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Psychopharmacology > Lecture 18: Antidepressants > Flashcards

Lecture 18: Antidepressants Flashcards

1
Q

dysthymia

A

relatively mild but prolonged symptoms that persist for at least two years

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2
Q

depression is the ___ most disabling disease in the world

A

4th

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3
Q

by 2020, depression will be the ___ leading cause of disability

A

2nd

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4
Q

WHO estimated that ___ people worldwide have depression

A

300,000,000

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5
Q

MDD responsible for __% of psychiatric hospitalizations

A

70

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6
Q

MDD responsible for __% of suicides

A

40

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7
Q

__ of the US population suffers per year

A

9-10%

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8
Q

__% of men and __% of women experience depression

A

10, 25

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9
Q

__% of cases are adequately treated per year

A

21

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10
Q

MDD is __ more common in 1st degree relatives of someone with depression

A

3x

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11
Q

classically, MDD was thought to be caused by ___

A

deficiency in monoamines (5HT, DA, NE)

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12
Q

problem with monoamine deficiency hypothesis

A

NT changes occur shortly after taking antidep, but clinical benefits develop slowly

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13
Q

now, interest is on long term action, specifically ___

A

2nd messengers and their fx

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14
Q

3 possible 2nd messenger effects

A
  1. protect neurons from damage due to injury or trauma
  2. promote and maintain health and stability of new neurons
  3. promote activity-dependent remodeling of existing cells; plasticity
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15
Q

neurogenic theory of depression; 2 discoveries

A
  1. neurons are able to repair/remodel themselves

2. adult brain can make new neurons

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16
Q

postnatal neurogenesis

A

brain making new neurons as an adult

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17
Q

stressful conditions can damage the ___

A

hippocampus

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18
Q

hippocampus shrinks in response to ___

A

corticosteroids

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19
Q

depression is now thought of as a ___

A

neurodegenerative disorder

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20
Q

stressful conditions reduce neurogenesis in __ (2)

A

hippocampus

frontal cortex

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21
Q

network hypothesis of antidepressants

A

recovery from depression is gradual process facilitated by structural guidance and rehab

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22
Q

2 possible pathways for antidep MoA starting with 5HT or NE reuptake inhibition

A
  1. 5HT4,6,7 / beta adrenergic - adenylyl cyclase - cAMP - cAMP dep protein kinase (PKA) - increase creb (cAMP response element binding protein) - BDNF (brain derived neurotrophic factor)
  2. 5HT2 / alpha1 adrenergic - Ca2+ dep kinases - CREB - BDNF
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23
Q

BDNF

A

brain-derived neurotrophic factor

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24
Q

CREB

A

cAMP response element-binding protein

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25
Q

PKA

A

cAMP-dependent protein kinase

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26
Q

what increases expression of adenylyl cyclase?

A

stimulation of 5HT4,6,7 or beta adrenergic

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27
Q

what increases expression of Ca2+ dependent kinases?

A

stim of 5HT2 or a1 adrenergic

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28
Q

adenylyl cyclase increases __

A

cAMP

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29
Q

cAMP increases ___

A

PKA

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30
Q

PKA increases ___

A

CREB

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31
Q

CREB increases __

A

BDNF

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32
Q

what does BDNF do? (3)

A
  1. trophic actions
  2. increased function
  3. synaptic remodeling
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33
Q

chronic stress decreases the expression of __ in the ___

A

BDNF, hippocampus

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34
Q

stress elevates levels of ___

A

glucocorticoids

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35
Q

what do glucocorticoids do?

A

reduce expression of BDNF

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36
Q

what does reduced expression of BDNF do?

A

atrophy or death or neurons

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37
Q

6 types of AD

A
  1. tricyclic
  2. MAOI
  3. atypical
  4. SSRIs
  5. dual action
  6. SNRIs
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38
Q

1st generation ADs

A

TCAs, MAOIs

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39
Q

1st TCA

A

imipramine

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40
Q

imipramine MoA

A

blocks presyn transporters for 5HT and NE

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41
Q

general TCA action

A

blocks presyn transporters for 5HT and NE

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42
Q

what were TCAs named for?

