Diarrhoea

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Diarrhoea

  1. 1. DIARRHOEA
  2. 2. DIARRHOEAIncrease in FREQUENCY, LIQUIDITY, VOLUME of stoolsStool weight more than/equal to 200 gm/day (western diet) or 450 gm/day (indian diet)
  3. 3. PSEUDO-DIARRHOEAIncreased frequency but with NORMAL VOLUMESeen due to local inflammation of rectum (IBS, proctitis)Patient passes small but frequent stools
  4. 4. TYPES OF DIARRHOEAACUTE: less than 2 weeksPERSISTENT: 2-4 weeksCHRONIC: more than 4 weeks
  5. 5. ACUTE DIARRHOEA
  6. 6. CAUSES90% INFECTIOUS !!!10% NON-INFECTIOUS
  7. 7. INFECTIOUS CAUSESTOXIN-INDUCED: No inflammation, no RBCs/WBCs in stools)INFLAMMATION OF BOWEL WALL: May have RBCs or/and WBCs in stools
  8. 8. TOXIN INDUCED- PRE-FORMED TOXINS (Staph aureus, B. cereus, C. perfringens)- ENTEROTOXINS (V. cholerae, ETEC, Kleb pneum)- ENTEROADHERENT (E. coli, GIARDIA, helminths, cryptosporidium)- CYTOTOXINS (C. difficile)
  9. 9. INFLAMMATORY DIARRHOEA• MILD – Usually viral (Rota, Norwalk)No WBC/RBC in stools• MODERATE – Superficial mucosal inflammation and involvement. No invasion. Bacterial mostly. WBC present in stool. No RBC(Salmonella, Campylobacter, CMV, Vibrio parahemolyticus)
  10. 10. INFLAMMATORY DIARRHOEA• SEVERE (INVASIVE) – Invasion of mucosal wall present. Both WBCs and RBCs (dyssentery) present in stoolsExamples – Shigella, EIEC - Entamoeba histolytica(invades mucosal wall and causes flasked shaped ulcers)
  11. 11. NON-INFECTIOUS CAUSESDRUGS: antibiotics, laxatives, NSAIDs, antacids, anti-HTn, theophyllinesTOXINS: Arsenic, Mushroom (Amanita), Organophosphates (stimulate Ach – insecticides)
  12. 12. NON-INFECTIOUS CAUSESISCHAEMIC COLITIS: due to lack of blood supply – mucosal loss – therefore WBCs and RBCs in stoolRADIATION: mucosal lossGVHDDIVERTICULITIS
  13. 13. INVx of acute caseStool examn: Ova (helminths – adhere mild), cyst (E. histolytica), WBC (inf. + 2 non-inf.), RBC (severe invasive), antigen (Rotavirus)USG Abdomen: reveals bunch of helminthsSerology: Abs seen in blood (E. histolytica)
  14. 14. M/m of acute case90% self-limitingESSENTIAL T/t – REHYDRATIONOral hydration suffices in most casesI.V. Fluids – NS may be preferred when BP low and low perfusion (chances of acidosis)RL – when K+ low
  15. 15. M/m of acute case10% need additional therapyANTI-MOTILITY – used when mild inflammation or non-infective, reduce water loss(given when no fever, non-RBC diarrhoea, moderate to severe dehydration) CHANCES OF RUPTURE OF INTESTINE IF SEVERE INVASIVE DIARRHOEA
  16. 16. ROLE OF ANTI-BIOTICSTemperature > 38.5 celsius(indicates mucosal invasion & has entered systemic circulation, severe)Presence of WBC/RBC (moderate- severe)Extremes of age (infants or > 65 yrs) – chances of septicemia
  17. 17. ROLE OF ANTI-BIOTICSNo improvement in 48 hoursIMMUNOCOMPROMISED (eg HIV) – coz in them diarrhoea can be a sign of septicemiaPatients of mechanical heart valves (I.E.-SEPTICEMIA-DIARRHOEA)New outbreak in community (to prevent spread)
  18. 18. CHRONIC DIARRHOEA
  19. 19. Chronic DiarrhoeaMore than 4 weeks duration90% non-infectiousOnly 10% infectiousClassified according to mechanism of diarrhoea
  20. 20. 1. SECRETORYDue to derangement of fluid & electrolyte transport across enterocytesEither failure to resorb or hypersecretion into lumen (Na+, K+, water)WATERY STOOLSPAINLESS DIARRHOEA
  21. 21. 1. SECRETORYPersists with FASTING (independent of oral intake)Low/absent stool osmolal gapStool Osmolal gap= Expected – calculated290-{cations+anions})290-2(cations)290-2(Na+K)
  22. 22. CausesInfectionsChronic alcoholHormonesIntestinal resectionSub-acute obstructionAddison’s diseaseStimulant laxatives
