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Pharmacology Spring Semester > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

SSRI drug names

A

Fluoxetine (Prozac)

Sertraline (zoloft)

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2
Q

SNRI drug name

A

Duloxetine

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3
Q

Tricyclic antidepressant names

A

Amitriptyline

Desipramine

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4
Q

MAOI drug name

A

Tranylcypromine

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5
Q

Other Antidepressant Drugs

A

Buproprion
Mirtazapine
Trazadone

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6
Q

Describe the delayed onset of ADD therapeutic effects

A

Mood only elevates once the drug level in the system has raised and stabilized (at about 4 days) and stayed high for another 6-8 days. This means you won’t feel better unless you are medication compliant and able to wait 2 full weeks for improvement.

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7
Q

Where is seratonin synthesized?

A

Mainly in ECL cells - Enterochromaffin-like

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8
Q

What enzyme breaks seratonin down?

A

Monoamine oxidase - MAO

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9
Q

What is metabolized into melatonin? Where does this happen?

A

Seratonin (5-HT) - Melatonin is made in the pineal gland.

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10
Q

SSRI mechanism of action

A

Block the Seratonin Reuptake Transporter (SERT) that brings Seratonin out of the synapse and into the nerve terminal.
They DO NOT affect other amines (like NE)
They DO NOT bind to any receptors.

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11
Q

SSRI in the CNS - acute effects and long-term adaptation

A

Acutely, more Seratonin in the synapse for longer. Over time, enhanced seratonergic transmission.

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12
Q

SSRI’s initial effects

A

CNS Stimulation - restlessness, GI upset, usually improves with time.

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13
Q

SSRI’s therapeutic response

A

Gradual improvement in most depressive symptoms in 1-6 weeks. positive response 70-80%

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14
Q

Non-depression indications for SSRI’s

A 
Anxiety D/O - phobia, panic, PTSD, OCD
Eating D/O - bulimia
PMDD
ADD/ADHD
And many more - off-label
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15
Q

SSRI’s ADME

A 
PO 
Protein bound
CYP3A4 - phase 2 glucoronidation
Some active metabolites
Renal Excretion
Long T 1/2
Kinetics are only important for toxic reactions - discontinuation reactions - worse with shorter T1/2 due to faster drop in levels.
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16
Q

SSRI adverse effects

A

Agitation, insomnia, GI problems, Headache, dizziness, fatigue, weight gain or loss,
Starting with a low dose will help with all of these except the worst one -
sexual dysfunction

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17
Q

SNRI mechanism of action

A

Block SERT - similar to SSRI’s.

At medium to high doses, they also block the NET - can increase BP at high dose.

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18
Q

Unique indication for SNRI’s

A

Neuropathic Pain

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19
Q

SSRI’s/SNRI’s overdose toxicity

A

Generally safe, but when combined with MAOI’s can lead to life threatening Seratonin Syndrome. - Hyperthermia, muscle rigidity, myoclonus, akathisia, hyperreflexia, fluctuating vital signs, and mental status.

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20
Q

What works better? SSRI’s or SNRI’s?

A

There is no evidence for differences in efficacy, but individuals may respond to one better than the other.

21
Q

What are some risks associated with Doluxetine?

A

Shorter t 1/2 - worse discontinuation syndrome
Hypertension at high dose.
Inhibitor of CYP2D6 - DDI’s, can enhance levels of other psychoactive medications.

22
Q

Trazodone mechanism of action

A

5-HT2A Receptor blockade (the receptor senses levels of seratonin in the synapse and signals a stop to secretion, so blocking it increases secretion), also a weak SERT blocker and a weak partial agonist at 5-HT1A

23
Q

Trazodone nontherapeutic mechanisms

A

Alpha 1 Antagonist - sedation

Active mtabolite mCPP -agonist at several 5HT receptors - unknown effects

24
Q

Trazodone Clinical Issues

A

Sedation, orthostatic hypotension, headache, risk of Priapism, CYP3A4 inhibition - DDI’s. Lower overall response than SSRI’s.

25
Q

Mirtazapine mechanism of action

A

Alpha 2 antagonist - Enhances NE release, causing increased NE neurotransmission.

