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RB Y3 2 Psychiatry > Pharmacology of Antidepressants > Flashcards

Pharmacology of Antidepressants Flashcards

1
Q

which drugs have the most effect in moderate depression

A

most of the drugs have a similar effect

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2
Q

which drugs are most effective in severe depression

A

TCAs

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3
Q

what are teh 3 cardinal symptoms of depression

A

anergia, low mood and anhedonia

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4
Q

outline the criteria for mild, moderate and severe depression

A
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5
Q

do AD work immediately?

A

no, take around 2-6 weeks

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6
Q

how long do depressive symptoms need to be present for for crtieria?

A

most of teh day for the past 2 weeks

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7
Q

are dosing adjustments amde for older patients?

A

yes, they dont need as large as an adult dose

usually start on half the adult dose

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8
Q

what happens if you start a patient on an AD and see no change?

A

assess after 4-6 weeks

increase dose and review in 2 weeks

if after 6 weeks at max/max tolerated dose there is still non/inadequate response - switch drug

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9
Q

if eg fluxoetine doesnt work cn you switch to citalopram?

A

no, must swittch AD class

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10
Q

how long after resolutionof symptoms must AD be continued for, and after recurrence

A

6-12 months

12-24 if recurrence

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11
Q

what happens if you stop AD too soon?

A

50% relapse

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12
Q

in which circumstances would AD be continued indefinitely?

A

3rd relapse, or very severe

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13
Q

what is the monoamine hypothesis

A

suggests that depression results from functionally deficient monoaminergic transmission in the CNS. although this is too simple to fully explain depression, pharmacological theory is based on increasing the monoaminergic transmission

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14
Q

endocrinology and depression

A

dexamethasone suppression test is abnormal in 1/3 patients - abnormally weak response of plasma cortisol to exogenous steroid

this may reflect monomaine transmission in the hypothalamus

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15
Q

what is the first derivative of serotonin

A

tyrptophan

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16
Q

what is noradrenaline made from

A
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17
Q

what is the role of monoamine oxidase enzyme

A

removes the neurotransmitters norpinehrine, serotonin and dopamine from the brain by reabsorbing them from teh synpatic clefr and breaking them down

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18
Q

mechanism of action of SSRIs

A

selectively inhibit the reuptake of serotonin from the synaptic cleft

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19
Q

which drug is used first line in depression

A

usually SSRI, individuals respond differently to different drugs

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20
Q

when are SSRIs taken

A

morning, reduce insomnia

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21
Q

use of SSRIs in teh elderly

A

avoid! they cause hyponatraemia and falls

22
Q

SSRIs and sexual function

A

can cause sexual dysfunction and failure of orgasm

23
Q

what effect do SSRIs have on weight

A

can cause anorexia

24
Q

drug for patient with depression and obesity?

A

fluoxetine causes weight loss

25
Q

drug interactions with SSRIs

A

there is an increased risk of GI bleeding if taken with NSAIDs

26
Q

which 2 SSRIs are best for patients who are worried about drug interactions

A

citalopram and sertralie have the lowest risk of interactions

27
Q

are there discontinuation symptoms with SSRIs?

A

yes, similar to AE

myoclonus too

28
Q

which SSRi is the safest in cardiac problems?

A

sertraline

29
Q

what is there an increased risk of with SSRIs, especially in teens

A

transient increase in self harm or suicidal ideation, more likely in younger person

30
Q

depression in the elderly

A

avoid SSRIs

half dose of TCA

31
Q

mechanism of action of TCAs

A

block the reuptake of monoamines into presynaptic terminals (mainly noradrenaline and serotonin)

32
Q

in which class of depresion are TCAs good

A

severe, and elderly

33
Q

what are the main AE of TCAs

A

they have anticholinergic effects as block M2 and M3 receptors in smooth muscle: bladder (urinary retention), vascular and airways, blurred vision, dry mouth, constipation

34
Q

do TCAs have an effect on weight?

A

cause weight gain

35
Q

when are TCAs taken

A

at night - they cause sedation

36
Q

what problems can teh sedation from TCA cause

A

daytime performance affected by drowsiness and difficulty concentrating

37
Q

what are the CVS side effects of TCAs

A

cause postural hypotension, tachycardia and in more severe cases arrhythmias

38
Q

what type of event would deem patients as having an increased arrhythmias risk, and so should avoid TCAs

A

eg post MI

39
Q

overdose of TCAs

A

are cardiotoxic

initially, excitement and delirium and convulsions

cardiac dysrhythmias (heart block)

40
Q

how does sudden death usually occur in TCA overdose

A

usually due to atrial fibrillation

41
Q

why should TCAs be avoided in those with suicidal intent

A

due to cardiotoxicity

42
Q

how do dual reuptake inhibitors work

A

block the reuptake of monoamines noradrenaline and 5HT into presynaptic terminals

43
Q

when are dual reuptake inhibitors taken

A

in the morning - insomnia

44
Q

what other use does duloxetine have

A

neuropathic pain and bladder instability (stres incontinence)

45
Q

when are dual reuptake inhibitors usually used

A

if SSRI hasnt worked

excellent in combination with mirtazapine

46
Q

in which cases may mirtazapine be considered first line

A

if patient has insomnia and or poor appetite

47
Q

does mirtazapine have a faster or slower onset than others

A

faster

48
Q

what substance should mirtazapine not be combined with

A

alcohol - can cause GI upset

49
Q

trazodone

A

monoamine receptor antagonist

50
Q

which drug can cause priapism

A

trazodone, MARA

51
Q
A

RB Y3 2 Psychiatry (12 decks)

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