II General Physical Examination


General Physical Examination

A general look at the patient may be extremely useful in defining the cause, associated complications, or assist in the differential diagnosis. In the following section, relevant physical signs are discussed in general and especially in relation to the gastrointestinal system.

Nutritional Status and Obesity

Obesity is being considered as a disorder of energy homeostasis. About 2 billion people worldwide may be obese or over weight. Excess body weight is one of the most important challenging public health problems, which almost affects everyone in three individuals.

Look at the patient as a whole and assess the nutritional status. A BMI gives a good idea about obesity, although it is not a direct measure of adiposity. BMI is the weight in Kg divided by the height in meters squared. In Asians, even a lower BMI is associated with higher risk; in elderly, it is reverse.

Body Mass Index (BMI)


BMI 18.5 to <25Kg/m2 is considered normal.


BMI 25 to <30Kg/m2 is considered over weight.


BMI 30 to <35Kg/m2 is considered obesity I.


BMI 35 to <40Kg/m2 is considered obesity II.


BMI >40Kg/m2 is considered obesity III.

Grade 1 overweight = BMI of 25–29.9 (23–25 for Asian population).

Grade 2 called obesity = BMI 30–39.9 (>25 for Asian population).

Grade 3 morbid obesity = BMI >40kg/m2.

BMI should be interpreted with caution as it is not a direct measure of adiposity. A waist circumference is done in addition to BMI in people with a BMI <35. The waist hip ratio (WHR) can also be used to predict the risk of the patient, especially in terms of heart disease. It is calculated by measuring the waist circumference midway between the costal margin and iliac crest divided by the maximum circumference around the buttock. A value >1 for males and >0.85 for females is associated with higher-risk insulin resistance, hypertension, diabetes, and dyslipidemia.

Look for Co-Morbidities in Obesity




Hypertension (weight loss of 1Kg is associated with a decrease of BP 3–6mmHg in systolic and 1–3mmHg diastolic pressure).


Heart disease.


Chronic lung disease.


Obstructive sleep apnea (sleep restriction associated with low leptin high ghrelin).


Chronic kidney disease.


Osteoarthritis, especially knees and back pain.


Cancer (increased risk of postmenopausal breast cancer).


Gallbladder disease is more common in obese.


GERD also increases with obesity.

An ideal goal is to lose no more than 0.5–1.0kg (1–2lb.) a week on a balanced healthy diet with regular physical activity and behavior change program. People should usually aim to lose a realistic 5 to 10 percent of their original weight.

Who should lose weight?

1. Overweight and obese individuals BMI >25.

2. Severely obese (BMI 35–39.9) can gain significant health benefits by losing excess weight, especially the patients with central obesity.

This is especially true if:

1. Positive family history of coronary heart disease.

2. Hypertension.

3. Dyslipidemia.

4. Diabetes mellitus.

Secondary Causes of Obesity


Hypothyroidism (slow metabolism) Rx subclinical does not reduce weight.


Cushing syndrome (central obesity).


Polycystic ovarian syndrome (50 percent are obese).


Medication-related (steroids, adrenergic antagonists, cyproheptadine sodium valproate, carbamazepine, lithium, tricyclic antidepressants, phenothiazines, thiazolidinediones, sulphonylureas, insulin).


Oral contraceptive use (uncommon).


Hypogonadism and GH deficiency (abdominal and visceral fat).


Eating disorders (bulimia nervosa, night-eating disorder).






Hypothalamic (ventromedial hypothalamus) obesity.


Genetic syndromes (e.g., Prader–Willi syndrome, Fröhlich syndrome, Laurence Moon–Biedl syndrome.

Obese people have a 60 percent chance of developing hypertension. Congestive cardiac failure increases twofold with a BMI greater than 30. IHD, stroke, diabetes, chronic kidney disease, and liver diseases are more common in obese individuals. Osteoarthritis, gout, gallbladder disease, dyslipidemia, and obstructive sleep apnea are more common in obese individuals. In any patient, it is important to do a base line screening, especially when weight is a problem.

Minimum Screening








Waist circumference.


Blood pressure.


Blood sugar fasting.


Fasting triglycerides.


Serum lipids.


Look for obstructive sleep apnea.


Look for medications that may increase weight.


Estimate the physical activity or inactivity.


Look for secondary causes of obesity.


Look for co-morbidities.


Family history.

Vitamins are organic compounds that humans cannot synthesize and need an external supply in limited small quantities. Vitamin C and all the groups of Vitamin B are all water soluble, while Vitamins A, D, E, and K are fat soluble.



Result of Deficiency


Vitamin A


Night blindness.


Vitamin B1


Beriberi, Wernicke’s encephalopathy.


Vitamin B2


Ariboflavosis (chilosis, glossitis).


Vitamin B3


Pellegra (dementia, diarrhea, dermatitis).


Vitamin B5

Pentothenic acid

Uncommon (paresthesia, acne).


Vitamin B6




Vitamin B7


Dermatitis or impaired growth.


Vitamin B9

Folic acid

Megaloblastic anemia, birth defects.


Vitamin B12


Megaloblastic anemia neuropathy.


Vitamin C

Ascorbic acid

Scurvy and bleeding gums.


Vitamin D


Rickets and osteomalacia.


Vitamin E




Vitamin K


Bruising and bleeding.


