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Pharm II Exam I > Antidepressants/Bipolar > Flashcards

Antidepressants/Bipolar Flashcards

1
Q

How does the therapeutic benefits of antidepressants differ in time from onset of administration in the blood?

A

Blood levels plateau in hours-days, but the therapeutic benefits are not seen until 2-6 weeks later (true for ALL antidepressants)

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2
Q

SSRI selectively block ____ transporter inhibiting reuptake of __________

A

SSRIs selectively block SERT inhibiting reuptake of serotonin (5-HT)

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3
Q

Serotonin is synthesized from _______

A

Tryptophan

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4
Q

Two examples of SSRIs are:

A

Fluoxetine (prozac) and Sertraline (zoloft)

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5
Q

What is the action of SERT that the SSRI blocks?

A

SERT is responsible for the reuptake of serotonin (SSRIs keep serotonin in the from being taken up; with time neuronal pathways adapt to enhance serotonergic transmission) Serotonin does not act directly at the NT receptor

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6
Q

Tranycypromine is classified under this drug category

A

MAOIs (monoamine oxidase inhibitors)

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7
Q

Amitriptyline and desipramine are classified under this drug category

A

TCAs (tricyclic antidepressants)

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8
Q

Duloxetine is classified under this drug category

A

SNRI

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9
Q

Fluoxetine and Sertraline are classified under this drug category

A

SSRI

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10
Q

Indications for SSRI

A 
Depression
Anxiety disorders (panic, phobias, PTSD, OCD)
Eating disorders
Prementrual dysmorphic disorder
ADD/ADHD
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11
Q

What are the effects of SSRIs (fluoxetine and sertraline) in the body?

A

Initially (hours-days): adverse effects such as CNS stimulation
Delayed (1-6 weeks): the therapeutic response kicks in and you see a GRADUAL improvement in depressive symptoms

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12
Q

SSRI ADME

A

A: oral
D: good absorption, 75-95% protein bound
M: oxidation by CYP3A4, metabolism of some SSRIs produces active metabolites
E: most have long half life (24 hrs)

Kinetics mostly important for toxic response, not therapeutic response (ie withdrawal is more likely with a shorter half life)

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13
Q

SSRI adverse effects

A 
CNS stimulation (insomnia, agitation)
GI problems (nausea, diarrhea, bleeding)
Sexual dysfuction - big one - (decreased libido, anorgasmia)

Minimize AE (except sexual dysfuction AE) by starting with lower doses

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14
Q

What would be problematic with prescribing an SSRI or an SNRI to a patient who is vegan?

A

If your patient isnt eating meat or fish, they aren’t synthesizing tryptophan as needed to make serotonin and the SSRI/SNRI wont be as effective

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15
Q

Mechanism of action of SNRI (duloxetine)

A

Very similar to SSRI by blocking SERT from reuptaking serotonin but also block norepinephrine at medium-high doses. Like SSRIs, SNRIs are selective in that they dont block the transmitter receptors, only working on transporters.

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16
Q

Unique indication for duloxetine

A

Neuropathic pain (also FDA-approved for generalized anxiety disorder, fibromyalgia and diabetic neuropathy)

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17
Q

Unique effect of duloxetine

A

Increases BP at high doses (also has a shorter duration and more withdrawal symptoms)

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18
Q

Can you overdose on SSRI/SNRIs?

A

Not easy to do bc of high TI, fatalities are rare UNLESS combined with other drugs like MAOIs (inhibit breakdown of serotonin) and then “serotonin syndrome” sets in: hyperthermia, muscle rigidity, hyperreflexia, myoclonus

Again, the unique AE for SNRIs is hypertension, especially with overdose

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19
Q

What are the efficacy differences between SNRIs and SSRIs?

A

No efficacy differences (no evidence)

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20
Q

What makes fluoxetine unique?

A

Takes a long time to stabilize the dose (to wash out drug)

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21
Q

What is the half life of duloxetine?

A

Shorter than the others - more likelihood of “discontinuation symptoms” ie withdrawal symptoms

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22
Q

Compare the drug-drug interactions between fluoxetine, duloxetine and sertraline

A

Fluoxetine and duloxetine both inhibit CYP2D6 and have the same potential for drug interactions
Sertraline has fewer drug interactions

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23
Q

What drug class is bupropion in?

