Term
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Definition
Indirect acting sympathomimetic; Local anesthetic
MOA: PNS- inhibits voltage gated Na+ channels; CNS- blocks uptake of DA, NE, serotonin
Produces an amphetamine-like effect that is shorter acting and more intense; RR = 5
Cocaine hydrochloride- water soluble (injected or absorbed through musical membrane); when heated in an alkaline solution- crack cocaine (smoked)
Penetrates brain quickly
Effects: rush; tachycardia, ventricular arrhythmia, appetite loss, hyperactivity, insomnia; increased risk of stroke, intracranial hemorrhage, MI, seizure; hyperthermia, coma/death |
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Term
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Definition
Indirect acting sympathomimetic
MOA: drug taken up via DAT/NET which causes increased release of dopamine and NE/serotonin from presynaptic neuron by reversal of transporters and preventing normal reuptake via NET/DAT/SERT/VMAT
RR = 5; Schedule II
Readily enters CNS; d-isomer is most potent
Treatment: ADHD-> increases mood and alertness
SE: insomnia, anorexia, tics, headaches, visual hallucinations, emotional lability, growth retardation
Contraindications: history of mania, psychosis, drug/alcohol abuse; closed angle glaucoma (increases alpha adrenergic receptor activation)
Drug Interactions: other sympathomimetics (increased BP/HR); MAO-I (hypertensive crisis); phenobarbital/phenytoin/tricyclic antidepressants (inhibits their metabolism)
Abuse: oral, smoked, or injected
Effects: alertness, euphoria, agitation, confusion, bruxism (tooth grinding), skin flushing, tachycardia, arrhythmia, HTN crisis, stroke
Withdrawal syndrome: dysphoria, drowsiness, irritability |
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Term
| Methamphetamine (N-methylamphetamine) |
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Definition
Indirect acting sympathomimetic
Higher ratio of central to peripheral actions compared to amphetamine |
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Term
| Methylphenidate (Ritalin) |
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Definition
Indirect acting sympathomimetic
Treatment: ADHD
MOA: increase in dopamine and NE levels by blocking
reuptake in presynaptic neuron via NET/DAT
Racemic mixture-> d-isomer is more potent; short, intermediate, or long acting
Schedule II
SE: insomnia, anorexia, tics, headaches, visual hallucinations, emotional lability, growth retardation
Contraindications: history of mania, psychosis, drug/alcohol abuse; closed angle glaucoma (increases alpha adrenergic receptor activation)
Drug Interactions: other sympathomimetics (increased BP/HR); MAO-I (hypertensive crisis); phenobarbital/phenytoin/tricyclic antidepressants (inhibits their metabolism) |
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Term
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Definition
Mixed-Acting Sympathomimetic
MOA: Beta1/Beta2-adrenergic receptor agonist and blocks NET/DAT
Higher bioavailability and duration of effects than catecholamines
Excreted in urine-> a significant fraction remains unchanged |
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Term
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Definition
Indirect acting sympathomimetic
Byproduct of tyrosine metabolism; found in fermented foods
MOA: increase synaptic levels of catecholamines by mimicking excitation of SNS; increases release
Use with caution in patients on MAO-A inhibitors-> normally degraded by MAO in liver
Low oral bioavailability b/c of first pass effect (concentration is reduced in liver); parenteral injection
Side effects: elevated BP |
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Term
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Definition
Indirect-Acting Sympathomimetics
MOA: inhibits both NE and dopamine transporters; increases interstitial concentrations not only of NE and dopamine, but also serotonin and glutamate while decreasing GABA levels
Used primarily to improve wakefulness in narcolepsy and some other conditions-> psychostimulant
Effects: increased BP and heart rate, though these are usually mild |
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Term
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Definition
Non-stimulant Sympathomimetic
Treatment: ADHD
MOA: increases NE transmission with no increase in dopamine by inhibiting NE reuptake by presynaptic NET
Slower onset than stimulant sympathomimetics
Metabolized by CYP2D6 isoenzyme (half life increased w/ CYP2D6 inhibitors)
Not controlled substance-> no increase in DA release = low potential for abuse
SE: abdominal pain, nausea, vomiting, decreased appetite, diarrhea, dizziness, somnolence; decreased mean height/weight in children
Drug interactions: MAO-I (hypertensive crisis) |
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Term
| Dexmethylphenidate (Focalin) |
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Definition
Sympathomimetic; d-isomer of methylphenidate
Treatment: ADHD
Given in half the dose of racemic methylphenidate
Schedule II
SE: insomnia, anorexia, tics, headaches, visual hallucinations, emotional lability, growth retardation
Contraindications: history of mania, psychosis, drug/alcohol abuse; closed angle glaucoma (increases alpha adrenergic receptor activation)
Drug Interactions: other sympathomimetics (increased BP/HR); MAO-I (hypertensive crisis); phenobarbital/phenytoin/tricyclic antidepressants (inhibits their metabolism) |
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Term
| Dextroamphetamine (Dexedrine) |
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Definition
Sympathomimetic; d-isomer of amphetamine
MOA: increased release of dopamine and NE from presynaptic neuron by reversal of transporters
Schedule II
Treatment: ADHD
SE: insomnia, anorexia, tics, headaches, visual hallucinations, emotional lability, growth retardation
Contraindications: history of mania, psychosis, drug/alcohol abuse; closed angle glaucoma (increases alpha adrenergic receptor activation)
Drug Interactions: other sympathomimetics (increased BP/HR); MAO-I (hypertensive crisis); phenobarbital/phenytoin/tricyclic antidepressants (inhibits their metabolism) |
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Term
| Lisdexamfetamine (Vyvanse) |
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Definition
Sympathomimetic
Pro-drug; d-amphetamine bonded to L-lysine
MOA: after ingestion, hydrolyzed to separate parts; increased release of dopamine and NE from presynaptic neuron by reversal of transporters
Less potential for abuse/toxicity; still Schedule II
SE: insomnia, anorexia, tics, headaches, visual hallucinations, emotional lability, growth retardation
Contraindications: history of mania, psychosis, drug/alcohol abuse; closed angle glaucoma (increases alpha adrenergic receptor activation)
Drug Interactions: other sympathomimetics (increased BP/HR); MAO-I (hypertensive crisis); phenobarbital/phenytoin/tricyclic antidepressants (inhibits their metabolism) |
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Term
| Amphetamine mixed salts (Adderall) |
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Definition
Indirect-Acting Sympathomimetic; Racemic form of amphetamine
MOA: increased release of dopamine and NE from presynaptic neuron by reversal of transporters
Schedule II
SE: insomnia, anorexia, tics, headaches, visual hallucinations, emotional lability, growth retardation
Contraindications: history of mania, psychosis, drug/alcohol abuse; closed angle glaucoma (increases alpha adrenergic receptor activation)
Drug Interactions: other sympathomimetics (increased BP/HR); MAO-I (hypertensive crisis); phenobarbital/phenytoin/tricyclic antidepressants (inhibits their metabolism) |
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Term
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Definition
SSRI antidepressant-> racemic mixture
MOA: allosteric inhibition of SERT
Treatment: MDD, anxiety disorders (GAD), PTSD, OCD, panic disorder, PMDD, bulimia/anorexia nervosa/obesity, premature ejaculation, autism
Metabolized to an active product-> norfluoxetine=> 1/2 life is 3X longer than parent drug
Highly lipophilic
SE: nausea, diarrhea; diminished sexual function; headache; insomnia/hypersomnia; weight gain
Drug Interactions: decreases metabolism/increases half life of atomoxetine by acting as CYP2D6 inhibitor |
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Term
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Definition
SSRI antidepressant
MOA: allosteric inhibition of SERT
Treatment: MDD, anxiety disorders (GAD), PTSD, OCD, panic disorder, PMDD, bulimia
High lipophilic
SE: nausea, diarrhea; diminished sexual function; headache; insomnia/hypersomnia; weight gain
Drug Interactions: decreases metabolism/increases half life of atomoxetine by acting as CYP2D6 inhibitor |
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Term
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Definition
SSRI antidepressant
MOA: allosteric inhibition of SERT
