‫بسم ال الرحمن الرحيم‬

GENERAL EXAMINATION
First, describe the general condition of the patient: his alertness,
consciousness, cooperation, orientation to time, place and persons, intelligence
and memory, then describe:
I- Built: According to age, height and weight (normal 10% above or lower).
Causes of stunted growth are:
a- Malnutrition (commonest type).
b- Malabsorption syndrome.
c- Chronic diarrhea.
d- Liver cirrhosis and bilharzial liver fibrosis.
e- Nephrotic syndrome (heavy albuminuria).
f- Congenital cyanotic hear diseases (chronic hypoxia).
g- Cystic fibrosis.
h- Chronic infections in childhood as tuberculosis and empyema.
i- Genetic disorders:
• Turner’s syndrome.
• Dwarfism.
• Mongolism.
• Achondroplasia.
j- Endocrinal disorders: Cretinism and pituitary infantilism.

II- Decubitus:
a- Squatting → Fallout’s tetralogy.
b- Semisitting (orthopneic) → left sided heart failure, pericardial
effusion, emphysema, ascites, asthma and respiratory failure.
c- Mohamed prayer position (leaning forward) → pericardial effusion
and mediastinal tumors.
d- Lying on the affected side → Pleurisy and lung abscess,
bronchiectasis and empyema with bronchopleural fistula (suppurative
lung syndromes to minimize expectoration).
e- Lying on healthy side (contralateral side) → moderate amount of
pleural effusion and pneumothorax (more blood is driven to healthy
lung with better ventilation/perfusion ratio).
f- Sitting up → Massive ascites.
g- Opithotonus → tetanus, meningitis and strychnine poisoning.
h- Lying on back with legs drawn up → Peritonitis.
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i- Hyperextension of neck → meningitis.

III- Appearance:
a- Acromegaly:
• Enlargement of tongue (macroglossia) and soft tissues of
the palate may produce obstructive sleep apnea.
• Hypertension may lead to left ventricular failure with
pulmonary edema and dyspnea.
• Increased intracranial tension due to pituitary tumors may
cause central alveolar hypoventilation.
b- Thyrotoxicosis:
• Retrosternal extension my cause dyspnea or mediastinal
syndrome due to compression of mediastinal structures.
• Dyspnea due to hyperkinetic circulatory state.
• Heart failure and arrhythmias produce dyspnea due to
pulmonary congestion.
c- Myxedema:
• Obstructive sleep apnea due to macroglossia.
• Central sleep apnea due to depression of the respiratory
center.
• Dyspnea due to obesity and hypoventilation.
• Dyspnea due to constipation and abdominal distension.
d- Cushing’s syndrome:
• Dyspnea due to muscle weakness and myopathy.
• Impaired diaphragmatic function (due to hypokalemia).
• Increased incidence of respiratory infections.
e- Toxic look:
• Pulmonary tuberculosis.
• Suppurative lung diseases.
f- Blue bloater: obesity, generalized edema, cyanosis, puffy
eyelids, and fish-mouth breathing → respiratory failure due to chronic
bronchitis.
g- Pink puffer: slim, cyanosis → respiratory failure due to α1
antitrypsin deficiency.
h- Cachectic: malignancy, malnutrition & chronic inflammatory
diseases.
i- Infantile: pituitary infantilism.
j- Tetanus: a certain smile (risus sardonicus).
k- Myasthenia gravis: weak smile and bilateral ptosis.

IV- Skull:
a) Acromegalic.
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b) Frontal baldness of myotonia dystrophica.

c) Microcephaly.
d) Alopecia areata → chronic suppuration.

V- Loss of hair from outer 1/3 of eye brow:

a- Myxedema.
b- Artificial.

VI- Exophthalmos:
a) Bilateral:
• Thyrotoxicosis.
• Congenital.
b) Unilateral:
• Cavernous sinus thrombosis.
• Leukemic infiltrations behind the eyeball.
• Arteriovenous aneurysm between cavernous sinus and internal
carotid artery.

