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66 Cards in this Set

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  • Back
What four congential abnormalities can you have in gut formation?
Omphalacele, gastrochises, malroation and duplication.
Which is more common atresia in an infant (of bowel) or stenosis?
Atresia is actually more common. With stenosis, lesions tend to occur from developmental failure, intrauterine vascular accidents, or intusssusceptions.
Failure of cloacal diaphgram to rupture gives you an imperforate anus.
What causes a meckel diverticulum?
Failure of involution of the viteline duct.
What defines hirschprungs, what are the two different types, what can you see?
No aurbuch's or meissner's plexus. Variable length is not innervated, in long segment disease can be up to entire intestine. There is familial inheritance. Most cases involve the rectum and sigmoid only.

You see proximal to the anganglionic segment, progressive dilation and hypertrophy,begining with the descending colon, sometimes getting to megacolon (15-20cm).
You can get mucosal inflammation when you have thinning.

You stain with Ach for the ganglions.

Males predominane 4:1.

10% of cases are kids with downs.

Neurological abnormalities with 5%.
What should you think when you see megacolon?
chagas, (the trypanasomes destroy the neurons of the bowel), organic obstruction of the bowel, toxic megacolon with IBD, or a functional psychosomatic disorder.
Which virus can look like celiac sprue?
Rotavirus, causes flattening of the villi.
What are the different mechanisms of enterocolitis?
You can have epithelial cell damage, you can have preformed toxins that act quickly, you can have toxigenic organisms which proliferate then give off an enterotoxin, you can have infection by enteroinvasive organisms which destroy the cells.
Other than toxins, how else can the bacteria destroy the epithelium?
They can destroy the epithelium by adhering to the mucosa.
What organisms do you have put out enterotoxins and what are two kinds.
Enteroxins, cause diarrhea and include cholera toxin and heat labile toxin from ETEC. These cause a secretory diarrhea. The shiga toxin and EHEC cause diret tissue damage.

Staph causes cytokine release.
How does EHEC and shigella cause diarrhea?
It causes direct tissue damage through a toxin which causes epithelial cell necrosis.
What kind of bacteria is shigella?
Shigella is a gram negative facultative anaerobe, it is remarkably contagious.
What kind of bacteria are salmonella?
They are flagellated, gram-negative bacteria that cause a self limited food borne and water-borne gastroenteritis, or a water bornesystemic illness (s typi does this).
What are the majr sources of salmonella in this country?
Contaminated beef and chicken.
This is from the salmonlla typhimuram and the salmonella enteridis.
What about systemic infection?
This is human to human, and usually associated with poor living conditions,caused by salmonella enteridis.
What does salmonella look like?
It is a flagellated gram negative orgaism.
What is campylbacter?
Campylobacter is a comma shaped gram negative organism once classified with vibrios.
Where do outbreaks of campylobacter usually come from?
They usually come from unpasteurized milk or contaminated water.
What are the three types of clinical outcomes you can have with campylobacter?
You can have diarrhea, dysentary or enteric fever. Post infectious you can have guillan burret syndrome as well as reiter's syndrome (as well as shigella).
What kind of morphological changes do you see in most bacterial causes of diarrhea?
You usually see a nonspecific pattern of damage to the surface epithelium, increased maturation adn an increased mitotic rate, hyperema and edema of the lamina propia, and variabl neutrophilic infiltration into the lamina propia and epithelial layer.
modest blunting in the small intestine, and preserval of mucosal architecture in the colon
What can you see in shigella?
You see enlargement of lymphoid follicles.
You can then get denudation of the mucosa.
What do you see with salmonella?
You tend to see blunted villi, vacular congestion, and mononuclear inflammation.
What possible nematodes can affect the bowel?
ascaris, necatur duodenal, strongyloidis, trichuria tricuria, enterobios.
What cestodes?
Taneia solia, Dip latum, Hymenolepsis nana.
What can happen in enteromaeba histolytica?
can get an infection, can go to brain, liver sometimes.
usually will get dysentary.
What kind of morphology do you get with G lambdia?
colon can be void or organisms, but you can get blunting, no villi, mixed infiltrate in the lamina propria. organisms ahve two nuclei. recurrence is common following antibiotics.
What happens with necrotizing enterocolitis?
transumural inflammation and/or necrosis at a segment along the bowel.
Describe AIDS enteropathy?
There is thought to be malabsorptive syndrome asssociated with direct viral aids.
What do you tend to see in GVHD?
first you see some apoptosis, then some sloughing.
What about radiatinon enterocolitis?
can present as mucosal damage, ischemic fibrosis, stricture.
Who gets diversin colitis?
rout en y, segments of short chain fatty acids.
What are the three most common causes of malapsorption?
celiac, pancreatic insufficiency, crohn's disease.
What should you look for in sprue?
blunting, increased chronic inflammatory infiltrate, deepening crypts.
What is the malignant risk?
non hodgkins, small intestinal adenocarcinoma, esophageal squamous cell carcinoma.
where do you see sprue in the si?
where do you see tropical sprue?
you tend to see this in all segments of the si? tend to have megaloblastic change (atypical enlargement of the nuclei of epithelial cells, reminescent of the changes)