It is a decrease in hemoglobin with or without a corresponding decrease in the total red blood cell count below a normal range given for the age, sex and race. Normal hemoglobin in adult males is 14–18g% while in females is 12.5–16.5g%.


Figure 2 Gross anemia (pale complexion is best seen under the lower eyelid)


The conjunctiva under the lower eyelids, tongue, hands, nails, and general complexion of the patient indicate the amount of pallor (Figure 2), which is usually proportional to the extent of anemia. Pale complexion without anemia is seen with severe vasoconstriction seen in advanced heart failure.


A good history can only be taken while keeping the etiological causes in mind. One can ask direct questions pertaining to each cause. A detailed history of dietary habits, episodes of any blood loss (especially melena or hematochezia), drug intake (especially aspirin and non-steroidal anti-inflammatory drugs), passage of worms in stools, gut operations and history of chronic diarrhea is essential to assess iron deficiency anemia. The commonest cause of anemia is blood loss, and in females, it is due to excessive menstrual loss. Ask details regarding the sites, amount, frequency, and duration of blood loss.

Recent studies indicate that IDA is associated with decreased work performance, behavioral changes, and intellectual deterioration via decreased monoamine oxidase activity and increased catecholamine activity, especially in children. Incidence of infection is increased due to reduced lymphocytes transformation, suppressed lymphokines production, and impaired bactericidal activity of polymorphonuclear cells. An increase in hemoglobin achieved with optimal replacement therapy with intravenous iron is 0.27g% per day, while that with oral iron is about 0.25g% per day.


Anemia may be classified according to etiological and pathological classifications. Morphological classification is based on size and chromatin content of red cells. Hypochromic and microcytic anemia is classically seen in iron deficiency and thalassemia (rarely with sideroblastic anemia and chronic disorders). Macrocytic anemia is seen with megaloblastic marrow in B12 and folic acid deficiency, with normoblastic marrow in alcoholics and polychromatophillic macrocytic in hemolysis. A normochromic and normocytic anemia is associated with chronic disorders, infections, malignancy, CRF, endocrine disorders, and connective tissue disorders. A leukoerythroblastic anemia is associated with leukemia, myelosclerosis, and metastatic carcinoma.

An etiological classification helps to formulate a plan of investigations and workup.

Blood Loss

Menstrual loss.

Gut: worms, peptic ulcer, varices, piles, and angiodysplasia.

Lung: hemoptysis for example, TB or tumor.

Kidney: hematuria for example, stones or tumors.

Dyserythropoietic Anemia




Aplastic: Autoimmune or idiopathic, drugs and chemicals, radiation, infections, and congenital.


Renal: Chronic renal failure.


Endocrine: Addison’s disease, thyroid, pituitary and parathyroid disease.


Marrow: Lymphomas, leukemia, and myelofibrosis.




Primary dyserythropoietic anemia is rare.


Secondary: Vitamin B12 and folic acid deficiency, Iron deficiency anemia, thalassemia, hemoglobinopathies, aplastic anemia, myelofibrosis, and leukemia.

Hemolytic Anemia




Sickle cell anemia, thalassemia, and other types of hemoglobinopathies.




Autoimmune hemolytic anemia, acquired hemolytic anemia, and microangiopathic hemolytic anemia.




Burns, G6PD deficiency, lead poisoning.

Other Causes of Anemia

Malaria, incompatible transfusion, infections (bacterial endocarditis, clostridia, hemophilus, salmonella, and meningococcus), and hypersplenism. Malignant hypertension, uremia, and tumors also rarely cause hemolysis.

The term megaloblastic change is used to describe marrow changes of Vitamin B12 or folic acid deficiency anemia. In macrocytic anemia, there are larger-sized RBCs (MCV >100fl) in the blood commonly seen in B12 or folic acid deficiency. Folic acid deficiency can occur acutely, while Vitamin B12 reserves may take several years to exhaust.

Causes of Folic Acid Deficiency


Decreased intake of green vegetables or increased use of alcohol.


Decreased absorption as in tropical sprue, coeliac disease, alcoholics, patient on hemodialysis, and with drugs (tetracyclines, oral contraceptives, anti-convulsants).


Increased requirement pregnancy, infancy, tumors, and exfoliative skin diseases.


Decreased utilization with folic acid antagonists like methotrexate, trimethoprim, and triamterene.

Causes of B12 Deficiency Anemia


Strict vegetarians.


Pernicious anemia and gastrectomy.


Malabsorption syndrome like ileal resection, tropical sprue, coeliac disease, chronic pancreatitis, intestinal lymphoma, and drugs like neomycin, alcohol, and colchicine, and so on.


Increased requirement as in pregnancy, tumors, and thyrotoxicosis.


Abnormal utilization (fish tape worm).

Other Causes of Macrocytic Anemia

Alcohol, chronic liver disease, myxedema, cytotoxic drugs, aplastic anemia, newborns, pregnancy, COPD, preleukemia, and reticulocytosis may be associated with macrocytosis.

Clinical Features

These are best divided into general features that are shared by all types of anemia, and specific features that are particular to the specific etiology of the anemia. It is important to suspect aplastic anemia when there is evidence of reduction of all the cell lines in the blood. The patient is pale with evidence of bruising, indicating thrombocytopenia, and there may also be evidence of infection indication leucopenia (Figure 3). Iron deficiency anemia is the commonest form of anemia and may be suspected when koilonychia, glossitis (Figures 3 and 4) or angular stomatitis is present.


