Pharm (Advanced) Flashcards
(138 cards)
amphetamine
Use: Narcolepsy, ADHD
MOA: Nervous system stimulant (incr. DA levels in CNS)
CI/Toxicity: Depresses appetite, ascorbic acid decr. absorption /alkaline incr. absorp.
methamphetamine
Use: Narcolepsy, Anorexiant, ADHD, Drug of abuse
MOA: Like amphetamine but higher central to peripheral effects (reaches CNS better than amphetamine w/ longer lasting effects)
CI/Toxicity:
- Schedule II stimulant, high degree of abuse
- toxic to nerve cells due to inhibiting DA reuptake & increasing synth
ephedrine
Use:
MOA: Activates β-receptors, Orally active, Long duration of action
CI/Toxicity: Cardiac problems
tyramine
Use: Normal byproduct of tyrosine metabolism
MOA:
-Metabolized by MAO in liver
- High first pass effect (low bioavailability)
- Indirect sympathomimetic when given parenterally → increased release of stored catecholamines
CI/Toxicity: Caution to those on MAOI → intensified effect → increased BP and HR
modafinil
Use: Promotes wakefulness (narcolepsy)
MOA: Psychostimulant w different structure and effects than amphetamines
-MOA not fully understood but inhibits DA and NE transporters → increased DA, NE, Serotonin, Glutamate, and decreased GABA
CI/Toxicity: Increased BP and HR
atomoxetine
Use: ADHD (adults + children)
- Does not increase alertness or motor activity
- Slower onset than stimulants
MOA: Non-stimulant compound
- Selective reuptake inhibitor of NE
- Incr. NE transmission
- Decr. sympathetic outflow in CNS and increased NE effects in periphery
- not a controlled substance, b/c it’s not a stimulant
CI/Toxicity: May be less effective than stimulants because it DOES NOT have DA effects.
- Avoid MAOIs
- *t1/2 goes from 5 hrs to 24 hrs in poor metabolizers
methylphenidate
Ritalin
Use: ADHD, Narcolepsy, Postural Orthostatic Tachycardia Syndrome
MOA: Piperidine class of compounds (amphetamine variant)
- Increases NE and DA levels in the brain.
- Reuptake inhibitors of monoamine transporters
- short acting w/ t1/2 3-5 hrs
CI/Toxicity: Facial tics, tachycardia,
Avoid MAOIs → avoid HTN crisis
dexmethylphenidate
Use: ADHD
MOA: D-enantiomer only,
- Blocks reuptake of DA, NE, via transporter blockade
- Available in short, intermediate, and long lasting formulas
CI/Toxicity: Facial tics, tachycardia,
Avoid MAOIs → avoid HTN crisis
dextroamphetamine
Use: ADHD
MOA: D-enantiomer only, Blocks reuptake of DA and NE
CI/Toxicity: Facial tics, tachycardia,
-C/I w/ cardiac abnormalities
Avoid MAOIs → avoid HTN crisis
lisdexamfetamine
Use: ADHD
MOA: Dextromphetamine + L-Lysine, Blocks reuptake of DA and NE
CI/Toxicity: Facial tics, tachycardia,
-C/I w/ cardiac abnormalities
Avoid MAOIs → avoid HTN crisis
amphetamine mixed salts
Adderall
Use: ADHD
MOA: mixture of d- and l-enantiomers attached to different salts
-Increased presynaptic release of DA, NE, 5HT via transporter reversal
CI/Toxicity: Facial tics, tachycardia,
Avoid MAOIs → avoid HTN crisis
valproic acid
aka: Depakene
Class: conventional anticonvulsant
Use: migraine headache prophylaxis
-Bipolar disorder
MOA: Unclear, may increase GABA or block Na channels
CI/Toxicity: nausea, fatigue, tremor, weight gain, hair loss, lipid abnormalities, hyperinsulinemia, hirsutism and menstrual disturbances. not recommended for use during pregnancy
phenobarbital
aka: Luminal
Class: conventional anticonvulsant
Use: sedation and relief of anxiety; amnesia; hypnosis; anesthesia; coma and respiratory depression; steeper dose-response relationship than benzodiazepines
