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Psych and Behavior > Segars Antidepressants and Mood Stabilizers > Flashcards

Segars Antidepressants and Mood Stabilizers Flashcards

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1
Q

SSRIs work by?

Whats the result?

A
  • inhibit pre-synaptic reuptake of Serotonin (via SERT)

- results in enhanced, prolonged serotonergic neurotransmission to post-synaptic receptors

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2
Q

Do TCAs or SSRIs have more side effects?

A

-TCAs affect more side effects

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3
Q

What are the 5 side effects of SSRIs?

A
  • Sexual dysfunction
  • GI issues
  • CNS sedation or insomnia
  • weight gain/loss
  • QT prolongation
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4
Q

What are the acute withdrawal symptoms of SSRIs or all categories of antidepressants for that matter?

How do we avoid this?

A
  • flu like symptoms (Malaise, lethargy, generalized aches)
  • taper patients off when switching drugs or stopping drugs
  • patients if they forget to take a dose look and feel like death, which is a good thing for compliance I guess
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5
Q

Sweating, Hyperreflexia, Akathisia/Myoclonus, Shivering/Tremors….what is this?

what causes this?

A
  • Serotonin Syndrome

- Patients on SSRIs or any drugs that affect serotonin

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6
Q

What’s the most serious effect of SSRIs that was even worse with the TCAs?

how to avoid?

A
  • suicide, when patients take all of their drug at once. Drinking alcohol makes death even more likely
  • avoid this w/ frequent follow up and asking them suicide questions
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7
Q

NMS: Neuroleptic Malignant syndrome

What drugs cause it?
what is it?
treatment?

A

-seen w/ dopaminergic antipsychotics

-HYPO-reflexia
NORMAL pupils
NORMAL/decreased bowel sounds

-Treatment is GIVING drug dantrolene

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8
Q

Serotonin Syndrome

what causes it?
what is it?
treatment?

A

-SSRIs, SNRIs, SARAs, TCAs

-HYPER-reflexia
Clonus
DILATED pupils
HYPER-active bowels

-treatment is stopping the drugs

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9
Q

What is the strongest SSRI with high risk of drug-drug CYP450 interaction?

A

-fluoxetine (broad and strong inhibitor)

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10
Q

What are the SSRIs are least likely to of drug drug CYP450 interaction?

A
  • Citalopram
  • Sertraline
  • these are mild inhibitors
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11
Q

Difference between secondary and tertiary TCA SNRIs?

A
  • secondary inhibit NE> 5-HT

- Tertiary inhibit NE=5-HT

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12
Q

How do SNRIs work?

A

-selectively inhibit the pre-synaptic reuptake of serotonin (via SERT) and Norepi (via NET)

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13
Q

Name 3 secondary TCAs

DAN

A
  • Despiramine
  • Amoxapine
  • Nortriptyline
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14
Q

Name 4 tertiary TCAs

DACI

A
  • Doxepin
  • Amitriptyline
  • Clomipramine
  • Imipramine
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15
Q 
ALL TCAs
Desvenlafaxine
Duloxetine
Venlafaxine
Levomilnacipran
A

SNRIs

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16
Q

SNRIs + DA

A

Amoxapine

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17
Q

Classic TCA side effects?

A

-3 Cs
Cardiotoxicity (conduction abnormalities)
Coma
Convulsion

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18
Q

What is the “Quinidine-like” effect?

A
  • TCA overdose
  • Class 1 antiarrhythmic
  • prolongs QRS complex
  • slows down phase 0 depolarization
  • Na channel blockade
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19
Q

NON-TCA SNRIs have?

A

-fewer side effects

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20
Q

Which SARAs act like SSRIs?

how do they work?

A
  • trazodone
  • Nefazodone

-act like SSRIs and selectively block post-synaptoc a1 receptors on noradrenergic (NE) neurons and post synaptic 5-HT 2a

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21
Q

How does the SARA Mirtazapine work?

A
  • selectively blocks pre-synaptic a2 receptors on noradrenergic (NE) and serotonergic (5HT) neurons
  • has no SERT/NET activity
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22
Q

How do NDRIs work?

example?

A
  • inhibits pre-synaptic reuptake of Norepi (via NET) and dopamine (via DAT)
  • some evidence of enhancing pre-synaptic release of NE and DA
  • Buproprion
23
Q

What are side effects of the SARAs?

A
  • CNS depression (Traz/Mir)
  • orthostatic hypotension (Traz)
  • weight gain (Mirt)
24
Q

side effects of buproprion which are generally stimulating?