Figure 3 Features of aplastic anemia showing pallor, bruising, and skin infection. Koilonychia in IDA shown on the right as flattening and early spooning of the nails


Figure 4 Features of iron deficiency anemia showing koilonychias and bald tongue

The specific features helpful in diagnosing iron deficiency, megaloblastic, and hemolytic types of anemia are given in Figure 5.


Figure 5 Clinical features of anemia are separated according to the etiology

IDA=Iron deficiency anemia, HA=hemolytic anemia

Laboratory Feature of Anemia

Iron Deficiency Anemia

1. The peripheral smear in Figure 6 shows hypochromia (pale red cells) and microcytosis (smaller size of red cells).

2. The serum iron levels are low and the TIBC is increased.

3. The red cell indices demonstrate a low MCV and MCH.


Figure 6 Peripheral smear of IDA and macrocytic anemia. On the left, hypochromic and microcytic smear; on the right, hyperchromic macrocitic picture with hypersegmented polymorph

4. Serum ferritin levels and bone marrow iron staining on biopsy give an indication of the total iron stores. Each microgram of ferritin in the serum is equivalent to 8mg of stored iron provided there is no liver injury as ferritin is an acute phase reactant.

5. Check for blood loss in stool, urine, and sputum. Also, check stool for ova and cyst.

6. Endoscopy, barium studies, rarely technetium-labeled RBC for Meckel’s diverticulum or chromium-labeled RBC studies for site of blood loss are required.

Macrocytic Anemia

1. Peripheral smear shows variability in size and shape of red blood cells. There is macrocytosis (Figure 6), increased MCV (>100fl), decreased reticulocytes, RBC inclusions (basophilic stippling and Howell–Jolly bodies), and hypersegmented polymorphs.

2. Marrow is hypercellular, megaloblastic with M/E (myeloid/erythroid) ratio becoming 1:1.

3. Indirect bilirubin and serum LDH are raised due to hemolysis. Beta leucine is increased in B12 deficiency only.

4. Serum B12 levels are less than 120pg./ml in B12 deficiency, while serum folate is <0.5 ng/ml in folic acid deficiency.

5. Cytokinetics: ineffective erythropoiesis and thrombopoiesis with intramedullary destruction of RBCs. There is a decreased production or delivery of WBCs.

6. Schilling test is done to check the amount of labeled B12 absorption in pernicious anemia.

7. Methylmalonic aciduria is an index of B12 deficiency and urinary formiminoglutamic acid is high in Vitamin B12 deficiency.


Figure 7 Patients with deep jaundice is likely to have obstruction or cholestasis


It is the yellowish discoloration of the skin and mucous membrane, clinically visible when bilirubin in the blood is usually greater than 3.0mg%. It is best seen in the sclera because of the affinity of bilirubin for the elastic tissue (Figure 7).


A rise in the serum bilirubin may be due to increased production of bilirubin (hemolytic jaundice), decreased conjugation in the liver (hepatic jaundice), or obstruction in biliary passages (obstructive jaundice). It should be differentiated form caroteinemia, which also produces a faint yellow discoloration while sparing the sclera.

A large portion of bilirubin is produced by breakdown of red blood cells. It combines with albumin in a ratio of 2:1 and is transported to the liver. This indirect or unconjugated bilirubin is insoluble in water and is not excreted in urine. After reaching the liver, it is taken up and conjugated with two molecules of glucuronide and excreted in bile as bilirubin diglucuronide. This conjugated bilirubin or direct bilirubin is water soluble, and it will be excreted in the urine if it diffuses back into the blood due to obstruction. Normally, it is excreted in the bile, and upon reaching the intestine, it is acted upon by intestinal bacteria and converted to urobilinogen (which undergoes enterohepatic circulation) or excreted in the feces as stercobilinogen. Urobilinogen, when present in the urine indicates patent biliary passages, or in other words, excludes obstructive jaundice. In hepatitis, at times, severe inflammation of the hepatocytes presses the small biliary passages, causing temporary obstruction. This results in itching, passage of whitish-gray stools, and absence of urobilinogen in the urine. This is called the cholestatic stage of viral hepatitis and only lasts a few weeks.

Hepatic jaundice is due to some liver insult commonly due to viral hepatitis or at times drugs (like INH, PAS, ethanol, carbon-tetrachloride, imipramine, phenytoin can cause liver injury), and rarely may be congenital (deficiency of specific enzymes). At times, severe inflammation in viral hepatitis may mechanically obstruct the small biliary passages, resulting in very high levels of bilirubin called cholestatic viral hepatitis.

Obstructive jaundice is a surgical problem because the cause of the obstruction has to be removed in order to achieve a cure. Whenever there is obstruction, it is associated with colicky pain in the right hypochondrium, fever with rigors, and chills due to infection and a rising jaundice. This triad of Charcot is characteristic of ascending cholangitis. The stool becomes pale due to absence of stercobilinogen, and there may be itching due to deposition of bile salts in the skin.

Causes of Obstructive Jaundice


Drugs like chlorpropamide, oral contraceptives, chlorpromazine, and anabolic steroids.


Primary biliary cirrhosis.


