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)
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)
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)
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
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..
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.
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