Intestinal Electrolyte & Water Absorption Flashcards
function organization of villus in the small intestine
*villi = absorptive zone
-brush border hydrolases
-solute & nutrient transporters
-low water permeability
*crypts = secretory zone
-little nutrient permeabiity
-high water permeability
the villus of the small intestine as an anatomic unit of absorption
*interior of villus contains network of blood vessels and a central lacteal (vessel for absorption of lymph)
*also contains actin filaments that rhythmically contract to cause microvillus movement that promotes absorption
general principles of intestinal electrolyte/water absorption and secretion
*water absorption in the small intestine is PASSIVE
*dependent on absorption of ions (Na+ and Cl-) and solutes (sugars, amino acids) into basolateral space
*water moves passively into the basolateral space to keep it isosmotic with plasma
*water enters capillaries along hydrostatic gradient
mechanisms of sodium absorption in the small intestine
*main driving force for water ABSORPTION
*proximal gut: Na+/H+ exchange & Na+/solute co-transport
*distal gut: coupled Na+/Cl- absorption & Na+ channels
mechanisms of chloride absorption in the small intestine
*whole gut: PD-dependent Cl- transport
*distal gut: coupled Na+/Cl- absorption & HCO3-dependent Cl- absorption
mechanisms of chloride secretion via CFTR in small intestine
*main driving force for water SECRETION
- serosal Na+/K+/Cl- cotransporter loads cells with chloride ions
- Na+ ions are pumped back out
- CFTR is an apical Cl- gate and channel
- multiple extracellular signals can open CFTR via cAMP and PKA (lets chloride OUT of the cells)
- Na+ ions passively follow Cl- ions via paracellular pathways
- water passively follows the increased flux of Cl- and Na+ ions (water exiting the cell)
mechanisms of potassium absorption in the small intestine
*proximal gut: driven by H2O absorption
*distal gut: active transport
mechanisms for potassium secretion in the gut
*mainly in the COLON
*active & passive transport
factors that stimulate electrolyte secretion and absorption in the small intestine
- circulating hormones
- enteroendocrine cells
- enteric neurons
- mast cells
- macrophages
diarrhea
*increase in the VOLUME & FREQUENCY of bowel movements with a change in the consistency of the stools
chronic diarrhea
sx lasting more than one month
etiologies of diarrhea
- infectious/inflammatory
- osmotic
- dysmotility
- secretory
infectious/inflammatory etiology of diarrhea
disruption of epithelial tight junctions allows electrolytes and water into lumen
osmotic etiology of diarrhea
presence of malabsorbed or non-absorbable osmoles keeps water in lumen
dysmotility etiology of diarrhea
decreased transit time through the gut lumen impairs effective absorption
secretory etiology of diarrhea
increased H2O entry into lumen due to increased Cl- or HCO3- secretion or decreased Na+ absorption
general history questions for diarrhea
- onset (acute/sudden vs. gradual)
- character
-consistency (soft, mushy, liquid)
-average # of stools/day
-volume - pattern
-continuous vs. intermittent
-postprandial
-nocturnal
examples of causes of infectious diarrhea
*invasive bacterial infections (salmonella, shigella, campylobacter, yersinia)
*bacterial toxins (C. diff, S. Aureus, toxigenic E. coli)
*enteropathic viral infections (rotavirus; norwark virus)
*parasites (giardia, cryptosporidium, etc)
history clues for infectious diarrhea
*recent travel or camping trips
*onset after meal at restaurant, outing, communal meal
*handling or consumption of raw or undercooked meats, poultry, seafood
*recent use of antibiotics (risk for C. diff)
*children in daycare
*use of well water
examples of causes of osmotic diarrhea
*ingestion of non-absorbable osmoles (Mg++ containing antacids; sugar alcohols)
*disaccharide malabsorption (lactase deficiency, fructose intolerance)
*selective fat malabsorption (gastric resection/bypass, pancreatic insufficiency, bile salt deficiency)
*global malabsorption (short bowel syndrome, mucosal diseases)
history clues for osmotic diarrhea
*use of Mg++ containing antacids
*ingestion of sugar alcohols (sugar free syrups, candies, gums)
*ingestion of dairy products
*GI surgery (RYGB, cholecystectomy)
*pancreatic disease
examples of causes of secretory diarrhea
*toxins (E. coli, CHOLERA, other vibrios)
*drugs (antroquinone laxatives, misoprostol, etc)
*bile salts (post-cholecystectomy, s/p ileal resection, SIBO)
*GI endocrine tumors
cholera & secretory diarrhea
*cholera toxin A irreversibly activates adenylate cyclase, increasing cAMP levels
*activates Cl- secretion via CFTR; Cl- pours out of enterocytes
*Na+ passively follows Cl-
*water passively follows the increased flux of Cl- and Na+
*cholera patients may produce up to 20 L/day of watery stool
*cholera toxin also inhibits non-nutrient Na+ and Cl- absorption by villus cells
note - solute-coupled Na+ absorption remains intact!
history clues for secretory diarrhea
*high volume, watery diarrhea
*NOCTURNAL DIARRHEA
*syncope, hypotension
*ER visits for rehydration
*hypokalemia
*hx of longstanding diabetes
examples of causes of dysmotility diarrhea
*increased motility (gastric bypass surgery, post-vagotomy, ileal or IC valve resection, hyperthyroidism)
*decreased motility (diabetic enteropathy, scleroderma, etc)
approach for diagnosis of chronic diarrhea
*stool analysis
*celiac & IBD serology
*endoscopy & biopsy
*radiology
*hydrogen breath tests
MOA for oral rehydration therapy (in tx of cholera, etc)
solute-coupled Na absorption with glucose
