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Pharmacology > Week 3 depression, anxiety, insomnia > Flashcards

Week 3 depression, anxiety, insomnia Flashcards

1
Q

What are the first line drugs for the treatment of depression?

A

SSRI, SNRI’s, Mirtazipine, Wellbutrin(bupropion)

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2
Q

What are the adverse effects of muscarinic drugs?

A

dry mouth, worsening of closed angle glaucoma, lethargy, constipation

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3
Q

What are the adverse effects of histaminergic drugs?

A

sedation and weight gain

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4
Q 
What drug class do these drugs fall into?
Paroxetine, fluoxetine, citalopram, escitalopram, sertraline
A

SSRI’s

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5
Q

what is the mechanism of action for SSRI drugs?

A

desensitization of the presynaptic 5HT1A autoreceptor. Stops the feedback loop that causes cells to reuptake serotonin. the outcome is increased bioavailability of intrinsic serotonin.

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6
Q

Why do SSRI’s require 4-6 weeks for therapeutic effect?

A

Desensitization of the 5-HTP1A receptor takes time therefore there is not immediate bioavailability of endogenous serotonin

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7
Q

What is the general halflife of SSRI drugs?

A

generally longer than other classes of drug.

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8
Q

why are bridge order important for SSIRI’s especially in anxiety patients?

A

Because the side effects of the medication are nearly immediate however therapeutic effects take weeks to months to show. activation is one side effect that tends to increase anxiety for these patients

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9
Q

what are the most common side effects of SSRI drugs?

A

GI: nausea, vomiting, diarrhea. insomnia, sexual dysfunction, migrains, and tension headaches.

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10
Q

what is a more rare side effect of SSRI drugs

A

EPS (akethesia, dystonia, parkinsonism, TD)

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11
Q

What risks are elderly patients more likely to show when taking SSRI?

A

Extra Pyrimidal effects and falls

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12
Q

SSRI’s have what effect on weight?

A

generally weight loss is seen especially in early treatment

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13
Q

Why do falls happen with SSRI’s?

A

Bradycardia may occurr

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14
Q

what bridge orders might help with sleep when initiating SSRI treatment?

A

Beta Blocker drugs generally help with sleep disturbances and restlessness

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15
Q

What SSRI has the highest chance of causing serotonin syndrome?

A

Paroxetine

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16
Q

What CYP enzyme are fluoxetine and paroxetine heavily metabolized by?

A

CYP2D6

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17
Q

What happens when combining tamoxifen with paroxetine or fluoxetine?

A

The anticancer drug tamoxifen is less effective

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18
Q

why do we avoid MAOI and SSRI?

A

because there is increased risk of serotonin syndrome.

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19
Q

how do you avoid Serotonin syndrome when switching between prozac and a MAOI?

A

allow for a 4-6 week washout period

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20
Q

What is the interaction between metoprolol and SSRI’s Prozac and paroxetine?

A

all are metabolized by the CYP2D6 enzyme. mixing these drugs causes an increase in the bio availability of metoprolol and can cause excessive effects of the beta blocker

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21
Q

What SSRI carry’s the most cardiac risks?

A

Citalopram

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22
Q

What cardiac event may occur when citalopram is used?

A

increase in the QT interval

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23
Q

What dose of citalopram is advised and why?

A

nothing over 40mg/day due to dose depended risk for QT prolongation

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24
Q

what dose of citalopram is recommended for elderly, or hepato compromised patients?

A

no more than 20mg/day

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25
Q

What SSRI is the only SSRI that requires renal adjusting?

A

Paroxetine

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26
Q

what type of adjustments should be made for SSRI drugs?

A

always hepatic adjustment and for paroxetine, renal adjustment

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27
Q

What is the most potent SSRI?

A

citalopram

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28
Q

Venlafazine, desvenlafaxine, and duloxetine fall into what drug class?

A

SNRI serotonin norepiniphrine re-uptake inhibitors

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29
Q

what is the MOA for SNRI drugs?

A

inhibit reuptake of serotonin and norepinephrine

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30
Q

What is the general half-life of SNRI drugs

A

5-12 hours

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31
Q

what adjustments are needed for SNRI drugs

A

renal AND hepatic adjustments are required for these drugs

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32
Q

what are the adverse effects of SNRI drugs?

A

similar to those of SSRI with more noradrenergic side effects

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33
Q

what noradrenergic side effects can be expected with SNRI’s and when does this occurr?

A

increased HR, dry mouth, dilated pupils, sweating, constipation

34
Q

Why is discontinuation syndrome more common in SNRIs than SSRI?

A

because the halflife is shorter. especially in venlafaxine and desvenlafaxine.

35
Q

what SNRI can interact with metoprolol and cause overabundance

A

duloxetine is a strong CYP 2D6 inhibitor similar to some SSRI’s it can cause interactions with metoprolol

36
Q

what is the MOA for mirtazipine?

A

alpha-2 receptor antagonism. causes RELEASE of serotonin and nor epinephrine.

