anesthetics, analgesics, and sedatives Flashcards

1
Q

opioids moa

A

presynaptic block of Ca2+ influx in response to an action potential; post-synaptic increase in K+ efflux causing hyperpolarization

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2
Q

opoid toxicity

A

respiratory depression, constipation, miosis

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3
Q

opioid toxicity treatment

A

naltrexone or naloxone

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4
Q

butorphanol moa

A

mu opioid partial agonist and kappa opioid receptor agonist

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5
Q

tramadol moa

A

very weak opioid agonist; also inhibits serotonin and norepinephrine repute

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6
Q

barbiturate moa

A

facilitates GABA action by increasing the duration of Cl channel opening

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7
Q

barbiturate adverse effects

A

respiratory and CV depression (can be fatal); CNS depression exacerbated by EtOH use; induces CYPs

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8
Q

benzodiazepine moa

A

facilitates GABA action by increases the frequency of Cl channel opening

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9
Q

benzodiazepine affect on sleep cycle

A

decreases REM sleep

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10
Q

short acting benzos

A

triazolam, oxazepam, and midazolam

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11
Q

treatment of benzodiazepine OD

A

flumazenil

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12
Q

zolpidem, zaleplon, and eszopiclone

A

act via the BZ1 subtype of the GABA receptor; lower risk of dependence

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13
Q

inhaled anesthetics

A

halothane, the “fluranes” and nitrous oxide

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14
Q

inhaled anesthetic effect

A

myocaridal depression, respiratory depression, nausea, increased cerebral blood flow

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15
Q

treatment of malignant hyperthermia

A

dantrolene

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16
Q

causes anesthetic that causes hepatotoxicity

A

halothane

17
Q

anesthetic that causes nephrotoxicity

A

methoxyflurane

18
Q

anesthetic that is pro-convulsant

A

enflurane

19
Q

causes malignant hyperthermia

A

inhaled anesthetics and succinylcholine

20
Q

ketamine moa

A

blocks NMDA receptors, produces dissociative anesthesia;

21
Q

ketamine effects

A

increases cerebral blood flow; stimulates the CV system;

22
Q

anesthetic that causes hallucinations

A

ketamine

23
Q

propofol moa

A

potentiates GABA

24
Q

propofol use

A

rapid anesthesia induction and short procedures

25
Q

local anesthetics moa

A

block Na channels by binding to a specific inner portion of the channel; preferentially bind to activated Na channels so must effective in rapidly firing neurons;

26
Q

order of loss with local anesthetics

A

pain , temp, touch, pressure;

27
Q

amide local anesthetics

A

have 2 I’s in the name

28
Q

ester local anesthetics

A

have only 1 I in the name

29
Q

depolarizing NM blocking drug moa

A

succinylcholine - strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction

30
Q

succinylcholine moa

A

strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction
phase I: prolonged depolairzation (no antidone; block potentiated by cholinesterase inhibitors)
phase II: repolarized but blocked; ACh receptors are available, but desensitized (antidote - cholinesterase inhibitors)

31
Q

nondepolarizing NM blockers

A

tubcurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

32
Q

nondepolarizing NM blockers moa

A

competitive antagonists at the ACh receptors

33
Q

reversal of NM block

A

cholinesterase inhibitors