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Neuro Exam 2 > Anti-depressants and Anxiolytics > Flashcards

Anti-depressants and Anxiolytics Flashcards

1
Q

Describe the mechanism of MAOIs

A

MAOIs = MAO (monoamine oxidase) inhibitors

  • inhibit MAOI enzyme on the mitochondrial membrane of the presynaptic cell
  • MAO breaks down DA, NE, and 5-HT (serotonin) => MAOIs cause increase in dopamine norepi and serotonin available in the synaptic cleft
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2
Q

Where in the brain is the origin of NE pathways?

A

Locus coeruleus

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3
Q

Where do serotonin pathways originate?

A

Raphe nucleus- project to the hippocampus and frontal cortex

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4
Q

Describe two ways that NE is removed from the synaptic cleft

A

(1) Reuptake by NET (NE transporters) then degraded inside presynaptic neuron by MAO
(2) Degraded by COMT = enzyme on the postsynaptic neural membrane

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5
Q

Do the anti-depressant properties come more from inhibition of the MAO-A or MAO-B enzyme?

A

Antidepression aspects more from the MAO-A inhibition

-while MAO-B inhibitors could be helpful to increase dopamine in the treatment of Parkinsons

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6
Q

Isocarborazid

A

MAO-inhibitor

-nonselective => blocks both MAO-A and MAO-B

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7
Q

Are MAO-inhibitors reversible?

A

No, they are suicide inhibitors => they completely inactivate the MAO enzyme

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8
Q

Main indication for MAOIs

A

-atypical depression/resistant depression

  • used also in MDD and dysthymia, but not first line b/c of side effect profile
  • then also used for panic disorders and some eating disorders (bulemia), then OCD, GAD, and headaches
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9
Q

What is the latency of some antidepressants, is this in all of them?

A

All antidepressants have this lag phase where it takes 4-6 weeks to see its maximum effect

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10
Q

What is the main toxicity of MAOIs?

A

Potentially lethal hypertensive crisis

-tons of food and drug interactions

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11
Q

Describe tyranine- why could eating cheese cause hypertensive crisis in pt on which anti-depressant medication?

A

Tyranine (in some cheeses) causes excess NE release, this excess NE is normally broken down by MAO

-pt on MAOI may not be able to handle this excess NE => NE can cause a dangerous increase in BP

=> tyramine can cause cerebral hemorrhage and death

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12
Q

What antidepressants can you not take together?

A

Can’t take MAOIs with either SSRIs or tricyclics

-MAOIs have ton of drug and food interactions

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13
Q

Why are MAOIs considered second line treatment for depression?

A

B/c of their food and drug interactions

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14
Q

How long after discontinuation of MAOIs could one start on an SSRI/TCA?

A

2 weeks- b/c need at least 2 weeks for the MAO enzyme to repopulate

-b/c MAOIs are suicide inhibitors so irreversible inhibition

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15
Q

Mechanism of tricyclic antidepressants

A

Tricyclics work by blocking the reuptake of 5-HT and NE at the synaptic cleft

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16
Q

Mechanism of the side effects of tricyclics

A

Due to its anti-cholinergic, anti-histamine, and anti-alpha adrenergic effects

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17
Q

Major indications for TCAs

A

MDD, panic disorder

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18
Q

Why may TCAs be used for bed wetting?

A

B/c of their anti-cholinergic effects

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19
Q

What is the most dangerous thing about TCAs?

A

Very narrow therapeutic index => high risk of overdose

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20
Q

What is a symptom of TCA overdose that also can be present at therapeutic ranges?

A

Cardiovascular toxicity (arrhythmia, conduction changes)

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21
Q

Side effects of anti-histaminergics

A

Weight gain, drowsiness

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22
Q

Side effects of anti-cholinergics

A

Constipation, dry mouth, blurred vision, drowsiness

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23
Q

Side effects of anti-alpha adrenergics

A

Dizziness and decreased BP

24
Q

Why did SSRIs vastly change the culture around depression?

A

Now that there was a safe drug for treatment that was just as effective, more ppl could be treated for depression => expanded who got treated for depression

25
Q

Indications for SSRIs

A
  • depression and dysthmia (used in less severe cases b/c of fewer side effects)
  • also anxiety and eating disorders
26
Q

Mechanism of SSRIs

A
  • blocks 5HT reuptake at both the dendrites and axons
  • increase in serotonin will desensitize and eventually downregulate the autoreceptors on the dendrites of the presynaptic cell, these autoreceptors act in the feedback loop => downregulation of autoreceptors leads to more 5HT release by the axon
27
Q

What may cause the delay in effect of Fluoxetine?

A

Fluoxetine = Prozac = SSRI

-downregulation of autoreceptors takes time => may add to the 4-6 week time until max effect

28
Q

Why would SSRIs cause mental agitation/anxiety in some cases?

A

Due to excess 5HT around which activates the 5-HT2A and 5-HT2C receptors

-excess serotonin doesnt just have one effect

29
Q

What one possible effect of SSRI toxicity?

