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Neuro Med > Exam 7: Mood disorder pharmacology > Flashcards

Exam 7: Mood disorder pharmacology Flashcards

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?

A

nonselective serotonin antagonist (cyproheptadine)

20
Q

What drug class do MAOIs potentiate? What occurs?

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?

A

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

22
Q

What drugs are classified as SSRIs?

A

Fluoxetine (prozac), sertraline (zoloft)

23
Q

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

A

selective inhibition of serotonin reuptake by CNS neurons

24
Q

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

A

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

25
Q

What are atypical dual/mixed action antidepressants?

A

Venlafaxine, duloxetine, mirtazaprine, bupropion

26
Q

What is the MOA of venlafaxine?

A

blocks 5HT and NE reuptake

27
Q

How is venlafaxine different from TCAs?

A

venlafaxine does not affect adrenergic, histaminergic or cholinergic receptors

28
Q

What are contraindications of patients when prescribing venlafaxine?

A

patients on MAOIs

29
Q

What is different about the dosing of venlafaxine from other antidepressants?

A

An increase in dose changes the uptake of a different monoamine. Lowest: 5HT, Middle: NE, Highest: DA

30
Q

What is the mechanism of action of mirtazapine?

A

Blocks presynaptic alpha 2 receptors on both adrenergic and serotonergic neurons, increasing NE and 5HT levels

31
Q

What is the mechanism of action of bupropion?

A

Enhances NE and DA neurotransmission: increases presynaptic release and inhibits postsynaptic reuptake

32
Q

What are adverse effects of bupropion?

A

CNS stimulation (agitation, anorexia, insomnia)

33
Q

What is the MOA of ketamine?

A

potent NDMA receptor antagonist, aiding in the release of glutamine in the frontal and prefrontal cortices of depressed patients

34
Q

Whree are neurons located that are responsible for release of serotonin and andidepressant effects?

A

raphe nucleus and receive input from the medial prefrontal cortex

35
Q

What drugs are used to treat bipolar disorder?

A

Lithium carbonate (eskalith), valproic acid (depakote), carbamazepine (tegretal)

36
Q

How long does it take to see the therapeutic effects of lithium?

A

5-21 days

37
Q

What is the most likely MOA of lithium?

A

involves effect of postsynaptic rather than presynaptic neuron, interfering with the production and release of IPD3 and DAG- both needed in amine neurotransmission

38
Q

What are adverse effects of lithium at therapeutic concentrations?

A

fatigue, muscular weakness, slurred speech, ataxia and fine tremor of the hands, excessive thirst and urination

39
Q

What are adverse effects of lithium at toxic doses?

A

impaired consciousness, possibly coma, muscular rigidity, hyperactive deep reflexes, market tremor and muscle fasciculations

40
Q

What are therapeutic uses of lithium?

A

manic phases of bipolar disorder, prevention of mood swings in patients prone to bipolar disorder, antidepressant effects in some patients

41
Q

What are anticonvulsants used to treat bipolar disorder?

A

valproic acid, carbamazepine

42
Q

What should never be used as a monotherapy for patients with bipolar disorder? Why? what should be given as well?

A

SSRIs; may cause rapid onset of mania, should be given a mood stabilizer

43
Q

Compare the use of valproic acid to lithium in the treatment of bipolar disorder?

A

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
Q

What is lurasidone used to treat?

A

bipolar disorder

45
Q

what is the mechanism of action of lurasidone?

A

D2 and 5HT2A receptor antagonists may be involved, precise mechanism is uknown

Neuro Med (39 decks)

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