1- Antidepressants Flashcards by Colleen Cahill

What are the hypotheses for the cause of depression and which is the most relevant?

Monoamine (most relevant)- all antidepressants increase amine neurotransmission

(others: neurotrophic, neuroendocrine

How well did you know this?

Not at all

Perfectly

How long does it take for antidepressants to have an effect?

2-3 weeks due to neuronal plasticity

(reuptake inhibited immediately but effects are delayed)

How well did you know this?

Not at all

Perfectly

What is the long-term effect of uptake inhibitors?

Antidepressants down-regulate auto-receptors, increasing firing rate of 5-HT neuron

How well did you know this?

Not at all

Perfectly

Antipressants only have effects if what?

Pt has chemical imbalances

How well did you know this?

Not at all

Perfectly

What is the general MOA for TCAs?

Inhibit re-uptake of NE and 5-HT, block alpha-adrenergic, histamine, and muscarinic receptors

How well did you know this?

Not at all

Perfectly

What is the use of TCAs?

Depression (one of last line), neuropathic pain, enuresis (smaller dose)

How well did you know this?

Not at all

Perfectly

TCAs are typically well absorbed where and how often are they given?

Well absorbed orally, given 1x daily @ bedtime

How well did you know this?

Not at all

Perfectly

What metabolizes TCAs?

CYP2D6 (drug interactions VERY common)

How well did you know this?

Not at all

Perfectly

TCAs + MAOIs has the potential to cause what drug interaction?

Serotonin syndrome (severe CNS toxicity)

How well did you know this?

Not at all

Perfectly

How do TCAs interact with SSRIs?

Compete for metabolism so can be toxic

How well did you know this?

Not at all

Perfectly

How do TCAs interact with amphetamine (sympathomimetic drugs)?

Cause HTN

How well did you know this?

Not at all

Perfectly

How do TCAs interact with alcohol or other CNS depressants?

Sedative actions

How well did you know this?

Not at all

Perfectly

TCAs can potentiate the effects of what drug class?

Anticholinergic

How well did you know this?

Not at all

Perfectly

Some of the SEs of TCAs include blockade of what receptors leading to what sxs?

Histamine receptor blockade: drowsiness, sedation,
Cholinergic blockade (PNS): dry mouth, urinary retention, impaired memory
𝜶1 receptor blockade: CV

How well did you know this?

Not at all

Perfectly

Aside from receptor blockades, what are the other SEs of TCAs?

Weight gain, analgesia, SIADH, sexual dysfunction, decrease is seizure threshold, tolerance

How well did you know this?

Not at all

Perfectly

What is the most serious complication a/w toxicity/ overdose of TCAs?

Cardiac toxicity (Torsades de pointes)

How well did you know this?

Not at all

Perfectly

Aside from cardiac toxicity, what are other effects of toxicity/ overdose with TCAs?

Prolonged QT interval, cardiac arrhythmias, respiratory depression

(can be fatal)

How well did you know this?

Not at all

Perfectly

Pt presents with toxicity/ overdose with TCAs. What is the tx for the Torsades de pointes?

Magnesium, isoproterenol, cardiac pacing

How well did you know this?

Not at all

Perfectly

Pt presents with toxicity/ overdose with TCAs. What is the tx for managing arrhythmias/ preventing seizures?

Lidocaine, propranolol, phenytoin

How well did you know this?

Not at all

Perfectly

Pt presents with toxicity/ overdose with TCAs. What is the tx for restoring acid/ base balance?

Sodium bicarb and potassium chloride

How well did you know this?

Not at all

Perfectly

Can TCAs be given in pregnancy?

YES

How well did you know this?

Not at all

Perfectly

Why is there limited use with TCAs?

Toxicity and potential overdose

How well did you know this?

Not at all

Perfectly

How are TCAs dosed?

Start @ low dose then increase → tapered gradually

How well did you know this?

Not at all

Perfectly

What is the benefit of using TCAs?

No euphoria/ low abuse potential

How well did you know this?

Not at all

Perfectly

Due to the fact that all TCAs are equally effective at treating depression, choice of drug is based on what?

Adverse effects

Are Amitriptyline and Imipramine secondary or tertiary amines?

Tertiary (serotonin \> NE)

What is the MOA of Amitriptyline and Imipramine and are they more or less potent than secondary amines?

Inhibit 5-HT reuptake Produce more seizures and more sedating than secondary amines

Are Nortriptyline and Desipramine tertiary or secondary amines?

Secondary (NE \> serotonin)

What is the MOA for Nortriptyline and Desipramine?

Block NE reuptake

What is the MOA for SSRIs?

Selectively inhibits 5-HT reuptake

What is the use for SSRIs?

Depression (DOC), panic disorder, OCD, social anxiety, bulimia, alcoholism, used in children/ teenagers

What is the DOC (class) for depression)

SSRIs

Where are SSRIs well absorbed and what is their half life?

Well absorbed by gut, t1/2 = 24-72hrs

What metabolizes SSRIs?

