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GI Week 5 > Liver Path 2 - Nelson > Flashcards

Liver Path 2 - Nelson Flashcards

1
Q

What is the early pathologic finding in liver of alcohol abuse?

A

Alcohol steatosis = fatty liver
Enlarged
Macrovesicular steatosis is seen microscopically (large lipid vacules)

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2
Q

Is alcoholic steatosis reversible?

A

Yes, with cessation of alcohol consumption

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3
Q

What are the 3 microscopic features of alcoholic hepatitis?

A

Liver cell injury = swelling/ballooning
Mallory Bodies
Neutrophilic inflammation

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4
Q

What are mallory bodies?

A

cytokeratin aggregates

Can be seen in other liver diseases such as NAFLD and PBC

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5
Q

What is the typical gross appearance of alcoholic cirrhosis? Early and late?

A

Early:

  1. enlarged
  2. Fatty
  3. Micronodular

Late:

  1. Shrunken
  2. Non-fatty
  3. Variable size nodules
  4. Choelstasis is usually present
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6
Q

2 big causes of death in alcoholic cirrhosis?

A
  1. Hepatic encephalopathy and coma

2. Massive GI tract hemorrhage (esophageal varices)

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7
Q

What patient population gets non-alcoholic fatty liver disease?

A 
Metabolic Syndrome
Obesity
Type 2 diabetes
Dyslipidemia
Insulin Resistance
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8
Q

Fibrosis + nodules = ?

A

Cirrhosis

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9
Q

What is primary biliary cirrhosis?

A

Autoimmune cholangiopathy characterized by progressive inflammatory destruction of small and medium sized intrahepatic bile ducts

May lead to cirrhosis

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10
Q

Which bile ducts are destroyed in primary biliary cirrhosis?

A

INTRAHEPATIC bile ducts!

Extrahepatic bile ducts are spared

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11
Q

Typical patient with PBC?

A

Middle aged females of northern european ancestry

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12
Q

Key diagnostic lab test for PBC?

A

AMA = antimitochodnrial antibodies

Elevated alkaline phosphatase and GGT

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13
Q

Insidious onset of fatigue and anicteric pruritis…. what do you think it is?

A

Primary biliary cirrhosis

May also get xanthomas, steatorrhea, vit. D. malabsorption-related osteomalacia

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14
Q

What causes secondary biliary cirrhosis?

A 
Secondary to any disorder causing prolonged EXTRAHEPATIC bile duct obstruction:
Stones
Tumor
Biliary Atresia
Cystic fibrosis
Choledochal cysts
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15
Q

What is primary sclerosing cholangitis?

A

Autoimmune cholangiopahty

Progressive, random, unever fibroinflammatory destruction of EXTRA and INTRAHEPATIC bile ducts

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16
Q

What distinguishing PBC and PSC?

A

PBC is only intrahepatic ducts

PSC is both intra and extra hepatic ducts

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17
Q

What disease is primary sclerosing cholangitis (PSC) assoicated with?

A

Ulcerative cholitis

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18
Q

What antibody is usually found in PSC?

A

p-ANCA

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19
Q

How does PSC appear on cholangiogram?

A

Beaded appearance

Demonstrates strictures and dilations of extrahepatic and intrahepatic bile ducts

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20
Q

Define hereditary hemochromotosis

A

Excessive iron absorption, resulting in the accumulation of iron in tissues, producing organ injury

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21
Q

Pathogenesis of herediatry hemochromotosis

A

Decreased synthesis of hepcidin leading to excessive intestinal iron absorption

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22
Q

Hereditary hemochormotosis has mutations in what gene? located on what chromosome?

A

HFE gene on chromosome 6

Most common mutation is C282Y

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23
Q

Classic triad for hemochromotosis?

A

Cirrhosis
Diabetes
Skin pigmenetation

24
Q

Best screening test for hemochromotosis?

A

Fasting transferrin saturation

25
Q

Treatment for hemochromotosis?

A

Clear excessive iron from tissues using phlebotomy or iron chelating agents

26
Q

Common cause of secondary hemochromotosis?

A

Parenteral iron overload (transfusions, iron-dextran injections)

27
Q

How does liver biopsy of secondary hemochromotosis differ from hereditary?

