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?

This is especially true if:

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.

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.

Anemia

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)

Examination

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.

Etiology

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.

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.

Clinical Features

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

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

Macrocytic Anemia

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

Jaundice

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.

Note

Figure 8 Clinical features of hemolytic and obstructive jaundice

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

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.

Pathogenesis

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

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

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

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).

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).

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.

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.

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

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

Prerequisites of Examination

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

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

Figure 33 Dilated veins on the abdomen

Figure 34 Loss of pubic hair in hypopituitrism and hypogonadism

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