I- Enophthalmos:
a. Horner’s syndrome.
b. Dehydration.
c. Shock.
d. Severe wasting.

II- Ptosis:
a- Unilateral:
• Horner’s syndrome (Pancoast’s tumor).
• 3rd nerve palsy.
• Local eye disease.
• Congenital.
b- Bilateral:
• Myasthenia gravis.
• Congenital heart diseases.
N.B: Lid lag and retraction in thyrotoxicosis.

VII- Puffy eyelids:

a- Chronic cough (commonest cause).
b- Renal diseases.
c- Mediastinal syndrome.
d- SVC thrombosis.
e- Myxedema.
f- Angioneurotic edema.
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g- Nutritional edema (hypoproteinemia).

h- Advanced right-sided heart failure.

III- Sclera:
a) Bluish discoloration in hypoproteinemia, congenital osteogenesis
imperfecta and gradually occurring anemias.
b) Jaundice.

IV- Conjunctiva:
a) Anemia (to be seen in lower lid because of the frequent affection of the
conjunctiva of the upper lid by trachoma).
b) Jaundice.
c) Inflammation.
d) Subconjunctival hemorrhage → severe hypertension, chronic coughs
and blood diseases.
e) Bitot’s spots → vitamin A deficiency.

V- Pupils:
a. Size: pin pointed pupils in pontine hemorrhage and opiate poisoning.
b. Equality: unilateral miosis → Horner’s syndrome
c. Regularity.
d. Reaction to light: Argyll-Robertson pupil (the pupil responds to
accommodation and not light).

VI- Nose:
a) Redness in tip: alcoholism, mitral stenosis and cold weather.
b) Working ala nasi: pneumonia, toxemia, nervousness, bronchial asthma
and respiratory failure.
c) Nasolabial fold: vitamin B2 deficiency → sulphur granules.
d) Bleeding nostrils: blood diseases, local conditions and severe
hypertension.
e) Any discharge from the nostrils.

VII- Pigmentation in butterfly area of face:

a- MS (malar flush)(red).
b- SLE (red).
c- Pellagra (brownish).
d- Pregnancy (brownish).

VIII- Lips:
a) Pallor: anemia.
b) Cyanosis: congenital heart diseases, cor pulmonale, heart failure
and arteriovenous fistula.
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c) Cheilosis: thiamine deficiency.

IX- Tongue:
a) Pallor: severe anemia.
b) Cyanosis: congenital heart diseases, cor pulmonale, heart failure
and arteriovenous fistula. Cyanosis in tongue is always of the
central type except in SVC obstruction where it is peripheral.
c) Tremors: nervousness, thyrotoxicosis and parkinsonism.
d) Dry: uremia, intestinal obstruction and in mouth breathers.
e) Generalized atrophy of papillae in pernicious anemia, iron
deficiency anemia and pellagra.
f) Absence of fur in heavy smokers and fungus infection.

X- Gums:
a) Blue line: lead poisoning.
b) Hypertrophy: monocytic leukemia and epanutin poisoning.

XI- Parotids:
a) Mumps.
b) Parotid tumors.
c) Parotid stones.
d) Liver cirrhosis.
e) Endemic parotiditis especially with ankylostoma infestation.

XII- Breath:
a) Diabetic ketoacidosis → acetone smell.
b) Uremia → ammonia smell.
c) Hepatic failure → fetor hepaticus (mossy smell).
d) Suppurative lung diseases → putrid smell.

