Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Psychopharmacology > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

What are the characteristics of depressive syndromes?

A

-characterized by presence of depressed mood

or

-loss of interest for most of the day (nearly every day for at least 2 weeks for major depression)

+

-associated clinical symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the associated clinical symptoms of depressive syndromes?

A
  • loss of energy
  • disturbed sleep
  • disturbed appetite
  • cognitive symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where do norepinephrine secreting neurons primarily originate from?

A
  • locus ceruleus
  • lateral tegmental areas
  • project widely to almost all areas of brain and spinal cord
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where do serotonergic neurons reside?

A
  • raphé nuclei in brainstem

- diffusely make contact with all areas of brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When was the first tricyclic antidepressants (TCA) introduced?

A

Imipramine

-1950s

Strong efficacy in treatment of psychotic depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name the tertiary amines.

A
  • imipramine
  • amitriptyline
  • clomipramine
  • doxepin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name the secondary amines.

A

Desipramine

-metabolite of imipramine

Nortriptyline

-metabolite of amitriptyline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the structure of TCAs.

A

Tricyclic structure

-two benzene rings on either side of a seven member ring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the categories of TCA side effects?

A
  • cardiac
  • anticholinergic effects
  • adrenergic
  • histamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe TCA cardiac effects.

A

Prolonged QT interval (QTc is corrected for heart rate)

  • slowing of intracardiac conduction by inhibiting sodium channels
  • may be associated with torsades de pointes (potentially fatal ventricular arrhythmia)

Avoid in patients with recent MI

May be associated with increase in CV disease
-even in those not known to have cardiac history prior to initiation

1 to 2 week supply may be fatal in overdose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe TCA anticholinergic effects.

A

Muscarinic acetylcholine receptor antagonism

  • dry mouth
  • urinary retention
  • constipation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe TCA adrenergic effects.

A

Peripheral α-1 adrenergic antagonism

-orthostatic hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe TCA histamine effects.

A

Histamine (H1) receptor antagonism

  • sedation
  • possible weight gain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is required before starting a TCA?

A

ECG

-to rule out any existing conduction abnormalities before starting therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In what patients should TCAs be avoided?

A

Patients with recent MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What may TCAs be associated with?

A

Increase in CV disease

-even in those not known to have cardiac history prior to initiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe TCA use for pain syndromes.

A

Mild to moderate analgesic effect in treatment of chronic pain syndromes

  • includes migraines
  • independent of effect on mood
  • efficacy starts at lower doses
  • response seen earlier than with depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why are TCAs dangerous in overdose?

A

1 to 2 week supply may be fatal in overdose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which TCAs are particularly effective for pain syndromes?

A
  • amitriptyline
  • clomipramine
  • seem more effective than SSRIs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is monoamine oxidase?

A

Enzyme

  • metabolizes monoamines (serotonin, NE, dopamine)
  • enzyme has two isomers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is MAO-A?

A
  • found in brain and intestines
  • metabolizes serotonin, NE, dopamine
  • MAO-A inhibition required for antidepressant effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is MAO-B?

A
  • found in brain and platelets

- primarily metabolizes dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What was the first available MAOI?

A

Iproniazide

  • anti-TB drug
  • discovered in 1950s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the currently available MAOIs?

A
  • tranylcypromine
  • phenelzine
  • isocarboxazid

Transdermal selegiline
-antiparkinsonian MAO-B selective agent (non-selective at higher doses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are MAOIs particularly effective for?

A

For patients with depressive syndromes also meeting criteria for atypical features (two of the following four):

  • hyperphagia
  • hypersomnia
  • heavy leaden feeling in the limbs
  • severe sensitivity to criticism or rejection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What substance do MAOIs have a dangerous interaction with?

A

Tyramine-containing foods

  • aged cheeses
  • red wines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the MAOI-tyramine interaction.

A

Can lead to adrenergic (hypertensive) crisis (increased sympathetic flow)

  • severe hypertension
  • headache
  • increased risk of stroke / cerebral hemorrhage
  • serotonergic side effects possible
  • orthostatic hypotension
27
Q

With what medications should MAOIs not be combined with?

A

Medications containing sympathomimetic properties

  • decongestants
  • amphetamines
  • epinephrine (often added to local anesthetics as vasoconstrictor)
28
Q

When combined with what drugs, can MAOIs cause serotonin syndrome?

A

Serotonergic drugs

-potentially fatal

29
Q

What are the initial symptoms of serotonin syndrome?

A

A

30
Q

What are latter symptoms of serotonin syndrome?

A

May lead to

  • delirium
  • seizures
  • coma
  • death
31
Q

What is the serotonin syndrome triad?

A
  • mental status changes
  • alterations in muscular tone
  • autonomic hyperactivity
  • not all may occur simultaneously
32
Q

How is serotonin syndrome managed?

A
  • hospitalization

- serotonin antagonists

33
Q

What is the washout period needed between MAOIs and other serotonergic drugs?