Treatment: MDD, anxiety disorders (GAD), PTSD, OCD, panic disorder, PMDD, bulimia, autism
High lipophilic; inhibitor of CYP3A4
SE: nausea, diarrhea; diminished sexual function; headache; insomnia/hypersomnia; weight gain |
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Term
Citalopram (Celexa)
Escitalopram (Lexapro) |
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Definition
SSRI antidepressant
Citalopram- racemic mixture
Escitalopram- S enantiomer of citalopram
MOA: allosteric inhibition of SERT
Treatment: MDD, anxiety disorders (GAD), PTSD, OCD, panic disorder, PMDD, bulimia
Highly lipophilic; not metabolized by P450s
SE: nausea, diarrhea; diminished sexual function; headache; insomnia/hypersomnia; weight gain |
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Term
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Definition
SSRI antidepressant-> racemic mixture
MOA: allosteric inhibition of SERT
Treatment: MDD, anxiety disorders (GAD), PTSD, OCD, panic disorder, PMDD, bulimia, premature ejaculation, autism
High lipophilic
SE: nausea, diarrhea; diminished sexual function; headache; insomnia/hypersomnia; weight gain |
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Term
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Definition
Selective SNRI antidepressant
MOA: bind and inhibit SERT > NET- low affinity
Treatment: MDD, pain disorder (fibromyalgia, neuropathy), generalized anxiety, urinary incontinence, vasomotor symptoms of menopause
Metabolized via CYP2D6 to desvenlafaxine; low protein binding
Once daily dose
SE: increased BP/HR; insomnia, anxiety, agitation; cardiac toxicity w/ overdose |
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Term
| Desvenlafaxine (Pristique) |
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Definition
Selective SNRI antidepressant- metabolite of Venlafaxine
MOA: bind and inhibit SERT and NET- low affinity
Treatment: MDD, pain disorder (fibromyalgia, neuropathy), generalized anxiety, urinary incontinence, vasomotor symptoms of menopause
Conjugated-> low metabolism=> excreted mostly unchanged in urine; low protein binding
Once daily dose
SE: increased BP/HR; insomnia, anxiety, agitation |
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Term
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Definition
Selective SNRI antidepressant
MOA: bind and inhibit SERT and NET- low affinity
Treatment: MDD, pain disorder (fibromyalgia, neuropathy), generalized anxiety, urinary incontinence, vasomotor symptoms of menopause
High protein bind; metabolized via CYP2D6 and CYP1A2
Well absorbed; once daily
SE: increased BP/HR; insomnia, anxiety, agitation |
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Term
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Definition
TCA antidepressant- tertiary amine
MOA: strong SERT and NET inhibitor
Treatment: depression that is unresponsive to other drugs, pain conditions, enuresis, insomnia
Highly anticholinergic
Well absorbed once daily dosing; long 1/2 life
Metabolized via demethylation, hydroxylation, glucuronidation, CYP2D6
SE: sedation; dry mouth, constipation, urinary retention, blurred vision, confusion, sexual effects; H1 antagonism (orthostatic hypotension); lethal in overdose |
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Term
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Definition
TCA antidepressant- secondary amine
Metabolite of imipramine
MOA: NE reuptake inhibitor
Treatment: depression that is unresponsive to other drugs, pain conditions, enuresis, insomnia
Less cholinergic but more potent than imipramine
Well absorbed once daily dosing; long 1/2 life
Metabolized via demethylation, hydroxylation, glucuronidation, CYP2D6=> lacks active metabolites
SE: sedation; dry mouth, constipation, urinary retention, blurred vision, confusion, sexual effects; H1 antagonism (orthostatic hypotension); lethal in overdose |
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Term
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Definition
TCA antidepressant- tertiary amine
MOA: SERT and NET inhibitor
Well absorbed once daily dosing; long 1/2 life
Metabolized via demethylation, hydroxylation, glucuronidation, CYP2D6=> active metabolite = nortriptyline
SE: sedation; dry mouth, constipation, urinary retention, blurred vision, confusion, sexual effects; H1 antagonism (orthostatic hypotension); lethal in overdose |
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Term
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Definition
TCA antidepressant- secondary amine
Metabolite of amitriptyline
MOA: reuptake inhibitor; NET > SERT
Well absorbed once daily dosing; long 1/2 life
Metabolized via demethylation, hydroxylation, glucuronidation, CYP2D6=> lacks active metabolites
SE: sedation; dry mouth, constipation, urinary retention, blurred vision, confusion, sexual effects; H1 antagonism (orthostatic hypotension); lethal in overdose |
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Term
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Definition
5-HT2A antagonist antidepressant
MOA: metabolite is a potent 5-HT2A antagonist; weak SERT>NET inhibitor; 5-HT1 agonist
Treatment: most commonly used as hypnotic for insomnia; major depression, anxiety disorders
Rapidly absorbed; extensive hepatic metabolism; low bioavailability; highly protein bound; short 1/2 life
SE: sedation; GI disturbances, othostatic hypotension |
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Term
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Definition
5-HT2A antagonist antidepressant
MOA: potent 5-HT2A antagonist; weak SERT/NET inhibitor
Treatment: major depression, anxiety disorder
Rapidly absorbed; extensive hepatic metabolism; low bioavailability; highly protein bound; short 1/2 life
Potent CYP3A4 inhibitor
SE: sedation, GI disturbances, orthostatic hypotension, hepatotoxicity |
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Term
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Definition
Unicyclic antidepressant
MOA: DAT >> NET inhibition; enhanced presynaptic catecholamine release
Treatment: depression, including seasonal depression; smoking cessation
Rapidly absorbed; extensive hepatic metabolism-> 3 active metabolites; biphasic elimination
SE: agitation; insomnia; anorexia; lacks sexual side effects |
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Term
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Definition
Tetracyclic antidepressant
MOA: alpha2 antagonist; enhanced NE and 5-HT release; 5-HT antagonist; antihistamine (H1 antagonist)
Treatment: unresponsive MDD
Metabolism- methylation then hydroxylation/glucuronidation; CYP2D6/3A4/1A2
SE: sedation; lacks sexual side effects |
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Term
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Definition
Tetracyclic antidepressant
MOA: potent NET inhibitor; weaker SERT inhibitor; also blocks D2 and muscarinic receptors
Treatment: unresponsive MDD; depression in psychotic patients
Rapidly absorbed; extensive hepatic metabolism-> metabolite = D2 blocker -> antipsychotic effects
SE: Parkinsonian symptoms |
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Term
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Definition
Tetracyclic antidepressant
MOA: potent NET inhibitor; weaker SERT inhibitor; anticholinergic
Treatment: unresponsive MDD
Well absorbed orally; extensive hepatic metabolism
SE: seizures |
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Term
Phenelzine (Nardil)
Tranylcypromine (Parnate) |
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Definition
MAOI antidepressant
Treatment: depression, social anxiety disorder
MOA: bind irreversibly and nonselectively to MAO-A and B
Well absorbed; extensive first pass effect; low bioavailability
SE: orthostatic hypotension; weight gain; sexual; insomnia; restlessness
Drug Interactions: any that increase serotonin/catecholamine levels (HTN crisis/serotonin syndrome); opioids (hyperpyrexic coma) |
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Term
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Definition
MAOI antidepressant
MOA: bind irreversibly and nonselectively to MAO-A and B
We'll absorbed; extensive first pass effect; low bioavailability
SE: orthostatic hypotension; weight gain; sexual; insomnia; restlessness |
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Term
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Definition
MAO-B inhibitor
MOA: irreversibly inhibits MAO-B; at higher doses becomes nonselective
Treatment: depression; Parkinson's Disease
We'll absorbed; extensive first pass effect; low bioavailability
Available transdermal, oral, and sublingual
Side effects: may inhibit MAO-A (in periphery) at higher doses; dyskinesias, psychosis, hallucinations; orthostatic hypotension; weight gain; sexual; insomnia; restlessness
Contraindications: SSRIs, tricyclic antidepressants, Meperidine-> all may cause stupor, rigidity, hyperthermia; may block serotonin metabolism-> restlessness, sweating, twitches, hyperreflexes, shivering, tremor, seizures, coma, death |
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Term
