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Spring Pharm Block 2 > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

Describe the broad physiologic goal of all antidepressant medications.

A

Increase the concentration of neurotransmitters in the synapse

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2
Q

By what mechanism do anti-depressants have their effect?

A

There is disagreement –> some say the increased concentration of the neurotransmitters in the synapse lead to the anti-depressive effect while others argue that the effect comes from down regulation of receptors on the pre-synaptic neuron.

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3
Q

What evidence is there that down regulation of receptors is the reason anti-depressant medications are effective?

A

Because anti-depressant medications take 3-4 weeks to be effective, meaning the down regulation of receptors is likely more responsible.

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4
Q

List neurotransmitters (NTs) found in the synapse of CNS neurons

A

Epinephrine, norepinephrine, serotonin, dopamine, acetylcholine

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5
Q

What are two ways the body removes neurotransmitters from the synapse?

A
  1. Reuptake: recycling NTs by pumping them back into the pre-synaptic neuron
  2. Enzymes: acetylcholinesterase and monoamine oxidase chew up NTs in the synapse
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6
Q

Which class of antidepressant medications is most effective?

A

No one class is more effective than another –> what determines use is side effects the patient experiences

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7
Q

What was the original class of antidepressant medications?

A

Monoamine oxidase inhibitors (MAOIs)

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8
Q

Name two MAOIs on the market today.

A

Phenelzine and Tranylcypromine

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9
Q

What is the mechanism of action of MAOIs?

A

They block action of monoamine oxidase thereby increase CNS synapse levels of epi, norepi, and dopamine

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10
Q

What are two isoforms of MAOIs and which has the most antidepressive effect?

A

MAO-A and MAO-B –> MAO-A has the greatest antidepressive effect

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11
Q

What is the GI related AE of MAOIs and how is it mitigated?

A

MAO in the colon metabolizes vasoactive substances that we eat (tyramine) before they enter the bloodstream. MAOIs allow absorption of these vasoactive chemicals. Patient must adhere to a special diet or suffer risk of hypertensive emergency and urgency.

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12
Q

List common AEs of MAOIs other than the GI related AE.

A

Many drug interactions, orthostatic hypotension, palpitations, tachycardia, erectile dysfunction

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13
Q

Differentiate between Phenelzine and Tranylcypromine and state how it is clinically relevant.

A

Phenelzine: more sedating –> prescribe to people with insomnia
Tranylcypromine: more activating –> prescribe to people that sleep too much

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14
Q

When, after discontinuing use of MAOIs, do you no longer worry about AEs?

A

3 weeks after stopping medication

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15
Q

When should MAOIs be combined with other antidepressant medications?

A

Only under care of psychiatrist –> mixing more than one drug class can lead to serotonin syndrome

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16
Q

T/F: MAOIs are considered first line therapy for depression.

A

False –> patients on an MAOI have issues

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17
Q

What are two medications previously discussed in class that have weak MAOI properties?

A

Linezolid (antibiotic) and St. John’s Wort (OTC antidepressant)

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18
Q

Describe the use and mechanism of tricyclic antidepressants (TCAs).

A
  • They are not commonly used –> they are dirty drugs (lots of side effects)
  • They indiscriminately block NT reuptake
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19
Q

Why are TCAs still kept on the market?

A

Off label uses such as insomnia (Anti-Ach sedation), neuropathic pain, enuresis (bed wetting)

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20
Q

What are the three primary results of TCA toxicity?

A
  1. Tonic-clonic seizures
  2. Cardiac arrhythmias
  3. Anti-cholinergic effects (constipation, dry mouth, urinary retention, sedation, tachycardia)
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21
Q

How should you counsel patients when starting them on a TCA?

A

Anti-Ach side effects will start immediately but the antidepressant effects will not be seen for three weeks

22
Q

What is the father of TCAs?

A

Imipramine

23
Q

What is the hallmark ECG finding of TCA toxicity and what is the antidote?

A

Toxicity causes QRS widening on the ECG. The antidote is Bicarbonate

24
Q

What are the two broad categories of TCAs?

