Usmle Step 1 Dit: Gastrointestinal

Front 1

Explain the liveranatomy

Back 1

Hepatic diverticulum grows off anterior part of distal foregut. Becomes: liver, biliary and head of pancreas.

Front 2

Major site of hematopoiesis during fetal life

Back 2

Liver

Front 3

Mesodermal hematopoeitic stem cells migrate from mesonephros to.......

Back 3

Liver at about 3 wks

Front 4

What are the 4 main functions of hepatocytes?

Back 4

Make proteins, metabolize toxins and drugs, storage, make bile and excrete bilirubin

Front 5

What proteins are made by hepatocytes?

Back 5

Coagulation factors, complement proteins, albumin, apolipoproteins, C-reactive protein, angiotensinogen, transferrin, ceruloplasmin

Front 6

What toxins and drugs are metabolized by hepatocytes?

Back 6

Cytochrome p450, UDP-glucouronyl transferase, ALT/AST, steroid hormones->inactive metabolites

Front 7

What substances are stored by hepatocytes?

Back 7

Glucose as glycogen, cholesterol and triglycerides (VLDL particles), minerals, vit b12, ADEK

Front 8

What is the portal triad composed of?

Back 8

Bile ductule, branch of portal vein, branch of hepatic artery

Front 9

In what direction does bile move in the liver?

Back 9

Away from central vein

Front 10

In what direction does blood flow move in the liver?

Back 10

Towards the central vein

Front 11

Hepatic zone affected first by viral hepatitis?

Back 11

zone I

Front 12

Hepatic zone that is highly oxygenated

Back 12

zone I

Front 13

Heaptic zone affected first by ischemia

Back 13

zone III

Front 14

Hepatic zone that contains cytochrome p450 system

Back 14

zone III

Front 15

Hepatic zone where ingested toxins like cocaine go

Back 15

zone I

Front 16

Hepatic zone where alcoholic hepatitis develops

Back 16

zone III

Front 17

Mildly decreased UDP glucuronosyltransferase conjugation. Asymptomatic or mild jaundice.

Back 17

Gilbert syndrome

Front 18

Absent UDP glucuronosyltransferase. Presents early in life, patients die withing a few years if not treated. Increased unconjugated bilirubin. DOES NOT respond to phenobarbital.

Back 18

Crigler-najjar syndrome, type I

Front 19

Mutated UDP glucuronosyltransferase. Mild version. Increased unconjugated bilirubin. Responds to phenobarbital.

Back 19

Crigler-najjar syndrome, type II

Front 20

What values of bilirubin are tested in labs and which are deduced?

Back 20

Labs give values of direct and total bilirubin. And indirect is deduced by total - direct.

Front 21

What are the principle symptoms of kernicterus?

Back 21

Chorea, cerebral palsy, hearing loss

Front 22

What is the treatment for kernicterus?

Back 22

Phototherapy

Front 23

Conjugated hyperbilirubinemia due to defectove liver excretion. Black liver. Benign.

Back 23

Dubin-Johnson syndrome

Front 24

Why is there black liver in one of the hereditary hyperbilirubinemias?

Back 24

Bilirubin gets trapped in hepatocytes

Front 25

Similar but even milder version of dubin-johnson syndrome

Back 25

Rotor syndrome

Front 26

Synonym for unconjugated bilirubin

Back 26

Indirect

Front 27

If there is too much unconjugated bilirubin in an infant...

Back 27

They may develop kernicterus (accumulation in the brain)

Front 28

What enzyme is responsible for conjugation of bilirubin?

Back 28

Glucouronyl transferase

Front 29

Why are new borns suceptible to jaundice?

Back 29

They have a reduced amount of UDP glucuronosyltransferase so they conjugate bilirubin as effectively

Front 30

Alcoholic liver disease with reversible changes, seen in heavy drinkers. Macrovesicular fatty changes

Back 30

Hepatic steatosis

Front 31

Alcoholic liver disease with swollen and necrotic hepatocytes with neutrophilic infiltration, mallory bodies. Seen in long-term consumption.

Back 31

Alcoholic hepatitis

Front 32

Alcoholic liver disease with micronodular, irregularly shrunken liver with scarring and fibrosis. Sclerosis around central vein (zone III)

Back 32

Alcoholic cirrhosis

Front 33

Hepatic encephalopathy is seen in

Back 33

Effects of liver cell failure

Front 34

Scleral icterus is seen in

Back 34

Effects of liver cell failure

Front 35

Esophageal and anorectal varices are seen in

Back 35

Effects of portal hypertension

Front 36

Testicular atrophy, gynecomastia, spider nevi, palmar erythema due to increased estrogen is seen in

Back 36

Effects of liver cell failure

Front 37

Peripheral edema and ascitis is seen in

Back 37

Effects of liver cell failure

Front 38

Hepato and/or spenlomegaly is seen in

Back 38

Effects of portal hypertension

Front 39

Upper GI bleed like hematoemesis and melena are seen in

Back 39

Effects of portal hypertension (esophageal varices)

Front 40

Caput medusae and ascitis (spontaneous bacterial peritonitis) is seen in

Back 40

Effects of portal hypertension

Front 41

Asterixis and fetor hepaticus is seen in

Back 41

Effects of liver cell failure

Front 42

Increased bleeding, PT and PTT

Back 42

Effects of liver cell failure

Front 43

What is the treatment for esophageal varices?

Back 43

- Octeotride (somatostatin agonist)

- Endoscopic banding of varices

- Propranolol or nadolol

- TIPS procedure (transjugular intrahepatic portosystemic shunt)

Front 44

What is the treatment for ascitis?

Back 44

Diuretics and paracentesis

Front 45

What is the treatment for cirrhosis?

Back 45

Diuretics, B-blockers, vitamin K, lactulose

Front 46

What is SAAG?

Back 46

Serum ascitis albumin gradient

Front 47

How is SAAG determined?

Back 47

[Albumin]serum - [Albumin]ascitis

Front 48

What does a SAAG of more or same as 1.1 represent?

Back 48

Portal hypertension

Front 49

What does a SAAG of less than 1.1 represent?

Back 49

Cancer, nephrotic syndrome, tuberculosis, pancreatitis, biliary disease, connective tissue disease