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TOXICOLOGY > HEPATOTOXICITY > Flashcards

HEPATOTOXICITY Flashcards

1
Q

LIST THE PHASE 1 RXN THAT CONVERTS XENOBIOTICS

A
  • TRANSFORMATION FROM LIPOPHILIC TO POLAR STAGE
  • OXIDATION
  • REDUCTION
  • HYDROLYSIS
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2
Q

PHASE 2 OF XYNOBIOTIC TRANSFORMATION

A
  • CONJUGATION
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3
Q

DISCUSS ZONE 1 OF LIVER BIOTRANSFORMATION

A
  • PERIPORTAL
    • most aerobic
    • contains glutathione
    • glutathione perioxidase
    • alcohol dehydrogenase
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4
Q

discuss zone 2 of liver cell damage

A
  • gradualtransformation from zone 1 to 3
    • contains something of both elements
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5
Q

discuss zone 3 of specific hepatic cell damage

A
  • least aerobic
  • contains CYP450
  • CYP450 REDUCTASE
  • ALSO PLACE OF LIPID SYNTHESIS
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6
Q

LIST THE CHEMICALS THAT CAUSES ZONE 1 DAMAGE IN LIVER

A
  1. COCCAINE
  2. ALCOHOL
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7
Q

LIST THE CHEMICALS THAT CAUSES AMAGE IN ZONE 2

A

SELDOMLY SPECIFIC

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8
Q

LIST THE CHEMICALS THAT CAUSES AMAGE IN ZONE 3

A
  • ccl4
  • benzo(a) pyrine
  • PCBs
  • aflatoxins
  • pyrrolizidine alkaloids,
  • acetaminophen
    a. o.
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9
Q

define cholestasis

A

Damage to canicula, causing hyperbilirubinemia

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10
Q

define steatosis and where it occurs

A
  • Triglyceride accumulation (zon3 damage)
  • also known as fatty liver degeneration
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11
Q

Dysfunctional scar tissue formation (stellate
cells)

A

cirrhosis

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12
Q

toxic response of liver to cholestasis

A
  • inhibition excretion of bile salts or phospholipids
  • inhibition excretion via MRP2 (anions, GSH,

bilirubin)

  • injury bile duct epithelium
  • bile duct occlusion (bile stones)
  • injury in hepatocytes
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13
Q

aflatoxin produced by aspegillosus spp. that produces toxins that hurt the joints of chicken

A

Cyclopiazonic acid

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14
Q

primary target organ by aflatoxin

A

liver

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15
Q

secondary effect of aflatoxin

A
  • reduced performance
  • reduced immunity
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16
Q

effects of aflotoxin on diets with low porteins

A

acute toxicity

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17
Q

effects of aflotoxin on diests with high proteins

A

Increase neoplastic foci

18
Q

effects of aflatoxin on diets with low vit. A

A

increased DNA adducts

19
Q

what are the risks for AFlo in milk

A

in high producing animals
animals with subclinical mastitis are at risk
Non-conventional species: buffalos, goats, mares?

20
Q

mainbiotransformation pathways of nicine bases

A
  • Hydrolysis: carboxylesterases
  • N-oxidation: mainly FMO’s
  • Dehydrogenation: CYP (3A, 2B/ 2C
21
Q

this liver cells are sensitive to reactive oxygen/nitrogen species

A

endothelial cells

22
Q

this cells promotes liver cirrhosis, but may also activate oval cells (liver regeneration)

A

kuffur cells

23
Q

which phase 1 activities are affected in liver function impairement

A
  • (CYP450, MFO)
  • mediated processing of hormones,
  • neuro-transmitters (COMT) is delayed or incomplete.
  • Drug metabolism (therapy) Is impaired (dose adjustment - minus 25% of the standard dose)
24
Q

which phase 11 liver activities are affected with liver function impairement

A
  • conjugation activities
    • UDP-GT
    • GST
    • ST
    • AND OTHERS
25
Q

THE MOST TOXIC AFLOTOXIN

A

AFLATOXIN B1

26
Q

POST MORTEM APPEARANCE OF LIVER

A
  • bile duct proliferation with pale livers (fatty liver syndrome)
  • Karyomegaly in hepatocytes Preneoplastic lesions
27
Q

WHICH ANIMALS ARE SENSITIVE TO Pyrrolizidine alkaloids

A
  • horses!
    • Cattle and sheep with copper toxicosis
28
Q

WHICH ANIMALS ARE SENSITIVE TO Biotransformation-based toxicity:

A

horse, cattle, rat, chicken, human

29
Q

WHICH ANIMALS ARE RESISTANT TO Biotransformation-based toxicity:

A

sheep, guinea pig, hamster, gerbil

30
Q

CLINICAL SYMPTOMS OF ACUTE Pyrrolizidine alkaloids TOXICITY

A
  • Liver failure (generally lethal)
    • icterus/jaundice
  • depression (hepato-encephalopathy)
  • edema, ascites
31
Q

OST MORTEM CHANGES IN ACUTE LIVER TOXICITY

A
  • extensive centri-lobular necrosis and hemorrhages,
  • karyomegaly
32
Q

CLINICAL SIGNS OF CHRONIC INTOXICATION WITH Pyrrolizidine alkaloids (PA)

A
  • Rough coat,
  • weight loss,
  • weakness
  • Anorexia,
  • production losses (milk)
  • Photosensitation
  • Liver palpation: small and dense (fibrosis)
33
Q

WHICH ENZYMES ARE ELEVATED IN Pyrrolizidine alkaloids

A
  • AST/ALT slighly increased,
  • GGT high
34
Q

WORKUP OF A PATIENT WITH Pyrrolizidine alkaloids INTOXICATION

A
  • identification of exposure,
  • PA analyses
  • Histological examonation of the liver (karyomegaly, portal necrosis)
35
Q

DISCUSS PROGNOSIS OF PYRROLIZIDIN INTOXICATION

A
  • Prognosis: poor (liver cirrhosis progresses even after cessation of exposure)
  • Caution: PAs are exerted in (dairy) milk PA’s accumulate in honey! Humans: progressive veno-occlusive liver injury with liver cirrhosis, no convincing evidence for carcinogenicity.
36
Q

DISCUSS Acetaminophen INTOXICATION IN CATS

A
  • (metabolism mediated sensitivity already at low doses)
  • Present predominantly methemoglobinemia
37
Q

DISCUSS ACETAMINOPHEN INTOXICATION IN DOGS

A

present clear signs of liver failure (at high, repetitive doses)

38
Q

DISCUSS ACETAMINOPHEN INTOXICATION IN HUMANS

A
  • liver function impairment (DILI – drug induced liver injury: auto-immune mechanism
  • Impairment of bile acid secretion – yellow stools
39
Q

measures to reduce liver injury

A
  1. Reduce exposure
  2. Reduce absorption
  3. Improve elimination
  4. Modulate biotransformation
40
Q

went up to page 14

A

TOXICOLOGY (4 decks)

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