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pharmacology > toxicology lect 8 > Flashcards

toxicology lect 8 Flashcards

1
Q

arises from a single or multiple exposure to an agent over 1-2 days

A

acute toxicity

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2
Q

occurs from repeated exposures of a agent over a period no longer than 3 months

A

subacute toxicity

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3
Q

occurs from repeated exposures over a period greater than 3 months

A

chronic toxicity

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4
Q

synergism effect of drugs

A

when two drugs that have the same effect are used together and the response is greater than what would be expected by adding the responses to the drugs used alone

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5
Q

effect of volume of distribution (Vd) of a toxin on the ability to purify a drug

A

the larger the Vd of a toxin the harder it is purify the blook through hemodialysis because the toxin is accumulated in the periphery

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6
Q

at very high and toxic concentrations, elimination process may become saturated and toxins or drugs normally elimited by first order kinetics become elimiated via what

A

zero order kinetics

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7
Q

what are the primary determinants of toxicity

A
  1. dose and dose rate
  2. duration of exposure (AUC)
  3. route of exposure
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8
Q

what is the mechanism of toxicity of cyanide

A

interfere with cellular energy function

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9
Q

necrosis

A
  • acute, traumatic premature death of cells in living tissue
  • caused by factors external to the cell or tissue
  • lack of a proper immune response leads to a buildup of dead tissue and cell debris
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10
Q

when is gastric lavage not recommended after acute poisoning

A
  • 4 hours after consumption
  • 30 min have elapsed since ingestion of a corrosive material
  • ingestion of hydrocarbon solvents
  • coma, stupor, delirium or convulsions are present
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11
Q

what is ipecac syrup used for

A

induces emesis; treatment of acute poisoning

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12
Q

what can be done to increase the rate of excretion following an acute poisoning

A
  • osmosis diuretics
  • alter urinary pH (bicarbonate, ammonium chloride)
  • hemodialysis and hemoperfusion

** small the Vd, the more effective the dialysis

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13
Q

what drug can be administered to reduce the absorption or enhance the elimination of chemicals

A

activated charcoal

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14
Q

what drug can be administered to reduce the absorption or enhance the elimination of bases

A

ammonium chloride: acidify urine

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15
Q

what drug can be administered to reduce the absorption or enhance the elimination of acids

A

sodium bicarbonate: alkalinize the urine

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16
Q

Dimercaprol chelates what metals

A

arsenic

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17
Q

penicillamine chelates what metal

A

copper

*used in Wilson’s disease and resistant cases of rheumatoid arthritis

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18
Q

Deferoxamine chelates what metal

A

iron

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19
Q

calcium disodium edetate chelates what metal

A

lead

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20
Q

what drug can be given to inactivate the toxins with acetaminophen poisoning

A

acetylcysteine

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21
Q

what drug is used to treat cholinesterase inhibitor poisons (OPs)

A

atropine

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22
Q

what drug is used to treat sodium nitrite, Na+ thiosulfate, and amyl nitrite poisoning

A

cyanide antidote

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23
Q

what drug is used to treat methanol or ethylene glycol poisoning

A

ethanol

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24
Q

what drug is used to treat ethylene glycol poisoning

A

fomepizole

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25
Q

mechanism of bleach (3-6% sodium hypochlorite in water) poisoning. what are the symptoms?

A
  • oxidative stress
  • symptoms
    • severe irritation
    • hypotension
    • delirium
    • coma
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26
Q

treatment of bleach poisoning

A

remove from skin by flooding with water

  • do not use emesis or lavage
  • use mik, melted ice cream or beaten eggs
  • antacids
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27
Q

mechanism of ethylene glycol poisoning

A
  • converted to oxalic acid by alcohol dehydrogenase
  • alters calcium homeostasis
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28
Q

symptoms of ethylene glycol poisoning

A
  • CNS depression
  • kidney damage due to calcium oxalate crystals
29
Q

treatment of ethylene glycol poisoning

A
  • gastric lavage
  • give ethanol IV
  • fomepizole- alcohol dehydrogenase inhibitor
30
Q

mechanism of botulinus toxin (produced by clostridium botulinum)

A

inhibits the release of Ach

31
Q

symptoms of of botulinus toxin

A
  • 8 hr to 8 days
  • vomiting
  • double vision
  • muscular paralysis
32
Q

treatment of of botulinus toxin

A
  • emesis, gastric lavage
  • draw blood to measure toxin concentration
  • give equine trivalent antitoxin (ABE)
33
Q

mechanism of organophosphate (parathion and malathion) poisoning (found in insecticides and pesticides)?

