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Neuro Med > Exam 7: Mood disorder pharmacology > Flashcards

Exam 7: Mood disorder pharmacology Flashcards

(45 cards)

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1
Q

Describe depression

A

Intense sadness, pessimistic worry, agitation, somatic concerns, sleep and eating disturbances, loss of drive, enthusiasm and libido, mental slowing

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2
Q

Describe mania

A

amplified energy, extremely elevated mood, rapid speech, racing thoughts, decreased need for sleep, hypersexuality, grandiosity, excessive interest in goal-directed activities

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3
Q

What is the hypothesis of the cause of depression?

A

changes in serotonin and norepinephrine signaling in brain, especially if they are deficient or receptors are insensitive

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4
Q

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

A

Antidepressants, Mood stabilizers

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5
Q

What are the drugs classified as antidepressants?

A

Tricyclic antidepressants, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, dual-mechanism drugs

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6
Q

What are the drugs classified as mood stabilizers?

A

lithium carbonate, anticonvulsants, atypical antipsychotics

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7
Q

What are the clinical effects of TCAs in depressed subjects?

A

elevation of mood after 2-3 weeks

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8
Q

What are the neurochemical effects of TCAs?

A

Block the reuptake of NE and 5-HT by nerve terminals, resulting in higher concentration of NT at receptors`

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9
Q

What TCA is NE-selective?

A

Desipramine

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10
Q

What TCA has both NE and 5HT action?

A

imipramine

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11
Q

What two drugs, taken together, can lead to toxicity?

A

Fluoxetine and any TCA

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12
Q

What liver enzyme metabolized TCAs?

A

CYP2D6

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13
Q

What drug is classified under MAOIs?

A

Phenelzine (Nardil)

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14
Q

What are the neurochemical effects of MAOIs (phenelzine)

A

Irreversibly blocks the oxidative deamination of monoamines, non-selectively inhibits both MAO-A and MAO-B

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15
Q

What monoamines does MAO-A metabolize?

A

NE and 5HT

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16
Q

What monoamines does MAO-B metabolize?

A

DA

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17
Q

What class of drugs should not be started until at least 14 days following discontinuation of MAOI? Why?

A

SSRIs; MAOIs bind irreversibly, it takes a while before protein synthesis can catch up for MAOI function to come back to normal

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18
Q

What is serotonin syndrome?

A

hyperthermia, muscle rigidity, tremors, autonomic instability, confusion, irritability, and agitation

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19
Q

What can be use to treat serotonin syndrome?

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A

nonselective serotonin antagonist (cyproheptadine)

20
Q

What drug class do MAOIs potentiate? What occurs?

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A

sympathomimetic amines such as tyramine (induces release of NE and epinephrine release from adrenergic nerve endings. Results in hypertensive crisis

21
Q

What types of foods must a patient on MAOI avoid?

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A

foods rich in tyramine (aged cheese, red wine, beer, bananas), ephedrine and pseudoephedrine

22
Q

What drugs are classified as SSRIs?

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A

Fluoxetine (prozac), sertraline (zoloft)

23
Q

What is the MOA of SSRIs (fluoxetine and sertraline)?

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A

selective inhibition of serotonin reuptake by CNS neurons

24
Q

What drug class should not be administered with fluoxetine? Why?

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A

Any TCA (desipramine, imipramine), Fluoxetine inhibits CYP2D6 leading to toxicity of TCAs

25
What are atypical dual/mixed action antidepressants?
Venlafaxine, duloxetine, mirtazaprine, bupropion
26
What is the MOA of venlafaxine?
blocks 5HT and NE reuptake
27
How is venlafaxine different from TCAs?
venlafaxine does not affect adrenergic, histaminergic or cholinergic receptors
28
What are contraindications of patients when prescribing venlafaxine?
patients on MAOIs
29
What is different about the dosing of venlafaxine from other antidepressants?
An increase in dose changes the uptake of a different monoamine. Lowest: 5HT, Middle: NE, Highest: DA
30
What is the mechanism of action of mirtazapine?
Blocks presynaptic alpha 2 receptors on both adrenergic and serotonergic neurons, increasing NE and 5HT levels
31
What is the mechanism of action of bupropion?
Enhances NE and DA neurotransmission: increases presynaptic release and inhibits postsynaptic reuptake
32
What are adverse effects of bupropion?
CNS stimulation (agitation, anorexia, insomnia)
33
What is the MOA of ketamine?
potent NDMA receptor antagonist, aiding in the release of glutamine in the frontal and prefrontal cortices of depressed patients
34
Whree are neurons located that are responsible for release of serotonin and andidepressant effects?
raphe nucleus and receive input from the medial prefrontal cortex
35
What drugs are used to treat bipolar disorder?
Lithium carbonate (eskalith), valproic acid (depakote), carbamazepine (tegretal)
36
How long does it take to see the therapeutic effects of lithium?
5-21 days
37
What is the most likely MOA of lithium?
involves effect of postsynaptic rather than presynaptic neuron, interfering with the production and release of IPD3 and DAG- both needed in amine neurotransmission
38
What are adverse effects of lithium at therapeutic concentrations?
fatigue, muscular weakness, slurred speech, ataxia and fine tremor of the hands, excessive thirst and urination
39
What are adverse effects of lithium at toxic doses?
impaired consciousness, possibly coma, muscular rigidity, hyperactive deep reflexes, market tremor and muscle fasciculations
40
What are therapeutic uses of lithium?
manic phases of bipolar disorder, prevention of mood swings in patients prone to bipolar disorder, antidepressant effects in some patients
41
What are anticonvulsants used to treat bipolar disorder?
valproic acid, carbamazepine
42
What should never be used as a monotherapy for patients with bipolar disorder? Why? what should be given as well?
SSRIs; may cause rapid onset of mania, should be given a mood stabilizer
43
Compare the use of valproic acid to lithium in the treatment of bipolar disorder?
Efficacy similar to lithium in many cases, superior to lithium for rapid-cycling bipolar disorder, appropriate first line use, can be combined with lithium in patients that don't respond to either
44
What is lurasidone used to treat?
bipolar disorder
45
what is the mechanism of action of lurasidone?
D2 and 5HT2A receptor antagonists may be involved, precise mechanism is uknown

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