Metabolized by and inhibit CYP450s (2D6) = many drug interactions

What is the result of inhibition of CYP3A4 and CYP2D6 with SSRIs?

Increased toxicity of TCAs and Phenytoin/ carbamazepine

How do SSRIs interact with MAOIs?

Serotonin syndrome

How do SSRIs interact with St Johns wort or amphetamines?

Serotonin syndrome

How do SSRIs interact with beta blockers?

Heart block and hypotension

How do SSRIs interact with codeine?

Fluoxetine inhibits conversion to active compound

How do SSRIs interact with Meperidine?

Increases 5-HT (potential for serotonin syndrome)

How do SSRIs interact with Tramadol?

Increased seizure risk

What are the SEs (although mild) of SSRIs?

CNS stimulation, sexual disinterest/ dysfunction, photosensitivity

Amitriptyline and Imipramine drug class?

TCAs

Nortriptyline and Desipramine drug class?

TCAs

Fluoxetine drug class?

SSRIs

Sertraline drug class?

SSRIs

Paroxetine drug class?

SSRIs

Citalopram drug class?

SSRIs

Escitalopram drug class?

SSRIs

What is the DOC for depression?

Citalopram

What is the use of Paroxetine?

OCD and social anxiety

T1/2 of Sertraline is how long and what is important about its elimination?

26 hours, extensive first pass metabolism

What drug in the SSRI class has the fewest drug interactions?

Sertraline

What SSRI is preferred in elderly?

Sertraline

Does Fluoxetine or Norfluoxetine (active metabolite of Fluoxetine) have a longer half life?

Fluoxetine = 2-3 days Norfluoxetine = 7-9 days)

What SSRI is most likely to inhibit CYP450 enzymes (CYP2D6)/ has the most drug interactions (ex. pain meds)?

Fluoxetine

Use of Fluoxetine should be cautioned in what patient population?

Diabetic pts (impairs blood glucose levels)

Venlafaxine drug class?

SNRIs

Duloxetine drug class?

SNRIs

What is the MOA for MAOIs?

Irreversibly inhibi MAOs (which metabolize NE, DA, 5-HT)

MAO-A metabolizes what and where (location)?

NE, DA, and 5-HT in both CNS and periphery

MAO-B metabolizes what and where (location)?

Selectively metabolizes DA in CNS but NOT in GI tract

What is the use of MAOIs?

Refractory depression (class of last choice)

What is the half life of MAOIs?

Long (effects persist after discontinuing drug)

How do MAOIs interact with sympathomimetic amines?

Severe hypertension (OTC cold/ cough meds)

How do MAOIs interact with any other drug that releases serotonin?

Serotonin syndrome → hyperpyrexia

What do MAOIs inhibit?

CYP450 enzymes (2D6)

What are the SEs of MAOIs?

* Hypertensive crisis (phenelzine), avoid foods w/ tyramine * Orthostatic hypotension * Weight gain (very common) * Anticholinergic

Phenelzine drug class?

MAOIs

Selegiline drug class?

MAOIs

What is the MOA of Phenelzine?

Inhibits both MAO-A and MAO-B → increases NE and 5-HT

What is true about the drug action of Phenelzine?

Actions persist longer than serum levels

Phenelzine is a substrate for what?

MAOs

What is the use of Phenelzine?

Refractory depression (drug of last choice due to serious SEs)

What is the MOA of Selegiline?

Selectively inhibits MAO-B → increases DA

What is true about the SEs of Selegiline?

Fewer than other MAOIs

In addition to depression, Selegiline can also be used for what?

Parkinson's (lower dose)

What is the MOA of Bupropion?

Inhibits DA reuptake

What is the use of Bupropion?

ADHD, alcoholism (decreases craving), ER for smoking cessation

What are the pharmacokinetics of Bupropion?

Extensive first pass metabolism, high protein binding, active metabolites

What are the SEs of Bupropion?

Seizures, CNS effects, cardiac

What is the MOA of Mirtazapine?

Blocks presynaptic alpha-2 receptors → increases release of NE and 5-HT

What is the use for Mirtazapine?

Eliminates SEs a/w SSRIs (anxiety, insomnia, nausea, sexual dysfunction)

What are the pharmacokinetics of Mirtazapine?

Metabolized by CYP450s, t1/2 = 20-40 hrs

What are the SEs of Mirtazapine?

Drowsiness/ sedation (may be advantage in depressed pts with insomnia and anxiety?

What is the MOA of Atomoxetine?

Selective inhibitor of NE reuptake

What is the use of Atomoxetine?

ADHD (first non-stimulant for tx), increase memory and attention Does not cause euphoria = good choice for addicts

What are the SEs of Atomoxetine?

GI distress, insomnia, liver damage (possible but rare)

What is the MOA for Trazodone?

5-HT2A receptor antagonist

What is the use of Trazodone?

Sleep aid, pain management

What are the pharmacokinetics of Trazodone?

Short t1/2, high first pass metabolism

What are the SEs of Trazodone?

Sedating (not good antidepressant), priapism (rare but serious)

1- Antidepressants Flashcards

(92 cards)