XIII- Generalized pigmentation:

a- Addison’s disease.
b- Pellagra.
c- Hodgkin’s disease.
d- Leukemia.
e- Thyrotoxicosis.
f- Neurofibromatosis.
g- Scabies.
h- Varicose ulcers (hemosiderin pigments).
i- CHF (severe edema with hemosiderin pigments).
j- Jaundice.
k- Purpura.
l- 2ry stage syphilis.
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XIV- Petichae:
• In infective endocarditis.
• In upper part of the chest and neck, retina, conjunctiva and palate
(SVC drainage areas).
• They are round, regular, with red margins and pale centers .
• They appear in crops and remain for a few days and then disappear.
• D.D:
1- Spider navi: ‫ ٭‬in the SVC drainage areas in patients with
liver cirrhosis, disappear by pressure on the center by a pen.
2- Flee bites: itchy, generalized, all red ● (no pale center) with
blood on clothes.

XV- Pallor: detected in mucus membranes of lips, lower lids (not upper lids
because of trachoma) and palms:
a- Anemia.
b- Malignancy.
c- Blood diseases.
d- Infective endocarditis.
e- Parasitic infestations.
f- Malnutrition.
g- Chronic infections.
h- Rheumatic fever.

XVI- Jaundice: yellow discoloration of the sclera and mucus membranes,

which is apparent clinically when level of serum bilirubin exceeds 2-3
mg%, causes are:
a- Cardiac causes (due to liver congestion):
• Right sided heart failure.
• Constrictive pericarditis.
• TS and TI.
b- Chest causes:
• Pulmonary infarction (hemolysis of blood).
• Liver affection secondary to antituberculous drugs.
• Cor pulmonale.
N.B: Rifampicin changes color of body secretion to orange.
c- Liver causes.
d- Blood causes as hemolytic anemia.

VIII- Cyanosis: It is bluish discoloration of the lips and mucus membranes due
to raised level of reduced hemoglobin in capillaries more than 5 gm%
(normally 1-2 gm%), so don’t say cyanosis with pallor. Normally:
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• O2 saturation of arterial blood → 95-99%.

• O2 saturation of venous blood → 70%.
• Cyanosis is apparent clinically when O2 saturation is below 80%.
• Types of cyanosis:
a. Central cyanosis: blood leaving the heart already contains the
required amount of reduced hemoglobin or abnormal hemoglobin
(Sulph and methemoglobin), causes are:
1- Secondary polycythemia:
 Congenital cyanotic heart diseases.
 Cyanotic cor pulmonale.
 Cushing’s syndrome.
 Renal carcinoma (↑ erythropoietin).
2- Primary polycythemia.
3- High altitudes.
4- Acute pulmonary edema.
5- Liver cirrhosis (porto-pulmonary shunts).
6- Methemoglobin due to nitrite toxicity.
7- Sulphemoglobin due to sulphonamide toxicity.
b. Peripheral cyanosis: blood leaving the heart contains the normal
amount of reduced hemoglobin, but as it reaches the peripheral
vessels rapid extraction of O2 occurs raising the amount of reduced
hemoglobin to more than 5gm% in the periphery, causes are:
1- Right sided heart failure.
2- Peripheral circulatory failure.
(Due to low cardiac output and stagnation of blood)
3- Peripheral vascular diseases:
 Raynaud’s disease.
 Burger’s disease.
 Acrocyanosis.
4- Cold weather.
c. Chemical cyanosis:
1- It is a type of central cyanosis.
2- It is reversible on stoppage of the drug.
3- It is due to nitrites → metHb (bluish color) or
sulphonamides → sulphHb (grayish color).
4- It is due to change of iron from the ferrous form to the
ferric form that cannot utilize oxygen.
d. Differential cyanosis: (cyanosis in LL and not in UL)
1- Eisenmenger PDA or reversal of shunt from pulmonary
artery to aorta due to elevation of the pulmonary artery
pressure secondary to increased flow or pulmonary
vasoconstriction.
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2- PDA + infantile coarctation of aorta (preductal type) due

to drop of blood pressure after the site of constriction so
blood passes from pulmonary artery to aorta.

