clinical toxicity I and II Flashcards

1
Q

what is the toxicidrome for opioids?

A

altered mental, decreased RR, decreased HR, BP, temperature, pinpoint pupils and decreased bowel sounds.

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2
Q

what are some common opioids

A

heroin, fentanyl, codeine, hydrocodone, meperidine, oxycodone, methadone

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3
Q

what to give in a opioid scenario

A

ABC/substrates. remove all obstructive process, assess and protect if necessary, IV fluids, O2 100%, dextrose/thiamine.

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4
Q

what drug can reverse an opioid OD

A

naloxone. competitive mu/delta/kappa antagonist. can precipitate withdrawal.

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5
Q

are higher or lower doses of naloxone needed for synthetic opioids

A

higher,

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6
Q

what are some natural opioids

A

morphine, codeine

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7
Q

what are some semi-synthetic opioids

A

heroin, oxycodone, hydromorphone

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8
Q

what are some fully synthetic opioids

A

meperidine, methadone, fentanyl.

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9
Q

what is characteristic of opioid withdrawal

A

flu-like symptoms nausea, vomit, piloerection, yawning. normal mental status

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10
Q

what are two other opioid reversal drugs

A

nalmefene and naltrexone

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11
Q

benzodiazepam toxidrome

A

depressed mental status, normal vitals

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12
Q

treatment for the benzodiazepam OD

A

supportive, ABCs, consider flunazenil

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13
Q

what is flunazenil

A

competitive non-selective benzodiazepam antagonist. only works for benzodiazepam, not the other sedative-hypnotics

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14
Q

do patients have to have a history of acetominophen ingestion to have a treatable level?

A

no. 1/500 w/o a history have a treatable level.

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15
Q

stage 1 acetominophen toxidrome

A

0-24hrs GI irritation, generally asymptom.

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16
Q

stage II acetominophen toxidrome

A

24-72 hours. LFT and renal function abnormalities, can have RUQ pain.

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17
Q

stage III acetominophen toxidrome

A

72-96 hrs. hepatic necrosis, can also show renal failure

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18
Q

stage IV acetominophen toxidrome

A

4days-2weeks. resolution of organ function

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19
Q

what is antidote for acetominophen poisoning

A

N-acetylcysteine. best if given within 8 hours of overdosr.. it is effective for all stages of toxicity.

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20
Q

when is NAC indicated for patients with acetominophen poisoning

A

a level unknown at the time of ingestion over the rumack-mathew nomogram. if the patient is showing signs og hepatotoxicity. when the APAP level will not be available within 8 hours of ingestion.

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21
Q

what are the signs of late APAP toxicity

A

prothrombin time > 200, serum Cr > 3.3. hepatic encephalopathy, blood pH < 7.3, factor VIII/V ratio > 30

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22
Q

what are two measures for the APAP toxicity that predict a poor prognosis

A

serum lactate elevation taken at various times throughout presentation. serum phosphate levels even more accurate. if the phosphate levels are elevated 2-3 days post OD >1.2 then that confers a poor prognosis

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23
Q

what are the mechanisms of NAC

A

supplies sulfhydryl groups, antioxidant. improves microcirculation, supplies glutathione and has antiinflammatory properties.

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24
Q

tricyclic antidepressants

A

anticholinergic, catechol reuptake inhibitors, alpha-adrenergic blocker, GABA antagonists, sodium channel blocker.

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25
what does the toxidrome for tricyclic antidepressant
elevated HR, widened pupils, dry mucous membranes, dry flushed skin, decreased bowel sounds.. (alpha-blockers can cause hypotension). widened QRS complex.
26
what is the antidote for tricyclic antidepressant toxicity
sodium bicarbonate, the alkalinization reduces the affinity for the TCA for its receptor and the sodium overcomes the sodium channel inhibitions. must careful to monitor the EKG and the blood pH
27
what is the anticholinergic toxidrome
mydriasis, dry-flushed skin, decreased bowel sounds, urinary retention, increased temperature, confusion, hallucination, seizures.
28
what are some common anticholinergics
atropine, diphenhydramine, scopolamine, meclizine
29
what is the antidote to anticholinergic
physostigmine -anticholinesterase.
30
when is physostigmine contraindicated
when there is TCA exposure. it causes asystole. there is muscarinic and nicotinic excess seen when the patient has not been exposed to anticholinergics.
31
what are the indications for using physostigmine
when there is pure anticholinergic, when there are CNS changes or peripheral, when there are no ECG findings suggesting that there is TCA exposure.
32
what do we treat with when we are unsure that the patient has ingested an anticholinergic
sedative-hypnotics. diazepam works great
33
what is the toxidrome for cholinergic
opposite of anticholinergic, miosis, salivation, bronchorrhea/spasm, fasciculations
34
what are some cholinergics
anticholinesterases (nerve gases, organophosphates, carbamates, physostigmine, neostigmine). cholinomimetics such as bethanechol
35
what is the antidote to cholinergic OD
atropine and some very high doses might be needed. pralidoxime which is an enzyme regenerator and reduces the excessive dosing of atropine.
36
what is the differential when metabolic acidosis
MUDPILES methanol, uremia, diabetic ketoacidosis, paraaldehyde/metformin, iron, lactate, ethylene glycol, salicylate.
37
what is the aim for treatment of methanol toxicity
to inhibit the ADH and then remove the toxic agent. usually given ethanol or fomepizole and dialysis..
38
what is the indication for hemodyalysis
methanol or ethylene glycol level > 25-50, metabolic acidosis, coma, hemodynamic instability
39
what is the differential for someone that is bradycardic and hypotensive
beta blockers, CCB, alpha-2 agonist, digoxin
40
CCB toxidriome
peripheral vasodilation, decreased sinus rate, slows AV conduction. decreased pulse, BP. normal temp and respirations.
41
is there increased or decreased ventricular contractility with CCB
decreased. it is a negative ionotrope.
42
why is there is brady cardia when CCB toxic
there is sinus node depression due to the negative chronotropy
43
what is the presentation of nifedipine and dihydropyridines toxicity
peripheral vasodilation, reflex tacycardia, there can hypotension.
44
what is the presentation of verapamil or diltiazem OD
hypotension (vasodilation, bradycardia), bradycardia (inhibition of the sinus node
45
what can be done for CCB OD
bowel irrigation, activated charcoal, IV, monitor
46
what are some treatments for CCB OD
calcium salts, glucagon, amrinone, dopamine, dobutamine, norepinephrine, isoproterenol, insulin.
47
what do B blockers do
negative inotrope/chronotrope, slow AV conduction. B(2) blockers cause bronchoconstriction and increased vascular resistance.
48
what is important to know about BB at high doses
the selectivity is lost in OD
49
what do BB do in OD?
mental status depression and seizures.
50
what does clonidine do
alpha-2 agonist there is a decrease in CNS sympathometic output. cross-reactive with alpha-1
51
what is the clinical presentation of clonidine OD
bradycardia, pinpoint pupils, CNS depression
52
what is the predistribution digoxin toxicity
nausea, vomit, hyperkalemia
53
what is the postdistribution digoxin toxicity
hypotension, bradycardia, arrhythmias, death
54
what is the antidote for digoxin tox
digibind -an antibody that binds digoxin
55
what is toxidrome for cocaine/amphetamines
CNS stimulation, agitation, hallucinations, seizures, increased muscle activity, temperature, CK, kidney injury. can cause decreased blood flow -angina, stroke, heart attacks.
56
what are PCP/ketamine/DM, what do they do?
dissociative anesthetics. depending on dose: Low: euphoria medium: agitation, anesthesia, increased strength high: CNS anesthesia
57
what can cause synthetic marjiuana cause
hyperadrenergic, seizures, paranoia
58
what does LSD/psilocybin do
alters perceptions and hallucinations. psychiatric illness
59
is LSD toxic
not inherently toxic. there are adverse effects related to experience
60
what are downers?
GABA agonists such as GHB, roofies, etc.