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
this chemical can lead to urinary excretion of toxin
sodium bicarbonate
26
2 main antidotes to administer for opiate intoxication
naloxone (Narcan) naltrexone (trexan)
27
antidote used for acetaminophen poisoning
N-acetylcysteine
28
antidote for atropine toxicity (can cross BBB)
physostigmine
29
antidote for methanol poisoning
ethanol
30
antidote for organophosphate poisoning
atropine and pralidoxime
31
antidote for metal poisoning (lead and iron)
metal chelators
32
a constellation of clinical signs that may suggest a particular type of ingestion
toxidrome
33
anticholinergic cholinergic sympathomimetic sedative hallucinogenic serotonergic
toxidromes
34
acute ingestion of acetaminophen happens with what dose in children
>200mg/kg
35
acute ingestion of acetaminophen happens with what dose in adults
6-7 g
36
N/V and anorexia are main presentations for what toxicity
acute acetaminophen toxicity
37
after 1-2 days, what levels rise that lead to liver necrosis and also acute renal failure can happen
AST and ALT
38
presents with N/V and worsening sx's and evidence of hepatic injury
chronic acetaminophen toxicity
39
how to dx acetaminophen toxicity:
at 4 hours after ingestion, obtain blood work (CMP)
40
how to tx acetaminophen toxicity
N-acetylcysteine (NAC) activated charcoal/sorbitol fluids; vitamin C
41
this toxicity is caused by GSH (glutathione) depletion
acetaminophen
42
this toxicity presents with vomiting, tinnitus, and ABG's show respiratory alkalemia and metabolic acidosis
acute salicylate toxicity
43
this toxicity presents with confused elderly patient and its harder to diagnose
chronic salicylate toxicity
44
how to dx salicylate toxicity:
check serum salicylate toxicity check ABG's (reveal respiratory alkalemia and metabolic acidosis)
45
how to tx salicylate toxicity:
get them to ICU sodium bicarbonate activated charcoal
46
exposure for iron toxicity
prenatal vitamins
47
mechanism that causes iron toxicity
ROS stress
48
presents w/ abd pain, vomiting and long term GI issues
iron toxicity
49
to dx iron toxicity:
serum iron and ferritin levels exposure hx
50
to tx iron toxicity:
deferoxamine (metal chelators)
51
exposure for lead toxicity:
paint
52
mechanism for lead toxicity:
binds SH groups and inhibits other enzymes
53
this toxicity is multi-system; N/V/ abd pain, peripheral neuropathy, chronic encephalopathy
lead toxicity
54
to dx lead toxicity:
exposure hx blood lead level
55
tx lead toxicity:
metal chelators (EDTA, dimercaprol)
56
what meds are used for bronchospasms/problems with breathing due to lung inflammation from gases, vapors, smoke inhalation (CO, ozone)
steroids (albuterol)
57
what is the treatment for cocaine toxicity
Labetalol: alpha and beta adrenergic blocker
58
this drug is an anticoagulant
warfarin
59
antidote for warfarin toxicity
Vitamin K1 (Phytonadione) "fight to not die-one"
60
inhibits Vitamin K action and is used in rodentocide to kill rodents
warfarin
61
progressive hypoxia leading to HA/V , syncope, seizures, coma
Carbon Monoxide toxicity
62
what do you treat carbamate poisoning with? (organophosphate poisoning)
Atropine, NOT pralidoxime
63
S-warfarin is a substrate for which enzyme
CYP2C9
64
R-Warfarin is a substrate for which enzyme
CYP3A4
65
S-Warfarin + cimetidine =
bleeding (cimetidine inhibits CYP2C9)
66
R-Warfarin + erythromycin =
bleeding (erythromycin inhibits CYP3A4)
67
this toxidrome includes: sleepiness/coma, decrease in HR, RR, and pupil diameter
opioid toxicity
68
basically this molecule binds Hb tightly, not allowing it to bind to O2
CO poisoning
69
this poisoning leads to agitation, increased HR, BP, temperature, and dilated pupils, even twitching
amphetamine poisoning
70
drug development phase that is used first in human volunteers
phase I
71
drug development phase that is used in patients (testing efficacy)
phase II
72
drug development phase that is a multi-site analysis (looking at different hospitals with patients who were administered drug); deals with dosing of drug
phase III
73
drug development phase that deals with after drug is approved (post marketing analysis)
phase IV
74
which 2 phases used for antineoplastic drugs
I and II
75
this drug has financial and operational incentive to be developed faster so that patients can get treatment (newer tx receiving more funding for research)
orphan drug
76
term used for not just 1 drug being taken by a patient but many; think meth
SPEED BALL
77
this age group has the highest incidental poisoning (accidental)
1-2 yr olds
78
this age group when poisoned are most likely to die
adults
79
the amount of a drug needed to produce an effective outcome 50% of the time
ED50
80
this poisoning is another organophosphate poisoning and we treat pt. with atropine and pralidoxime
Parathion poisoning
81
how do you know if you are giving correct amount of atropine?
lungs clear on auscult BP systolic >80 HR>80
82
the concentration of ligand required to occupy 50% of binding sites (measure of binding affinity)
Kd
83
how well a drug can activate full response on receptor
kx (effect)
84
this antagonist lessens function of enzyme(receptor) and decreases max response and shifts ED50 to the right
allosteric antagonist
85
decrease in the maximum response (b/c # of agonist binding sites decrease
non-competitive antagonists (pseudo-irreversible antagonist
86
measure of binding affinity b/t antagonist and receptor
Ki
87
competes with primary agonist just shifts ED50 to the right (tries to overcome by increasing conc. of agonist)
competitive antagonist
88
decreases the response of the receptor from its baseline (level of activity) all by itself
inverse agonist
89
shifts curve to left and makes agonist more potent; binds to a distinct site (not same site as ligand)
allosteric agonist
90
binds to same site as ligand and activates receptor
primary agonist