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54 Cards in this Set
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Question: Drug treatment with fluoxetine is initiated for major depression. What should you tell the PT?
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They have CNS stimulating effects: may cause agitation, anxiety, jitters, and insomnia. Therefore, don't take SSRIs in the evening. Muscle cramps and twitches. May take 2 weeks or more to become effective.
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Question: Concerning the proposed MOA of antidepressant drugs, what is accurate?
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MOA of bupropion is unknown--doesn't inhibit NE or 5-HT.
Downregulation of adrenoceptors with TCA and MAOIs Nefazodone block 5-HT receptors in CNS. Selegiline is a selective inhibitor of MAO-B, the enzyme that form that metabolizes dopamine. |
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Question: What is likely to occur with doxepin, a TCA?
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TCA: block NE reuptake and block alpha receptors.
Sedation and atropine-like effects: mydriasis and dry mouth are common. Urinary retention. They lower the threshold for seizures. |
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Question: A PT taking fluoxetine wishes to stop taking the drug due to it affecting his sexual performance. He is also trying to overcome a dependency on tobacco. What is the DOC?
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Bupropion.
It is the least likely antidepressant to affect sexual performance. TI is also used in withdrawal of nicotine dependence. |
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Question: What is correct about using antidepressant drugs?
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MAOIs: although used infrequently, are more likely to be effective in depression with attendant anxiety, phobic features, hypochondriasis.
SSRIs: associated with weight loss. |
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Question: A PT taking 30 x the daily recommended dosage of amitriptyline presents to the ER.
What are the signs and symptoms of the PT likely to be observed. In severe tricyclic antidepressant OD, it would be of minimal value to? |
TCAs have anticholinergic effects: increased body temperature, decreased bowel sounds, tachycardia, dilated pupils. Hypotension occurs frequently due to antagonisms of alpha receptors.
Coma and shock. Minimal value: initiate hemodialysis (to hasten drug elimination) 3 C's: Coma, Convulsion, Cardiac problems are the most common causes of death. |
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Question: What is the antagonist of 5-HT2 receptors used widely for insomnia?
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Trazodone.
Others: Triazolam and zolpidem are effective hypotonic drugs. |
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Question: An female PT is treated with a BZ due to the death of her husband. She didn't like the daytime sedation. She is rather infirm for her age (80) and has poor eyesight. Her symptoms are not abating, and what is the recommended DOC for this PT?
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Paroxetine or another SSRI
Older PTs are more sensitive to antidepressants that cause sedation, atropine like adverse effects or postural hypotension. TCAs and MAOI have many autonomic SE; mirtazapine and trazodone are highly sedating. |
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Question: SSRIs are much less effective than tricyclic antidepressants in the management of?
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Chronic pain of neuropathic origin.
SSRIs are not useful for this. They have clinical effectiveness equivalent or superior to that of TCAs. |
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Question: Compared with other antidepressant drugs, mirtazapine has the distinctive ability to act as an antagonist of?
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Alpha2 receptors.
This facilitates NE and 5-HT release by opposing feedback. Also blocks H1; therefore very sedating. Also blocks 5-HT2 and 5-HT3 |
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Question: What drug is of value for OCD?
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Clomipramine
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Question: What drug has est. clinical use for ADHD, enuresis, and management of chronic pain?
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Imipramine.
Is a backup for ADHD behind methylphenidate. |
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Question: Inadequate of treatment for breast cancer with tamoxifen has occurred when PTs have been on?
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Fluoxetine, since it inhibits CYP450.
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What are the tricyclic antidepressants? MOA?
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Imipramine, amitriptyline
Also: desipramine, nortriptyline, clomipramine, doxepin. Inhibits reuptake of NE and serotonin |
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What are the two groups of heterocyclics?
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Serotonin-norepinephrine reuptake inhibitor (SNRIs): venlafaxine, duloxetine
5-H2 receptor antagonists: nefazodone, trazodone Miscellaneous heterocyclic agents: amoxapine, bupropion, maprotiline, and mirtazapine. |
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What are the SSRIs?
They have minimal inhibitory effect on what? |
Fluoxetine, paroxetine, sertaline, citalopram
NE transport, or blocking actions on adrenergic and cholinergic receptors. |
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What are the monoamine oxidase (MAO) inhibitors? MOA?
