Pharm 2 Flashcards
before rxing NMB, what are 2 things you must make sure of? are NMB analgesics or anesthetics?
pt on ventilator AND sedated before giving NMB. no, they just paralyze muscles
MOA vs reversed by vs indications NMB
nondepol competitive antag or depol agonist vs chEI vs intracavitary procedures, endotrach intub, vent; convuls: epi, electroconvulsive therapy, local anesthetic tox, tetanus, malig hyperthermia
MOA vs indic succinylcholine
AchR agonist –> depol postsynaptic membrane like Ach –> excite motor end plate –> but can cause flaccid paralysis –> do 2 phase vs induct NM blockade, adjunct gen anes, rapid seq intub
phase 1 vs 2 of succinylcholine
very short; cont depol, bolus, augmented by chEI vs cont infusion or rpt dosing, prolonged end plate depol w/ gradual repol –> resistant to further depol –> tachyphylaxis, reversed by chEI
ADME succinylcholine
rapid on/off, IV/IM; distributed in extracell fluid; 80% hydrolysis, plasma pseudocholinesterase makes succinylmonocholine –> succinic acid + choline –> inactive (not metab by AchE); 10% renal elim
CI vs BBW succinylcholine
acute phase injury (burns, skel muscle denerv), malig hyperthermia, skel muscle myopathies/UMN injury vs cardiac arrest from hyperkal rhabdo
DI succinylcholine
aminoglycosides, inhaled anesthetics –> malig hyperthermia, atra/pancuronium, digoxin, donepezil, lidocaine/procainamide
highest to lowest risk of malig hyperthermia meds. what is malig hyperthermia? tx?
isoflurane > sevo > des > en > halothane. abnl Ca2+ release –> skel musc ctx, rigid, heat, metabolic acidosis, tachy, inc CO2. dantrolene
AE succinylcholine
H/oTN, br/tachy, inc IOP, musc fasc, postop myalgia; cardiac arrhythmia & arrest d/t hyperkal rhabdo & renal failure => BBW
MOA vs indic competitive nondepol AchR antag. know the meds & their differences
keep AchR in closed or nonfxnal position; paralytic effects last longer vs muscle denerv, MG, critically ill pts. cis/atra, pan, roc, vecuronium; Lec 18, slide 25
AE nondepol NMB
aspiration, bronchospasm, dec hypoxic drive, postop residual curarization –> injurious airway & resp fxn compromise. DOES NOT PROVIDE SEDATION, if given: w/draw NMB then w/ sedation
DI nondepol NMB
aminoglycoside abx, inhaled anes, polypeptide abx, procainamide, Ca2+ channel blockers
EMG vs acceleromyography
periph n stim, surrogate for action on diaphragm, interrater variability vs more objective, train of 4 ratio, reduce incidence of unexpected PORC
MOA vs indic vs AE vs DI vs CI neo/pyridogistine
AchEI –> counteracts neuromuscular blockade of nondepol blockers vs reverse NM blockade vs DUMBBELLs, bradyrhythmia; give atropine to minimize DUMBBELLs vs succinylcholine, glucocorticoids vs bowel/blad obstruction
MOA vs AE vs DI sugammadex
bind tightly to steroid of roc/vecuronium –> dec free fraction in plasma vs pruritus, urticaria, anaphylaxis, cardiac arrest/brady vs binds to other steroid hormones even progesterone –> backup for ocp
what is a sedative-hypnotic drug?
sedative –> dec anxiety; hypnotic –> produce drowsiness & maintain sleep. all cause CNS depression x/ buspirone & propranolol
5 C’s of addiction. addiction vs dependence?
compulsive, chronic, cont despite harm, impaired ctrl, craving. loss of ctrl in self-limiting intake of drug vs w/drawal syndrome after abrupt cessation of drug
what kind of receptors are GABAa vs MT1/2 vs OX1/2 aka hypocretin 1/2 vs H1 receptors?
Cl- channel vs GPCR in suprachiasmatic nucleus –> bind melatonin or MRAs –> sleep or sedation vs Gq & Gi –> release GABA and gluE vs Gq –> IP3/DAG in CNS
what is the GABA receptor? 3 subtypes?
gamma-aminobutyric acid; inhibitory NT –> hyperpol –> more difficult for neuron to fire. A = activates Cl- channel to hyperpol neurons; B = G protein to hyperpol; C = GABA is 10-100x more potent
benzos w/drawal sxs. how to tx?
sz, adrenergic stim, autonomic instability, flumazenil (w/ caution). more benzos, taper slowly