Central cyanosis Peripheral cyanosis

1- Site: Under surface of tongue Extremities: hands, nose
and nail bed
2- Temperature: Hot (peripheral Cold (peripheral
vasodilatation) vasoconstriction)
3- Clubbing: Present Absent
4- Femoral O2: Below 80% Normal
5- O2 therapy: Improves cyanosis due No improvement of
to lung disease only cyanosis

XVII- Neck Examination:

a. Trachea:
• Shifted to site of lesion: Lung or pleural fibrosis or lung collapse.
• Shifted to opposite side: pleural effusion, pneumothorax, lung
tumors or thyroid swelling.
b. Thyroid:
 Describe the enlargement if present.
 Percuss upper border of sternum for retrosternal extension.
 Palpate lower border while swallowing for retrosternal extension.
 Palpate for systolic thrill (thyrotoxicosis).
 Auscultate for systolic bruit (thyrotoxicosis).
c. Lymph nodes:
 Site, consistency, borders, tenderness, matted or discrete and the

presence or absence of sinuses.

 Other lymph node enlargement e.g. axillary, inguinal or mediastinal

(D’Espine sign).
 If present, Check for:

 Liver and spleen enlargement.

 Purpuric rash.
 Sternal tenderness.
 Bleeding tendency.
 Fever.
 Important causes of lymphadenopathy are:

 Lymphoma.
 Leukemia.
 Infections.
 Tuberculosis.
 Secondaries.
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 Hodgkin’s disease.
 Local causes as tonsillitis.
d. Neck pulsations:

Arterial Pulsations Venous Pulsations

1- Not obliterated on pressure Obliterated on pressure
2- Single wave Wavy (A and V waves)
3- Synchronous with heart beat V wave synchronous and A wave
asynchronous with heart beat
4- In anterior triangle of neck In posterior triangle of neck
(medial to sternomastoid) (lateral to sternomastoid)
5- Easily felt than seen Easily seen than felt
6- No effect with respiration Change with respiration
7- Don’t change with position Change with position

1- Causes of arterial pulsations in neck (pulse pressure > 60 mmHg):

1- Systolic ↑ and diastolic ↓:
• AI.
• PDA.
2- Systolic ↑ and diastolic normal:
• Atherosclerosis of ascending aorta.
• Thyrotoxicosis.
• Complete heart block.
3- Systolic ↑ and diastolic ↑:
• Systemic hypertension.
4- Systolic normal and diastolic ↓(hyperkinetic circulation):
• Severe anemia.
• Fevers.
• Pregnancy.
• A-V fistula.
• Liver cell failure.
• Paget’s disease of bone.
2- Examination of neck veins:
• Congested neck veins only:
i. SVC thrombosis.
ii. Aortic aneurysm causing mediastinal syndrome.
iii. Mediastinal tumor.
(These causes are usually associated with dilated veins on chest wall)
iv. Constrictive pericarditis.
v. Cardiac tamponade.
• Pulsating neck veins:
i. Prominent V wave in tricuspid incompetence.
ii. Absent A wave in atrial fibrillation.
iii. Prominent A wave in:
 TS.
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 Severe PS.
 Severe pulmonary hypertension.
 Complete heart block (giant A wave due to
simultaneous contraction of atrium and ventricle
against a closed tricuspid valve.
 Nodal rhythm.
 Atrial flutter.
• Congested pulsating neck veins:
i. Right sided heart failure.
ii. Increased intrathoracic pressure e.g. emphysema.
iii. Increased intra-abdominal pressure e.g. massive ascites.
iv. Constrictive pericarditis.
v. Pericardial effusion.
• Technique of neck veins examination:
i. Normal venous pressure is from 3-13 cmH2O.
ii. Site patient 90° and if the column of blood is seen above
the clavicle (sometimes upper level cannot be determined)
→ severe congested neck veins and usually associated with
dilated veins on chest wall → SVC obstruction
iii. If not seen, lie patient 45° to see whether it is normal or
there is increase in venous pressure.
iv. If more than 2 cm above clavicle → congested neck veins
→ look to the upper level of vein to see pulsations:
 Inspiratory emptying → Rt. Sided heart failure.
 Inspiratory filling and steep Y descend →
constrictive pericarditis.
v. We can measure the venous pressure clinically by a line
drawn horizontally from the upper level of the vein (while
the patient is sitting 45°) then measure the distance from
that line to the sternal angle and add 5 (distance between
the sternal angle and midatrial point).

