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IM16.1-17 | Diarrheal Disorders — Practice Quiz
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A 25-year-old woman presents with large-volume watery stools (6–8 per day) for 2 days, no blood, no fever, and no tenesmus. Stool osmotic gap is measured at 40 mOsm/kg. Which pathophysiological mechanism is MOST consistent with this presentation?
Correct. A stool osmotic gap <50 mOsm/kg indicates that the stool water composition is accounted for by measurable electrolytes, which is the hallmark of secretory diarrhoea. Cholera is the prototype: cholera toxin activates adenylyl cyclase, raising cAMP, which opens CFTR chloride channels — producing massive chloride-driven water secretion without mucosal invasion (hence no blood, no fever). The SGLT1 co-transporter is not affected by cholera toxin, which is why WHO ORS (glucose-coupled sodium absorption) remains effective.
Stool osmotic gap = measured osmolality - 2×(stool Na + stool K). Gap <50 = secretory; gap >125 = osmotic. Secretory diarrhoea is large-volume, watery, persists with fasting, no blood, low osmotic gap — prototype: cholera.
A stool osmotic gap <50 mOsm/kg points to secretory diarrhoea — the stool is isotonic with plasma but driven by active electrolyte secretion, not by an unabsorbed solute (osmotic gap >125) or mucosal invasion (which would cause blood/fever).
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A 30-year-old man presents with acute diarrhoea that resolves completely when he fasts for 24 hours. Stool osmotic gap is 140 mOsm/kg. Which of the following is the MOST likely cause?
Correct. An osmotic gap >125 mOsm/kg indicates that unabsorbed, osmotically active solutes are retaining water in the bowel lumen. The diarrhoea resolving with fasting is the clinical hallmark of osmotic diarrhoea. Lactase deficiency is the commonest cause in adults: unabsorbed lactose (disaccharide) generates the osmotic load. Cholera and ETEC produce secretory diarrhoea (gap <50) which does NOT resolve with fasting.
Osmotic diarrhoea: resolves with fasting, high osmotic gap (>125), cause is unabsorbed solute — lactose intolerance, sorbitol, Mg-antacids. Secretory: persists with fasting, low osmotic gap (<50).
Diarrhoea that resolves completely with fasting + high osmotic gap >125 = osmotic diarrhoea. The unabsorbed solute generates the osmotic load. Secretory diarrhoea (cholera, ETEC) persists during fasting and has a low osmotic gap.
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A 40-year-old farmer presents with bloody mucoid stools, fever (38.5°C), tenesmus, and lower abdominal cramps for 3 days. Stool microscopy shows RBCs and pus cells. Which term BEST describes this clinical syndrome?
Correct. Dysentery is defined by blood and/or mucus in stool, indicating mucosal invasion and inflammation. The additional features — fever, tenesmus, lower abdominal pain, and pus cells on microscopy — confirm invasive/inflammatory diarrhoea. This presentation is caused by organisms that invade the colon (Shigella, Entamoeba histolytica, Campylobacter, enteroinvasive E. coli). The management differs critically from watery diarrhoea: antimotility agents (loperamide) are CONTRAINDICATED in dysentery.
Dysentery = blood and/or mucus in stool. Diarrhoea = ≥3 loose/liquid stools/day without blood. Duration classification: acute <2 wk, persistent 2-4 wk, chronic >4 wk. Antimotility agents (loperamide) are absolutely contraindicated in dysentery.
Blood and mucus in stool + fever + tenesmus = dysentery (not diarrhoea). The distinction is critical: antimotility agents are contraindicated in dysentery. Dysentery implies colonic mucosal invasion; watery diarrhoea implies secretory or osmotic mechanism without mucosal damage.
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A 5-year-old child is brought with watery diarrhoea for 2 days. Examination shows sunken eyes, dry mouth, skin pinch retracts in 2 seconds, and the child is irritable. There is no severe dehydration. According to the WHO IMCI dehydration plan, which rehydration strategy is APPROPRIATE?
Correct. Sunken eyes, dry mouth, irritability, and slow skin pinch (retraction in 2 seconds) indicate SOME dehydration (not severe — no lethargic/unconscious, no sunken fontanelle, skin retracts but not >2 seconds). This matches WHO Plan B: 75 mL/kg low-osmolarity ORS (245 mOsm/L; Na 75, glucose 75, K 20, Cl 65, citrate 10 mmol/L) over 4 hours under supervised facility care. Plan C (IV Ringer's Lactate 30 mL/kg in 30 min then 70 mL/kg) is for severe dehydration (limp, unconscious, no radial pulse).
