Neurology Flashcards
selegiline
selective inhibitor of MAO-B, which preferentially metabolizes dopamine over NE and 5HT –> increasing the availability of dopamine
use: adjunctive agent to L-dopa in treatment of PD
toxicity: may enhance adverse effects of L-dopa
memantine
Alzheimers drugs- nmda antagonist; helps prevent excitotoxicity mediated by ca2+
toxicity: dizziness, confusion, hallucinations
donepezil, galantamine, rivastigmine
ach esterase inhibitors for tx of Alzheimers
toxicity: nausea, dizziness, insomnia
reserpine + tetrabenazine
amine depleting for Huntington’s
haloperiodol
dopamine receptor antagonist for Huntington’s
sumatriptan
5HT(1b/1d) agonist –> vasoconstriction, inhibition of trigeminal activation and vasoactive peptide release
use: acute migraine, cluster headache attacks
toxicity: coronary vasospasm (contraindicated in pts with CAD or Prinzmetal’s angina), mild tingling
succinylcholine
used for muscle paralysis in surgery or mechanical ventilation, selective for motor nicotinic receptor
depolarizing agent
What are nondepolarizing agents used for muscle paralysis in surgery or mechanical ventilation?
tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium
competitive antagonist that competes with Ach for receptors
reversal of blockade- neostigmine, edrophonium, and other cholinesterase inhibitors
dantrolene
used for tx of malignant hyperthermia, which is caused by inhalation anesthetics (except N2O) and succinylcholine
also used to treat neuroleptic malignant syndrome (toxicity of antipsychotic drugs)
mechanism: prevents release of ca2+ from sarcoplasmic reticulum of skeletal muscle
What are PD drugs that agonize dopamine receptors?
bromocriptine, pramipexole, ropinirole (non-ergot); non-ergots are preferred
What are PD drugs that increase dopamine?
amantadine (increase release)
L-dopa/carbidopa (converted to DA in CNS)
What are PD drugs that prevent dopamine breakdown?
selegine (selective MAOB inhibitor); entacapone, tolcapone (COMT inhibitors)
What are PD drugs that curb excess cholinergic activity?
benztropine (antimuscarinic, improves tremor and rigidity but has little effect on bradykinesia)
for essential or familiar tremors: use B-blocker
L-dopa/carbidopa
mechanism: increase level of dopamine in brain, L-dopa can cross BBB and is converted by dopa decarboxylase in the CNS to dopamine
carbidopa- peripheral decarboxylase inhibitor to increase bioavailability of L-dopa in the brain and to limit peripheral side effects
use: PD
toxicity: arrhythmias from peripheral conversion of dopamine; long term use can produce dyskinesia, akinesia between doses
thiopental
IV anesthetic barbibuate
high potency, high lipid solubility, rapid entry into brain –> induction of anesthesia and short surgical procedures
effect terminated by rapid redistribution into tissue and fat, decreased cerebral blood flow
midazolam
benzodiazepine IV anesthetic
most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics
may cause severe postoperative respiratory depression, decreased BP (treat overdose with flumazenil) and amnesia
arylcyclohexylamines (ketamine)
PCP analog that acts as dissociative anesthetics, blocks NMDA receptors
cause disorientation, hallucination and bad dreams
increases cerebral blood flow
What opiates are used as IV anesthetics?
morphine, fentanyl used with other CNS depressants during general anesthesia
propofol
used for rapid anesthesia induction and short procedures, less postoperative nausea than thiopental
potentiates GABA(A)
What are some local anesthetics?
esters- procaine, tetracaine
amides- lidocaine, mepivacaine, bupivacaine
(amides have 2 I’s in name)
How do local anesthetics work?
block Na channels by binding to specific receptors on inner portion of channel, preferentially bind to activated na channels so most effective in rapid firing neurons
3* amine local anesthetics penetrate membrane in uncharged form then bind to ion channels as charged form
order of nerve blockade: pain > temp > touch > pressure
usually given with vasoconstrictors to enhance local action- decrease bleeding, increase anesthesia by decreased systemic concentration
toxicity: CNS excitation, severe CV toxicity (bupivacaine), hypertension, hypotension and arrhythmias (cocaine)
What are some benzodiazepines?
diazepam, lorazepam, traizolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam
Benzodiazepams: mechanism, clinical use, toxicity
facilitate gaba (A) action by increasing frequency of Cl- channel opening, decreased rem sleep, most have long half-lives and active metabolites
use: anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification ( especially alcohol withdrawal), night terrors, sleep walking, general anesthetic (amnesia, muscle relaxation), hypnotic
(insomnia)
toxicity: dependence, additive CNS depression effects with alcohol, less risk of respiratory depression and coma than with barbiturates
treat overdose with flumazenil (competitive antagonist at gaba benzodiazepine receptor)
What are some nonbenzodiazepine hypnotics?
zolpidem (ambien), zaleplon (sonata), eszopiclone (lunesta)
mechanism: act via the BZ1 receptor subtype and is reversed by flumazenil
clinical use: insomnia
toxicity: ataxia, headaches, confusion. short duration bc of rapid metabolism by liver enzymes. unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnesic effects, lower dependence risk than benzodiazepines
