Pharm Antidepressants

Front 1

Question: Drug treatment with fluoxetine is initiated for major depression. What should you tell the PT?

Back 1

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.

Front 2

Question: Concerning the proposed MOA of antidepressant drugs, what is accurate?

Back 2

MOA of bupropion is unknown--Increases NE and dopamine, but 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.

Front 3

Question:What is likely to occur with doxepin, a TCA?

Back 3

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.

Front 4

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?

Back 4

Bupropion.

It is the least likely antidepressant to affect sexual performance. TI is also used in withdrawal of nicotine dependence.

Front 5

Question: What is correct about using antidepressant drugs?

Back 5

MAOIs: although used infrequently, are more likely to be effective in depression with attendant anxiety, phobic features, hypochondriasis.

SSRIs: associated with weight loss.

Front 6

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?

Back 6

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.

Front 7

Question: What is the antagonist of 5-HT2 receptors used widely for insomnia?

Back 7

Trazodone.

Others: Triazolam and zolpidem are effective hypotonic drugs.

Front 8

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?

Back 8

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.

Front 9

Question: SSRIs are much less effective than tricyclic antidepressants in the management of?

Back 9

Chronic pain of neuropathic origin.

SSRIs are not useful for this. They have clinical effectiveness equivalent or superior to that of TCAs.

Front 10

Question: What drug is of value for OCD?

Back 10

Clomipramine

Front 11

Question: Compared with other antidepressant drugs, mirtazapine has the distinctive ability to act as an antagonist of?

Back 11

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

Front 12

Question: What drug has est. clinical use for ADHD, enuresis, and management of chronic pain?

Back 12

Imipramine.

Is a backup for ADHD behind methylphenidate.

Front 13

Question: Inadequate of treatment for breast cancer with tamoxifen has occurred when PTs have been on?

Back 13

Fluoxetine, since it inhibits CYP450.

Front 14

What is the amine hypothesis of mood, and what are 4 problems with this theory?

Back 14

Brain amines (NE and 5-HT) function in the expression of mood.

Postmortem studies do not show decrease NE or 5-HT; antidepressant change brain amine within hours, but weeks to become affective; most antidepressants DOWNregulate amine receptors; 1 antidepressant, buproprion, have minimal effects of brain NE or 5-HT

Front 15

What are the tricyclic antidepressants? MOA?

Back 15

Imipramine, amitriptyline

Also: desipramine, nortriptyline, clomipramine, doxepin.

Inhibits reuptake of NE and serotonin

Front 16

What are the two groups of heterocyclics?

Back 16

Serotonin-norepinephrine reuptake inhibitor (SNRIs): venlafaxine, duloxetine

5-H2 receptor antagonists: nefazodone, trazodone

Miscellaneous heterocyclic agents: amoxapine, bupropion, maprotiline, and mirtazapine.

Front 17

What are the SSRIs?

They have minimal inhibitory effect on what?

Back 17

Fluoxetine, paroxetine, sertaline, citalopram

NE transport, or blocking actions on adrenergic and cholinergic receptors.

Front 18

What are the monoamine oxidase (MAO) inhibitors? MOA?

Back 18

Phenelzine, tranylcypromine, isocarboxazid, selegiline (selective MAO-B-inhibitor)

IMAO 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.

Front 19

How is mirtazapine different than other heterocyclic antidepressants?

Back 19

Inhibits alpha2 receptors and 5-HT2 receptors, thereby increasing the release of NE and serotonin.

Front 20

How are SNRIs different from TCA's?

Back 20

They lack significant blocking effects on peripheral receptors: H2, muscarinic, or alpha receptors.

Front 21

Long-term use of tricyclics and MAOIs, but not SSRIs lead to?

Back 21

Downregulation of beta-receptors

Front 22

What are the clinical uses of TCAs?

Imipramine, clomipramine, trazodone, amitriptyline

Back 22

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.

Front 23

SNRIs are used for?

Back 23

Venlafaxine: GAD

Duloxetine: diabetic peripheral neuropathy.

Also, major depression, chronic pain, fibromyalgia, menopausal symptoms.

Note: Duloxetine has a greater effect on NE.

Front 24

SSRIs are used for?

Back 24

Depression, OCD (also clomipramine, a TCA), bulimia, social phobias, eating disorders, premenstrual dysphoric disorder, PTSD, GAD, panic disorders, anxiety, alcohol dependence

Front 25

What are the SE of TCAs?

Back 25

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.

Front 26

SE of SSRIs?

Back 26

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.

Front 27

What is the treatment for serotonin syndrome? Associated with?

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?

Back 27

Cyproheptadine (5-HT2 receptor antagonist). Occurs with SSRIs with MAOI, or anything that increases serotonin.

Nortriptyline, a secondary TCA that has less anticholinergic effects.

NaHCO3

Front 28

What are the characteristics of OD and the TRI-C's with TCAs?

Back 28

OD: agitation, delirium, convulsions, coma, respiratory depression and ciruclatory collapse, hyperpyrexia, severe arrhythmias.

Tri-C's: Convulsions, Coma, Cardiotoxicity (arrhythmias) are characteristic.

Front 29

SE of:

Mirtazapine

Trazodone

Bupropion

Maprotiline

Venlafaxine

Back 29

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

Front 30

SE of MAOI?

Contraindicated in?

Back 30

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)

SSRIs or meperidine (prevents serotonin syndrome)

Front 31

Sedation is mainly caused by?

Less common with?

Back 31

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.

Front 32

Who are antagonistic of muscarinic receptors?

Back 32

TCA, but marked with amitriptyline

Front 33

CV effects occur mainly from?

Back 33

TCAs: alpha-blockers that produce hypotension and depression of cardiac conduction.

Venlafaxine: elevated BP and HR

Front 34

What drugs lower the threshold for seizures?

Back 34

TCAs and MAOIs

Also SSRIs