Flashcards in diarrhea Deck (98):
which NT are released by enteric neurons?
VIP and Ach. both stimulate epithelial cells to secrete chloride
what are 2 other secretagogues that are released from local enteroendocrine cells
what do bile salts do to secretion?
what does aldosterone do to the gut?
increases expression of transporters for Na reabsorption
what effect does increased motility have on absorption
what effect does inflammation have on absorption
it increases secretion and decreases absorption
definition of acute diarrhea
less than 4 weeks
what is the typical clinical course of viral or bacterial diarrhea?
self-limited of lecithin 7 day
what is the most likely cause of infectious diarrhea that lasts longer than 7 days
is chronic diarrhea likely to be infectious?
how is osmotic diarrhea classified
increased osmotic load tot eh intestines decreases the absorptive capacity because of gradient. there is NO increased secretion. if the osmotic load is not presented to the intestines then there is no diarrhea. t
what syndromes cause an osmotic diarrhea
malabsorption and maldigestion. there are typically no nocturnal episodes.
how to calculate the osmolar gap of the feces
stool gap: 290 - 2x (Na + K)
what if the stool osmolar gap is < 50 and the Na+ > 90
what if the stool osmolar gap is >125 and the stool Na <60
what are the two disorders that are characteristic of endogenous osmotic diarrhea caused by intraluminal maldigestion?
cholestasis and pancreatic insufficiency
what are the two things that can cause endogenous osmotic diarrhea due to mucosal malabsoprtion
enteropathies and rugs
what can cause exogenous osmotic diarrhea with post mucosal obstruction
what is characteristic of cholestasis?
decreased bile salts and fat malabsoprtion
what is characteristic of pancreatic insufficiency
maldigestion/malabsoprtion of carbohydrates and lipids
celiac diease, lactose intolerance, infections
gluten enteropathy that causes mucosal inflammation in the proximal bowel. there is villous atrophy and decreased surface area for absorption
decreased lactase in surface absorptive cells. the lactose load causes fermentation and thus an increase in the osmotic load.
how do infections cause enteropathies
damage to the brush border causes malabsorption. giardia, cryptosporidium, isospora, strongyloides, MAI, rotavirus.
infiltrate that causes lymphatic obstruction that causes lymphangiectasia
rapid intestinal transit causes malabsorption
what happens in small bacterial overgrowths
deconjugation of bile salts leads to steatorrhea, there is carbohydrate malabsorption, protein malabsorption, and altered bowel motility
where is bicarb secretion most prominent and what is the mechanism
in the proximal duodenum and is an electroneutral mechanism with chloride. through the CFTR channels.
what stimulates carbonate secretion?
cAMP, cGMP, calcium
what causes secretory diarrhea
when there is an increased chloride secretion resulting in fluid losses exceeding absorptive capacity
what are the causes of secretory diarrhea
can be infectious or non. usually not related to food intake because there are nocturnal episodes seen.
what is the stool osmolar gap in secretory diarrhea
what are the clinical syndromes
hypokalemia and hypochlorydia
what tumors can cause secretory diarrhea.
VIPoma, medullary carcinoma of the thyroid, systemic mastocytosis, villous adenoma, gastrinoma (zollinger-ellison syndrome)
bile salt diarrhea caused by what. what two syndromes of BSD does this cause? what are their mechanisms
disease or resection of the terminal ileum. causes 2 different syndromes of BSD 1.) decreased bile acid absorption and pool leading to fat malabsorption and steatorrhea 2.) there is increased bile salt acid delivered to the colon which induces a secretory diarrhea.
what are the labs for decreased bile acid absorption and pool?
serum bile acids are low, fecal bile acids are low. stool + fat.
what are the labs when there is increased bile salt acid delivered tot he colon?
serum bile acids will be normal and the fecal bile acids will be high
how do we diagnose bile salt diarrhea?
C-triolein breath test
what is bile salt diarrhea treated with?
what does inflammation do to cause diarrhea?
affects the mucosal integrity and transport proteins. inflammatory mediators affect the secretion/reabsorption balance.
what happens to the intestine in chronic inflammation?
fibrosis and villous atrophy
what are some causes that incite inflammation in the bowel?
infection, autoimmunity, chemical, vascular.
what kinds of infectious diarrhea are there?
toxin mediated, enteroadherant, invasive.
examples of preformed exotoxins
bacillus cereus, staph aureus, clostridium perfringens
what are the two types of endotoxins?
enterotoxin and cytotoxin
which organisms are enterotoxins?
ETEC (enterotoxigenic e coli), vibrio cholera.
which organisms are cytotoxins?
