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16 Cards in this Set
- Front
- Back
Clonidine/Guanfacine
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Alpha-2 Adrenergic Receptor Agonists
Guanfacine newer, longer half-life, less sedation side effects Dry mouth/eyes, fatigue, sedation, dizziness, nausea, **hypotension**, constipation. Do not give to adults with BP <90/60 or with cardiac arrhythmias, especially bradycardia |
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Propranolol Type
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Beta-Blockers. Propranolol, Nadolol, Pindolol, Labetolol, Atenolol, Metoprolol, and Acebutolol
B1 = B2 affinity: Propranolol, Nadolol, Pindolol B1 > B2 affinity: Metoprolol, Atenolol, Acebutolol B2 Selective has fewer pulmonary and vascular effects, but use with caution in asthmatic patients b/c still has some B2 activity |
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Beta-Blocker Side Effects
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CONTRAINICATED in Asthma, insulin-dependent DM, CHF, vascular disease, angina, hyperthyroidism. If must give, use B1 agonist.
1) Cardiovascular - Hypotension, Bradycardia, Dizziness, CHF 2) Respiratory - Asthma 3) Metabolic - Hypoglycemia (worsened in diabetics on insulin) 4) GI - Nausea, diarrhea, abominal pain 5) Sexual Dysfunction - impotence 6) Neuropsychiatric - Lassitude, fatigue, dysphoria, insomnia, vivid nightmares 7) Rare - Raynaud's Phenomenon, Peyronie's Disease 8) Withdrawal Syndrome - Rebound worsening of preexisting angina pectoris when beta blockers are discontinued |
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Gabapentin
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Anticonvulsant
Indirectly increases brain GABA levels. Well absorbed but dose has upper limit b/c saturation of neutral amino acid membrane transporter. Excreted unchanged in urine. |
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Pregabalin
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Anticonvulsant
Believed to work by inhibiting release of excess excitatory neurogransmitters, presumably by binding to the alpha-2-delta subunit protein of voltage-dependant Ca channel in brain and spinal cord. Also increases neuronal GABA levels. Binding affinity 6x more potent for alpha-2-delta subunit then Gabapentin Longer half-life then Gabapentin |
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Topiramate
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Anticonvulsant
Selective inhibitor of Glu AMPA receptors, blocks Na+ receptors, indirect GABAergic activity. Potentiates action of GABA at non-benzodiazepine, non-barbiturate-sensitive GABA(A) receptor 1.5% patients develop renal calculi Non-dose related adverse events - psychomotor slowing, dizziness, somnolence, ataxia, nystagmus, parasthesias Dose-related adverse events - fatigue, nervousness, poor concentration, confusion, taste perversion, depression, anorexia, anxiety, mood problems, weight loss, tremor. |
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Tiagabine
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Anticonvulsant
Potent and selective reuptake inhibitor of GABA. Also mild blocking effects of H1, serotonin I(B) benzodiazepine, and chloride channel receptors Reports of seizures in patients w/o epilepsy Sedation, cognitive impairment, ataxia, dizziness, tremor, parasthesias, confusion, depression. Teratogenic in rat studies. Lower doses should be used in hepatic impairment - metabolized by P450 |
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Zonisamide
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Anticonvulsant
Blocks sodium channels and may weakly potentiate dopamine and serotonin activity. Also inhibits carbonic anhydrase. May block calcium channels. Can elevate hepatic alkaline phosphatase, increase BUN and creatinine. 4% patients develop kidney stones. Weight loss common. Is a sulfonamide, thus may cause fatal rash and blood dyscrasias though these are rare drowsiness, cognitive impairment, etc |
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Levetiracetam
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Anticonvulsant
Poorly understood mechanism, appears to indirectly enhance GABA inhibition. Drowsiness, dizziness, ataxia, diplopia, memory impairment, apathy, and parasthesia. Some patients develop behavioral disturbances during Tx, and hallucinations can occur. Suicidality noted in few patients during clinical trials. |
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Barbituates
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Mechanism involves GABA receptor-benzodiazepine receptor-chloride ion channel complex.
High abuse/addiction potential, narrow therapeutic range. Development of tolerance (compared to benzos) Paradoxical dysphoria, hyperactivity, cognitive distoration |
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Benzodiazepines
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a
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Buproprion
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Norepinephrine and Dopamine reuptake inhibitor. Does NOT interact with serotonin.
Absence of serotonin effect = less risk of sexual dysfxn or sedation Headache, insomnia, dry mouth, tremor, and nausea. Minimal dose dependent risk of seizure (0.05% at 300mg, the same as other anti-depressants. 0.1% at 400mg) Relatively safe in overdose, very few deaths reported. Seizures in 1/3 of all ODs. Patients with severe anxiety or panic disorder should NOT be started on Buproprion. B/c of potentiating effects on dopaminergic neurotransmission, can cause psychotic symptoms including hallucination, delusions, catatonia and delerium. |
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Buproprion interactions and labs
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1) Increases plasma concentration venlafaxine and decrease in its main metabolite, O-desmethylvenlafaxine. Not significant changes with other SSRIs.
2) With Lithium may rarely cause CNS toxicity including seizures. 3) DO NOT co-administer with MAOIs due to possibility of inducing hypertensive crisis. Must wait 14 days after discontinuing MAOI before starting Buproprion 4) In Parkinson patients, may allow for lower doses of dopaminergic drugs, although can produce psychotic symptoms, delerium and dyskinesia when co-administered with dopaminergic agents 5) Carbamazepine may decrease plasma levels of Buproprion, and Buproprion may increase plasma levels of valproic acid 6) May cause false-positive result on urinary amphetamine screen |
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Mirtazapine
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Unique among drugs for major depression in that it increases both norepinephrine and serotonin through a mechanism other than reuptake blockade (as in TCAs an SSRIs) or monoamine oxidase inhibition (as in phenelzine or tranylcypromine)
Mechanism is antagonism of central presynaptic alpha-2-adrenergic receptors and blockade of postsynaptic serotonon 5-HT(2) and 5-HT(3) receptors. Alpha-2-adrenergic antagonism causes increased firing of norepinephrine and serotonin neurons. Reduces nausea an diarrhea, compared to other rugs likely to cause it. Side effects include sedation/somnolence and increased appetite. Almost always given before sleep (~50% have sedation) |
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Mirtazapine interactions
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Can potentitate the sedation of alcohol and benzodiazepines. Should NOT be used within 14 days of a MAOI.
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Trazodone
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Weak inhibitor of serotonin reuptake and potent antagonist serotonin 5-HT(2A) and 5-HT(2C) receptors. Active metabolite is m-chlorophenylpiperazine (mCPP) which is an AGONIST at 5-HT(2C) receptors.\
mCPP has been associated with migraine, anxiety, and weight loss. Adverse effects partially mediated by alpha-1-adrenergic receptor antagonism. SEDATION - too sedating at therapeutic doses hence why it did not achieve widespread use. Extensively used at low doses as alternative to hypnotic agents, particularly to counteract frequent sleep disturbances with SSRIs. Other side effects - orthostatic hypotension, dizziness, headache and nausea. |