1. DIARRHOEA

2. DIARRHOEAIncrease in FREQUENCY, LIQUIDITY, VOLUME of stoolsStool weight more than/equal to 200 gm/day (western diet) or 450 gm/day (indian diet) 3. PSEUDO-DIARRHOEAIncreased frequency but with NORMAL VOLUMESeen due to local inflammation of rectum (IBS, proctitis)Patient passes small but frequent stools 4. TYPES OF DIARRHOEAACUTE: less than 2 weeksPERSISTENT: 2-4 weeksCHRONIC: more than 4 weeks 5. ACUTE DIARRHOEA 6. CAUSES90% INFECTIOUS !!!10% NON-INFECTIOUS 7. INFECTIOUS CAUSESTOXIN-INDUCED: No inflammation, no RBCs/WBCs in stools)INFLAMMATION OF BOWEL WALL: May have RBCs or/and WBCs in stools 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. INFLAMMATORY DIARRHOEA MILD Usually viral (Rota, Norwalk)No WBC/RBC in stools MODERATE Superficial mucosalinflammation and involvement. Noinvasion. Bacterial mostly. WBCpresent in stool. No RBC(Salmonella, Campylobacter, CMV,Vibrio parahemolyticus) 10. INFLAMMATORY DIARRHOEA SEVERE (INVASIVE) Invasion ofmucosal wall present. Both WBCsand RBCs (dyssentery) present instoolsExamples Shigella, EIEC- Entamoeba histolytica(invades mucosal wall and causesflasked shaped ulcers) 11. NON-INFECTIOUSCAUSESDRUGS: antibiotics, laxatives, NSAIDs, antacids, anti-HTn, theophyllinesTOXINS: Arsenic, Mushroom (Amanita), Organophosphates (stimulate Ach insecticides) 12. NON-INFECTIOUS CAUSESISCHAEMIC COLITIS: due to lack of blood supply mucosal loss therefore WBCs and RBCs in stoolRADIATION: mucosal lossGVHDDIVERTICULITIS 13. INVx of acute caseStool examn: Ova (helminths adhere mild), cyst (E. histolytica), WBC (inf. + 2 non-inf.), RBC (severe invasive), antigen (Rotavirus)USG Abdomen: reveals bunch of helminthsSerology: Abs seen in blood (E. histolytica) 14. M/m of acute case90% self-limitingESSENTIAL T/t REHYDRATIONOral hydration suffices in most casesI.V. Fluids NS may be preferred when BP low and low perfusion (chances of acidosis)RL when K+ low 15. M/m of acute case10% need additional therapyANTI-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. ROLE OF ANTI-BIOTICSTemperature > 38.5 celsius(indicates mucosal invasion & hasentered systemic circulation,severe)Presence of WBC/RBC (moderate-severe)Extremes of age (infants or > 65yrs) chances of septicemia 17. ROLE OF ANTI-BIOTICSNo improvement in 48 hoursIMMUNOCOMPROMISED (eg HIV) coz in them diarrhoea can be a sign of septicemiaPatients of mechanical heart valves (I.E.-SEPTICEMIA-DIARRHOEA)New outbreak in community (to prevent spread) 18. CHRONIC DIARRHOEA 19. Chronic DiarrhoeaMore than 4 weeks duration90% non-infectiousOnly 10% infectiousClassified according to mechanism of diarrhoea 20. 1. SECRETORYDue to derangement of fluid & electrolyte transport across enterocytesEither failure to resorb or hypersecretion into lumen (Na+, K+, water)WATERY STOOLSPAINLESS DIARRHOEA 21. 1. SECRETORYPersists 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. CausesInfectionsChronic alcoholHormonesIntestinal resectionSub-acute obstructionAddisons diseaseStimulant laxatives 23. INFECTIONS Chronic Shigellainfection destroys mucosal cells CHRONIC ALCOHOL damagesenterocytes and their functions INTESTINAL RESECTION aftersurgery, decreased area forreabsorption of Na & K SAIO Proximal part has compensatoryincrease in peristalsis and moresecretion. Therefore may haveincreased bowel motion 24. STIMULANT LAXATIVES Biscodyl,Senna, Castor oil - They irritate mucosa and causehypersecretion ADDISONS DISEASE aldosteronedeficiency HORMONAL - VIPoma - ZES (increased HCl due to increasedgastrin damages cells, also volume ofacid more, presents as secretorydiarrhoea) 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. NOTE SOMATOSTATIN INHIBITS INTESTINALSECRETIONSTHEREFORE,SOMATOSTATINOMADOESNT CAUSE DIARRHOEA 27. 2. OSMOTICDue to presence of osmotically active agent in lumen which draws H20 leading to diarrhoeaDue to water drawn into the lumen, distension PAINFUL DIARRHOEAStops with FASTINGStool osmolal gap increased 28. CausesOsmotic 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. CausesNon-absorbable carbohydrate in lumen. Eg:- LACTULOSE (used in hep.enceph)- SORBITOL (in sugar-free syrups) 30. 3. STEATORRHEAStool fat excretion > 6%MC manifestation of any malabsorptionClinically BULKY, FOUL- SMELLING, GREASY/OILY STOOLS, HARD TO WASH AWAYCauses:- Any cause of lipid malabsorption 31. INTRALUMINAL PHASEDEFECTSLIPASE DEFECT:- Deficiency (chronic pancreatitis) Inactivation of lipase (in acidicmedium like ZES) 32. INTRALUMINAL PHASEDEFECTSIMPAIRED MICELLE FORMATION Decreased bile synthesis (cirrhosis) Decreased bile secretion intrahepatic(PBC) or extrahepatic (stricture, tumor,stone in CBD) Deconjugation of bile bacteria induodenum (BOGS) Defective enterohepatic circulation indisease of ileum bile salts lost (TB,Crohns, Tropical sprue) 33. MUCOSAL PHASE DEFECT Mucosal loss (no re-esterification)Eg:- Celiac sprue Deficiency of lipoprotein (chylomicrons not formed)Eg:- Abetalipoproteinemia 34. DEFECT OF LYMPHATICS Tumour, TB, Filariasis (fat not absorbed - lost in urine CHYLURIA) Congenital (lymphatics not functional) Eg:- intestinal lymphangiectasias 35. 4. INFLAMMATORYMECHANISMS:Exudation of leukocytesIncreased secretion due to PGsIncreased motility due to cytokines (like IL-2) released from inflammatory cellsCLASSICAL TRIAD OF FEVER, PAIN & BLOOD IN STOOLS 36. CausesIBD (UC, Crohns d/s)Eosinophilic gastroenteritis (deposits of eosinophils in sub- mucosa)Chronic GVHDChronic radiation 37. 5. DYSMOTILITYDIARRHOEADue to rapid transit time or increased intestinal motilityEg 1:- due to nerves (autonomic neuropathy as in diabetes mellitus)Eg2:- due to hormones (hyperthyroidism) 38. 6. FACTITIOUS DIARRHOEAOften due to osmotic laxatives (self-induced)Commonly seen in young females and students 39. INVxStool osmolal GapHormonal 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 testTFT, Blood sugar