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Pathoma > 11.3 Liver > Flashcards

11.3 Liver Flashcards

1
Q

Jaundice

A

Yellow discoloration of the skin due to increased serum bilirubin

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2
Q

What is the breakdown of heme?

A

Heme -> Porphyrin -> Unconjugated bilirubin -> Conjugated bilirubin

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3
Q

Jaundice in Extravascular Hemolysis

A

Increased UCB which overwhelms the conjugating ability of the liver

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4
Q

Jaundice in the Newborn

A

Newborn liver has a low UGT activity to conjugate bilirubin - increased UCB

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5
Q

Jaundice in Gilbert Syndrome

A

Lowered UGT activity due to an autosomal recessive mutation - but are usually asymptomatic with increased UCB levels

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6
Q

Jaundice in Crigler-Najjar Syndrome

A

Absence of UGT - causes increased UCB leading to kernicterus and is usually fatal

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7
Q

Jaundice in Dubin-Johnson Syndrome

A

Autosomal recessive deficiency of bilirubin canalicular transport protein - increased CB with a pitch dark black liver

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8
Q

Jaundice in Biliary Tract Obstrction

A

Blockage of bile release leading to increased CB/decreased urine urobilinogen/increased alkaline phosphatase

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9
Q

Jaundice in Viral Hepatitis

A

Inflammation disrupts hepatocytes and small bile ductules - increase in BOTH CB and UCB

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10
Q

What are 2 consequences of extravascular hemolysis?

A
  • Dark urine

- Increased risk of bilirubin gallstones

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11
Q

What is a serious consequence of newborn jaundice?

A

UCB is fat soluble and can deposit in the basal ganglia, causing kernicterus - neurological deficits

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12
Q

What is Rotor Syndrome?

A

It has the same signs as Dubin-Johnson Syndrome but without the liver discoloration

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13
Q

What are some of the signs of biliary tract obstruction?

A
  • Dark urine
  • Pruritis
  • Hypercholesterolemia
  • Steatorrhea
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14
Q

Viral Hepatitis

A

Inflammation of the liver parenchyma usually from hepatitis virus

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15
Q

What are non-hepatitis viruses that can cause hepatitis?

A

EBV and CMV

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16
Q

What does chronic hepatitis tend to involve?

A

Portal Tract

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17
Q

Transmission of HAV

A

Travelers via fecal-oral transmission

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18
Q

Transmission of HBV

A

Parenteral transmission via childbirth, sex, IV drugs

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19
Q

Transmission of HCV

A

Parenteral transmission especially with blood transfusion

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20
Q

Transmission of HEV

A

Contaminated water or undercooked seafood

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21
Q

What does HEV in a pregnant woman indicate?

A

Fulminant Hepatitis

22
Q

How does HDV infection occur?

A

It is dependent on HBV for infection

23
Q

What is the first serologic marker for HBV infection with acute hepatitis?

A

HBsAG

24
Q

What are the protective Ab against HBV?

A
  • HBcAB

- HBsAB

25
Q

What Ag of HBV indicates infectivviy?

A

HBeAG

26
Q

What type of hepatitis most often leads to chronic hepatitis?

A

HCV

27
Q

What are the 2 mechanisms of HDV infection?

A
  • Superinfection (on an existing HBV infection) -> MORE SEVERE
  • Coinfections
28
Q

Cirrhosis

A

Disruption of normal hepatic parenchyma by bands of fibrosis and regenerative nodules of hepatocytes

29
Q

What is the key mediator of fibrosis seen in cirrhosis?

A

Stellate cells. They release TGF-b to mediate this.

30
Q

What is the main consequence of cirrhosis?

A

Portal HTN

31
Q

Alcohol-Related Liver Disease

A

Damage to the hepatic parenchyma due to consumption of alcohol - most common cause of liver disease in the West

32
Q

What are some of the clinical signs of alcohol-related liver disease?

A
  • Fatty liver
  • Alcoholic hepatitis
  • Cirrhosis
33
Q

Alcoholic Hepatitis

A

Direct damage to hepatocytes often seen with bing drinking

34
Q

What is the mediator of the damage in alcoholic hepatitis?

A

Acetaldehyde

35
Q

What are Mallory bodies?

A

Damaged intermediate filaments in the hepatocytes

36
Q

What pattern of enzymes will be seen with alcoholic hepatitis?

A

AST is greater than ALT - AST is in the mitochondria

37
Q

Nonalcoholic Fatty Liver Disease (NAFLD)

A

Same signs as in the alcoholic version, but WITHOUT exposure to alcohol

  • Fatty liver
  • Hepatitis
  • Cirrhosis
38
Q

What is NAFLD associated with?

A

Obesity

39
Q

Hemochromatosis

A

Excess body iron deposition that can cause cirrhosis - damage from the generation of free radicals - often due to HFE mutation

40
Q

What does the presence of lipfuscin in cells indicate?

A

Aged though wear and tear

41
Q

Wilson Disease

A

Autosomal recessive mutaiton in ATP7B gene in ATP-mediated Cu transport - Cu builds up in the hepatocyes

42
Q

When will hemochromatosis present? What about Wilson?

A

Hemochromatosis - Late young adulthood

Wilson - Childhood

43
Q

What is the treatment of Wilson disease?

A

D-penicillamine

44
Q

Primary Biliary Cirrhosis

A

Autoimmune granulomatous destruction of intrahepatic bile ducts

45
Q

Who is the classic patient of primary biliary cirrhosis?

A

Middle aged women

46
Q

What Ab will be seen in primary biliary cirrhosis?

A

Anti-mitochondrial Ab

47
Q

Primary Sclerosis Cholangitis

A

Inflammation and fibrosis of intrahepatic and extra hepatic bile ducts

48
Q

What is the appearance of primary sclerosing cholangitis on imaging?

A

“Beaded” in uninvolved regions which are dilated

49
Q

What is primary sclerosis cholangitis associated with?

A
  • Ulcerative coititis

- p-ANCA is often positive

50
Q

Reye Syndrome

A

Fulminant liver failure and encephalopathy in children with viral illness who take aspirin

51
Q

Hepatic Adenoma

A

Benign tumor of hepatocytes that is associated with oral contraceptives

52
Q

What is a serum tumor marker for hepatocellular carcinoma?

A

Alpha-fetoprotein

Pathoma (119 decks)

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