IX- Blood pressure:

a. Normal B.P. varies with age and the maximum normal for middle-aged
subject is 150/90. Normally, 5% of the population has hypotension
(systolic B.P. below 100 mmHg).
b. Methods of recording B.P.:
• Oscillatory: Mercury oscillates with beginning of the systolic pressure.
• Palpatory:
1- To attain a rough idea about the systolic B.P.
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2- To avoid the auscultatory gap (in hypertensive patients).

• Auscultatory:
1- To determine the systolic and diastolic B.P.
2- First component heard is the systolic B.P.
3- 5th phase of Kortokoff’s sounds is the diastolic B.P.
c. Uses of the sphygmomanometer:
1- To record B.P.
2- To elicit carpo-pedal spasm of latent tetany.
3- To detect increased capillary fragility (Hess test).
4- To elicit pulsus alternans.
5- To confirm pulsus paradoxus (↓ in systolic B.P. more than 10
mmHg during deep inspiration).
6- Diagnostic test in deep venous thrombosis (not used now for fear of
dislodgement of the thrombus).
7- Rotating tourniquets in acute pulmonary edema to relieve
pulmonary congestion (old method, not used now).
8- Record the B.P. in lower limbs in cases of:
 Aortic incompetence (Hill’s sign: B.P. in LL > UL by more than
15 mmHg, which is the normal difference).
 Coarctation of the aorta (B.P. in LL < B.P. in UL).
d. Low diastolic B.P. is seen in:
1- Hemorrhage.
2- Gastroenteritis.
3- Addison’s disease.
4- Postural hypotension.
5- Burns.

XVIII- Temperature:
a. Normal range from 36.6 to 37.2 °C. It is measured through the oral,
axillary (add ½ degree) or rectal routes (subtract ½ degree).
b. Normally, every rise of 1 °C increases pulse by 10-15 b/m.
c. Tachycardia out of proportion to rise of temperature in:
1- Rheumatic carditis.
2- Diphtheria (due to toxic myocarditis).
3- Viral myocarditis.
d. Slower heart rate than expected for a given temperature:
1- Typhoid fever.
2- Meningitis.
3- Viral infections.
e. The course of fever is described as:
1- Continuous fever: temperature always high and doesn’t fluctuate
more than 1 °C in 24 hours e.g pneumonia & 2nd week of typhoid.
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2- Remittent fever: temperature always high but variation between

morning and evening is bigger than 1 °C e.g. empyema and T.B.
3- Intermittent fever: fever occurs in bouts of several days
alternating with afebrile periods e.g. malaria & collagen diseases.
4- Relapsing fever: short periods of fever alternating with short
periods of normal temperature.

XIX- Pulse:
a. Rate:
1- Normal rate 60-90 b/m.
2- Tachycardia → if more than 90 b/m.
3- Bradycardia → if less than 60 b/m.
b. Rhythm:
1- Regular: normal sinus rhythm.
2- Irregular:
 Regular irregularity: ventricular premature beats.

 Irregular irregularity:

• Atrial fibrillation.
• Multiple ventricular premature beats:
 Bigeminy: normal beat followed by a dropped or weak beat.
 Trigeminy: 2 normal beats followed by a dropped beat.

