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What is a unique histological feature of the Duodenum?
Brunner's glands.
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What are Brunner's glands?
Produce mucus-rich bicarbonate secretion to protect from chyme, provide enzymatic buffer zone, lubricate mucosa.
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Where does the Jejunum begin?
Ligament of Treitz.
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What is a unique histologic feature of the Ileum?
Peyer's patches.
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What are peyer's patches?
Gut associated lymphoid tissue (GALT) as immune surveillance.
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What are the layers in the small intestine (in to out)?
- Mucosa, muscularis mucosa, submucosa, muscularis propria, serosa.
- What is Gastroschisis?
- Extrusion of intestines due to failure of part of abdominal wall to form.
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Which is the most common site of SI atresia?
Duodenum - associated with Down's syndrome.
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What is a Meckel's diverticulum, where is it most common?
- Remnant of omphalomesenteric duct
- , proximal to Ileocecal valve (IC).
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What is the difference between atresia and stenosis?
Atresia is complete (not-formed), stenosis is incomplete narrowing.
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What are the four most common causes of bowel obstruction?
Hernia, adhesion, intussesception, volvulus.
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What are the four major categories of diarrhea causes?
Secretory, osmotic, exudative, malabsorption, motility disorders.
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What are the two most important viral pathogens leading to gastroenteritis?
Rotavirus, Norwalk virus -- preferentially affect small bowel.
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What type of diarrhea does Giardia lamblia cause?
Malabsorptive -- ingest cysts in water contaminated by feces.
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What is pancreatic insufficiency associated with?
Alcoholism/chronic pancreatitis, cystic fibrosis.
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What is the genetic association with celiac disease?
HLA-DQ2 and DQ8.
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What are three autoantibodies associated with gluten sensitive enteropathy (GSE)?
Gliadin, endomyseal, tTG.
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Classic presentation of celiac sprue?
Diarrhea, weight loss, fatigue.
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What is a pathologic feature of GSE?
Blunting of villi, itraepithelial lymphocytosis.
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What are the two main types of IBD?
Crohn's disease, ulcerative colitis.
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What is Crohn's disease?
Systemic inflammatory disorder with prominent GI involvement.
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What sort of inflammation does crohn's have?
Transmural inflammation, affects all layers -- and also patchy.
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What is the usual progression of ulcerative colitis?
Starts in rectum (distal colon) and works it's way proximally.
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Where do adenocarcinomas of SI usually arise?
Duodenum, ampullary -> jaundice.
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What mutations do GI stromal tumors contain?
c-Kit, PDGFRa -- CD117.
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What is a carcinoid tumor?
Neoplasms of neuroendocrine cells capable of generating (secreting) bioactive molecules.
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Which carcinoid tumors are more likely to be malignant?
SI and colonic (as opposed to appendiceal and rectal - usually benign).
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What are some symptoms of carcinoid syndrome?
- Vasomotor disturbances, intestinal hypermotility, asthmatic bronchoconstrictive attacks, hepatomegaly, niacin deficiency systemic fibrosis, cardiac involvement.
- Pancreatic development involves fusion of?
- ventral and dorsal primordia.
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What is pancreas divisum?
Failure of duct systems to fuse - main duct drains head and rest drains through minor sphincter -- 3-10% -- may lead to pancreatitis.
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What is annular pancreas?
Pancreas wraps around duodenum -- obstruction.
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Most cases of acute pancreatitis are related to?
Alcohol or biliary tract disease (Stones).
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What is the cardinal manifestation of acute pancreatitis?
Abdominal pain - may be referred to upper back.
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What are some lab findings of acute pancreatitis?
Elevated amylase and lipase, hypocalcemia.
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What characterizes chronic pancreatitis, associated with?
Chronic inflammation and fibrosis with irreversible organ damage - chronic alcoholism.
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Autoimmune pancreatitis is related to?
IgG4 Sclerosing disease.
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What separates autoimmune pancreatitis from pancreatic cancer?
IgG4 and responds to steroids.
