaethesia).
Contralateral inferior quadrantanopia.
Gerstmann's syndrome (lesion of the dominant lobe):
Dyscalculia: inability to perform mental arithmetic.
Dyslexia: inability to read.
Dysgraphia: impairment of writing.
Figner agnosia.
Right-left disorientation.
Lesion of the non dominant lobe:
Constructional apraxia.
Dressing apraxia.
Sensory inattention/neglect.
Spatial disorientation.
Memory impairment.
Contalateral superior quadrantanopia.
Receptive (Wernicke's) aphasia: lesion of the dominant lobe.
Complex partial seizures.
Complex hallucinations (olfactory, auditory).
Auditory agnosia: inability to recognize auditory stimuli.
Contralateral dense hemiplegia with contralateral upper motor neuron facial palsy (uncrossed
hemiplegia).
Contralteral hemisensory loss.
Lacunar lesions:
Pons:
Ipsilateral 6th and 7th nerves palsies (Conjugate/horizontal gaze palsy).
Contalateral hemiplegia and hemisensory loss.
Medulla oblongata:
Ipsilateral 9th, 10th, 11th and 12th nerves palsies.
Contralateral hemiplegia.
Alternating analgesia: loss of pain and temperature on one side of the face and the
opposite side of the body.
Lateral medullary syndrome: (Wallenberg's syndrome)
Ipsilateral 9th and 10th nerves palsies.
Ipsilateral Horner's syndrome (descending autonomic nerves).
Ipsilateral ataxia and nystagmus (cerebellar signs).
Ipsilateral loss of pain and temperature on the face.
Contralateral loss of pain and temperature on one half of the body.
Features of raised intracranial pressure: (headache, vomiting, seizures, visual disturbances and
papilloedema).
Hemiplegia.
Radial nerve: {arises from the posterior cord of the brachial plexus (C5-8)}
Ulnar nerve: {arises from the medial cord of the brachial plexus (C8-T1)}
Claw hand (extension of the proximal phalanges and flexion of the distal phalanges)
Wasting and paralysis of small muscles of the hand (except lateral two lumbricals).
Wasting and paralysis of hypothenar muscles.
Sensory loss to the medial one and a half fingers (palmar and dorsal surface).
Lesion at the elbow: as above+ radial deviation of the wrist.
Median nerve: {arises from the medial and lateral cords of the brachial plexus (C5-T1)}
Foot drop.
Weakness of foot dorsiflexion.
Weakness of foot eversion.
Weakness of extensor hallucis longus.
Sensory loss over the dorsum of the foot and the lower lateral part of the leg.
Wasting of the anterior tibial and peroneal muscles.
High- stepping gait.