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