Carcinoma of liver or metastatic liver disease can cause biliary obstruction.


Post-hepatic causes, for example, gallstones, post-operative strictures of bile duct, and cancer bile duct (cholangiocarcinoma), cancer of gallbladder or head of pancreas, and periampullary tumors.


Choledochal cyst.


Parasites in the CBD or pressure from outside, for example, lymph nodes.


Congenital bile duct defects (bleary atresia).




Sclerosing cholangitis.


Rarely, jaundice in a hemiplegic patient may be predominantly seen on the non-hemiplegic or normal side.

Carotenemia appears as a yellow tinge of the skin in hypothyroidism or patients consuming excessive carrots.

Patients with severe uremia may are quite pale, and the sallow complexion may have superficial resemblance to jaundice.


Figure 8 Clinical features of hemolytic and obstructive jaundice

Causes of Hemolytic Jaundice


Congenital hemolytic anemia like hereditary spherocytosis, thalassemia, and sickle cell anemia.


Autoimmune hemolytic anemia (warm and cold antibody-induced) and microangiopathic anemia.


Acquired infective causes like malaria, infectious mononucleosis, and mycoplasma pneumonia.


Drugs like methyldopa, quinine, quinidine, pencillamine, hydralazine, and so on.


Mismatched transfusion, connective tissue disorders, uremia, malignancies, and G6PD deficiency.


R arely, hypersplenism or paroxysmal nocturnal hemoglobinuria.


Figure 9 Thalassemic patient with jaundice, typical facies (prominent cheeks) also had hepatosplenomegaly


It is characterized by bulbous enlargement of the distal phalanx of one or more fingers and toes (Figures 10 and 11) due to an increase in soft tissue. There is loss of angle between the base of the nail and the adjacent skin (Figure 11), fluctuation at the nail bed, and increased curvature of the nail (Figure 11). It is usually painless, bilateral, and often reversible.


Figure 10 Clubbing in a patient with inflammatory bowel disease and cirrhosis of the liver

Clinical Presentation

Clubbing usually first develops in the thumb and index finger and later involves the other fingers. Early clubbing may be detected by measuring the transverse diameter of index finger at the base of nail divided by diameter at distal interphalyngeal joint. Normally, it is one or less; more than one signifies clubbing. The normal angle between the nail plate and the skin overlying the proximal end of the nail is 160° or less. Proliferation under the nail plate causes the angle to increase above 160° and often exceeds 180°. This is appreciated with the finger at the level of the eyes (profile sign, Figure 11). The edge of a paper placed parallel to the long axis of the nail normally reveals a triangular area toward the base of the nail. A diamond-shaped area is also revealed when two nails are held back to back, as shown in Figure 11. These triangular or diamond-shaped areas are lost in early clubbing. The normal root of the nail lies against bone (DIPJ), but with clubbing, the root of the nail is separated from the underlying bone by connective tissue and edema. This spongy material makes the base of the nail to float when rocked from side to side or in the longitudinal direction (floating sign). In advanced cases, there is a warm club-like swelling of the distal phalanx.


Figure 11 Different methods for the demonstration of clubbing

In relation to gastrointestinal disease, it is seen in about one-third of the patients with cirrhosis. Rarely, with development of hepatopulmonary syndrome, there may be associated cyanosis. Clubbing is also seen in inflammatory bowel diseases and celiac disease. Clubbing is divided into various stages, with different signs appearing as severity of clubbing increases.

Clinical Stages of Clubbing



Loss of normal angle (160 to 170) between the nail and the soft tissue around its bed. It actually becomes 180 or greater and is the initial sign.


Shiny appearance of adjacent skin.


Fluctuation and softening of the nail bed causes rocking of the nail on palpation.


Increased convexity of the nail in both longitudinal and vertical direction.



Clubbed or bulbous appearance of the finger tips.


Local warmth and signs of inflammation appear with involvement of the proximal bone.


Longitudinal striations and friable nails are nonspecific late signs.


It is not well understood, but the prerequisite seems to be peripheral vasodilatation and A-V anastomosis due to proposed substances like prostaglandins, ferritin, adenosine triphosphate, 5-hydroxytryptamine, and bradykinin. Proliferation and edema of connective tissue between the skin and the nail bed results in loss of normal angle and increased sponginess of the nail base causing clubbing.

Causes of Clubbing

Insidious onset of clubbing over months may be due to inflammatory causes, but rapidly progressive clubbing may be seen in malignant diseases. In children, congenital heart disease, cystic fibrosis, and lung infection are often considered. In adults, the two most common causes are infections and intrathoracic neoplasm. Clubbing only in the toes may be seen in PDA with reversal of shunt. Unilateral clubbing may be seen with aneurysm of the aorta and large vessels, apical lung tumors, in hemiplegia and axillary tumors. Clubbing may also be idiopathic or associated with trauma.

Other Types of Clubbing

When clubbing is associated with subperiosteal new bone formation (resembling elm bark) in the distal diaphysis of the long bones of extremities, it is called hypertrophic osteoarthopathy. Lung and pleural tumors account for one-third of the cases. The affected area appears inflamed, painful, and edematous. Acropachy is an alternate name for clubbing and in Graves’ disease; it is called thyroid acropachy. In this condition, there may be associated onycholysis. Pseudoclubbing is the term applied when the nail appears to be clubbed, but in reality, there is only increased nail curvature usually with chronic paronychia or abscess of the pulp space. This can be confirmed by placing the thumbs of the patient back to back as aforementioned. In true clubbing, a diamond-shaped empty space is lost, while it is present normally and in pseudoclubbing.


