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Pharmacology > Antidepressant Agents > Flashcards

Antidepressant Agents Flashcards

1
Q

What is it called when depression and mania occur simultaneously? What is it called when you have rapid switching between these two different states?

A

Mixed mood state

Called rapid cycling, often from hypomania to depression

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2
Q

What is dysthymia?

A

A less severe but long-lasting form of depression

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3
Q

What are the diagnostic criteria for depression?

A

AD to SIGECAPS for two week period

At least 1 of two major criteria (AD)
Anhedonia and Dysphoria - inability to feel pleasure and depressed mood

At least 5 of the minor criteria (SIGECAPS)
Sleep - increased or decreased
Interest - decreased
Guilt - increased
Energy - decreased
Concentration - decreased
Appetite - increased or decreased
Psychomotor depression
Suicide ideation
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4
Q

How long is a typical major depressive episode, and what is the greatest predictor of them?

A

6 to 24 months, number of prior episodes predicts likelihood of developing subsequent ones

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5
Q

What is the monoamine receptor hypothesis of depression and how does this correlate with treatment?

A

Decreased levels of NE / 5-HT leads to upregulation of receptors as a compensatory mechanism.

Treatment is effective after long-term increase in 5-HT and/or NE levels leads to downregulation of receptors once more, and a return to equilibrium

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6
Q

What treatment is recommended in patients with MDD and a high suicide risk / treatment resistant depression or depression in pregnancy? Side effects?

A

Electroconvulsive therapy

Amnesia around time of ECT, confusion, muscle aches

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7
Q

What is the mechanism of action of St. John’s wort and its drug interaction of concern?

A

It has some mild MAO-inhibiting properties as herbal treatment for mild / moderate depression.

Induces CYP3A4

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8
Q

What is the difference between MAO-A and MAO-B?

A

MAO-A - present in GI tract and liver, preferentially metabolizes 5-HT and NE, linked to depression
MAO-B - present in platelets and lymphocytes, preferentially metabolizes DA

Both will metabolize tyramine, but MAO-A inhibitors most important in GI tract (restrict diet here)

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9
Q

What are the two clinically important MAO inhibitors? What is their mechanism of action?

A
  1. Tranylcypromine - try a sip of wine
  2. Phenelzine - funnel leading into bottle of wine

They nonselectively bind and irreversibly inhibit MAO-A and MAO-B

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10
Q

What is the clinical indication for MAO inhibitors and who is it most useful in?

A

Second-line treatment for MDD which is treatment-resistant. Most useful in those with other complications like significant anxieties, phobias, or hypochondriasis

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11
Q

What serious syndromes can happen from food / drug interactions with MAO? Why?

A

Hypertensive crisis and serotonin syndrome

Hypertensive crisis because tyramines are normally metabolized by MAO-A, and work similar to amphetamines by inhibiting / reversing VMAT and causing catecholamine overload

Serotonin syndrome is due to buildup of 5-HT in the synapse, especially with other SSRI’s / SNRI’s

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12
Q

What is one strange cardiovascular side effect of MAOI’s which has not been explained? What are the other general side effects beside this?

A

Orthostatic hypotension -> strange because it causes NE buildup.

Other side effects are otherwise the same as SSRI’s

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13
Q

What are the important tricyclic antidepressants?

A

Imipramine
Desipramine
Clomipramine

Think of “imprint” from dodgeball

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14
Q

What is the mechanism of action of TCA’s? What other receptors do they inactivate?

A

Primary:
Blockage of NE and 5-HT reuptake, and blockade of 5-HT2 subtypes

Secondary: "Dirty drugs" - blockade of:
H1 receptor - swatting bee dodgeball
alpha1 receptor - alpha1 cupcake candle
M1 receptor - anticholinergic tea party
Na channels - peanut stand, heart effects
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15
Q

What are the clinical indications of TCA’s?

A

Major depressive disorder - second line due to toxicity

Chronic pain syndromes - i.e. migraine bell, diabetic neuropathy diasweeties

OCD - kid compulsively sorting marbles

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16
Q

What TCA is given for OCD?

A

Clomipramine

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17
Q

What are the contraindications of TCA’s and why?

A

Prostatism / narrow angle glaucoma - anticholinergic effects
Post-MI and heart block - anticholinergic effects
Bipolar disorder -> can lead to a switch syndrome (mania after depressive episode)

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18
Q

What are the adverse effects of TCA’s not in overdose?

A
  1. Weight gain
  2. Anticholinergic effects
  3. Cardiovascular effects - tachycardia (M1), orthostatic hypotension (alpha 1), conduction delay and arrhythmias (Na channel)
  4. CNS - drowsiness / lethargy (H1), lowers seizure threshold - shaking kid
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19
Q

What are the features of TCA overdose?

