GI Flashcards
etiology of gastric and duodenal ulcers?
gastric: direct invasion and damage in body of stomach, duodenal: decreased somatostatin, increased gastrin, increased acid
2 actions of fibrates and SE?
fibrate: PPAR-a activator, increased hydrolysis of VLDL and increased beta oxidation of fatty acids, leading to lower triglycerides. can cause gall stones by preventing bile salt formation by inhibiting cholesterol 7 alpha hydroxylase
woman with persistent noninflammatory diarrhea that gets better with somatostatin. diagnosis?
VIPoma
what is enteropeptidase?
a brush border enzyme that activates trypsinogen to trypsin, which aids in lipid and protein digestion
young ish man with pancreatitis, CT shows pancreatic divisum. what is this? explain embryology
ventral bud forms the main pancreatic duct, rest of the pancreas in the dorsal bud. in normal development the buds fuse at 8 weeks, but in pancreatic divisum it remains divided, separate ductal systems–> pancreatitis
why do you get gallstones in crohn’s disease?
bile acid absorption is at terminal ileum, which crohn’s disease affects often. decreased bile acid absorption leads to higher cholesterol:bile acid ratio in bile increases, leading to gallstones
2,3 aVF ST elevations in boy in soccer pain with chest pain, increased serum methionine, what amino acid is essential for this patient?
cysteine. dx is homocysteineuria, the build up of homocysteine causes thrombosis including in the coronary arteries. due to decreased amounts of cystathionine synthase, which prevents cysteine formation from homocysteine.
RTA, seatbelt bruising, and retroperitoneal bleeding. where is the source?
pancreas contusion
infant botulism vs adult botulism
c. botulinism spores ingestion leading to floppy baby and lethargy vs preformed toxin ingestion from canned food
what can be used to test brushborder enzyme function independent of pancreatic activity, in patient with pancreatic resection due to chronic pancreatitis and mass
d-xylose- monosaccharides are readily absorbed. polysaccharides need to be digested by amylase first
multiple hypodense regions in liver, with massive hyperdense area next to it
mets to liver (more common than HCC) and oral contrast in stomach
most common benign mass in liver
cavernous hemangioma- blood filled spaces wth single epithelial layer in the liver
woman with chronic diarrhea that is uncomplicated, started on diphenoxylate, what is that?
its an opioid that slows motility, given tgt with atropine (to prevent addiction) SE is biliary colic because it constricts sphincter of oddi
oral vs intramuscular antibody, which Ig concetntration is markedly different?
IgA
excess mast cells in the skin positive for CD117, KIT, have what effect on GIT?
gastric hypersecretion because of histamine activating the proton
pneumobilia, gallstones and abdo pain and vomiting
gallstone ileus triad, gets stuck in ileum after fistula formation because ileum is the narrowest
how does TPN cause gallstones
decreased CCK production, gallbladder hypomotility
crohn’s disease effect on colonic architecture
thickening of muscularis mucosae, causing strictures, and fat creeping
fingertip ulcers, calcifications, telangiectasias and severe heartburn. dx and mechanism of heartburn?
CREST of systemic sclerosis- fibrous replacement of muscularis of lower esophagus
colon polyp, which has worst prognosis?
lymph node invasion. not lamina propria because its like basement membrane (in-situ) and the lymph drain in muscularis mucosae
signet ring carcinoma what type is this?
diffuse type of gastric carcinoma, linitis plastica because invades the wall because lack of E-cadherin. the other type is infiltrative- glands involvement
fatty cells in the villi of intestinal epithelium, dx
abetalipoproteinemia, cannot make apoB contiaing lipoproteins, which means cannot collect fat from enterocytes
autopsy looks like FAP of the liver, what is dx?
cirrhosis, due to fibrosis and regnerataive parenchymal nodules
some grain in china lead to p53 mutation, which cancer how?
aflatoxin made by aspergillus, infects grain, tgt with hep B is predisoposing to HCC
nocturnal cough, basal zone hyperplaisa, eos, lamina propira papillae elongatino, gets better with pantoprazole, dx?
GERD, relaxation and incompetence of GEJ
profuse watery diarrhea in HIV patient, mucosal biopsy shows inflammatory infiltrate in lamina propria and pathogens lining the epithelium, dx and usual location
cryptosporidium parvum, usually in small intestine
1 week ago had cholecystectomy in mexico, comes back with jaundice and fever and mild hypotension, dies two days later- liver biopsy shown, what is dx and mechanism? and what will be associated sign?
PT decrease. fulminant hepatitis due to inhaled halothane (used anesthetic worldwide), leading to acute liver injury. Other things like albumin and palmar erythema are late signs for CLD, but for acute liver injury, factor VII has shortest halflife
hematemesis, ulcer at the posterior wall of the duodenal bulb, which artery does it affect?
gastroduodenal from the common hepatic from celiac trunk. anterior wall of duodenum would lead to perforation
adenoma to carcinoma sequence regulated by what?
normal to early adenoma is APC/b-catenin, early adenoma to late adenoma is KRAS gene, late adenoma to carcinoma is TP53
what enzyme is involved in making pigment stones?, where is it produced?
beta-glucuronidase. produced by injured hepatocytes or from bacteria (c. sinensis) is common in East Asia), rmb glucoronides is what is conjugated to bilirubin. so cleaving this makes in unconjugated bilirubin, which is more susceptible to pigment stone formation
how does HBV allow for HDV infection?
HbSAg covers the HDV particles so it can infect hepatocytes