Figure 12 Causes of clubbing are given in various systems in descending order of importance

Peripheral Edema

It is the collection of fluid in the interstitial space due to either altered Starling’s forces or blockage of venous outflow. In relation to GIT, edema may be seen in cirrhosis of liver, malabsorption syndromes, and protein losing enteropathies.

Examination: Look for edema at dependent parts of the body, that is, around the ankle (sacrum in bed bound patients). A constant pressure when applied against a bony prominence for about 10 s leaves a pit, which gradually fills up. This is seen when about 4 kg of fluid has already collected. If the pit remains for a shorter period (less than 30 to 40s), the cause is likely due to hypoalbuminemia (fast edema). A cardiac cause is essentially ruled out when the venous pressure is normal and the pit stays for longer period (more than 40 s) unless diuretics have been used (called slow edema). Similarly, edema limited to the face or hands is not seen with cardiac cause. In general, edema may be generalized with cardiac disease, liver disease, kidney disease, and other causes of hypoalbuminemia. Local causes are due to venous or lymphatic obstruction or vascular leakage or increased permeability.


Figure 13 Pitting edema shown in fluid overload conditions

Causes of Edema


CVS: congestive cardiac failure, right heart failure, and constrictive pericarditis.


Liver: chronic liver disease and cirrhosis.


GIT: malabsorption and protein losing enteropathies.


Kidney: chronic renal disease and nephrotic syndrome.


Lung: cor-pulmonale.


Drugs: calcium antagonists.


Others: allergy and angioedema, premenstrual edema, tight undergarments, wet beriberi, severe obesity, cyclic edema.


Hypoalbuminemia: malnutrition.


Unilateral edema: DVT, tumor, or lymph node causing obstruction.


Lymphatic obstruction: When gross, it may also pit (filariasis, Milroy’s disease, congenital lymphedema, malignant lymphatic invasion.

Disease-Focused Examination

In cirrhosis, signs of liver cell failure may appear, but quite often, one may not find any sign, even with advanced liver disease. General examination may reveal, spider angioma, jaundice, palmer erythema, and bruising. There may be clubbing, leuconychia, Dupuytren’s contracture, gynecomastia, and testicular atrophy.

Rarely, a sweet, fecal smell (fetor hepaticus) is noticed in the breath of those with end-stage liver disease (due to dimethyl sulfide). Asterixis or hepatic flap is demonstrable in early to late hepatic encephalopathy. The patient is asked to fan out the fingers of the outstretched hands, with wrist extended for 10 to 15s. There is coarse, irregular flexion and extension of the fingers with lateral movements. It is due to false neurotransmission and inability to maintain posture and tone. It may also be seen in advanced cardiac, renal, and respiratory failure and severe electrolyte disturbance and overdoses.


Figure 14 Spider angioma in cirrhosis with raised central area and branching capillaries


Figure 15 Leuconychia (white ban across the nail in hypoalbuminemia) on the left, and clubbing associated with white nails is seen in a case of cirrhosis on the right

Dupuytren’s contracture (Figure 16) is the cord like thickening of the palmer fascia, resulting in fixed flexion of the lateral fingers, especially the ring finger. It is usually bilateral and associated with consumption of alcohol. It is not a sign of cirrhosis from other causes.


Figure 16 Dupuytren’s contracture in a patient with alcoholic cirrhosis (left) and palmer erythema (redness predominant over the thenar and hypothenar eminences) in chronic liver disease. The soles of the feet may be similarly involved. Palmer erythema may also be seen in pregnancy, thyrotoxicosis, rheumatoid, and polycythemia

In primary biliary cirrhosis, itching (from deposition of bile pigments in the skin) is an early feature; therefore, scratch marks may be visible along with hyperpigmentation and jaundice (also see page 79). Hyperlipidemia may be associated with deposition, especially around the eyes called xanthelasma (Figure 17).


Figure 17 Xanthelasma along the margin of the eye due to hyperlipidemia and bruising in Vitamin K deficiency

Features of chronic malabsorption include generalized weight loss and asthenia. Various deficiencies are associated with suggestive clinical features, like calcium and Vitamin D (bone pain and deformity); protein (poor wound healing, failure to grow, and leukonychia); Vitamin K (bruising); Vitamin A (night blindness); Vitamin B12 (paresthesia and numbness); Vitamin B1 (weakness and lassitude; Vitamin B6 (dermatitis, diarrhea, and dementia and iron deficiency (koilonychia)).

In Peutz–Jegher’s syndrome, brownish-black pigmented spots around the mouth occur. The patient presents with chronic diarrhea due to intestinal polyposis (in the stomach, small bowel, and large bowel).

In celiac disease, chronic diarrhea may be associated with an extremely itchy bullous rash on the extensor surfaces called, dermatitis herpatiformis (Figure 18).

Inflammatory bowel disease may be associated with large joint arthritis, especially of the knees, liver involvement with sometimes signs of chronic liver disease, clubbing, eye involvement with scleritis and uveitis, and skin involvement with erythema nodosum and pyoderma gangrenosum (Figure 19). This is an angry-looking ulcerating lesion of the skin, with blackish areas representing gangrene seen in inflammatory bowel disease.


