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Pharm Test 3 > Depression and Bipolar Disorder > Flashcards

Depression and Bipolar Disorder Flashcards

1
Q

Serotonin-Selective Reuptake Inhibitors (SSRI)

A

Fluoxetine (Prozac)

Sertraline (Zoloft)

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2
Q

Serotonin-Norepinephrine Reuptake Inhibitors (SNRI)

A

Duloxetine (Cymbalta®)

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3
Q

Tricyclic antidepressants

A

Amitriptyline (Elavil®)

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4
Q

Monoamine oxidase inhibitor (MAOI)

A

Phenelzine (Nardil)

Selegiline (Emsam)

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5
Q

Atypical Antidepressants

A

1) Bupropion (Wellbutrin, BuSpar®) – blocks NET, DAT, may increase DA and NE release
2) Mirtazapine (Remeron) – alpha-2 adrenergic, 5HT2, 5HT3 receptor antagonist

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6
Q

3 Types of depression

A

i. Reactive Depression – short-term pharmacotherapy only if necessary

ii. Major Depression – antidepressants are most effective here. Usually requires
long term treatment of 6 months +, potentially for years.

iii. Bipolar Depression – a complex disorder that is treated with antidepressants
(controversial) , anti-manic drugs (lithium, valproate, carbamazepine,
lamotrigine) and sometimes antipsychotics.

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7
Q

Major Depressive Disorder

A

MDD is a Syndrome.
Includes Mood, but also Vegetative, Cognitive, Impulse control, Behavioral
and Somatic features.

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8
Q

Why is the diagnosis for MDD frequently missed?

A

Misinformation and stigma limit treatment; e.g., depression is due to emotional weakness, bad parenting, sinful behavior, etc.

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9
Q

What is the monoamine theory of depression?

A

Depression results from a functional deficit of monoamine transmitters at certain sites in the brain while mania results from functional excess.

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10
Q

Sites of antidepressant drug actions

A 
NET- NE transporter
SERT- serotonin transporter
MAO- monoamine oxidase
5HTR- Serotonin receptors
a1AR- alpha 1 adrenergic receptors
BAR- beta adrenergic receptors
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11
Q

Selective Serotonin Reuptake Inhibitors (SSRI) do what?

A

selectively inhibit the serotonin transporter (SERT), blocking serotonin reuptake into nerve terminals.

-These drugs increase the levels of serotonin in the synaptic cleft.

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12
Q

Serotonin-Norepinephrine Reuptake Inhibitors (SNRI) do what?

A

inhibit SERT and the norepinephrine transporter (NET), blocking 5HT and NE reuptake into nerve
terminals.

-These drugs increase the levels of both serotonin and norepinephrine in
the synaptic cleft.

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13
Q

The Tricyclic Antidepressants (TCA) do what?

A

inhibit SERT and NET, blocking 5HT
and NE reuptake into nerve terminals.

-These drugs also increase the levels of both
serotonin and norepinephrine in the synaptic cleft.

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14
Q

Bupropion inhibits the dopamine transporter (DAT) and NET. Bupropion increases what?

A

the levels of both dopamine and norepinephrine in the synaptic cleft. The importance of dopamine in depression is not clear, but several drugs that are effective antidepressants act to increase synaptic dopamine levels.

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15
Q

Inhibition of 5HT2 receptors is most 1_________. Receptor inhibition blocks presynaptic regulation (inhibition) of neurotransmitter release, leading to
2._________ release of 5HT and so increases synaptic levels.

A
  1. Important

2. Increased

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16
Q

True or False? Although the monoamine hypothesis cannot completely explain the etiology of
depression, pharmacological manipulation of monoamine transmission remains the
most successful therapeutic approach.

A

TRUE!!!!

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17
Q

True or false? While pharmacological effects of antidepressants (increased NT availability are immediate, the therapeutic effects of these compounds are immediate as well.

A

False: the therapeutic effects of these compounds TAKE SEVERAL WEEKS to develop. The onset of therapeutic effect coincides with a compensatory down regulation in receptors.

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18
Q

What is the prototype SSRI?

A

Fluoxetine

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19
Q

Mechanism of action for fluoxetine?

