Non-infectious Diarrhea

Question 1

Difference btwn acute & chronic non-infectious diarrhea?

Answer 1

acute: < 4 weeks, chronic > 4 wks

Question 2

If non-infectious diarrhea is large volume where is the damage likely coming from & why?
What kind of bowel movements would these patients have?

Answer 2

SI b/c it does most of the water absorption

they’d have large, painless diarrhea

Question 3

Which would improve with fasting, osmotic or secretory non-infectious diarrhea?

Answer 3

osmotic improves w/ fasting

Question 4

what’st he mechanism for secretory diarrhea?

Answer 4

there’s a net secretion of anions (chloride or bicarb) or net inhibition of sodium absorption

Question 5

What’s the MC cause of secretory diarrhea? specifics about that?

Answer 5

Enterotoxins produced by bacteria like cholera, E coli and shigella

Question 6

Other than enterotoxins, what 3 other things can cause secretory diarrhea?

Answer 6

1. peptides like gastrin, VIP & 5-hydroxytrytamine (5-HT)
2. Loss of absorptive surface like in short bowel syndrome, celiac sprue or IBD
3. Rapid intestinal motlility like in IBS or hyperthyroidism

Question 7

what’s VIP and how’s it involved in secretory diarrhea?

Answer 7

Vasoactive Intestinal Peptide

NT in peripheral & central NS that causes secretion of Cl and bicarb by intestinal epithelia

Question 8

What’s VIPoma? what’s another name for it? what’s the common SE?

Answer 8

tumor that secretes VIP leads to loss of bicarb (decreasing pH) in stool water leading to metabolic acidosis, assoc w/ 1-3 L stools/day w/ dehydration

Aka Watery diarrhea hypokalemia achlorhydria (WDHA) syndrome
S/S: Hypokalemia: colon preserves sodium (to try and compensate for fluid loss from SI) but loses K in exchange

Question 9

What can cause non-infectious osmotic diarrhea? (4 things)

Answer 9

ingestion of :

1. cations
2. anions
3. sugars (like dissacharides like lactose)
4. sugar alcohols like sorbitol that’s in sugar free foods

Question 10

what’s the MOA of non-infectious osmotic diarrhea?

Answer 10

ions overwhelm the system & saturate their transporters so draws water out to equalize

Question 11

what kind of saccharides can and can’t be absorbed?

Answer 11

Monosaccharides can be aborbed

Diassacharides cannot so need disaccharidases to break them down

Question 12

where is lactase located? what happens w/ its deficiency?

Answer 12

brush border of SI cells

can’t break lactose into glucose and galactose so can’t absorb lactose leading to osmotic diarrhea

Question 13

Which would have electrolyte imbalance, osmotic or secretory non-infectious diarrhea?

Answer 13

secretory diarrhea

Question 14

whats the stool osmotic gap and what do you use it for?

Answer 14

290 mOsm/kg - 2(Na+K) (stool levels)
use it to determine secretory vs osmotic diarrhea
Small osmotic gap < 50: secretory diarrhea (b/c large secretion of Na & K in stool)
large osmotic gap > 100: osmotic diarrhea

Question 15

what’s the difference btwn maldigestion and malabsorption? what could they lead to?

Answer 15

Maldigestion: pancreatic exocrine insufficiency and lack of bile (like in chronic pancreatitis or CF) lead to inability to breakdown food
Malabsorption: mucosal diseases (like Celiac) likes to inability to absorb nutrients
they could lead to steatorrhea

Question 16

what’s the MC cause of steatorrhea & when would it occur? what else might you see with it?

Answer 16

pancreatic insufficiency but not until only 10% or < of pancreas function is left
might also see weight loss (malabsorption of fat) and fat soluble vit deficiency (vit A, D, E & K)

Question 17

what are 3 ways to test for pancreatic insufficiency?

Answer 17

1. stool test - qualitative or quantitative fecal fat
2. secretin stimulation test - secretin stimulates pancreas, aspirate duodenal contents & measure bicarb output (rarely performed b/c complex)
3. fecal elastase activity

Question 18

what’s Celiac sprue?
what would it lead to?
what would an endoscopy & histo loop like?

Answer 18

autoimmune disorder occurs w/ ingestion of gluten (Ab against gliadin and tissue transglutaminase)
Leads to SI inflammation, vili atrophy and malabsorption
Scope would see scaloped duodenal folds; histo: inflammation, decreased pili & hyperplastic crypts

Question 19

how would celiac present in childhood?

Answer 19

failure to thrive, hypotonia, abd distension

Question 20

how would celiac present in adulthood?

Answer 20

diarrhea, bloating, dermititis herpetaformis (vesicular lesions, puritic), iron def anemia (b/c prox SI), osteopenia

Question 21

when would bile acid induce diarrhea?

Answer 21

w/ ileal resection or disease b/c of loss of transporters leads to increased bile acid in colon > 3-5 mmol/L which can inhibit electrolyte absorption and stimulate secretion

Question 22

what’s microscopic colitis and what are the 2 main types?

Answer 22

histologic chronic mucosal inflammation w/ gross healthy looking colonic mucosa
2 types: collagenous colitis and lymphocytic colitis

Question 23

What’s collagenous colitis? what can cause it?

what would histo look like?

Answer 23

type of microscopic colitis
Cause: NSAIDs, SSRIs
Histo: irregularly thickened subepithelial collagen bands & mixed inflam cells (lymph, plasma & eosinophils) in lamina propria

Question 24

what’s lymphocytic colitis? what can cause it?

what would histo look like?

Answer 24

type of microscopic colitis
Cause: SSRIs, BBs, bisphosphonates, statins
Histo: increased intraepithelial lymphocytes w/ no mucosal architectural distortion

Question 25

what’s the Rome III criteria for IBS?

Answer 25

recurrent abd pain at least 3 days/mo in last 3 mo assoc w/ 2+ of the following:

1. improved w/ defecation
2. onset assoc w/ change in stool frequency
3. onset assoc w/ change in stool form (appearance)

Question 26

what’s the different categories for IBS?

Answer 26

1. diarrheal predom IBS (loose/watery stools > 25% & hard < 25%)
2. Constipation predom IBS (hard > 25%, loose < 25%)
3. Mixed IBS - hard & loose both > 25%)

Question 27

what are the 4 important afferent inputs to the vomiting center?

Answer 27

1. Chemoreceptor trigger zone (postrema): in 4th ventricle, outside BBB, D2, opoids, & seratonin, NK1 receptors
2. Vestibular: motion sickness via CN 8, M1, H1 receptors
3. GI: vagal & spinal afferents, seratonin receptors, GI mucosal irritation by chemo, radiation, distension, infection leads to serotonin release for vagal afferent input into vomtingchenter & chemoreceptor trigger zone
4. CNS: psychiatric, stress and anticipatory vomiting

Question 28

where is the vomiting center located?

Answer 28

nucleus of tractus solitarius in the medulla