Figure 18 Dermatitis herpatiformis in a patient with coeliac disease


Figure 19 Pyoderma gangrenosum in a patient with ulcerative colitis

It may involve any part of the body. It is seen especially in ulcerative colitis, but occasionally in Crohn’s disease (CD).

In acute hemorrhagic pancreatitis, bruising around the umbilicus is called Cullen’s sign (Figure 30) and in the flank is called Gay Turner’s sign.

In the skin, in relation to gastrointestinal diseases, one may find pigmentation associated with chronic liver disease in hemachromatosis, Peutz–Jegher’s syndrome, malabsorption syndrome, Cronkhite–Canada syndrome. Acanthosis may be associated with carcinoma of the stomach. Flushing along with diarrhea and wheezing is seen in carcinoid syndrome. Glucagonoma may be associated with migratory necrolytic rash. In hereditary hemorrhagic telangiectasia, skin telangiectasis may be associated with GI bleeding. Porphyria in association with alcoholic liver disease may be associated with vesicles on exposed skin surface. Tight skin with loss of wrinkles and calcification in systemic sclerosis maybe associated with dysphagia and bacterial over growth syndrome. Bruising is seen in chronic liver disease and is due to a defective Vitamin K-dependent coagulation factors. Hypersplenism may be associated with thrombocytopenia and a petechial rash. Pruritus in obstructive jaundice and chronic kidney disease is associated with scratch marks on the skin. Cyanosis in relation to GI disease may rarely be associated with hepatopulmonary syndrome.

On the hands, one may find some signs of chronic liver disease like clubbing, leukonychia, spider angioma, palmer erythema, bruising, Dupuytren’s contracture, or asterixis. Clubbing may also be seen in inflammatory bowel disease and malabsorption syndromes in relation to gastroenterology. The hands may be pale like the complexion with anemia related to gastrointestinal blood loss in a host of diseases.

In the eyes, one may find jaundice, uveitis (ulcerative colitis and CD), and Biot’s spots (Figure 20) with night blindness, in Vitamin A deficiency. Anemia is seen in a variety of GI causes. Kayser–Fleischer ring may be seen in Wilson’s disease (Figure 20) associated with signs of chronic liver disease.


Figure 20 Kayser–Fleischer ring on the left seen as an outer rim of golden brown color around the outer cornea. The patient also had jaundice from chronic liver disease. Biot spot in Vitamin A deficiency is seen at 9 o’clock on the sclera on the right

Examination of the neck involves looking for lymph nodes, thyroid enlargement, thyroglossal cyst, large blood vessels, trachea and esophageal abnormalities, and any other swellings. Left supraclavicular lymph node enlargement is associated with carcinoma of the stomach or lung and gastrointestinal malignancies and is called Virchow’s lymph node. Lymphadenopathy, especially in the neck, may be the first feature of lymphoma. Goiter may be associated with thyrotoxicosis or myxedema. In relation to GIT, the former is associated with hypermotility and the latter with hypomotility and at times, ascites. Medullary carcinoma of the thyroid may be associated with diarrhea; thyroid abnormalities may occur in chronic active hepatitis.


Figure 21 A young male with bull neck in lymphoma on the left (it may also be seen in children with diphtheria). Goiter in a female on the right

Oral Examination

This includes a detailed look at the lips, teeth, tongue, tonsils, and throat. A torch, tongue depressor, and disposable gloves are all that may be required during the examination. A careful look may provide valuable clues to the diagnosis or presence of complications.

Examination of Lips

Appear blue in cyanosis and pale in anemia.

Aphthous ulcers on the inner surface of lips.

Angular stomatitis (fissure at the angle of mouth) seen in iron riboflavin deficiency.

Cleft lip or its repair may be obvious.

Herpes labialis (reddish crusted vesicles).

Cheilosis (seen in iron deficiency anemia).

Ulcer (may be due to cancer).

Pigmentation (in Peutz–Jegher’s syndrome).

Chancre (small firm indurated lesion in syphilis).

Examine the inside of the mouth with a torch and a tongue depressor. Inspect the buccal mucosa, gums, teeth, and tongue. Also, carefully look at the pillars of fauces, uvula, and the tonsils. Look for changes in color, abnormal growths or masses, ulcers, and abnormal odor. Bad orodental hygiene may be the source of many problems. Bleeding gums are commonly due to gingivitis. Whitish spots on the buccal mucosa (Koplik spots) opposite the second molar may be seen in measles. Leukoplakia is a premalignant disorder, where the buccal mucosa may appear like a homogenous or nodular white patch that cannot be rubbed off. Biopsy confirms the diagnosis. Red velvety lesion (erythroplasia) of the mouth, even when asymptomatic, is more likely to be carcinoma in situ or invasive carcinoma, than the white lesion. Any chronic ulcerative lesions that fail to heal in one to two weeks should be considered potentially malignant.

Examination of Teeth and Gums

Look for caries of the teeth.

Tar deposition in heavy smokers.

Tetracycline staining (yellow-gray bands).

Pigmentation of gums in Addison’s disease.

Blue line on the gums indicates lead toxicity.

Hyperplasia of the gums is seen in chronic gingivitis and chronic phenytoin use.

Peg-shaped and notched upper incisor teeth (Hutchinson’s teeth).

Examine the tongue inside the mouth and then after protruding. Look for the shape, size, wasting, and involuntary movements. Inspect the tongue more closely on protrusion and look for deviation.

Examination of Tongue

Geographical tongue is a normal variant.

Fissured tongue may be a normal variant.

Anemia can be accessed from the pallor.

Central cyanosis is seen on the under surface of tongue.

White curd-like deposits occur in fungal infection or candida, but blackish deposits are seen with other fungi.

Excessive coating (fur) occurs in smokers.

Strawberry tongue is seen in scarlet fever.

Dry tongue may indicate dehydration or seen in Sjogren’s or sicca syndrome.

Generalized papillary atrophy occurs in pernicious anemia and IDA.

Wasted flaccid and ipsilaterally deviated tongue is seen in lower motor neuron hypoglossal palsy, for example, bulbar palsy. A weak and spastic tongue is seen in pseudobulbar palsy and upper motor neuron lesion of the hypoglossal nerve.

Fasciculation may be seen in bulbar palsy.

Tremor may be seen in thyrotoxicosis.

Carcinoma of the tongue especially occurs on the side and under surface as growth or ulcer.

Red beefy tongue is seen in Vitamin B6, B12 deficiency and nicotinic acid poisoning.

Bald and pale tongue may be seen in pernicious anemia.

Aphthous ulcers are seen in bad orodental hygiene and CD.

Macroglossia is seen in acromegaly and amyloidosis.

Ulcers of the tongue may be seen in celiac disease, Reiter’s disease, Behcet’s disease, CD, and in syphilis. Carcinoma of the tongue may also present as an ulcer.


Figure 22 Magenta tongue is seen especially in riboflavin (Vitamin B2) deficiency (left). A geographical tongue is a normal variant and should be differentiated from oral candidiasis or thrush, which usually has a layer or coating like pseudo-membrane. This curdled milk-like membrane can be whipped away, which leaves an erythematous mucosa


Figure 23 Coated tongue seen on the left may be normal or associated with many fevers, especially typhoid. On the right, the tongue is deviated to the right and that half is showing some wasting. This is seen in lower motor neuron hypoglossal nerve palsy


Figure 24 Patient on the left has hereditary hemorrhagic telangiectasia. They may bleed especially from gastrointestinal tract due to presence of similar lesions. On the right, leukoplakia close to the left tip of the tongue is seen as a whitish patch

Examination of the throat is mandatory, as it is one of the commonest sites of infection. It includes a look at the orodental hygiene, tongue, pharynx, and tonsils. Throat is a known source of sinus, chest, and ear problems. A simple group-A beta hemolyticus streptococcal infection may lead on to rheumatic fever and permanent cardiac disability.

Examination of the Throat


Aphthous ulcers are well-demarcated ulcers with red margins seen anywhere on the mucous membrane.


Deviation of the uvula to the healthy side on saying “ah” occurs in vagal palsy.


Herpes zoster infection of the trigeminal or glossopharyngeal nerve is associated with vesicles in the area of distribution.


Malignancy is recognized by an irregular hard growth, infiltration, and or ulceration. There is lymph node enlargement in the area of drainage.

A white patch in the throat may be due to multiple causes depending on the history. It may be simply follicular tonsillitis or may be a serious infection like diphtheria. The differential diagnosis of this appearance is given as follows:


Figure 25 Petechae are seen on the palate in a case of infectious mononucleosis

White Patch in the Throat


In acute follicular tonsillitis, the enlarged tonsil has areas of visible pus.


In infectious mononucleosis, the enlarged tonsil is covered by a whitish membrane.


In candidiasis, there is patchy white curd-like membrane or whitish spots.


In diphtheria, the grayish membrane readily bleeds on attempted removal.

Clinical Examination: Inspection

Prerequisites of Examination

1. Introduce yourself, take permission, and explain briefly to the patient what you are about to do, and that you will not hurt him or her.

2. The patient should be lying down supine in a comfortable position and in good light.

3. The head may be supported with a small pillow.

4. Hands are kept by the side, while the face is turned to the opposite side.

5. Legs are kept straight. The knees may be flexed, but this does not relax the abdominal muscles.

6. The patient breathes quietly with his mouth open.

7. The urinary bladder should be recently emptied.

8. Exposure of the abdomen should be adequate according to the age, sex, and culture, from mid-thorax to pubis.

9. Start to look at the abdomen from the foot end moving toward the right side, getting ready to palpate the abdomen. Also, examine the sides of the abdomen and the back with the patient sitting.

The abdomen is artificially divided into four or nine quadrants for reference purpose to localize the disease anatomically (Figure 26). This is useful for differential diagnosis, as any localizing features may pint to a cause in the underlying anatomical structures.


Figure 26 The artificial regions of the abdomen

After having met the prerequisites, one should comment on the following features on inspection.

Parameters of Inspection


Shape of abdomen.


Abdominal movements.


Epigastric pulsations.


Pigmentation and rashes.




Prominent veins.


Visible peristalsis.


Pubic hair.




Hernial orifices.


Scars and tap marks.


Surgical incisions.


Figure 27 The patient has general abdominal swelling with localized fullness, especially in the epigastrium (on the left). Gross abdominal distension due to ascites with striae due to stretching seen on the right

A diagrammatic representation of the findings on inspection is advisable. An example is given as follows.


Figure 28 The scheme of general physical examination of GIT

Causes of Abdominal Distention


Abnormal masses or enlarged viscera.


Free or encysted fluid in the abdomen.


Fetus in the hypogastrium.


Flatus or gas.


Fat, that is, obesity.




Figure 29 Swelling in the right hypochondrium was a tumor in the liver. On the right, there is fullness in the left hypochondrium. This was due to massive splenomegaly

2. Abdominal Movements

Normal movement during quiet breathing in females is thoracoabdominal (abdomen forms a concavity during inspiration), but is abdomino-thoracic (abdomen bulges out during inspiration) in males and infants of either sex. The patient uses the diaphragm for breathing when there is chest pain (pleurisy), intercostal nerve paralysis, or ankylosing spondylitis. Conversely, the patient uses more chest muscles when there is large ascites, peritonitis, abdominal tumors, liver abscess, or any because that restricts or limits the diaphragmatic movement. The indrawing of the anterior abdominal wall during inspiration (paradoxical movement) may be seen when the patient is voluntarily doing it, or rarely, in paralysis of the diaphragm.

3. Epigastric Pulsations

They are either due to transmission form the aorta, the heart, or rarely from aneurysmal dilatation of an artery.

Causes of Epigastric Pulsations


Thin built (transmission from aorta).


Aneurysm of abdominal aorta.


Hyperkinetic right ventricle.


Mass in front of aorta (carcinoma stomach).


Pulsatile liver in tricuspid regurgitation.

4. Pigmentation and Rashes

Localized pigmentation (erythema abigne) may be seen with repeated heat applications or infrared radiation to relieve the pain. Primary biliary cirrhosis, hemochromatosis, and malabsorption syndromes may be associated with generalized pigmentation.

(a) Bruising in the flanks may be seen in acute hemorrhagic pancreatitis (Gray Turner’s sign). If similar bruising is present around the umbilicus, it is termed Cullen’s sign (Figure30). Bruising may also be seen in chronic liver disease.


Figure 30 Bruising around the umbilicus in acute hemorrhagic pancreatitis is called Cullen’s sign (similar bruising in the flanks is called Gray Turner’s sign)

(b) Rose spots are small (pin head size), red blanchable spots (Figure 31), found sparsely on the abdomen or back, in typhoid fever. In paratyphoid fever, they are larger in size and greater in number.

(c) Linea nigra is a brown-black-pigmented streak between umbilicus and symphysis pubis, seen in pregnancy, especially in multiparous women.


Figure 31 Typical rose spots are seen as pink-red spots on the abdomen as shown


Figure 32 Striae due to stretching in a patient history of gross ascites

Causes of Striae




Gross ascites.


Cushing’s syndrome.


Gross obesity.

6. Prominent Veins

Prominent veins on the abdomen are most commonly seen in portal hypertension (Figure 33). Standing makes the veins more prominent due to the effect of gravity. Emptying the vein with the fingers and releasing one side at a time may determine the direction of flow, by noting the time taken to refill. The flow is in the direction that takes less time to refill. Normal venous drainage is from the umbilicus toward each quadrant, that is, centrifugally.


Figure 33 Dilated veins on the abdomen

Causes of Prominent Veins


Portal obstruction in cirrhosis of the liver is associated with normal blood flow. Rarely, a periumblical swelling with dilated veins (caput medusa) is seen.


In inferior vena-caval obstruction, the blood flow of the dilated veins is upward toward the thorax.


In superior vena-caval obstruction, blood flow of dilated veins is toward the groin.


Figure 34 Loss of pubic hair in hypopituitrism and hypogonadism

9. Umbilicus

Normal umbilicus is inverted and located centrally, somewhat nearer to pubic symphysis, than the xiphi-sternum. An everted and transverse slit “smiling” umbilicus is seen in abdominal distension from any cause, but most commonly with a large ascites. An umbilicus that has shifted upward, with a longitudinal slit, is seen in large ovarian cyst or tumors.

10. Hernial Orifices

Inspect the inguino-femoral regions in privacy. While standing, ask the patient to cough, to look for hernias. Examine the area along the recti muscles and umbilicus for hernia, which develop due to weakness of the abdominal wall (for radiology, see Figure 74).

11. Scars and Tap Marks

Previous abdominal surgical procedures are recognized by a typical scar. Occasionally, they are associated with fibrotic bands that may be responsible for intestinal obstruction. A history of operations, like nephrectomy, may necessitate adjustment of the doses of certain drugs or splenectomy, (patient is predisposed to pneumococcal and salmonella septicemia) may help in patient management. Tiny needle puncture marks on the abdomen are evidence of attempted paracentesis. Larger marks may be due to laparoscopic procedures or surgical incisions. Incision scars may be the site of herniation, abdominal pain, infection, fistula, and discharge. It is also important to remember that operations on the gut may result in indigestion, diarrhea, or malnutrition, and deficiency of vitamins.


Figure 35 A patient with gross ascites and bandaged after taping on the left, and edema involving the testis and penis on the right


Figure 36 Common abdominal incisions

Clinical Examination: Palpation

Initial Requirements

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Jul 29, 2019 | Posted by in GASTROENTEROLOGY | Comments Off on II General Physical Examination

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