Path General Liver

Front 1

common genetic defect in uptake/conjugation of UCB (↓ UGT1A1)

Back 1

Gilbert syndrome

Front 2

genetic disorders with decreased to absent conjugating enzymes (UGT1A1 - uridine diphosphate-glucuronosyltransferase)

Back 2

Crigler-Najjar syndromes

Front 3

defect in uptake, conjugation of UCB, and secretion of CB

Back 3

viral heptiatis

Front 4

how does viral hepatitis affect urine bilirubin and urine UBG?

Back 4

both are increased

Front 5

how is UBG produced?

Back 5

intestinal bacteria convert CB to UBG

Front 6

prodrome of viral hepatitis

Back 6

fever, painful hepatomegaly
serum transaminases increase steadily
atypical lymphocytosis

Front 7

infective particles of HBV

Back 7

HBeAg and HBV-DNA

Front 8

non-protective antibody for HBV
remains positive in acute infection

Back 8

anti-HBc-IgM (anti-HBV core AB IgM)

Front 9

only marker present during window phase of HBV infection

Back 9

anti-HBc-IgM

Front 10

protective antibody against HBV

Back 10

anti-HBs (anti-HBV surface AB)

Front 11

marker of immunization after HBV vaccination or recovery from past infection

Back 11

anti-HBs (anti-HBV surface AB)

Front 12

where does the conjugation of bilirubin occur?

Back 12

liver

Front 13

genetic defect in secretion into intrahepatic bile ducts
black pigment in hepatocytes

absent transport protein for bilirubin glucuronides (↑ CB)

asymptomatic but chronically jaundiced

Back 13

Dubin-Johnson syndrome

Front 14

genetic defect in secretion into intrahepatic bile ducts
NO black pigment in hepatocytes (↑ CB)

Back 14

Rotor's syndrome

Front 15

describe normal bilirubin metabolism

Back 15

UCB is conjugated in the liver
CB is secreted into the common bile duct and enters the duodenum
bacteria convert CB to UBG
20% of the UBG returns to the blood (90% goes to the liver and 10% goes to the kidneys, ending up in the urine)
the other 80% spontaneously oxidizes to urobilin

Front 16

how does extravascular hemolysis affect AST, ALT, ALP, GGT?

Back 16

since AST is found in RBCs,
AST ↑

Front 17

is ALT or AST higher in alcoholic hepatitis? why?

Back 17

AST is higher b/c alcohol damages mitochondria, which is where AST is normally located

Front 18

how does obstructive liver disease affect ALT, AST, ALP, GGT? how does it affect the stool?

Back 18

ALP & GGT are markedly increased
AST & ALT are slightly increased
stool is pale b/c CB doesn't enter the duodenum to be converted to UBG

Front 19

where is ALP found?

Back 19

bile duct epithelium & hepatocyte canalicular membranes

Front 20

where is ALT and AST found?

Back 20

ALT is found in the cytosol
AST is in mitochondria

Front 21

specific enzyme for liver cell necrosis

Back 21

ALT

Front 22

increased GGT and ALP

Back 22

liver cholestasis

Front 23

what increases GGT?

Back 23

obstruction to bile flow
induction of CYP450 (alcohol)

Front 24

what does α-Fetoprotein (AFP) indicate?

Back 24

hepatocellular carcinoma

Front 25

transmission of Hep. A

Back 25

fecal-oral
shellfish

Front 26

transmission of Hep. E

Back 26

fecal-oral (waterborne)

Front 27

transmission of Hep. G

Back 27

parenteral

Front 28

indicates HCV infection or recovery

Back 28

anti-HCV-IgG

Front 29

positive RIBA (recombinant immunoblot assay) & HCV RNA indicate

Back 29

infection

Front 30

positive RIBA and negative HCV RNA indicate

Back 30

recent recovery

Front 31

anti-HBc-IgG + anti-HBs

Back 31

recovered from HBV

Front 32

anti-HBs only

Back 32

immunized

Front 33

A 25 y/o woman presents with fever, jaundice, and hepatosplenomegaly. Lab results reveal positive serum ANA (antinuclear AB) test & anti-smooth muscle AB's

Back 33

autoimmune hepatitis

Front 34

neonatal hepatitis is multifactorial, but it can be associated with what infection and inborn error of metabolism?