A

2nd = iron initially accumulates in the KUPFFER CELLS, NOT HEPATOCYTES

28
Q

What is Wilson’s disease?

A

Disorder of cooper metabolism resulting in impaired secretion of copper as ceruloplasmin as well as impaired excretion of copper into bile

29
Q

Mutation in Wilson’s disease?

A

Mutation in ATP7B gene on chromosome 13

Defective copper-transporting ATPase protein

30
Q

Diagnostic test for Wilson’s disease?

A

Low ceruloplasmin levels

Increased 24 hour urinary copper excretion

31
Q

What can be seen on eye exam in Wilson’s disease?

A

Kayser-Fleischer rings

Copper ring deposits in eye

32
Q

When should you consider Wilson’s Disease in your differential?

A

Liver disease in anyone

33
Q

What do you see in Wilson’s disease on liver biopsy?

A

Increased hepatic copper

34
Q

Define alpha-1-antirypsin deficiency

A

Abnormally low levels of A1AT which primarily inhibits neutrophil elastase (A1AT is a protease inhibitor)

35
Q

How does pathogenesis of lung and liver injury differ in A1AT deficiency?

A

Liver disease is related to the ACCUMULATION of A1AT in hepatocytes

Lung = secondary to anti-protease/protease imbalance

36
Q

What do you see on liver biopsy in A1AT deficiency?

A

Cirrhosis with PAS + globules

**misfolded gene product protein aggregates in heptocellular ER

37
Q

Two main categories of drug induced liver injury?

A
  1. Direct hepatotoxicity = toxic to liver in a predictable, dose dependent fashion
  2. Unpredictable hepatotoxicity =
    - not all exposed develop injury
    - toxic reactions may relate to metabolism of drug or propensity of drug to develop immune response
38
Q

What should you always include in a differential diagnosis for any form of liver disease?

A

Exposure to toxin or therapeutic agent!!

39
Q

What would you expect if there is an outlfow problem (circulatory liver disorder in hepatic vein)

A

Centrilobular congestion

40
Q

Budd-Chiari Syndrome

A

Hepatic Vein thrombosis with centrilobular congestion and necrosis

**Absence of JVD

41
Q

What can cause nutmeg liver?

A

Budd-Chiari Syndrome

Right sided heart failure?

42
Q

Sinusoidal obstruction syndrome

A

Presence of obstructive, non-thrombotic lesions of the small (central) hepatic veins in patients exposed to radiation and/or hepatoxins

43
Q

Biliary atresia

A

Complete or partial obstruction of the lumen of the extrahepatic biliary tree within the first 3 months of life

44
Q

Top 2 leading causes of granulomatous hepatitis?

A
  1. Idiopathic (50%)

2. Sarcoidosis (22%)

45
Q

Define HELLP syndrome

A

Hemolysis
Elevated Liver enzymes
Low Platelets

During pregnancy

46
Q

3 pregnancy associated liver diseases?

A

Preeclampsia
Acute fatty liver
Intrahepatic cholestasis

47
Q

What is preeclampsia?

A

maternal hypertension
Proteinuria
Peripheral edema
Coagulation abnormalities

48
Q

What do AST and ALT really tell you? Do they measure hepatic function?

A

NO!!! Elevations in these enzymes reflect hepatocellular damage

49
Q

What lab tests mark cholestasis?

A

Alakline Phosphatase

GGT

50
Q

What markers actually reflect global hepatic function?

A

Albumin
Prothrombin Time
Clotting factors (Factor V levels)

*true hepatic synthesis

51
Q

Which is more specific to liver ALT or AST?

A

ALT!!! more specific to liver

AST is present in heart, muscle, brain, and kidneys too

52
Q

AST > ALT suggests?

A

Alcoholic hepatitis

53
Q

ALT > AST suggests?

A

Viral hepatitis

54
Q

What is the primary stimulus for ALP production?

A

Bile duct obstruction

Can also see rise in bone disease

55
Q

What test can assist if ALP rise is due to bone of liver?

A

GGT!

Associated with biliary epithelium

56
Q

Do reasons for doing a liver biopsy?

A

Determine etiology of liver disease

Determine extent of damage to the liver

GI Week 5 (12 decks)

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