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indirect-acting sympathomimetic agent
MOA: block reuptake of neurotranmitters by NET---increase synaptic activity
drug interactions:
potency increased when used w/ MOA inhibitors
short-acting with immediate effects (w/in 30 mins)
Side effects:
facial tics, tachcardia
usually give in a racemic mixture
indirect-acting sympathomimetic
MOA: increase presynaptic release of neurotransmitters through NET
side effects: drug of abuse (b/c activates rewards centers in brain.
usually given as a racemic mixture:
indirect-acting sympathomimetic
MOA: increase presynaptic release of neurotransmitters through NET
often used in asthma
mild stimulant 
dose-related rise in blood pressure
indirect-acting sympathomimetic
MOA: similar to amphetamine but shorter and more intense.
prevent reuptake of DA into neurons at pleasure centers of the brain
effects: local anesthtic w/ peripheral sympathomimetic action.

indirect sympathomimetics similar to NE
MOA: "releaser" of catecholamines
MOA: effects central alpha1B receptors also GABAergic, glutaminergic + serotonergic synapses.
can be used for narcolepsy
MOA: reuptake inhibitor
not a stimulant
side effects: decreased grwth, nausea, and sedation.

more stuff:  onset is slower
1. indirect-acting sympathomimetics
what are the two main MOA types?
2.  What must drug must be avoided when taking these drugs?
1. releasers and reuptake inhibitors
2.  MAO inhibitors
general effects of indirect-acting sympathomimetics
not much CNS effects except for amphethemines and ephedrine

eyes: contraction and mydriasis ( alpha agonists and including phenylephrine

bronchi: rlelaxes it (Beta 2 agnonist) most efficient drugs for the purpose

GI: relaxation

increases hrt rate
what biochemical pathway each receptor is coupled to?
1. alpha 1
2. alpha 2
3. dopamine
4. beta receptor
1. Gq, activate IP3 AND DAG
2. Gi, inhibit adenylyl cyclase
3. Gi reduce cAMP (more imp in brain)
4. Gs stimulate adenylyl cyclase
similar to methylphenidate
onset w/in one hour
taken in 2 doses
excretion increased by acidifying the urine
MOA, side effects, seizure type
Drug class: anticonvulsant

keeps inactivated vg-Na+ channels in active state
seizure types:
partial seizures-simple and complex, partial with secondarily generalized tonic-clonic seizure, generalized seizure- tonic-clonic only
side effects:
drowsiness, stupor, coma, convulsions, respiratory depression, aplastic anemia
valproic acid
drug classs: anti-convulsant
older generation

MOA: block vg Na+ channels in inactive state and blocks t-type Ca2+ channels
increases amt of GABA that can be recovered from the brain by inducing GABA synthetic enzyme and inhibiting GABA degradative enzyme
seizure type use:
all types

elimintation: low doses is first order
higher doses are zero order

GI symptoms, sedation
other: has interactions with other anticonvulsants
drug class: anticonvulsant, hyantoins

MOA: block Na+ channels in inactive state

side effects: CNS depression, arrhythmas
also low doses have first order kinetics of elimination and higher doses have zero order of elimination which means levels in blood can increase rapidly

Drug categories: used for migraines

activates 5-HT receptors on trigeminal nerve endings and cerebral/meningeal vesels; also have vasoconstriction properties side effects: mild. dizziness, muscle weakness
contraindication: patients w/ coronary artery disease, angina

more stuff:
duration of action shorter than migraine itself
ergot alkaloids
MOA and drugs in class

Drug categories: used for migraines MOA: activates 5-HT receptors on the trigeminal nerve endings and cerebral/ meningeal vessels.  has vasoconstrictive properties.  Also partial agonist activity at alpha adrenergic receptors and DA receptors.

Includes: erogotamine, methylsergide
Drug class: ergot alkaloid; used for migraines

MOA: same as general

more stuff:
more effective for when given during prodrome of attack
has long-lasting vasoconstriction when taken repeatedly
Drug interactions:
usually given with caffiene to increase absorption
Drug category: used for migranes for this phase

MOA: blocks Ca+ channels and has NO activity against 5-HT receptors
used along with erogotamine to increase absorption
Drug class: ergot alkalod; used Tfor migraines

MOA: safe as general

more stuff: safer than ergotamine
doesn't work with treating active migraine episodes
Drug class: anticonvulsant (older), barbituate
similar to phenobarbital (b/c it is a metabolite of said compound)
binds to GABA-A Cl channel receptors to increase duration of channel opening thereby causing synaptic inhibition

side effects:

seizure type: partial with secondarily generalized tonic-clonic seizure and generalized tonic-clonic seizure

Drug class: anticonvulsant (older), barbituate

binds to GABA-A Cl channel receptors to increase the duration of open state

seizure types: same as its metabolites
partial seizures-partial w/ secondarily generalized tonic-clonic seizures and generalized tonic-clonic seizures

side effects:
Drug class:
anticonvulsant (older), benzodiazepine

binds to GABA-A Cl channels and increases the freq of opening

side effects: drowsiness and lethargy ( not listed in pwrpt)

seizure type: usfeful for myoclonic seizures in children
drug class: anticonvulsant (older), barbituate


binds to GABA-A Cl channels increase freq of opening

side effects:
drowsiness,tolerance and lethargy (not listed in pwrpt)

seizure type:
drug class: anticonvulsant (newer)