A

their structure

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43
Q

monoamine hypothesis of mania and depression

A

depression from deficiency of NE and 5HT; excess leads to mania

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44
Q

MAOI mech of action

A

block enzyme MAO that metabolizes and regulates amount of amine transmitters in nerve terminal

45
Q

difference between MAOI and TCAs

A

TCAs inhibit reuptake, MAOIs inhibit degradation

46
Q

3 TCA clinical limitations

A
  1. slow onset
  2. side effects
  3. cardiotoxic/overdose fatality
47
Q

3 second gen compounds

A
  1. trazodone (desyrel)
  2. bupropion (wellbutrin)
  3. venlafaxine (effexor)
48
Q

4 TCAs

A
  1. imipramine (tofranil)
  2. desipramine (norpramin)
  3. nortriptyline (pamelor, aventil)
  4. clomipramine (anafranil)
49
Q

when were SSRIs invented?

A

1980s-1990s

50
Q

first SSRI

A

prozac

51
Q

has availability of SSRIs reduced the number of treatment resistant patients?

A

no

52
Q

are SSRIs more efficacious?

A

no, but fewer side effects

53
Q

6 SSRIs

A
  1. fluoxetine (prozac)
  2. sertraline (zoloft)
  3. paroxetine (paxil)
  4. citalopram (celexa)
  5. fluvoxamine (luvox)
  6. escitalopram (lexapro)
54
Q

when were TCAs and MAOIs introduced?

A

1950s-1960s

55
Q

prototypic TCA

A

imipramine (tofranil)

56
Q

pharmacologically active metabolite of imipramine

A

desipramine (norpramin)

57
Q

2 MoAs of imipramine/desipramine

A
  1. block presyn reuptake transporter for 5HT and NE

2. block postsynaptic receptors for histamine, ACh, and NE (alpha adrenergic)

58
Q

blockade of histamine receptors results in ___

A

drowsiness/sedation

59
Q

blockade of AChRs results in (6)

A
  1. confusion
  2. memory and cognitive impairments
  3. dry mouth
  4. blurred vision
  5. increased HR
  6. urinary retention
60
Q

blockade of NE receptors results in ___

A

fx blood pressure, can cause orthostatic hypertension

61
Q

nortriptyline and desipramine have ___ than other TCAs

A

less sedation and fewer anticholinergic side fx

62
Q

half life of imipramine

A

10-20h

63
Q

3 TCAs other than imipramine

A
  1. desipramine (norpramin)
  2. nortriptyline (pamelor, aventil)
  3. clomapramine (anafranil)
64
Q

4 limitations of TCAs

A
  1. slow onset
  2. side fx
  3. cardiotoxic arrhythmias
  4. non universal efficacy
65
Q

surprisingly, TCAs can be effective ___

A

analgesics

66
Q

MAO effect on GI tract

A

breaks down tyramine

67
Q

effect of elevated tyramine

A

increase blood pressure, possible heart attack/stroke

68
Q

trazodone was __ second gen

A

3rd

69
Q

most common trazodone side effect

A

drowsiness

70
Q

trazodone MoA

A

not very potent 5HT and NE reuptake blocker

71
Q

trazodone effect on sex

A

may improve sex, but has risk of priapism

72
Q

trazodone has ___ half life

A

short

73
Q

clomipramine (anafranil) is structurally similar to ___, but has greater effect on __

A

TCAs; more 5HT reuptake effect

74
Q

clomipramine and its active metabolite also inhibit ___

A

NE

75
Q

clomipramine is classified as a ___

A

mixed serotonin-NE reuptake inhibitor

76
Q

MoA of SSRIs

A

block presynaptic transporter for 5HT

77
Q

___ is least selective for 5HT, and ___ is most selective

A

prozac, celexa

78
Q

which receptor is the basis of therapeutic effect of all SSRIs?

A

5HT1

79
Q

stimulation of 5HT2 receptors thought to be responsible for (5)

A
  1. insomnia
  2. anxiety
  3. agitation
  4. sexual dysfunction
  5. serotonin syndrome
80
Q

2 effects at 5HT1

A

antidepressant, anxiolytic

81
Q

effect at 5HT3

A

nausea

82
Q

are SSRIs fatal in OD?

A

no

83
Q

SSRIs can inhibit ___, causing what dangerous result?

A

CYP450

possibly dangerous reactions with other meds

84
Q

5 concerns with SSRIs

A
  1. serotonin syndrome
  2. withdrawal
  3. sexual dysfunction
  4. long term may cause cog impairment
  5. fetal effects
85
Q

serotonin syndrome (5)

A
  1. cog disturbance (confusion, hypomania)
  2. agitation/restlessness
  3. autonomic dysfunction (fever, diarrhea, tachycardia)
  4. neuromuscular impairment (ataxia, twitching)
  5. visual hallucinations
86
Q

what percent of patients develop SSRI withdrawal?

A

60%

87
Q

6 core fx of withdrawal from SSRIs

A
  1. flulike symptoms
  2. nausea
  3. insomnia
  4. imbalance
  5. sensory disturbances (shocks)
  6. hyperarousal
88
Q

___% of depression patients with SSRIs experience sexual dysfunction

A

80%

89
Q

5 other side fx of SSRIs

A
  1. suicidality
  2. sleep disturbance
  3. apathy
  4. physiological symptoms (nausea, coma, muscle cramps, GI bleeding)
  5. pregnancy warning
90
Q

drug most associated with serotonin syndrome, psychosis, temper, delusions, discontinuation

A

paxil

91
Q

fluvoxamine (luvox) sturctural derivative of ___

A

prozac

92
Q

large dose of citalopram associated with ___

A

ECG irregularities, seizures

93
Q

which drug causes problems for liver? which causes least problems?

A

prozac

celexa

94
Q

escitalopram is the ___ of celexa

A

therapeutically active optical isomer of celexa

95
Q

lexapro is __ as potent as celexa

A

2x

96
Q

first dual-action antidep

A

TCAs

97
Q

venlafaxine MoA

A

mixed 5HT-NE reuptake inhibitor

98
Q

duloxetine/cymbalta MoA

A

blocks reuptake of 5HT and NE

99
Q

mirtazepine (remeron) MoA

A

increases presyn release of NE and 5HT

  1. blocks central alpha2 autoreceptors, increasing NE
  2. blocks adrenergic heteroreceptors located on 5HT neuron terminals, which usu inhibit 5HT release (only 5HT1 receptors, because mirtazepine blocks 5HT2 and 5HT3)
100
Q

problem with remeron

A

causes drowsiness bc of action on histamine; appetite increase/weight gain

101
Q

MoA bupropion

A

dopamine-norepinephrine reuptake inhibitor

102
Q

are SNRIs better than placebo?

A

no

103
Q

STAR*D study

A

sequenced treatment alt to releive depression

104
Q

results of STAR*D

A

zoloft and escitalopram may have slight advantages, though modest benefits over others

105
Q

combinations of ___ and ___ are being explored.

A

combo of SSRI and 5HT2 receptor antagonist

106
Q

ketamine MoA

A

NMDAR antagonist

107
Q

3 benefits of ketamine

A
  1. response in hours
  2. promotes synaptogenesis
  3. effective in 70% of patients
108
Q

problem with ketamine

A

best route is IV

109
Q

novel approach to depression

A

effort to manipulate hypothalamic-pituitary-adrenal (HPA) axis

Psychopharmacology (22 decks)

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