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Psych Pharm > Antidepressants and Mood Stabilizers > Flashcards

Antidepressants and Mood Stabilizers Flashcards

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1
Q

What are the core symptoms of depression?

A
  • persistent sad, anxious, tense, empty mood
  • feelings of hopelessness, pessimism
  • feelings of guilt, worthlessness, helplessness
  • persistent physical symptoms that don’t respond to treatment such as headaches, digestive disorders, and chronic pain
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2
Q

What are the vital signs of depression?

A
  • difficulty concentrating, remembering, making decisions, loss of interest or pleasure in hobbies and activities, decreased energy, fatigue, being slowed down, insomnia, oversleeping, thoughts of death of suicide, suicide attempts, restlessness
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3
Q

What are the classifications of depression?

A
  1. Reactive (secondary) - 60%, mainly core symptoms
  2. Major depressive disorder (endogenous) - 25%, core and vital symptoms, peak onset 20-40. Responsive to antidepressant drugs and ECT
  3. Bipolar Disorder (manic) - 15%, alternating episodes of depression and mania. treated w/ mood stabilizers and antidepressants
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4
Q

Biogenic Amine hypothesis

A
  1. functional deficit in monoamines thought to cause depression
  2. NE and 5HT increase immediately but takes weeks = therapeutic lag
    - delayed effect b/c of beta receptors, cAMP, and serotonergic neurotransmission, neurogenesis
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5
Q

What receptors can be targeted at presynaptic areas? post synaptic?

A
  1. presynaptic : MAOI, NE works at alpha 2 AR, 5HT works at 1D/2A, TCA’s inhibit reuptake as well as SNRI and SSRI
  2. Postsynaptic : TCAs act at alpha 1 AR
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6
Q

What is the BBW for antidepressants?

A

risk of suicidal thinking to all everyone, closely monitored especially during initial weeks of treatment

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7
Q

What are some other common problems in antidepressant therapy?

A
  1. placebo effect
  2. St john’s warts for mild to moderate depression - no more effective than placebo and interferes w/ various medications
  3. Pharmacogenomics or resistance to antidepressant treatment - many of the drugs are substrates for ABCB1 at the BBB liming drug to accumulate in brain and have its effects.
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8
Q

What are the antidepressants that are substrates of MDR1?

A

citalopram, venlafaxine, paroxetine, amitriptyline

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9
Q

MOA of TCAs

A
  • inhibit reuptake of 5HT and NE into presynaptic terminals
  • potentiates and prolongs actions of these neurotransmitters
  • also blocks mAch, 5HT, and Histamine receptors
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10
Q

ADE of TCAs

A
  1. orthostatic hypotension - alpha AR antagonism
  2. blurred vision, worsening of narrow-angle glaucoma, dry mouth, constipation, urinary retention, tachycardia, confusion - antagonism of mAchR
  3. sedation - antagonism of histamine and alpha AR
  4. metabolic/endocrine - weight gain, sexual disturbances
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11
Q

TCA overdose symptoms

A
  • overall low TI

- CV effets, acidosis, delirium, seizures

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12
Q

PK of TCA

A
  • most incompletely absorbed due to 1st pass
  • high lipid solubility and distribution to brain and fat
  • highly bound to plasma protein (high Vd)
  • tricycling ring subject to oxidation (CYP2D6) and conjugation
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13
Q

drug interactions of TCA

A
  • EtOH and other sedatives, antiparkinson drugs, antipsychotic drugs, biogenic amines, competition for plasma protein binding
  • can block effects of clonidine
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14
Q

MOA of trazodone

A
  • mod inhibition of 5HT reuptake but mainly 5HT2a antagonist and 5HT1a partial agonist
  • short half life
  • inhibits CYP 3A4
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15
Q

MOA of mirtazepine

A
  • enhances release of 5HT and NE by antagonizing presynaptic alpha-2ARs. Also antagnoizes 5HT2 receptors
  • potent antihistamic = sedation
  • increased weight gain
  • less GI and sexual disturbances than SSRIs
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16
Q

MOA of bupropion

A
  • weak blocker of DAT, SERT, and NET
  • active metabolite is NE reuptake blocker
  • also used in smoking cessation
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17
Q

ADE of bupropion

A
  • agitation, anxiety, restlessness, risk of seizure
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18
Q

MOA of Venlafaxine

A
  • inhibits 5HT and NE reuptake
  • devoid of antihistaminergic, anticholinergic, and antiadrenergic properties
  • doesn’t have TCA like side effects
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19
Q

ADE of venlafaxine

A

HTN, sweating dizziness, nausea, anxiety

20
Q

MOA of duloxetine

A

SNRI

  • most potent available
  • highly bound to plasma
  • metabolized by CYP2D6 and CYP 1A2
21
Q

