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SN13 SHORT NOTE 5M

Write a short note on chronic diarrhoea and malabsorption.

General Medicine · Final Professional

Definitions

Diarrhoea is the passage of loose or watery stools three or more times daily, or more frequently than is normal for the individual, and is more precisely defined by a stool weight exceeding 200 g/day. Chronic diarrhoea persists for more than 4 weeks.

Malabsorption is impaired absorption of nutrients, resulting from defects in digestion (maldigestion), mucosal absorption, or transport of absorbed nutrients.

Classification of Chronic Diarrhoea

TypeMechanismEffect of fastingExamples
OsmoticNon-absorbed solute draws water into the lumenSTOPS with fastingLactose intolerance, magnesium-containing antacids and laxatives, sorbitol, coeliac disease
SecretoryActive secretion of electrolytes and waterCONTINUES during fasting; nocturnalCholera and enterotoxins, VIPoma, carcinoid, bile acid malabsorption, microscopic colitis, medullary thyroid carcinoma
Inflammatory / exudativeMucosal inflammation, blood and pusContinuesInflammatory bowel disease, invasive infection, intestinal tuberculosis, ischaemic colitis, radiation enteritis
Fatty (steatorrhoea)Maldigestion or malabsorption of fatReducedCoeliac disease, chronic pancreatitis, bacterial overgrowth, tropical sprue, giardiasis
Motility-relatedRapid transitVariableIrritable bowel syndrome, diabetic autonomic neuropathy, hyperthyroidism, post-surgical (short bowel, post-vagotomy)

Causes of Malabsorption

LevelCauses
Luminal (maldigestion)Chronic pancreatitis and pancreatic insufficiency, cystic fibrosis, bile salt deficiency (cholestasis, ileal resection, small intestinal bacterial overgrowth), Zollinger–Ellison syndrome (acid inactivation of lipase)
MucosalCOELIAC DISEASE, TROPICAL SPRUE, giardiasis, intestinal tuberculosis, Crohn's disease, Whipple's disease, lymphoma, amyloidosis, radiation enteritis, HIV enteropathy, lactase deficiency
Post-mucosal (transport)Intestinal lymphangiectasia, lymphoma, tuberculosis of mesenteric nodes, constrictive pericarditis
AnatomicalShort bowel syndrome, gastrectomy, blind loop with bacterial overgrowth, fistulae

Clinical Features

  • Diarrhoea with steatorrhoea — bulky, pale, offensive, greasy stools that float and are difficult to flush.
  • Weight loss despite adequate intake; failure to thrive in children.
  • Abdominal bloating, distension, flatulence and cramps.
  • Consequences of specific deficiencies — worth reciting in an answer as they demonstrate understanding:
  • Iron, folate, B12 → anaemia (microcytic, macrocytic or dimorphic)
  • Vitamin D and calcium → osteomalacia, bone pain, proximal myopathy, tetany
  • Vitamin K → bruising and prolonged prothrombin time
  • Vitamin A → night blindness, xerophthalmia
  • Protein → oedema and hypoalbuminaemia
  • Zinc → dermatitis, poor wound healing; B-complex → glossitis, angular stomatitis, neuropathy
  • Red flags requiring urgent investigation: nocturnal diarrhoea, rectal bleeding, weight loss, anaemia, fever, onset over the age of 50, and a family history of malignancy or inflammatory bowel disease. Their absence, with a long history and stable weight, points towards irritable bowel syndrome.

Investigations — a Stepwise Approach

Step 1 — basic:

CBC (anaemia and its type), ESR and CRP, renal function and electrolytes, liver function and albumin, calcium and phosphate, INR, thyroid function, iron studies, vitamin B12 and folate, and blood glucose.

Step 2 — stool:

Microscopy for ova, cysts and parasites (particularly *Giardia*, which requires multiple samples or duodenal aspirate), stool culture, *C. difficile* toxin, faecal fat estimation or a qualitative Sudan stain, faecal calprotectin (raised in inflammatory, normal in functional disease — a valuable discriminator), and faecal elastase (low in pancreatic insufficiency).

Step 3 — targeted:

  • Coeliac serology — IgA anti-tissue transglutaminase (tTG) with total IgA (to exclude IgA deficiency, which causes false negatives). The patient must be eating gluten at the time of testing.
  • Hydrogen breath tests — for lactose intolerance and small intestinal bacterial overgrowth.
  • Upper GI endoscopy with duodenal biopsy — for coeliac disease, tropical sprue, giardiasis and Whipple's disease.
  • Colonoscopy with ileoscopy and biopsies — for inflammatory bowel disease, intestinal tuberculosis, malignancy, and microscopic colitis (which requires biopsy of macroscopically normal mucosa).
  • Imaging — CT or MR enterography, barium follow-through; CT abdomen for pancreatic disease and lymphadenopathy.
  • Gut hormone profile (VIP, gastrin, chromogranin A, urinary 5-HIAA) for suspected neuroendocrine tumour.

