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54 Cards in this Set

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Drugs in this Lecture
MAOI: tranylcypromine//

TCAs: imipramine, desipramine, amitriptyline, duloxetine.//

SSRIs: fluoxetine, sertraline, venlafaxine, duloxetine.//

Misc ADs: trazodone, buropion, mirtazapine.//

Bipolar: lithium, valproic acid, carbamazepine, Lamotrigine.//
Depression: Unipolar
'major depressive disorder', lasts 4-12 months, remit spontaneously but if untreated, likely to recur).//

Most common in 4th decade. many don't seek treatment. //

70% respond to ADs.//
It's acronym for depressive sxs.//

Sleep disturbance, loss of Interest, Guilty feelings, decrease Engergy and Concentration, Appetitie, Psychomotor agitation, Suicidal thoughts.//
What is theoretical mechanism of ADs?
There is Biogenic Amine theory, and Neurogenesis hypothesis.
Biogenic Amine Theory?
seeks to correct NE and/or serotonin deficiency. //

Evidence in favor: most ADs increase amine levels, amine depletion can cause depressive sx (e.g. via Reserpine inactivating VMAT).//

Evidence against: some drugs though increase amine level are still poor ADs, amine blockers often don't affect mood, new ADs don't alter amine level. Time discrepancy: clinical improvements takes 2-6 weeks.//
Neurogenesis hypothesis?
states that depression results from impaired hippocampal neurogenesis. ADs act by increasing neurogenesis and decreasing cell death in hippocampus. This explains the Time Discrepancy.//

in favor: depressed pts display reduced hippocampal mass, stress hormones which cause depression reduce neurogenesis, many ADs stimulate hippocampal neurogenesis, hippocampal neurogenesis inhibition prevent AD efficacy.//

evidence against: some ADs (TMS) do not alter neurogenesis, decreased neurogenesis and depression can be dissociated, most evidence not from humans.//
Monoamine Oxidase Inhibitors
not usually first line ADs due to side effects.//

tranylcypromine, phenelzine, selegiline (MAO-B inhib: now in patch, fewer food restrictions).//
MAOIs neurochemical effects?
block metabolism of amines by IRREVERSIBLY inhibiting MAO-A and MAO-B.
MAOIs Clinical effects
acute first few days: CNS stimulation, agitation, euphoria.//

Chronic 2-6 wks: improvement of sx of depression, CNS activation remains but lessened.//

MAOI other indications: panic disorder, agoraphobia
uncommon, results in hyperthermia, shock and seizures. Tx with supportive therapy.
MAOI interractions?
avoid indirect sympathomimetics incl. TYRAMINE, amphetamine, bupropion, L-Dopa.//

Should not be taken with SSRIs, which may result in Serotonin Syndrome.//
What's Serotonin Syndrome?
rare but fatal, serotonin toxicity caused by co-administration of drugs with different mech. of elevating brain serotonin levels (MAOI and SSRIs, also MDMA (ecstasy) plus MAOI)./
What are Sx of Serotonin Syndrome?
mental confusion, cognitive effects, hyperpyrexia, tachycardia, hypertension, mausea, diarrhea, muscle twitching.
Which antibiotic shouldn't be taken with MAOIs?
Linezolid, because it's a MAO inhibitor as well.
Tricyclic antidepressants (TCAs): Tertiary amines
Tertiary amines have higher affinity for SERT than NE-T. They are SERT blockers, inhibiting reuptake of 5-HT//

e.g. imipramine, amitriptyline
TCAs: Secondary Amines
Higher affinity for NE-transporter (NET) than SERT.//

e.g. desipramine, nortriptyline.
What's different about imipramine and amitriptyline compared to the secondary armines, desipramine and nortriptyline???
So, the tertiary drugs, imipramine is metabolized to secondary amine drug desipramine.//

Similarly amitriptyline gets metabolized to nortriptyline.//

The signifance is that initially the tertiary amine drugs act at SERT, then once metabolized, work at NET blockage.//
TCAs: Neurochemical Effects
blockade of neuronal reuptake of NE and or 5-HT, raising synaptic level of biogenic amines. //

TCA's also block receptors such as muscarinic, alpha1, H1 resulting in side effects.//

Amaxopine (2 drug)also blocks D2 receptors, efficacy in psychotic depression.//
TCAs: Clinical effects
acute: drowsy, dysphoric, anxious, autonomic effects.//

choronic: improvement of most sx of depression (70% response rate). Side effects from receptor blockage diminish overtime. Mood elevation is NOT euphorial**.
Other indications for TCAs?
panic disorder, OCD (clopiramine only), anxiety/phobias, chronic neuropathic pain, ADHD, migraine prophylaxis.//
TCAs adverse effects:
secondary have better side effect profile than tertiary amines. Most effects due to receptor blockade, big issue in compliance.
Common side effects of TCAs per organ system
CNS: sedation, vascular: orthostatic hypotension (alpha1 block), heart: tachycardia, anticholinergic: dry mouth, confusion, vegetative: increased appetite and weight gain, sexual dysfunction.//

amoxapine: additional extrapyramidal effects, tardive dyskinesia.//
very low TI, cause fatal arrhythmias, acidos, seizures, paralysis, coma.//

careful at dispensing to suicidal pts.//
TCAs OD tx:
supprotive, gastric lavage, physostigmine, antiseizure (diazepam or phenytoin).//

Taper after chronic use.//
TCAs interractions
effects increased by: neuroleptics, methylphenidate, oral contraceptives, some SSRIs.//

decreased by: barbiturates, carbamazepine, rifampin.//

TCA potentiate effects of anticholinergics, sympathomimetics, alcohol and other CNS depressants. //
Serotonin Selective Reuptake Inhibitors (SSRIs):
selectively block reuptake of 5-HT. Sertraline also cause some blocking of DAT-1. More specific so less side effects.