A

irreversible cholinesterase inhibitor

34
Q

symptoms of organophosphate poisoning

A

SLUD

  • salvation
  • lacrimation
  • urination
  • defecation
35
Q

chronic exposure of organophosphate poisoning may contribute to what disease

A

parkinsons disease

36
Q

treatment of organophosphate poisoning

A

atropine to block cholinergic effects

37
Q

mechanism of organochlorine pesticide (DDT, Dieldrin) poisoning

A

interfere with the inactivation of sodium channel and enhance neuron excitability causing rapid repetitive firing

38
Q

symptoms of organochlorine pesticide (DDT, Dieldrin) poisoning acute and chronic exposure

A
  • acute:
    • CNS stimulation
    • tremors
  • chronic
    • association with brain CA, tesicular CA, non-hodgkin’s lymphoma, alzheimers
39
Q

treatment after organochlorine pesticide (DDT, Dieldrin) poisoning

A

none, symptomatic

40
Q

mechanism of chlorophenoxy compounds (TCDD): 2,3,7,8 tetrachloro-p-dioxin (herbicide) poisoning

A

agonist for aryl hydrocarbon (AH) receptor, induces gene expression

41
Q

mechanims of paraquat poisoning

A

oxidative stress

42
Q

symptoms of paraquat poisoning

A
  • hematemesis
  • ocular surface toxicity; skin irritant
  • pulmonary edema and fibrosis
43
Q

treatment of paraquat poisoning

A
  • lavage, cathartics, charcoal
44
Q

mechanism of carbon tetrachloride (CCl4) poisoning

A

metabolized by a CYP450 to free radicals -> apoptotic cell death

45
Q

symptoms of carbon tetrachloride (CCl4) poisoning

A
  • CNS depression
  • cardiac arrhythmias
  • liver and kidney damage
  • carcinogenic
46
Q

treatment of carbon tetrachloride (CCl4) poisoning

A

remove contaminated clothing and treat symptoms

47
Q

mechanism of mineral acid (corrosive) poisoning

A

oxidative stress

48
Q

symptoms of mineral acid (corrosive) poisoning

A
  • inflammation and necrosis of GI tract
  • hypovolemic shock due to massive hemorrhage
49
Q

treatment of mineral acid (corrosive) poisoning

A
  • do not use gastric lavage or emetic compounds
  • dilute acid with water
  • milk of magnesia
50
Q

mechanism of arsenic (heavy metal) poisoning

A

binds to SH groups on metabolic enzymes, increased oxidative stress

51
Q

acute and chronic symptoms of arsenic (heavy metal) poisoning

A
  • acute
    • G.I. effects; CNS effects, ventricular arrhythmias
  • chronic
    • polyneuritis, nephritis, cardiac failure, liver cirrhosis
52
Q

treatment of arsenic (heavy metal) poisoning

A

dimercaprol

53
Q

mechanims of lead poisoning

A

oxidative stress

*primarily bound to erythrocytes, redistributed and accumulates in other tissues, especially bone

54
Q

neuromuscular effects of lead poisoning

A

wrist drop and ankle drop

55
Q

treatment of lead poisoning

A

chelation (edetate calcium disodium)

56
Q

mechanismof iron poisoning

A

oxidative injury; corrosive effect in GI tract

57
Q

symptoms of iron poisoning

A
  • severe G.I irritation
  • mucosal block is destroyed
  • hypotension, shock
58
Q

treatment of iron poisoning

A

deferoxamine

59
Q

mechanism of copper poisoning

A

redox cycles, increases oxidative stress

60
Q

wilson’s disease

A

genetic disorder in which the body cannot eliminate copper and it accumulates in tissue

61
Q

treatment of copper poisoning

A

penicillamine

62
Q

mechanism of asbestos

A
  • redox cycles, increases oxidative stress
  • chronic inflammatory action
63
Q

treatment of asbestos poisoning

A

symptomatic

64
Q

mechanism of carbon monoxide poisoning

A

impairs ability of oxyhemoglobin to transport O2

65
Q

treatment of carbon monoxide poisoning

A

administer O2 by best means available

66
Q

mechanism of cyanide poisoning

A

complexes with ferric iron of cytochrome oxidase, produces cellular anoxia by inhibiting oxygen utilization in mitochondria

67
Q

treatment of cyanide poisoning

A
  • rapid
  • cyanide antidote = sodium nitrite or amyl nitrite
  • then give sodium thiosulfate and rhodanese
68
Q

symptoms of chronic lead poisoning

A

CNS effects: hyperirritability, behavior disturbances and intellectual deficits, finally coma and intractable convulsions

69
Q

Role of Rhodanese in cyanide metabolism

A

CN- + S (thiosulfate) → SCN- (excreted)

pharmacology (9 decks)

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