(tropics iexcept jamiaca)

maladsorption usually becomes apparent within days or weeks after.
What kind of host reaction do you get in whipple disease?
you don't get a reaction in whipple disease.
What kind of changes do you see in PAS/
you tend to see whippelii in the epithelial cells, macrophages, neutrophils. also in the lymph nodes... you get opstruction.. maybe this is repsonsible for malabsorption.
What is the initialy presentationoften in whipple disease?
What do you need to see teh organisms, tropheryma whippelli?
What types of changes do you see in abetalipoproteinemia?
you get vacuolization because without betalipropotein, can't make chylomicron.
What is thought to be the etiology of IFBD?
Inflammatory reaction for genetic predisposed of commensal organisms.
What genes are associated with CD?
NFKb, and NOD2.
What are the findings of crohn?
sharply delminted typically transmural involvement of the bowel by an inflammatory process, noncaseating granulomas, fissuring with formation of the fitulae.
Is crohn's disease associated with smoking?
What kind of morphology do you have?
serosa is granular and dull gray and often the mesenteric fat wraps around teh bowel surface. the mesentary is thickened. Intestinal wall is thick, with hypertrophy of the muscularis propia. sharp demarcation of diseased bowel segments fromuninolved. focal ulcers, loss of nomral ulcers with linear ulcers which tend to be oriented along the axis.

you get neutrophilic nfammation, chronic mucosal damage, villus bluntin, branching crypts with irregularit. metaplasia with gastric antrum, paneth cells. ulceration (superficial, or deep), trnasmural inflammation affecting all layers (chronic inflammatory cel), noncaseating granulomas. fibrosis...
cam have localized vasculitis.
what kind of hepatic effects an you get fro ibd?
you can have psc or hepatic pericholangitis.
Do you have mucosal thickening of the bowel?
What do you need to look for in UC and chrohn's?
the degree ofdyspl;asia.
What do you tend to see more in uc than crohn's?
crpt abcess.
What are the three types of bowel infarction?
You can have mural, transmural and mucosal infarction.
Which of the three types is caused by mechanical compromise of the vessel, how about flow problems?
What kind of gross changes do you see with an infarcted bowel?
in arterial occlusions, you tend to get very well demarcated hemorrhage, in vascular not so much. you get sloughing of the mucosa, which in 1-4 days will become gangrenous.

mucosal and submucosal bowel is a somewhat lessor form of this. mucosal can only be tips...
Where do you tend to see angiodysplasia?
You tend to se this in the duodenum, where you have the most strain.
What is the most common obstruction point in the intestine?
smal intestine
how can you tell congenital from acquired diverticulosis?
congenital has all 3 layers, acquired is partial.
What is the relative frequency of tumors in the small intestine?
1%, a sig decrease from before.
Where do adenomas most frequently occur?
ampulla of vader
people with fap are frequently with issues.
What are risks for adenocarcinoma?
Other conditions with increased risk for small intestinal adenocarcinoma, celiac disease, FAP, hereditary nonpolyposis colorectal cancer, PJ syndrome.
what is the prognosis?
usually tumors have invaded the bowel wall; however, a wide en bloc excision of these cancers yields about a 70% five year survival rate.
What are the tumors (benign ) in the si and colon?
hyperplastic polyps, hamartomatous polyps(juvenile polyps, peutz-jeghers polyps), inflamatory polyps, lymphoid polyps.
What kind of neoplastic lesions can you have in the small intestine and the colon?
benign adenoma, malignant adenocarcinoma, carcinoid tumor, and anal zone carcinoma.
What kind of mesenchymal lesions can you have?
GIST, lipoma, neuroma, and angioma, kaposi sarcoma.
What do you look for in a peutz jeghers?
Patient's will have hyperpigmentation in the lips, all 3 layers making the polyp with smooth muscle going into the glands.
What are people with peutz jeghers at increased risk for?
lung, overy, pancreas, breast cancer.
What are the criteria for adenomas?
tubuler over 75%, >50% villous architicture is villous, 25-50% is tubulovillous
What is worrisome, what is not worrisome as far as gross features on adenomas?
<1cm tubular adenomas is rare to have cancer, >4 cm villous is high risk (40%)