NASH/ASH & DILI Flashcards

1
Q

AFLD

A

Alcoholic Fatty Liver Disease

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2
Q

NAFLD

A

Non-Alcoholic Fatty Liver Disease

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3
Q

ASH

A

Alcoholic Steatohepatitis

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4
Q

NASH

A

Non-Alcoholic Steatohepatitis

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5
Q

accumulation of triglyceride within hepatocyte cytoplasm; risk factors are metabolic syndromes and excessive alcohol consumption; NOT associated with inflammation or hepatocyte ballooning; REVERSIBLE with exercise and weight loss

A

Steatosis

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6
Q

Steatosis is reversible with…

A

Exercise

Weight loss

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7
Q

Alcoholic and Non-Alcoholic fatty liver disease are distinguished by histologic features (True or False)

A

False; must be done through clinical history/etiology

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8
Q

NAFLD and AFLD encompass both simple steatosis and steatohepatitis (True or False)

A

True

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9
Q

fat accumulation in hepatocytes WITH inflammation, hepatocyte ballooning and fibrosis

A

Steatohepatitis

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10
Q

In addition to steatosis, what histologic features do you see in NASH and ASH?

A

Lobular inflammation, hepatocytes ballooning and fibrosis

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11
Q

hepatocyte finding in steatohepatitis; cells are larger with pale swollen cytoplasm with clumps of cytoskeleton filaments, and a more rounded contour

A

Hepatocyte Ballooning

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12
Q

As cirrhosis evolves in the setting on steatohepatitis, steatosis often becomes less apparent and is sometimes absent entirely (True or False)

A

True

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13
Q

High triglycerides, Low HDL, Insulin resistance, Obesity, and HTN are risk factors for metabolic syndrome that can cause

A

Non-Alcoholic Fatty Liver Disease

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14
Q

How can adipose tissue contribute to the progression of steatohepatitis?

A

Adipose tissue are actually active (can release a variety of pro-inflammatory factors

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15
Q

How does Chronic Alcohol consumption contribute to Alcoholic Fatty Liver Disease

A

1) Endotoxin activates Kupffer cells to release cytokines
2) ETOH metabolism requires heavy O2 consumption (hypoxia)
3) Production of acetaldehyde (damages liver proteins and stimulates immune response)

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16
Q

dense, eosinophilic aggregates of clumped cytoskeleton microfilaments in hepatocytes; seen in BOTH alcoholic and non-alcoholic steatohepatitis (far LESS in non-alcoholic though)

A

Mallory-Denk bodies (Mallory’s Hyaline)

17
Q

(NASH/ASH) is the most common chronic hepatic disorder in Western nation, sometimes silent until well advanced, with minimal to no abnormal LFTs

A

NASH

18
Q

The AST:ALT ratio for alcohol related Fatty Liver Disease/Steatohepatitis

A

> 2

19
Q

Treatment for NAFLD

A
  1. Diet and exercise

2. Tx underlying metabolic syndrome

20
Q

Diagnosis of Alcoholic Liver Disease

A
  1. H & P (identify alcoholism)
  2. AST:ALT >2
  3. Elevated GGT
  4. Histologic findings
21
Q

Two main categories for drug-induced liver injury

A

Direct: injury due to drug metabolites
Indirect: Drug-induced immune mediated injury

22
Q

Histologic features of Drug-Induced Immune-Mediated liver injury

A
  1. Inflammation with EOSINOPHILS

2. Numerous apoptotic hepatocytes (acidophil bodies)

23
Q

Notorious drug that cause toxic liver injury

A

Acetaminophen (Tylenol)

24
Q

Histologic features of Toxic-Injury to the liver (due to a drug metabolite)

A
  1. Centrilobular necrosis with hepatocytes showing eosinophilic staining
  2. Normal hepatocytes showing numerous mitotic figures (regenerating cells)
25
Q

What are some drugs notorious for drug-induced liver injury

A
  1. Antibiotics
    - amoxicillin
  2. NSAIDs
    - Ibuprofen
    - acetaminophen