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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 TCAs?

A 
Amitryptiline
Imipramine
Nortriptyline
Clomipramine
Desipramine
Doxepin
Protriptyline
Trimipramine
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2
Q

What are the Atyptical antidepressants?

A 
Bupropion
Venlafaxine
Desvenlafaxine
Duloxetine
Amoxapine
Maprotiline
Mirtazapine
Trazodone
Nefazodone
Vorioxetine
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3
Q

What are the SSRIs?

A 
Citalopram
Escitalopram
Fluoxetine
Paroxetine
Sertraline
Fluvoxamine
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4
Q

What are the MAOIs

A

Tranylcypromine
Isocarboxazid
Phenelzine

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5
Q

What are the mood stabilizers?

A

Lithium
Valproate
Carbamazepine

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6
Q

Which drug can cause symptoms of depression?

A

Reserpine

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7
Q

How do antidepressants produce an antidepressant effect?

A

Increase levels of monoamines.

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8
Q

What is the immediate effect of antidepressants?

A

Increase NE and 5-HT

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9
Q

What is the black box warning for all antidepressants?

A

Suicidal Ideation in patients up to 24 years old.

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10
Q

What herbal extract is often used by patients in Europe and the US to treat depression? Is it effective?

A

St. John’s Wort is an extract from Hypericum perforatum. It is no more effective than placebo (does not really work)

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11
Q

Patients taking St. John’s Wort for depression need to be counseled to avoid taking this if they are also taking medicine for which diseases.

A 
Particularly HIV, but also for:
heart disease 
seizures
cancers
organ transplant rejection
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12
Q

Norepinephrine acts on which presynaptic receptor? What is the effect?

A

Inhibits a2AR. Enhances 5-HT and NE release.

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13
Q

What disorders are TCAs indicated for?

A 
Major Depression
Pain
Anxiety Disorders
ADHD
Nocturnal Enuresis
Depression associated with Schizophrenia
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14
Q

What is the main Mechanism of Action of TCAs?

A

Inhibit reuptake of serotonin via SERT and Norepinephrine via NET pre-synaptically. Inhibits a1AR post-synaptically.

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15
Q

What are secondary MoAs for TCAs?

A

blocks mACh, %-HT, and Histamine receptors

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16
Q

What are the clinical affects a person taking TCAs may experience.

A

Acutely: drowsy, dysphoric, anxious, cognition impaired

Chronically (2-8 weeks): Improved clinical symptoms, but will continue to experience dysphoria.

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17
Q

What are adverse effects of TCAs due to the primary MoA? Why?

A

Orthostatic Hypotension and sedationdue to a-AR antagonism

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18
Q

What are adverse effects of TCAs due to the secondary MoA? Why

A

Secondary MoA: Blurred vision, worsening of narrow-angle glaucoma, dry mouth, constipation, urinary retention, tachycardia, confusion, due to mAChR antagonism.
Sedation due to histamine and a-AR antagonism
weight gain and sexual disturbances

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19
Q

What side effects will a person experience when they overdose (OD) on TCAs?

A

TCAs have low therapeutic Index, patients will experience:
Cardio effects including arrhythmia, direct myocardial depression, and worsening of CHF.
Also experience Acidosis, delirium and seizures

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20
Q

Describe pharmacokinetics of TCAs

A

Incompletely absorbed due to first pass metabolism.
High lipid solubility, goes to brain and fat.
Highly protein bound, high Vd, long t1/2

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21
Q

Which drugs or drug classes potentiate the effects of TCAs?

A

Alcohol and other sedatives.

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22
Q

Which drugs inhibit effect of TCAs? Why?

A

Antiparkinson drugs
Antipsychotic drugs
Biogenic Amines
These drugs compete for plasma protein binding

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23
Q

The effect of which drug (one in particular) is blocked by TCAs?

A

Cloinidine

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24
Q

Which atypical antidepressant is an analog of Loxapine?

A

Amoxamine

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25
Q

What is the MoA of Amoxamine? What are the side effects? What is it used for?

A

Mixed Inhibition of NET>SERT>DAT.

