Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

pharmacology unit 6 > clinical toxicity I and II > Flashcards

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are some common opioids

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what drug can reverse an opioid OD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

are higher or lower doses of naloxone needed for synthetic opioids

A

higher,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are some natural opioids

A

morphine, codeine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are some semi-synthetic opioids

A

heroin, oxycodone, hydromorphone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are some fully synthetic opioids

A

meperidine, methadone, fentanyl.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is characteristic of opioid withdrawal

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are two other opioid reversal drugs

A

nalmefene and naltrexone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

benzodiazepam toxidrome

A

depressed mental status, normal vitals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

treatment for the benzodiazepam OD

A

supportive, ABCs, consider flunazenil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is flunazenil

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

stage 1 acetominophen toxidrome

A

0-24hrs GI irritation, generally asymptom.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

stage II acetominophen toxidrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

stage III acetominophen toxidrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

stage IV acetominophen toxidrome

A

4days-2weeks. resolution of organ function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the mechanisms of NAC

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

tricyclic antidepressants

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what does the toxidrome for tricyclic antidepressant

A

elevated HR, widened pupils, dry mucous membranes, dry flushed skin, decreased bowel sounds.. (alpha-blockers can cause hypotension). widened QRS complex.

26
Q

what is the antidote for tricyclic antidepressant toxicity

A

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
Q

what is the anticholinergic toxidrome

A

mydriasis, dry-flushed skin, decreased bowel sounds, urinary retention, increased temperature, confusion, hallucination, seizures.

28
Q

what are some common anticholinergics

A

atropine, diphenhydramine, scopolamine, meclizine

29
Q

what is the antidote to anticholinergic

A

physostigmine -anticholinesterase.

30
Q

when is physostigmine contraindicated

A

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
Q

what are the indications for using physostigmine

A

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
Q

what do we treat with when we are unsure that the patient has ingested an anticholinergic

A

sedative-hypnotics. diazepam works great

33
Q

what is the toxidrome for cholinergic

A

opposite of anticholinergic, miosis, salivation, bronchorrhea/spasm, fasciculations

34
Q

what are some cholinergics

A

anticholinesterases (nerve gases, organophosphates, carbamates, physostigmine, neostigmine). cholinomimetics such as bethanechol

35
Q

what is the antidote to cholinergic OD

A

atropine and some very high doses might be needed. pralidoxime which is an enzyme regenerator and reduces the excessive dosing of atropine.

36
Q

what is the differential when metabolic acidosis

A

MUDPILES methanol, uremia, diabetic ketoacidosis, paraaldehyde/metformin, iron, lactate, ethylene glycol, salicylate.

37
Q

what is the aim for treatment of methanol toxicity

A

to inhibit the ADH and then remove the toxic agent. usually given ethanol or fomepizole and dialysis..

38
Q

what is the indication for hemodyalysis

A

methanol or ethylene glycol level > 25-50, metabolic acidosis, coma, hemodynamic instability

39
Q

what is the differential for someone that is bradycardic and hypotensive

A

beta blockers, CCB, alpha-2 agonist, digoxin

40
Q

CCB toxidriome

A

peripheral vasodilation, decreased sinus rate, slows AV conduction. decreased pulse, BP. normal temp and respirations.

41
Q

is there increased or decreased ventricular contractility with CCB

A

decreased. it is a negative ionotrope.

42
Q

why is there is brady cardia when CCB toxic

A

there is sinus node depression due to the negative chronotropy

43
Q

what is the presentation of nifedipine and dihydropyridines toxicity

A

peripheral vasodilation, reflex tacycardia, there can hypotension.

44
Q

what is the presentation of verapamil or diltiazem OD

A

hypotension (vasodilation, bradycardia), bradycardia (inhibition of the sinus node

45
Q

what can be done for CCB OD

A

bowel irrigation, activated charcoal, IV, monitor

46
Q

what are some treatments for CCB OD

A

calcium salts, glucagon, amrinone, dopamine, dobutamine, norepinephrine, isoproterenol, insulin.

47
Q

what do B blockers do

A

negative inotrope/chronotrope, slow AV conduction. B(2) blockers cause bronchoconstriction and increased vascular resistance.

48
Q

what is important to know about BB at high doses

A

the selectivity is lost in OD

49
Q

what do BB do in OD?

A

mental status depression and seizures.

50
Q

what does clonidine do

A

alpha-2 agonist there is a decrease in CNS sympathometic output. cross-reactive with alpha-1

51
Q

what is the clinical presentation of clonidine OD

A

bradycardia, pinpoint pupils, CNS depression

52
Q

what is the predistribution digoxin toxicity

A

nausea, vomit, hyperkalemia

53
Q

what is the postdistribution digoxin toxicity

A

hypotension, bradycardia, arrhythmias, death

54
Q

what is the antidote for digoxin tox

A

digibind -an antibody that binds digoxin

55
Q

what is toxidrome for cocaine/amphetamines

A

CNS stimulation, agitation, hallucinations, seizures, increased muscle activity, temperature, CK, kidney injury. can cause decreased blood flow -angina, stroke, heart attacks.

56
Q

what are PCP/ketamine/DM, what do they do?

A

dissociative anesthetics. depending on dose:
Low: euphoria
medium: agitation, anesthesia, increased strength
high: CNS anesthesia

57
Q

what can cause synthetic marjiuana cause

A

hyperadrenergic, seizures, paranoia

58
Q

what does LSD/psilocybin do

A

alters perceptions and hallucinations. psychiatric illness

59
Q

is LSD toxic

A

not inherently toxic. there are adverse effects related to experience

60
Q

what are downers?

A

GABA agonists such as GHB, roofies, etc.

pharmacology unit 6 (45 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions