Antidepressant Drugs Flashcards

1
Q

the timeline for diagnosis of major depressive disorder is after how long

A

2 weeks

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2
Q

what are the 2 types of depression

A

reactive/secondary
endogenous

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3
Q

what is the difference between reactive/secondary and endogenous depression in terms of treatment response

A

reactive/secondary- transient and responds to treatment
endogenous- responds to treatment but recurrence is high

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4
Q

5-HT mainly used what type of receptor

A

GPCR

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5
Q

what does the amine hypothesis of depression say

A

depression is due to the deficiency of amount and functions of 5-HT, NE, and DA neurons

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6
Q

the amine hypothesis of depression was based on what antihypertensive drug

A

reserpine

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7
Q

how does reserpine act which is used to further the amino hypothesis of depression

A

reserpine acts by blocking the transportation of monoamines into the pre-synaptic vesicles, leading to the inactivation of MAO enzymes= monoamine depletion in CNS

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8
Q

what does the neurotrophic hypothesis of depression say

A

neurotrophic factors (ex: brain derived neurotrophic factor) are needed for neural plasticity, resilience and neurogenesis

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9
Q

what is the relationship between brain derived neurotropic factor and depression

A

depressed patients have a decrease in BDNF

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10
Q

amygdala __ CRF release, hippocampus __ CRF release

A

stimulates
inhibits

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11
Q

what is the relationship between stress, CRF, ACTH, cortisol, and BDNF

A

stress= increased CRF, ACTH, and cortisol
high cortisol= decreased BDNF
decreased BDNF=depression

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12
Q

what are the 3 possible effects of action of antidepressant drugs

A

inhibit uptake of NE and 5-HT
inhibit MAO
block presynaptic alpha2 autoreceptors

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13
Q

what are 3 secondary adaptive changes as a result of antidepressant drug use

A

desensitization of presynaptic NE and 5-HT receptors
increase neurogenesis
increase BDNF transcription

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14
Q

monoamine oxidase is an intracellular enzyme present in __

A

neurons

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15
Q

what is the function of monoamine oxidase

A

prevents accumulation of neurotransmitters outside the vesicle

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16
Q

selegiline as a MAO inhibitor inhibits __

A

irreversibly inhibits MAO-B

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17
Q

MAO inhibitors mechanism of action

A

inactivation of MAO
=decreased monoamine clearance
=increased NE, 5-HT, and dopamine

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18
Q

what is the effect of inhibition of MAO in the liver and gut

A

decreases the metabolism of tyramine, increasing drug-food interactions

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19
Q

what drug class is preferred in atypical or refractory depression

A

MAO inhibitors

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20
Q

why are MAO inhibitors rarely used in clinical practice compared to SSRIs (3)

A

more side effects
potential for food-drug interactions
restriction of tyramine rich foods

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21
Q

what are the 3 main adverse effects of MAO inhibitors

A

postural (orthostatic) hypotension
weight gain
sexual dysfunctions

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22
Q

MAO inhibitors can cause drug-drug interactions in use with…

A

drugs that increase NE
drugs with alpha agonists
tyramine rich foods
SSRIs, TCAs

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23
Q

what is the cheese reaction that can occur when MAO inhibitors are used with tyramine rich foods

A

excessive release of NE
–>hypertensive crisis, tachycardia, cardiac arrythmias

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24
Q

what must be done to avoid serotonin syndrome when using MAOIs and SSRIs

A

both require a washout period of 2 weeks prior to other drug use

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25
Q

what antidepressant class is used if patients don’t respond to SSRIs

A

tricyclic antidepressant (TCA)

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26
Q

tricyclic antidepressant (TCA) mechanism of action

A

increases NE and 5-HT by blocking transporters at presynaptic terminals leads to increased concentration of NE and 5-HT in the synaptic cleft

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27
Q

what drug class can be used in those with depression and Parkinson’s disease

A

TCA

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28
Q

what are 4 adverse effects of TCA

A

antimuscarinic effects
cardiac arrythmia
alpha-1 blocker
histamine blocker

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29
Q

how can TCA use lead to cardiac arrythmia

A

inhibition of fast Na+ channels

30
Q

what are 3 symptoms of TCA toxicity

A

coma, convulsions, cardiotoxicity

31
Q

what can be done to minimize withdrawal syndromes and cholinergic rebound effects with TCAs

A

tapering of dose

32
Q

TCAs are contradicted in (3)

A

angina
arrhythmias
benign prostatic hyperplasia

33
Q

TCAs reduce efficacy of what class of drugs

A

antihypertensives (alpha2 agonists)

34
Q

what is used to treat cardiac toxicity in TCA use

A

sodium bicarbonate

35
Q

how does sodium bicarbonate work to reduce the toxic effects of TCAs

A

displaces TCAs from cardiac sodium channels, preventing their blockage

36
Q

what is the mechanism of action of amoxapine

A

it’s a TCA which blocks 5-HT2 and dopamine D2 receptors

37
Q

what is an adverse effect of amoxapine

A

parkinsonian syndrome

38
Q

what drug is used to treat depression with agitation/anxiety

A

Maprotiline TCA

39
Q

what drug is used to treat depression and insomnia

A

Maprotiline

40
Q

what drug class is preferred for OCD

A

SSRI

41
Q

what can the TCA amitriptyline be used for

A

neuropathic pain

42
Q

doxepin is a TCA that can be used for __ and __ in addition to depression

A

hypnotics
pruritus

43
Q

what is the mechanism of action of SSRIs

A

selectively inhibit prejunctional serotonin transporter to block the reuptake of serotonin

44
Q

SSRIs require __ weeks to improve mood but don’t reach maximum benefit until __ weeks

A

2
12

45
Q

what is the effect of antidepressants on BDNF

A

increases

46
Q

why are SSRIs more preferred than TCAs for depression

A

SSRIs lack anticholinergic, alpha blocking, and antihistamine properties

47
Q

how does the SSRI fluoxetine work

A

inhibits activation of Tamoxifen (antiestrogen) into an active metabolite

48
Q

what drugs are preferred over fluoxetine due to having less interactions

A

citalopram
escitalopram

49
Q

with fluoxetine, how long must be waited after discontinuation before starting MAO inhibitors

A

4 weeks

50
Q

what are 3 adverse effects of SSRIs

A

sexual dysfunction
rebound/discontinuation syndrome
SIADH–>hyponatremia

51
Q

why is less rebound/discontinuation syndrome seen less with fluoxetine

A

its a long acting metabolite

52
Q

how do SSRIs differ from SNRIs

A

SSRIs block alpha1 adrenergic, muscarinic, and histamine receptors
SNRIs do not

53
Q

what drug class is preferred in depression with chronic pain conditions and also neuropathic pain

A

SNRIs

54
Q

what is an adverse effect of the SNRI Venlafaxine

A

hypertension

55
Q

the SNRI Duloxetine is not preferred in patients with what 2 conditions

A

hepatic insufficiency
end stage renal disease

56
Q

what is the mechanism of action of trazodone

A

5-HT2 presynaptic receptor antagonist
–>increased 5HT release

57
Q

trazadone has __ blocking activity and __ blocking activity

A

alpha1
H1

58
Q

what are 3 effects of alpha1 blocking activity by trazodone

A

priapism
cardiac arrythmia
postural hypotension

59
Q

what is the effect of H1 blocking activity by trazodone

A

produces mode sedation, useful in insomnia

60
Q

what drug is preferred in depression with agitation and insomnia

A

trazodone

61
Q

what drug is preferred for sleep over benzodiazepines due to the lack of tolerance of dependence

A

trazodone

62
Q

nefazodone adverse effect

A

hepatotoxicity

63
Q

what is the mechanism of action of buproprion

A

blocks reuptake of NE and DA

64
Q

unlike other antidepressants, buproprion has little risk of causing ___

A

sexual dysfunction

65
Q

bupropion can cause __ or __ with toxicity

A

seizures
insomnia

66
Q

what is the mechanism of action of mirtazapine

A

inhibition of presynaptic alpha2 receptors increases NA and 5-HT release

67
Q

what drug is used in depression with anorexia

A

mirtazapine

68
Q

what drug class is used for bulimia

A

SSRI

69
Q

what drugs can be used for treatment resistance major depression

A

atypical antipsychotics+SSRIs or SNRIs

70
Q

what antidepressant has rapid effect within 24 hours

A

ketamine-like drugs (esketamine)

71
Q

what is the mechanism of action of ketamine like esketamine

A

blocks presynaptic NMDA receptors

72
Q

what antidepressant can be used in postpartum depression

A

brexanolone