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Definition
Treatment of mild to moderate depression
MOA: inhibition of SERT, NET, and DAT; down regulate cortical beta adrenoceptors; up regulate 5-HT2 receptors; binds GABA receptor; reduces IL-6
Taken in a dried, hydroalcoholic form
May also inhibit some viruses and neoplasms
SE: photosensitization; hypomania, mania, autonomic arousal
Drug Interactions: antidepressants/stimulants-> serotonin syndrome; digoxin, OC, cyclosporine, HIV drugs, warfarin, irinotecan, theophylline, anticonvulsants |
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Term
| Chlorpromazine (Thorazine) |
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Definition
Typical Antipsychotic
MOA: blockade of D2, α-adrenergic, muscarinic, H1 histaminic, and 5-HT receptors
alpha1 = 5-HT2A > D2 > D1; low potency
Excreted in urine weeks after last dose
Toxicity: medium EPS; sedation; hypotension; deposits in cornea/lens |
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Term
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Definition
Typical Antipsychotic
MOA: blockade of D2, α-adrenergic, muscarinic, H1 histaminic, and 5-HT receptors
Toxicity: cardiotoxicity (prolonged QT interval); deposits in retina; overdose can be lethal |
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Term
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Definition
Typical Antipsychotic
MOA: blockade of D2, α-adrenergic, muscarinic, H1 histaminic, and 5-HT receptors
Treatment: Schizophrenia; Tourette's syndrome
D2 > 5-HT2A; high potency
Available in parenteral form
Toxicity: high EPS |
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Term
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Definition
Typical Antipsychotic
MOA: blockade of D2, α-adrenergic, muscarinic, H1 histaminic, and 5-HT receptors
D2 >> 5-HT2A; high potency
Toxicity: medium EPS; sedation; hypotension |
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Term
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Definition
Typical Antipsychotic
MOA: blockade of D2, α-adrenergic, muscarinic, H1 histaminic, and 5-HT receptors
Treatment: Schizophrenia, Tourette's syndrome
D2 > alpha1 > D4 > 5-HT2A > D1 > H1; high potency
Available in parenteral form
Toxicity: very high EPS; torsade; sedation; dry mouth; blurred vision; GI |
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Term
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Definition
Atypical Antipsychotic; 2nd line drug
MOA: blocks 5-HT2 and D2 receptors
Treatment: Schizophrenia; indicated to reduce risk of suicide
Low affinity for D2 receptor; D4 = alpha1 > 5-HT2A > D2 = D1; medium potency
Relapse after discontinuation is rapid and severe
Toxicity: very low EPS; hypotension; agranulocytosis; lowered seizure threshold; diabetes; increase in lipid levels; weight gain; myocarditis |
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Term
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Definition
Atypical Antipsychotic; 2nd line drug
MOA: blocks 5-HT2 and D2 receptors
Treatment: manic phase of bipolar disorder; aggression/self-injury in children; +/- Schizophrenic symptoms
Low affinity for D2 receptor; 5-HT2A > H1 > D4 > D2 > alpha1 > D1; high potency
Toxicity: very low EPS; sedation; weight gain; lowered seizure threshold; diabetes; increased lipid levels |
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Term
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Definition
Atypical Antipsychotic
MOA: blocks 5-HT2 and D2 receptors
Treatment: manic phase of bipolar disorder; +/- Schizophrenic symptoms
Low affinity for D2 receptor; H1 > alpha1 > M1,3 > D2 > 5-HT2A; low potency
Toxicity: very low EPS; sedation |
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Term
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Definition
Atypical Antipsychotic
MOA: blocks 5-HT2 and D2 receptors
D2 << 5-HT2A; high potency
Treatment: OCD, aggression/self-injury in children
Toxicity: low EPS; elevated prolactin |
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Term
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Definition
Atypical Antipsychotic
MOA: blocks 5-HT2 and D2 receptors
D2 < 5-HT2A; medium potency
Toxicity: very low EPS; prolonged QT interval |
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Term
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Definition
Atypical Antipsychotic
MOA: partial D2-receptor agonist; 5-HT2A antagonist; 5-HT1A partial agonist
Low affinity for D2 receptor; D2 = 5-HT2A > D4 > alpha1 = H1 >> D1; high potency
High occupancy of D2 receptors but lacks EPS due to 5-HT antagonism/partial agonism
Toxicity: very low EPS |
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Term
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Definition
Adrenergic-neuron blocking agent
Sympatholytic; effects CNS and PNS
MOA: inhibits vesicular monoamine transporter (VMAT) irreversibly, resulting in depletion of catecholamine stores by inability to fill vesicles w/ NE, DA, and serotonin
Treatment: tardive dyskinesia-> interferes w/ dopaminergic function; HTN; antipsychotic
Oral w/ long duration
Toxicity: Parkinsonian syndromes; sedation, lassitude (mental exhaustion); nightmares; depression; diarrhea; GI cramps and increases gastric acid secretion
Contraindications: depression-> may worsen; peptic ulcer-> b/c of increase gastric acid |
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Term
Benztropine (Cogentin)
Trihexyphenidyl (Artane) |
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Definition
Muscarinic Receptor Antagonist
Treatment: parkinsonism associated w/ antipsychotic use-> improve tremor and rigidity
MOA: potent inhibition of dopamine reuptake by DAT
Short lived effects
SE: sedation, dry mouth, urinary retention; poorly tolerated by the elderly |
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Term
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Definition
Mood Stabilizer
Treatment: prophylaxis or manic phase of bipolar disorder; also recurrent endogenous depression, schizoaffective disorder, and unipolar depression
MOA: suppresses inositol signaling by inhibiting inositol monophosphatase (IMPase) which prevents recycling; inhibits glycogen synthase 3 (GSK-3); inhibits NE sensitive adenylyl cyclase; uncouples GPCRs
Virtually complete oral absorption; peak [plasma] = 30min-2hr; no protein binding/no metabolism-> excreted unchanged in urine; 5 days for steady state concentrations
Slow onset of actions- may require a concominant antidepressant; at high concentrations may displace Na+; renal clearance is decreased during pregnancy
SE: tremor, mentalconfusion (toxic levels); decreased thyroid function; polydipsia/polyuria; diabetes insipidus; renal toxicity; edema; bradycardia-tachycardia syndrome; acneiform eruptions; teratogenic (also transferred in breast milk); leukocytosis
Drug Interactions: diuretics/newer NSAIDs-> reduces renal clearance; neuroleptics (antipsychotics)-> increased extrapyramidal symptoms; ECT-> Li+ lowers seizure threshold and causes prolonged seizures |
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Term
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Definition
Anticonvulsant; Mood Stabilizer
Treatment: absence, myoclonic, partial, and tonic-clonic seizures; bipolar disorder-> mania
MOA: Anticonvulsant=> induces closure of the inactivation in activated Na+ channels in depolarizing neurons, preventing further depolarization; also blocks voltage-gated Ca2+ T-type channels; also reduces metabolism of GABA by inhibiting GABA transaminase and succinc semialdehyde dehydrogenase and promotes GABA synthesis by glutamic acid decarboxylase; BPD=> may inhibit GSK-3 activity and promote gene expression through inhibition of histone deacetlyase
Rapid, complete oral absorption; hepatic metabolism (UGT/beta-oxidation>CYP2C9) w/ minor renal excretion
High bound to albumin; some metabolites are as potent as parent
SE: GI, sedation, ataxia, tremor, rash, alopecia, weight gain, hepatitis (rare); teratogenic
Drug Interactions: inhibits metabolism of phenytoin/phenobarbital (CYP2C9) and lamotrigine (UGT); increases carbamazepine metabolism and is VA metabolism is increased by carb.; displaces drugs bound to albumin-> phenyotin; clonazepam-> induces absence status epilepticus (rare) |
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Term
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Definition
Anticonvulsant; Mood Stabilizer
Treatment: partial and complex tonic-clonic seizures; bipolar disorder-> acute mania or prophylaxis; tics
MOA: Anticonvulsant=> induces closure of the inactivation in activated Na+ channels in depolarizing neurons, preventing further depolarization; BPD=> inositol depletion
Slow/erratic oral absorption; hepatic enzyme and renal excretion-> must monitor function of both; can induce its own metabolism
SE: stupor/coma, irritability, convulsions, respiratory depression, vertigo, blurred vision, nausea/vomiting, aplastic anemia, water retention; teratogenic
