neuro Flashcards
alpha agonists for glaucoma?
epinephrine (a1) and brimonidine (a2)
decrease aqueous humor synthesis (a1 via vasoconstriction)
don’t use a1 in acute angle glaucoma - mydriasis!
** SEs: blurry vision, ocular hyperemia, foreign body sensation, ocular allergic rxns, ocular pruritus
beta blockers for glaucoma?
timolol, betaxolol, carteolol
decrease aqueous humor synthesis
** no pupillary/visual SEs
diuretic for glaucoma?
acetazolamide
inhibition of CA –> decreased aqueous humor synthesis
** no pupillary/visual SEs
cholinomimetics for glaucoma?
direct: pilocarpine, carbachol
indirect: physostigmine, echothiophate
increase aqueous humor outflow - contraction of ciliary mm and open trabecular meshwork
- pilocarpine for emergencies - very effective
- SEs: miosis and cyclospasm
prostaglandin for glaucoma?
latanoprost = PGF(2alpha)
increases outflow of aqueous humor
** darkens iris color
opioid MOA?
agonists at mu, delta (enkephalin), kappa (dynorphin) rcptrs
open K and chlose Ca channels –> decreased synaptic transmission
inhibit Ach, NE, 5HT, glu, substance P release
butorphanol?
kappa opioid rcptr agonist and partial mu agonist
–> analgesia
used in sever pain
causes less respiratory depression
- w/d sx if pt also taking full agonist
- not easy to reverse OD with naloxone
tramadol?
weak opioid agonist
inhibits 5HT and NE reuptake
SEs similar to opioids
** decreases sz threshold, risk of serotonin syndrome
1st line for absence sz?
ethosux
1t line for status epilepticus?
BZOs (acute)
phenytoin (ppx)
1st line for simple partial sz?
carbamazepine
1st line for complex partial sz?
carbamazepine
1st line for tonic-clonic sz?
carbamazepine, phenytoin, VPA
ethosuximide?
absence sz
MOA: blocks thalamic T-type Ca channels
SEs: fatigue, GI distress, H/A, itching, SJS
BZOs?
status epilepticus, eclampsia sz (after Mg)
MOA: increase GABAa action
SEs: sedation, resp depression, tolerance, dependence
phenytoin?
everything except absence; fosphenytoin = parenteral
MOA: increase Na channel inactivation
SEs: nystagmus, diplopia, ataxia, gingival hyperplasia, hirsutism, teratogenesis, drug-induced lupus, CYP450 induction, SJS
** zero order kinetics
carbamazepine?
partial and tonic-clonic sz, trigeminal neuralgia
MOA: increased Na channel inactivation
SEs: diplopia, ataxia, blood dsycrasias, hepatotoxic, induction of CYP450, SIADH, SJS
VPA?
everything except status; + myoclonic sz, BPD
MOA: increased Na channel inactivation, inhibit GABA transaminase –> increased GABA
SEs: Gi distress, hepatotoxicity, NT defects, tremor, weight gain
gabapentin?
partial sz, peripheral neuropathy, postherpetic neuralgia
MOA: inhibits high-voltage activated Ca channels
SEs: sedation, ataxia
phenobarb?
partial and tonic clonic sz
MOA: increased GABAa action
SEs: sedation, tolerance, cardioresp depression, induction of CYP450
** 1st line in neonates
topamax?
partial and tonic-clonic sz, migraine prevention
MOA: blocks Na channels, increases GABA
SEs: sedation, mental dulling, kidney stones, weight loss
lamictal?
everything except status
MOA: blocks voltage-gated Na channels
SEs: SJS if not titrated slowly
levetiracetam?
partial and tonic-clonic
unknown MOA: maybe GABA/glu related?
tiagabine?
partial sz
MOA: inhibit GABA reuptake
vigabatrin?
partial sz
MOA: irreversible inhibition of GABA transaminase
barbiturate MOA?
increased duration of Cl channel opening –> decreased neuron firing –> GABAa facilitation
** contraindicated in porphyria
barbiturate toxicity?
resp and cardio depression
CNS depression
induces CYP450
BZO MOA?
increase freq of Cl channel opening –> GABA facilitation
ATOM = short acting (alpraz, triaz, oxaz, midaz)
zolpidem, zaleplon, eszopiclone?
nonBZO hypnotics
MOA: BZ1 subtype of GABA rcptr
tox: ataxia, HA, confusion; rapid metab by liver; modest day-after psychomotor depression
decreased blood solubility of anesthetic means what?
rapid induction and recovery time
increased lipid solubility of anesthetic means what?
increased potency
MAC?
min alveolar conc required for 50% of pts not to move with incision
MAC = 1/potency
effects of inhaled anesthetics?
myocardial and respiratory depression
nausea/emesis
increased cerebral blood flow, decreased cerebral metabolic demand
which inhaled anesthetic is hepatotoxic?
halothane
which inhaled anesthetic is nephrotoxic?
methoxyflurane
which inhaled anesthetic is proconvulsant?
enflurane
which anesthetic causes expansion of trapped gas in body cavity?
N2O
which inhaled anesthetic does NOT cause NMS?
N2O
thiopental?
high potency, high lipid solubility
effect terminated by rapid redistrib into tissue
DECREASES cerebral blood flow
midazolam?
IV BZO - used for endoscopy
may cause severe postop resp depression and hypoT, anterograde amnesia
ketamine?
block NMDA rcptr
cardiovascular stimulant
disorientation, hallucination, bad dreams
INCREASES cerebral blood flow
propofol?
sedation in ICU, rapid anesthesia induction, short procedures
potentiates GABA
how do you tell the amides from the esters (local anesthetic)?
amides have 2 Is in the name
MOA of local anesthetic?
block Na channel (bind rcptr on inner portion)
preferentially bind activated Na channels
how does infected tissue affect anesthetic needs?
more acidic –> alkaline anesthetic cannot penetrate membrane –> need MORE
order of nerve blockade (small vs large, myelinated vs not)?
small –> large
myelin –> no myelin
overall: small myelin –> small unmyelin –> large myelin –> large unmyelin
order of sensory loss in anesthetic use?
pain
T
touch
pressure
which local anesthetic causes cardiovascular toxicity?
bupivicaine
which local anesthetic causes methemoglobinemia?
benzocaine
succinyl choline?
ACh rcptr agonist –> sustained depol –> paralysis
- in phase I, can’t reverse; block potentiated by AChE inhib
- in phase II, can reverse with AChE inhib
** complications: hypercalcemia, hyperkalemia, malignant hyperthermia
nondepolarizing paralytics?
tubucurarine, atracurium, vecuronium, etc
- competitive antag, compete with ACh
reverse with neostigmine + atropine; edrophonium, AChE inhib
dantrolene?
prevents Ca release from SR
used in malig hyperthermia and NMS
baclofen?
GABAb agonist at spinal cord –> skel mm relaxation
used in mm spasms
cyclobenzaprine?
centrally acting skel mm relaxant
similar to TCAs
used in mm spasms
dopa agonists?
bromocriptine = ergot
non-ergot (betteR) = pramipexole, ropinirole
amantadine?
increases dopa release and decreases reuptake
used in PD, influenza A, rubella
** toxicity: ataxia, livedo reticularis
L-dopa + carbidopa?
L-dopa can cross BBB; carbidopa prevents peripheral conversion to dopa –> increased availability and decreased peripheral SEs
** toxicity: arrhythmias; long term –> on-off phenomenon (dyskinesia after admin) and akinesia b/w doses
selegiline?
centrally acting; MAO-B inhibitor - prevents dopa breakdown into 3MT
adjunct to L-dopa
** may enhance adverse L-dopa effects
entacapone, tolcapone?
COMT inhibition: prevent L-dopa degradation to 3OMD
entacapone: peripheral
tolcapone: peripheral and central
memantine?
NMDA rcptr antag
used in AD
helps prevent excitotoxicity
** toxicity: dizziness, confusion, hallucinations
donepezil, galantamine, rivastigmine, tacrine?
AChE inhibitors
used in AD
** nausea, dizziness, insomnia
NT changes in Huntington?
decreased GABA, ACh
increased dopa
Huntington tx?
tetrabenazine and reserpine: inhibit VMAT - limit dopamine vesicle packaging and release
haldol - D2 antagonist
triptan MOA?
5HT1b/1d agonists
inhibit trigeminal n activation
prevent vasoactive peptide release
induce vasoconstriction
triptan toxicity?
coronary vasospasm - contraindicated in CAD, Prinzmetal
mild paresthesias
