Neuro - Pharm Flashcards
(32 cards)
Describe the indications and MOA for valproate
first line: long-term treatment for tonic-clonic generalized seizures
- also for focal seizures, absence epilepsy, myoclonic seizure, migraine PPX, bipolar
MOA: inhibits GABA transaminase = increases GABA
- decreases neuronal excitability + inactivated Na and Ca channels
What is the MOA and AEs of valproate?
MOA: inhibits GABA transaminate -> increases GABA
- decreases neuronal excitability + inactivates Na and Ca chanels
- GI upset, dizziness
- tremor, ataxia, sedation
- alopecia
- weight gain
- teratogenic: neural tube defects
CONTRAINDICATED IN PREGNANCY
What is carbamazepine’s indications and MOA?
indications:
first line: focal seizures, trigeminal neuralgia
MOA: inactivates vg-Na channels
- inhibits APs + decreases synaptic transmission
What is the MOA for carbamazepine and what are its AEs?
MOA: inactivates vg-Na channels
- inhibits APs + decreases synaptic transmission
AEs
- NVD
- DRESS syndrome
- Tertatogenicity - first trimester (cleft palate)
- Stevens-Johnson
- folate deficiency
- ataxia
What are the indications for ethosuximide and what is its MOA?
indications: first-line treatment for absence seizures
MOA: inhibition of vg-Ca channels in neurons of the thalamus
What is the MOA and AEs for ethosuximide?
MOA: inhibition of vg-Ca channels in neurons of the thalamus
AEs
- GI symptoms
- Stevens-Johnson
- fatigue
- headache, dizziness
- increased serum levels of phenytoin
What is the MOA and AEs for phenytoin and fosphenytoin?
MOA: inactivates Na channels
zero-elimination drug
AEs
- hirsutism
- hyperpigmentation
- gingival hyperplasia
- Drug-induced SLE
- SJS
- DRESS
- hypothyroidism
What is MOA and indication for phenobarbital?
indications:
- first line for neonates
MOA: GABA A agonist
- increases GABA action
What are the MOA and indication for benzodiazepines?
indications
- first line for status epileptics
MOA: indirect GABA A agonist
- increased GABA action
What are the indications and MOA of lamotrigine?
indications
- first-line: long-term therapy of focal seizures
MOA: inhibition of vg-Na channels = decrease glutamate release
What interactions does lamotrigine have?
coadministration with carbamazepine, phenobarbital, and phenytoin increase clearance of lamotrigine
What is the MOA and indications of gabapentin?
second-line for focal seizures
postherpetic neualgia
peripheral neuropathy
MOA: inhibition of P/Q type Ca-channels
- decreased Ca intracellular flow = decreased glutamate release
What are the indications and MOA for vigabatrin? What is its AE?
adjunctive therapy for refractory seizures
mono therapy for infantile spasm
MOA: inhibits GABA transaminase irreversibly
- increases GABA
can cause irreversible vision loss
What is the indication and MOA for topiramate? What drug-drug interactions does it have?
focal and generalized tonic-clonic seizures
migraine ppx
idiopathic intracranial HTN
MOA: blocks vg-Na channels = increases GABA
decreases OCP efficacy
What are the indications and MOA for amtriptyline?
indications:
PPX for tension headache
moderate to severe migraine
cluster headaches
MOA: tricyclic antidepressant - tertiary amine
- inhibition of 5HT and NE reuptake in the synaptic cleft
What is the indications and black box warning for amtriptyline?
indications
- PPX for tension headaches
- moderate to severe migraine
- cluster headache
Black box warning - no use < 24 due to suicidal ideation
What are the CYP450 inducers and inhibitors?
inducers
- Carbamazepine
- Phenytoin
- phenobarbital
inhibitors - valproate
What is the depolarizing NMJ blockers?
succinylcholine
- fasted onset of action among neuromuscular blockers: 60 seconds
What are the clinical uses for NMJ blockers?
laryngeal intubation
artificial ventilation
intraoperative skeletal muscle relaxation
All cause respiratory arrest + require artificial ventilation
What is the MOA of succinylcholine? What is its onset and duration?
MOA: depolarizing NMJ-blocer
- binds to ACh receptors + prolongs depolarization at motor end plate
- causes flaccid paralysis
Duration of action:
- onset: 60 seconds - fastest NMJ
- duration: 5-10 minutes
What are the MOA and AEs of succinylcholine?
MOA: depolarizing NMJ blocker
- binds to ACh receptors + prolongs depolarization at motor end place
- causes flaccid paralysis
AEs
- malignant hyperthermia
- hyperkalemia: contraindicated in burns, rhabdo, stroke, SCI
- hypercalcemia
- deficiency of plasma cholinesterase
What are the MOA for the non depolarizing NMJ blockers?
NONDEPOLARIZING NMJ blockers
competitive antagonists: compete with ACh to bind with nicotinic ACh receptors at the motor end plate
- prevents depolarization
What is the short acting non depolarizing NMJ blocker? What is its indication?
Mivacurium
indicated for tracheal intubation
What is mivacurium and what is its AEs?
short acting non depolarizing NMJ blocker
AEs: histamine release
- rash
- bronchospasm
- hypotension