Drug Interactions: oral contraceptives-> induces CYP3A4 which metabolizes OC; phenobarbital/phenytoin/valproic acid-> increase carbamazepine metabolism by CYP3A4; propoxyphene/fluoxetine-> inhibit carb. metabolism; phenytoin/valproic acid/lamotrigine/tiagabine/topiramate-> metabolism increased by carbamazepine; haloperidol-> carb. decreases efficacy of haloperidol |
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Term
| Chlordiazepoxide (Librium) |
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Definition
Sedative-Hypnotic- benzodiazepine
MOA: enhances Cl- inflow through GABA-A receptor channels in the presence of GABA by increasing frequency of inflow
Decrease latency of sleep onset, increase stage 2 of NREM sleep, and decrease duration of REM and stage 4 NREM sleep
Long duration of action
Active metabolites; erratic IM bioavailability
SE: dependence, CNS depression, anterograde amnesia, teratogenic |
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Term
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Definition
Anticonvulsant; Sedative-Hypnotic-> benzodiazepine
Treatment: status epileptics; sleep disorders; used IV in anesthesia
MOA: enhances Cl- inflow through GABA-A receptor channels in the presence of GABA by increasing frequency of inflow
Decrease latency of sleep onset, increase stage 2 of NREM sleep, and decrease duration of REM and stage 4 NREM sleep
Hydroxylated to an active metabolite-> oxazepam
Given IV; long duration of action; erratic IM bioavailability
SE: CV and respiratory depression; drowsiness; dependence, CNS depression, anterograde amnesia, teratogenic |
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Term
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Definition
Sedative-Hypnotic- benzodiazepine
MOA: enhances Cl- inflow through GABA-A receptor channels in the presence of GABA by increasing frequency of inflow
Decrease latency of sleep onset, increase stage 2 of NREM sleep, and decrease duration of REM and stage 4 NREM sleep
Long duration of action
Metabolite of diazepam and chlordiazepoxide
SE: dependence, CNS depression, anterograde amnesia, teratogenic |
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Term
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Definition
Sedative-Hypnotic-> active metabolite of desmethyldiazepam (and therefore diazepam and chlordiazepoxide)
Use: ethanol detoxification; sleep disorders
MOA: positive modulator of GABA-A receptor-> increased frequency of channel opening=> attenuates withdrawal symptoms
Decrease latency of sleep onset, increase stage 2 of NREM sleep, and decrease duration of REM and stage 4 NREM sleep
Intermediate duration of action
Not effected by decreased liver function
SE: dependence, CNS depression, anterograde amnesia, teratogenic |
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Term
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Definition
Sedative-Hypnotic- benzodiazepine
MOA: enhances Cl- inflow through GABA-A receptor channels in the presence of GABA by increasing frequency of inflow
Decrease latency of sleep onset, increase stage 2 of NREM sleep, and decrease duration of REM and stage 4 NREM sleep
Active metabolites w/ long 1/2 life
SE: daytime sedation, dependence, CNS depression, anterograde amnesia, teratogenic |
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Term
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Definition
Sedative-Hypnotic- benzodiazepine
MOA: enhances Cl- inflow through GABA-A receptor channels in the presence of GABA by increasing frequency of inflow
Decrease latency of sleep onset, increase stage 2 of NREM sleep, and decrease duration of REM and stage 4 NREM sleep
Rapid absorption and onset; short duration of action
SE: daytime anxiety, dependence, CNS depression, anterograde amnesia, teratogenic; behavioral disinhibition, delirium, aggression, violence |
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Term
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Definition
Sedative-Hypnotic- benzodiazepine
MOA: enhances Cl- inflow through GABA-A receptor channels in the presence of GABA by increasing frequency of inflow
Decrease latency of sleep onset, increase stage 2 of NREM sleep, and decrease duration of REM and stage 4 NREM sleep
Treatment: sleep disorders, panic disorders, agoraphobia
Rapid oral absorption; intermediate duration of action
SE: dependence, CNS depression, anterograde amnesia, teratogenic |
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Term
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Definition
Intravenous Anesthetic; Sedative-Hypnotic- barbiturate
MOA: enhances Cl- inflow through GABA-A receptor channels by increasing duration of inflow
Used to induce anesthesia; rapid onset and rapid recovery-> very lipid soluble; rapidly redistributes to fat/muscle
Ok to use in patients w/ increased intracranial pressure
SE: teratogenicity; respiratory/cardiac depression; decreased cerebral metabolism/oxygen utilization/blood flow; reduce hepatic/renal blood flow w/o loss of function
Contraindications: porphyrias-> increases ALA synthase |
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Term
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Definition
Sedative-Hypnotic- barbiturate
MOA: enhances Cl- inflow through GABA-A receptor channels by increasing duration of inflow; inhibit glutamate AMPA receptors
SE: teratogenicity
Contraindications: porphyria |
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Term
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Definition
Anticonvulsant; Sedative-Hypnotic- barbiturate
Treatment: generalized tonic-clonic and partial seizures; sedation/hypnosis
MOA: enhances Cl- inflow through GABA-A receptor channels by increasing duration of inflow; inhibits glutamate AMPA receptors
Low toxicity; low cost
Complete but slow oral absorption; hepatic enzyme and renal excretion; long elimination half life (4-5days)-> elimination increased by alkalization of urine
SE: sedation (but tolerance develops); nystagmus, ataxia, irritability; teratogenic
Drug Interactions: oral contraceptives-> induces CYP3A4 which metabolizes OC; valproic acid/carbamazepine-> competes for metabolism
Contraindications: porphyria |
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Term
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Definition
Hypnotic
MOA: selective GABA agonist that enhances Cl- inflow through GABA-A receptor channels
Decreases REM sleep; shortens sleep latency and prolongs total time spent in sleep
Metabolized by hepatic CYP3A4 to inactive metabolites
Available in biphasic release that provides sustained drug levels for sleep maintenance
Rebound insomnia occurs at higher doses
SE: anterograde amnesia; day after somnolence; teratogenicity |
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Term
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Definition
Hypnotic
MOA: selective GABA agonist that enhances Cl- inflow through GABA-A receptor channels
Decreases latency of sleep onset w/ little effect on sleep time and REM/NREM
Metabolized by aldehyde dehydrogenase and CYP3A4 to inactive metabolites
Acts rapidly w/ short 1/2 life-> use for patients who awake early in sleep cycle
Rebound insomnia occurs at higher doses
SE: teratogenicity |
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Term
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Definition
Hypnotic
MOA: selective GABA agonist that enhances Cl- inflow through GABA-A receptor channels
Increases total sleep time; increases stage 2 NREM sleep, and decreases REM sleep
Metabolized by hepatic CYP3A4 to inactive metabolites
Long 1/2 life
SE: teratogenicity |
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Term
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Definition
Hypnotic
MOA: melatonin receptor MT1 and MT2 agonist in suprachiasmatic nucleus
Treatment: sleeping difficulty-> reduces latency of persistent sleep
Rapid oral absorption w/ high 1st pass metabolism (CYP1A2)-> active metabolite w/ longer 1/2 life
SE: dizziness, somnolence, fatigue, decreased testosterone, increased prolactin; teratogenicity
Drug Interactions: fluoxamine-> inhibits metabolism; rifampin-> reduces plasma levels
Contraindications: liver dysfunction |
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Term
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Definition
Anxiolytic
MOA: 5-HT1A and D2 partial agonist
Relieves anxiety w/o causing sedation, hypnosis, euphoria; no rebound anxiety or withdrawal
Slow onset; rapidly absorbed orally w/ high 1st pass metabolism-> metabolites w/ alpha-adrenergic blocking actions
Not used for acute attacks-> takes >1wk for effect
SE: nonspecific chest pain, tachycardia, palpitations, dizziness, nervousness, tinnitus, GI distress, mydriasis, paresthesias; teratogenic
Drug Interactions: MAOIs-> elevate BP |
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Term
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Definition
Benzodiazepine antagonist
MOA: competitive GABA-A receptor antagonist at benzodiazepine binding site
Treatment of overdose-> blocks actions of benzodiazepines, eszopiclone, zaleplon, and zolpidem
