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PHRM 845 > L67-68 Watts antidepressants > Flashcards

L67-68 Watts antidepressants Flashcards

1
Q

3 types of depression and rough estimate of prevalency

A

reactive (60%)
Major depressive (25%)
Bipolar affective (15%)

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2
Q

some physiological clinical features of depression

A

decreased sleep
appetite changes
fatigure
psychomotor dysfxn

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3
Q

some psychological clinical features of depression

A

dysphoric mood
worthlessness
guilt
loss of interest/pleasure *

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4
Q

2 cognitive clinical features of depression

A

decreased concentration
suicidal ideation

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5
Q

“biogenic amine” hypothesis of depression:
- _________ causes depression by depleting ___ and ___ from vesicles

A

reserpine
NE
5HT

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6
Q

“biogenic amine” hypothesis of depression:
agents that increase ___ and ___ are effective for treating depression

A

5HT and NE

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7
Q

“biogenic amine” hypothesis of depression:
Genetic polymorphisms in ____ promotor

A

SERT

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8
Q

“biogenic amine” hypothesis of depression:
Alterations in ________ and __ receptors

A

5HT1A/2C and a2

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9
Q

neuroendocrine hypothesis of depression thing Watts said to know

A

know that HPA axis is involved and it is overactivity of HPA axis that causes excessive release of CRF (causes core depressive sxs)

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10
Q

CRF acts on _____ receptors which leads to disruption of what 2 things

A

CRF1 receptors, sleep and sexual behaviors

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11
Q

3rd neurotrophic hypothesis of depression key message according to Watts

A

Brain-derived neurotrophic factor (BDNF) is critical in neural plasticity, resilience, and neurogenesis

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12
Q

dendritic ________ start to disappear in depression

A

sprouts

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13
Q

Integration of hypotheses of depression (shit he wants us to know)
____ and ____ abnormalities regulate BDNF levels

A

HPA
steroid

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14
Q

Integration of hypotheses of depression (shit he wants us to know)
Hippocampal glucocorticoid receptors are activated by _____ during stress which (increases/decreases) BDNF

A

cortisol
decrease

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15
Q

Integration of hypotheses of depression (shit he wants us to know)
chronic activation of _____ receptors increases BDNF signaling

A

monoamine

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16
Q

Integration of hypotheses of depression (shit he wants us to know)
chronic activation of monoamine receptors leads to a downregulation of the ____ axis

A

HPA

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17
Q

how long does it take most antidepressants to show effects?

A

days to weeks
(next slide says 2-3 weeks)

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18
Q

what two neurotransmitters are normally degraded by monoamine oxidase

A

NE and 5HT

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19
Q

MAOis cause more NE and 5HT released from ______ into the _______

A

vesicles
synapse

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20
Q

2 non-selective MAOi’s

A

phenelzine (nardil)
Tranylcypromine (parnate)

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21
Q

2 MAO-B selective drugs

A

selegiline (eldepryl/ensam)
Safinamide (xadago)

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22
Q

1 MAO-A selective drug

A

Moclobemide (manerix)

23
Q

Reversible
A. MAO-A
B. MAO-B

A

both

24
Q

used in europe but not here yet
A. MAO-A
B. MAO-B

A

A. MAO-A

25
Q

6 severe side effects of MAOi’s

A

headache
drowsiness
dry mouth
weight gain
hypotension
sexual dysfxn

26
Q

avoid what food for what purpose in MAO’is

A

tyramine bc of hypertensive crisis risk

27
Q

2 MAOi interactions with OTCs

A

cold preparations, diet pills

28
Q

3 drug classes that interact with MAOi’s

A

TCA
SSRI
L-DOPA

29
Q

what main herbal product has MAOi activity and should be avoided

A

st johns wort

30
Q

Site of Action of Reuptake Blockers:
Orthosteric site -> _____ binds

A

serotonin

31
Q

Site of Action of Reuptake Blockers:
allosteric sites -> _____

A

antidepressants bind here and block NE and 5HT into synapse

32
Q

4 indications for TCAs

A

depression
panic disorder
chronic pain
enuresis

33
Q

Why is OD/toxicity extremely dangerous in TCAs

A

depressed pts more likely to be suicidal *

34
Q

TCA/Tertiary Amine/Secondary Amine MOA

A

inhibit NE and 5HT reuptake via NET and SERT

35
Q

Also act as H1, a1, and antimuscarinic agonists
A. Tertiary amine TCAs
B. Secondary amine TCAs

A

A. Tertiary amine TCAa

36
Q

causes less general side effects than the other as a whole
A. Tertiary amine TCAs
B. Secondary amine TCAs

A

B. Secondary amine TCAs

37
Q

Imipramine:
Tert or Sec amine

A

tertiary

38
Q

Amitriptyline:
Tert or Sec

A

Tertiary

39
Q

imipramine metabolized into __________?

A

desipramine (a secondary amine)

40
Q

Amitriptyline metabolized into ________?

A

nortriptyline, a secondary amine

41
Q

Used for enuresis and ADHD
A. Imipramine
B. Amitriptyline
C. Clomipramine
D. Doxepin

A

A. Imipramine

42
Q

Clomipramine:
Tert or Sec

A

Tertiary

43
Q

Doxepin
Tert or Sec

A

Tertiary

44
Q

Used for OCD
A. Imipramine
B. Amitriptyline
C. Clomipramine
D. Doxepin

A

C

45
Q

Desipramine
Tert or Sec

A

secondary

46
Q

Nortriptyline
Tert or Sec

A

secondary

47
Q

Maprotiline
Tert or Sec

A

secondary

48
Q

Better at targeting NET than SERT
A. Tertiary
B. Secondary

A

B. Secondary -> there is an “n” in secondary

49
Q

T or F: Opening Serotonin transporter pumps is a part of the MOA of SSRIs

A

false, they get blocked to keep 5HT in synapse longer

50
Q

I (cole) know the ssris so i’m skipping cards on that just so anyone else looking at this knows

A

sorry

51
Q

highlighted side effect of SSRIs

A

anxiety for some reason

52
Q

Vilazodone
A. SSRI + 5HT1A partial agonist
B. 5HT2 Antag/ SERT inhibitor

A

A

53
Q

Vortioxetine
A. SSRI + 5HT1A partial agonist
B. 5HT2 Antag/ SERT inhibitor

A

A

54
Q
A

PHRM 845 (34 decks)

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