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95 Cards in this Set

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Blocks inactive NaV.
For generalized tonic clonic seizures.
Not a central depressant.
Reduces spread by targeting excessively active regions.
Gingival hyperplasia is most common side effect.
Blocks inactive NaV.
For generalized tonic clonic seizures and post herpetic neuralgia
Side effects include drowsiness, renal and hepatic, blurred vision.
For generalized tonic clonic seizures.
Currently not used much in favor of valproate.
Non-slsective CNS depressant.
Limits seizure spread, elevates spread, preventing recurrence of febrile-induced seizures.
Phenobarbital (barbituate)
Used to interrupt Status Epilepticus.
Diazepam (benzodiazepine)
Blocks rapidly inactivating T-type Ca++ channels.
For generalized absence seizures primarily, also for myoclonic seizures.
Side effects include GI distress, drowiness, and may cause seizures in pts with major motor epilepsy.
Block NaV. Some T-type Ca++ channels and GABA uptake also blocked.
For generalized absence and generalized tonic clonic.
Few CNS side effects. Good drug!
Valproic Acid (Valproate)
Blocks CaV and maybe NaV.
Excellent in neuropathic pain and low-level disorders.
Fewer side effects than most antiepileptics.
(Structural analog of GABA, but not a GABA agonist)
Strongly blocks NaV
For complex partial seizures.
Can be used as an adjuvant.
Glycine antagonists at NMDA receptors.
Possibly blocks NaV.
For generalized tonic cloin and partial seizures.
Inhibits GABA uptake in to neurons.
For partial seizures.
Blocks NaV.
Enhances efficacy of GABA, blocks AMPA.
For patial seizures.
Mechanism of action unknown.
For long term treatment of anxiety, especially in the elderly.
For insomnia.
Short half-life.
For generalized anxiety disorder and panic/phobia disorder.
Use a low dose for daytime anxiety.
Medium half life.
For generalized anxiety disorder, panic/phobia disorders, and insomnia.
Use a low dose for daytime anxiety.
Use a high dose for insomnia.
Long half life.
Reversible depression of all excitable tissue, though CNS is most sensitive.
Small doses are hyperalgesic.
Short acting.
Side effects are hangover (extended CNS depression), paradoxical excitement, hepatic enzymatic drug interactions, withdrawl is bad.
Acts on benzodiazepine site on GABA receptor, but not a benzodiazepine.
For insomnia. Cannot relive anxiety at high doses.
Tolerance not much of an issues.
Used to treat chronic alcoholism.
Inactivates aldehyde dehydrogenase, allowing acetylaldehyde to accumulate.
Used for fever, as a vehicle, skin disinfectant, prevent decubitus ulcers.
Antidote to methanol poisoning.
Enhances GABA, inhibits NMDA, enhances 5HT3
5-HT B/D agonist.
For acute migraines.
Potent vasoconstrictor of vessel SMC.
Reduces secondary pain flow to thalamus.
Side effects are minor, but contraindicated in pts with CAD.
Non-selective for 5HT, Da, and alpha adrenergic receptors. Theraputic effects likely from 5-HT1 receptors.
For acute treatment of frequent moderate migraines or infrequent severe migraines.
Side effects are nausea and vomiting in 10% of pts, may exacerbate angina, not for the pregnant.
Serotonergic antagonist.
For migraine prophylaxis.
Side effects - can cause retroperitoneal fibrosis that requires discontinuation of treatment for 1 month every 6 months.
Possible AD prophylaxis. 2 year treatment reduced AD risk by 55% in elderly who took drugs before, had no prior AD symptoms.
Possible AD prophylaxis.
Reduces AD risk by 79% in one study.
Hypercholesterolemia correlates with increased AD incidence in later life.
Possible AD prophylaxis.
Thought to reduce AD by reducing hypertension.
A butrylcholinesterase inhibitor.
Was the prototype AD drug.
Non-selective PNS and CNS inhibitor.
Short half-life, must be given 4 times daily.
Side effects are cholinergic in nature.
Causes direct hepatic damage.
CNS-selective acetylcholinesterase inhibitor.
Drug of choice for AD pts NOT ON multi-drug regimens.
Long half life - once daily.
Side effects are cholinergic in nautre.
No direct hepatic damage.
Metabolized by a cytochrome P450 isoensyme. Risk of adverse drug interactions high.
CNS-selective acetylcholinesterase inhibitor.
Drug of choice for AD PTS ON multi-drug regimens.
Inhibitor medium length - take 2 daily.
Side effects are cholinergic.
Metabolized by cholinesterases so reduced risk of drug interactions.
Reduced hepatotoxicity.
Non-selective CNS and PNS acetylcholinesterase inhibitor.