COELIAC DISEASE AND TROPICAL SPRUE — the two key mucosal diseases

Coeliac disease is a T-cell-mediated immune reaction to gluten in genetically susceptible individuals (HLA-DQ2/DQ8), causing villous atrophy, crypt hyperplasia and intraepithelial lymphocytosis in the proximal small bowel. It is considerably more common in India than was once thought, particularly in the wheat-eating north.

  • Features: diarrhoea, steatorrhoea, weight loss and anaemia; but also silent or atypical presentations — isolated iron deficiency anaemia, short stature, delayed puberty, infertility, osteoporosis, unexplained transaminitis, and neurological symptoms.
  • Dermatitis herpetiformis — an intensely itchy, blistering rash on the extensor surfaces — is its cutaneous manifestation.
  • Associations: type 1 diabetes, autoimmune thyroid disease, Down syndrome, IgA deficiency.
  • Diagnosis: serology followed by duodenal biopsy (Marsh classification), both while on a gluten-containing diet.
  • Treatment: a STRICT, LIFELONG GLUTEN-FREE DIET — excluding wheat, barley and rye (oats are usually tolerated). Involve a dietitian; correct nutritional deficiencies; monitor with serology and repeat biopsy where response is poor. Non-adherence is the commonest cause of persistent symptoms; refractory disease raises the possibility of enteropathy-associated T-cell lymphoma.

Tropical sprue — a malabsorption syndrome of unknown aetiology (probably post-infective with bacterial overgrowth), occurring in residents of and visitors to the tropics, including large parts of India. It causes diarrhoea, steatorrhoea, weight loss, and megaloblastic anaemia from B12 AND folate deficiency. Biopsy shows partial villous atrophy affecting the entire small bowel (unlike the proximal predominance of coeliac disease). It responds to prolonged tetracycline with folic acid and vitamin B12 — a distinction of considerable practical importance, since it is treatable with antibiotics rather than dietary exclusion.

Management Principles

1. Treat the specific cause — gluten-free diet, antibiotics for bacterial overgrowth and tropical sprue, pancreatic enzyme replacement for pancreatic insufficiency, antimicrobials for giardiasis and tuberculosis, immunosuppression for inflammatory bowel disease.

2. Correct nutritional deficiencies — iron, folate, B12, fat-soluble vitamins (A, D, E, K), calcium, magnesium and zinc.

3. Nutritional support and dietetic input; lactose avoidance where secondary lactase deficiency is present.

4. Symptomatic — antidiarrhoeals only when infection and inflammation have been excluded; bile acid sequestrants for bile acid diarrhoea.

5. Monitor weight, nutritional markers, and bone density.

DANGER / REMEMBER

In India, chronic diarrhoea with weight loss demands that you exclude intestinal tuberculosis — which classically involves the ileocaecal region and mimics Crohn's disease closely on imaging and endoscopy. The distinction matters enormously: giving steroids or anti-TNF therapy for presumed Crohn's disease to a patient with intestinal tuberculosis can be catastrophic, causing dissemination. Look for caseating granulomas, positive AFB and CBNAAT on biopsy, and a supportive chest X-ray and Mantoux, and where doubt persists, a therapeutic trial of antitubercular therapy with careful reassessment is often the safer course.

All questions in Hepatology / GIT

  1. Q1Discuss the aetiology, serology, clinical features, complications and management of viral hepatitis. ★
  2. Q2Discuss the aetiology, clinical features, complications, investigations and management of cirrhosis of the liver. ★
  3. Q3Discuss the causes, clinical assessment and management of upper gastrointestinal bleeding. ★
  4. Q4Discuss the aetiology, clinical features, severity assessment, complications and management of acute pancreatitis. ★
  5. SN1Write a short note on the approach to jaundice and interpretation of liver function tests.
  6. SN2Write a short note on acute liver failure.
  7. SN3Write a short note on non-alcoholic fatty liver disease and alcoholic liver disease.
  8. SN4Write a short note on portal hypertension and ascites.
  9. SN5Write a short note on hepatic encephalopathy.
  10. SN6Write a short note on hepatorenal syndrome.
  11. SN7Write a short note on spontaneous bacterial peritonitis and secondary peritonitis.
  12. SN8Write a short note on amoebiasis — intestinal and hepatic.
  13. SN9Write a short note on Wilson's disease.
  14. SN10Write a short note on the clinical approach to hepatomegaly and splenomegaly.
  15. SN11Write a short note on peptic ulcer disease, Helicobacter pylori and Zollinger-Ellison syndrome.
  16. SN12Write a short note on gastro-oesophageal reflux disease.
  17. SN13Write a short note on chronic diarrhoea and malabsorption.
  18. SN14Write a short note on inflammatory bowel disease.
  19. SN15Write a short note on acute infective diarrhoea — cholera and bacillary dysentery.
  20. SN16Write a short note on lower gastrointestinal bleeding.

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