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Clin Med II - GI > Liver Duval Lecture > Flashcards

Liver Duval Lecture Flashcards

1
Q

What are the different types of hepatic injury?

A
  • Inflammation (hepatitis)
  • Degeneration
  • Necrosis
  • Fibrosis (irreversible)
  • Cirrhosis (irreversible)
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2
Q

What are the irreversible types of hepatic injury?

A
  • Fibrosis

- Cirrhosis

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3
Q

What are the different types of hepatocyte degeneration?

A
  • Ballooning
  • Foamy
  • Steatosis
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4
Q

Describe ballooning degeneration of hepatocytes

A
  • Swollen cells with clumped chromatin

- Toxic, immune

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5
Q

Describe foamy degeneration of hepatocytes

A
  • Swollen cells with diffuse foamy appearance

- Retained biliary material

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6
Q

Describe steatosis

A
  • Fatty degeneration of hepatocytes
  • Microvesicular (ETOH, Reyes, AFLP)
  • Macrovesicular (ETOH, DM, obesity)
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7
Q

What are the different types of hepatocyte necrosis?

A
  • Coagulative
  • Apoptosis
  • Lytic
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8
Q

Describe coagulative necrosis

A
  • Poorly stained cells, “mummified”

- Ischemic

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9
Q

Describe apoptosis of hepatocytes

A
  • Toxic, immune

- Councilman bodies

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10
Q

Describe lytic necrosis

A

Hydropic degeneration (osmotic swelling)

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11
Q

Describe bilirubin metabolism (pathology)

A
  1. Breakdown of senescent RBCs
  2. Bind to serum albumin
  3. Hepatocellular uptake
  4. Glucuronides excreted into bile
  5. Deconjugation in gut to urobilinogens
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12
Q

Describe unconjugated (indirect) hyperbilirubinemia (pathology)

A
  • Water insoluble, tightly bound to albumin
  • Cannot excrete in urine
  • Toxic (kernicteris)
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13
Q

Describe conjugated (direct) hyperbilirubinemia (pathology)

A
  • Water soluble, loosely bound to albumin
  • Excreted in urine
  • Nontoxic
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14
Q

What can cause unconjugated hyperbilirubinemia (pathology)?

A
  • Increased production (e.g. hemolytic anemia)
  • Decreased uptake
  • Decreased conjugation (e.g. hepatitis)
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15
Q

What can cause conjugated hyperbilirubinemia (pathology)?

A
  • Decreased excretion

- Impaired bile flow (e.g. obstruction)

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16
Q

What are disorders a/w jaundice (pathology)?

A
  • Physiologic in newborns
  • Crigler Najjar I
  • Crigler Najjar II
  • Gilbert syndrome
  • Dubin Johnson syndrome
  • Rotor’s syndrome
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17
Q

What is Crigler Najjar I?

A
  • A/w jaundice
  • Increased unconjugated bilirubin due to lack of enzyme UGT
  • Fatal
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18
Q

What is Crigler Najjar II?

A
  • A/w jaundice
  • Increased unconjugated bilirubin due to partial enzyme defect
  • Nonfatal
19
Q

What is Gilbert Syndrome?

A
  • A/w jaundice

- Mild increased unconjugated due to reduced enzyme activity and impaired uptake

20
Q

What is Dubin Johnson syndrome?

A
  • A/w jaundice

- Increased conjugated bilirubin due to defective excretion

21
Q

What is Rotor’s syndrome?

A
  • A/w jaundice

- Asymptomatic increased conjugated bilirubin due to defective uptake and excretion

22
Q

What causes cholestasis (pathology)?

A
  • Hepatocellular dysfunction

- Biliary obstruction

23
Q

Morphology of cholestasis

A
  • Bile stained liver
  • Foamy degeneration
  • Distension/proliferation of upstream bile ducts
  • Bile lakes
  • Ultimately, fibrosis and cirrhosis
24
Q

Features of cholestasis (pathology)

A
  1. Enlarged hepatocytes
  2. Dilated canaliculi
  3. Apoptosis
  4. Bile pigment in Kupffer cells
  5. Bile duct proliferation
  6. Bile retention
  7. Periportal degeneration
25
Q

How much destruction of the liver needs to occur to produce hepatic failure?

A

80-90%

26
Q

Morphology of hepatic failure

A
  • Massive necrosis (viral, toxic, immune)
  • Chronic liver disease
  • Necrosis absent (Reyes, TCN, AFLP)
27
Q

Describe hepatic encephalopathy (pathology)

A
  • Metabolic disorder of CNS/neuro
  • Severe loss of hepatic function
  • Shunting of blood around diseased liver
28
Q

Describe hepatorenal syndrome (pathology)

A
  • Renal failure in setting of liver failure
  • Reduced urine output
  • Hyperosmolar urine with low Na
29
Q

Morphology of liver cirrhosis

A
  • Bridging fibrosis
  • Regenerative nodules
  • Diffuse architectural disruption
30
Q

Causes of portal HTN (pathology)

A
  • Prehepatic (thrombosis of portal vein, splenomegaly)
  • Intrahepatic (cirrhosis, fatty change)
  • Posthepatic (R HF, pericarditis)
31
Q

What are non-hepatic viruses that can cause hepatitis?

A
  • EBV
  • CMV/herpes
  • Yellow fever
  • Adeno, rubella, entero
32
Q

IgM antiHAV in Hepatitis A indicates:

A

Acute infection

33
Q

IgG antiHAV in Hepatitis A indicates:

A

Immunity

34
Q

What are the different states of clinical viral syndromes?

A
  • Carrier state
  • Asymptomatic infection
  • Acute infection
  • Chronic infection
  • Fulminant
35
Q

Acute infection by viral hepatitis consists of which stages?

A
  • Incubation
  • Symptomatic pre-icteric
  • Symptomatic icteric
  • Convalescence
36
Q

Morphology of acute hepatitis

A
  • Mixed inflammation
  • Ballooning degeneration
  • Cholestasis
  • Councilman bodies
  • Fatty change
37
Q

Morphology of chronic hepatitis

A
  • Early: portal inflammation
  • Progression: periportal and bridging inflammation
  • Late: post-necrotic cirrhosis
38
Q

Describe fulminant hepatitis (pathology)

A
  • Onset of disease to encephalopathy in 2-3 weeks

- MC viral (HBV more than HCV)

39
Q

Morphology of fulminant hepatitis

A
  • Diffuse or random areas of necrosis
  • Shrunken organ
  • Scarring
  • Post-necrotic cirrhosis
40
Q

Describe autoimmune hepatitis (pathology)

A
  • Chronic hepatitis with immune abnormalities
  • MC female
  • Responds to immunosuppression
41
Q

How can toxic liver injury occur (pathology)?

A
  • Direct toxicity of agent
  • Conversion to toxic species
  • Immune mediated injury
42
Q

Morphology of steatosis alcoholic liver disease

A
  • Micro or macrovesicular
  • Initially centrilobular
  • Large, yellow, soft, greasy
  • Completely reversible with abstinence
43
Q

Morphology of alcoholic hepatitis

A
  • Ballooning degeneration
  • Mallory bodies
  • Polys
  • Fibrosis
44
Q

Morphology of alcoholic cirrhosis

A
  • Brown, shrunken, nonfatty
  • Micronodular to mixed micro/macro (Laennec’s)
  • Only 10-15% of alcoholics, females MC
  • Cirrhosis can develop without having prior steatosis/hepatitis

Clin Med II - GI (17 decks)

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