MOA: GABA analog but MOA is unknown may promote nonvesicular GABA reslease and/or bind a protien in cortical membranes w/ an AA sequence similar to L type vg Ca2+ channels
seizure types:
all partial seizures w/andw/o secondary generalization

side effects: somnolence, fatigue (mild)
drug class: anticonvulsant (newer)

MOA: inhibits GAT-1 (GABA transporter) thereby inhibiting reuptake into glia cells and neurons

side effects:
dizziness, tremor, somnolence (mild)

therapeutic use: all partial seizures w/or w/o a generalized tonic-clonic seizure
drug classs: anticonvulsant

works similar to gabapentin (so we don't really know).  might bind to protein in cortical membranes w/ an AA seq similar to L type Ca2+ channels

therapeutic use:
? prbly all partial seizures

side effects:
prbly somnolence and fatigue (mild)
drug class: anticonvulsant (newer)

blocks Na+ channels ( reduces the currents in crebellar granule cells)
and activates K+ channels

somnlence, weight loss (mild)

therapeutic use:
everything but abscence seizures
drug class: anticonvulsant (newer)

blocks Na+ channels
may cause inhibition of glutamate release due to effects on Na+ channels
dizziness, GI symptoms (mild)

therapeutic use:preferred treatment for ALL types of seizures (INCLUDING abscence)
factors involved in epilepsy treatment
1. oral contraceptive effieciency is reduced.
1a.  phenytoin, phenobarbital, and valproate associated w/ teratogenic effects
2. avoid taking more than one drug at a time
MOA, seizure type, side effects
binds to t-type Ca2+ channels inhibits them in thalamic neurons
seizure type:
Absence seizures
side effects: GI symptoms, sedation
drug class: anticonvusant (newer)

inhibit T-type CA currents and Na+ channel blocker

toxicity: well tolerated
somnolence, fatigue (mild)

therapeutic uses:
against all partial seizures with and w/o secondarily generalized tonic-clonic seizures
drug class: sedative-hypnotic/anxiolytic
MOA: same as other benzos
elimination: long-acting
drug class: sedatives/anxiolytics
MOA: same as others
elimination: long-acting
drug class: sedative/anxiolytic (benzodiazepine)
MOA: same as other benzos
elimination: intermediate acting
drug class: anxiolytics/sedatives (benzodiazepine)
MOA: same as other benzos
elimination: long-acting
drug class: anxiolytics/sedatives (benzodiazepine)
MoA: same as other benzos
elimination: short-acting (only one)
drug class: anxiolytics/ sedatives
MOA: same as other benzos
elimintation: intermediate-acting
drug class: hypnotic (imidazopyridine)
MOA: works similar to benzos.  receptor agnoist
effects: primarily hypnotic, acts rapidly, less amnesia and day-after somnolence than zolpidem and benzos
elimination: short half-life
drug class: hypnotic (pyrazolopyrimidine)

MOA: binds to benzodiazepine binding sites on GABA-A receptors but is NOT a benzo

effects: amnesia w/higher doses
abrupt discontinuation=rebound insomnia
less risk of tolerance/dependence perhaps
drug class: hypnotic

MOA: melatonin receptor agnoist
no direct action on GABA-A recpetors

drug effects: reduces latency to sleep w/ no rebound nsomnia or withdrawal syndromes
elimination: forms active metabolite that has long half-life
drug class: sedative-hypnotics

MOA: not a benzo but has similar MOA

effects on EEG/sleep:
increases total sleep time
increase stage 2 non-REM sleep (preferred)
low doses-little on sleep patterns
high doses-decreases REM sleep

elimination: long half-life

less amnesia and day-after somnolence vs. zolpidem and benzos

drug class: benzodiazepine antagonist

effects: block actions of benzos, eszopiclone, zaleplon, and zolpidem and inverse agonist but not barbituates
compare and contrast barbiturates and benzodiazepines
low doses of both result in sedation to hypnosis.  High doses of barbituates causes anesthesia to coma but benzos don't
valerian root
drug class: anxiolytics

Therapeutic use: used more as a sedative/hypnotic than as a anxiolytic.

chemical makeup includes:
sesquiterpenes, iridoids, alkaloids, and more stuff

toxicity: rarely happens
migraine, GI prbs

drug interactions: potentiates sedative effects of barbiturates, anesthetics and other CNS depressants
used in combo w/ St. John's wort

more stuff:  less prone to causing drowsiness than barbituates
benzodiazepines in general
MOA: bind to BZ binding site (gamma binding site nxt to alpha) on GABAA Cl channels
require GABA to exert effects
increases freq of channel openings

drug effects: chronic use can cause tolerance by inducing down-regulation of BZ binding sites and dependence

drug interactions:
CNS depression is additive when taken w/ EtOH, opiods, anticonvulsants, phenothiazines
may also have enhanced CNS depression w/ antihistamines, anti-hypertensives, tricyclic antideperesants

effects on sleep
decreses time spent in slow wave sleep
total sleep time increased by increasing time spent in stage 2 of sleep
increases number of cycles of REM sleep and decreases amt of time spent in REM
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