A

Secondary Amines: desipramine, nortriptyline, exs

Tertiary Amines: amitriptyline, imipramine, exs

25
Q

Which TCAs are more well tolerated by patients?

A

Secondary because the tertiary amines are typically metabolized into the secondary amines. Tertiary amines stay around longer.

26
Q

Patients with what past medical history should have TCAs prescribed cautiously?

A

Seizure patients –> TCAs decrease seizure threshold

27
Q

What class of antidepressant medications is most commonly prescribed?

A

Selective Serotonin Reuptake Inhibitors (SSRIs)

28
Q

What is the father of SSRIs?

A

Fluoxetine

29
Q

Name SSRIs (other than the father of the class) commonly prescribed

A

Paroxetine, Sertraline, Citalopram, Fluvoxamine, Escitalopram

30
Q

Compare the AEs of SSRIs to the AEs of TCAs and MAOIs

A

Fewer AEs than other antidepressants –> no anti-ach effects or cardiovascular effects

31
Q

What is the primary AE associated with SSRIs?

A

Erectile dysfunction

32
Q

T/F: SSRIs are commonly lethal in overdose.

A

False: A patient would have to take a lot of SSRIs to overdose

33
Q

Other than depression, what other pathology is SSRIs used for?

A

Anxiety

34
Q

What is an increasingly common risk associated with SSRIs?

A

Suicidal ideation –> fluoxetine most common

35
Q

Describe serotonin syndrome.

A

Confusion, sweating, fever, rigidity, tachycardia, hypotension, and possibly death that typically results when two agents that increase serotonin levels are combined or begun in succession without an adequate washout period

36
Q

List two SSRIs that also have some serotonin 1-a receptor agonism and state how this is clinically relevant.

A

Vilazodone and Vortioxetine –> cause more down regulation of receptors and thus may be more potent than other SSRIs

37
Q

What are the advantages of prescribing Vilazodone?

A

Causes less erectile dysfunction and has no effect on weight (SSRIs tend to cause weight gain)

38
Q

What is the mechanism of bupropion?

A

It is a weak inhibitor of dopamine reuptake with no effect on norepinephrine or serotonin

39
Q

What is the major advantage of prescribing bupropion?

A

No effect on sexual function

40
Q

What is the common off-label use of bupropion?

A

Smoking cessation and other addiction disorders

41
Q

What is the major AE associated with bupropion?

A

Decreases seizure threshold –> cannot use in PMH of seizure or in eating disorders (hyponatremia decreases seizure threshold)

42
Q

Describe the mechanism of action of trazodone?

A

It is a weak SSRI and an antagonist of one specific type of serotonin receptor.

43
Q

What is the most common use of trazodone?

A

Insomnia –> the drug is highly sedating

44
Q

What AEs are associated with trazodone

A

Orthostatic hypotension (fall risk) and priapism (rare)

45
Q

Name three drugs that are Serotonin Norepinephrine Reuptake Inhibitors (SNRIs)

A

Venlafaxine, Duloxetine, and Levomilnacipran

46
Q

What was the first SNRI and what are its risks of use?

A

Venlafaxine –> causes HTN and increased lipids. Not great for patients with vascular disease

47
Q

Differentiate venlafaxine from desvenlafaxine.

A

Desvenlafaxine is the same drug but is dosed qd where venlafaxine is multiple doses per day

48
Q

Differentiate duloxetine from venlafaxine.

A

Duloxetine is an SNRI with less norepinephrine activity

49
Q

What are the primary uses of duloxetine other than as an antidepressant?

A

Peripheral neuropathy, fibromyalgia, and urinary incontinence

50
Q

What is the disadvantage of duloxetine?

A

High cost

51
Q

Name and describe three miscellaneous antidepressant medications.

A
  1. Mirtazapine: highly sedating
  2. St John’s Wort: herbal antidepressant
  3. Amphetamines: may be added to antidepressant meds in low doses for severe depression
52
Q

What is different about the way St. John’s Wort can be marketed?

A

Because it is an herbal, company cannot make the claim that it is an antidepressant. They can only say it may reduce depression.

Spring Pharm Block 2 (7 decks)

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