C. diff, enterohemorrhagic e coli (O157:H7)
which organisms are enteroadherent?
enteropathogenic e coli, enteroadherent e coli, giardia, cryptosporidium, helminths
which organisms are minimally invasive ?
roatvirus, norwalk virus, cryptosporidium, cyclospora
which organisms are moderately invasive?
salmonella, campylobacter, vibrio parahemilyticus
which organisms are severely invasive?
shigella, enteroinvasive e coli, entamoeba histolytica
which types give the worst nausea/vomiting and diarrhea?
preformed toxins, enterotoxins and invasives.
which give the most abdominal pain
what are the invasive's known for?
fever. although can be rough in nausea/vomiting, abdominal pain, fever and diarrhea.
what are organisms that we can catch from food?
aureus, bacillus cereus, perfringens, botulinum.
s aureus, toxins? where do we get it? prognosis?
multiple enterotoxins, poultry and milk products. usually self limited
bacillus, toxins? where do we get it? prognosis?
2 toxins: causes either emesis or diarrhea. typically self-limited
what is the vomiting bacillus associated with?
chinese fried rice unrefrigerated or improperly stored rice that heated up and eaten.
what is the bacillus diarrhea associated with?
meatballs. among other products.
c. perfringens, toxins? where do we get it? prognosis?
mild-to-severe enteritis necroticans from poorly cooked pork
clostridium botulinum, toxins? where do we get it? prognosis?
preformed toxin canned food. initial nausea/vomiting, diarrhea, descending paralysis and constipation
how does v cholera toxin work?
activation of adenylate cyclase c AMP cftr and expulsion of cl-
what is the pathogenesis and result of enterotoxigenic e coli?
travelers diarrhea. there is no invasion. causes watery diarrhea through labile toxin-cAMP or heat stable gAMP activation of CFTR expelling Cl-
what is the pathogenesis and result of enteropathogenic e coli?
there is attachment and effacement. this causes watery diarrhea
who does enteropathogenic e coliusually affect?
this typically affect newborns and children
what is the pathogenesis and result of enteroaggregative e coli?
attach to enterocytes by fimbreai. intrinsic proteases disrupt the cytoskeleton and cause exfolitation. results in bloody diarrhea
who is primarily affected by enteroaggregative e coli?
children and the immunosuppressed
enterohemorrhagic e coli
most common pathogen isolated from bloody diarrhea. comes from undercooked meat such as hamburger, roar beef, salami. most important reservoir is cattle.
what are the two virulence factors of hemorrhagic e coli
adherence factors and shiga-like toxins.
what is the inoculum for hemorrhagic e coli
what is incubation period for hemorrhagic e coli
what are the clinical symptoms of hemorrhagic e coli
severe abdominal cramping, initial non bloody diarrhea, that progresses to bloody stools later.
what are additional pathologies and flow chart associated with EHEC
there is enterocyte damage from attachment and effacement; due to the production of toxins there is endothelial damage, platelet aggregation, microvascular thrombi which leads to ischemic colitis and renal dysfunction.
where is EHEC most often found on colonoscopy? what does it show?
in the right colon. segmental colitis
what does EHEC cause in children?
what is the treatment for EHEC
conservative. antibiotics have been shown to worsen the outcome probably due to the release of more toxin.
what is the most common cause of gastroenteritis in the US? what does it cause?
viral illness, causes a mixed of secretory and osmotic.
what is the most common virus? where does it infect in the body?
norwalk or norovirus. upper small intestine.
what is the most common ivirus in children?
shigella from where?
what does shigella cause?
dysentery like illness. colon and TI involved. some produce toxins.
salmonella from where?q
where does salmonella infect?
distal ileum, colon,
who is at higher risk for salmonella?
sickle cell patients
where we get campylobacter?
what does campylobacter give us/
colitis in association with GBS
what does yersinia cause
ileitis, colitis, mesenteric adenitis, pseudoappendicitis, enterotoxin.
what is the most common cause of diarrhea in practice?
spurious diarrhea from impacted stool.
how do we treat spurious diarrhea?
stool fat in mucosal disease and why?
<9.5/100g stool. this is because there is more water malabsorption so its diluted.
pancreatic disease stool fat?
>9.5 due to the fat malabsorption
what is one of the most important things in the treatment of diarrhea?
rehydration! both oral and IV are effective. oral rehydration formulas are superior to fruit juices/gatorade and colas.
second line therapy?
anti motility agents. although they are typically not given with features of toxemia such as fevers, or bloody diarrhea.
what are adsorbents?
such as bismuth or pectin bind enterotoxins has bactericidal and antiinflammatory properties.
are antibiotics recommended in O157:H7?