Uncertain clinical use, potentiates nicotinic receptor, which is one possible use.
Considered an AD drug.
No direct hepatic toxicity.
NMDA receptor antagonist.
Can slow deterioration in AD alone and with Donepezil.
Just FDA approved in US.
Blocks NE reuptake in CNS and peripherally.
For mood elevation in special cases. Beware side effects.
Side effects - orthostatic hypotension, tachycardia, arrhythmia, sedation, anticholinergic effects, weight gain.
Suicide can be achieved by taking a weeks supply.
Blocks degradation of NE, DA, 5-HT, other amines.
For atypical depression and major depression when other drugs are not effective or appropiate.
Side effects - hepatotoxicity, potentiates sympathomimetic amines, hyperreflexia, and convulsions.
Tyramine reaction occurs - avoid wine and cheese.
Selectively inhibits 5-HT reuptake.
For mood elevation in 1-3 weeks.
Also for OCD, atypical depression, panic disorder, bulemia, with other drugs for bipolar.
Side effects - Sexual dysfunction, slow onset, 10% get naseua and diarrhea, suicidal thinking in adolescents, contraindicated in anorexics.
Inhibits reuptake of NE and 5-HT
Fewer side effects than tricyclics.
Similar side effect profile to SSRIs.
Short half life.
5-HT reuptake inhibitor. Also a partial agonist at 5-HT1aR.
Used for depression with insomnia, anxiety, and agitation.
Side effects - marked sedation, dizziness, hypotension, naseua.
5-HT reuptake inhibitor that is also a 5-HT2 antagonist.
Produces non-sedating mood elevation.
For depressed people with fatigue.
Inhibits DA and NE reuptake.
For depression, especailly with psychomotor retardation.
For treatment of nicotine addiction.
Low side effects, include nervousness and insomnia.
Alpha 2 antagonist and 5-HT 2 + 3 receptor antagonist.
Mood elevation but has sedative and anxiolytic effects.
Side effects similar to TCAs.
For treatment of acute mania (with benzodiazepine), manic phases of manic-depressive illness, mood swings of manic-depressive prone pts, anti-depressant effect in some.
Side effects - fatigue, muscular weakness, slurred speech, ataxia, thirst, urination.
Tolerance eventually develops to many side effects.
Stimulates hyptocretin/orexin neurons, predominantely in hypothalamus.
For narcolepsy, shift-work sleep disorder, possibly useful for ADHD in future.
Low abuse liability.
Fewer classicla stimulant side effects
Selective NE reuptake inhibitor.
For ADHD in children and 1st and only drug for ADD in adults.
Not a stimulant.
Side effects - hepatoxicity, decreased appetite, insomnia, sexual issues.
Antagonize adenosine receptors, levels of which may signal fatigue.
For bronchial asthmas - relax smooth muscle, with asprin for headaches, with ergots for migraine - improve their absorption.
Side effects - nervousness, insomnia, excessive respiratory stimulation, tolerance, but modest withdrawl.
Evoke release and inhibit reuptake of NE and 5-HT. Also have effects on DA.
First-line drug in ADHD. Also used in nacrolepsy and previously used in obesity.
Competes with NE for reuptake transporter and VMAT.
Causes wakefulness, tremor, dilated pupils.
Blocks reuptake of biogenic amines, especially dopamine.
Principle use is as anesthetic in upper respiratory tract. Vasoconstricts and reduces secretions.
Causes wakefulness, tremor, dilated pupils.
Evoke release and inhibit reuptake of NE and 5-HT. Also have effects on DA.
Used for narcolepsy. Can be used for ADHD, but is not first-line.
Competes with NE for reuptake transporter and VMAT.
Causes wakefulness, tremor, dilated pupils.
Causes pleasure (dopamine), appetite supression (norepinephrine), cognitive enhancement (acetylcholine), memory (vasopressin), mood modultion (serotonin), anxiety reduction (beta-endorphin)
Blocks NE reuptake. Effective in aiding smoking cessation. Has some side effects.
Blocks DA and NE reuptake. Effective in aiding smoking cessation. Has few side effects.
CB1 receptor antagonist.
Helps stop you from smoking weed. And has some use in getting you off the coke, morphine, booze, and food.
Precursor to DA.
Crosses BBB to enter brain and is metabolized to DA.
Used to treat parkinsonism.
Only 5% actually gets in brain because 95% is converted to DA in periphery and later to NE.
Causes peripheral DA and NE toxicity - orthostatic hypertension, nasea, dyskinesia, psychosis (dopamine in limbic and corticol areas).
Has been tried to be given to treat parkinsonism.
Given orally will make you vomit.
Will not cross BBB and causes vomiting when in periphery.
