anesthetics, analgesics, and sedatives Flashcards
opioids moa
presynaptic block of Ca2+ influx in response to an action potential; post-synaptic increase in K+ efflux causing hyperpolarization
opoid toxicity
respiratory depression, constipation, miosis
opioid toxicity treatment
naltrexone or naloxone
butorphanol moa
mu opioid partial agonist and kappa opioid receptor agonist
tramadol moa
very weak opioid agonist; also inhibits serotonin and norepinephrine repute
barbiturate moa
facilitates GABA action by increasing the duration of Cl channel opening
barbiturate adverse effects
respiratory and CV depression (can be fatal); CNS depression exacerbated by EtOH use; induces CYPs
benzodiazepine moa
facilitates GABA action by increases the frequency of Cl channel opening
benzodiazepine affect on sleep cycle
decreases REM sleep
short acting benzos
triazolam, oxazepam, and midazolam
treatment of benzodiazepine OD
flumazenil
zolpidem, zaleplon, and eszopiclone
act via the BZ1 subtype of the GABA receptor; lower risk of dependence
inhaled anesthetics
halothane, the “fluranes” and nitrous oxide
inhaled anesthetic effect
myocaridal depression, respiratory depression, nausea, increased cerebral blood flow
treatment of malignant hyperthermia
dantrolene
causes anesthetic that causes hepatotoxicity
halothane
anesthetic that causes nephrotoxicity
methoxyflurane
anesthetic that is pro-convulsant
enflurane
causes malignant hyperthermia
inhaled anesthetics and succinylcholine
ketamine moa
blocks NMDA receptors, produces dissociative anesthesia;
ketamine effects
increases cerebral blood flow; stimulates the CV system;
anesthetic that causes hallucinations
ketamine
propofol moa
potentiates GABA
propofol use
rapid anesthesia induction and short procedures
local anesthetics moa
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;
order of loss with local anesthetics
pain , temp, touch, pressure;
amide local anesthetics
have 2 I’s in the name
ester local anesthetics
have only 1 I in the name
depolarizing NM blocking drug moa
succinylcholine - strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction
succinylcholine moa
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)
nondepolarizing NM blockers
tubcurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium
nondepolarizing NM blockers moa
competitive antagonists at the ACh receptors
reversal of NM block
cholinesterase inhibitors