Flashcards in FA Neuro Pharm Deck (98):
Mu-opioid receptor partial agonist and kappa opioid receptor agonist; produces analgesia
Very weak opioid agonist; also inhibits serotonin and NE reuptake (used for chronic pain)
Facilitates GABAa action by increasing DURATION of Cl- channel opening, thus decreasing neuron firing (barbiturates increase duration). Contraindicated in porphyrias.
Facilitate GABAa action by increasing FREQUENCY of Cl- channel opening. Decrease REM sleep,
Act via the BZ1 subtype of the GABA receptor. Effects reversed by flumazenil.
Block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons.
Prevents the release of Ca2+ from the SR of skeletal muscle
Selectively inhibits MAO-B, which preferentially metabolizes dopamine over norepinephrine and 5-HT, thereby increasing the availability of dopamine
NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+)
Donepezil, galantamine, rivastigmine
Inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release
5-HT1B/1D agonist. Inhibits trigeminal nerve activation; prevents vasoactive peptide release; induces vasoconstriction. Half-life < 2 hrs
Increases Na+ channel inactivation, zero-order kinetics
Increases Na+ channel inactivation
Increases Na+ channel inactivation, increases GABA concentration by inhibiting GABA transaminase
Primarily inhibits high-voltage-activated Ca2+ channels; designed as GABA analog
Blocks thalamic T-type Ca2+ channels
Increases GABAa action
Blocks Na+ channels and increases GABA action
Blocks voltage-gated Na+ channels
Unknown; may modulate GABA and glutamate release
Increases GABA by inhibiting reuptake
Increases GABA by irreversibly inhibiting GABA transaminase
Decreases aqueous humor synthesis via vasoconstriction
Tox: Mydriasis; do NOT use in closed-angle glaucoma
Alpha2 agonist that decreases aqueous humor synthesis
Tox: Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic run, ocular pruritus
5 classes of drugs that can be used for glaucoma
1. alpha agonists
2. beta blockers
4. cholinomimetics (direct and indirect)
What beta blockers can be used for glaucoma?
Timolol, betaxolol, carteolol
What diuretic can be used for glaucoma?
What alpha agonists can be used for glaucoma?
Decreases aqueous humor synthesis via inhibition of carbonic anhydrase
Two direct cholinomimetics that can be used for glaucoma
pilocarpine and carbachol
two indirect cholinomimetics that can be used for glaucoma
physostigmine and chothiophate
What drug do you use in a glaucomic emergency?
pilocarpine - very effective at opening meshwork into canal of Schlemm
What is the mechanisms of cholinomimetics in treatment of glaucoma?
Increased outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
What are the side effects of cholinomimetics in treatment of glaucoma?
miosis and cyclospasm (contraction of ciliary muscle)
What prostaglandin is useful in glaucoma treatment?
what is the mechanism of latanoprost?
increased outflow of aqueous humor
darkens color of iris
agonist at mu receptors
agonist at delta receptors
agonist at kappa receptors
what opioid is used for cough suppression?
what opioid is used for diarrhea
opioid analgesic mechs
act as agonists at opioid receptors to (open K+ channels, close Ca2+ channels) --> decreased synaptic transmission Inhibit release of ACh, NE, 5-HT, glutamate, substance P
naloxone or naltrexone
mu opioid PARTIAL receptor agonist and kappa opioid receptor agonist; produces analgesia
severe pain (migraine, labor); causes less respiratory depression that full opioid agonists
can cause opioid withdrawal sx is pt is also taking full opioid agonist (competition for opioid receipts). OD not easily reversed w. naloxone
very weak opioid agonst; also inhibits serotonin and NE reuptake (works on multiple NTs - "tram it all" in with tramadol).
opioid tox, decreases seizure threshold, serotonin syndrome
blocks thalamic T-type Ca2+ channels
Ethosuximide causes Fatigue, GI distress, Headache, Itching, stevens-Johnson
facilitate GABA(A) action by increasing the DURATION of chloride channel opening, thus decreasing neuron firing (barbiDURATes increase DURATion). Contraindicated in porphyria
sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)
respiratory and CV depression (can be fatal!); CNS depression (exacerbated by EtOH); dependence; drug interaxns (INDUCES P450!).
none! supprotive - assist respiration and maintain BP
phenobarbital, pentobarbital, thiopental, secobarbital
facilitate GABA(A) action by increasing FREQUENCY of chloride channel opening, decrease REM sleep
highest addictive potential, shortest acting benzos
status epilepticus tx
competitive antagonist at GABA benzo receptor
Non benzo hypnotic examples
act via the BZ1 subtype of the GABA receptor
miminal alvelolar concentration required to prevent 50% of subjects from moving in response to noxious stimulus (e.g. skin incision)
inhaled anesthetic with hepatotoxicity
inhaled anesthetic with nephrotoxicity
inhaled anesthetic that is proconvulsant
inhaled anesthetic that can cause expansion of trapped gas in a body gravity?
the one inhaled anesthetic that doesn't cause malignant hyperthermia
what besides inhaled anesthetics can cause malignant hyperthermia
tx malignant hypertension
prevents the release of Ca2+ from SR of skeletal muscle
what causes neuroleptic malignant syndrome?
IV anesthetic barbiturate
IV anesthetic benzo
PCP analogs that act as dissociative anesthetics, Block NMDA receptors. CV stimulants. Cause disorientation, hallucination, and bad dreams. Increases cerebral BF
Used for sedation in ICU, rapid anesthesia induction, and short procedures. Less post operative nausea than thiopental. Potentiates GABA(A).
local anesthetic esters
procaine, cocaine, tetracaine
local anesthetic amides
lidocaine, mepivacaine, bupivacaine,
local anesthetic mechanism
blocks Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons. Teritiary amine local anesthetics penetrate membrane in uncharted form, then bind to ion channels in charged form.
Strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction
succinylcholine (depolarizing nueromuscular blocking drug)
reversal of non depolarizing neuromuscular blockade?
neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors)
How to treat Parkinson dz?
Levodopa w/ carbidopa
Selegiline (and COMT inhibitors)
arrythmias from increased peripheral formation of catecholamines. long term use can lead to dyskinesia following administration ("on off phenomenon"), akinesia between doses
how to treat alzheimers?
memantine (NMDA receptor antagonist)
AChE inhibitors (donepezil, galantamine, rivastigmine)
dizziness, confusion, hallucinations
AChE inhibitor tox
nausea, dizziness, insomnia
NT changes in HD?
decreased GABA and ACh,
tetrabenazamine and reserpien;
tetrabenazine and reserpine mech
inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release
dopamine receptor antagonist
5HT1b/1D agonist. INhibts trigeminal nerve activation; prevents vasoactive peptide release; induces vasoconstriction. Half-life < 2 hours
acute migraine, cluster headache