Acts rapidly w/ short 1/2 life (.7-1.3hrs)-> may require multiple doses
SE: agitation, confusion, dizziness, nausea, seizures, cardiac arrhythmia |
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Term
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Definition
Herbal supplement; Sedative-Hypnotic
Treatment: mild to moderate insomnia or anxiety
Reduces sleep latency; greater effect in poor sleepers (good sleepers show no efficacy)
SE: increased sleepiness on awakening; dizziness withdrawal w/ sudden cessation; headache; GI
Drug Interactions: may potentiate effects of benzodiazepines, anesthetics, and CNS depressants |
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Term
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Definition
Inhalational General Anesthetic
MOA: activate GABA-A receptor Cl- channels; may also antagonize NMDA receptor; may also increase K+ channel conductance and decrease nACh receptors conductance
Low solubility; rapid onset and recovery; MAC >100%
Incomplete anesthetic; no metabolism
Effects: decrease metabolic rate of brain; decrease renal filtration and blood flow; decrease hepatic blood flow
Toxicity: postoperative nausea and vomiting; decreased methionine synthase-> megaloblastic anemia |
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Term
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Definition
Inhalational General Anesthetic
MOA: activate GABA-A receptor Cl- channels; may also increase K+ channel conductance and decrease nACh receptors conductance
Low solubility; rapid onset and recovery
Metabolism-> formation of F-; also degraded by CO2 in anesthesia machine yielding compound A=> renal damage
Effects: decrease mean arterial pressure (decreased vascular resistance); decreased tidal V w/ increased respiratory rate; decrease metabolic rate of brain and increase cerebral blood flow; decrease renal filtration and blood flow; decrease hepatic blood flow; uterine muscle relaxant
Toxicity: decreased renal filtration |
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Term
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Definition
Inhalational General Anesthetic
MOA: activate GABA-A receptor Cl- channels; may also increase K+ channel conductance and decrease nACh receptors conductance
Moderate-high solubility; medium rate of onset and recovery
Effects: decrease mean arterial pressure (decreased vascular resistance); decreased tidal V w/ increased respiratory rate; decrease metabolic rate of brain and increase cerebral blood flow; decrease renal filtration and blood flow; decrease hepatic blood flow; uterine muscle relaxant
Toxicity: tachycardia |
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Term
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Definition
Inhalational General Anesthetic
MOA: activate GABA-A receptor Cl- channels; may also increase K+ channel conductance and decrease nACh receptors conductance
Moderate-high solubility; medium rate of onset and recovery
Renal metabolism-> formation of F-=> decreased renal concentrating ability
Effects: decrease mean arterial pressure (decreased CO); decreased tidal V w/ increased respiratory rate; decrease metabolic rate of brain and increase cerebral blood flow; decrease renal filtration and blood flow; decrease hepatic blood flow; uterine muscle relaxant
Toxicity: decreased renal filtration |
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Term
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Definition
Inhalational General Anesthetic
MOA: activate GABA-A receptor Cl- channels; may also increase K+ channel conductance and decrease nACh receptors conductance
High solubility; medium rate of onset and recovery
Oxidative metabolism-> formation of trifluoroacetic acid, Br-, and Cl-; further metabolized-> chlorotrifluoroethyl free radical which interacts w/ hepatic membrane=> induced hepatitis
Effects: decrease mean arterial pressure (decreased CO); decreased tidal V w/ increased respiratory rate; decrease metabolic rate of brain and increase cerebral blood flow; decrease renal filtration and blood flow; decrease hepatic blood flow; uterine muscle relaxant
Toxicity: bradycardia; hepatotoxicity-> hepatitis (esp. obese) |
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Term
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Definition
Intravenous Anesthetic- benzodiazepine
MOA: increases frequency of GABA-A channel openings
Used for balanced anesthesia and conscious sedation; slow onset and recovery
Reaches sedative plateau inadequate for surgical anesthesia but posses anxiolytic and amnesic properties-> preanesthetic
Water soluble but becomes lipid soluble at physiologic pH-> crosses BBB readily
Can be given IV, IM, orally, rectally
Effects: marked amnesia
Recovery can be accelerated w/ flumazenil |
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Term
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Definition
Intravenous Anesthetic; only IV anesthetic w/ both anesthetic and analgesic properties
AKA angel dust, Hog, Special K
MOA: noncompetitive antagonist of NMDA receptors
Moderately rapid onset and recovery
Dissociative anesthetic state-> catatonia, amnesia, and analgesia w/ or w/o loss of consciousness
Highly lipophilic; hepatic metabolism followed by renal and biliary excretion
Effects: CV stimulation, increased cerebral blood flow, emergence reactions impair recovery-> disorientation, illusions, vivid dreams=> less if given diazepam/midazolam/propofol
SE last ~1hr: hallucinations, separation of mind and body; stupor and coma, increased BP, impaired memory, chronic exposure may lead to long lasting psychosis
RR = 1
Pure form = white crystalline powder; also in liquid, capsule or pill; snorted, ingested, injected, or smoked
Contraindications: increased intracranial pressure |
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Term
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Definition
Intravenous Anesthetic
Induction agent: rapid onset and recovery; also used for prolonged sedation
Antiemetic properties
Rapid hepatic metabolism; excreted in urine
Effects: hypotension; elevated serum lipid levels; respiratory depression; pain at the site of injection is the commonest effect |
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Term
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Definition
Intravenous Anesthetic
Rapid onset and moderately fast recovery
Provides CV stability and minimal respiratory depression
Extensively metabolized in liver
Effects: decreased steroidgenesis; involuntary muscle movement; pain at injection site; postop nausea and vomiting; adrenocortical suppression |
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Term
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Definition
Opioid
Treatment: chronic, severe pain; acute pulmonary edema
MOA: μ-receptor agonist; histamine releasing effect
Available in slow release form (MSContin)
Metabolized in liver by conjugation->M3G/M6G metabolites have significant analgesic and hypnotic effect; M3G = neuroexcitatory (inhibit GABA); M6G = analgesic (> than morphine)
Renal > biliary excretion
Decreases respiratory and heart rate
Given oral, parenteral, rectal
SE: nausea, vomiting, pruritus, sphincter of Oddi spasm; disruption of sleep patterns
Contraindications: renal failure (metabolite build up) |
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Term
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Definition
Opioid
Illegal; IV, smoked, snorted
Highly lipid soluble (crosses BBB); deacytelated to active metabolites (6-monoacetyl morphine & morphine)
Euphoria lasts seconds to minutes, followed by hour of sedation-> wears of in 3-5hrs
SE: analgesia, euphoria, respiratory depression, vomiting, disruption of hypothalamic-pituitary-gonadal/hypothalamic-pituitary-adrenal axes (irregular menses/sexual performance problems)
Combinations: speedball = heroin+cocaine (cocaine reduces opiate withdrawal; heroin reduces irritability)
Withdrawal is brief (5-10days) and intense |
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Term
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Definition
Opioid
MOA: partial μ-receptor agonist
Treatment: severe pain; cough suppressant
Reduced first pass metabolism
Hepatic metabolism by CYP2D6-> metabolite of greater potency (morphine)
Can also be used as a cough suppressant
Given oral or parenteral |
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Term
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Definition
Opioid
MOA: partial μ-receptor agonist
Treatment: chronic, severe pain
Reduced first pass metabolism; available in slow release form (OxyContin)
Long-acting slow release version is abused by breaking the tablet-> making the full dose immediately available=> euphoria
Hepatic metabolism by CYP2D6-> metabolite of greater potency
Given oral |
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Term
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Definition
Oxycodone w/ acetominophen
MOA: partial μ-receptor agonist w/ analgesic
Given orally |
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Term
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Definition
