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PFM: Biweekly Exam 3 > Clinical Toxicology and Toxidromes > Flashcards

Clinical Toxicology and Toxidromes Flashcards

1
Q

what detoxifies acetaminophen

A

glutathione

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2
Q

this led by CYP450s may lead to products with more or less potential for toxicity

A

biotransformation

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3
Q

_____ may be a locus of detoxification or bioactivation

A

absorption

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4
Q

_____ often determines site of toxicity

A

distribution

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5
Q

promotion of this can be a therapeutic strategy

A

elimination of toxin

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6
Q

what age group has highest incidence of acute poisoning

A

1-2 yr olds

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7
Q

most common reason for poisoning by kids

A

unintentional

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8
Q

most common reason for poisoning by adults

A

intentional- suicide

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9
Q

this age group deals with analgesics and sedatives as poison

A

adults

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10
Q

this age group uses household cleaning supplies and cosmetics as poison

A

children

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11
Q

the opiate epidemic (what yr did all drugs increase in consumption)

A

2014

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12
Q

drug to administer if suspected fentanyl overdose

A

naloxone

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13
Q

highest prevalence of drug overdose

A

fentanyl and related drugs

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14
Q

what 2 things are the leading cause of pediatric accidental poisoning fatalities

A

iron and pesticides

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15
Q

this toxicity deals with the drug’s normal pharmacology, but just too high of dose/amount

A

pharmacologic toxicity

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16
Q

ex. metoprolol toxicity=heart block

A

pharmacologic toxicity

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17
Q

type of toxicity where our body is producing an effect that the drug is not made to do by itself (ex. acetaminophen-fever/ibuprofen-hives)

A

pathological toxicity

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18
Q

ex. of genotoxicity

A

radiation; cancer agents

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19
Q

ex. of drug-drug interactions that can lead to toxicity

A

inhibition or induction of CYP450

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20
Q

abnormal reactivity to a chemical peculiar to a given individual (ex. anaphylaxis from giving drug)

A

idiosyncratic drug rxns

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21
Q

final common effect of many toxins that is done by apoptosis or necrosis

A

cell death

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22
Q

3 main steps to manage a poisoned patient:

A
  1. monitor vital signs (O2, fluids);ABC’s
  2. obtain history (what they were doing to bring them in here)
  3. perform toxicologically-oriented patient exam
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23
Q

tx of this is support vital functions, slow drug absorption, and promote excretion

A

poison management

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24
Q

one way to get rid of toxin by absorption in GI tract is____ and combine it with _____ to make them excrete it

A

activated charcoal; sorbitol

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25
Q

this chemical can lead to urinary excretion of toxin

A

sodium bicarbonate

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26
Q

2 main antidotes to administer for opiate intoxication

A

naloxone (Narcan)
naltrexone (trexan)

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27
Q

antidote used for acetaminophen poisoning

A

N-acetylcysteine

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28
Q

antidote for atropine toxicity (can cross BBB)

A

physostigmine

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29
Q

antidote for methanol poisoning

A

ethanol

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30
Q

antidote for organophosphate poisoning

A

atropine and pralidoxime

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31
Q

antidote for metal poisoning (lead and iron)

A

metal chelators

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32
Q

a constellation of clinical signs that may suggest a particular type of ingestion

A

toxidrome

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33
Q

anticholinergic
cholinergic
sympathomimetic
sedative
hallucinogenic
serotonergic

A

toxidromes

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34
Q

acute ingestion of acetaminophen happens with what dose in children

A

> 200mg/kg

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35
Q

acute ingestion of acetaminophen happens with what dose in adults

A

6-7 g

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36
Q

N/V and anorexia are main presentations for what toxicity

A

acute acetaminophen toxicity

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37
Q

after 1-2 days, what levels rise that lead to liver necrosis and also acute renal failure can happen

A

AST and ALT

38
Q

presents with N/V and worsening sx’s and evidence of hepatic injury

A

chronic acetaminophen toxicity

39
Q

how to dx acetaminophen toxicity:

A

at 4 hours after ingestion, obtain blood work (CMP)

40
Q

how to tx acetaminophen toxicity

A

N-acetylcysteine (NAC)
activated charcoal/sorbitol
fluids; vitamin C

41
Q

this toxicity is caused by GSH (glutathione) depletion

A

acetaminophen

42
Q

this toxicity presents with vomiting, tinnitus, and ABG’s show respiratory alkalemia and metabolic acidosis

A

acute salicylate toxicity

43
Q

this toxicity presents with confused elderly patient and its harder to diagnose

A

chronic salicylate toxicity

44
Q

how to dx salicylate toxicity:

A

check serum salicylate toxicity
check ABG’s (reveal respiratory alkalemia and metabolic acidosis)

45
Q

how to tx salicylate toxicity:

A

get them to ICU
sodium bicarbonate
activated charcoal

46
Q

exposure for iron toxicity

A

prenatal vitamins

47
Q

mechanism that causes iron toxicity

A

ROS stress

48
Q

presents w/ abd pain, vomiting and long term GI issues

A

iron toxicity

49
Q

to dx iron toxicity:

A

serum iron and ferritin levels
exposure hx

50
Q

to tx iron toxicity:

A

deferoxamine (metal chelators)

51
Q

exposure for lead toxicity:

52
Q

mechanism for lead toxicity:

A

binds SH groups and inhibits other enzymes

53
Q

this toxicity is multi-system; N/V/ abd pain, peripheral neuropathy, chronic encephalopathy

A

lead toxicity

54
Q

to dx lead toxicity:

A

exposure hx
blood lead level

55
Q

tx lead toxicity:

A

metal chelators (EDTA, dimercaprol)

56
Q

what meds are used for bronchospasms/problems with breathing due to lung inflammation from gases, vapors, smoke inhalation (CO, ozone)

A

steroids (albuterol)

57
Q

what is the treatment for cocaine toxicity

A

Labetalol: alpha and beta adrenergic blocker

58
Q

this drug is an anticoagulant

59
Q

antidote for warfarin toxicity

A

Vitamin K1 (Phytonadione) “fight to not die-one”

60
Q

inhibits Vitamin K action and is used in rodentocide to kill rodents

61
Q

progressive hypoxia leading to HA/V , syncope, seizures, coma

A

Carbon Monoxide toxicity

62
Q

what do you treat carbamate poisoning with? (organophosphate poisoning)

A

Atropine, NOT pralidoxime

63
Q

S-warfarin is a substrate for which enzyme

64
Q

R-Warfarin is a substrate for which enzyme

65
Q

S-Warfarin + cimetidine =

A

bleeding (cimetidine inhibits CYP2C9)

66
Q

R-Warfarin + erythromycin =

A

bleeding (erythromycin inhibits CYP3A4)

67
Q

this toxidrome includes: sleepiness/coma, decrease in HR, RR, and pupil diameter

A

opioid toxicity

68
Q

basically this molecule binds Hb tightly, not allowing it to bind to O2

A

CO poisoning

69
Q

this poisoning leads to agitation, increased HR, BP, temperature, and dilated pupils, even twitching

A

amphetamine poisoning

70
Q

drug development phase that is used first in human volunteers

71
Q

drug development phase that is used in patients (testing efficacy)

72
Q

drug development phase that is a multi-site analysis (looking at different hospitals with patients who were administered drug); deals with dosing of drug

73
Q

drug development phase that deals with after drug is approved (post marketing analysis)

74
Q

which 2 phases used for antineoplastic drugs

75
Q

this drug has financial and operational incentive to be developed faster so that patients can get treatment (newer tx receiving more funding for research)

A

orphan drug

76
Q

term used for not just 1 drug being taken by a patient but many; think meth

A

SPEED BALL

77
Q

this age group has the highest incidental poisoning (accidental)

A

1-2 yr olds

78
Q

this age group when poisoned are most likely to die

79
Q

the amount of a drug needed to produce an effective outcome 50% of the time

80
Q

this poisoning is another organophosphate poisoning and we treat pt. with atropine and pralidoxime

A

Parathion poisoning

81
Q

how do you know if you are giving correct amount of atropine?

A

lungs clear on auscult
BP systolic >80
HR>80

82
Q

the concentration of ligand required to occupy 50% of binding sites (measure of binding affinity)

83
Q

how well a drug can activate full response on receptor

A

kx (effect)

84
Q

this antagonist lessens function of enzyme(receptor) and decreases max response and shifts ED50 to the right

A

allosteric antagonist

85
Q

decrease in the maximum response (b/c # of agonist binding sites decrease

A

non-competitive antagonists (pseudo-irreversible antagonist

86
Q

measure of binding affinity b/t antagonist and receptor

87
Q

competes with primary agonist just shifts ED50 to the right (tries to overcome by increasing conc. of agonist)

A

competitive antagonist

88
Q

decreases the response of the receptor from its baseline (level of activity) all by itself

A

inverse agonist

89
Q

shifts curve to left and makes agonist more potent; binds to a distinct site (not same site as ligand)

A

allosteric agonist

90
Q

binds to same site as ligand and activates receptor

A

primary agonist

PFM: Biweekly Exam 3 (20 decks)

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