Back 34

CMV
α1-antitrypsin deficiency

Front 35

A 4 y/o child who just had chickenpox is now in a coma. Chem-7 reveals low glucose. She also has an enlarged, fatty liver. What was the likely cause?

Back 35

Reye syndrome caused by aspirin (acetylsalicylic acid)

Front 36

what is the mechanism behind Reye syndrome?

Back 36

mitochondrial damage causes disruption of the urea cycle (↑ in serum ammonia) and defective β-oxidation of FAs

Front 37

what is the cause of acute fatty liver of pregnancy?

Back 37

abnormal β-oxidation of FAs

Front 38

most common cause of fulminant hepatic failure

Back 38

viral hepatitis

Front 39

what characterizes fulminant hepatic failure

Back 39

acute liver failure with encephalopathy within 8 weeks of hepatic dysfunction

Front 40

most common drug-induced cause of fulminant hepatic failure

Back 40

acetaminophen (Tylenol)

Front 41

What are mallory bodies & when do you see them?

Back 41

intracytoplasmic eosinophilic inclusions; seen with sustained long-term consumption of alcohol

Front 42

what do you see histologically with alcoholic hepatitis?

Back 42

swollen and necrotic hepatocytes with neutrophilic infiltration
mallory bodies

Front 43

what do you see histologically with alcoholic cirrhosis?

Back 43

brown, micronodular, shrunken, non-fatty liver
granular appearance
sclerosis around central vein

Front 44

upper limit of the liver is at what level

Back 44

5th intercostal space

Front 45

what constitutes the left hemiliver

Back 45

quadrate lobe (inferior) & greater part of caudate lobe

Front 46

which lobe corresponds to segment I?

Back 46

caudate

Front 47

which zone is located closest to the terminal hepatic vein (furthest from the hepatic a.)

Back 47

zone 3 (centrilobular)

Front 48

which zone is closest to the hepatic a.?

Back 48

zone 1

Front 49

what is the role of stellate cells and where are they found?

Back 49

storage and metabolism of vitamin A
also deposit collagen leading to fibrosis and cirrhosis
found in the space of Disse

Front 50

steatosis

Back 50

accumulation of triglycerides within hepatocytes

Front 51

describe the appearance of liver cells in ischemic coagulative necrosis

Back 51

liver cells are poorly stained and often have lysed nuclei

Front 52

describe hepatocytes that have undergone apoptosis

Back 52

hepatocytes round up to form shrunken, pyknotic (condensed chromatin), and intensely eosinophilic cells containing fragmented nuclei

Front 53

describe lytic necrosis and what is it the result of

Back 53

hepatocytes osmotically swell & rupture; outcome of ballooning degeneration

Front 54

Pt. presents with jaundice, itching, and nodules in her fingers?

Back 54

cholestasis presents with jaundice, pruritis, and xanthomas

Front 55

liver is shrunken
affected areas are soft, muddy-red or bile-stained

Back 55

fulminant hepatitis

Front 56

eosinophilic cytoplasm (ground glass)

Back 56

carrier state for HBV

Front 57

symptoms shared by acute & chronic hepatitis

Back 57

fatigue, malaise, anorexia, jaundice

Front 58

findings associated with chronic liver disease

Back 58

spider angiomas,
palmar erythema,
mild hepatosplenomegaly,
hepatic tenderness

Front 59

liver abscesses are associated with

Back 59

fever
RUQ pain
tender hepatomegaly
possibly jaundice

Front 60

oral contraceptives cause what liver pathology?

Back 60

cholestasis