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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
Indications for SSRIs
- depression and dysthmia (used in less severe cases b/c of fewer side effects) - also anxiety and eating disorders
26
Mechanism of SSRIs
- 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
What may cause the delay in effect of Fluoxetine?
Fluoxetine = Prozac = SSRI | -downregulation of autoreceptors takes time => may add to the 4-6 week time until max effect
28
Why would SSRIs cause mental agitation/anxiety in some cases?
Due to excess 5HT around which activates the 5-HT2A and 5-HT2C receptors -excess serotonin doesnt just have one effect
29
What one possible effect of SSRI toxicity?
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
What drug exhibits discontinuation syndrome?
SSRIs Discontinuation syndrome = headache, irritability, irritabiliy and fatigue upon abrupt discontinuation => taper down dose over a couple weeks
31
What are some theories as to why serotonin may increased suicidal behavior?
- antidepressants may throw pt in hypomania - akathisia (motor restlessness) can be very disturbing - physical symptoms (energy/drive) improve before mental symptoms
32
Are serotonin and norepi -ergic drugs more likely to help in the treatment of (a) anxiety (b) obsession (c) low energy
Serotonin more helpful against anxiety and depression, while norepi more helpful to increase attention and energy
33
What are SNRIs
= serotonin-norepinephrine reuptake inhibitors | -block serotonin and NE reuptake pumps
34
What anti-depressant drug has been shown to be useful against fibromyalgia
SNRIs (serotonin-norepi reuptake inhibitors)
35
Which anti-depressant has akathisia as a potential side effect?
SSRIs
36
Which anti-depressant has been used for smoking cessation/
NDRI = norepi dopamine reuptake blockers -b/c dopamine very involved in the reward pathways
37
Which is the only anti-depressant w/o a potential side effect of weight gain? Why is this ironic?
NDRI = norepi dopmaine reuptake inhibitors -ironic b/c contraindicated in pts w/ eating disorders due to increase risk of seizures
38
Which antidepressant doesn't have a risk of sexual side effects
NDRIs = norepi dopmaine receptor inhibitors
39
What drug a first line ADHD drug that can sometimes be used for depression?
NRIs = norepi reuptake inhibitors
40
What are some side effects of NRIs?
Norepi reuptake inhibitors (treats ADHD in the US, depression in Europe) Side effects = tremor, agitation, HTN, and tachycardia
41
Which receptor is responsible for the anti-depressive properties of SSRIs?
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
What are NaSSAs? Mechanism?
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
For what population is Mirtazapine highly useful in?
Mirtazapine = NaSSA -NaSSAs can cause sedation and increased appetite => typically used in the elderly
44
Which antidepressant may result in Priaprism
Priaprism = painful and persistent erection of the penis (very dangerous) -rare side effect of SARIs = serotonin antagonist and reuptake inhibitor
45
What drugs are first line to treat anxiety?
Benzodiazepines
46
(a) How do barbituates and benzodiaepines work on the GABA receptor? (b) How does the mechanism differ?
(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
Why are barbituates no longer first line for anxiety?
- narrow therapeutic index - high addiction risk - depress all levels of the CNS: depress respiratory drive
48
Name 3 anxiety disorders
- GAD - OCD - panic disorder
49
What are benzos used to treat?
Anxiety disorders (GAD, panic disorder, OCD) and insomnia -also alcohol withdrawal
50
What is the main side effect of benzos?
Sedation, ataxia => don't operate heavy machinery
51
Why do you need to taper down the dose of benzos?
B/c discontinuation can be painful and withdrawal can be deadly
52
What cognitive disorder may benzos be linked to?
Correlated w/ increased risk of Alzheimer's | but no proof of causation
53
Which benzo receptor would you target to just have the sedation effects?
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
What are the advantages and disadvantages of Buspirone vs. Benzos to treat GAD?
Buspirone = 5-HT1A agonist Advantages: no abuse potential, no tolerance or withdrawal, fairly well tolerated Disadvantages: still takes 2-3 weeks before effect
55
How does Ramelton help induce sleep?
= 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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