This document provides guidance on performing a general physical examination. It outlines examination of various body systems including build and stature, nutrition, facial appearance, eyes, nose, ears, oral cavity, neck, skin, extremities, and edema. For each system, it describes relevant physical findings, conditions they may indicate, and diagnostic approaches. The focus is on performing a thorough yet efficient exam to identify any abnormalities.

1. GENERAL PHYSICAL
EXAMINATION
 CHAIRPERSON – Dr. Praveen Kusubi
 STUDENT – Dr. Akshata

2.  1. General Built and Stature
 2. Nutrition
 3. Facial appearance
 4. Eyes
 5. Nose
 6. Ears
 7. Oral cavity
 8. Neck
 9. Skin
 10. Extremities
 11. Peripheral edema

3. 1. GENERAL BUILD AND
STATURE
 Indices of build and stature
1. Height, lower and upper segments
2. Arm span
3. Body mass index
4. Waist circumference

6. HEIGHT:SHORT STATURE
Height below 3rd centile or more than 2SD below the median
height for age and sex.
 Normal variant
 Familial short stature
 Constitutional growth delay
 Pathological
Proportionate
 Prenatal
 1. Intrauterine growth retardation
 2. Antenatal infection in mother (TORCH*, syphilis, AIDS)
 3. Antenatal consumption of alcohol, tobacco, heroin
 4. Chromosomal disorders (Down’s syndrome, Turner’s
syndrome).

7. SHORT STATURE:
1. Malnutrition (Protein-energy malnutrition, anorexia nervosa)
2. Endocrine disorders (growth hormone deficiency, hypothyroidism, congenital
adrenal hyperplasia, precocious puberty)
3. Cardiovascular disorders (cyanotic and acyanotic congenital heart disease, early
onset rheumatic heart disease)
4. Respiratory disorders (Kartagener’s syndrome, cystic lung disease, childhood
asthma)
5. Renal disorders (renal tubular acidosis, renal rickets, nephrotic syndrome, chronic
pyelonephritis)
6. Blood disorders (chronic anaemia like thalassemia or sickle cell anaemia,

8. SHORT STATURE:
 Disproportionate
 Rickets
 Skeletal dysplasia (kyphosis, lordosis, scoliosis)
 Defective bone formation (osteopetrosis, osteogenesis imperfecta)
 Defective cartilage growth (achondroplasia, multiple cartilagenous
exostosis

11. TALL STATURE:
2 SD or Height > 6feet

16. WEIGHT:Classification of Overweight and
Obesity by Body Mass Index (BMI) in Adults

17. INDICATORS:
 Body mass index (Quetelet's index) = Weight (kg)/
Height(m)(2)
 Ponderal index = Height (cm) /Cube root of body weight
(kg)
 Brocca index = Height (cm) -100
(For example, if a person's height is 160 cm, his
idealweight

20. SKIN FOLD THICKNESS:

23. NUTRITION:
 PEM: It may be primary due to inadequate intake of protein or
secondary due to defective intake or digestion, or absorption, or
altered metabolism and increased demand
 Defective intake
 Defective digestion and absorption
 Defective utilisation
 Excessive loss of nutrients
 Altered metabolism
 Increased requirements

34. FACE:
i. Hypertelorism
ii. Epicanthic folds
iii. Broad flat nose
iv. Low set ears
v. Thick lips
vi. Abnormal teeth
vii. Short neck
viii. Low hair line

39. EYES:
 HYPERTEROISM:- This refers to wide set
eyes i.e. distance between the two eyes is
more than the size of one eye.
 CAUSES:
 Noonan syndrome
 Turner syndrome
 LEOPARD (multiple lentigines) syndrome
 Hurler syndrome
 William syndrome
 Klippel-Feil syndrome

40. EYE:
 EYE BROWS AND EYE LASHES:
 Hypothyroidism
 Secondary syphilis
 Leprosy
 Generalized alopecia

41. EYE:
 PTOSIS:
 This is drooping of the upper lid to a level that
covers >2 mm of the superior cornea.

42. PTOSIS:
 1. CONGENITAL:
 (i) simple
 (ii) complicated
 2. ACQUIRED:
 (i) neurogenic:3rd nerve palsy,Horner’s
syndromeMultiple sclerosis
 (ii) myogenic: Myasthenia gravis,Snake
bite,Myotonic dystrophy,Eaton lambert myasthenic
syndrome,Oculo-pharyngial muscular dystrophy
 (iii) aponeurotic
 (iv) mechanical

43. EYE SIGNS IN
HYPERTHYROIDISM:

44. EYE:
 EYE BALL:
 Proptosis /Exophtholmos
 Pulsating
 Intermittent-orbital varix
 Enophtholmos
 Nystagmus

45. CAUSES FOR EXOPHTHALMOS:
 Exophthalmic ophthalmoplegia and staring
with lid lag seen in thyrotoxicosis .
 Pulsatile exophthalmos and pulsating
earlobes occur in severe TR.
 It is rarely seen in severe myopia, chronic cor
pulmonale and in normal individuals as
congenital anomaly

46. EYE: CAUSES OF PROPTOSIS

47. CONJUNCTIVA:
 Pallor
 Icterus
 Phlyctenular keratoconjunctivitis
 Bitot’s spots
 Petechiae (lower eye lid)/subconjuctival
hemorrhages in infective endocarditis

48. SCLERA:
● Jaundice or icterus, which is observed in CHF,
large pulmonary infarct, hemolysis due to
prosthetic valves, sometimes in calcified valves.
● Blue sclera noted in osteogenesis imperfecta,
Marfan synfrome, Ehlers-Danlos syndrome, and
may also be familial.

49. CORNEA:
Corneal Arcus
Arcus senilis
KF ring
Corneal clouding
Keratoconjunctivitis sicca

50. IRIS:
 Brushfields spots
 Heterochromia of iris
 Rubeosis iridis
 Uveitis

51. Scleritis/episcleritis/Uveitis
 Rheumatoid arthritis
 SLE
 Behçet's disease
 Ankylosing spondylitis
 Crohn's disease.
 Ulcerative colitis.
 Sarcoidosis

52. PUPILS:
 Number(polycoria)
 Location(corectopia)
 Size –Miosis/Mydriasis
 Color
 Pupillary reactions

53. LENS:
 Subluxation/Dislocations
 Cataract:Metabolic abnormalities:
Poorly controlled diabetes.
Phosphofructokinase
deficiency.
G6PD deficiency.
Hyperuricaemia
Systemic disease:
Muscular dystrophy.
Atopic dermatitis.
Neurofibromatosis
Congenital rubella
Hypoparathyroidism

56. EARS:
Ear findings Conditions
Low set ears Noonan syndrome
Turners syndrome
Klippel-Feil syndrome
Down syndrome
Cornelia de Lange syndrome
Rubintein – Taybi syndrome
Defomed ears Polychondritis
Ear lobe crease CAD
Deafness Turners syndrome
Klippel fleil syndrome
Rubella
Multiple lentigines syndrome
Jervell and Lange-Nielson syndrome

58. NOSE:
Nose findings Conditions
Broad flat nose Cornelia de Lange
syndrome
Down syndrome
William syndrome
Hurlers syndrome
Broad nose Acromegaly
Thin beaked nose Robinstein- Taybi
syndrome

60. LIPS:
Findings Conditions
Pallor Anemia
Cyanosis CHD
Thick lips Hurler syndrome
Acromegaly
Myxedema
Cretin
Absent philtrum FAS
Capillary pulsations AR
Rhagades Congenital syphilis