MOA:
- Bind to specific GABAA receptor subunits at CNS neuronal synapses increasing duration of GABA-mediated chloride ion channel opening
- Enhance membrane hyperpolarization
CI/Toxicity:
carbamazepine
aka: Tegretol
Class: conventional anticonvulsant
Use: Simple & complex partial seizures & generalized tonic- clonic seizures
-Bipolar disorder
MOA: Slows rate of recovery of Na+ channels from inactivation
CI/Toxicity: aplastic anemia
phenytoin
aka: Dilantin
Class: conventional anticonvulsant
Use: All types of partial & tonic- clonic seizures
* Not absence seizures
MOA: Slows rate of recovery of Na+ channels from inactivation. *Half life increases with concentration
CI/Toxicity: Cardiac toxicity; CNS depression
diazepam
aka: Vailum
Class: conventional anticonvulsant
Use: effective for status epilepticus, but it has a short duration of action & isn’t used as much
MOA:
- Enhance GABA- mediates synaptic inhibition via the GABAA receptor (incr frequency of GABA- activated Cl- channels)
- At higher conc’n, reduces high- freq firing of neurons
CI/Toxicity:
clonazepam
aka: Klonopin
Class: conventional anticonvulsant
Use: useful in absence & myoclonic seizures in children (but tolerance develops after 1- 6 months)
MOA:
- Enhance GABA- mediates synaptic inhibition via the GABAA receptor (incr frequency of GABA- activated Cl- channels)
- At higher conc’n, reduces high- freq firing of neurons
CI/Toxicity:
primidone
Class: conventional anticonvulsant (barbiturate)
Use: Effective against partial seizures & generalized tonic- clonic seizures
MOA: Like that of phenytoin (Slows rate of recovery of Na+ channels from inactivation)
CI/Toxicity:
ethosuximide
aka: Zarontin
Class: newer anticonvulsant
Use: Primary agent for tx of absence seizures
* Not for tonic- clonic seizures
MOA: Reduces low threshold Ca2+ currents (T- type currents) in thalamic neurons
CI/Toxicity:
gabapentin
aka: Neurontin
Class: newer anticonvulsant
Use: Effective for partial seizures, w/ & w/o secondary generalization when used in addition to other anti- seizure meds
MOA: Bind to protein in cortical membrane w/ an a.a. sequence identical to Ca2+ subunit α2δ1; full MOA is unclear
CI/Toxicity:
pregabalin
aka: Lyrica
Class: newer anticonvulsant
Use: Effective for partial seizures, w/ & w/o secondary generalization when used in addition to other anti- seizure meds
MOA: Bind to protein in cortical membrane w/ an a.a. sequence identical to Ca2+ subunit α2δ1; full MOA is unclear
CI/Toxicity:
tiagabine
aka: Gabitril
Class: newer anticonvulsant
Use: Add on therapy for partial seizures in adults (w/ or w/o secondary generalization)
MOA: Inhibits the GABA transporter, GAT-1, & thereby reduces GABA uptake into neurons & glia
CI/Toxicity:
topiramate
aka: Topamax
Class: newer anticonvulsant
Use: Partial & primary generalized seizures, migraine prophylaxis
MOA:
- Reduces VG Na+ currents in cerebellar cells & may act on the inactivated state of the channel
- Activates a hyperpolarizing K+ current, enhancing postsynaptic GABAA- receptor currents
- Limits activation of the AMPA- kainite- subtype of glutamate receptor
CI/Toxicity:
lamotrigine
aka: Lamictal
Class: newer anticonvulsant
Use: Monotherapy & add- on therapy for partial & secondarily generalized tonic- clonic seizures
MOA:
- Blocks sustained repetitive firing & delays recovery from inactivation of Na+ channels
- May have other MOAs that explain its broader spectrum of use than phenytoin & carbamazepine
CI/Toxicity: