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DABT > Liver Tox C&D 8 > Flashcards

Liver Tox C&D 8 Flashcards

1
Q

13-1 Major function of liver and consequences of impaired hepatic functions
Nutrient homeostasis

A

Function:
Nutrient homeostasis

Examples:
Glucose storage and synthesis
Cholesterol uptake

Consequences of impaired functions:
Hypoglycemia, confusion
Hypercholesterolemia

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2
Q

13-1 Major function of liver and consequences of impaired hepatic functions
Filtration of particulates

A

Function:
Filtration of particulates

Examples:
Products of intestinal bacteria (eg, endotoxin)

Consequences of impaired functions:
Endotoxemia

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3
Q

13-1 Major function of liver and consequences of impaired hepatic functions
Protein synthesis

A

Function:
Protein synthesis

Examples:
Clotting factors
Albumin
Transport proteins (eg, very low density lipoproteins)

Consequences of impaired functions:
Excess blessing
Hypoalbuminemia, ascites
Fatty liver

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4
Q

13-1 Major function of liver and consequences of impaired hepatic functions
Bioactivation and detoxification

A

Function:
Bioactivation and detoxification

Examples:
Bilirubin and ammonia
Steroid hormones
Xenobiotics

Consequences of impaired functions:
Jaundice, hyperammonemia-related coma
Loss of secondary male sex characteristics
Diminished drug metabolism
Inadequate detoxification
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5
Q

13-1 Major function of liver and consequences of impaired hepatic functions
Formation of bile and biliary secretion

A

Function:
Formation of bile and biliary secretion

Examples:
Bile acid-dependent uptake of dietary lipids and vitamins
Bilirubin and cholesterol
Metals (eg, Cu and Mn)
Xenobiotics

Consequences of impaired functions:
Fatty diarrhea, malnutrition, Vitamin E deficiency
Jaundice, gallstones, hypercholesterolemia
Mn-induced neurotoxicity
Delayed drug clearance

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6
Q

13-2 What representative toxins give rise to the following type of hepatobiliary injury?
Fatty liver

A

Representative toxins:

Amiodarone, CCl4, ethanol, fialuridine, tamoxifen, valproic acid

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7
Q

13-2 What representative toxins give rise to the following type of hepatobiliary injury?
Hepatocyte death

A

Representative toxins:

Acetaminophen, allyl alcohol, Cu, dimethylformamide, ethanol

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8
Q

13-2 What representative toxins give rise to the following type of hepatobiliary injury?
Immune-mediated response

A

Representative toxins:

Diclofenac, ethanol, halothane, tienilic acid

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9
Q

13-2 What representative toxins give rise to the following type of hepatobiliary injury?
Canalicular cholestasis

A

Representative toxins:

Chlorpromazine, cyclosporin A, 1,1-dichlorothylene, estrogens, Mn, phalloidin

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10
Q

13-2 What representative toxins give rise to the following type of hepatobiliary injury?
Bile duct damage

A

Representative toxins:

Alpha-naphthylisothiocyanate, amoxicillin, methylenedianiline, sporidesmin

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11
Q

13-2 What representative toxins give rise to the following type of hepatobiliary injury?
Sinusoidal disorders

A

Representative toxins:

Anabolic steroids, cyclophosphamide, microcystin, pyrrolizidine alkaloids

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12
Q

13-2 What representative toxins give rise to the following type of hepatobiliary injury?
Fibrosis and cirrhosis

A

CCl4, ethanol, thioacetamide, vitamin A, vinyl chloride

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13
Q

13-2 What representative toxins give rise to the following type of hepatobiliary injury?
Tumors

A

Aflatoxin, androgens, arsenic, thorium dioxide, vinyl chloride

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14
Q

13-3 Factors in the Site-specific injury of representative hepatotoxicants

Site:
Zone 1 hepatocytes (vs Zone 3)

A

Representative toxicants:
Fe (overload)
Allyl alcohol

Potential explanation for site-specificity:
Preferential uptake and high oxygen levels
Higher oxygen levels for oxygen-dependent bioactivation

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15
Q

13-3 Factors in the Site-specific injury of representative hepatotoxicants

Site: Zone 3 hepatocytes (vs Zone 1)

A

Representative toxicants:
CCl4
Acetaminophen
Ethanol

Potential explanation for site-specificity:
More P450 isozyme for bioactivation
More P450 isozyme for bioactivation and less GSH for detoxification
More hypoxic and greater imbalance in bioactivation/detoxification reactions

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16
Q

13-3 Factors in the Site-specific injury of representative hepatotoxicants

Site: Bile duct cells

A

Representative toxicants:
Methylenedianiline, sporidesmin

Potential explanation for site-specificity:
Exposure to the high concentration of reactive metabolites in bile

17
Q

13-3 Factors in the Site-specific injury of representative hepatotoxicants

Site: Sinusoidal endothelium (vs hepatocytes)

A

Representative toxicants:
Cyclophosphamide, monocrotaline

Potential explanation for site-specificity:
Greater vulnerability to toxic metabolites and less ability to maintain glutathione levels

18
Q

13-3 Factors in the Site-specific injury of representative hepatotoxicants

Site: Kupffer cells

A

Representative toxicants:
Endotoxin, GdCl3

Potential explanation for site-specificity:
Preferential uptake and then activation

19
Q

13-3 Factors in the Site-specific injury of representative hepatotoxicants

Site: Stellate cells

A

Representative toxicants:
Vitamin A
Ethanol (chronic)

Potential explanation for site-specificity:
Preferential site for storage and then engorgement
Activation and transformation to collagen-synthesizing cell

20
Q

13-4 Examples of drugs with known idiosyncratic hepatotoxicity:

Immune-mediated (allergic) idiosyncratic hepatotoxicity

A 
Diclofenac (analgesic)
Halothane (anesthetic)
Nitrofurantoin (antibiotic)
Phenytoin (anitconvulsant)
Tienilic acid (diuretic)
21
Q

13-4 Examples of drugs with known idiosyncratic hepatotoxicity:

Nonimmune-mediated (nonallergic) idiosyncratic hepatotoxicity

A 
Amiodarone (antiarrhythmic)
Bromfenac (analgesic)- withdrawn from market
Diclofenac (analgesic)
Disulfiram (alcoholism)
Isoniazid (antituberculosis)
Ketoconazole (antifungal)
Rifampicin (antimicrobial)
Troglitazone (antidiabetes)- withdraen from market
Valproate (anticoncvulsant)

DABT (6 decks)

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