A

Bupropion is a dopamine reuptake inhibitor, part of the subclass of newer ADDs

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24
Q

What drug class is trazodone in?

A

Trazodone is a 5-HT1A (serotonin autoreceptor) receptor antagonist, part of the subclass of newer ADDs

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25
Q

What drug class is mirtazapine in?

A

Mirtazapine is an alpha2 autoreceptor antagonist, part of the subclass of newer ADDs

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26
Q

Indication for Trazodone

A

Sedative properties with no anticholinergic effects

27
Q

Indication for Bupropion

A

smoking cessation

28
Q

Indication for Mirtazapine

A

Strong sedative properties - has some anticholinergic effects

29
Q

Trazodone mechanism

A

5-HT2A receptor blockade = major therapeutic mechanism (weak SERT blocker and weak partial agonist at 5-HT1A- increases 5-HT). 5HT2A is an autoreceptor that downregulates norepinephrine production if 5-HT levels are high in synapse (so drug effect is to increase synaptic NE)

Active metabolite mcPP works as agonist at several 5-HT receptors= non-therapeutic mechanism

30
Q

Trazodone AE

A

sedation and orthostatic hypotension (also risk of priapism and headache)

31
Q

Mirtazapine mechanism

A

Potent alpha2 antagonist (blocks autoreceptor- enhances NE release) = major therapeutic mechanism
Potent H1 antagonist: sedation = non-therapeutic mechanism
Weak antagonist at muscarinic and alpha1 (leads to side effects)

32
Q

Mirtazapine AE

A

Sedation (also weight gain, dizziness, dry mouth, constipation)

33
Q

Bupropion mechanism

A 
Block DAT (dopamine) and NET (norep): therapeutic mechanism
Potent antagonist at nicotinic alpha3beta4 receptor - may contribute to use in smoking cessation - non-therapeutic mech
34
Q

Bupropion AE

A

CNS stimulation, potential for seizures (higher risk in patients with eating disorders)

35
Q

Advantages for Bupropion

A

Far fewer sexual side effects, unique mechanism may help in some treatment-resistant patients

36
Q

Amitriptyline is a ______ amine, while desipramine is a _____ amine

A

Amitriptyline is a tertiary amine, while desipramine is a secondary amine (both are tricyclic antidepressants)

37
Q

TCA (amitriptyline and desipramine) mechanism

A

Block neuronal reuptake pumps for both 5-HT/Serotonin (SERT) and NE (SERT and NET) AND blocks receptors for NTs (muscarinic cholinergic, a1 adrenergic, H1 histamine)
Desipramine - blocks NET
Amitriptyline blocks SERT (tertiary amines metabolized to secondary amines; effect of tertiary amines is blocking reuptake of both amines)

38
Q

TCA AE

A 
Initial AE: drowsiness, autonomic symptoms (dry mouth, constipation), anxiety, dysphoria, difficulty in concentration
Longer AE:
Heart - arrythmias
Vascular - orthostatic hypotension
Autonomic - dry mouth, constipation
CNS - sedation
Vegetative - increased appetite, weight gain
Sexual dysfunction
39
Q

TCA ADME

A

Can produce active metabolites
Long half life (24+ hours)
Again, kinetic differences important for toxicity only

40
Q

TCAs: Overdose toxicity

A

Low TI makes them dangerous in overdose
Desipramine has less side-effects and a higher TI than amitriptyle
Tx: supportive; lavage; lidocaine for arrhythmias

41
Q

MAOI (tranylcypromine) mechanism

A

Irreversibly inhibit monoamine oxidase

42
Q

MAOI (tranylcypromine) indications

A

Good for “atypical depression”

Normally 3rd line drugs: dangerous drug and food interactions

43
Q

MAOI (tranylcypromine) ADME

A

Lots of drug-drug interactions:
With sympathomimetics: headache, increased BP
with merperidine, dextromethorphan: serotonin syndrome, severe toxicity and fatalities
With SSRIs/SNRIs/TCAs/trazadone: serotonin syndrome - changes drugs is difficult! Allow 2-5 weeks after cessation to start new drug (and 2 weeks before putting someone on MAOIs)

44
Q

Why should you tell a patient on tranylcypromine to limit their cheese and wine?

