IM16.{1-3,6,15} | Diarrheal Disorder Foundations — Summary & Reflection

KEY TAKEAWAYS

Diarrhoea = ≥3 loose/liquid stools per day. Dysentery = blood and/or mucus in stool — distinct entity with different management. Duration: acute <2 wk / persistent 2–4 wk / chronic >4 wk.

Four mechanisms:
- Secretory: cAMP/cGMP-driven CFTR activation → large-volume watery stools, no blood, no fever, low osmotic gap, PERSISTS with fasting. Prototype: cholera (rice-water stools)
- Osmotic: non-absorbable solute retains water → moderate-volume, ceases with fasting, HIGH osmotic gap
- Inflammatory/invasive: mucosal invasion → blood/pus/mucus + fever + tenesmus + faecal leucocytes. Prototype: Shigella, E. histolytica
- Malabsorptive: impaired nutrient absorption → fatty/floating/pale stools, multi-nutrient deficiency, chronic course. Prototype: coeliac, tropical sprue

Dehydration (WHO): Plan A (no dehydration) = ORS at home; Plan B (some dehydration: sunken eyes + thirsty + slow skin pinch) = 75 mL/kg ORS over 4 hr supervised; Plan C (severe: lethargic + very slow skin pinch) = IV Ringer's Lactate 100 mL/kg. WHO ORS: 245 mOsm/L, Na 75, glucose 75, K 20, Cl 65, citrate 10 mEq/L.

Chronic consequences: fat-soluble vitamin deficiencies (A, D, E, K), hypoalbuminaemia, iron-deficiency anaemia, B12/folate deficiency, zinc deficiency, osteoporosis.

Crohn's vs UC: CD = transmural, skip lesions, any GI segment, fistulae, non-caseating granulomas; UC = mucosal-only, continuous from rectum, colon-only, crypt abscesses. UC first-line = mesalamine; surgery curative in UC, for complications only in CD. Exclude intestinal TB before immunosuppressants in India.

REFLECT

Consider the two opening vignettes: the young man from West Bengal with rice-water stools and the woman with bloody mucoid stools and tenesmus. By now you can name the mechanisms (secretory vs inflammatory), identify the likely pathogens (V. cholerae vs Shigella or E. histolytica), describe the risk of dehydration (catastrophic in cholera, less immediate in dysentery), and outline the initial management (IV rehydration vs antibiotics). Now think one step deeper: why does cholera produce no fever while Shigella does? (The answer lies in whether the pathogen invades the mucosa and triggers an inflammatory cytokine response, or acts purely via toxin secretion from the gut lumen.) How would your management change if the man with rice-water stools was a 75-year-old man with known ischaemic heart disease who cannot tolerate a rapid IV bolus? Reflecting on these edge cases — where the standard algorithm meets individual patient factors — is what converts the knowledge you have built in this SDL into clinical judgement.