GI Week 2 Flashcards
Question: Which of the following is true about fatty liver disease (alcoholic and nonalcoholic)?
- NASH can be distinguished from ASH by the presence of Mallory bodies
- Progression of both: fibrosis -> steatosis -> steatohepatitis -> liver failure/HCC
- Two “hits” are needed for NAFLD: fat accumulation and oxidative stress to hepatocytes
- Total parenteral nutrition and jejuno-ileal bypass are protective against the development of fatty liver disease
Answer: C. One more “hit” is needed to progress from steatosis (fat accumulation) to steatohepatitis (fatty liver with inflammatory changes)
Other: NASH and ASH are indistinguishable on histology. Fatty liver disease progression occurs in the following manner: steatosis -> steatohepatitis -> fibrosis -> liver failure/HCC. Non-alcoholic fatty liver is commonly associated with TPN and jejuno-ileal bypass (not protective).
Learning objective = Apply the above liver injury pathways and consequences to the following condition: fatty liver disease (alcoholic and nonalcoholic) (SM 137b: Liver Histology and Basic Pathology)
Question: What is the best imaging modality for initial evaluation of the following organs/conditions:
Gallbladder
Bowel motility
Bowel obstruction
Infection/masses/inflammation
Answer:
Gallbladder: ultrasound
Bowel motility: fluoroscopy
Bowel obstruction: Xray abdominal series
Infection/masses/inflammation: give IV or oral contrast (CT)
Learning objective = To be able to choose which radiologic imaging modality is most appropriate for GI motility issues, including acute bowel pathology; and To be able to choose which radiologic imaging is most appropriate for liver, gallbladder and pancreatic pathology. (SM 145b: Imaging of the GI System)
Question: Which of these is true about control of gallbladder contraction and biliary secretion?
- Cholecystokinin release leads to the contraction of the sphincter of Oddi
- Acetylcholine leads to skeletal muscle contraction of the gallbladder
- Nutrient sensing in the esophagus leads to cholecystokinin release and downstream effects
- Cholecystokinin leads to smooth muscle contraction of the gallbladder
Answer: D. CCK causes contraction of the gallbladder smooth muscle, which leads to secretion of a bolus of bile
Other: A – CCK leads to eventual relaxation of the sphincter of Oddi. B – ACH leads to smooth muscle contraction of the gallbladder. C – nutrient sensing in the duodenum causes CCK release
Learning objective = Describe the mechanisms whereby the gall bladder concentrates bile, and the endocrine mechanism stimulating gall bladder contraction and the secretion of bile through the sphincter of Oddi into the small intestine. (SM 144b: Bile Salts and the Absorption of Lipids)
Question: A 39-year-old African-American man comes to the physician because of anorexia, malaise, dark urine and upper abdominal discomfort. His temperature is 37.9ºC (100.2ºF). Physical examination shows scleral icterus and moderate right upper quadrant tenderness. The liver is palpable below the right costal margin. Laboratory studies show:
HBsAg: positive
HBsAb: negative; Anti-HBc IgM: positive; HBeAg: positive
Which of the following will most likely change in his serologic findings when this patient enters the window period?
- He will become HBcAg-positive
- He will become HBc IgG-positive
- He will become HBsAb-positive
- He will become HBsAg-negative
Answer: D. This patient has acute hepatitis B. The “window period” refers to that period in infection when neither hepatitis B surface antigen (HBsAg) nor its antibody (HBsAb) can be detected in the serum of the patient. It is an immunologically mediated phenomenon caused by the precipitation of antigen-antibody complexes in their zone of equivalent concentrations and, thereby, their removal from the circulation.
Because of this, the first thing that will happen in the window period is that the serum will become negative for the surface antigen (HBsAg) as that antigen is precipitated out of the serum by developing levels of its specific antibody (HBsAb). Serologic tests conducted during the window period will be positive for HBcAb and HBeAb.
Question source: https://www.ama-assn.org/residents-students/usmle/usmle-step-1-prep-change-serologic-findings-when-entering-window-period (modified to remove answer choice C from this site’s original question)
Question: What is the affected protein/gene for these bilirubin metabolism disorders and what type of hyperbilirubinemia (indirect or direct) is present?