A

TYRAMINE in these foods can cause drug interactions and lead to acute hypertensive crisis

45
Q

MAOI (tranylcypromine) AE

A

overdose (when combined with other drugs): agitation, delirium, shock, coma, seizures, hyperthermia

46
Q

Which ADDs cause pregnancy risks?

A

Tranycypromine (contraindicated)
Fluoxetine, sertraline (slight risk of rare fetal malformations, category C)
Amitriptyline (possible risk of limb malformation)

Note that ALL drugs on our list are cat C or worse (duloxetine, bupropion, mirtazapine, trazodone). Untreated maternal depression is also associated with LBW and delayed fetal development. May want to just keep her on a C category ADD.

47
Q

What is the only drug that has received FDA approval for use in children with major depressive disorder?

A

Fluoxetine

48
Q

What is the first-line treatment for major depression?

A

SSRIs, SNRIs and bupropion

49
Q

All antidepressants require how many weeks for complete clinical effect?

A

1-6 weeks

50
Q

What is the response rate for most antidepressants?

A

60-80% response rate (suggestions that blocking both SERT and NET is better remains unproven)
However, lower overall response rate with trazodone and bupropion

51
Q

What four drugs are used for bipolar disorders?

A

Lithium, olanzapine, valproate (divalproex), and lamotrigine

52
Q

What drugs are appropriate for acute manic emergencies?

A

Key is sedation

  • Antipsychotics- olanzapine
  • Anticonvulsants - valproate
53
Q

What drugs are appropriate for bipolar maintenance?

A

Mood stabilizers

  • Lithium carbonate
  • Anticonvulsants - valproate, Iamotrigine
  • Atypical antipsychotics - olanzapine
54
Q

Drug of choice for maintenance therapy of bipolar disorder

A

Lithium (mech of action unclear)

55
Q

Should you use antidepressants to treat bipolar disorder?

A

No, use mood stabilizers. Can cause significant problems in switching from depression to mania (initial presentation of depressive episode could be either major depression or bipolar disorder)

56
Q

Lithium indications

A

Depression, schizoaffective disorder (both as an adjunt)

Generally do not give lithium for acute manic emergencies (insufficient calming effects alone)

57
Q

Lithium ADME

A

A: absorbed well orally
D: slow release preperations are useful to minimize toxic peaks
M: not known
E: excreted in urine, 80% of filtered is reabsorbed, altering clearance can alter blood levels, narrow TI indicates blood level monitoring

58
Q

Lithium drug interactions

A

Any drug that increases lithium excretion will decrease lithium blood levels (mannitol, acetazolamide, theophylline)
Sodium and lithium use the same transporter, so an increase in sodium excretion causes a decrease in lithium excretion, leading to increased lithium levels and therefore toxicity

59
Q

Lithium toxicity

A

TI very low, overdose can occur with normal therapy - often due to changes in renal clearance
>2 mEq/L considered toxic

60
Q

What anticonvulsants are being used as adjuct with lithum for maintenance?

A

Valproic acid and Iamotrigine
Becoming first line for treating bipolar II
If used as monotherapy (without lithium) for maintenance, unknown efficacy with severe BP

61
Q

Iamotrigine unique indication and side effects

A

Unique indication: anti-depressant (unproven for other anticonvulsants). Study found that lithium more effective for mania and Iamotrigine better for preventing depression = use in combo!
Side effects: Stevens-johnson syndrome rash - less common

62
Q

Olanzapine indication and AE

A

Indication: bipolar I, especially for manic emergencies

Side effects: weight gain/diabetes type 2 risk (potential problem for all atypical antipsychotics)

63
Q

Benzodiazepines indication

A

Acute treatment of manic episodes and for treating the anxiety often associated with bipolar disorder

64
Q

Why might you use another mood stabilizer over lithium?

A

Quicker response, safer (larger TI), better tolerated in many pts, may prevend “kindling” effect (suppress subsequent episodes), efficacy very good in milder disease forms (especially bipolar II)

However, efficacy may be lower in severe disease (Iamotrigine is the exception bc it is better at treating depressive episodes than lithium)

Pharm II Exam I (5 decks)

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