Oxycodone w/ aspirin
MOA: partial μ-receptor agonist w/ analgesic
Given orally |
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Term
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Definition
Opioid
MOA: partial μ-receptor agonist
Hepatic metabolism by CYP2D6-> metabolite of greater potency
Given orally |
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Term
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Definition
Hydrocodone w/ acetaminophen
MOA: partial μ-receptor agonist w/ analgesic
Given orally |
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Term
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Definition
Hydrocodone w/ ibuprofen
MOA: partial μ-receptor agonist w/ analgesic
Given orally |
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Term
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Definition
Opioid
MOA: μ-receptor agonist
Treatment: severe pain
Metabolized by conjugation to H3G-> CNS excitatory
Given oral, parenteral, rectal |
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Term
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Definition
Opioid
MOA: μ-receptor agonist
Treatment: severe pain
Given parenteral or rectal |
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Term
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Definition
Opioid
MOA: μ-receptor agonist
100X more potent than morphine; often used as anesthetic adjunct-> slow onset and recovery
Intermediate duration of action (30min)-> lengthens w/ infusion
Metabolized in liver/intestinal mucosa by CYP3A4 w/ renal and biliary excretion
When used w/ doperidol and N2O-> neuroleptanesthesia
Given buccal transmucosal, transdermal (patch), parenteral, PCA
SE: decreased respiratory and heart rate; muscle rigidity; nausea, vomiting, pruritus, truncal rigidity |
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Term
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Definition
Opioid
MOA: μ-receptor agonist; antimuscarinic effects; can block 5-HT reuptake
Produces excitation/confusion; used as anesthetic adjunct
Metabolized in liver w/ biliary and renal excretion
Decreases respiratory and heart rate
Common drug of abuse among health professionals
Given oral or parenteral
SE: nausea, vomiting, pruritus, reduces shivering, tachycardia
Contraindications: renal failure (metabolite may cause seizures); incidences where tachycardia would be a problem; MAOIs due to 5-HT reuptake inhibition-> serotonin syndrome |
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Term
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Definition
Opioid
MOA: weak μ-receptor agonist
Given orally
Low analgesic activity; banning is under consideration |
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Term
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Definition
Opioid
MOA: weak μ-receptor agonist; inhibits NE and 5-HT reuptake
Treatment: mild to moderate pain; labor pain
Given orally
No effects on respiratory and CV systems
Hepatic metabolism w/ renal excretion
Toxicity: seizures, nausea, vomiting, dizziness, dry mouth, sedation, headache
Contraindications: epilepsy; MAOIs |
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Term
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Definition
Opioid
MOA: μ-receptor antagonist; κ-receptor agonist
Given parenterally
Ceiling effect to respiratory depression-> but when it does occur may be naloxone resistant
SE: psychotomimetic effects |
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Term
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Definition
Opioid
MOA: μ-receptor partial agonist; κ-receptor agonist
Given oral or parenteral
SE: psychotomimetic effects |
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Term
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Definition
Opioid
MOA: μ-receptor partial agonist; strong κ-receptor agonist
Given parenteral or intranasal |
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Term
| Buprenorphine (Buprenex, Subutex, Suboxone) |
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Definition
Opioid
Treatment of heroine addiction
MOA: partial agonist at μ opioid receptor-> stronger affinity than abused opioids; antagonist at κ-receptor-> induces positive mood; antagonist at δ-receptor
Minimal withdrawal symptoms, low potential of overdose, long acting, blocks heroin effects (e.g. euphoria)
Long 1/2 life (40hrs)
Sublingually active, but potential to be dissolved & injected-> schedule III; given orally or parenterally
Buprenorphine-naloxone=> oral; naloxone blocks potential buprenorphine high if taken IV
SE: psychotomimetic effects
Contraindications: pregnancy; benzodiazepine use; breathing/lung problems; kidney/gallbladder problems; head injury; mental disorders; adrenal/thyroid disfunction; enlarged prostate; urination problems
Drug Interactions: alcohol/benzodiazepines/fluvoxamine-> increased buprenorphine effects; naltrexone/partial opioid agonists-> risk of withdrawal |
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Term
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Definition
Treatment of heroin addiction and opioid overdose
MOA: selective μ-receptor antagonist; blocks the mild subjective high that may be produced by buprenorphine (or other opiates) alone
Reverses opioid effects in 1-3minutes-> normalizes respiration, consciousness, pupil size, bowel activity
Orally inactive (i.e. in combination w/ buprenorphine); IV-> precipitates an opioid withdrawal syndrome (antagonist precipitated withdrawal)
Short duration of action (1-2hrs)
SE: itching, nausea, vomiting |
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Term
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Definition
Serotonin Agonist
Treatment: acute migraine; cluster headaches
MOA: agonist of 5-HT1D/1B receptors on presynaptic trigeminal nerve endings to inhibit release of vasodilating peptides; may prevent vasodilation and stretching of pain endings and causes vasoconstriction
Duration of effect often shorter than migraine-> multiple doses; expensive
Given oral, nasal, subcutaneous; onset = 1.5hrs
SE: altered sensations; dizziness; muscle weakness, neck pain; injection site reactions; chest pain
Contraindications: coronary artery disease-> may cause coronary artery spasm |
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Term
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Definition
Ergot Derivative
Treatment: migraine
MOA: partial agonist of alpha adrenoceptors, 5-HT2, and DA receptors; agonist of 5-HT1D/1B receptors; vasoconstrictor
Dissociates very slowly-> long lasting effects
Effective when given during prodrome-> less effective if delayed; caffeine facilitates absorption
Oral, sublingual, rectal suppository, inhaler
No more than 6mg orally/attack; no more than 10mg/week
SE: overdose = severe, prolonged vasospasm |
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Term
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Definition
Ergot Derivative
Treatment: migraine
MOA: 5-HT2 receptor partial agonist; agonist of 5-HT1D/1B receptors; vasoconstrictor
Prophylaxis; inaffective for active migraine
W/drawn for toxicity |
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Term
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Definition
Derived from opium poppy or are synthetic derivatives
Treatment of acute and severe chronic pain; produces euphoria; illegal use
MOA: activates μ opiate receptor (GPCR) which inhibits adenylyl cyclase; chronic exposure causes weakening of inhibition = increased cAMP = increased CREB = increased dynorphin-> inhibition of GABAergic inhibitory interneurons => disinhibition of DA neurons
RR = 4
SE: in patient w/o pain-> nausea, vomiting, sedation
Withdrawal: caused by loss of suppression of locus ceruleus-> irritability; increased sensitivity to pain; nausea, aches, insomnia, pupillary dilation, sweating, piloerection, tachycardia, diarrhea, increased BP, fever
Drug Interactions: sedative-hypnotics-> increased CNS/respiratory depression; antipsychotic tranquilizers-> increased sedation, accentuates CV effects; MAOIs-> hyperpyrexic coma, HTN |
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Term
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Definition
Treatment: HTN, opiate detoxification; tics
MOA: alpha-2 adrenergic agonist
Opiate detox: decreases adrenergic neurotransmission in locus ceruleus-> less withdrawal symptoms, except for aches and craving
Oral
SE: orthostatic hypotension; sedation; diarrhea |
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Term
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Definition
Opioid
Treatment: chronic, severe pain; most successful form of detox off of short acting opiates (heroin)
MOA: slow acting μ opioid receptor agonist-> induces receptor endocytosis=> decreased tolerance and dependence
Orally active, slow-onset w/ long duration of action-> reduced likelihood of inducing euphoria/withdrawal symptoms
Oral once daily; metabolized by hepatic CYP3A4/2B6 to active metabolites
Withdrawal is slow in onset and lasts long
Benefits of use during pregnancy may outweigh hazards