A

-2 week washout period

34
Q

What is the washout period needed between MAOIs and vortioxetine?

A

-3 week washout period

35
Q

What is the washout period needed between MAOIs and fluoxetine?

A
  • 5 week washout period after stopping fluoxetine

- norfluoxetine has long half life

36
Q

What drugs have serotonergic activity?

A
  • SSRIs/SNRIs
  • TCAs
  • buspirone
  • triptans
  • cyclobenzaprine
  • dextromethorphan
37
Q

What opiates have serotonergic activity?

A
  • meperidine
  • methadone
  • tramadol
38
Q

What are possible mild early side effects of SSRIs (that can be minimized by starting the SSRI at a low dose and increasing the dose gradually)?

A
  • GI upset
  • sweating
  • headaches
  • jitteriness
  • sedation
39
Q

What may continuation of SSRIs be associated with?

A

Reversible sexual side effects (in 2-73% of patients)

  • delayed ejaculation
  • decreased libido
  • ED
40
Q

What are some medical risks of SSRIs?

A
  • anticoagulant effects (greater risk of bleeding syndromes)
  • worsening osteoporosis; increased risk of falls in elderly; 2-fold increase risk of fractures
  • may lead to hyponatremia
  • cataract formation
41
Q

Which SSRI is associated with significant weight gain?

A

Paroxetine

To a lesser extent, citalopram

42
Q

What adverse effect is citalopram associated with?

A

Dose related QTc prolongation

43
Q

Which SSRIs are LEAST likely to inhibit hepatic enzymes?

A
  • citalopram
  • escitalopram
  • followed by sertraline
44
Q

In what situation may SSRIs be less effective or ineffective compared to placebo?

A

Treatment of depression with concomitant alcohol abuse or dependence

45
Q

What is a risk of using SSRIs in patients with a vulnerability to bipolar disorder?

A
  • can induce mania in the short term
  • overall mood instability in the long term
  • younger depressed patients may be incorrectly diagnosed with unipolar depression (may exhibit manic symptoms later)
46
Q

What has SSRI use been associated with in kids, adolescents, and young adults up to 25yo?

A

Increased risk of treatment emergent suicidality

-may be due to increased agitation or activation as a side effect or mixed manic symptoms

47
Q

What side effects of TCAs are the SNRIs expected not to have with a similar efficacy?

A
  • anticholinergic
  • antihistaminic
  • hypotensive
  • significant cardiac effects
48
Q

How does venlafaxine act at lower doses?

A

Less than 150mg

-primarily serotonergic

49
Q

What side effect does venlafaxine have at higher doses?

A

Mild to moderate dose related hypertension

50
Q

What are some advantages of Pristiq over the parent compound?

A
  • once daily starting dose is the target dose

- metabolism is independent of liver cytochrome enzymes

51
Q

How does duloxetine act throughout its entire dosage range?

A

Dual action

-may increase blood pressure but less pronounced effect

52
Q

How does duloxetine compare to the SSRIs and venlafaxine as an antidepressant?

A

Less tolerable overall without any advantages in efficacy

53
Q

Describe duloxetine use for pain syndromes?

A
  • does NOT have a clinically significant effect on pain symptoms in most depressed patients
  • is effective and has FDA approval for diabetic neuropathy pain and fibromyalgia
54
Q

How is levomilnacipran compare to the SNRIs?

A

Significantly greater selectivity for norepinephrine reuptake inhibition

55
Q

How does bupropion work?

A

Dopamine reuptake inhibition

-may also inhibit NE reuptake

56
Q

Describe bupropion’s side effect profile.

A
  • can have mild stimulant like properties
  • can decrease appetite
  • non sedating
  • shortening of QT interval
57
Q

What two side effects that bupropion does NOT have are the most common reasons for non adherence?

A
  • sexual side effects

- weight gain

58
Q

What is a major side effect of bupropion?

A

Can lower seizure threshold

59
Q

What are conditions that can increase seizure risk?

A
  • eating disorders

- active withdrawal from alcohol / BDZ

60
Q

What drugs may increase bupropion levels?

A

2D6 inhibitors

  • paroxetine
  • fluoxetine
61
Q

Which antidepressant is LEAST likely to cause mania in bipolar patients?

A

Bupropion

62
Q

How does bupropion compare to SSRIs for anxiety symptoms in depressed patients?

A

Comparable benefit

63
Q

What is the MOA of mirtazapine?

A

Antagonist at alpha-2-adrenergic autoreceptors

  • causes an increase in NE and serotonin release
  • blocks certain serotonergic post synaptic receptors
64
Q

What effects does mirtazapine have?

A
  • can improve appetite (5HT3 and H1 antagonism)
  • sleep (through H1 antagonism)
  • can be helpful in acutely depressed with poor oral intake and insomnia
65
Q

What is nefazodone’s MOA?

A

Post synaptic 5HT2 antagonist

-weak serotonin and NE reuptake inhibition

Psychopharmacology (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions