Term
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Definition
Class: anti-parasitic, kinetoplastid drug
Mechanism: unknown
Clinical use: African "sleeping sickness" (T. BRUCEI) @ HEMOLYTIC STAGE
Adverse effects: malaise, nausea, fatigue, headache
Administration: slow IV infusion
Distribution: binds to plasma proteins tightly
Excretion: renal, caution in impaired |
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Term
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Definition
Class: anti-parasitic, kinetoplastid drug
Mechanism: unknown
Clinical use: Africant sleeping sickness (T. Brucei) @ hemolytic stage |
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Term
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Definition
Class: anxiolytics, barbiturate
Mechanism: allosteric agonist at GABA(A) receptors, enhance duration of transmission; inhibit glutamate receptors
Clinical use: induction of anesthesia; SEIZURES
Adverse effects: impaired cognitive and motor function, small therapeutic index, overdose risk w/ other depressants, tolerance, abuse
Distribution: rapid CNS conc. induces anesthesia, short duration before redistrtibute |
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Term
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Definition
Class: anxiolytics, barbiturate
Mechanism: allosteric agonist at GABA(A) receptors, enhance duration of transmission, inhibit glutamate receptors
Clinical use: induction of anesthesia
Adverse effects: impaired cognitive and motor function, small therapeutic index, risk of overdose, tolerance, abuse
Distribution: rapid rise in CNS induces anesthesia, short duration before redistribution |
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Term
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Definition
Class: anxiolytics, barbiturate
Mechanism: allosteric agonist at GABA(A) receptors, enhance duration of transmission, inhibit glutamate receptors
Clinical use: induction of anesthesia
Adverse effects: impaired cognitive and motor fx, small therapeutic index, overdose risk, tolerance, abuse
Distribution: rapid rise in CNS induces anesthesia, short duration before redistribution |
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Term
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Definition
Class: anxiolytics, benzodiazepines
Mechanism: positive allosteric modulator at GABA(A) receptors, enhance transmission and hyperpolarization
Clinical use: ANESTHESIA
Contraindications: sleep apnea
Advantages: rapid onset, relatively high therapeutic index, low risk of drug interactions, minimal CNS or ANS effects
Adverse effects: PSYCHOMOTOR DEPRESSION, residual daytime sedation, tolerance to hypnotic effect, risk of dependence, depression of CNS w/ other depressants, amnestic effects, abuse
Elimination: <6hr |
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Term
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Definition
Class: anxiolytics, benzodiazepines
Mechanism: positive allosteric modulator at GABA(A) receptors, enhance transmission and hyperpolarization
Clinical use: epilepsy, anxiety
Contraindication: sleep apnea
Advantages: rapid onset, high TI, low risk drug intrxns, minimal CNS and ANS effects
Adverse effects: PSYCHOMOTOR DEPRESSION, residual daytime sedation, tolerance to hypnotic effect, risk of dependence, depression of CNS w/ other depressants, amnestic effects, abuse
Elimination: 6-12hr |
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Term
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Definition
Class: anxiolytics, benzodiazepines
Mechanism: positive allosteric modulator at GABA(A) receptors, enhance transmission and hyperpolarization
Clinical use: anxiety
Contraindication: sleep apnea
Advantages: rapid onset, high TI, low risk of drug interxn, minimal effects on CNS and ANS
Adverse effects: PSYCHOMOTOR DEPRESSION, residual daytime sedation, tolerance to hypnotic effect, dependence risk, CNS depression w/ other depressants, amnestic effect, abuse
Elimination: 6-20hr |
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Term
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Definition
Class: anxiolytics, benzodiazepines
Mechanism: positive allosteric modulator of GABA(A) receptors, enhance transmission and hyperpolarization
Clinical use: insomnia
Contraindications: sleep apnea
Advantages: rapid onset, high TI, low risk drug interxn, minimal effects on CNS and ANS
Adverse effects: PSYCHOMOTOR DEPRESSION, residual daytime sedation, tolerance to hypnotic effect, dependence risk, CNS depression w/ other depressants, amnestic effect, abuse
Elimination: <6hr |
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Term
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Definition
Class: anxiolytics, benzodiazepines
Mechanism: positive allosteric modulator at GABA(A) receptors, enhance transmission and hyperpolarization
Clinical use: anxiety
Contraindications: sleep apnea
Advantages: rapid onset, high TI, low drug interxn, minimal effects of CNS and ANS
Adverse effects: PSYCHOMOTOR DEPRESSION, residual daytime sedation, tolerance to hypnotic effects, dependence risk, depression of CNS w/ other depressants, amnestic effect, abuse
Elimination: >20hr |
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Term
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Definition
Class: anxiolytics, Z drugs
Mechanism: allosteric agonist at GABA(A) receptor, enhance transmission
Clinical use: insomnia, anxiety
Advantages: rapid onset, modest-day after psychomotor depression, some amnestic effects, low risk of tolerance
Adverse effects: depression of CNS on own and worse w/ other depressants; COMPLEX SLEEPING BEHAVIORS |
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Term
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Definition
Class: anxiolytics, Z drugs
Mechanism: allosteric agonist at GABA(A) receptors, enhance transmission
Clinical use: insomnia, anxiety
Advantages: rapid onset, modest day-after psychomotor depression, amnestic effects, low risk of tolerance
Adverse effects: depression of CNS by self or with other depressants; COMPLEX SLEEPING BEHAVIORS |
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Term
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Definition
Class: anxiolytics, Z drugs
Mechanism: allosteric agonist at GABA(A) receptors, enhances transmission
Clinical use: insomnia, anxiety
Advantages: rapid onset, modest day-after effects, amnestic effects, low tolerance risk
Adverse effects: depression of CNS by self or with other depressants; COMPLEXT SLEEPING BEHAVIORS |
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Term
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Definition
Class: ~anxiolytics, benzodiazepine antagonist
Mechanism: antagonist at benzodiazepine site of GABA(A) receptor
Clinical use: benzodiazepine overdose, shorten recovery following anesthesia with benzodiazepines; NOT COMMON DUE TO ADVERSE EFFECTS
Adverse effects: seizures, agitation, confusion, dizziness, nuause; CAN PRECIPITATE BENZO WITHDRAWAL SYMPTOMS |
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Term
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Definition
Class: anxiolytics,
Mehcanism: partial agonist at 5-HT1A receptor, also D2, does not bind GABA receptors
Clinical use: generalized anxiety disorder
Advantage: lack of sedative/hypnotic/euphoric effects, lacks anticonvulsants and muscle relaxing effects; does not impair psychomotor performance; minimal abuse liability
Adverse effects: delayed action |
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Term
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Definition
Class: anxiolytics
Mechanism: agonist at melatonin recpetors, modulate circadian rhythms
Clinical use: insomnia characterized by difficult w/ sleep onset; only sedative-hypnotic not a schedule drug
Advantages: minimal potential for abuse, no rebound insomnia, no withdrawal
Adverse effects: minor
LOW EFFICACY |
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Term
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Definition
Class: anxiolytics
Mechanism: antihistamine with some anticholinergic effects
Clinical use: allergies, night-time sleep aid
Adverse effects: long half-life, sedation next day, anticholinergic adverse effects
ROUTINE USE FOR INSOMNIA NOT RECOMMENDED |
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Term
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Definition
Class: anxiolytics, antidepressant
Mechanism: serotonin reuptake inhibitor, serotonin receptor antagonist, alpha receptor antagonist, histamine receptor antagonist
Clinical use: depression, off-label-insomnia
Advantage: lack of abuse potential, shorter half-life than TCA (less daytime sedation), less antimuscarinic activity than TCAs
Adverse effects: tolerance to sedating effect, daytime drowsiness, discontinuation syndrome |
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Term
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Definition
Class: antidepressant, tricyclic
Mechanism: increase levels of NE and 5HT in synaptic cleft by blocking reuptake
Clinical use: mood disorders, panic disorders, GAD, PTSD, OCD, pain disorders
Contraindication: MAO-I coadministration
Adverse effects: anticholinergic effect, antiadrenergic effects, influence Na+ channels (CARDIAC ARRHYTHMIAS), HISTAMINE BLOCKADE, MAY PRECIPITATE MANIA IN BIPOLAR
Absorption: oral
Distribution: easy CNS, bound to plasma proteins
Metabolism: signif. first pass, NORTTRIPTYLINE as metabolite active anti-depress
Elimination: conjugate and renal |
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Term
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Definition
Class: antidepressant, tricyclic
Mechanism: increase NE and 5HT in synaptic cleft by inhibiting reuptake
Clinical use: mood disorders, panic disorders, GAD, PTSD, OCD, pain disorders, ENURESIS IN KIDS
Contraindication: MAO-I
Adverse effects: wide effects (histamine, cholinergic and alpha receptor actions), down regulate monoamine receptors, interact w/ Na+ channel (CARDIAC ARRHYTHMIAS), HISTAMINE BLOCAKE, MAY PRECIPITATE MANIA IN BIPOLAR
Absorption: oral
Distribution: easy CNS, plasma protein bound
Metabolism: signif. first pass to active metabolite DESIPRAMINE as antidpress
Elimination: conjugate and renal |
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Term
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Definition
Class: antidepressant, SSRI
Mechanism: inhibit 5HT reuptake w/o significant effect on NE and DA re-uptake
Clinical use: depression, OCD
Contraindications: MAO-I coadministration
Adverse effects: few than other classes
Absorption: oral
Metabolism: P450 system, inhibit P450s
T1/2: 24hrs |
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Term
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Definition
Class: antidepressant, SNRI
Mechanism: inhibition of 5Ht and NE reuptake
Clinical use: depression
Advantage: minimal inhibitory action at P450 enzymes
Adverse effects: nausea, dizziness, insomnia, sedation, SEXUAL DYSFUNCTION, constipation; high dose increase BP |
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Term
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Definition
Class: antidepressant, SNRI
Mechanism: inhibition of NE and 5HT reuptake
Clinical use: depression
Contraindication: hepatic insufficiency, end stage renal disease
Adverse effects: nausea, dry mouth, constipation, diarrhea, vomiting, insomnia, dizziness, somnolence, sweating, SEXUAL DYSFUNCTION
Absorption: delayed by food
Distribution: plasma proteins
Metabolism: hepatic, lots
Elimination: 12 hrs |
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Term
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Definition
Class: antidepressant, heterocyclic
Mechanism: unknown, decrease nicotine craving
Clinical use: depression
Adverse effects: headache, nausea, tachycardia, restlessness, dry mouth, sweating, tremor, seizure at high doses
Elimiation: 20hr half-life |
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Term
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Definition
Class: antidepressant, heterocyclic
Mehcanism: blocks presynaptic a2 autoreceptors, increases NE transmission, blocks 5HT2 and 5HT3 receptors
Clinical use: depression
Adverse effects: antihistamine (sedative), increased appetite and weight gain |
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Term
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Definition
Class: antidepressant, MAO-I
Mechanism: inhibits MAO (A&B), decrease monoamine breakdown; elevates modd, suppress REM, stimulate CNS
Clinical use: atypical depression with phobia or psychotic features
Adverse effects: HYPERTENSIVE CRISIS IF NOT AVOID TYRAMINE, orthostatic hypotension, dry mouth, blurred vision, weight gain, HEPATOTOXICITY, may precipitate mania in bipolar, use limited due to complicated dietary restriction
Absorption: oral
Distribution: readily cross BBB
Metabolism: P450 to active metabolite
Elimination: renal |
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Term
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Definition
Class: antidepressant, new MAO-I
Mechanism: reversible inhibitors of MAO-A, safer, slightly less efficacious
Clinical indication: depression
Adverse effects: hypertensive crisis when combined with other anti-depressants or stimulants, migraine meds, certain herbs or cold meds
NOT APPROVED IN US |
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Term
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Definition
Class: antidepressant, herb
Mechanism: hypericin inhibits MAO-A and MAO-B, hyperforin inhibits 5HT/Ne/DA reuptake
Clinical indications: mild to moderate depression
Adverse effects: dizziness, rash, photosensitization, hypomania, autonomic arousal, serotoning syndrome slight risk |
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Term
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Definition
Class: antidepressant
Mechanism: unknown, attenuates signaling via receptors coupled to PIP2, interferes with re-synthesis of PIP2
Clinical use: 1* BP, adjuvant to antidepressants for MDD
Contraindication: pregnancy - teratogenic