26
Q

Mirtazapine nontherapeutic mechanisms

A

Potent H1 antagonist - sedation

Weak antagonist at muscarinic and alpha 1 - leading to adrenergic and cholinergic side effects.

27
Q

Mirtazapine Clinical Issues

A

Sedation, weight gain, dizziness, anticholinergic action.
May help in some treatment resistant patients.
CYP inhibition

28
Q

Buproprion Therapeutic mechanism

A

Blocks DAT (dopamine) and NET. DA effects are unique.

29
Q

Buproprion nontherapeutic mechanisms

A

Weak alpha 1 and histamine antagonist, strong antagonist at nicotinic receptor - smoking cessation.

30
Q

Buproprion Clinical Issues

A

CNS stimulation, anxiety, insomnia, weight loss, headache, SEIZURES
Few sexual side effects - unique mechanism of action.
Overall lower response rates, may worsen anxiety.

31
Q

Tricyclics mechanism of action

A

Block SERT and NET.
Desipramine - prefers NET
Amitriptyline - Prefers SERT

Bock a variety of receptors - Side effects muscarinic, cholinergic, alpha 1 adrenergic, h1 histamine.

32
Q

TCA’s - Initial effects

A

Initially - drowsiness, dry mouth, constipation, anxiety, dysphoria, difficulty concentrating.

33
Q

TCA’s - delayed response

A

Gradual improvement of most depressive symptoms - positive responses in 80%

34
Q

TCA ADME

A

Long T 1/2, some active metabolites, kinetic differences don’t matter, except for the severity of the toxic response when stopping or switching drugs.

35
Q

What works better, TCA’s, or SSRI’s

A

No evidence for difference, but individuals may respond better to one than the other.

36
Q

TCA adverse effects

A

There are a lot, and noncompliance is common.
NE - tachycardia, palpitations, orthostatic hypotension, delayed orgasm,
Cholinergic - heart block, dry mouth, constipation, urinary retention, blurred vision
Anticholinergic - sedation, confusion, memory impairment, hallucinations
Antihistimine - increased appetite, weight gain.

37
Q

TCA overdose toxicity

A

Low TI due to cardiac arrythmias, although desipramine is better than amitriptyline.
Also acidosis, delerium hyperpyrexia, seizures, paralysis, coma.

38
Q

Treatment for TCA overdose

A

Supportive, lavage, and lidocaine for arryhthmias.

39
Q

MAOIs mechanism of action

A

Irreversibly inhibit Monoamine Oxidase. Increased NE and 5HT in synapse.

40
Q

MAOI’s - behavioral and clinical effects

A

Initially - stimulation, agitation, euphoria.

1-6 weeks - stimulation decreases, depression improves.

41
Q

MAOI Indications

A

3d line - used for atypical depression.

42
Q

MAOI interactions

A

Many drugs are partially detoxified by MAO, so MAOI’s increase levels - lots of DDI’s
Meperidine and Dextromethorphan - Seratonin syndrome, possible fatality
SSRIs, SNRIs, TCA’s, Trazadone - can cause seratonin sydrome when switching to them from MAOI’s - allow at least 2 weeks before starting the new med.

43
Q

MAOI dietary restriction - what is it and why?

A

TYRAMINE - in cheese, wine, and other foods. Can cause acute hypertensive crisis.

44
Q

MAOI adverse effects

A 
CNS stimulation
Postural hypotension
GI distress
Sexual Dysfunction
Overdose - uncommon, can cause hyperthermia, shock, coma, seizures.
45
Q

Use of antidepressants in pregnancy

A

Tranylcypromine - significant risk. Avoid.
Fluoxetine, sertraline - Category C.
Amitriptyline - possible risk.

46
Q

What drug can you use for children with major depressive disorder? What is the risk of ADD use in children?

A

Fluoxetine - Monitor for worsening depression, and suicidal ideation.

47
Q

Considerations in ADD choice

A

Tolerance of adverse effects - compliance

Most have similar efficacy, but you don’t know which one is best for your patient until you try.

48
Q

Poor response to ADD drugs - what do you do?

A 
Check the 5 D's
Dose
Duration
Diagnosis
Other Drugs
Different treatment - cognitive behavioral, psychotherapy, etc.

Pharmacology Spring Semester (8 decks)

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