61. GUMS:
 GUMS:
1. Gum hyperplaisa - Phenytoin toxicity
2. Cyanosis- CHD

62. TEETHS:
 Hutchinsonian teeth

Peg shaped teeth: Hurlers syndrome,william
syndrome,congenital syphilis

Mulberry molars

Wide spaced teeth

Stained teeth:
tobacco staining,
chronic betel /leaf chewing,
fluorosis,
Pink teeth in porphria
Tetracycline
Brown teeth in kernicterus,teeth caries,osteogenesis
imperfecta

64. TONGUE:
Tongue findings Condition
Colour-
Blue
Scarlet red
Magenta
Black
Pale tongue
Cyanosis
Niacin
Riboflavin deficiency
Actinomycosis
IDA Shock
Macroglossia Acromegaly
Myxedema
Downs syndrome
Hurler syndrome
Cretin
Glossoptosis Pierre Robin syndrome

68. PALATE:
Palate findings Conditions
High arched palate Marfans syndrome
Pierre Robin syndrome
Cleft/perforated palate Tertiary syphilis
Velocardiofacial syndrome
Tuberculosis
Pierre Robin syndrome

69. NECK:
Short neck Webbed neck Low hair line
Klippel-Feil syndrome Noonan syndrome Noonan syndrome
Morquios syndrome Edwards syndrome Edwards syndrome
Turners syndrome Turners syndrome
Cornelia de Lange
syndrome

70. PALLOR
 Pallor (paleness) is the waxy appearance of skin and mucous
membrane.
 It depends on thickness and quality of skin, and quality and amount
of blood in the capillaries.

71. SITES TO LOOK FOR
PALLOR
1. Lower palpebral conjunctiva (retract the lower eyelids
downward and ask the patient to look upwards — both eyes
at a time).
2. Tongue, specially the tip and the dorsum.
3. Mucous membrane of palate.
4. Nail-beds (press the pulp to see the redness of nail-bed).
5. Palms, soles and general skin surfaces.

73. Causes of pallor:
Pallor without
anemia ?

74. CYANOSIS
 Kyanos –dark blue color , osis- condition
 Def – Bluish discoloration of the skin and
mucous membrane due to presence of
increased amount of reduced haemoglobin
>4g/dl or Haemoglobin derivatives in the
capillary blood

75. TYPES OF CYANOSIS
 A) CENTRAL CYANOSIS
 B) PERIPHERAL CYANOSIS
 C) Others- Enterogenous,
Mixed
Diffrential cyanosis

76. CENTRAL CYANOSIS:

77. Central Cyanosis
PATHOPHYSIOLOGY
 Decreased arterial oxygen saturation(80-85%) due to
imperfect oxygenation of blood in lungs or admixture of
venous and arterial blood
 Sites- Tongue
Inner aspect of lips
Mucous membrane of gum,palate,cheeks
Lower palpebral conjunctiva
Others-Nasal and Rectal Mucous membrane
Retina

78.  Mechanism- Hypoxic hypoxia
 Causes- Cynotic heart disease
Acute pulmonary edema
Eisenmengers syndrome
Acute severe asthma
COPD, Cor pulmonale
Resp failure ,Resp depression
Lobar pneumonia
Fibrosing alveolitis
Tension pneumothorax
Acute laryngeal edema
Acute pulmonary thromboembolism
Pulmonary artetiovenous fistula

79. PERIPHERAL CYNOSIS

80. Peripheral Cyanosis
Sites- Tip of nose
Ear lobules
Outer aspect of lips,chin,cheek
Tip of fingers and toes
Nail bed of fingers and toes
Palms and soles

81.  Causes of Peripheral cyanosis
a) Exposure to cold air or cold water
b) Congestive cardiac failure
c) Frost bite
d) Raynaud’s phenomenon
e) Shock or peripheral circulatory failure
f) Venous obstruction-SVC Syndrome
g) Hyperviscosity syndrome-MM,Polycythemia,Macroglobulinaemia
h) Arterial obstruction
i) Cryoglobulinaemia-Abnormal globin-gel low temp
j) Mitral stenosis
k) Septicaemia

