Pharmacology Flashcards
neostigmine
cholinergic agonist
quaternary acetylcholinesterase (does not cross BBB)
reverses anesthetic paralysis
SLUDGE
pyridostigmine
cholinergic agonist
long(est) acting acetylcholinesterase, quaternary (does not cross BBB)
preferred drug in myasthenia gravis
SLUDGE
physostigmine
cholinergic agonist
tertiary acetylcholinesterase (does cross BBB = CNS effects)
antidote for atropine
SLUDGE, convulsions, coma
pralidoxime
cholinergic ANTagonist
regenerates acetylcholinesterase
treats OD on cholinergic agonists
anti-SLUDGE
benzocaine
local anesthetic, ester
topical-only anesthetic
if internal use, serious methylglobinemia –> cyanosis
tetracaine
local anesthetic, ester
long-duration LA used for spinal anesthesia
mechanism of action of all local anesthetics
blocks Na+ channels on nociceptive receptors, especially small and unmyelinated neurons
adverse events of all local anesthetics if they are administered IV
v tach, v fib, other potential arrythmias, heart block, bradypenia, hypotension, convulsions, coma, possible death
lidocaine
local anesthetic, amide
most commonly used LA, intermediate duration, can be topical, injected subQ, spinal anesthesia
bupivicaine
local anesthetic, amide
long duration, used for epidurals
heart problems are especially severe if IV
atropine
anti-cholinergic muscarinic antagonist
blocks downstream muscarinic signalling (G-protein pathway)
has CNS effects, antidote to acetylcholinesterase inhibitors (anti-SLUDGE), treats bradycardia, bedwetting, pupil dilation
can cause tachycardia, hyperthermia, delirium, dizziness, anti-SLUDGE
scopolamine
anti-cholinergic muscarinic antagonist
blocks downstream muscarinic signalling (G-protein pathway)
long-acting and has CNS effects - prevents vomiting from motion sickness, surgery, etc.
sedation, confusion, anti-SLUDGE
glycopyrrolate
anti-cholinergic muscarinic antagonist
blocks downstream muscarinic signalling (G protein pathway)
similar to atropine, but in PNS only: anti-acetylcholinesterase, bradycardia, etc.
like atropine, tachycardia, anti-SLUDGE (no CNS side effects like delirium, dizziness, hyperthermia)
botox
anticholinergic
cleaves SNAREs that are needed for neurotransmitter vesicle fusion to pre-synaptic membrane, so ACh is not released
spasm, strabismus, dystonia, hyperhydrosis (execs sweating), tension/migraine headache, cosmetics
3-6 months duration
pilocarpine
cholinomimetic muscarinic agonist
direct muscarinic agonist = directly binds to muscarinic receptor and induces G protein signalling
ciliary contraction in glaucoma, tear and salivary gland production in Sjorjen’s syndrome
SLUDGE
tubocurarine
non-depolarizing NMJ blocker (curare)
nicotinic receptor competitive antagonist (binds active site) without depolarizing post-synaptic membrane
no longer used d/t many side effects, but is the parent compound for other curares
atracurarium
non-depolarizing NMJ blocker (curare)
as with other curares, nicotinic receptor competitive antagonist (blocks active site) without post-synaptic membrane depolarization
no CNS effects, intermediate-acting time
anesthetic paralysis and intubation
of currently used curares, most likely to cause side fx: widespread histamine, PNS neurotoxin (e.g. seizure)
rocurarium
non-depolarizing NMJ blocker (curare)
as with other curares, non-depolarizing nicotinic receptor competitive antagonist
no CNS effects, short-acting
anesthetic paralysis
similar side fx to other curares but less extreme d/t more quickly metabolized
succinylcholine
depolarizing NMJ blocker
step 1: ACh mimetic, causes widespread vasiculations
step 2: desensitization/receptor fatigue
step 3: broken down by plasma pseudocholinesterase
rapid onset (<1 min) and short duration (<10 min)
in genetically susceptible individuals (pseudocholinesterase mutations), effects can last for several hours
sugammedex
NMJ blockade reversal
releases/sequesters non-depolatorizing NMJ blocker from active site of nicotinic receptor, restoring normal signalling. sugammedex-curare complex then excreted renally.
reverses effects of non-depolarizing NMJ blockers
reasonably safe, fast-acting
aspirin
non-selective COX inhibitor, primarily COX1
IRREVERSABLE acetylation by acting as a steric block on COX.
anti platelet in addition to normal NSAID antiinflammatory antipyretic analgesic fx
Aspirin itself is rapidly excreted (within an hour) but effects last as long as it takes to make new COX/platelets
possible Reye’s syndrome in kids but this is being questioned now
Most GI effects of the NSAIDs because it is most partial to COX1; also, renal compromise and salycism