Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
30 Cards in this Set
- Front
- Back
What is one proposed etiology of depression that invloves synaptic receptors?
|
Depression may be caused by an elevated B/a1 ratio. Therapy reverses this ratio.
|
|
What happens to a1, a2 and B receptors during the start of anti-depressant therapy?
|
a2 and B receptors are desensitized at the synapse while a1 receptors are not.
|
|
Phenelzine
|
MAO inhibitor.
|
|
Tranylcypromine
|
MAO inhibitor
|
|
Selegiline
|
Selective MAOb inhibitor
|
|
What neurotransmitters are degraded by MAOa?
|
Norepinephrine and Seratonin
|
|
What neurotransmitters are degraded by MAOb?
|
Dopamine
|
|
Why do most anti-depressants cause a 2-3 week lag phase before they are effective?
|
During this period a2 and B receptors are desensitized.
|
|
What are the toxic effects of MAOIs?
|
1. Postural hypotension due to a desensitization.
2. Insomia and impotence due to excessive autonomic stimulation 3. Potentailly fatal hypertensive crisis after ingestion of tyramine or sympathomimetic drugs like ephedrine or phenylpropanolamine. |
|
What is the effect of mixing meperidine and an MAOI?
|
May cause hyperreflexia and convulsions.
|
|
Do TCAs produce CNS stimulation?
|
No. TCAs actually cause sedation or fatigue especially during the first few weeks of treatment, followerd by some mood elevation.
|
|
Amitriptyline
|
Tricyclic Antidepressant
|
|
Imipramine
|
Tricyclic Antidepressant
|
|
What is the mechanism of TCAs?
|
They inhibit re-uptake pumps, increasing the synaptic concentration of Norepinephrine and Seratonin.
|
|
What are the sympathomimetic effects of TCAs?
|
Arrythmia, tremor and insomnia
|
|
What are the antihistaminic effects of TCA's
|
Initail sedation but tollerance soon develops.
|
|
What are the antimuscarinic effects of TCAs?
|
dry mouth, blurred vision, tachycardia, urinary retention.
|
|
What are the effects of mixing TCAs with drugs that interfere with hepatic metabolism?
(antipsychotics) |
Enhanced toxic effects of TCAs
|
|
What are the effects of mixing TCAs with drugs that increase hepatic metabolism?
(barbituates) |
May produce additive sedation effects.
|
|
Trazadone and Nefazodone
|
Anitdepressants that inhibit serotonin > norepi uptake.
|
|
Venlafaxine
|
Seratonin>>>NE pump inhibitor. Used to treat major depression
|
|
Buproprion
|
Unknown mechanism. Contraindicated in patients taking Zyban for smoking cessation.
|
|
Amoxapine
|
Antipsychotic with antidepressant effect.
|
|
Maprotiline
|
Potent NE reuptake inhibitor
|
|
Mirtazipine
|
Blocks serotonin and a2 receptors. Also blocks H1 receptors and produces sedation. May also cause weight gain
|
|
What are the 4 main SSRIs?
|
Fluoxetine, Sertaline, Paroxetine, and Fluvoxamine.
|
|
What are the side effects associated with SSRIs?
|
Nausea, insomnia, anxiety, decreased libido. Secondary to excessive serotonin.
|
|
What is the promary use of Lithium?
|
Stabilization of mood swings. Very effective in preventing manic episodes.
|
|
How is Lithium eliminated from the body?
|
It is excreted entirely by the kidney. Na loading causes an increase lithium secretion. Na depletion causes lithium retention.
|
|
What is the effect of mixing Thiazides and Lithium?
|
Causes Lithium toxicity due to renal excretion of Na and Litium retention. NSAIDS also increase Lithium reabsorption.
|