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What is a tumor marker for pancreatic cancer?
CA19-9, more useful to follow treated patients.
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What is the composition of bile salts, function?
Cholates - breakdown of cholesterol in liver, detergents to dissolve dietary fat.
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With malabsorption due to disruption of bile salts, one becomes deficient in what vitamins?
ADEK (fat soluble).
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What is the yellow color in bile, what is it composed of?
Bilirubin, breakdown of hemoglobin.
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What does ERCP stand for, what is it?
Endoscopic retrograde cholangiopancreatography - inject dye through pancreatic and bile ducts to image.
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Who does Primary biliary cirrhosis usually affect, describe the onset?
Middle age women F:M 6:1, insidious, asymptomatic onset.
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What is the primary presentation of PBC?
Asymptomatic elevation of LFT's (alkaline phosphatase) and cholesterol.
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What antibody is positive in 90-95% of PBC cases?
Anti-mitochondrial antibody.
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What is primary biliary cirrhosis?
Progressive destruction (autoimmune?) of small bile ducts in liver.
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What are the first symptoms experienced in PBC?
Pruritis, fatigue, abdominal discomfort -> skin pigmentation, xanthelasma, steatorrhea, vit. D malabsorption.
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PBC patients have increased risk to develop?
Hepatocellular carcinomas.
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What is the major cause of death in PBC?
Liver failure, second is massive variceal hemorrhage and infection.
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What is the treatment of PBC?
Ursodeoxycholic acid, liver transplant in end stage disease.
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What is usually the cause of secondary biliary cirrhosis?
Prolonged obstruction of extrahepatic biliary tree.
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What is Primary Scleorsing Cholangitis (PSC)?
Inflammation and obliterative fibrosis of intra and extra-hepatic bile ducts.
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What is PSC associated with?
IBD- 70% of cases -- especially ulcerative colitis.
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What is the appearance of bile ducts in PSC on cholangiography?
Beaded ducts.
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What is alagille syndrome?
AD disorder, characterized by paucity of interlobular bile ducts - systemic.
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What are some other effects of alagille syndrome?
Chronic cholestasis, cardiac anomalies, butterfly vertebrae, posterior embryotoxon, dysmorphic facies.
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Usual presentation of Alagille syndrome, morbidity?
Jaundice, CV symptoms, failure to thrive before 6 months -- liver disease.
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What is Caroli's disease?
Segmental dilatation of large intrahepatic bile ducts.
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What two things is Caroli's disease associated with?
Caroli's syndrome, Polycystic kidney disease.
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What is Caroli's syndrome?
Congenital hepatic fibrosis - portal tract fibrosis.
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Caroli's disease increases the risk of?
Cholangiocarcinoma (up 7%).
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What are four congenital biliary abnormalities?
Absence of gallbladder, duplication of gallbladder, aberrant location of gallbladder, agenesis of any part of hepatic or bile ducts.
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What is cholelithiasis, what is their composition?
Gallstones, most (90%) cholesterol, 10% calcium bilirubinate (pigmented stones).
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What are the four contributing factors to gallstones?
Supersaturation, gallbladderhypomotility, crystal nucleation, accretion within gallbladder mucosa.
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What are some risk factors for cholelithiasis?
Pregnancy, obesity, rapid weight loss, prolonged fasting, Oral contraceptives, DM, cirrhosis.
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Usual clinical presentation of cholelithiasis?
Biliary colic - intense, dull pain in RUQ, constant for 1-4 hrs - can radiate to back or right scapula.
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Which is the most common biliary cancer?
Gallbladder cancer.
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What is the treatment for cholelithiasis?
Silent: observation, symptomatic: cholecystectomy, alternative to surgery: ursodeoxycholic acid.
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What are choledochal cysts?
Congenital dilation of Common Bile duct, presents usually before age 10.
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What triad is suggestive of hepatobiliary or pancreatic malignancy?
Cholestasis, abdominal pain, weight loss.
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When do symptoms arrive from cholangiocarcinoma?
Upon obstruction of biliary drainage system.
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