Mood Disorder Pharmacology Flashcards Preview

Neuro Block 5 > Mood Disorder Pharmacology > Flashcards

Flashcards in Mood Disorder Pharmacology Deck (44)
Loading flashcards...

In general, how is unipolar depression different from bipolar disorder?

unipolar depression is characterized by episodes of depression, separated by periods of euthymia

bipolar disorder is characterized by episodes of depression (briefer) followed by episodes of mania


What is the prevalence of depression?

1 in 10 patients seen in primary care!

it's the 4th most common compaint

***Note that 70% of medical care over-utilizers have at some time in their lives had a diagnosis of major depression


What hypothesis is the make idea fo neurochemical basis of affective disorders?

the amine hypothesis


Describe the amine hypothesis for affective disorers.

certain levels of amine NTs and receptor sensitivity are necessary for normal mood
 (NE, 5HT, DA)

Depression occurs if receptors are insensitive or if amine synthesis, storage, or release is deficient

Mania occurs if there is an excess of NT or a receptor hypersensitivity


What ist he major issue with the amine hypothesis of mood disorders?

there's a mismatch between the time course of treatment:

neurochemical effects can occur in 1-2 days, while clinical improvement takes 10-21 days


What are the two general drug classes for treatment of mood disorders?


mood stabilizers


What percentage of patients do not respond to initial antidepressant therapy?



What effects do tricyclic antidepressants cause in normal, non-depressed, subjects?

NO stimulation of mood elevating effect

you get antimuscarinic effects: dry mouth, blurred vision, constipation, urinary retention, sleepiness and light headedness


What is the effect of TCAs in depressed subjects?

elevation of mood only after 2-3 weeks

50% experience dry mouth and tachycardia


What is the mechanism of the TCAs

block the reuptake of NE and/or 5HT by nerve terminals

some are NE selective and others are NE/5HT mixed action

This results in higher concentration of the NTs at their receptors


What are the adverse effects of the TCAs

orthostatic hypotension

antimuscarini effects (especialy in elderly patients): acute confusional state, constipation, glaucoma

weight gain

tachycardia and increased tendency for arrhythmias with high doses


What are some drug interactions you'll see with the tricyclic antidepressants?

1. they'll potentiate central depressants like alcohol, sedatives, and opioids

2. the antimuscarinic effects may delay gastric emptying time, so you get increased inactivation of levodopa in treating parkinsonism


What do MAOIs do?

they irreversibly block the oxidative deamination of monoamines like NE and 5HT


What's the difference between MAOa and MAOb?

MAOa metabolizes NE and 5HT in the brain and gut

MAOb metabolizes DA in the blood platelets


How long do you have to wait for changes to be seen with MAOIs?

the NTs change in 24-48 hours, but it takes 3+ weeks for clinical effect


Why are MAOIs used more for treating symptomatically?

the therapeutic index is very low - only 5!

usually hospitalize 1 week too


What is the major concen for drug interaction with the MAOIs?

They will potentiate sympathomimetic amins

especially indirect acting amines like tyramine

tyramine is usually metabolized by hepatic MAO, but ifyou take an MAOI, tyramine will build up and enter systemic circulation

it enhances release of catecholamines from peripheral and central nerve terminals and the adrenal medulla

this results in massive adrenergic stimulation that can cause a hypertensive crisis


What option is available in Europe to lower the incidence of interaction with tyramine?

they have approved selective and reversible MAOa inhibitors called Brofaramine and maclobemide

they don't inhibit all the MAO, so you don't get the interaction


What are some major examples of SSRIs?

fluoxetine = prozac

sertraline = zoloft

citalopram = celexa

escitalopram = lexapro


What are the adverse effects of SSRIs and how are they different from the TCAs and MAOIs?

nausea, diarrhea, weight LOSS, sexual dysfunction

stimulation - anxiety, nervousness, insomnia

They are unusual in that they're NOT sedating



What is the black box marning for fluoxetine?

they can increase suicidal thinking in children, adolescence and young adults


Which serotonin receptor probably contributes to the clinical improvement seen with SSRIs?

5-HT 2a


What is the difference between an autoreceptor and a heteroreceptor?

autoreceptors are acted on by 5HT to inhibit the addition release of 5HT

Heteroreceptors are acted on by NE to inhibit the release of 5-HT


What are hte 4 major atypical antidepressants?

velafaxine (effexor)

duloxetine (cymbalta)

Mirtazapine (Remeron)

Buproprion (wellbutrin)


What is the mechanism of action for venlafaxine (effexor)?

it's a selective 5HT and NE reuptake inhibitor (SNRI)


If Venlafaxine also blocks serotonin and norepinephine reuptake, why is it different than the TCAs?

Venlafaxine does NOT affect the adrenergic receptors, histaminergic receptors or cholinergic receptors

this means it has far fewer side effects


Although efficacy of most antidepressants doesn't increase with increasing dose, it does with venlafaxine. Why?

because it affects different NTs at different doses

lowest = serotonin

middle = norepinephrine

hihest = dopamine


What is desvenlafaxine (pristiq) and is it more effective than venlafaxine (effexor)?

It's an active metabolite of venlafaxine

it's not any more effective- the patent for venlafaxine was up in 2010, so they played the system


What's the mechanism of action for mirtazapine (remeron)?

It blocks presynaptic alpha2 receptors on adrenergic and serotonergic neurons, so you increase NE and 5HT levels


What is the mechanism of action for buproprion (wellbutrin)?

it affects boht NE and DA transport in th eneurons