82. Differentiation of Cyanosis
FEATURES CENTRAL PERIPHERAL
Sites Tongue and Oral cavity Tongue uneffected
Handshake Warm Cold
Application of warmth No change Warmth-Cyanosis
Decrease
Cold- Cyanosis
Increase
Application of pure
oxygen
For 10 min
Cyanosis may improve No response
Clubbing and
Polycythemia
Usually Present Absent
Pulse Volume Normal or High Low
Dyspnoea Often Breathless Absent

83. Enterogenous Cyanosis
 Due to presence of excessive Sulphaemoglobin>0.5g/dl
or Methaemoglobin >1.5g/dl
 Causes- Hereditary Haemoglobin M disease
Poisoning by aniline dyes
Drugs like nitrates and nitrites
Carboxyhaemoglobinaemia
Confirmed- Spectroscopic examination

84. JAUNDICE
 Yellowish discolouration of skin and mucous
membrane due to excess amount of bilirubin
present in the blood.
 Clinical jaundice-S.bilurubn-3mg/dl
 Latent jaundice-S.bilurubin-1-3mg/dl

85. Sites
 Upper bulbar conjunctiva
 Under surface of tongue
 Mucous membrane of palate
 Palms and Soles
 General skin surface

86. JAUNDICE

87. D/D of jaundice
 Carotenaemia
 Atabrine toxicity
 Diffuse Xanthomatosis
 Muddy sclera
 Old subconjunctival haemorrhage

88. Features of Haemolytic Anaemia
 Acholuric urine
 Stool-High color
 Jaundice-Lemon yellow tinge (as s.bil<6mg/dl)
 Anaemia
 Splenomegaly
 May have typical facies(chipmunk facies in
thalassaemia)
 Reticulocytosis

89. Features of Obstructive jaundice
 Urine-Deep yellow
 Stool-Pale or clay colored with Steatorrhoea
 Jaundice-Greenish-yellow
 Generalised pruritis
 Sinus bradycardia
 Xanthelasma
 Petechiae,purpura or echymosis-Vit k def
 Gall bladder my be palpable
 Prolonged case- Osteomalasia,bone pain,fracture-Hepatic
osteodystrophy
 Rarely hepatospleenomegaly,h/o fever ,pain abd

90. Features of Hepatocellular jaundice
 Urine-Yellowish
 Stool-High colored and become pale
 Orange yellow tinge bulbar conjunctiva
 Anorexia,nausea,vomiting,fever may be present before jaundice
 Tender hepatomegaly is frequent
 Variable pruritus
 Bleeding manifestations
 h/o affection of other member of the family or locality

92. Fluctuating jaundice
 Gilbert syndrome
 Stone impaction in CBD
 Periampullary carcinoma
 Haemolytic anaemia
 Dubin johnson syndrome

93. SKIN:
SKIN MANIFESTATION CONDITION
Bronze pigmentation Hemochromatosis
Café au luit spots Von Recklinghausen’s
disease
Multiple lentigines LEOPARD syndrome
Angiofibromas Tuberous sclerosis
Erythema marginatum Rheumatic fever
Janeway lesions and Oslers
nodes
Infective endocarditis

95. SKIN:
SKIN
MANIFESTATION
CONDITION
Coarse skin Myxedema
Hyperextensible and
rubber like skin
Ehler- Danlos
syndrome
Plucked chicken
appearance
Pseudoxanthoma
elasticum
Moist silky skin Hyperthyroidism

101.  EXTREMITIES/ LIMBS
1. Digits
2. Nails
3. Feet
4. Joints

102. EXTREMITIES AND LIMBS:
Digits description Disease
a. Arachnodactyly Marfan syndrome
b. Polydactyly Ellis-van Creveld and
Laurence-Moon-Biedl
syndromes
c. Syndactyly Ellis-van Creveld and
Laurence-Moon-Biedl
syndromes
d. Clindactyly Down, Ellis-van Creveld and
Hurler’s syndromes
e. Brachydactyly Down and Turner syndromes,
hyperparathyroidism