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Phenelzine, tranylcypromine, isocarboxazid, selegiline (selective MAO-B-inhibitor)
MAO is a presynaptic enzyme responsible for metabolizing NE and serotonin (MAO A) and dopamine (MAO B). Therefore, MAOI increase the level of the amines in the presynaptic nerve. |
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How is mirtazapine different than other heterocyclic antidepressants?
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Inhibits alpha2 receptors and 5-HT2 receptors, thereby increasing the release of NE and serotonin.
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What are the two SNRIs and how are they different from TCA's?
What are the SNRIs SE? |
Venlafaxine, duloxetine.
They lack significant blocking effects on peripheral receptors: H2, muscarinic, or alpha receptors. SE: increase BP is the most common; also stimulant effects, sedation, nausea. |
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Long-term use of tricyclics and MAOIs, but not SSRIs lead to?
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Downregulation of beta-receptors
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What are the clinical uses of TCAs?
Imipramine, clomipramine, trazodone, amitriptyline, and bupropion |
Imipramine: enuresis
Clomipramine: OCD Trazodone: to treat insomnia by causing sedation Amitriptyline: neuropathic pain Bupropion: aid in smoking cessation Major depression (backup), fibromyalgia, phobic disorders (compared with alprazolam), chronic pain. |
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SNRIs are used for?
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Venlafaxine: GAD
Duloxetine: diabetic peripheral neuropathy. Also, major depression, chronic pain, fibromyalgia, menopausal symptoms. Note: Duloxetine has a greater effect on NE. |
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SSRIs are used for?
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Depression, OCD (also clomipramine, a TCA), bulimia, social phobias, eating disorders, premenstrual dysphoric disorder, PTSD, GAD, panic disorders, anxiety, alcohol dependence
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What are the SE of TCAs?
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Think of their MOA:
Sedation (blocks histamine); sympathomimetic effects (tachy, sweating, agitation, insomnia); atropine-like effects (urinary retention, blurred vision, constipation, dry mouth, hallucinations and confusion); alpha-blocker effects (orthostatic hypotension); cardiac arrhythmias. Note: additive depression of CNS with other central depressants: ethanol, barbiturates, BZ, opioids. |
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SE of SSRIs?
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Sexual dysfunction (decrease libido, difficulty with orgasm), GI upset.
Serotonin syndrome: hyperthermia, muscle rigidity, CV collapse, flushing, diarrhea, seizures. Note: paroxetine is associated with increase suicidal ideation. |
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When TCA anticholinergic SE, such as confusion and hallucination, occur in the elderly, what drug should be used instead?
CV toxicity with TCAs is treated with what? |
Nortriptyline, a secondary TCA that has less anticholinergic effects.
NaHCO3 |
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What are the characteristics of OD and the TRI-C's with TCAs?
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OD: agitation, delirium, convulsions, coma, respiratory depression and ciruclatory collapse, hyperpyrexia, severe arrhythmias.
Tri-C's: Convulsions, Coma, Cardiotoxicity (arrhythmias) are characteristic. |
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SE of:
Mirtazapine Trazodone Bupropion Maprotiline Venlafaxine |
Increase appetite and weight gait, sedation.
Sedation, priapism, postural hypotension. Seizures at high dosages (and in bulimic PTs), stimulant effects (tachycardia, insomnia). Amoxapine also causes seizures. Sedation, orthostatic hypotension. Dose-dependent increase in BP and HR |
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SE of MAOI?
Contraindicated in? |
Hypertensive crisis with sympathomimetic tyramine ingestion (wine and cheese) and beta-agonists; CNS stimulation.
MAOIs typically lower BP with long term usage (increase NE in presynaptic terminal causes autonomic sympathomimetic effects) Contraindicated in: SSRIs or meperidine (prevents serotonin syndrome) |
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Sedation is mainly caused by?
Less common with? |
TCA, mirtazapine (heterocyclic), and trazodone (5-HT2 sold as a sleeping aid)
Less common with MAOIs, SSRIs, and bupropion since they cause CNS stimulating effects. |
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Who are antagonistic of muscarinic receptors?
Out of the TCAs, which one is the least sedating, and has a lower seizure threshold? |
TCA, but marked with amitriptyline (a tertiary amine, which has more anticholinergic SE than do secondary amine like nortriptyline).
Desipramine. |
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CV effects occur mainly from?
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TCAs: alpha-blockers that produce hypotension and depression of cardiac conduction.
Venlafaxine: elevated BP and HR |
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What drugs lower the threshold for seizures?
