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