Toxicity: respiratory depression, constipation, miosis, tolerance, dependence, withdrawal
Drug Interactions: alcohol/benzodiazepines/fluvoxamine/naltrexone-> increase methadone effect; carbamazepine-> decreased effect; partial opioid agonist-> risk of withdrawal |
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Term
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Definition
Cannabinoid; active substance = THC
MOA: agonist of cannabinoid-1 (CB1R) G(io)PCR-> disinhibition of DA neurons by inhibition of GABA neurons in VTA
RR = 2
1/2-life = 4hrs; onset = minutes; maximum effect = 4hrs
Effects: feeling of wellbeing, euphoria/relaxation; grandiosity, altered perception of passage of time; drowsiness, diminished coordination, memory impairment; visual hallucinations, increased appetite, decreased nausea, relief of chronic pain
Withdrawal syndrome: restlessness, irritability, mild agitation, insomnia, nausea, cramping |
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Term
| Gamma hydroxybutyrate (GHB) |
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Definition
aka liquid ecstasy, grievous bodily harm, date rape drug
MOA: weak agonist of GABA-B receptor-> disinhibition of DA neurons by inhibiting inhibitory GABA neurons
Odorless; rapidly absorbed after ingestion; max concentration = 20-30minutes; 1/2 life = 30minutes
Effects: euphoria, enhanced sensory perception, amnesia; sedation/coma |
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Term
| Lysergic acid diethylamide (LSD) |
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Definition
Hallucinogen
MOA: partial agonist of 5-HT2A receptor-> IP3-> increased glu transmission to pyramidal neurons in prefrontal cortex by enhancing excitatory input from thalamus
RR = 1; neither dependence nor addiction
Tachyphylaxis- repeated exposure leads to rapid tolerance
Oral; onset = 30minutes; lasts 6-12hrs
Effects: shape and color distortion, hallucinations, dizziness, nausea, paresthesias, blurred vision; reexperience up to several years later
Can induce abortion |
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Term
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Definition
Hallucinogen
MOA: partial agonist of 5-HT2A receptor
RR = 1
Effects: shape and color distortion, hallucinations, dizziness, nausea, paresthesias, blurred vision; reexperience up to several years later |
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Term
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Definition
CNS Depressant
MOA: binds multiple receptors- GABA-A, 5-HT3, nACh, NMDA, Kir3 channels
RR = 3
SE: motor incoordination, sleepiness, suppression of inhibitory systems; thiamine deficiency
Drug interactions: produces cross-tolerance to other sedatives (benzodiazepines) -> when used together overly increases sedation; tricyclic antidepressants; zolpidem
Detox: oxazepam, carbamazepine, disulfiram, naltrexone, acamprosate
Withdrawal Syndrome: craving, tremor, nausea, sleep disturbance, tachycardia, HTN, sweating, seizures, hallucinations, delirium tremens (rare) |
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Term
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Definition
Use: ethanol detoxification
MOA: competitive inhibitor of NMDA glu receptor
Low SE and low potential for abuse
SE: arrhythmia, altered BP, headache, insomnia, impotence, hallucinations in elderly |
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Term
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Definition
Use: ethanol detoxification
MOA: blocks aldehyde dehydrogenase (ADH) metabolism of etoh-> accumulation of acetaldehyde = flushing, respiratory difficulties, vomiting, and BP drop upon alcohol ingestion |
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Term
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Definition
Use: ethanol and heroine detoxification
MOA: competitive μ-opiate receptor antagonist-> blocks reinforcing properties by inhibiting drug stimulated dopaminergic pathways
Success is linked to a polymorphism of μ opioid receptor; long acting (1/2 life 10hrs); oral administration
Reverses opioid effects in 1-3minutes-> normalizes respiration, consciousness, pupil size, bowel activity
No agonist effects |
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Term
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Definition
Sedative-Antianxiety and Anticonvulsants
MOA: enhances Cl- inflow through GABA-A receptor channels in the presence of GABA by increasing frequency of inflow (not duration) on inhibitory interneurons-> disinhibition of DA neurons
Oral or IV administration
Use: decrease the time to onset of the deeper stages of sleep; ethanol detoxification
RR = 3
Effects: euphoria
Withdrawal syndrome: irritability, insomnia, phono/photophobia, depression, muscle cramps, seizures; tapers off w/in 1-2weeks |
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Term
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Definition
Nicotinic cholinergic receptor agonist
MOA: agonist of alpha4beta2 nAChR-> excitation of DA neurons in VTA; ionotropic receptor- increased Na+ influx and depolarization
Highly lipophilic-> penetrates BBB, well absorbed across skin
RR = 4
Withdrawal syndrome: irritability, sleep problems |
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Term
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Definition
Treatment: tobacco dependence
MOA: alpha4beta2 nicotinic acetylcholine receptor partial agonist-> greater affinity than nicotine w/ less stimulated dopamine release
Oral; excreted virtually unchanged in urine
SE: nausea, abnormal dreams, constipation, vomiting, flatulence, xerostomia (dry mouth); may exacerbate psychiatric illnesses; suicidal ideation
Contraindications: pregnancy
Drug Interactions: cimetidine-> decreases renal clearance of varenicline |
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Term
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Definition
Anticonvulsants
MOA: enhance GABA-A mediated influx of Cl- to prevent depolarization |
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Term
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Definition
Ex. nitrates, ketones, hydrocarbons
Effects: euphoria
Taken by sniffing, huffing, bagging
Nitrous oxide- binds NMDA receptors
Fuel additives- enhance GABA-A function
Poppers (amyl nitrate)- produce smooth muscle relaxation and enhance erection
Benzene/Toluene- white matter lesions
Prevalent in children and young adults |
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Term
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Definition
aka angel dust, Hog, Special K
Dissociative anesthetic
MOA: noncompetitive antagonist of NMDA receptors
Effects last ~1hr: hallucinations, separation of mind and body; stupor and coma, increased BP, impaired memory, chronic exposure may lead to long lasting psychosis
RR = 1
Pure form = white crystalline powder; also in liquid, capsule or pill; snorted, ingested, injected, or smoked |
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Term
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Definition
Club drug aka roofies aka date rape drug
Benzodiazepine
MOA: GABA-A agonist
Colorless, odorless, tasteless
Repeated use can lead to tolerance/dependence; detox can be life threatening
SE: sedation, anterograde amnesia, incapacitation when combined w/ ethanol |
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Term
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Definition
Dissociative drug
Cough suppressant found in OTC medications
MOA: NMDA glu receptor antagonist-> blocks inhibitory pathways
SE: distort perception of sight/sound, produce feelings of detachment; do not generally produce hallucinations
Drug Interactions: MAO-Is-> motor restlessness, tremor, hyperpyrexia, death=> due to potentiation of 5-HT transmission by blocking reuptake |
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Term
3,4-methylenedioxymethamphetamine (MDMA)
aka Ecstasy |
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Definition
MOA: reverses transport at serotonin transporters (SERT) and to a lesser degree DAT/NET
Effects: fostered feelings of intimacy and empathy w/o impairing intellectual abilities; hyperthermia, serotonin syndrome (mental status change, autonomic hyperactivity, neuromuscular abnormalities), seizure
Oral; w/ repeated use serotonin depletion can become permanent
Withdrawal syndrome: depression lasting up to several weeks, increased aggression |
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Term
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Definition
Stimulant
MOA: adenosine receptor antagonist
Prevents sleep |
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Term
Donepezil (Aricept)
Rivastigmine (Exelon)
Galantamine (Razadyne) |
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Definition
Anticholinesterase
Treatment: Alzheimer's disease
In AD, loss of cholinergic neurons results in decrease of choline acetyltransferase (synthesizes ACh)
MOA: cholinesterase inhibitor-> increase cholinergic activity