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TCAs and MAOIs
Also SSRIs |
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What drug is used to treat:
Alcohol withdrawal Anorexia/bulimia Anxiety ADHD Atypical depression |
BZ
SSRIs BZ, SSRIs Methylphenidate (Ritalin), amphetamine (Dexedrine) MAO inhibitors |
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What drug is used to treat:
Bipolar disorder Depression Depression with insomnia OCD Panic disorder |
Mood stabilizers: lithium, valproic acid, carbamazepine, atypical antipsychotics
SSRIs, SNRIs, TCAs Mirtazapine SSRIs, clomipramine SSRIs, TCAs, BZ |
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What drug is used to treat:
PTSD Schizophrenia Tourette's syndrome Social phobias |
SSRIs
Antipsychotics Antipsychotics (haloperidol) SSRIs |
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What is the MOA of methylphenidate?
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Increase presynaptic NE vesicular release (like amphetamines).
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What are the antipsychotics, and their MOA?
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Haloperidol, trifluoperazine, fluphenazine, thioridazine, chlorpromazine (haloperidol + "-azine's).
Block dopamine D2 receptors (increases cAMP) |
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What are the antipsychotics used for?
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Schizophrenia, (primarily positive symptoms), psychosis, acute mania, Tourette's syndrome.
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What are the SE of antipsychotics?
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Highly lipid soluble and stored in body fat.
Extrapyramidal system SE hyperprolactinemia leading to galactorrhea SE from blocking muscarinic dry mouth, constipation), alpha (hypotension), and histamine (sedation) receptors. Neuroleptic malignant syndrome, tardive dyskinesia |
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What is neuroleptic malignant syndrome, and how do you treat it?
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Rigidity, myoglobinuria, autonomic instability, hyperpyrexia.
Dantrolene, agonist (e.g., bromocriptine) |
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Which antipsychotics have a high potency, and which ones have a low potency? What is the consequence of each one?
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High potency: haloperidol, trifluoperazine, fluphenazine.
Low potency: thioridazine, chlorpromazine High potency has neurologic SE while low potency do not. |
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What are the SE of chlorpromazine and thioridazine
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Chlorpromazine: corneal deposits
Thioridazine: retinal deposits. Note: The "C" in Corneal goes with "C"hlorpromazine. The "T" in reTinal goes with "T"hioridazine. |
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Evolution of extrapyramidal system.
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4 h: acute dystonia (muscle spasm, stiffness, oculogyric crisis)
4 d akinesia (parkinsonian symptoms) 4 wk akathisia (restlessness) 4 mo tardive dyskinesia. |
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What is the FEVER with neuroleptic malignant syndrome?
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Fever
Encephalopathy Vitals unstable Elevated enzymes Rigidity of muscles |
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What are the atypical antipsychotics? MOA?
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Olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone.
Blocks 5-HT2, alpha, H1, and dopamine receptors |
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What are the atypical antipsychotics used for?
What about olanzapine, that blocks to the antipsychotics. |
For both positive and negative symptoms of Schizophrenia.
Olanzapine: OCD, anxiety disorder, depression, mania, Tourette's syndrome. |
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What are the SE of atypical antipsychotics?
Olanzapine/clozapine Clozapine |
Fewer extrapyramidal and anticholinergic SE than traditional antipsychotics.
Olanzapine/clozapine: significant weight gain. Clozapine: agranulocytosis (requires weekly WBC monitoring). |
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What lithium MOA and clinical use.
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Possibly inhibition of phosphoinositol cascade.
Mood stabilizer for bipolar; blocks relapse, and acute manic events. Also SIADH. |
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What is the LMNOP side effects of lithium?
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L: lithium SE:
M: Movement (tremor) N: Nephrogenic diabetes insipidus O: hypOthyroidism P: Pregnancy. Heart block, teratogenesis. Narrow therapeutic window requires close monitoring of serum levels. |
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Buspirone MOA? Clinical use?
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Stimulates 5-HT1a receptors
GAD. Does not cause sedation, addiction, or tolerance. Does not interact with alcohol (vs. barbiturates, BZ). |
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Antidepressants:
What inhibits NE reuptake? Inhibits alpha2 receptors? Inhibits 5-HT reuptake? |
TCA, maprotiline
Mirtazapine SSRIs, trazodone. |
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What is the treatment for serotonin syndrome? Associated with?
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Cyproheptadine (5-HT2 receptor antagonist). Occurs with SSRIs with MAOI, or anything that increases serotonin.
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What are MAO inhibitors used for?
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Atypical depression, anxiety, hypochondriasis.
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