A

Other than craziness from anticholinergic effect:

3 C’s

Coma
Convulsions - seizures, agonist to GABA-A receptor?
Cardiotoxicity - Na channel interference can cause prolonged QRS and QT -> leads to TdP arrhythmia

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20
Q

How should TCA overdose be managed?

A

IV diazepam to control seizures, and gastric lavage if possible to flush out TCA’s. Otherwise, treatment is supportive.

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21
Q

Why are SSRI’s the first line treatment for depression?

A

They have no receptor blocking properties, lack cardiotoxic effects, and are safe in overdose

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22
Q

Which SSRI is most selective but has dose-dependent cardiac effects and what is the effect?

A

Citalopram / escitalopram

QT prolongation

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23
Q

List the major SSRIs?

A
  1. Fluoxetine - Fly Out
  2. Citalopram / Escitalopram -The City
  3. Fluvoxamine
  4. Paroxetine - Parrot Air
  5. Sertraline - DeSERT
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24
Q

Which SSRI is most associated with weight gain?

A

Paroxetine

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25
Q

What are the other indications for SSRI’s other than depression?

A 
Bipolar depression
OCD - dwight with his stapler
PTSD - dogtags
Anxiety disorders - guy hiding behind desk + anxious worker, + the scream screensaver
Bulimia - woman at desk
PMDD (premenstrual dysphoric disorder)
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26
Q

What are the CNS, GI, and sexual side effects of SSRI’s?

A

CNS - stimulant effect - can cause insomnia, anxiety, agitation, and restlessness
GI - NVD
Sexual dysfunction - big one, delayed orgasm, decreased libido, decreased arousal anorgasmia

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27
Q

What are the dosing strategies used to manage SSRI-induced sexual dysfunction?

A

Reduce the dosage or permitting “drug holidays” -> skip doses on the weekends

28
Q

What major medication is considered an NDRI?

A

Bupropion -> NET DAT ball pro

Norepinephrine dopamine reuptake inhibitor

29
Q

What are the clinical indications for bupropion?

A

Firstline treatment in depressed patients not responsive to SSRI
Augmentation therapy for SSRI/SNRI
Antidote to SSRI-induced sexual dysfunction

30
Q

Why might bupropion be superior to SSRI’s / SNRI’s in some cases?

A

Not associated with sexual dysfunction or weight gain

31
Q

What are the adverse effects of bupropion? How does this relate to contraindication?

A

Can cause insomnia, nightmares, anxiety, and seizures

Contraindicated (seizure risk) for patients with history of CNS tumor, seizures, head trauma, or eating disorders - think of girls having a seizure with their eating disorders on the basketball court in sketchy

32
Q

What are the two major SNRI’s?

A

Duloxetine (dual copier / scanner) and venlafaxine (fax machine)

33
Q

Other than depression, what are SNRI’s good for treating?

A

Neuropathic pain (diasweeties machine with broken cord) as well as fibromyalgia (fiber bars)

34
Q

What is duloxetine also particularly good for?

A

Diabetic neuropathy and chronic musculoskeletal pain (back pain or knee pain)

35
Q

Other than the typical SSRI side effects, what are two extra side effects which can be troublesome in SNRI’s?

A
  1. Nausea

2. Hypertension (due to increased NE, think of the guy working on the fax machine with steam coming from his ears)

36
Q

What drug is a SPARI and what does that mean? What is its mechanism?

A

Serotonin 1A Partial Agonist / Reuptake Inhibitor

Vilazodone

37
Q

What is Vilazodone used for?

A

Augmentation therapy for increasing tolerability of SSRIs / SNRI’s

Lacks the sexual dysfunction and weight gain

38
Q

What drug class is trazodone in? Mechanism of action?

A

Trazodone trombone

In the SARI class - Seratonin antagonist / Reuptake Inhibitor

Antagonizes the 5-HT-2 receptors in specific (basketball number 52), also the alpha 1 receptor (burnt out alpha1 lighter) and H1 receptor (bee being swatted on head of player)

39
Q

What does trazodone do at low and high doses?

A

Low doses - hypnotic - antagonizes the receptors without enough serotonin to cause stimulation
High doses - antidepressant

40
Q

What are the main clinical indications of trazodone?

A
  1. Augmentation therapy for SSRI/SNRI to reduce insomnia, allowing better sleep
  2. Treatment of insomnia alone

Rarely used as monotherapy

41
Q

What are the side effects for trazodone / one good non-side effect?

A

Orthostatic hypotension (alpha 1 antagonist), priapism (drug is sometimes called trazabone)

It lacks sexual side effects!

42
Q

What does NaSSA stand for and what drug falls in this class?

A

Noradrenergic and Specific Serotonin Antagonist

Mirtazapine

43
Q

What serotonin receptors are responsible for anxiety, anorexia, insomnia, sexual dysfunction, nausea, and GI problems?

A

5-HT-2: Anxiety, insomnia, sexual dysfunction, anorexia

5-HT-3: Nausea, GI problems

44
Q

What is the mechanism of action of Mirtazapine?

