1. Diarrhoea can be acute (<2 weeks), persistent (2-4 weeks), or chronic (>4 weeks). Acute diarrhoea is usually infectious and caused by toxins or intestinal inflammation. 2. Chronic diarrhoea is usually non-infectious and can be secretory, osmotic, inflammatory, due to dysmotility, or factitious. Common causes include infections, medications, lactose intolerance, IBD, thyroid disorders, and laxative abuse. 3. Evaluation involves stool tests to identify infectious causes or evaluate for malabsorption, and blood tests to check for hormonal or metabolic abnormalities underlying chronic diarrhoea.

1. DIARRHOEA

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. PSEUDO-DIARRHOEA
Increased frequency but with
NORMAL VOLUME
Seen due to local inflammation
of rectum (IBS, proctitis)
Patient passes small but
frequent stools

4. TYPES OF DIARRHOEA
ACUTE: less than 2 weeks
PERSISTENT: 2-4 weeks
CHRONIC: more than 4 weeks

5. ACUTE DIARRHOEA

6. CAUSES
90% INFECTIOUS !!!
10% NON-INFECTIOUS

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. 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 mucosal
inflammation and involvement. No
invasion. Bacterial mostly. WBC
present in stool. No RBC
(Salmonella, Campylobacter, CMV,
Vibrio parahemolyticus)

10. INFLAMMATORY
DIARRHOEA
• SEVERE (INVASIVE) – Invasion of
mucosal wall present. Both WBCs
and RBCs (dyssentery) present in
stools
Examples – Shigella, EIEC
- Entamoeba histolytica
(invades mucosal wall and causes
flasked shaped ulcers)

11. NON-INFECTIOUS
CAUSES
DRUGS: antibiotics, laxatives,
NSAIDs, antacids, anti-HTn,
theophyllines
TOXINS: Arsenic, Mushroom
(Amanita), Organophosphates
(stimulate Ach – insecticides)

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. 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. 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. 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. 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. 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. CHRONIC DIARRHOEA

19. Chronic Diarrhoea
More than 4 weeks duration
90% non-infectious
Only 10% infectious
Classified according to mechanism
of diarrhoea

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. 1. SECRETORY
Persists with FASTING
(independent of oral intake)
Low/absent stool osmolal gap
Stool Osmolal gap=
Expected – calculated
290-{cations+anions})
290-2(cations)
290-2(Na+K)

22. Causes
Infections
Chronic alcohol
Hormones
Intestinal resection
Sub-acute obstruction
Addison’s disease
Stimulant laxatives

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.  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.  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 INTESTINAL
SECRETIONS
THEREFORE,
SOMATOSTATINOMA
DOESN’T CAUSE DIARRHOEA

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. 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. Causes
Non-absorbable carbohydrate in
lumen. Eg:
- LACTULOSE (used in hep.enceph)
- SORBITOL (in sugar-free syrups)

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

32. INTRALUMINAL PHASE
DEFECTS
LIPASE DEFECT:-
 Deficiency (chronic pancreatitis)
 Inactivation of lipase (in acidic
medium like ZES)

33. INTRALUMINAL PHASE
DEFECTS
IMPAIRED 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)

34. MUCOSAL PHASE DEFECT
 Mucosal loss (no re-esterification)
Eg:- Celiac sprue
 Deficiency of lipoprotein
(chylomicrons not formed)
Eg:- Abetalipoproteinemia

35. DEFECT OF LYMPHATICS
 Tumour, TB, Filariasis (fat not
absorbed - lost in urine –
CHYLURIA)
 Congenital (lymphatics not
functional) Eg:- intestinal
lymphangiectasias

36. 4. INFLAMMATORY
MECHANISMS:
Exudation of leukocytes
Increased secretion due to PGs
Increased motility due to cytokines
(like IL-2) released from
inflammatory cells
CLASSICAL TRIAD OF FEVER,
PAIN & BLOOD IN STOOLS

37. Causes
IBD (UC, Crohn’s d/s)
Eosinophilic gastroenteritis
(deposits of eosinophils in sub-
mucosa)
Chronic GVHD
Chronic radiation

38. 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)

39. 6. FACTITIOUS
DIARRHOEA
Often due to osmotic laxatives
(self-induced)
Commonly seen in young females and
students

40. 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