Peripheral decarboxylase inhibitor.
Used with another drug to treat parkinsonism.
Circumvents peripheral DA toxicity and blocks Vitamin B effect.
Best treatment for PD.
Increases life expectancy with minimal side effects.
No resistance develops.
Some peripheral side effects are present - orthostatic HTN, nausea, vomiting, dyskinesis, pyschiatric effects.
Sinemet (Levodopa and Carbidopa)
Blocks action of ACh.
Early drug used to treat PD, enhance motion by stimulating caudate.
Side effects - especially in elderly - low theraputic index, sedation, delerium, tachycardia, anti-salivation, anti-lacrimation, anti-urination, anti-defication (SLUD).
Peripheral COMT inhibitors.
COMT is the enzyme that breaks down L-DOPA. Decreases L-DOPA elimination.
Used to extend Sinemet duration of action and decrease it's on/off and weaning off effects. One of these drugs can cause liver failure - which one?
Tolcapone (liver failure) and Entacapone.
D2 agonist and partial D1 agonist/antagonist.
Used to aid Sinemet in late-stage PD, used alone in early PD, can also treat associated hyperprolactinemia (pituitary D2 receptros block prolactin secretion)
Dopamine D1/D2 agonist.
Used to aid Sinemet in late-stage PD and used along in early PD.
Incidence of side effects lower than with D2 agonists.
Possibly aleviates on/off phenomenon, due to prolonged action.
Moderate half-life.
Enhances DA release of Substantia Nigra, blocks glutamate.
Used to aid Sinemet in late-stage PD and can be used alone in early stage.
Side effects similar to anti-cholinergics.
Started as anti-viral.
Inhibits metabolism of brain DA to DOPAC via MAO-B inhibition.
Provides mild symptomatic relief, expensive.
Has uncertain neuroprotective effect.
Dopamine D3>D2 agonist.
Used to aid Sinemet in late-stage PD and can be used alone in early PD.
Can also be used with restless leg syndrome.
Side effects include sleep attacks, hallucination, dyskinesia, nausea. Somewhat more effective than bromocyptine.
No ergoline-like side effects.
Pramipexole and Ropinirole
Powerful D1/D2 agonist.
Used to rescue PD patients rapidly from the off-state.
Administed IV, sublingual, rectally, intranasal, pen-injection.
Strong D2 receptor antagonist.
Used to treat psychosis.
High sedative, moderate hypotensive, low motor side-effects.
A phenothiazine with high anti-cholingergic and anti-adrenergic properties so pseudoparkonism side effect is not present.
Can cause Neuroleptic Malignant Syndrom (NMS).
Strong D2 receptor antagonist.
Used to treat psychosis.
Low sedative, low hypotensive, high motor side-effects.
High pseudoparkinsonism and tardative dyskinesia motor side effects.
A phenothiazine, but low anticholinergic properties so
Strong D2 receptor antagonist.
Low sedative, low hypotensive, high motor-side effects.
High pseudoparkinsonism and tardative dyskinesia motor side effects.
A butyrphenone, so more D2 selective.
Strong D2 and strong 5HT2 receptor antagonist.
Used to treat psychosis.

Can possibly increase anxiety and depression.
Strong 5-HT2 antagonist and weak D2 antagonist.
Atypical anti-psychotic drug of choice of the moment.
Strong anti-cholinergic, so few to no motor side-effects.
Causes potentially fatal agranulocytosis in up to 3% of patients - so monitor blood.
May partly relieve tardive dyskinesia.
Strong 5-HT2 and weak D2 antagonist.
Used to treat psychosis.
Low to none motor side effects.
Possible new best atypical anti-psychotic.
No risk of aganulocytosis!
Strong 5-HT2 and weak D2 antagonist.
Used to treat psychosis.
Low to none motor side effects.
Also used to alleviate dopaminergic treatment-induced psychosis/hallucinations in PD.
Strong 5-HT2 and weak D2 antagonist.
Used to treat psychosis.
Low to none motor side-effects.
May not cause weight gain like other psychotics.
Side effect: Prolonged QT interval.
Mild presynaptic D2 agonist (reduced DA release from substantia nigra) and postsynaptic D2 antagonist (reduced DA effects on striatum).
Low to no motor side effects.
Milder action and inhibition of DA release which appears to prevent motor side effects and tardive dyskinesia.
May not cause weight gain like other psychotics.
Good analgesic, weak anesthetic.
Rapid uptake and elimination.
High MAC.
No odor, no metabolism, no hepatic toxicity.
Little cardiac or respiratory depression.
Can easily distend air spaces.
Nitrous Oxide
Effective anesthetic at low concentrations.
Causes hepatic necrosis.