Drugs: fluoxetine (prozac), sertraline (zoloft), venlafaxine (effexor), duloxetine (cymbalta).
How are venlafaxine, and duloxetine different?
different in that they inhibit reuptake of 5-HT and NE (and to a lesser extent, DA). So, they aren't really SERT selective, but grouped with SSRIs because their clinical profile is similar to SSRIs.
SSRIs: clinical effects
actue: CNS stimulation, anxiety, agitation.//

chronic: improvement of depression, CNS activatin remains but anxiety usually resolves. //
SSRIs: Other indications?
panic disorder, OCD, eating disorders (e.g. bulimia)
SSRIs adverse effects?
headache, GI upset, sexual dysfunctininsomina.//

Much safer in OD. High TI. Should taper off drug because of withdrawal especially with venlafaxine.
SSRIs interractios
fluoxetine and paroxetine inhibit p450 enzymes and slow metabolism for many drugs e.g.: TCAs, lithium, warfarin, theophylline.//

Fluoxetine inhibits 2D6 and 3A4, and 2C9.//

If taken together with MAOIs, can cause serotonin syndrome.//
Misc. Antidepressants
drugs: trazodone, bupropion, mirtazapine (rameron)
Trazadone and nefazodone:
weak inhibition of 5-HT reuptake, some NE reuptake, blocks post-synaptic 5-HT2 receptors ***.//

side effects: cause blockade of other receptors (alpha 1, H1, 5-HT BUT NOT MUSCARINIC.//
blocks DA reuptake, also blocks NE and 5HT uptake. Little activity at blocking receptors, so least side effects.//

blockage fo alpha 2 and 5-HT presynaptic receptors > increase NE and 5-HT.//

Little effects on reuptake system.

side effects: very potent H1-R blocker, therefore Sedative properties.
Other indications?
Bupropion: treate nicotine addiction/withdrawals
Misc. ADs: adverse effects?
In general, fewer side effects:

trazodone: sedation

bupropion: agitation, weight loss.

Mirtazapine: sedation, weight gain, dry mouth, constipation.//
How about in Children?
precipitate suicidal thoughts (SSRIs). Only drug approved is Fluoxetine (prozac) in children.
What's the efficacy of ADs?
if used properly, most generally have a 70% efficacy.
Treatment of different types of depression?
spec. dx of depression not critical except:

unipolar vs. bipolar, atypical depression (MAOIs first line), pschotic depression (also requires antipsychotics), anxious depression (may benefit from benzodiazepine).//

Dose is gradually increased over several weeks to minimize side effects.//
What are the first line drugs for most physicians in depression?
What to do if there's a poor response to ADs in a pt?
5 D's: Dose, Duration, Dx, Adjunct Drugs, Different Treatment.
What's 'atypical depression'?
These pts have sx of agitation, weight gain, somnolence.
Def. Bipolar Disorder
episodes of full mania that may alternate with episodes of major depression. aka Manic Depression
Def. Bipolar II disorder
has recurrent episodes of major depression with HYPOMANIA.
Tx of acute manic episodes
Not with Lithium alone, use antipsychotics, sedatives, antiseizure drugs
Tx of bipolar depression
Care needs to be taken with Rx not to push the patient in to Mania. Use ADs with mood stabilizers (olanzapine and fluoxetine, lamotrigine, quetiapine).
What are some Maintainance drugs?
used in chronic tx, prevents reoccurences, mood stabilization) Drug: lithium, antiseizure drugs (valproic acid, carbamazepine, lamotrigine)
Lithium Mech?
interferes with metabolism of inositol phophates, inhibit glycogen synthase kinse 3
Uses for Lithium?
long term bipolar maint., as adjunct in unipolar and schizoaffective disorders.

Lithium is NOT effective in acute manic episodes.//
Adverse effects of Lithium?
tremor, edema, polydypsia, polyuria, GI irritation.
OD of Lithium?
low TI, so must monitor. vomiting, nausea, ataxia, seizures etc etc.

Tx : suportive, osmotic diuretic, dialysis.//
Lithium pharmakokinetics.
well absorbed, 5% excreted in urine, 80% filtered is reabsobed (changes with age and Na levels in the body)., short t1/2.//

Aim is .5-1.0 mEq/L.//
Lithium drug interractions?
Increased levels: due to decreased secretions - sodium-depleting diuretics (thiazides), ACE-I, NSAIDS, can increase chance of Li. Tox.//

Decreased Li: due to increased urine excretion -- mannitol, acetazolamide, theophylline.