You are on page 1of 1

PATHOPHYSIOLOGY OF CHOLERA

Precipitating (modifiable):
Predisposing (non-modifiable):  Long-term antacid use
 Poverty  Improper sanitation
 Environment  Improper food handling
 Blood type O  Malnutrition

Ingestion of food contaminated with V. cholerae

Goes to stomach

Mostly: killed by acidity of the stomach Some: survives and colonize small intestine

Produces enterotoxins (exotoxin)

Destruction and irritation of mucosal B subunits of V. cholerae binds to GM1


lining of small intestine ganglioside receptors (G-protein receptors)

TENESMUS Hyperactive BS
A subunit is released into the cell

Altered bleeding ulceration Abdominal


digestion & cramps Stimulates adenylate cyclase
reabsoption

weakness
cAMP

Inhibits Na+ and Cl- absorption by microvilli Secretion of Cl- by the crypt cells

Water goes out from cell to “rice-watery”


intestinal lumen DIARRHEA

Fluid & electrolyte imbalance Dry skin


Poor skin turgor
Dry mouth, tongue
Sunken, glassy eyes
Dehydration Cold-clammy
stupor

Hypovolemic shock Decreased circulating blood volume

HypoTachyTachy

Decreased renal perfusion

Renin release Decreased GFR

Combines with angiotensinogen Decreased urine output

Angiotensin I

Angiotensin I to Angiotensin II by ACE

vasoconstriction Aldosterone secretion ADH secretion

@farr_awaaaay

You might also like