Can result in a hepatitis in rare cases.
Little airway irritation.
Slow uptake and elimination.
Good anesthetic and muscle relaxant.
Pungent odor - bronchoiritating with laryngospasm.
No renal, low metabolism with only reported liver toxicity.
Stable cardiac rhythm and rate.
Vasodilates and reduces systemic vascular resistance.
Good anesthetic.
Rapid uptake and elimination.
Generally used for matentience of anesthesia.
Minimal systemic and side effects.
High incidence of coughing and laryngospasm, raises airway resistance.
Protective airway responses come back quickly and general recovery is quick after discontinuation.
Good anesthetic.
Rapid uptake and elimination.
Generally used for inductgion of anesthesia.
Minimal systemic and side effects.
No coughing or layngospasm, lowers airways resistance.
Strong vasodilation.
Rocovery longer and expensive.
Anesthetic similar to isoflurane with renal toxicity.
Smells bad like isoflurane.
Used for normal amnesia and normal outpatient anestesia.
No analgesia.
Unpredictable hypnosis.
Strong amnesia.
Enhances GABA function. Unlike others, can be reversed.
Used for a cerebral protective operation because it decreases cerebral metabolic rate for oxygen.
Low pain on injection compared to other drug in class.
Used for low cost induction.
No analgesia. (Or possibly hypo-algesia in low doses).
Strong hypnosis.
Weak amnesia.
Enhances GABA function.
Cardiac depressant.
Can be used for a cerebral protective operation because it decreases cerebral metabolic rate for oxygen. Slightly worse for perfusion pressure and ICP than other agent used for same thing.
No analgesia.
Strong hypnosis.
Moderate amnesia.
Enhances GABA function.
Painful on injection.
Minimal hangover and nice anti-emetic effect.
Used for normal analgesia when lower doses are needed.
Also used to help lessen pain peri-operatively and chronic pain.
Used in low blood pressure emergencies and for long procedures.
Strong analgesia.
Moderate hypnosis with hallucinations in some groups.
Moderate amnesia.
Raises systemic blood pressure.
Bad side effect - increases ICP.
Stable with a context sensitive half life.
Competivie inhibitor of NMDA.
Not painful on injection.
Only drug safe with porphyria.
Used for brief procedures like cardioversion and electroconvulsive therapy.
Cadiac depressant.
Enhances GABA function.
No analgesia.
Strong hypnosis.
Weak amnesia.
Used on patients with cardiac disease because its only anesthetic that has no effect on Cardiac system and also used for brief procedures like cardioversion and electroconvulsive therapy.
Only IV anesthetic that does not cause histamine release.
Enhances GABA function.
No analgesia.
Strong hypnosis.
Weak amnesia.
Blocks normal stress-induced cortisol and cannot be used in the ICU when pts are under high stress.
Painful on injection.
Used as sedative in ICU.
Also used as an adjuvant.
Also used to potentiate anesthesia, assist with intubation, and as a general anesthetic when you don't need deep levels (ie patient can talk).
Alpha 2 agonist.
Problems - slow onset, hypotension, bradycardia, pain on injection.
Function like Midazolam, but has an aqueous base, so more pain on injection so not used. Can be reversed.
Amide class LA.
Associated with nerve toxicity when used as a nerve block and has ability to difuse through bone.
Amide class LA.
Often used for post-op analgesia (Marcaine block).
Extensive protein binding, so long acting but slow onset.
As 0.5% solution with epi.
Amide class LA.
1.5% with epi.
Long acting due to high protein binding.
Greater lipid solubility, so more potent.
Onset 3-5 min, length 5-10 hours.
Amide class LA.
Used commonly world-wide.
Very safe.
2% concentration with vasoconstrictor.
Can use pupal anesthesia test for pain.
Use with epinephrine.
Can have allergy to catecholamine give with it, but not the druf itself.
Can have complications with liver or renal disease.
Amide class LA.
Used as 3% solution without vasoconstrictor.
Inherently a mild vasoconstrictor (safe to inject at areas with end organ circulation)
Good for cardiac pts where you want to avoid catecholamines.
Quick onset (30 sec to 4 min) and short duration (half hour).
Works for 60 min as a block.
Sulfite free.

As a 2% concentration with levonordefrin (vasoconstrictor), can use for 1 to 5.5 hours.
Amide class LA.
High PKA so slow onset.
Ester class LA.
Used in ENT cases.
Ester class LA.
Most commonly used in this class.
Ester class LA.
Potent vasoconstrictor.
Also used in dentristy.
Cardiac patients should receive less than max full dose.
Mildly potent vasoconstrictor.
Acts on alpha sites.
Cardiac patients should receive less than max full dose.