Pharmacology of antidepressants

Question 1

What are the two types of mood disorders

Answer 1

Unipolar (depression) and Bipolar (manic-depressive)

Question 2

T/F: Mood disorders are episodic

Answer 2

True

Question 3

What are the tertiary TCAs, what type of inhibiton does it favor

Answer 3

Imipramine, Amitriptyline, Doxepin, Trimipamine, Clomipramine/ greater Serotonin reuptake inhibition

Question 4

What are the secondary TCAs, what type of inhibiton does it favor

Answer 4

Despiramine, Nortriptyline, Protriptyline/ greater norepinephrine reuptake inhibition

Question 5

What is the chronic effects of TCAs, what is the theory behind it

Answer 5

Desensitization, decrease in beta-adnergic receptors and serotonin receptors/ Desensitization leads to delayed therapeutic antidepressant response

Question 6

What are the TCA therapeutic effects

Answer 6

Antidepressant activity (specific mood-elevating effect), antipanic activity, antiobsessional activity (5-HT inhibition), sedation in non-depressed individuals

Question 7

What receptors are antagonized by TCAs

Answer 7

muscarinic receptors, alpha-1 norepinephrine receptors, histamine-1 and histamine-2 receptors

Question 8

What side effects of TCAs are due to antagonizing histamine receptors

Answer 8

weight gain and drowsiness

Question 9

What side effects of TCAs are due to muscarinic receptors

Answer 9

Constipation, blurred vision, dry mouth, urinary retention, memory impairment

Question 10

What side effects of TCAs are due to antagonizing alpha-1 receptors

Answer 10

Dizziness, orthostatic hypotension

Question 11

What are other side effects of TCAs

Answer 11

Tremor (beta-adnergic stimulation), cardiac arrhythmias with seizures and coma (Sodium channel blockade)

Question 12

T/F: TCAs are associated with high suicide potential

Answer 12

True

Question 13

What are the selective serotonin reuptake inhibitors

Answer 13

Fluoxetine, Sertraline, Paroxetine, Citalopram, Escitalopram

Question 14

What is the MOAs of nefazadone and trazodone

Answer 14

Inhibition of serotonin uptake carrier, antagonism of serotonin receptors, antagonism of alpha-1 adnergic receptors, chronically down-regulates receptors

Question 15

What are the side effects of nefazadone and trazodone

Answer 15

Sedation (most prominent), dry mouth (alpha adnergic antagonism), hyptotension, hepatoxicity (nefazodone BBW), trazodone (painful priapism)

Question 16

T/F: Nefazadone and Trazadone have antimuscarinic activity

Answer 16

False: Nefazodone and Trazodone has NO ANTIMUSCARINIC activity

Question 17

What atypical antidepressent is similar to nefazodone and trazodone, whats the difference

Answer 17

Vilazodone, partial serotonin 1A agonist activity

Question 18

What NDRI not only takes up norepiphrine but at high enough concentrations dopamine as well, what happens when chronically used, side effects

Answer 18

Bupropion/ down-regulates beta-adnergic receptors/ mild psychomotor agitation, insomnia, seizures

Question 19

What are the dose-dependent MOAs of venlafaxine

Answer 19

Inhibition of serotonin uptake carrier (low doses), inhibiton of norepinephrine carrier ( medium doses), inhibition of dopamine carrier (high doses), down regulates those receptors

Question 20

What are the side effects of venlafaxine

Answer 20

Increased diastolic blood pressure (NE stimulation), Nausea (serotonin 3 mediated)

Question 21

T/F: Venlafaxine has no antagonism of muscarinic, alpha-adnergic, or histamine 1 receptors

Answer 21

True

Question 22

What is the active metabolite of venlafaxine, what makes it different

Answer 22

Desevenlafaxine, NOT a substrate for CYP 2D6

Question 23

What receptors does Mirtazapine antagonize, therapeutic effects

Answer 23

alpha2-adnergic, serotonin-2, serotonin-3, histamine-1, antianxiolytic and antidepressant

Question 24

What are the side effects of mirtazapine

Answer 24

weight gain and drowsiness

Question 25

What is the MOA of maprotiline, side effects

Answer 25

Selective NE uptake inhibition, chronically: down regulates receptors/ sedation (histamine-1 antagonism), orthostatic hypotension (alpha-1 antagonism), seizures

Question 26

What the MAO inhibitors

Answer 26

Phenelzine (hydrazine), Isocarboxizid (hydrazide), tranylcypromine (amphetamine derivative), moclobemide (reversible MAO inhibitor)

Question 27

T/F: MAO inhibitors only increase the amount of dopamine present

Answer 27

False: Due to MAO-inhibitors there is an accumulation of norepinephrine, dopamine, and serotonin in the synaptic cleft

Question 28

What are the pharmacologic effects

Answer 28

Mood-elevating action in depressed patients, mild stimulant action in non-depressed individuals, antipanic action, antiarcoleptic action

Question 29

What is the tyramine effect associated with MAO inhibitors

Answer 29

Tyramine that is usually metabolized by MAO is not leading to severe hypertension due to build-up

Question 30

What are drug-drug interactions for MAO inhibitors

Answer 30

Pseudoephedrine, SSRIs (serotonin syndrome), Meperidine

Question 31

T/F: At subanesthetic doses, ketamine can exert immediate antidepressant effect in patients with resistant bipolar or unipolar depression with IMMEDIATE reduction in suicidal thoughts

Answer 31

True

Question 32

What does ketamine cause when subanesthetic doses are given

Answer 32

Release of glutamate