A

Mechanism of action: highly selective inhibition of 5HT reuptake (serotonin transporter –SERT). >300-fold selective for SERT over NET.

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20
Q

Therapeutic uses for fluoxetine

A

Therapeutic uses.

(1) MAJOR DEPRESSIVE DISORDER
Initially produces little or no improvement.
Adaptation of the 5HT systems require time.
However, most side effects begin.

After 3-8 weeks the therapeutic effects appear.
Tolerance develops to most side effects.
Sexual dysfunction side effects may begin.

If no improvement after 6-8 weeks, try another antidepressant

Fluoxetine also approved for treatment of:

(2) Obsessive Compulsive Disorder
(3) Bulimia Nervosa
(4) Panic Disorder
(5) Premenstrual dysphoric disorder

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21
Q

Fluoxetine inhibits ________. It undergoes ____________ metabolism.

A

2D6; First pass

22
Q

What is the black box warning on antidepressants?

A

increased risk of suicidal thinking and behavior in children, adolescents and young adults. Appears to be short term risk.

23
Q

These side effects are at what type of receptors:
(i) Agitation
(ii) Akathesia.
(iii) Initial anxiety. Overall SSRI effect is anxiolytic.
(iv) Panic attacks
(v) Insomnia. Disrupt slow wave sleep.
Can develop myoclonus.
(vi) Sexual dysfunction (20-40%)
Anorgasmia, delayed orgasm, decreased libido, impotence. May continue
after drug cessation.

A

5HT2 receptors - tolerance develops to most

24
Q

These side effects are at why type of receptors:

(i) Nausea
(ii) Gastrointestinal distress
(iii) Diarrhea
(iv) Headache
(v) Weight loss – does not seem to return.

A

5HT3 receptors – tolerance develops.

25
Q

Can you name some Rebound effects from rapid withdrawal of SSRIs?

A

Dysphoria, agitation, anxiety, confusion, seizures, paranoia.

Fluoxetine is one of the least likely to cause rebound effects.

26
Q

What is The most commonly prescribed SSRI

A

Sertraline (Zoloft®): 25 or 50 mg/day  200 mg/day for all uses.

27
Q

Sertraline appears to be BETTER/POORLY tolerated (fewer SE) than fluoxetine.
Sertraline may be more efficacious in severe ____________?

A
  1. Better

2. Depression

28
Q

What is the mechanism of action for Duloxetine (Cymbalta®)?

A

Mechanism of action: inhibition of 5HT and NE reuptake: 7-fold selective for SERT over
NET. This is similar to the selectivity of the TCAs.
Duloxetine is approved for treatment of several pain conditions as well.

29
Q

Therapeutic uses for Duloxetine (Cymbalta®)?

A

(1) Major depressive disorder
(2) Generalized anxiety disorder
(3) Diabetic peripheral neuropathy (pain)
(4) Fibromyalgia (pain)
(5) Chronic musculoskeletal pain (pain)

30
Q

Pharmacokinetics for Duloxetine (Cymbalta®)?

A

(1) Well absorbed orally. Peak concentration 6-10 h.
(2) Food slows absorption
(3) Metabolized by CYP 1A2 and 2D6.
Inhibits CYP 2D6. (Blocks tamoxifen activation).
(4) Metabolites are inactive.
Half-life = 11-12 hr.

31
Q

True or false? The side effects for Duloxetine (Cymbalta®) are similar to SSRIs?

A

True

32
Q

What is one big major complication for SNRIs?

A

Narrow angle glaucoma

33
Q

Mechanism of action for Amitriptyline (Elavil®)?

A

Mechanism of action: inhibition of 5HT and NE reuptake: 8-fold selective for SERT over
NET

34
Q

Therapeutic uses for Amitriptyline?

A

Therapeutic uses.

(1) Major depressive disorder
(2) Used off-label for many indications involved with pain (migraine prophylaxis, diabetic
neuropathy) .

35
Q

Pharmacokinetics for Amitriptyline?

A

Well absorbed after oral administration

(a) Metabolized primarily by CYP 2D6, demethylation.
(b) Half is metabolized to nortriptyline (Aventyl®, Pamelor®)
(c) Further metabolites of amitriptyline and nortriptyline are active
(d) Half-life = 30 hr for active metabolites.