37
Q

What are the adverse effects of mirtazipine

A

dry mouth, sedatio, weight gain, elevated cholesterol, anticholinergic effects.

38
Q

What are the serious side effects of wellbutrin

A

lowered seizure threshold, psychosis and cognitive function issues

39
Q

What is the MOA of Bupropion?

A

inhibiting reuptake of norephinephrine and dopamine

40
Q

Wellbutrin is different from the other major classes of antidepressants because of what reason?

A

it does not have any effect on serotonin, only norepinephrine and dopamine

41
Q

What is the half life of wellbutrin

A

10-21 hours

42
Q

What kind of metabolic adjustments are required for wellbutrin

A

renal and hepatic

43
Q

What dose of wellbutrin is especially noted with seizures?

A

doses over 45mg/day

44
Q

what patient populations should avoid use of wellbutrin

A

pt’s with seizure history, anorexia or bulemia

45
Q

what mediations should wellbutrin not be given with and why

A

fluoxetine, paroxetine, sertraline, despiramine. because of theirCYP2D6 inhibition

46
Q

how should wellbutrin be titrated

A

slowly, avoid rapid titration

47
Q

What drug antidepressant drug classes cause bleeding risk?

A

SSRI and SNRI’s

48
Q

what is the medication treatment for post-partum depression?

A

brezanolone which must be given over 60 hour continuous infusion at the hospital with constant monitoring

49
Q

how does the dosing of prozac for depression differ from the dosing for anxiety

A

generally depression initial dosing is at 20mg but for anxiety the treatment starts at 10mg

50
Q

how soon do SSRI and SNRI’s take to have effect on anxiety

A

2-4 weeks

51
Q

what is the antidote for benzodiazepines

A

flumazenil

52
Q

patients with what conditions should avoid the use of benzodiazepines

A

patient’s with COPD and sleep apnea

53
Q

what are the preferred anti-anxiety benzodiazepines for elderly adults

A

oxazepam and lorazepam

54
Q

what birth defect are benzodiazepines associated with

A

cleft palate

55
Q

what is one major compliance drawback with buspirone for anxiety

A

it must be given in divided doses

56
Q

what is the MOA of buspirone

A

agonist of the 5-HT1 a receptor which reduces the firing of serotonin neurons

57
Q

what is the usual onset of effect for buspirone

A

2-3 week s

58
Q

what are common adverse effects of buspirone

A

transient anxiety, HA, dizziness, abodominal pain and nausea

59
Q

what are the four major classes of sleep medication

A

benzodiazepines, orexin receptor agonist, NBRA and melatonin receptor agonists

60
Q

what length of time should sleep medications be prescribed for?

A

2-4 weeks with PRN use

61
Q

what is the course length for sleep benzodiazepines

A

7-10 days with PRN use

62
Q

what is the ideal benzodiazepine for sleep in elderly populations?

A

temazepam

63
Q

after how long do patient’s develop tolerance to benzodiazepines?

A

4 weeks

64
Q

for long acting benzodiazepines how long does dependency and rebound insomnia occurr

A

2-4 weeks

65
Q

for short acting agents how long does benzodiazepine dependence and rebound insomnia tak?

A

days to weeks

66
Q

what is the MOA for NBRA

A

agonism of the gaba receptor the major inhibitory receptor in the body

67
Q

what popular drug fits into the NBRA category

A

ambien

68
Q

what are the side effects of NBRA medications

A

HA< dizziness, sonmnolence, GI upset, and low birth weight in pregnancy

69
Q

eszipiclone is a NBRA with what special side effect

A

dry mouth and foul taste in mouth

70
Q

what benefits to NBRA’s have over benzodiazepines despite similar mechanism?

A

less sleep cycle disruption, less abuse risk, less withdrawal, tolerance and next day effects, less rebound insomnia

71
Q

what is Ramelteon?

A

Ramelteon is a melatonin receptor agonist

72
Q

what is the MOA of ramelteon (MRA)

A

regulating sleepiness and phase shift from day to night by activating the melatonin receptors 1 and 2

73
Q

Can ramelteon be used in patient’s with COPD and sleep apnea

A

it is generally safer for these patients.

74
Q

patient’s on ramelteon should avoid what kinds of diet

A

high fat diet

75
Q

can patient’s with alcohol use disorder use ramelteon

A

yes

76
Q

what is the MOA for orexin receptor antagonists lemborexant and vucorexant

A

antagonizes orexin receptors. orexin usually causes wakefulness, these drugs block it and inhibit wakefulness

77
Q

what are the adverse effects of lemborexand and suvorexant?

A

sleep paralysis, hypnagogic and hynoponbic effects and cataplexy effects

78
Q

lumborexant and suvorexant should not be taken at what point in the night

A

when the patient has <7 hours to sleep

79
Q

orexin antagonists should be taken with what regard to food?

A

take on an empty stomach

80
Q

what is the safest prescription sleep medication for elderly patients?

A

ramelteon

Pharmacology (5 decks)

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