Adverse effects: GI, ataxia, confusion, convulsions, tremors, HYPOTHYROIDISM, RENAL TOXICITY, dry mouth, polydipsia, polyuria, leukocytosis
Absorption: oral, rapid
Distribution: wide
Elimination: kidney |
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Term
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Definition
Class: anticonvulsant
Mechanism: prolongs the inactivated state of Na+ channels
Clinical use: reduces symptoms during maanic and depressive episodes, seizures, trigeminal neuralgia
Adverse effects: acute intox that can lead to resp. depression stupor or coma; SEVERE LIVER TOXICITY, APLASTIC ANEMIA, AGRANULOCYTOSIS, drowsiness, ataxia, nystagmus, vomiting
ABsorption: oral, well
Metabolism: P450 system, INDUCES P450 ENZYMES, ACCELERATES ITS OWN METABOLISM |
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Term
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Definition
Class: anticonvulsant
Mechanism: prolongs inactivated sate of Na+ channels; suppress Ca influx through T-type channels; may increase GABA concentrations in brain
Clinical use: bipolar disorder
Contraindication: pregnancy
Adverse effects: nausea, vomit, tremor, sedation, weight gain, liver toxicity
Absorpion: oral
Distribution: 90% plasma protein bound
Metabolism: extensively by liver P450s |
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Term
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Definition
Class: antipsychotics
Mechanism: D2 receptor blockade; also blocks alpha1, histamine and ACh receptors
Clinical uses: schizophrenia, psychotic disorders, manic phase of BP
Adverse effects: RISK OF TARDIVE DYSKENSIA IS LOW, sedation, orthostatic hypotension, anticholinergic effect
Drug interactions: intensify responses to CNS depressants (anti-histamines, benzos or barbituates), can intensify response to anticholinergic drugs
Absorption: PO, IM or IV, high first pass, F oral = 30%
T1/2- biphasic, initial 2hrs, terminal 30hrs
Excretion: renal, as metabolites |
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Term
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Definition
Class: antipsychotics, atypical
Mechanism: D1 and D2 blockade; less D2 antag than typical antipsychotics, potent antagonist at some serotonin receptors
Clinical use: MOST EFFECTIVE DRUG FOR SCHIZOPHRENIA but reserved for pts who don't respond to others
Contraindication: other drugs that can suppress bone marrow fx (anticancer drugs)
Adverse effects: AGRANULOCYTOSIS, seizures, weight gain, myocarditis, sedation, orthostatic hypotension, anticholinergic effects
Absorption: rapid, oral
Distribution: 95% plasma protein bound
Metabolism: extensive
Excretion: feces and urine
T1/2 - 12 hrs |
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Term
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Definition
Class: antipsychotics
Mechanism: D2 receptor blockade
Clinical use: Schizophrenia, psychotic disorders, Tourrette's syndrome
Adverse effects: EXTRAPYRAMIDAL EFFECTS FREQUENT, RISK OF TARDIVE DYSKINESIA IS HIGH, prolong QT interval, ARRHYTHMIAS
Absorption: PO(60%), or IM
Metabolism: extensive hepatic
Excrete: urine as parent drug and metabolite
T1/2-20hrs |
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Term
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Definition
Class: antipsychotics, atypical
Mechanism: more potent antagonist at 5HT2 receptors than DA
Clinical use: schizophrenia, psychotic disorers
Adverse effects: sedation, orthostatic hypotension, anticholinergic effects, weight gain, hyperglycemia and diabetes induction
T1/2-21-54hrs |
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Term
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Definition
Class: antipsychotics, atypical
Mechanism: antagonist at D2 and 5HT2 receptors; potent at alpha receptors
Clinical use: schizophrenia, other psychotic disorders
Adverse effects: weight gain, abuse potential
T1/2 - 6hrs |
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Term
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Definition
Class: antipsychotics, atypical
Mechanism: VERY HIGH AFFINITY AT D2 AND 5HT2 RECEPTORS, little to no anticholinergic actions
Clinical use: schizophrenia and psychotic disorders
Adverse effects: higher incidence of extrapyramidal effects at higher doses, prolongs QT, weight gain,
T1/2 - 20hrs |
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Term
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Definition
Class: antipsychotics, atypical
Mechanism: antagonist at D2 and 5HT2 receptors, moderate SSRI-like activity
Clinical use: schizophrenia and psychotic disorders
Adverse effects: prolong QT
T1/2 - 2.5hr IM, 7hr PO |
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