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Pharm III Unit I > 5 Antidepressants > Flashcards

5 Antidepressants Flashcards

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1
Q

DSM-V Criteria for Major Depression

A

A. Five or more of the following during a 2 week period:

  1. Depressed mood most the day, nearly EVERY DAY
  2. Markedly diminished interest or pleasure in all, or almost all activities
  3. Weight loss or weight gain, or decrease or increase in appetite nearly EVERY DAY
  4. Insomnia or hypersomnia nearly EVERY DAY
  5. Psychomotor agitation or retardation nearly EVERY DAY
  6. Fatigue or loss of energy nearly every day
  7. Feelings of worthlessness or inappropriate guilt nearly EVERY DAY
  8. Diminished ability to think or concentrate or indecisiveness
  9. Recurrent thoughts of death, thought or plans of suicide

B. Sx cause significant impairment in cognitive, social, and occupational function

C. Sx are not due to the physiological effects of a substance or medical condition

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2
Q

PET scans of patients with depression show…

A

Decreased overall brain activity

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3
Q

What is the neurotrophic hypothesis of depression?

A

Deficits in nerve growth factors (BDNF) —> structural changes and neuronal loss in the brain, especially the hippocampus and frontal cortex

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4
Q

What is the Neuroendocrine Hypothesis of depression?

A

Dysregulation of the HPA axis —> altered glucocorticoid function

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5
Q

What is the biogenic amine hypothesis of depression?

A

Abnormal neurtotransmission of dopamine, NE, and serotonin

Evidence for it: Treatment with reserpine depletes NE —> depression

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6
Q

All antidepressants increase…

A

Amine neurotransmission

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7
Q

Why do antidepressants take 2-3 weeks to be fully effective?

A

Due to neuronal plasticity - it takes time for you brain to adjust to the increased amount of neurotransmitters

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8
Q

What are the different antidepressant targets?

A
  1. TCAs inhibit the reuptake of NE and 5HT
  2. SSRIs selectively inhibit the reuptake of 5HT
  3. SNRIs inhibit the reuptake of NE and 5HT
  4. DA reuptake inhibitors (Bupropion)
  5. MAOIs inhibit the metabolism of NE, DA, and 5HT
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9
Q

How does normal reuptake of 5HT work?

A

5HT levels in the synapse are modulated by reuptake and presynaptic inhibition

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10
Q

What do uptake inhibitors do to 5HT levels?

A

5HT levels in synapse will increase BUT so does feedback inhibition, thus balancing synaptic amine levels

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11
Q

What is the long-term effect of reuptake inhibitors?

A

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

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12
Q

MOA for Tricyclic Antidepressants

A

Inhibit the re-uptake of NE and 5HT

Also block alpha-adrenergic, histamine, and muscarinic receptors

No euphoria/low abuse potential

Take 2-4 weeks to have effect

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13
Q

How are TCAs used?

A

Depression

Chronic pain (TMJ), fibromyalgia

Enuresis

(Limited use due to toxicity and potential overdose)

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14
Q

Examples of TCAs

A

Amitriptyline (Elavil) and Imipramine (Tofranil)
• Tertiary amines
• Primarily inhibit 5HT reuptake
• Produce more seizures than secondary amines
• More sedating than secondary amines

Nortriptyline (Pamelor) and Desipramine (Norpramin)
• Secondary amines
• Primarily block NE reuptake

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15
Q

Tertiary amines primarily block ________ reuptake while Secondary amines primarily block _________ reuptake

A

Tertiary = 5HT

Secondary = NE

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16
Q

How are TCAs prescribed?

A

Generally started at a low dose then increased

All TCAs are equally effective at treating depression

Choice of TCA is based on adverse effects

All antidepressants should be tapered gradually if possible

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17
Q

TCA pharmacokinetics

A

Well-absorbed orally

Variable and long half-lives (10-90 hours)

They are generally given once a day at bedtime

Metabolized by CYP2D6 - drug interactions VERY common

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18
Q

Side effects of TCAs

A

Weight gain

Histamine receptor blockade - sedation/fatigue

Cholinergic blockade - blurred vision, tachy, constipation, urinary retention, dry mouth, palpitations, impairment of memory

Alpha receptor blockade - cardiac depression and arrhythmias, postural hypotension, dizziness, reflex tachycardia

Analgesia

SIADH —> water intoxication and hyponatremia

Sexual dysfunction

Decrease in seizure threshold

Tolerance develops to sedation, postural hypotension and anticholinergic effects

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19
Q

Can TCAs be used in pregnancy?