36
Q

TCAs: Mechanisms of adverse effects? Consider TCAs as 5 drugs in 1.

A

(a) Serotonin Reuptake Inhibitor
(b) Norepinephrine Reuptake Inhibitor
(c) Acetylcholine Muscarinic Receptor Antagonist
(d) Alpha‐1 Adrenergic Receptor Antagonist
(e) Histamine Receptor Antagonist

37
Q

True or false? TCAs are toxic? Acute poisoning is common and potentially life-threatening?

A

True

38
Q

What do you treat TCA overdose with?

A

Sodium bicarbonate

39
Q

Mechanism of action for Phenelzine (Nardil®)?

A

Mechanism of action: Irreversible inhibition of monoamine oxidase (MAO) A & B
(non-selective suicide substrate). The pharmacologic effects continue after drug
has been cleared.

40
Q

Pharmacokinetics for Phenelzine (Nardil®)?

A

Pharmacokinetics

(1) Rapidly absorbed after oral administration.
(2) Transformed by acetylation in the liver.
(a) 50% of the population are slow acetylators.
(b) Dosage titration is slow.

41
Q

List two most common side effects for Phenelzine (Nardil®)?

A

(1) Orthostatic hypotension - common

(2) Sedation - common

42
Q

MAOIs may lead to the “cheese reaction” because MAO metabolizes what?

A

Tyramine

43
Q

Mechanism of action for Selegiline (Emsam®

: transdermal patch)?

A

Mechanism of action: Irreversible inhibition of monoamine oxidase (MAO) A & B –
suicide substrate. Pharmacologic effects continue after drug has been cleared.
Selegiline at anti-depressant doses inhibits MAO-A and MAO-B. MAO-A is the
therapeutic site for anti-depressant action.

44
Q

Pharmacokinetics for Selegiline (Emsam®

: transdermal patch)

A

Pharmacokinetics
(1) 25-30% absorbed with transdermal patch.
(2) Metabolized primarily by CYP 2B9. Metabolites are active
(N-desmethylselegiline, amphetamine, methamphetamine).
(a) Half-life 18-25 hr transdermally.
(b) Regeneration of enzyme requires new protein synthesis (< 2 weeks).

45
Q

Mechanism of action for Bupropion (Wellbutrin®) –

A

Mechanism of action: inhibition of dopamine transporter (DAT) and NET, selective for
DAT over NET. May increase DA and NE release from terminals.

46
Q

Pharmacokinetics for Bupropion (Wellbutrin®)

A

Pharmacokinetics
Well absorbed after oral administration
(a) Metabolized by CYP 2B6.
(b) Half-life = 11-24 hr for bupropion and active metabolites.

47
Q

True or false? Bupropion (Wellbutrin®) can be used off label to treat sexual dysfunction due to other antidepressants, especially SSRIs?

A

True

48
Q

The mechanism of action for Mirtazapine (Remeron®) is complex:

(1) Antagonist at presynaptic alpha-2 adrenergic receptors: increases release of both
___ and ___.

(2) Antagonist at 5HT2 and 5HT3 receptors.
(a) Inhibition of presynaptic 5HT2 receptors increases release of __ and __.
(b) Inhibition of 5HT3 receptors has an ____-______ effect (cf. ondansetron).

(3) Antagonism of histamine H1 receptors produces ________ and ______ ____.

A

(1) Antagonist at presynaptic alpha-2 adrenergic receptors: increases release of both
5HT and NE.

(2) Antagonist at 5HT2 and 5HT3 receptors.
(a) Inhibition of presynaptic 5HT2 receptors increases release of DA and NE.
(b) Inhibition of 5HT3 receptors has an ANTI-EMETIC effect (cf. ondansetron).

(3) Antagonism of histamine H1 receptors produces SEDATION and WEIGHT GAIN.

49
Q

Major Side effect for Mirtazapine?

A

Somnolence

50
Q

What drug is a mood stabilizer?

A

Lithium, antiepileptic drugs

51
Q

Mechanism of action of lithium?

A

Not clear. Alters intracellular signaling pathways. Inhibits NE and DA release indirectly. Alters ion transport in cells.

Pharm Test 3 (8 decks)

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