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Pharm III Unit I > 5 Antidepressants > Flashcards

5 Antidepressants Flashcards

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
Q

What happens if you combine TCAs and amphetamines?

A

May cause hypertension

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26
Q

TCAs can potentials the sedative actions of ….

A

Alcohol and CNS depressants

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27
Q

TCAs can potentials the effects of …

A

Anticholinergic drugs

28
Q

What are the different SSRIs mentioned in this lecture?

A 
Fluoxetine (Prozac)
Sertraline (Zoloft)
Paroxetine (Paxil)
Citalopram (Celexa)
Escitalopram (Lexapro)
29
Q

Uses for SSRIs

A 
Depression
Panic disorder
OCD (***Paxil***)
Social anxiety (***Paxil***)
Bulimia
Alcoholism
Children and Teenagers
30
Q

Which SSRI is most likely to have drug interactions?

A

Fluoxetine (Prozac)

Inhibits CYP450s

Also, it impairs blood glucose in diabetics

Long half life (2-3 days)

31
Q

Which SSRI is least likely to interact with other drugs

A

Sertraline (Zoloft)

Preferred in the elderly

Half life of 26 hours and extensive first-pass elimination

32
Q

Which SSRI is currently the DOC for depression?

A

Citalopram (Celexa) or Escitalopram (Lexapro)

Low incidence of pharmacokinetic interactions and side effects

33
Q

MOA for SSRIs

A

Selectively inhibits 5HT reuptake

Take 2-3 weeks to be effective

34
Q

Pharmacokinetics for SSRIs

A

Well absorbed by gut

Half-life = 24-72 hours

Metabolized by CYP2D6

Inhibits CYP450s - many drug interactions**

35
Q

SSRI side effects

A

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
Q

SSRIs + TCAs =

A

Inhibition of metabolism of TCAs —> increased toxicity

37
Q

SSRIs + phenytoin and carbamazepine =

A

Increased levels and toxicity

38
Q

SSRIs + MAOIs =

A

Serotonin Syndrome

39
Q

SSRI + St. John’s Wort or amphetamines =

A

Serotonin syndrome

40
Q

SSRIs + beta blockers =

A

May result in heart block and hypotension

41
Q

SSRIs + Opioids

A

Codeine - fluoxetine inhibits conversion to the active compound

Meperidine - increases 5HT —> potential for serotonin syndrome

Tramadol - increased risk of seizures

42
Q

What are SNRIs?

A

Serotonin-NE Reuptake Inhibitors

More side effects than SSRIs

43
Q

How are SNRIs used?

A

Depression

Neuropathic pain

Post menopausal hot flashes

44
Q

Venlafaxine (Effexor) is a _______ that may increase________.

A

SNRI

Increase BP

45
Q

Duloxetine (Cymbalta) is an SNRI that may…

A

Cause hepatotoxicity

Cause bilateral acute angle-closure glaucoma

46
Q

MOA for MAOIs

A

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
Q

What should be know about Phenelzine (Nardil)?

A

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
Q

Drug of last choice for depression

A

Phenelzine (Nardil) - MAOI

49
Q

What do we need to know about Selegiline (Deprenyl)?

A

Selectively inhibits MAO-B —> increased DA

Used in Parkinson’s

Fewer side effects

50
Q

How are MAOIs used?

A

For depression which doesn’t respond to other drugs

51
Q

What are the pharmacokinetics of MAOIs?

A

Long half life

Effects persist after discontinuing drug

52
Q

Side effects of MAOIs

A

Hypertensive crisis (Phenelzine) - AVOID tyramine

Tremors, sedation or excitation and insomnia

Orthostatic hypotension

Weight gain (common)

Anticholinergic effects - blurred vision, dry mouth etc

53
Q

What dietary advice should you give to you patient when prescribing an MAOI?

A

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
Q

What happens when you mix MAOIs with OTC cold and cough meds

A

If they contain sympathomimetic amines (phenylephrine, ephedrine, amphetamines) can lead to severe hypertension

55
Q

Mixing what drugs with MAOIs will get you some sweat serotonin syndrome?

A

Meperidine
Dextromethorphan
TCAs
SSRIs

All can lead to hyperpyrexia

56
Q

Because MAOIs can also inhibit CYP450s, they can…

A

Affect metabolism of SSRIs, Ca2+ blockers, etc

57
Q

What is the MOA for Bupropion (Wellbutrin)?

A

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
Q

What is the extended release form of Bupropion?

A

Zyban - used for smoking cessation

59
Q

What are the pharmacokinetics of Bupropion?

A

Extensive first-pass metabolism and high protein binding

Active metabolites

60
Q

Side effects of Bupropion (Wellbutrin)

A

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
Q

MOA for Mirtazapine (Remeron)

A

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
Q

Side effects of Mirtazapine (Remeron)

A

Blocks histamine receptors —> drowsiness as a predominant side effect

63
Q

What is the first non-stimulant treatment for ADHD?

A

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
Q

What is Trazodone (Desyrel)

A

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
Q

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?

A

Trazodone (Desyrel) - it can cause priapism

66
Q

How does St. John’s Wort (Hypericin) work?

A

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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