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Psych Pharm > Anti-depressants & Mood Stabilizers (TCAs & Atypicals) > Flashcards

Anti-depressants & Mood Stabilizers (TCAs & Atypicals) Flashcards

1
Q

Definition of depression?

A

Affective disorder w/ emotional, cognitive, behavioral, somatic regulation

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2
Q

Definition of depression?

A

Affective disorder w/ emotional, cognitive, behavioral, somatic regulation

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3
Q

Core syndrome?

A

Persistent emotion, guilt, untreatable physical symptoms

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4
Q

Pathophys of depression?

A

Decrease of monoamines (NE & serotonin)

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5
Q

When do anti-depressants take clinical effect?

A

Takes weeks

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6
Q

BBW for all anti-depressants & mood disorders?

A

<24 y/o you should monitor changes in depression, suicidal thinking, unusual behavior

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7
Q

What is reactive or secondary depression? What are its symptoms? What is its tx?

A

it is secondary to loss, drugs, alcohol, other psychiatric disorders. Symptoms: Core syndrome. Tx: remits spontaneously + responds to Rx

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8
Q

What is major depressive disorder? Symptoms? Tx?

A

Recurrent. Symptoms: core syndrome + vital signs. Tx: anti-depressants + ECT

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9
Q

What is bipolar disorder (manic depression)? Symptoms? Tx?

A

Mania + depression episodes. Symptoms: increased elation, irritable, less sleep needed, grandiose notions, increased talking. Tx: mood stabilizers + anti-depressants

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10
Q

What are the issues with pharmacogenomics?

A

ABC (MDR1/P-gp) @ BBB –> decreased access to brain

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11
Q

What drugs are substrates for MDR1?

A

Citalopram, Paroxetine, Amitriptyline, Venlafaxine

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12
Q

Non-substrates for MDR1?

A

Mirtazapine, fluoxetine

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13
Q

What are the TCAs?

A

Amitriphyline, Imipramine, Nortriptyline

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14
Q

What do the TCAs treat?

A
  • Major depression
  • Bedwetting (Imipramine)
  • OCD (Clomipramine)
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15
Q

MOA of TCAs?

A

decrease reuptake of 5HT and NE into presynaptic terminals –> increased actions of neuroTx + change receptor profile with treatment

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16
Q

What else do the TCAs do?

A

block ACh, 5-HT, histamine receptors (these are the basis of ADEs)

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17
Q

Are the TCAs highly lipid soluble?

A

Yes, the get into the brain and into fat

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18
Q

Are the TCAs protein bound?

A

Yes, they have a high volume of distribution and a long half life

19
Q

Describe the metabolism of TCAs?

A

Tertiary amines –> secondary amines via demethylation (imipramine –> desipramine; amitriptyline –> nortriptyline)
-Metabolized via CYP2D6

20
Q

What are the acute effects of TCAs?

A

drowsy + decreased cognition

21
Q

chronic effects of TCAs?

A

increased cognition; NOT euphoria

22
Q

DDIs w/ TCAs?

A

EtOH, other sedatives; TCAs block clonidine

23
Q

ADEs of TCAs?

A
  1. Orthostatic hypoTN (antagonism of alpha-adrenergic receptors)
  2. Anti-DUMBBELLS + CI Glaucoma (antagonism of ACh receptors)
  3. Sedations (antagonism of histamine + alpha adrenergic receptors)
  4. Metabolic/Endocrine: gain weight + sexual disturbance
24
Q

TCAs have a low TI. What does OD cause?

A

Arrhythmia, cardiac failure, CHF

  • Acidosis, delirium, seizure
  • FA says Tri-C’s: Coma, Convulsions, Cardiotoxicity
25
Q

What are the atypical anti-depressants?

A

Amoxamine, Maprotiline, Trazadone/Nefazodone, Mirtazepine, Bupropion, Venlafaxine, Duloxetine
*BoopMir MapTraz & Amox VenDul

26
Q

Atypical anti-depressants treat?

A

Major depression

27
Q

Amoxapine MOA?

A

Basically a TCA that is a dopamine antagonist

28
Q

Amoxamine ADE?

A

DA antagonism –> extrapyramidal effects (Parkinsonism)

29
Q

Maprotiline MOA?

30
Q

Maprotiline ADE?

A

seizures, sedation, orthostatic hypoTN

31
Q

Trazodone, Nefazodone use?

A

used for depression assc w/ anxiety + sleep disturbance

32
Q

Traz, Nefaz MOA?

33
Q

Traz, Nefaz PK? ADE?

A

CYP3A4 inhibitor; short half life. Nefazodone has been largely discontinued due to hepatotoxicity

  • FA: sedation, nausea, priapism, ortho hypoTN
  • *Called Trazabone (priapism)
34
Q

Mirtazepine MOA?

A

alpha 2 receptor antagonist –> increased release of 5HT + NE

35
Q

Mirtazepine ADE?

A

Antagonizes 5HT-2 recpetors; sedation (anti-histaminergic); weight gain. Less GI & sexual disturbance than SSRIs

36
Q

Bupropion is also used for?

A

Smoking cessation; formulated for slow release

37
Q

Bupropion MOA?

A

weak DA, 5HT, NE reuptake inhibitor; metabolites = SNRI

38
Q

Bupropion ADE?

A

increases monoamines –> restlessness, anxiety, seizures

39
Q

Venlafaxine MOA?

A

SSRI + SNRI w/ no antihistamine, anti-ACh, anti-adrenergic properties (avoid TCA ADEs)

40
Q

Venlafaxine ADE?

A

small sustained HTN

41
Q

Duloxetine MOA? A unique thing about it?

A

SNRI; it is the most potent SNRI available

42
Q

PK of duloxetine?

A

50% bioavailability; 95% protein bound; CYP2D6 metabolized

43
Q

Vilazodone MOA?

A

potent 5HT1a partial agonist and SSRI

Psych Pharm (10 decks)

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