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Stack #215175
| Question | Answer |
|---|---|
| phenelzine | nardil non selective irreversible MAO-I |
| tranylcypromine | parnate- non selective irreversible MAO-I |
| isocarboxazide | marplan- non selective irreversible MAO-I |
| selegiline | eldepryl selective MAOI-B irreversible MAO-I |
| rasagiline | selective MAOI-B(concentration dependent)irreversible |
| moclobemide | aurorix, manerix selective MAO-A inhibitors RIMA's reversible |
| brofaromine | selective MAO-A inhibitors RIMA reversible |
| linezolide | selective MAO-A inhibitor that is an antibiotic |
| carbamazepine Tegretolanticonvulsant | mild to moderate inhibitor of reuptake so interacts with MAOI but < SSRI |
| opioid analgesics meperidine, methadone, tramadol | interaction with MAOI |
| dextromethorphan, decongestants or weight-loss products that contain ephedrine, pseudoepidrine, phenylpropanolamine and amphetamines are | drugs that could cause serotonin syndrome |
| amitriptyline | elavil TCA increase NE, and 5-HT tertiary amine |
| clomipramine | anafranil TCA increase NE and 5HT tertiary amine |
| doxepin | adapin, TCA increase NE and 5-HT tertiary amine |
| imipramine | tofranil, TCA icnrease NE and 5-HT tertiary amine |
| amoxapine | ascendine TCA secondary amine ONLY NE |
| desipramine | norpramine TCA secondary amine only NE |
| maprotiline | ludiomil TCA secondary amine only NE |
| nortriptyline | pamelor TCA secondary amine only NE |
| other receptors that TCA have effects on | muscarinic 1 cholenergic side effects, adrenergic alpha 1 moderatly selective, histamine 1. They have no effect on adrenergic beta receptors |
| cocaine | just blocks the reuptake of NE and 5HT |
| amphetamine | compets for transport vessicle gets pushed back out in space |
| TCA has more prominent effects on | NE than 5-HT and no effec on DA reuptake |
| clinically relevant adverse effects of inhibition of NE reuptake | increase NE in cleft leads to increase heart rate via intrinsic anticholinergic properties that increase sinus node. prolonged PR/QRS/QT ventricular fibrillation, ortostatic hypotension |
| anticholnergic effects of TCA overdose | dry mouth, blurred vision, dilated pupils, urinary retention, absent bowel sounds, pyrexia (fever), myocloni twitching |
| orthostatic hypotension is the most troublesome and most common cardio effect of TCA adn MOAIS because of falls. the ones that cause this the most are | imipramine the tertiary amines cause more severe orthostatic hypoetnsion than the secondary amines |
| The 5HT 1a receptors are located where | somato dendrictic receptors, theses are the auto receptors |
| the 5HT 1D auto receptors are located where | on the terminal axon to regulate serotonin release. these are different than the 1B/1D receptors in the trigeminal ganglia that are not autoreceptors |
| Mirtazapine (remeron) | atypical (mixed action) |
| mianserin (bolvidon) | atypical mixed action tetracyclic antidepressants less anticholinergic effects, serotonin-related side effects & adrenergic SE (such as orthostatic hypotension and sexual dysfunction) Antihistaminic SE of drowsiness and weight gain are prominent. |
| the adrenergic side effects are from which blockade | serotonergic |
| how long dose it take to see beneficial effects | 4-6 weeks because adaptive changes must occur |
| where is the noradrendergic tract | The most prominent noradrenergic (ie, norepinephrine-containing) nucleus is the locus ceruleus in the pons, which account for over 40% of noradrenergic neurons in the rat brain. |
| the dopamine tracts are | nigrostriatal, mesocortical, mesolimbic, tuberanfundibular, raphe nucleus |
| serotonin | raphe nucleus |
| The primary reinforcing and behavioral-stimulant effects of amphetamine, however, are linked to | enhanced dopaminergic activity, primarily in the mesolimbic dopaminergic pathway. |
| monoamine transporters | These are the dopamine transporter (DAT), serotonin transporter (SERT), and the norepinephrine transporter (NET) in the outer cell membrane and the vesicular monoamine transporter (VMAT1 and VMAT2) in the membrane of intracellular vesicles. |
| Ne binds | alpha 1 adrenergic on 5ht cell bodies alpha 2 heteroreceptors on 5HT presynaptic never terminal, and alpha 2 auto receptors on its on presynaptic nerve terminal |
| what does mirtazepine work faster | due to teh blockade of alpha 2 in the CNS. this is the autoreceptor. blockade of this receptor doesn't allow the natural NT to bind & negatively feedback & stop presynaptic release. blocks both the alpha 2 auto & heteroreceptors increase both NE and 5HT |