Atrial fibrillation Ventricular premature beats

1 Rapid rate Normal
-
2 No compensatory pause Compensatory pause
-
3 No effect on exercise ↓ on exercise
-
4 ECG ECG
-

 A-V block: dropped beats at pulse.

c. Character:
1- Collapsing pulse (water hammer pulse):
• Definition: a pulse of sudden upstroke and a sudden down-stroke
best felt at the forearm with the arm raised.
• Causes: all causes of arterial pulsations in neck (Depends on a wide
pulse pressure).
2- Plateau pulse:
• Definition: a pulse with a slow upstroke, low amplitude, a slow
down-stroke and a prolonged duration.
• Causes: aortic stenosis (associated with heaving sustained apex).
3- Pulsus bisferiense:
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• Definition: a pulse with 2 palpable peaks.

• Causes:
 AI with AS.
 Severe AI.
4- Pulsus paradoxus:
• Definition: it is a diminution of the volume of pulse at the end of
deep inspiration due to pooling of blood in the pulmonary vessels.
It occurs normally and the diminution doesn’t exceed 10 mmHg. It
is detected by the sphygmomanometer. It is usually associated with
congested pulsating neck veins in early stages and congested non-
pulsating in late stages.
• Causes: constrictive pericarditis and pericardial effusion.
5- Pulsus bigeminy:
• Definition: a normal beat followed by a dropped or weak beat.
• Causes:
 Myocardial infarction.
 Myocarditis.
 Digitalis toxicity.
6- Pulsus deficit:
• Definition: the apical heart rate is more than the pulse rate and the
difference is the deficit. It is due to early depolarization of the
ventricles, this leads to contraction (felt at the apex) without enough
pressure to open the aortic valve, therefore blood will not pass to
the radial pulse.
• Causes:
 Rapid atrial fibrillation.
 Multiple ventricular premature beats.
7- Pulsus alternans:
• Definition: a strong beat followed by a weak beat. It is detected by
the sphygmomanometer as duplication of the heart beat below
systolic blood pressure. It is due weakness of myocardial fibers,
part of them contract at one time while in the next all contract. It is
differentiated from pulsus bigeminy by:
 The time relation between the normal and the weak beats
(weak beat occurs exactly in between 2 normal beats, while
in bigeminy the premature beat is nearer to the previous
normal beat and is followed by a compensatory pause).
 Its persistence after exercise.
• Causes: left ventricular failure with myocardial infarction.
d. Volume: it is the amplitude of the wave of arterial pulsation and it
depends on wide pulse pressure i.e. more than 60 mmHg.
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1) Large volume: all causes of arterial pulsations in neck.

2) Small volume: (pulse pressure < 30 mmHg)
 All obstructive valvular diseases.
 Constrictive pericarditis.
 Pericardial effusion.
 Rapid arrhythmias.
 Shock.
e. Equality: unequal in volume and timing:
1) Peripheral embolism.
2) Aortic aneurysm.
3) Unilateral cervical rib.
4) Pancoast’s tumor.
5) Infantile coarctation of the aorta with PDA (delayed femoral pulse
more than radial pulse).
f. Peripheral pulsations: the status of the dorsalis pedis, anterior and
posterior tibial, popliteal, femoral, radial, brachial, carotid and superficial
temporal arteries. Diminished peripheral pulsations in:
1. Peripheral embolism: acute pain and signs of poor perfusion.
2. Saddle shaped embolism: at abdominal aortic bifurcation. It
manifests with acute pain in LL and signs of poor perfusion to
LL. It is treated by i.v heparin and embolectomy by Fogarty’s
catheter with in the first 24 hs.
3. Leriche syndrome: extensive thrombosis and atherosclerosis of
abdominal aortic bifurcation. It is common in diabetes. It
manifests by chronic pain in lower back, buttocks, back of LL
and calf muscles and impotence. It is diagnosed by
aortography and treated by bypass grafting (Dacron or Teflon
graft).
4. Coarctation of the aorta.
5. Burger’s disease (thromboangitis obliterans).
6. Extensive atherosclerosis.
7. 10% of normal persons have aberrant dorsalis pedis artery.

X- Respiration:
a. Normal rate: 14-18/minute.
b. Ratio of pulse to respiration is 4:1.
c. In pneumonia ratio 3:1 or less.