A

Yep

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20
Q

Why do you get analgesia when taking TCAs?

A

Results from activation of descending noradrenergic pathways in the spinal cord (NE acts on alpha2 receptors to decrease glutamate input into pain pathway going to brain)

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21
Q

What happens to you if you overdose on TCAs?

A

Primarily CARDIO toxic

Torsade de pointes
Prolonged QT interval
Cardiac arrhythmias
Severe hypotension
Agitation, delirium
Seizures, hyperpyrexia
Coma, shock, metabolic acidosis
Respiratory depression
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22
Q

How do you treat a TCA overdose?

A

Cardiac monitoring and supportive care

Gastric lavage and activated charcoal

Magnesium, isoproterenol, and cardiac pacing for Torsades de pointes

Lidocaine, propranolol, phenytoin to manage arrhythmias and/or prevent seizures

Sodium bicarb and potassium chloride to restore acid/base balance

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23
Q

Combining TCAs with MAOIs can…

A

Result in SEROTONIN SYNDROME

Severe CNS toxicity manifested by hyperpyrexia, convulsions, and coma

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24
Q

Should you combine TCAs and SSRIs?

A

No, you dummy

They compete for metabolism, thus combo can lead to toxic levels of TCAs

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25
What happens if you combine TCAs and amphetamines?
May cause hypertension
26
TCAs can potentials the sedative actions of ....
Alcohol and CNS depressants
27
TCAs can potentials the effects of ...
Anticholinergic drugs
28
What are the different SSRIs mentioned in this lecture?
``` Fluoxetine (Prozac) Sertraline (Zoloft) Paroxetine (Paxil) Citalopram (Celexa) Escitalopram (Lexapro) ```
29
Uses for SSRIs
``` Depression Panic disorder OCD (***Paxil***) Social anxiety (***Paxil***) Bulimia Alcoholism Children and Teenagers ```
30
Which SSRI is most likely to have drug interactions?
Fluoxetine (Prozac) Inhibits CYP450s Also, it impairs blood glucose in diabetics Long half life (2-3 days)
31
Which SSRI is least likely to interact with other drugs
Sertraline (Zoloft) Preferred in the elderly Half life of 26 hours and extensive first-pass elimination
32
Which SSRI is currently the DOC for depression?
Citalopram (Celexa) or Escitalopram (Lexapro) Low incidence of pharmacokinetic interactions and side effects
33
MOA for SSRIs
Selectively inhibits 5HT reuptake Take 2-3 weeks to be effective
34
Pharmacokinetics for SSRIs
Well absorbed by gut Half-life = 24-72 hours Metabolized by CYP2D6 Inhibits CYP450s - many drug interactions****
35
SSRI side effects
Mild - less autonomic side effects and risk of arrhythmia compared to TCAs GI: nausea, loss of appetite, constipation Weight loss or gain possible CNS stimulation (anxiety/insomnia) with fluoxetine or sertraline Sedation more likely with other drugs Sexual disinterest/dysfunction Photosensitivity
36
SSRIs + TCAs =
Inhibition of metabolism of TCAs —> increased toxicity
37
SSRIs + phenytoin and carbamazepine =
Increased levels and toxicity
38
SSRIs + MAOIs =
Serotonin Syndrome
39
SSRI + St. John’s Wort or amphetamines =
Serotonin syndrome
40
SSRIs + beta blockers =
May result in heart block and hypotension
41
SSRIs + Opioids
Codeine - fluoxetine inhibits conversion to the active compound Meperidine - increases 5HT —> potential for serotonin syndrome Tramadol - increased risk of seizures
42
What are SNRIs?
Serotonin-NE Reuptake Inhibitors More side effects than SSRIs
43
How are SNRIs used?
Depression Neuropathic pain Post menopausal hot flashes
44
Venlafaxine (Effexor) is a _______ that may increase________.
SNRI Increase BP
45
Duloxetine (Cymbalta) is an SNRI that may...
Cause hepatotoxicity Cause bilateral acute angle-closure glaucoma
46
MOA for MAOIs