A
  • agitation
  • insomnia
  • weight loss (from depression probably)
  • seizure
25
Q

How do MAOIs work?

Are oral agents reversible or irreversible?

A
  • inhibition of MAO (A/B) increases levels of monoamines in neuronal vesicles and increase amounts of NE, 5-HT, and DA released
  • irreversible
26
Q

Phenelzine
Isocarboxazid
Tranylcypromine
Selegiline

A

MAOIs

27
Q

Which MAOI comes in patch form?
How does it work?
How strong is it?

A
  • selegiline
  • B-selective unless at high dose
  • it is the safest MAOI
28
Q

Side effects of MAOIs?

A
  • orthstatic hypotension
  • sexual dysfunction
  • weight gain
  • insomnia/agitation/nervousness
29
Q

What syndrome and crisis can be caused by MAOIs?

A
  • serotonin syndrome

- hypertensive crisis

30
Q

What must happen before starting a patient on an MAOI?

A
  • must be off other therapies due to the risk of serotonin syndrome or hypertensive crisis
  • be careful starting MAOIs after giving fluoxetine because it takes 5 weeks to leave system instead of the average 2 weeks
31
Q

What is the cause of MAOI hypertensive crisis?

which MAOI probably wont cause this?

A
  • inhibition of MAO-A in the GI leading to a buildup of tyramine
  • Selegiline probably wont cause this because it minimally blocks MAO-A in the GI tract
32
Q

-eating wine and cheese followed by……

headache, vomit/nausea, sweating, nosebleed, tachycardia, chest pain, vision change, SOB, confusion….is what?

A

-MAOI hypertensive crisis

33
Q

What class of drugs most likely causes anticholinergic effects?

examples?

A
  • TCAs

- Clomipramine and amitriptyline

34
Q

What class of drugs most likely causes drowsiness?

what two random exceptions do too?

A

-TCAs
ie Amitriptyline and Clomipramine

  • exceptions
  • atypical agent: Mirtazapine
  • SARA: Trazodone
35
Q

What classes of drugs most likely causes insomnia/agitation?

A
  • SSRI: fluox and Sert
  • atypical: Buproprion
  • SARA: Vilazodone
  • TCA: Amoxapine
  • MOAI: Trany and Isocarb
36
Q

What classes of drugs most likely cause orthostatic hypotension?

A
  • > > TCAs: >Imipramine and < Nortriptyline
  • MAOI: phenelzine
  • SARA: Trazodone
37
Q

What classes of drugs most likely cause QT prolongation?

A

-»TCAs

38
Q

What classes of drugs most likely cause weight gain?

A

-»TCAs
…nortriptyline and deslpramine have lowest risk

-atypical: mirtazapine

39
Q

What classes of drugs most likely cause Sexual dysfunction?

A
  • > > SSRIs
  • TCAs
  • MAOI (not selegeline)
40
Q

How long does depression therapy take to work?

A
  • takes weeks

- in about 3-4 weeks you usually see 50% reduction in symptoms

41
Q

Single agent treatment rarely/always achieves remission

A

-rarely

42
Q

When do you bail out on a drug?

A

-8-9 weeks without improvement

43
Q

All depression drugs must be _______ when taking a patient off of them

A

-titrated downward

44
Q

Carbamazepine
Lamotrigine
Divalproate/Valproic Acid

A

Anti-Seizure agents used for mood stabilizers

45
Q

How does lithium work?

A
  • inhibits calcium dependent and depolarization provoked release of NE and DA
  • inhibits G protein receptors both Gi and Gs
46
Q

Side effects of Lithium?

How?

A
  • polyuria (polydipsia)
  • Nephrogenic Diabetes Insipidus!!!!

-Li competes with Na in the kidneys for reabsorption

47
Q

Why isn’t Lithium used?

A
  • diabetes insipidus

- NARROW theraputic window

48
Q

What drugs interact with Lithium

A
  • ACEIs
  • NSAIDs (>lisinopril)
  • Diuretics (> thiazides)
49
Q

Lithium can be used for what?

A
  • acute phase and maintenance of mania/bipolar 1 disorder
  • augmentation in unipolar depression
  • off label: like clozapine it reduces risk of suicide
50
Q

Carbamazepine is used for what?

A

-acute and maintenance TX for acute mania and mixed episodes (Bipolar 1)

51
Q

What is Carbamazepine dangerous?

A

-major CYP450 inducer

52
Q

What does Lamotrigine treat?

A

-only maintenance of Bipolar 1 and 2

53
Q

What does Divalproex/valproic acid treat?

A

-acute Bipolar w/o psychotic features

Psych and Behavior (10 decks)

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