Pharmacology/Psychiatry - Antidepressants Flashcards

1
Q

Re-uptake inhibitors immediate action?

A

Increase levels of neurotransmitters = more opportunity to bind to receptor

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2
Q

Re-uptake inhibitors delayed action?

A

Down-regulation of neurotransmitter receptors

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3
Q

What might explain the reason for time needed to see antidepressant effect?

A

Re-uptake inhibitor delayed action - down-reg of NT receptors

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4
Q

Sustained antidepressant therapy is also associated with increase in production of what?

A

BDNF - brain derived neurotrophic factor

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5
Q

Antidepressant suicide risk is increased in which populations (in general)?

A

Children, adolescents, and adults up to 24 yo.

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6
Q

What are SNRI’s? Examples?

A

Serotonin and Norepinephrine Re-uptake Inhibitors
- Ex: Tricyclic Antidepressants (TCA) - amitriptyline
- Ex: Venlafaxine

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7
Q

What are SSRI’s? Example?

A

Selective Serotonin Re-uptake Inhibitors
- Ex: Fluoxetine

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8
Q

What are MAOI’s? Example?

A

Monoamine Oxidase Inhibitors
Ex: Trazodone

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9
Q

One of the first types of antidepressants discovered?

A

TCAs

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10
Q

Mechanism of TCAs?

A

They are classified as SNRI’s = block the re-uptake of serotonin and norepinephrine so they can hang around in synaptic cleft and exert their effects

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11
Q

Adverse effects of TCAs?

A

Block receptors for M-receptors, alpha-1 and Histamine-1 receptors

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12
Q

Adverse effect of blocking M-receptors? (4)

A
  • Salivary glands = dry mouth
  • Intestines = constipation
  • Bladder = urinary retention
  • Pupil = dilation
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13
Q

Adverse effect of blocking alpha-1 receptors on blood vessels? (3)

A
  • Orthostatic hypotension
  • Sedation
  • Sexual dysfunction
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14
Q

Adverse effects of blocking histamine-1 receptors? (2)

A
  • Weight gain
  • Drowsiness
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15
Q

Sexual dysfunction is caused by serotonin acting on what receptor?

A

5-HT2a receptors

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16
Q

What can TCA overdose lead to?

A

Life-threatening cardiac arrhythmias

17
Q

How does Venlafaxine differ from TCA’s?

A
  • it also weakly inhibits dopamine re-uptake
  • has less significant alpha-1, H-1 and M-1 block
18
Q

Most commonly prescribed antidepressant class?

A

SSRI’s

19
Q

Adverse effects of SSRI’s?

A
  • Often related to M, alpha-1 and H-1 block but typically more mild than TCAs (except sexual dysfunction)
20
Q

SSRI’s have the potential to cause what?

A

Serotonin syndrome

21
Q

Triad of sx of serotonin syndrome?

A
  • Altered mental status
  • Autonomic hyperactivity
  • Neuromuscular abnormalities
22
Q

Altered mental status ex?

A

Agitation

23
Q

Autonomic hyperactivity ex?

A

Patient is often hot and sweating with a fast HR and high BP

24
Q

Neuromuscular abnormalities ex?

A

Hyper-reflexia and clonus are particularly common in lower extremities

25
Q

Medication to interfere with serotonin action in serotonin syndrome?

A

Cyproheptadine

26
Q

Symptomatic treatment of serotonin syndrome?

A

Treat with benzodiazepines

27
Q

Therapeutic mechanism of MAOI’s?

A

Block monoamine oxidase = enzyme that metabolizes norepinephrine -> higher levels of norepinephrine

28
Q

When can MAOI’s induce a hypertensive crisis?

A

when combines with foods containing tyramine

29
Q

Medication that inhibits serotonin re-uptake but is NOT considered an SSRI?

A

Trazodone

30
Q

Trazodone acts directly as an antagonist at what serotonin receptors?

A

5-HT2A receptors

31
Q

Adverse effects of Trazodone?

A
  • H1-block and potent alpha-1 block = strong sedative
  • Weight gain (minimal)
32
Q

Antidepressant Bupropion? what is the non-anti-depressant version used for?

A

Antidepressant = Wellbutrin
Smoking cessation therapy = Zyban

33
Q

Wellbutrin mechanism of action?

A

Weak inhibition of norepinephrine and dopamine reuptake

34
Q

Adverse effects of Wellbutrin?

A

Dose related seizure risk