Irreversibly inhibit MAO (Monoamine Oxidase), which metabolize NE, DA, and 5HT MAO-A metabolizes all three in both the CNS and periphery MAO-B selectively metabolizes DA in the CNS but NOT in the GI tract
47
What should be know about Phenelzine (Nardil)?
Inhibits both MAO-A and MAO-B Increases NE and 5HT (and DA) Actions persist longer than serum levels Also a substrate for MAOs Used for depression that hasn’t responded to other drugs (DRUG OF LAST CHOICE)
48
Drug of last choice for depression
Phenelzine (Nardil) - MAOI
49
What do we need to know about Selegiline (Deprenyl)?
Selectively inhibits MAO-B —> increased DA Used in Parkinson’s Fewer side effects
50
How are MAOIs used?
For depression which doesn’t respond to other drugs
51
What are the pharmacokinetics of MAOIs?
Long half life Effects persist after discontinuing drug
52
Side effects of MAOIs
Hypertensive crisis (Phenelzine) - AVOID tyramine Tremors, sedation or excitation and insomnia Orthostatic hypotension Weight gain (common) Anticholinergic effects - blurred vision, dry mouth etc
53
What dietary advice should you give to you patient when prescribing an MAOI?
Avoid foods with tyramine (red wine, beer, aged cheese) Tyramine causes release of amines and with limited metabolism by MAO-A, can lead to severe hypertension
54
What happens when you mix MAOIs with OTC cold and cough meds
If they contain sympathomimetic amines (phenylephrine, ephedrine, amphetamines) can lead to severe hypertension
55
Mixing what drugs with MAOIs will get you some sweat serotonin syndrome?
Meperidine Dextromethorphan TCAs SSRIs All can lead to hyperpyrexia
56
Because MAOIs can also inhibit CYP450s, they can...
Affect metabolism of SSRIs, Ca2+ blockers, etc
57
What is the MOA for Bupropion (Wellbutrin)?
Inhibits DA, and to a minimal extent, NE and 5HT reuptake May work where others haven’t. Sometimes combined with SSRIs Used in ADHD, alcoholism (decreases craving)
58
What is the extended release form of Bupropion?
Zyban - used for smoking cessation
59
What are the pharmacokinetics of Bupropion?
Extensive first-pass metabolism and high protein binding Active metabolites
60
Side effects of Bupropion (Wellbutrin)
Seizures - contraindicated in patients with a history of seizures CNS effects - anxiety, insomnia, restlessness, tremor, psychosis Cardiac - tachycardia Sexual dysfunction side effects are rare
61
MOA for Mirtazapine (Remeron)
Blocks presynaptic alpha2 receptors which inhibit release of NE and 5HT —> increased release of NE and 5HT Blocks 5HT-2a and 5HT-3 receptors Eliminates side effects associated with SSRIs - anxiety, insomnia, nausea, sexual dysfunction May be an advantage in depressed patients with insomnia and anxiety
62
Side effects of Mirtazapine (Remeron)
Blocks histamine receptors —> drowsiness as a predominant side effect
63
What is the first non-stimulant treatment for ADHD?
Atomoxetine (Strattera) Selective inhibitor of NE reuptake Does not cause euphoria so good choice for addicts May increase memory and attention Side effects - most common are GI distress and insomnia Liver damage rare but possible
64
What is Trazodone (Desyrel)
5HT-2a receptor antagonist Short half life and high first pass metabolism SEDATING - not good antidepressant, more often used as a sleep aid or for pain management Side effects - sedation, dizziness, hypotension, nausea and priapism
65
Dude walks into the ER with a boner that’s lasted all day. He says he just started taking a new med for going to sleepy time. What do you think he was taking?
Trazodone (Desyrel) - it can cause priapism
66
How does St. John’s Wort (Hypericin) work?
May be effective in mild depression Mechanism uncertain - may block reuptake or inhibit MAO Causes photosensitivity DO NOT combine with other antidepressants - can cause serotonin syndrome May prolong the effects of general anesthetics Efficacy of oral BC, digoxin, protease inhibitors and warfarin reduced due to increased metabolism

Pharm III Unit I (9 decks)

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