A

Alpha-2 antagonist -> increases NE and serotonin in the synapse

H1 antagonist: insomnia at night but possible daytime sleepiness

Antagonizes 5-HT-2 and 5-HT-3: Less nausea, GI, insomnia, and anxiety

Net effect is boosted 5-HT to 5-HT-1 receptor: decreased depression

45
Q

What are some side effects of mirtazapine?

A

Blocks 5-HT-2: may cause weight gain (fat guy watching the game)

Histamine blockage can cause sedation (fat guy sleeping)

46
Q

What are the major clinical indications of mirtazapine?

A

Depression in elderly patients with insomnia + weight loss - can cause sedation + weight gain

Also augmentation for SSRI / SNRI due to lack off sexual dysfunction (people kissing on megatron)

47
Q

What class of drugs is Nefazodone in and what does it share all its characteristics with?

A

SPARI - like trazodone

48
Q

What are the side effect differences between TCAs and newer SSRIs/SNRI’s?

A

TCAs: Sedation, anticholinergic, orthostatic hypotension, and weight gain

SSRIs: Agitation/insomnia, GI effects, and sexual dysfunction

49
Q

What antidepressants have the shortest half lives and why? What is their elimination?

A

SNRI’s, because they are the only antidepressants which are not highly protein bound to act as a reservoir

All are renally eliminated after hepatic metabolism

50
Q

What antidepressant has the longest halflife, why, and what must be done before switching to a MAOI? What period is sufficient for others?

A

Fluoxetine

  • has active metabolites
  • need to wait 5 weeks for plasma concentration to drop to guarantee no serotonin syndrome
  • 2 weeks is enough for others (5 drug half lives minimum)
51
Q

What are bupropion, nefazodone, duloxetine, and all SSRI’s known for?

A

Inhibition of CYP450 enzymes and increased plasma concentrations, which could lead to hypertensive crisis or serotonin syndrome

52
Q

What is the treatment for MAO-induced hypertensive crisis and a few symptoms?

A

Phentolamine - alpha1/alpha2 antagonist

high BP, headache, nausea / vomiting / sweating, dilated pupils, chest pain

53
Q

What types of cold medications are contraindicated with MAOs?

A

Sympathomimetics like pseudoephedrine and phenylephrine

54
Q

What are the clinical features of serotonin syndrome? When does this most often occur?

A

Hyperpyrexia (high temp), hyperreflexia, hypertension, agitation, tremor, tachycardia, and myoclonus

Any serotonin reuptake blocking agent (including drugs of abuse like cocaine, and dextromethorphan / linezolid) + a MAO-Inhibitor

55
Q

What should be done to treat serotonin syndrome?

A

Muscle relaxants, antiseizure drugs, and the 5-HT antagonist called cyproheptadine (silly pranks prohibited in sketchy)

56
Q

How long should trial therapy for an antidepressant last to see if it works? Why?

A

8-12 weeks

Takes 2-4 weeks to see improvement at all, and 6-8 weeks to see full effect

57
Q

What are the three phases of MDD and their approximate lengths?

A
  1. Acute treatment phase - 3 months
  2. Continuation treatment phase - 4-9 months
  3. Maintenance phase - variable
58
Q

Through what phases of MDE (major depressive episode) should you be treated and why?

A

Acute and continuation phase -> dropping of treatment during continuation phase could result in a relapse depression (most MDE’s last 6 months or longer). For this reason, most patients should take antidepressants for at least a year

59
Q

Give three scenarios in which life treatment for MDD during the maintenance phase is warranted?

A
  1. Three or more previous MDE’s - 3 strikes and you’re on
  2. Two or more MDE’s and greater than age 50
  3. One or more MDE and greater than age 60
60
Q

What are two reasons why we taper SSRI’s / SNRI’s with short half lives (other than fluoxetine)?

A
  1. Withdrawal syndrome is decreased, which includes - insomnia, anxiety, fatigue, mood changes, and GI disturbances
  2. If gradual tapering shows early signs of depression, dose can be restored without risk of having to start over on 8-12 week clock
61
Q

What is the general treatment algorithm for antidepressants if they arent working?

A

first line SSRI/SNRI/NDRI monotherapy -> augmentation therapy i.e. SSRI + NDRI -> second line monotherapy -> ECT / Vagus nerve stimulation

62
Q

What SSRI’s are safest and most dangerous in pregnancy?

A

Safest - Fluoxetine and citalopram

Dangerous - Paroxetine, particularly ASDs and VSDs of the heart

63
Q

What antidepressants are approved in children under 18?

A

Fluoxetine and escitalopram

64
Q

Are all antidepressants currently out equally effective in treating depression?

A

Yes, actually. Just need to worry about side effects

65
Q

For patients with psychotic depression, what should they be on?

A

An antipsychotic medication combined with antidepressant

Pharmacology (54 decks)

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