XI- Hands:
a) Cold hands → low cardiac output failure and fear.
b) Warm hands → high cardiac output failure e.g. thyrotoxicosis and
beriberi.
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c) Tremors → congenital, nervousness, senility, parkinsonism,

alcoholism, thyrotoxicosis, disseminated sclerosis, uremia and
hepatic and respiratory failure.
d) Palm:
1. Palmar erythema → liver cell failure and collagen diseases.
2. Sweating palms → neurosis.
3. Subcutaneous nodules → rheumatoid arthritis.
4. Ulnar nerve → thickened in leprosy.
e) Shape of hands:
1. Spade hand → acromegaly.
2. Claw hand → ulnar paralysis.
3. Long fingers →congenital arachnodactyly.

XII- Nails:
a. Spooning (koilonychia) → iron deficiency anemia.
b. Capillary pulsations → aortic incompetence.
c. Splinter hemorrhage → subacute bacterial endocarditis.
d. Cyanosis.
e. Pulp of fingers → Osler’s nodes → subacute bacterial endocarditis.

XIII- Clubbing of fingers:

A. Definition: it is bulbous enlargement of the soft tissues of the terminal
phalanges with over curving of the nail bed in longitudinal and transverse
directions.
B. Degrees:
• 1st degree: obliteration of the angle of nail bed detected clinically by:
 Looking tangentially to the nail bed.
 Palpating the nail bed by the index finger to detect softening and
yielding of tissues under the nail.
nd
• 2 degree: convexity of the angle of the nail bed (Parrot’s peak).
• 3rd degree: drum stick appearance.
• 4th degree: pulmonary osteoarthropathy (widening and thickening of
the ends of long bones). Sometimes the 4th degree is not included in the
degrees of clubbing.
C. Mechanisms and etiology:
1) Bilateral causes:
 Anoxemic clubbing (bluish in color):
i. Congenital cyanotic heart diseases e.g. Fallout’s tetralogy.
ii. Cyanotic cor pulmonale.
iii. High altitudes.
 Toxemic clubbing (pale in color):
i. Infective endocarditis.
ii. Suppurative lung syndromes.
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iii. Bronchial carcinoma.

iv. Primary biliary cirrhosis.
v. Ulcerative colitis.
vi. Polyposis of the colon.
 Miscellaneous:
i. Familial.
ii. Occupational.
iii. Mesothelioma.
iv. Thyrotoxicosis especially if there is malignant exophthalmos.

2) Unilateral causes:
i. Cervical rib.
ii. Pancoast’s tumor.
iii. Aortic aneurysm.
iv. Infantile coarctation of the aorta.
3) Clubbing in lower limbs only (differential clubbing):
i. Eisenmenger PDA.
ii. Infantile coarctation of the aorta with PDA.
4) Reversible clubbing: Mesothelioma (fibrous type) clubbing subsides
after surgical removal of the tumor.

XIV- Lower limbs: check for:

1) Edema:
 Unilateral or bilateral.
 Pitting or non-pitting.
 Extent up to sacral region (by pressure on the coccyx), abdomen
(by pinching the abdominal wall) and chest wall (by pressure
upon a rib or sternum).
 Puffiness of the eyelids and edema of the face.
 Signs of inflammation (thrombophlebitis and cellulites).
N.B. Edema of lower limbs always precedes ascites except in tricuspid
incompetence, constrictive pericarditis & pericardial effusion: ascites precox.
2) Tenderness in calf muscles → deep venous thrombosis and peripheral
neuritis.
3) Rashes.
4) Clubbing, spooning and cyanosis.
5) Pulsations.
6) Tophi of gout.
7) Hairs: loss of hairs → chronic ischemia.

XV- Congenital malformations:

a. Webbing of the neck and cubitus vulgus → Turner’s syndrome.
b. Kyphosis, tall, polydactyly and pectus excavatum → Marfan’s syndrome.
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