A

Serotonin syndrome = predictable consequence of excess serotonin

-increased heart rate, sweating, abdominal pain, diarrhea- large range of symptoms but include possible shock and death

30
Q

What drug exhibits discontinuation syndrome?

A

SSRIs

Discontinuation syndrome = headache, irritability, irritabiliy and fatigue upon abrupt discontinuation

=> taper down dose over a couple weeks

31
Q

What are some theories as to why serotonin may increased suicidal behavior?

A
  • antidepressants may throw pt in hypomania
  • akathisia (motor restlessness) can be very disturbing
  • physical symptoms (energy/drive) improve before mental symptoms
32
Q

Are serotonin and norepi -ergic drugs more likely to help in the treatment of

(a) anxiety
(b) obsession
(c) low energy

A

Serotonin more helpful against anxiety and depression, while norepi more helpful to increase attention and energy

33
Q

What are SNRIs

A

= serotonin-norepinephrine reuptake inhibitors

-block serotonin and NE reuptake pumps

34
Q

What anti-depressant drug has been shown to be useful against fibromyalgia

A

SNRIs (serotonin-norepi reuptake inhibitors)

35
Q

Which anti-depressant has akathisia as a potential side effect?

A

SSRIs

36
Q

Which anti-depressant has been used for smoking cessation/

A

NDRI = norepi dopamine reuptake blockers

-b/c dopamine very involved in the reward pathways

37
Q

Which is the only anti-depressant w/o a potential side effect of weight gain?

Why is this ironic?

A

NDRI = norepi dopmaine reuptake inhibitors

-ironic b/c contraindicated in pts w/ eating disorders due to increase risk of seizures

38
Q

Which antidepressant doesn’t have a risk of sexual side effects

A

NDRIs = norepi dopmaine receptor inhibitors

39
Q

What drug a first line ADHD drug that can sometimes be used for depression?

A

NRIs = norepi reuptake inhibitors

40
Q

What are some side effects of NRIs?

A

Norepi reuptake inhibitors (treats ADHD in the US, depression in Europe)

Side effects = tremor, agitation, HTN, and tachycardia

41
Q

Which receptor is responsible for the anti-depressive properties of SSRIs?

A

5-HT1A receptors = post-synaptic site of action of therapy for antidepressants
-where the excess serotonin works on for anti-depressive and anti-anxiety effects

42
Q

What are NaSSAs?

Mechanism?

A

NaSSA = Noradrenaline and specific serotonergic antidepressant

  • increases NE
  • increases 5-HT at the 5-HT1A receptor (good for anti-depressive and anti-anxiety purposes)
  • blocks the other serotonin receptors => no GI side effects, no sexual dysfunction etc
43
Q

For what population is Mirtazapine highly useful in?

A

Mirtazapine = NaSSA

-NaSSAs can cause sedation and increased appetite => typically used in the elderly

44
Q

Which antidepressant may result in Priaprism

A

Priaprism = painful and persistent erection of the penis (very dangerous)

-rare side effect of SARIs = serotonin antagonist and reuptake inhibitor

45
Q

What drugs are first line to treat anxiety?

A

Benzodiazepines

46
Q

(a) How do barbituates and benzodiaepines work on the GABA receptor?
(b) How does the mechanism differ?

A

(a) Both work as allosteric agonists of the GABA receptor => bind at the non-active site to increase the effect of GABA

(b) Barbituates work to increase duration of GABA receptor opening and can work w/o GABA input.
Benzos work to increase the frequency of GABA receptor opening and cannot work w/o GABA input => are more safe.

47
Q

Why are barbituates no longer first line for anxiety?

A
  • narrow therapeutic index
  • high addiction risk
  • depress all levels of the CNS: depress respiratory drive
48
Q

Name 3 anxiety disorders

A
  • GAD
  • OCD
  • panic disorder
49
Q

What are benzos used to treat?

A

Anxiety disorders (GAD, panic disorder, OCD) and insomnia

-also alcohol withdrawal

50
Q

What is the main side effect of benzos?

A

Sedation, ataxia => don’t operate heavy machinery

51
Q

Why do you need to taper down the dose of benzos?

A

B/c discontinuation can be painful and withdrawal can be deadly

52
Q

What cognitive disorder may benzos be linked to?

A

Correlated w/ increased risk of Alzheimer’s

but no proof of causation

53
Q

Which benzo receptor would you target to just have the sedation effects?

A

Benzo 1 receptor is for sedation (=> target w/ Ambien and Sonata to treat insomnia)

Benzo 2 receptor is for anxiolysis and muscle relaxation (no pure benzo 2 agonist yet)

54
Q

What are the advantages and disadvantages of Buspirone vs. Benzos to treat GAD?

A

Buspirone = 5-HT1A agonist

Advantages: no abuse potential, no tolerance or withdrawal, fairly well tolerated

Disadvantages: still takes 2-3 weeks before effect

55
Q

How does Ramelton help induce sleep?

A

= melatonin receptor agonist, but no proof that it’s any better than melatonin OTC
-no abuse or dependence

Neuro Exam 2 (4 decks)

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