  23. 23.  INFECTIONS – Chronic Shigella infection destroys mucosal cells CHRONIC ALCOHOL damages enterocytes and their functions INTESTINAL RESECTION – after surgery, decreased area for reabsorption of Na & K SAIO – Proximal part has compensatory increase in peristalsis and more secretion. Therefore may have increased bowel motion
  24. 24.  STIMULANT LAXATIVES – Biscodyl, Senna, Castor oil - They irritate mucosa and cause hypersecretion ADDISON’S DISEASE – aldosterone deficiency HORMONAL - VIPoma - ZES (increased HCl due to increased gastrin damages cells, also volume of acid more, presents as secretory diarrhoea)
  25. 25.  HORMONAL- Calcitonin (Medullary thyroid Ca)- Histamine (Mastocytosis)- Prostaglandins (Villous adenoma of colon) – also causes severe hypo K+- Serotonin (Carcinoid)NOTE: Niacin is needed to form tryptophan. In case of pellagra, the intermediates are unable to form tryptophan and are converted to serotonin.THEREFORE, SECRETORY DIARRHOEA IN PELLAGRA
  26. 26. NOTE – SOMATOSTATIN INHIBITS INTESTINALSECRETIONSTHEREFORE,SOMATOSTATINOMADOESN’T CAUSE DIARRHOEA
  27. 27. 2. OSMOTICDue to presence of osmotically active agent in lumen which draws H20 leading to diarrhoeaDue to water drawn into the lumen, distension – PAINFUL DIARRHOEAStops with FASTINGStool osmolal gap increased
  28. 28. CausesOsmotic Laxatives (MgSO4 or Al containing) – Mild action, so more abuse potential than stimulants (which cause severe irritation)LACTASE DEFICIENCY (“MILK INTOLERANCE”/ “MILK ALLERGY”)Lactose not broken down and therefore no absorption..
  29. 29. CausesNon-absorbable carbohydrate in lumen. Eg:- LACTULOSE (used in hep.enceph)- SORBITOL (in sugar-free syrups)
  30. 30. 3. STEATORRHEAStool fat excretion > 6%MC manifestation of any malabsorptionClinically – BULKY, FOUL- SMELLING, GREASY/OILY STOOLS, HARD TO WASH AWAYCauses:- Any cause of lipid malabsorption
  31. 31. INTRALUMINAL PHASE DEFECTSLIPASE DEFECT:- Deficiency (chronic pancreatitis) Inactivation of lipase (in acidic medium like ZES)
  32. 32. INTRALUMINAL PHASE DEFECTSIMPAIRED MICELLE FORMATION Decreased bile synthesis (cirrhosis) Decreased bile secretion – intrahepatic (PBC) or extrahepatic (stricture, tumor, stone in CBD) Deconjugation of bile – bacteria in duodenum (BOGS) Defective enterohepatic circulation in disease of ileum – bile salts lost (TB, Crohn’s, Tropical sprue)
  33. 33. MUCOSAL PHASE DEFECT Mucosal loss (no re-esterification)Eg:- Celiac sprue Deficiency of lipoprotein (chylomicrons not formed)Eg:- Abetalipoproteinemia
  34. 34. DEFECT OF LYMPHATICS Tumour, TB, Filariasis (fat not absorbed - lost in urine – CHYLURIA) Congenital (lymphatics not functional) Eg:- intestinal lymphangiectasias
  35. 35. 4. INFLAMMATORYMECHANISMS:Exudation of leukocytesIncreased secretion due to PGsIncreased motility due to cytokines (like IL-2) released from inflammatory cellsCLASSICAL TRIAD OF FEVER, PAIN & BLOOD IN STOOLS
  36. 36. CausesIBD (UC, Crohn’s d/s)Eosinophilic gastroenteritis (deposits of eosinophils in sub- mucosa)Chronic GVHDChronic radiation
  37. 37. 5. DYSMOTILITY DIARRHOEADue to rapid transit time or increased intestinal motilityEg 1:- due to nerves (autonomic neuropathy as in diabetes mellitus)Eg2:- due to hormones (hyperthyroidism)
  38. 38. 6. FACTITIOUS DIARRHOEAOften due to osmotic laxatives (self-induced)Commonly seen in young females and students
  39. 39. INVxStool osmolal GapHormonal assays (serum gastrin levels, calcitonin)Stool pH (acidic if lactose in stools, but alkaline if due to laxatives like MgSO4)72 hour stool fat quantitative testTFT, Blood sugar

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