Extrapyramidal SA due to DA receptor antagonism. Used for depression in Psychotic patients.

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26
Q

What is the MoA of Maprotiline? What is the possible SA?

A

SNRI.

Incresed risk of seizure

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27
Q

What is the primary and secondary MoA of Trazodone?

A

Primary: 5-HT2a antagonist and 5-HT1a partial agonist.
Secondary: Moderate inhibition of SERT

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28
Q

What is Trazodone used for?

A

Treatment of depression characterized by anxiety and sleep disturbances.

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29
Q

What is the half life and metabolism profile of Trazodone?

A

Short t1/2 (2-9 hours) and CYP3A4 metabolism

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30
Q

What drug is similar to Trazodone but is largely discontinued? Why is it discontinued?

A

Nefazodone. Largely discontinued due to hepatic toxicity.

31
Q

What is the MoA of Vilazodone?

A

Potent 5-HT1a partial agonist and SSRI

32
Q

What is the MoA of Mirtazepine?

A

(Analog of Mianserin). Enhances release of seretonin and NE by antagonizing presynaptic a-2AR.
Antagonizes 5-HT2 receptors.
Potent antihistaminic (sedating)

33
Q

What are the expected SAs of Mirtazepine?

A

Increased weight gain

Less GI and sexual SAs than SSRIs

34
Q

What is the MoA of Bupropion?

A

Weak blocker of DAT, SERT, and NET

It’s active metabolite is an NE reuptake blocker

35
Q

What is the major SA of Bupropion?

A

Seizure

36
Q

How is Bupropion administered?

A

given as divided doses or slow release formulation. Medium t1/2

37
Q

Other than mood alteration, what is Bupropion used for?

A

Smoking cessation

38
Q

What is the MoA of Venlafaxine?

A

SSRI and SNRI has a short t1/2 (4-10 hours)

39
Q

What are the SAs of Venlafaxine?

A

TCA-like SAs. Produces small, sustained hypertension, sweating, dizzyness, nausea, and anxiety

40
Q

What is the most potent SNRI available?

A

Duloxetine (100x more potent than Venlafaxine)

41
Q

What are the pharmacokinetic properties of Duloxetine?

A

Highly protein bound.
Metabolized by CYP2D6 and CYP1A2
T1/2 is about 12 hours

42
Q

What is the MoA of Vortioxetine?

A

Serotonin modulator and stimulator.
Potent blocker of SERT
High efficacy partial agonis at 5-HT1a receptors
Partial agonist of 5-HT1b
Antagonist of 5-HT1d, 3a, and 7 receptors
Weak blocker of NET and B1-AR

43
Q

What are SSRIs used for?

A

First line therapy for Major Depression and PTSD.

Also used for OCD, social anxiety disorder, ADHD and some eating disorders

44
Q

Why do SSRIs have a better history of compliance?

A

More tolerable SAs due to negligible activity at mACh and Histamine receptors.

45
Q

What is the MoA of SSRIs?

A

Selective inhibition of SERT.

Potentiate and prolong the action of 5-HT

46
Q

What are the acute and chronic effects of SSRIs?

A

Acute: CNS stimulation, anxiety, agitation

Chronic (2-6 weeks): Improvement of most or all clinical symptoms, CNS activation remains.

47
Q

What are the Adverse effects of SSRIs?

A

Nausea, decreased libido, sexual dysfunction.

Low incidence of cardiovascular and anticholinergic effects. Higher therapeutic index!

48
Q

Which SSRI has the longest t1/2 and can be administered weekly?

A

Fluoxetine

49
Q

Which CYPs metabolize SSRIs and which CYPs are inhibited by SSRIs?

A

2D6, 2C19 and 3A4 metabolize

2d6 and 2C19 are inhibited

50
Q

Which class of drugs are contraindicated with administration of SSRIs? Why?

A

MAOIs

Will cause serotonin syndrome

51
Q

What is the cause of seretonin syndrome?

A

Onset within 24 hours of overdose or concurrent MAOI. Caused by overstimulation of 5-HT1A receptors in central grey midbrain and medulla.
Also triggered by increased 5-HT release (amphetamines, MDMA) or via 5-HT agonist (LSD, Buspirone, L-tryptophan)

52
Q

What are the symptoms of serotonin syndrome?

A 
Hyperpyrexia
Hyperreflexia
tremor
shivering
myoclonus
agitation
seizures
confusion
delirium
cardiovascular collapse
coma
53
Q

What are MAOIs used for?

A

patients unresponsive to treatment with other antidepressants and for whom ECT is not suitable.
Also used for panic disorder and agoraphobia

54
Q

What is the mechanism of action of MAOIs?

A

Block metabolism of monoamines by IRREVERSIBLE inhibition of MOA-A and MAO-B in nerve terminals.

55
Q

What are the acute and chronic clinical effects of MAOIs?

A

Acute: CNS stimulation, agitation, euphoria
Chronic: CNS activation remains, all others resolve

56
Q

What are the AEs of MAOIs?

A 
sleep disturbances (increased arousal)
orthostatic hypotension
weight gain
sexual dysfunction
57
Q

What substances are contraindicated with MAOIs?

A 
tyramine foods (cheese)
sympathomimetic drugs (cold remedies, diet aids, stimulants)= cause acute hypertensive rxn
Meperidine and Dextromethorphan= cause hyperpyrexia, delirium, convulsions, coma, and DEATH!!!
SSRIs= Seretonin Syndrome
58
Q

What are the mood stabilizers used for?

A

Maintenance of manic depression

59
Q

What is the MoA of Lithium?

A

Li inhibits inositol phosphate signaling (hypothesized)

60
Q

What are the pharmacokinetics of Li?

A

Rapid absorption (30 min-2hr peak)
Complete absorption (6-8hr)
Distributes to total body water, some in bone
Cleared in urine, no metabolism

61
Q

What are some AEs and things to worry about with Li?

A

NARROW THERAPEUTIC INDEX!!!
Cat. D
Neuro: tremor, ataxia, hyperactivity, aphasia, sedation, fatigue
Glands: edema, mild hypothyroidism
Renal: Polydipsia, polyuria, nephrogenic Diabetes Insipidus
Cardiac: Bradycardia-Tachycardia (sick sinus)
other: acne, folliculitis, exacerbates psoriasis
Beware patients who are dehydrated as this will increase drug serum concentrations

62
Q

What drugs are contraindicated with Li?

A

diuretics and NSAIDS (renal problems)

63
Q

What other mood-stabilizers can you give either alone or with Li?

A

Valproate and Carbamazepine

64
Q

What is first line therapy for bipolar disorder?

A

Lithium

although, milder forms may be treated with anticonvulsants

65
Q

What is Valproic Acid used for?

A

absence, myoclonic, partial, and tonic-clonic seizures.
Drug of choice in absence seizures accompanied with tonic-clonic seizures.
and of course, mild forms of bipolar disorder

66
Q

What is the MoA of Valproate?

A

Inhibits voltage gated Na channels by stabilizing the inactivated state of the channel. Also blocks T-type Ca channel (to lesser extent)
Stimulate GABA synthesis and inhibit GABA degredation
May increase K conductancies at high dose

67
Q

Drug Interactions of Valproate?

A

Valproate inhibits its own metabolism and the metabolism of other CYP2C metabolized drugs

68
Q

SAs of Valproate?

A

Hepatotoxicity (need liver function tests)
Sedation
Nausea, abdominal pain, and heartburn (common)

69
Q

What are the clinical uses of Carbamazepine?

A

Drug of choice for partial seizures.

also used for: generalized tonic-clonic seizure, and trigeminal neuralgia

70
Q

What is the MoA of Carbamazepine?

A

Inhibits Na channels

71
Q

Pharmacokinetics of Carbamazepine?

A

100% absorbed from GI tract
Metabolized by CYP3A4 to active metabolite.
Slow clearance

72
Q

Drug Interactions with Carbamazepine?

A

Induces CYP2C and 3A families, and induction of UGTs.

73
Q

SAs of Carbamazepine?

A

Aplastic Anemia
Drowsiness (high doses)
Diplopia and ataxia (common)
Mild GI upset

Psych Pharm (3 decks)

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