105. NAILS:
Abnormal nails Conditions
Nail stripes Chronic constrictive
pericarditis
Dysplastic nails Ellis-van Creveld syndrome
Plummer nails Hyperthyroidism
Square/broad nails Acromegaly, cretin
Koilonychias Iron deficiency anemia
Splinter hemorrhage Infective endocarditis
Clubbing Cyanotic congenital heart
disease infective
endocarditis, myxoid tumor

106. Nail changes:
 Beau’s lines
 Mees’s lines
 Lindsay nail/half and half nails
 Yellow nail
 Blue nail
 Black nail
 Green nail
 Brown nail

107. Nail changes:
 Pitting of nails
 Brittle nails
 Egg shell nails
 Racket nails
 Plummer sign
 Koenen sign

109. FOOT:
Foot abnormality Conditions
Pes cavus Friedrichs ataxia,
peroneal muscular
atrophy
Pes planus Marfans syndrome
Rocker bottom foot Edwards syndrome
Bow legs Achondroplasia
OI
Rickets osteomalacia
Sabre tibia- congenital
syphilis
Knock knees Ellis-van Creveld and
Laurence-Moon-Biedl
syndromes

111. CLUBBING
 Defn- Is the bulbous swelling of the terminal
part of the fingers and the toes with an
increase in the soft tissue mass and increased
anteroposterior ,transverse diameter of the nail
due to proliferation of subungual connective
tissue ,interstitial edema, and dilatation of
arterioles and capillaries

112. CLUBBING:

113. Digital index- Objective measurement of clubbing
Circumference at nail bed is divided by the
circumference of the distal interphalangeal joint
The individual ratio of 10 fingers are added and
now divided by 10
If > 1 clubbing to be present

114. GRADING OF CLUBBING
 Grade I –Increased fluctuation of nail bed with loss of
onychodermal angle
 Grade II –Increase in AP and Transverse diameter of the nails as
well as nail become smooth and glossy with loss of longitudinal
ridge
 Grade III – Increased pulp tissue,Parrot beak/Drumstick
 Grade IV – Wrist and ankle swelling due to HOA

115. HYPERTROPHIC PULMONARY OSTEOARTHROPATHY
• Subperiosteal new bone formation at the lower end of
radius,ulna,tibia
• Swelling ,Pain in wrist , ankle, elbow and knee
•Also other bones like ribs ,clavical,scapula may be affected
• Seen in Bronchogenic carcinoma(Squamous)
• Familial(Pachydermoperiostitis) or Idiopathic

116. Mechanisms of clubbing
 Neurogenic-Vagal stimulation
 Humoral- GH,PTH,Estrogen,Bradykinin,PG
 Ferritin - Decreased
 Hypoxia-Persistent hypoxia causes opening of deep AV fistula of
the terminal phalanx
 Toxic-SBE
 Metabolic-Thyrotoxicosis
 PDGF-Released secondary to infection(latest and most acceptable)

117. CAUSES OF CLUBBING
 Cardiovascular
 Pulmonary
 Gastrointestinal
 Congenital
 Unilateral
 Unidigital
 Miscellaneous
 pseudoclubbing

118. Pseudoclubbing
 Subperiosteal bone resorption of terminal
phalanges
Seen in
Scleroderma
Acromegaly
Hyperparathyrodism
Leprosy
People working with vinyl chloride

119. OEDEMA
 Accumulation of excessive amount of tissue
fluid in the subcutaneous tissue(or serous
sac)due to increase in extravascular
component of the ECF resulting in swelling of
tissue

120.  Total body water- 60% of body wt
 Total body water-
2/3 ICF + 1/3 ECF(3/4 IF +1/4 Plasma)

121. MECHANISM

122. Mechanism of edema
 Low plasma oncotic pressure-
Hypoprotienaemia
 High capillary hydrostatic pressure-CCF ,DVT
 Increased capillary permiability-Acute
inflammation ,Amlodipine
 Obstructed lymphatic drainage-
Filariasis,Radiation