Orally active; adequate penetration of CNS; benefit is modest and temporary
SE: nausea/vomiting, diarrhea, peripheral cholinomimetic effects
Contraindications: other drugs that inhibit cytP450s |
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Term
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Definition
NMDA antagonist
Treatment: Alzheimer's disease; vascular dementia
Excititoxic activation of NMDA glu receptors and decreased glu uptake, both by Aβ, may contribute to disease pathology
MOA: noncompetitive blockade of NMDA receptors by directly blocking the ion channel in a voltage dependent fashion (channel must be open for efficacy) w/ moderate affinity-> decreased glu; also antagonist of 5-HT3 receptors-> promotes learning and memory
SE: better tolerated and less toxic than cholinesterase inhibitors
Complete oral absorption; excreted unchanged in urine
Drug Interactions: excretion is pH dependent, avoid drugs that make urine alkaline-> carbonic anhydrase/NaHCO3; dextromethorphan/ketamine-> NMDA antagonists |
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Term
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Definition
Anticonvulsant
Treatment: absence seizures
MOA: blocks voltage-gated Ca2+ T-type channels in thalamic neurons
Complete oral absorption; low plasma binding
SE: GI; CNS depression, euphoria, headache, Parkinsonlike symptoms, photophobia, aplastic anemia, skin reactions |
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Term
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Definition
Anticonvulsant
Metabolized to phenobarbital and phenylethylmalonamide (PEMA)-> all 3 are active anticonvulsants
MOA: induces closure of the inactivation gate of activated Na+ channels in depolarizing neurons, preventing further depolarization
Oral; metabolized by oxidation and conjugation/excretion
SE: sedation and GI if given too quickly; drowsiness
Drug Interactions: oral contraceptives-> induces CYP3A4 which metabolizes OC |
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Term
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Definition
Anticonvulsant
Treatment: partial, complex, and generalized tonic-clonic seizures
MOA: induces closure of the inactivation gate of activated Na+ channels in depolarizing neurons, preventing further depolarization
Extensively bound in plasma (albumin); metabolized by hepatic CYP2C9
Half-life increases w/ higher concentrations (changes from first to zero order kinetics-> small dosage changes cause large plasma changes)
Abolishes tonic phase but may exaggerate clonic phase; taken orally (rapid or extended release)
SE: CNS depression, arrhythmias, gingival hyperplasia; teratogenic
Drug Interactions: valproic acid displaces bound phenytoin and competes for metabolism-> marked increase in free drug; warfarin is metabolized by same CYP-> bleeding disorder; oral contraceptives-> phenytoin induces CYP3A4 which metabolizes OC; carbamazepine-> enhances phenytoin metabolism and its metabolism is enhanced by phenytoin |
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Term
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Definition
Anticonvulsants-> benzodiazepine
Treatment: absence (in kids) and myoclonic seizures-> tolerance develops in 1-6months; tics
MOA: enhances Cl- inflow through GABA-A receptor channels in the presence of GABA by increasing frequency of inflow (not duration)
Oral or IV; very short plasma 1/2 life-> 1 hr
Status epileptics may be induced w/ abrupt discontinuation
SE: orally-> drowsiness, lethargy; hypotonia, dysarthria, dizziness; hyperactivity, irritability; weight changes; IV-> CV and respiratory depression |
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Term
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Definition
Anticonvulsant
Treatment: partial seizure w/ and w/o secondary generalization when used w/ other anticonvulsants; migraine, Bipolar disorder, chronic pain
MOA: acts presynaptically to promote release of GABA through a nonvesicular manner; bind presynaptic voltage gated Ca2+ channels and prevent activation
High solubility-> readily crosses BBB; absorbed orally but not metabolized and does not bind plasma proteins
Short 1/2-life-> 4-6hrs
SE: well tolerated; somnolence, dizziness, ataxia, fatigue |
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Term
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Definition
Anticonvulsant and Analgesic
Treatment: conjunctive therapy of partial seizure w/ or w/o secondary generalization
MOA: acts presynaptically to promote release of GABA through a non vesicular manner; bind presynaptic voltage gated Ca2+ channels and prevent activation
Oral; not metabolizes-> excreted in urine largely unchanges
SE: somnolence, dizziness, ataxia, headache, tremor |
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Term
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Definition
Anticonvulsant
Treatment: add on therapy for refractory partial seizures w/ or w/o secondary generalization
MOA: inhibits GABA transporter GAT-1-> reduces neuronal/glial uptake of GABA
Oral; extensively bound; metabolized by CYP3A
SE: mild; dizziness, somnolence, tremor
Drug Interactions: phenobarbital/phenytoin/carbamazepine-> decrease 1/2 life
Contraindications: generalized absence epilepsy |
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Term
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Definition
Anticonvulsant
Treatment: partial and primary generalized seizures; monotherapy for refractory partial epilepsy and refractory generalized tonic-clonic seizures; Lennox-Gastaut syndrome
MOA: induces closure of the inactivation in activated Na+ channels in depolarizing neurons, preventing further depolarization; also activates a hyperpolarizing K+ current, enhances postsynaptic GABA-A receptor current, limits activation of AMPA channels, weak carbonic anhydrase inhibitor
Oral; mostly renal excreted unchanged; metabolized by hydroxylation, hydrolysis, and glucuronidation
SE: mild; somnolence, fatigue, weight loss, nervousness, renal calculi
Drug Interactions: reduces plasma estradiol so may require higher oral contraceptive doses; carbamazepine causes increased metabolism |
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Term
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Definition
Anticonvulsant
Treatment: mono or add on therapy of partial and secondarily generalized tonic-clonic seizures in adults; absence seizure; Lennox-Gastaut syndrome (seizures, mental retardation); bipolar disorder
MOA: induces closure of the inactivation in activated Na+ channels in depolarizing neurons, preventing further depolarization; also may prevent glutamate release
Anti-folate properties; oral absorption; metabolized by glucuronidation
SE: dizziness, ataxia, blurred vision, nausea/vomiting, rash; Stevens-Johnson syndrome; DIC
Drug Interactions: phenytoin/carbamazepine/phenobarbital-> reduces 1/2 life and concentration; decreases plasma concentrations of valproic acid and VA increases [plasma] of lamotrigine; increases concentration of carbamazepine metabolites |
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Term
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Definition
Anticonvulsant
Treatment: partial seizures or refractory epilepsy
MOA: induces closure of the inactivation in activated Na+ channels in depolarizing neurons, preventing further depolarization; blocks voltage-gated Ca2+ T-type channels
Oral; long 1/2-life-> 63hrs; mostly renal excretion
SE: mild; somnolence, ataxia, nervousness, fatigue
Drug Interactions: phenobarbital/phenytoin/carbamazepine-> decrease plasma concentration of zonisamide; lamotrigine-> increases concentration |
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Term
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Definition
Antiviral Nucleoside Analog
Use: HSV-1&2 > VZV > EBV/CMV/HHV-6
Activation by 3 phosphorylations: mono-P by viral thymidine kinase; di- & tri-P by host cell enzymes
MOA: inhibits viral DNA syntheses by competing for deoxyGTP for viral DNA polmerase and irreversibly binding DNA template while initiating chain termination
Selective activity only in infected cells
Oral- low bioavailability; reduces duration of symptoms, frequency of viral shedding, and number of lesions (requires higher dose for VZV)
IV- HSV encephalitis, neonatal infection, immunocompromised
Topical- less effective for primary therapy, not effective against genital herpes
Renal excretion
MOR: altered thymidine kinase or DNA polymerase
SE: well tolerated; nausea, vomiting, headache; renal/neuro toxicity |
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Term
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Definition
Specific immune globulins prepared from donors immunized against specific toxins
MOA: provide passive immunization by transfer of high titer Abs
Used in cases of immunodeficiency, exposure, or when disease is present
Protection lasts 1-3 months
Treatment: rabies, hepatitis B, tetanus, VZV, CMV, respiratory syncytial virus, Rh imcompatibility
SE: risk of infusion acquired disease |
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