| which receptors do mirtazapine block | antagonist at presynaptic alpha2-autoreceptors and postsynaptic 5-HT2 and 5-HT3 receptors with some mild inhibitory properties at serotonin reuptake transporters. blocking postsynaptic 5-HT2 receptors may relieve ejaculatory difficulties |
| nefazodone blcoks which receptors | 5HT2 |
| trazodone blocks | 5HT2 and has alpha 1 effect |
| would not be desirable choices for obese patients | certain antidepressants (e.g., TCA, paroxetine, mirtazapine) are associated with significant weight gain and |
| if a depressed patient is sleeping and eating excessively, and possesses little energy or motivation | bupropion |
| mirtazapine has antihistaminergic effects and an increase in noradrenergic effects why still sedation | at lower dose it is considered to be quite sedating. higher daily doses (>30 mg) are less sedating owing to an increase in noradrenergic effects. |
| other side effects of mirtazapine are | In addition to the substantial risk of increasing appetite and total body weight, mirtazapine has also been associated with significant increases in total cholesterol and triglycerides |
| Bupropion and mirtazapine | appear unlikely to affect cardiac rhythm or induce arrhythmias in susceptible patients. |
| TCA are associated with | causing arrthymias |
| which to not use is hypertensive patients | venlafaxine and bupropion |
| decribe the effects of MAO on the heart | do not seem to affect rhythm significantly, although they generally do slow heart rate and can cause or worsen orthostatic hypotension. |
| bupropion has therectical concern of causing | hypoglycemia in patients |
| Because carbamazepine has a narrow therapeutic index and is metabolized by multiple isoenzymes within the cytochrome P450 system, antidepressants that may inhibit its clearance and raise plasma levels, such as....should be avoided | duloxetine (CYP 2D6), fluoxetine (CYP 2D6 and 3A4), and paroxetine (CYP 2D6), should be avoided |
| whicha antidepressant are better choose when woried about CYP interactions | one may opt for an SSRI less likely to inhibit metabolic pathways (e.g., sertraline, citalopram) or venlafaxine. |
| which antidepressant are the best choice when diabetes are of concern | an SSRI that is unlikely to induce weight gain or potentiate drug interactions may be a prudent choice. Such agents would include sertraline, citalopram, or escitalopram. |
| bad choice for diabets needing SSRI are | Several antidiabetic meds are metabolized via 2C9 (tolbutamide, glyburide, glipizide, rosiglitazone), and the admin of certain SSRIs (fluoxetine or fluvoxamine) may potentiate their effects. Some sulfonylureas are metabolized via the CYP 3A4 isoenzyme |
| which drugs are discouraged in elderly and why | anticholinergic effects of certain antidepressants (TCA, paroxetine) may discourage their use in elderly patients suffering from narrow angle glaucoma, chronic constipation, or urinary hesitancy. |
| others drugs that cause MAO inhibition interfering with the degradation of the meperidine and is manifested by agitation, hyperthermia, and circulatory collapse | Other narcotic analgesics such as meperidine, methadone, and tramadol may also trigger this reaction. Codeine and hydrocodone do not appear to have this effect when combined with MAOIs. |
| Foods that absolutely should not be consumed with nonselective MAOIs include | aged cheeses, concentrated yeast extracts, fava beans, and sauerkraut. |
| adverse effects associated with nonselective MAOI | Orthostatic hypotension, weight gain, edema, and sexual dysfunction are common during MAOI therapy. with the MAOIs, the mechanism is believed to be a direct sympatholytic effect because both the lying and the standing systolic BP readings are decreased |
| which of the antidepressant are least protein bound | venlafaxine |
| which cause the most agitation and insomia | fluoxetine, bupropion, sertraline |
| symptoms of dyscontinuation syndrome | dizziness, nausea, paresthesias, anxiety/insomnia, flu like symptoms onset is 36-72 hours and last from 3-7 days |
| which are the high to moderate cyp 1A2 inhibitors | fluvoxamine, fluoxetine, and paroxetine need to avoid if smoke |
| which are the hig to moderate cyp 2c9 2c19 and 3A4inhibitors | fluoxetine fluvoxamine |
| which drugs are high to moderate cyp 2D9 inhibitors | paroxetine, fluoxetine, duloxetine, bupropion,/ citalopram, escitalopram adn sertraline |
| which drugs are INDUCERS of 1A2 | cigarettes, caffeine, st. johns wort |
| which drugs are induces of CYP 2c9/19 | st. john's wort |
| which drugs are induces of 2D9 | carbamzepine, rifampin, phenytoin, phenobarbital, |
Created by:
lainylaina