Liver Pathology Flashcards

1
Q

What is ballooning degeneration?

What are conditions in which it occurs? (3)

A

Ballooning degernation is depletion of ATP with loss of volume control

It results from severe cell injury including ischemia, cholestasis, toxicity due to alcohol

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2
Q

What are causes of macrosteatosis? (list)

A

Obesity, alchol, drugs/toxins, HepC, ischemia, TPN, CF, metabolic

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3
Q

What are causes of microsteatosis?

A
Fatty liver of pregnancy
Drugs (valproate)
Toxins
Inherited diseases
Reye's syndrome
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4
Q

What are causes of unconjugated hyperbilirubinemia?

A

Physiologic jaundice
Bilirubin overproduction: hemolysis, hematomas, dyserythropoiesis
Diminished bilirubin uptake (RH failure)
Inherited disorders: UGT1A1- Cigler Najjar and Gilbert Syndrome

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5
Q

What is kernicterus?

A

Complication of severe unconjugated hyperbilirubinemia– circulating free bilirubin crosses BBB and desposits within neurons of basal ganglia

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6
Q

What are some of the pathologic appearances of cholestasis in liver? (3)

A

Feathery degeneration of hepatocytes

Rosetting/psuedoglandular arrangement of hepatocytes in prolonged cholestasis

Portal expansion and bile duct proliferation in obstructive cholestasis

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7
Q

What are two major types of hepatocellular necrosis?

A

Cytolytic: irreversible ballooning of hepatocytes due to defective osmotic regulation resulting in cell swelling/death. Toxic cause

Coagulative: architecture of dead tissue preserved; results from ischemic damage

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8
Q

Describe the difference between confluent and zonal necrosis

A

Confluent: Death of groups of adjacent hepatocytes (“like a geographic area”)

Zonal: confluent necrosis that exhibits a zonal distribution in the lobule

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9
Q

What are the lab measurements that are taken to evaluate liver disease?

A

Hepatocyte integrity: AST, ALT, LDH
Biliary function: BR, bile acids, canalicular enzymes (Alk-Phos, GGT)
Synthetic function: Albumin, coagulation factors, ammonia

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10
Q

What is the mechanism for chronic injury outcome?

A

Chronic injury==>Kipper cell activation==>Activation of stellate cells==>liver fibrosis==>Cirrhosis

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11
Q

Describe the gross/histological appearance of cirrhosis

What are the leading cause of cirrhosis?

A

Gross: parenchymal nodules surrounded by fibrous tissue
Histo: islands of parenchyma with tons of fibrotic tissue between

Leading causes: HepB/C, NAFLD, alcoholic liver disease

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12
Q

Acute Liver Failure:

What are most common causes? What are complications of liver failure? (2)

A

Common causes: Viral hepatitis (worldwide), acetaminophen overdose (West)

Complications include cerebral edema/intracranial hypertension

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13
Q

Describe the histological appearance of acetaminophen toxicity

A

Confluent coagulative necrosis involving mid-zones (II/III)

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14
Q

Describe gross and histological appearance for fulminant liver failure

A

Gross: significantly shrunken liver
Histo: parenchymal loss results in central vein and portal tract looking very similar due to reticulin collapse (“accordion collapse of veins”)

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15
Q

Contrast the morphological features of acute vs. chronic hepatitis

A

Acute: Ballooning degeneration, apoptosis, cholestasis, little mononuclear infiltrate

Chronic: Bridging necrosis, dense mononuclear infiltrate, fibrosis of portal veins

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16
Q

Describe the etiologies associated with variety of inflammatory cell types

A
Hepatotropic viruses: lymphocytes
Bacteria: neutrophils
Mycobacteria/fungi: granulomas
Autoimmune: lymphocytes/plasma cells
Drugs: eosinophils
Transplant rejection: eosinophils and lymphocytes
17
Q

Describe the histological features for acute hepatitis (2)

A

Hepatocellular injury with lobular inflammation

Giant cells

18
Q

What are types of necrosis observed with severe acute hepatitis? (2)

A

Confluent necrosis due to parenchymal collapse

Bridging necrosis resulting in portal-portal or portal-central linking

19
Q

What are etiologies of granulomatous hepatitis (5)

A
Infections: TB
Foreign body reactions
Drug reactions
Autoimmune disease
Primary biliary cirrhosis
20
Q

What are the etiologies for chronic hepatitis? (4)

A

Chronic viral hepatitis
Autoimmune hepatitis
Metabolic diseases: A1antitrypsin deficiency or Wilson’s disease
Drugs

21
Q

What do grade and stage measure in liver biopsy of chronic hepatitis case?

A

Grade: severity of inflammation and cellular injury
Stage: extent of fibrosis

22
Q

What is interface activity?

A

Interface activity refers to inflammation/hepatocellular injury at border between portal tract and the lobule (“limiting plate”)

23
Q

Describe morphological features of HepB vs. HepC

A

Both: lobular and portal infiltration
HepB: Evidence of antigen on staining (surface/core antigen), ground glass hepatocytes (accumulation of HepB surface protein)

HepC: More pronounced fat infiltration (steatosis)

24
Q

Describe epidemiology of autoimmune hepatitis

A
Female preponderance (70-90%)
Association with other autoimmune diseases (PSC)
25
Q

What are the difference types of autoimmune hepatitis (2)

A

Type I: anti-SMA/ANA with peak incidence 16-30yo

Type II: anti-LKM, peak incidence 10yo

Type II is more aggressive

26
Q

Describe the histology of autoimmune hepatitis?

A

chronic hepatitis (lobular hepatitis) with plasma cell infiltrate