Intestinal Electrolyte & Water Absorption Flashcards

1
Q

function organization of villus in the small intestine

A

*villi = absorptive zone
-brush border hydrolases
-solute & nutrient transporters
-low water permeability

*crypts = secretory zone
-little nutrient permeabiity
-high water permeability

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2
Q

the villus of the small intestine as an anatomic unit of absorption

A

*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

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3
Q

general principles of intestinal electrolyte/water absorption and secretion

A

*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

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4
Q

mechanisms of sodium absorption in the small intestine

A

*main driving force for water ABSORPTION
*proximal gut: Na+/H+ exchange & Na+/solute co-transport
*distal gut: coupled Na+/Cl- absorption & Na+ channels

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5
Q

mechanisms of chloride absorption in the small intestine

A

*whole gut: PD-dependent Cl- transport
*distal gut: coupled Na+/Cl- absorption & HCO3-dependent Cl- absorption

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6
Q

mechanisms of chloride secretion via CFTR in small intestine

A

*main driving force for water SECRETION

  1. serosal Na+/K+/Cl- cotransporter loads cells with chloride ions
  2. Na+ ions are pumped back out
  3. CFTR is an apical Cl- gate and channel
  4. multiple extracellular signals can open CFTR via cAMP and PKA (lets chloride OUT of the cells)
  5. Na+ ions passively follow Cl- ions via paracellular pathways
  6. water passively follows the increased flux of Cl- and Na+ ions (water exiting the cell)
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7
Q

mechanisms of potassium absorption in the small intestine

A

*proximal gut: driven by H2O absorption
*distal gut: active transport

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8
Q

mechanisms for potassium secretion in the gut

A

*mainly in the COLON
*active & passive transport

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9
Q

factors that stimulate electrolyte secretion and absorption in the small intestine

A
  1. circulating hormones
  2. enteroendocrine cells
  3. enteric neurons
  4. mast cells
  5. macrophages
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10
Q

diarrhea

A

*increase in the VOLUME & FREQUENCY of bowel movements with a change in the consistency of the stools

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11
Q

chronic diarrhea

A

sx lasting more than one month

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12
Q

etiologies of diarrhea

A
  1. infectious/inflammatory
  2. osmotic
  3. dysmotility
  4. secretory
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13
Q

infectious/inflammatory etiology of diarrhea

A

disruption of epithelial tight junctions allows electrolytes and water into lumen

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14
Q

osmotic etiology of diarrhea

A

presence of malabsorbed or non-absorbable osmoles keeps water in lumen

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15
Q

dysmotility etiology of diarrhea

A

decreased transit time through the gut lumen impairs effective absorption

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16
Q

secretory etiology of diarrhea

A

increased H2O entry into lumen due to increased Cl- or HCO3- secretion or decreased Na+ absorption

17
Q

general history questions for diarrhea

A
  1. onset (acute/sudden vs. gradual)
  2. character
    -consistency (soft, mushy, liquid)
    -average # of stools/day
    -volume
  3. pattern
    -continuous vs. intermittent
    -postprandial
    -nocturnal
18
Q

examples of causes of infectious diarrhea

A

*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)

19
Q

history clues for infectious diarrhea

A

*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

20
Q

examples of causes of osmotic diarrhea

A

*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)

21
Q

history clues for osmotic diarrhea

A

*use of Mg++ containing antacids
*ingestion of sugar alcohols (sugar free syrups, candies, gums)
*ingestion of dairy products
*GI surgery (RYGB, cholecystectomy)
*pancreatic disease

22
Q

examples of causes of secretory diarrhea

A

*toxins (E. coli, CHOLERA, other vibrios)
*drugs (antroquinone laxatives, misoprostol, etc)
*bile salts (post-cholecystectomy, s/p ileal resection, SIBO)
*GI endocrine tumors

23
Q

cholera & secretory diarrhea

A

*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!

24
Q

history clues for secretory diarrhea

A

*high volume, watery diarrhea
*NOCTURNAL DIARRHEA
*syncope, hypotension
*ER visits for rehydration
*hypokalemia
*hx of longstanding diabetes

25
Q

examples of causes of dysmotility diarrhea

A

*increased motility (gastric bypass surgery, post-vagotomy, ileal or IC valve resection, hyperthyroidism)
*decreased motility (diabetic enteropathy, scleroderma, etc)

26
Q

approach for diagnosis of chronic diarrhea

A

*stool analysis
*celiac & IBD serology
*endoscopy & biopsy
*radiology
*hydrogen breath tests

27
Q

MOA for oral rehydration therapy (in tx of cholera, etc)

A

solute-coupled Na absorption with glucose