SSRI MOA

A

selective inhibition of SERT - potentiate and prolongs action of 5HT

22
Q

Clinical effects of SSRIs

A
  1. acute - CNS stimulation, anxiety, agitation

2. Chronic - improvement of most or all clinical symptoms, CNS activation remains

23
Q

ADE of SSRIs

A

Nausea, decreased libido, sexual dysfunction

  • lower incidence of CV and anticholinergic effects
  • high TI (decreased risk of overdose)
  • increased risk of birth defects w/ paroxetine
24
Q

PK of SSRIs

A
  • high protein binding
  • long half life
  • most metabolized by CYP2d6, 2C19, 3A4 and can exhibit weak to strong inhibition of 2D6 and 2C19
25
Q

drug interactions for SSRIs

A
  • MAOIs contraindicated (must wait at least 2 weeks)
26
Q

MAOI examples

A

Phenelzine: MAOA
Selegiline: MAOB

27
Q

what is serotonin syndrome?

A
  • onset w/in 24 hours of overdose or concurrent MAOI. due largely to overstimulation of 5HT1A receptors in central grey and medulla
  • hyperpyrexia, hyperreflexia, tremor, shivering, myoclonus, agitation, seizures, confusion, delirium, CV collapse, and coma
28
Q

What are some things that can cause serotonin syndrome?

A
  • increased 5HT release (amphetamines, MDMA)

- 5HT agonists (LSD, buspirone, L-trp)

29
Q

SSRI examples

A 
Citalopram
Fluoxetine
Paroxetine
Sertraline
Fluvoxamine
30
Q

indications for MAOI

A
  • when pt is unrepsonsive to treatment w/ other antidepressant and for whom ECT is not suitable.
  • also used in panic disorder and agoraphobia
31
Q

MOA of MAOI

A

blocks oxidative metabolism of monamines by irreversible inhibition of MAO-A and MAO-B in nerve terminals

32
Q

Clinical effects of MAOI

A
  1. acute - CNS stimulation, agitation, possibly euphoria

2. chronic - improvement of most or all symptoms, CNS activation remains

33
Q

ADE of MAOI

A

sleep disturbance, orthostatic hypotension, weight gain, some sex dysfunction

34
Q

PK of MAOI

A
  • inactivated by acetylation
  • daily dosing required
  • generally well absorbed from GI tract
35
Q

drug interactions for MAOI

A
  • foods w/ high amounts of tyramine (cheese)
  • sympathomimetic drugs –> acute hypertensive reaction
  • meperidine, dextromethorpham –> hyperpyrexia, delirium, convulsions, coma, death
  • SSRIs
36
Q

mood stabilizer drugs

A
  • lithium
  • valproate
  • carbamazepine
37
Q

Lithium MOA

A
  • poorly understood. 1st line for bipolar disorder
  • possibly via inhibition of IP signaling
  • also inhibits nt-stimulated AC activity
38
Q

ADE of Lithium

A
  • very narrow therapeutic window
    toxic effects at > 1.5mEq/L
  • neurologic/ psych - tremor, ataxia, hyperactivity, aphasia, sedation, fatigue
  • edema, mild hypothyroidism
  • polydipsia, polyuria (nephrogenic DI)
  • bradycardia - tachycardia
  • acne, folliculitis, exacerbates psoriasis
39
Q

drug interactions for Li

A
  • diuretics and NSAIDS
40
Q

anticonvulsants for bipolar disorder

A
  • may be used to treat milder forms of bipolar disorder
  • able to increase dose faster, quicker response, better TI than Li
  • less experience, efficacy questionable in severe disease
  • used usually in combo w/ Li or anti-psychotics
41
Q

MOA of valproate

A
  • inhibits Na channels by stabilizing inactivated state
  • blocks Ca channel
  • stimulates GABA synthesis and inhibits GABA degeneration
  • at high doses, increases resting K conductances
42
Q

drugs interactions of valproate

A
  • inhibits its own metabolism and of other 2C drugs
43
Q

ADE valproate

A

nausea, ab pain, heartburn

  • sedation
  • hepatotoxicity
44
Q

MOA of carbamazepine

A
  • inhibits Na channel
45
Q

PK of carbamezpine

A
  • 70% bound to plasma protein
  • distributes slowly
  • metabolized by CYP3A4 to active metabolite
46
Q

drug interactions of carbamazepine

A
  • enhances metabolism of many drugs via induction of cyp2C and 3A and UGTs
47
Q

ADE carbamazepine

A
  • diplopia (double vision) and ataxia
  • mild GI upset, unsteadiness
  • at high doses drowsiness
  • rash common idiosyncratic rxn
  • aplastic anemia

Psych Pharm (7 decks)

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