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Clin Med II - GI > Liver Duval Lecture > Flashcards

Liver Duval Lecture Flashcards

(44 cards)

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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?

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

What is Gilbert Syndrome?

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A
  • A/w jaundice

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

20
Q

What is Dubin Johnson syndrome?

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A
  • A/w jaundice

- Increased conjugated bilirubin due to defective excretion

21
Q

What is Rotor’s syndrome?

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A
  • A/w jaundice

- Asymptomatic increased conjugated bilirubin due to defective uptake and excretion

22
Q

What causes cholestasis (pathology)?

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A
  • Hepatocellular dysfunction

- Biliary obstruction

23
Q

Morphology of cholestasis

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

Features of cholestasis (pathology)

Study These Flashcards
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
How much destruction of the liver needs to occur to produce hepatic failure?
80-90%
26
Morphology of hepatic failure
- Massive necrosis (viral, toxic, immune) - Chronic liver disease - Necrosis absent (Reyes, TCN, AFLP)
27
Describe hepatic encephalopathy (pathology)
- Metabolic disorder of CNS/neuro - Severe loss of hepatic function - Shunting of blood around diseased liver
28
Describe hepatorenal syndrome (pathology)
- Renal failure in setting of liver failure - Reduced urine output - Hyperosmolar urine with low Na
29
Morphology of liver cirrhosis
- Bridging fibrosis - Regenerative nodules - Diffuse architectural disruption
30
Causes of portal HTN (pathology)
- Prehepatic (thrombosis of portal vein, splenomegaly) - Intrahepatic (cirrhosis, fatty change) - Posthepatic (R HF, pericarditis)
31
What are non-hepatic viruses that can cause hepatitis?
- EBV - CMV/herpes - Yellow fever - Adeno, rubella, entero
32
IgM antiHAV in Hepatitis A indicates:
Acute infection
33
IgG antiHAV in Hepatitis A indicates:
Immunity
34
What are the different states of clinical viral syndromes?
- Carrier state - Asymptomatic infection - Acute infection - Chronic infection - Fulminant
35
Acute infection by viral hepatitis consists of which stages?
- Incubation - Symptomatic pre-icteric - Symptomatic icteric - Convalescence
36
Morphology of acute hepatitis
- Mixed inflammation - Ballooning degeneration - Cholestasis - Councilman bodies - Fatty change
37
Morphology of chronic hepatitis
- Early: portal inflammation - Progression: periportal and bridging inflammation - Late: post-necrotic cirrhosis
38
Describe fulminant hepatitis (pathology)
- Onset of disease to encephalopathy in 2-3 weeks | - MC viral (HBV more than HCV)
39
Morphology of fulminant hepatitis
- Diffuse or random areas of necrosis - Shrunken organ - Scarring - Post-necrotic cirrhosis
40
Describe autoimmune hepatitis (pathology)
- Chronic hepatitis with immune abnormalities - MC female - Responds to immunosuppression
41
How can toxic liver injury occur (pathology)?
- Direct toxicity of agent - Conversion to toxic species - Immune mediated injury
42
Morphology of steatosis alcoholic liver disease
- Micro or macrovesicular - Initially centrilobular - Large, yellow, soft, greasy * Completely reversible with abstinence
43
Morphology of alcoholic hepatitis
- Ballooning degeneration - Mallory bodies - Polys - Fibrosis
44
Morphology of alcoholic cirrhosis
- 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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