anesthetics, analgesics, and sedatives Flashcards
(33 cards)
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