WHO ORS (low-osmolarity, 245 mOsm/L): Na 75, glucose 75, K 20, Cl 65, citrate 10 mmol/L. Plan A = home ORS; Plan B = 75 mL/kg supervised × 4 hr (some dehydration); Plan C = IV RL 100 mL/kg (30+70 mL/kg) for severe dehydration.
Sunken eyes + dry mouth + skin pinch 2 seconds + irritability = SOME dehydration → WHO Plan B (75 mL/kg ORS over 4 hours supervised). Plan A is for no dehydration; Plan C with IV Ringer's Lactate is for severe dehydration with circulatory compromise.
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A 60-year-old man with chronic diarrhoea for 3 months presents with peripheral oedema, glossitis, angular cheilitis, and a low serum albumin. D-xylose absorption test is abnormal. Which small bowel pathology is MOST likely?
Correct. The combination of chronic diarrhoea, malabsorption (abnormal D-xylose absorption — D-xylose is absorbed exclusively by the small bowel mucosa; an abnormal test specifically indicates small bowel mucosal disease), hypoalbuminaemia, and nutritional deficiency signs (glossitis, angular cheilitis) points to villous atrophy of the small bowel mucosa. Coeliac disease (gluten-sensitive enteropathy) is the prototype. Diagnosis requires serum anti-tTG IgA and duodenal biopsy showing villous atrophy + crypt hyperplasia. Treatment is strict lifelong gluten-free diet.
Chronic diarrhoea + malabsorption + nutritional deficiencies + abnormal D-xylose = small bowel mucosal disease. Coeliac disease: anti-tTG IgA, duodenal biopsy, gluten-free diet. D-xylose specifically tests small bowel absorptive capacity.
Abnormal D-xylose absorption specifically indicates small bowel mucosal disease (D-xylose requires intact small bowel mucosa). Combined with nutritional deficiency signs + hypoalbuminaemia, this pattern points to coeliac disease (villous atrophy). IBS has no malabsorption.
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During a history from a patient with acute diarrhoea, which feature MOST SPECIFICALLY points toward Entamoeba histolytica rather than Shigella as the causative organism?
Correct. Amoebiasis (E. histolytica) characteristically presents with insidious onset, bloody stools (classically 'red currant jelly'), MINIMAL fever, and may cause hepatic amoebic abscess (right hypochondrial pain, liver enlargement). The portal of entry is contaminated water/food (faeco-oral). Shigellosis presents with explosive onset, high fever, household clustering (low infectious dose), and severe tenesmus — more acute and fulminant. The liver enlargement points specifically to extra-intestinal amoebic spread.
India pathogens in dysentery: E. histolytica (amoebic) — insidious, minimal fever, liver abscess risk, metronidazole 400-800mg TDS × 5-10 days. Shigella — explosive, high fever, household spread, low inoculum. Giardia — steatorrhoea, bloating, no blood.
Amoebic dysentery features: insidious onset, bloody stools with minimal fever, potential liver abscess formation (right upper quadrant). Shigella: explosive onset, high fever, household contacts affected (very low infectious dose). Minimal fever + liver signs = amoebiasis.
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A 35-year-old woman with a 6-week history of abdominal cramps and 4–6 loose stools daily shows RBCs and pus cells in stool. Stool culture is negative. Colonoscopy reveals continuous mucosal inflammation from rectum to splenic flexure with a sharp demarcation proximally. Biopsy shows crypt abscesses. Which diagnosis is MOST consistent?
Correct. Ulcerative colitis (UC) is characterised by continuous mucosal inflammation that always involves the rectum and extends proximally in a contiguous pattern with sharp proximal demarcation. Histology shows crypt abscesses and goblet cell depletion. Crohn's disease has skip lesions (non-contiguous), transmural inflammation, granulomas, and can involve any part of the GI tract from mouth to anus (often terminal ileum). Intestinal TB can mimic Crohn's (ileocaecal area, skip lesions); amoebic colitis has overlapping features but serology and biopsy differentiate.
UC vs Crohn's: UC = continuous from rectum, mucosal only, crypt abscesses, no granulomas. Crohn's = skip lesions, transmural, may have granulomas, terminal ileum common, can involve anywhere from mouth to anus. UC surgical option = curative colectomy; Crohn's surgery = non-curative.
Continuous colonic inflammation from rectum proximally + sharp demarcation + crypt abscesses = Ulcerative Colitis. Crohn's disease shows skip lesions (discontinuous), transmural involvement, may have granulomas, and frequently involves the terminal ileum.
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A microbiologist shows a stool wet-mount to a final-year student. The preparation shows pear-shaped trophozoites with two nuclei, a central axostyle, and falling-leaf motility. Which organism is being demonstrated?
Correct. Giardia lamblia trophozoites are distinctive on wet-mount: pear-shaped (piriform), bilaterally symmetrical with two nuclei (giving a face-like appearance), a central axostyle rod, and characteristic tumbling or falling-leaf motility. Entamoeba histolytica trophozoites are irregular amoeboid forms with a single nucleus and may contain ingested red blood cells. Giardia causes steatorrhoea and bloating (not dysentery), lives in the proximal small intestine, and is treated with metronidazole or tinidazole.
Stool microscopy identification: Giardia = pear-shaped, 2 nuclei, falling-leaf motility, sucking disc. E. histolytica = irregular amoeboid, single nucleus, ingested RBCs in trophozoites. E. histolytica cysts = 4 nuclei, cigar-shaped chromatoid bodies.
Pear-shaped trophozoite + two nuclei + central axostyle + falling-leaf motility = Giardia lamblia. E. histolytica trophozoites are irregular amoeboid forms with a single nucleus, often containing ingested RBCs in invasive disease. Giardia causes malabsorption/steatorrhoea; E. histolytica causes dysentery.
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In the microbiology laboratory, a dark-field or phase-contrast preparation from a stool suspension of a cholera patient shows organisms with characteristic rapid darting motility in a comma-shaped bacillus. This is the classic appearance of which preparation?
Correct. The hanging-drop preparation is the classic rapid diagnostic technique for Vibrio cholerae. A drop of watery stool is placed on a coverslip, inverted over a depression slide, and examined by dark-field or phase-contrast microscopy. Vibrio cholerae appears as comma-shaped (vibrio) organisms with characteristic rapid darting or 'shooting-star' motility. This technique is used in outbreak settings where culture may not be immediately available. Inhibition of motility by specific antiserum (O1 or O139) confirms the diagnosis.
Hanging-drop preparation for V. cholerae: stool suspension in dark-field or phase-contrast microscopy. Rapid darting/shooting-star motility of comma-shaped bacilli. Inhibited by O1/O139 antiserum. Rapid point-of-care diagnosis in outbreak settings.
The hanging-drop preparation is specific for Vibrio cholerae: comma-shaped organisms with rapid shooting-star motility visible under dark-field or phase-contrast microscopy. Motility inhibition with O1/O139 antiserum confirms the diagnosis. This is the rapid field diagnostic for cholera outbreaks.
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A 28-year-old HIV-positive man (CD4 count 150 cells/microL) has chronic diarrhoea for 6 weeks. Stool modified acid-fast stain shows small (4–6 micrometre) oocysts. Which of the following antiparasitic regimens is MOST appropriate for the causative organism?
Correct. Small (4-6 micrometre) oocysts on modified acid-fast stain = Cryptosporidium parvum. Cryptosporidiosis is an AIDS-defining illness when CD4 <200. In immunocompetent hosts, nitazoxanide (500 mg twice daily for 3 days) is effective and self-limiting. However, in severely immunocompromised patients (CD4 <100-200), nitazoxanide has limited efficacy and the disease becomes chronic and life-threatening. The single most important intervention is immune reconstitution via effective antiretroviral therapy (NACO Treat-All, TLD first-line). Metronidazole is not effective against Cryptosporidium; albendazole treats microsporidiosis.
Cryptosporidium: modified acid-fast stain, 4-6 micrometre oocysts. Immunocompetent = self-limiting, nitazoxanide. Immunocompromised (HIV CD4 <200) = chronic, life-threatening; ART for immune reconstitution is primary treatment. NACO Treat-All applies to all HIV patients.
Modified acid-fast stain small oocysts (4-6 micrometre) = Cryptosporidium. In HIV/AIDS (CD4 <200), nitazoxanide has limited benefit; antiretroviral therapy for immune reconstitution is the cornerstone of management. Metronidazole treats amoebiasis and giardiasis, not cryptosporidiosis.
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