Gilbert’s syndrome
Crigler-Najjar syndrome
Dubin Johnson syndrome
Answer:
Gilbert’s syndrome: uridine diphosphate glucuronyl gene (UDP-GT), mild indirect hyperbilirubinemia
Crigler-Najjar syndrome: Type I = complete absence of UDP-GT, very high indirect hyperbilirubinemia; Type II: partially active UDP-GT, indirect hyperbilirubinemia
Dubin Johnson syndrome: canalicular transporter of conjugated bilirubin, mild conjugated hyperbilirubinemia
Learning objective = Identify specific diseases that cause jaundice in the newborn infant (SM 134b: Approach to the Newborn with Suspected Liver Disease)
Question: What are the “5 F’s” of cholesterol stones and acute cholecystitis?
Answer: Fat, Female, Fair (Caucasians), Fertile (premenopausal), Forty (and above)
The 5 F’s describe the risk factors for developing cholesterol gallstones (which are 80% of the GS seen in the US) and of developing acute calculous cholecystitis (accounts for 90% of the cases of acute cholecystitis)
Learning objective = Define acute cholecystitis and complications of gallstones. (SM 136b: Pathology of Gallbladder and Biliary Tract)
Question: Fill in the blanks about Gilbert’s disease: presents with elevated ________ bilirubin, which is increased under conditions of ______________ , and has _________ clinical consequences. It occurs due to an abnormality of the TATA box of the ____________ gene
Answer:
Fill in the blanks about Gilbert’s disease: presents with mildly elevated unconjugated bilirubin, which is increased under conditions of fasting, exertion, and infections, and has _no_ clinical consequences. It occurs due to an abnormality of the TATA box of the __\_bilirubin-UDP-GT___ gene
Learning objective = Learn about Gilbert’s disease and how it can serve as a model for hepatic metabolic functions (SM 135b: Biliary Tract Disorders)
Question: Which of these is true about α1-antitrypsin (α1-AT) deficiency?
- α1-AT is a protease secreted by the liver into the blood
- The PiMM variant leads to a severe reduction in α1-AT
- Increased α1-AT leads to increased alveolar destruction in the lungs
- α1-AT activity normally inhibits elastase activity in the lungs
- Treatment of α1-AT deficiency is exogenous supplementation of α1-AT
Answer:
D. α1-AT normally inhibits elastase.
Others: a) α1-AT is a protease inhibitor. b) the PIZZ variant leads to a severe reduction in α1-AT (PiMM = wild-type, PiSS = moderate reduction w/ no symptoms; PiMZ = codominant intermediate level of α1-AT)
c) Decreased α1-AT leads to increased alveolar destruction in the lungs
e) lung transplantation is the treatment for α1-AT deficiency, and the healthy liver will produce functional α1-AT
Learning objective = Describe the genetic defect and clinical consequences of a1-antitrypsin deficiency (SM 138b: Pathology of Metabolic liver disease and viral hepatitis)
Question: Which of these is true about liver cancers?
- Cholangiocarcinoma is associated with elevated levels of hormones
- Macronodular cirrhosis has a higher risk of developing into HCC than micronodular
- 80-90% of primary tumors of the liver are benign hepatic adenomas
- Metastatic tumors of the liver usually present as a solitary mass in a background of cirrhosis
Answer: B – cirrhosis of the liver present in ~85% of all HCC: macronodular > micronodular
Others: a) hepatic adenoma (benign) is associated with elevated levels of hormones (oral contraceptives, contraceptive steroids). c) 80-90% of primary tumors of the liver are HCC. d) Metastatic tumors of the liver usually present without cirrhosis. (HCC usually presents as a solitary mass in a background of cirrhosis)
Learning objective = Describe the pathway leading to hepatocellular carcinoma (HCC). (SM 140b: Cirrhosis and Liver Cancer)
Question: Identify these key steps in the progression of precursor lesions in the pancreatic ducts to pancreatic carcinoma. What does PanIN stand for?
Answer:
PanIN = Pancreatic intraepithelial neoplasia
Learning objective = Describe precursor lesions in the pancreatic ducts and Why is prognosis in patients with pancreatic carcinoma is so poor. (SM 141b: Pathology of Pancreatic Disorders)
Question: Label these vessels and the 5 lettered spots where varices can form (A-E)
Learning objective = Explain why varices form and the approaches to treatment (SM 143b: Complications of Cirrhosis)
