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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
What is the MoA of Amoxamine? What are the side effects? What is it used for?
Mixed Inhibition of NET>SERT>DAT. | Extrapyramidal SA due to DA receptor antagonism. Used for depression in Psychotic patients.
26
What is the MoA of Maprotiline? What is the possible SA?
SNRI. | Incresed risk of seizure
27
What is the primary and secondary MoA of Trazodone?
Primary: 5-HT2a antagonist and 5-HT1a partial agonist. Secondary: Moderate inhibition of SERT
28
What is Trazodone used for?
Treatment of depression characterized by anxiety and sleep disturbances.
29
What is the half life and metabolism profile of Trazodone?
Short t1/2 (2-9 hours) and CYP3A4 metabolism
30
What drug is similar to Trazodone but is largely discontinued? Why is it discontinued?
Nefazodone. Largely discontinued due to hepatic toxicity.
31
What is the MoA of Vilazodone?
Potent 5-HT1a partial agonist and SSRI
32
What is the MoA of Mirtazepine?
(Analog of Mianserin). Enhances release of seretonin and NE by antagonizing presynaptic a-2AR. Antagonizes 5-HT2 receptors. Potent antihistaminic (sedating)
33
What are the expected SAs of Mirtazepine?
Increased weight gain | Less GI and sexual SAs than SSRIs
34
What is the MoA of Bupropion?
Weak blocker of DAT, SERT, and NET | It's active metabolite is an NE reuptake blocker
35
What is the major SA of Bupropion?
Seizure
36
How is Bupropion administered?
given as divided doses or slow release formulation. Medium t1/2
37
Other than mood alteration, what is Bupropion used for?
Smoking cessation
38
What is the MoA of Venlafaxine?
SSRI and SNRI has a short t1/2 (4-10 hours)
39
What are the SAs of Venlafaxine?
TCA-like SAs. Produces small, sustained hypertension, sweating, dizzyness, nausea, and anxiety
40
What is the most potent SNRI available?
Duloxetine (100x more potent than Venlafaxine)
41
What are the pharmacokinetic properties of Duloxetine?
Highly protein bound. Metabolized by CYP2D6 and CYP1A2 T1/2 is about 12 hours
42
What is the MoA of Vortioxetine?
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
What are SSRIs used for?
First line therapy for Major Depression and PTSD. | Also used for OCD, social anxiety disorder, ADHD and some eating disorders
44
Why do SSRIs have a better history of compliance?
More tolerable SAs due to negligible activity at mACh and Histamine receptors.
45
What is the MoA of SSRIs?
Selective inhibition of SERT. | Potentiate and prolong the action of 5-HT
46
What are the acute and chronic effects of SSRIs?
Acute: CNS stimulation, anxiety, agitation | Chronic (2-6 weeks): Improvement of most or all clinical symptoms, CNS activation remains.
47
What are the Adverse effects of SSRIs?
Nausea, decreased libido, sexual dysfunction. | Low incidence of cardiovascular and anticholinergic effects. Higher therapeutic index!
48
Which SSRI has the longest t1/2 and can be administered weekly?
Fluoxetine
49
Which CYPs metabolize SSRIs and which CYPs are inhibited by SSRIs?
2D6, 2C19 and 3A4 metabolize | 2d6 and 2C19 are inhibited
50
Which class of drugs are contraindicated with administration of SSRIs? Why?
MAOIs | Will cause serotonin syndrome
51
What is the cause of seretonin syndrome?
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
What are the symptoms of serotonin syndrome?
``` Hyperpyrexia Hyperreflexia tremor shivering myoclonus agitation seizures confusion delirium cardiovascular collapse coma ```
53
What are MAOIs used for?
patients unresponsive to treatment with other antidepressants and for whom ECT is not suitable. Also used for panic disorder and agoraphobia
54
What is the mechanism of action of MAOIs?
Block metabolism of monoamines by IRREVERSIBLE inhibition of MOA-A and MAO-B in nerve terminals.
55
What are the acute and chronic clinical effects of MAOIs?
Acute: CNS stimulation, agitation, euphoria Chronic: CNS activation remains, all others resolve
56
What are the AEs of MAOIs?
``` sleep disturbances (increased arousal) orthostatic hypotension weight gain sexual dysfunction ```
57
What substances are contraindicated with MAOIs?
``` 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
What are the mood stabilizers used for?
Maintenance of manic depression
59
What is the MoA of Lithium?
Li inhibits inositol phosphate signaling (hypothesized)
60
What are the pharmacokinetics of Li?
Rapid absorption (30 min-2hr peak) Complete absorption (6-8hr) Distributes to total body water, some in bone Cleared in urine, no metabolism
61
What are some AEs and things to worry about with Li?
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
What drugs are contraindicated with Li?
diuretics and NSAIDS (renal problems)
63
What other mood-stabilizers can you give either alone or with Li?
Valproate and Carbamazepine
64
What is first line therapy for bipolar disorder?
Lithium | although, milder forms may be treated with anticonvulsants
65
What is Valproic Acid used for?
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
What is the MoA of Valproate?
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
Drug Interactions of Valproate?
Valproate inhibits its own metabolism and the metabolism of other CYP2C metabolized drugs
68
SAs of Valproate?
Hepatotoxicity (need liver function tests) Sedation Nausea, abdominal pain, and heartburn (common)
69
What are the clinical uses of Carbamazepine?
Drug of choice for partial seizures. | also used for: generalized tonic-clonic seizure, and trigeminal neuralgia
70
What is the MoA of Carbamazepine?
Inhibits Na channels
71
Pharmacokinetics of Carbamazepine?
100% absorbed from GI tract Metabolized by CYP3A4 to active metabolite. Slow clearance
72
Drug Interactions with Carbamazepine?
Induces CYP2C and 3A families, and induction of UGTs.
73
SAs of Carbamazepine?
Aplastic Anemia Drowsiness (high doses) Diplopia and ataxia (common) Mild GI upset

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