123. Clinically edema demonstration
 Inspect leg for swelling
 Apply firm pressure
 Look for -Sacral edema
Parietal edema
Puffy face
Puffy lower eyelids
Scrotal edema

124. Clinical classification of
Oedema
Pitting oedema
CCF
Cirrhosis
Nephrotic syndrome
Hypoproteinaemia with severe anaemia
Pericardial effusion
Constrictive pericarditis
Drugs
Venous obstruction
Beriberi
Epidemic dropsy

125. PITTING EDEMA

126. PITTING EDEMA

128. LYMPHADENOPATHY
 Significant lymphadenopathy:
 Generalised lymphadenopathy:
 Persistent generalised
lymphadenopathy:CAUSES?

129. Points to be Noted while
Examining Lymph Nodes
• Site
• Size of the largest and smallest gland
• Number of nodes enlarged
• Consistency (soft, firm or hard)
• Tenderness
• Mobility
• Matted or discrete
• Fixity to skin and condition of the overlying skin
• Generalized or localized
• Adjacent groups of nodes
• Lesions in the areas of drainage
• Lymphedema

133. CAUSES OF LYMPHADENOPATHY
INFECTIOUS
Viral
Infectious mononucleosis syndromes
(EBV, CMV), infectious
hepatitis, herpes simplex, herpesvirus-6,
varicella-zoster virus, rubella,
measles, adenovirus,
bacterial streptococci, staphylococci, cat-scratch
disease, brucellosis,
tularemia, plague, chancroid,
melioidosis, glanders, tuberculosis,
atypical
mycobacterial infection, primary and
secondary syphilis, diphtheria,
leprosy,
fungal histoplasmosis, coccidioidomycosis,
paracoccidioidomycosis

134. chlamydia lymphogranuloma venereum,
trachoma
Parasitic
Ricketssiae
Toxoplasmosis, leishmaniasis,
trypanosomiasis, filariasis
scrub typhus, rickettsialpox, Q fever
IMMUNOLOGICAL Rheumatoid arthritis
b. Juvenile rheumatoid arthritis
c. Mixed connective tissue disease
d. Systemic lupus erythematosus
e. Dermatomyositis
f. Sjogren’s syndrome
g. Serum sickness
DRUG HYPERSENSITIVITY diphenylhydantoin, hydralazine,
allopurinol,
primidone, gold, carbamazepine, etc

135. MALIGNANCY Hematologic—Hodgkin’s disease,
non-Hodgkin’s lymphomas, acute
or
chronic lymphocytic leukemia,
hairy cell leukemia, malignant
histiocytosis,
amyloidosis
b. Metastatic—from numerous
primary sites
STORAGE DISRDERS Gaucher’s, Niemann-Pick, Fabry,
Tangier
OTHERS Castleman’s disease (giant lymph
node hyperplasia)
b. Sarcoidosis
Histiocytic necrotizing
lymphadenitis (Kikuchi’s disease)
Familial Mediterranean fever

136. Causes of Generalized
Lymphadenopathy
 Infections: Miliary tuberculosis, infectious
mononucleosis, Human immunodeficiency virus (HIV)
infection, German measles, filariasis secondary syphilis,
trypanosomiasis (not present in India).
 Other inflammatory disease: Systemic lupus
erythematosus, rheumatoid disease, hypersensitivity
reactions.
 Neoplastic diseases: Lymphomas, acute leukemias,
chronic lymphatic leukemia, blast crisis of chronic
myelogenous leukemia.
 Other conditions: Sarcoidosis, adverse reactions to
drugs like dilantin sodium.

137. THANK YOU

138. REFERENCES
HARRISON’S INTERNAL MEDICINE – 20th
edition
GOLWALLA – 15 th Edition
HUTCHISONS CLINICAL METHOD
MACLEODS CLINICAL METHODS
MEDICINE UPDATE 2020
ALAGAPPAN – 5th Edition