Liver Pathology 1

Question 1

Jaundice

Answer 1

• -Yellow discoloration of skin from retention of bilirubin

- -Shows when total serum bilirubin approaches 2-3 mg/dl

Question 2

Icterus

Answer 2

Yellow discoloration of sclera from retention of bilirubin

Question 3

Bilirubin metabolism

Answer 3

Reticuloendothelial cells convert heme to bilirubin–> transported to liver and complexed to albumin–> conjugated w/glucuronic acid in liver cells –> excreted in bile

Question 4

Unconjugated bilirubin

Answer 4

• -Water insoluble
• -Bound to albumin
• -Toxic to tissues
• -Not excreted in urine

Question 5

Conjugated bilirubin

Answer 5

• -Water soluble
• -Not tightly bound to albumin
• -Not toxic to tissues
• -Excreted in urine when present at high levels

Question 6

Cholestasis

Answer 6

Impaired secretion of bile

Question 7

Causes of unconjugated hyperbilirubinemia

Answer 7

• -Increased bilirubin production (hemolysis)
• -Impaired hepatic bilirubin uptake (Gilbert Syndrome)
• -Impaired bilirubin conjugation ( Crigler-Najjar syndrome)

Question 8

Causes of conjugated hyperbilirubinemia

Answer 8

• -Extrahepatic cholestasis (biliary obstruction)
• -Intrahepatic cholestasis
• -Excretion defect (Dubin-Johnson syndrome, Rotor syndrome)

Question 9

Physiologic neonatal jaundice

Answer 9

• -Unconjugated hyperbilirubinemia
• -Normal neonatal alt. in bilirubin metabolism including increased bilirubin production, decreased bilirubin clearance (immature UDP-glucuronosyltransferase) and increased enterohepatic circulation.

Question 10

Tx for physiologic neonatal jaundice

Answer 10

Phototherapy

Question 11

Organ system affected by high bilirubin?

Answer 11

–Bilirubin can deposit in brain (bilirubin induced neurologic dysfunction)

Question 12

Gilbert’s syndrome

Answer 12

–Decreased gluconyltransferase activity–> Increased unconjugated bilirubin w/o overt hemolysis. No clinical consequences.

Question 13

Gilbert syndrome inheritance and how common is it?

Answer 13

• -Autosomal recessive or autosomal dominant.

- -Very common

Question 14

Lab findings in Gilibert syndrome

Answer 14

Increased unconjugated bilirubin

Question 15

Hepatocellular cholestasis morphology

Answer 15

Bile within hepatocytes, feathery degeneration of hepatocytes

Question 16

Canalicular cholestasis morphology

Answer 16

Canalicular bile stasis, feathery degeneration of hepatocytes

Question 17

Acute cholangitis morphology

Answer 17

• -Extrahepatic biliary obstruction
• -canalicular bile stasis
• -bile within distended bile ducts
• -feathery degeneration of hepatocytes
• -portal tract edema
• -bile duct proliferation w/in portal tracts
• -ascending cholangitis

Question 18

Hepatitis A virus

Answer 18

• -Preferentially infects liver cells
• -Doesn’t cause chronic hepatitis
• -Injury due to cellular immune response
• -Majority asymptomatic

Question 19

What forms of hepatitis have vaccines available?

Answer 19

• -A

- -B

Question 20

How is hepatitis A diagnosed?

Answer 20

Serology

Question 21

Hepatitis B virus

Answer 21

• -Preferentially infects liver cells
• -Potential to cause chronic hepatitis
• -Injury due to cellular immune response
• -Virus in fluids and blood

Question 22

How is hepatitis B transmitted?

Answer 22

Parenteral, sexual/close contact, perinatal

Question 23

Hepatitis A presentation

Answer 23

• -Most asymptomatic
• -Some present with acute hepatitis
• -1% develop acute liver failure and may die

Question 24

Hepatitis B diagnosis

Answer 24

Serology (include nucleic acid testing if necessary)

Question 25

Hepatitis B presentation

Answer 25

- -70% asymptomatic - -30% develop clinical hepatitis - -90% resolve - -0.1-0.5% develop acute fulminant hepatitis with liver failure and may die

Question 26

Carrier state for hepatitis B

Answer 26

- -Persistent HBV infection w/o necroinflammatory disease - -Typically occurs from result of exposure at childbirth or exposure as a young child - -+ HBsAg > 6 months

Question 27

What indicates recovery from chronic HBV infection?

Answer 27

Negative test for HBsAg

Question 28

Delta hepatitis virus (HDV)

Answer 28

- -Can have acute coinfection with HBV and HDV (will look like HBV) - -Acute coinfection usually transient and self-limited. - -Can convert mild chronic HBV into acute liver failure, cause acute hepatitis to occur in HBV carrier, lead to chronic hepatitis

Question 29

In patients with HBV, when should HDV testing be considered?

Answer 29

- -Risk factors (IV drug use, from endemic country) - -Unusually severe or protracted acute hepatitis - -Acute hepatitis of undetermined origin in chronic HBV carrier

Question 30

Hepatitis C RNA type, transmission, and cell type preferentially infects

Answer 30

- -Single stranded RNA - -Spread parenteral (primarily blood), sexual/close contact, and rarely perinatally). - -Liver cells

Question 31

What causes hepatocellular injury in HCV?

Answer 31

--Patients cellular immune response and subsequent lysis of cells

Question 32

Do most people with HCV develop chronic or acute hepatitis?

Answer 32

Chronic (80%) | --accounts for almost half of liver disease in US.

Question 33

What do some HCV patients develop?

Answer 33

Extrahepatic autoimmune manifestations/syndromes (Cryoglobulinemia, membranoproliferative glomerulonephritis, thyroiditis)

Question 34

How do you diagnose HCV?

Answer 34

HCV antibody screen and reflex to HCV RNA by PCR--> Anti-HCV antibodies develop approx. 10 wks after infection, but don't confer recovery or immunity

Question 35

How do you diagnose HDV?

Answer 35

Nucleic acid testing to detect viral DNA

Question 36

How do you diagnose HEV?

Answer 36

Serology

Question 37

Hepatitis E virus (HEV)

Answer 37

- -Preferentially infects liver cells - -Hepatocellular injury due to patients cellular immune response - -Very prevalent in underdeveloped countries, rare in US - -Doesn't cause chronic hepatitis - -Generally self limited

Question 38

What group of ind. with HEV have a higher mortality rate?

Answer 38

Pregnant women