Pharmacology of Antidepressants Flashcards

(51 cards)

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
drug interactions with SSRIs
there is an increased risk of GI bleeding if taken with NSAIDs
26
which 2 SSRIs are best for patients who are worried about drug interactions
citalopram and sertralie have the lowest risk of interactions
27
are there discontinuation symptoms with SSRIs?
yes, similar to AE myoclonus too
28
which SSRi is the safest in cardiac problems?
sertraline
29
what is there an increased risk of with SSRIs, especially in teens
transient increase in self harm or suicidal ideation, more likely in younger person
30
depression in the elderly
avoid SSRIs half dose of TCA
31
mechanism of action of TCAs
block the reuptake of monoamines into presynaptic terminals (mainly noradrenaline and serotonin)
32
in which class of depresion are TCAs good
severe, and elderly
33
what are the main AE of TCAs
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
do TCAs have an effect on weight?
cause weight gain
35
when are TCAs taken
at night - they cause sedation
36
what problems can teh sedation from TCA cause
daytime performance affected by drowsiness and difficulty concentrating
37
what are the CVS side effects of TCAs
cause postural hypotension, tachycardia and in more severe cases arrhythmias
38
what type of event would deem patients as having an increased arrhythmias risk, and so should avoid TCAs
eg post MI
39
overdose of TCAs
are cardiotoxic initially, excitement and delirium and convulsions cardiac dysrhythmias (heart block)
40
how does sudden death usually occur in TCA overdose
usually due to atrial fibrillation
41
why should TCAs be avoided in those with suicidal intent
due to cardiotoxicity
42
how do dual reuptake inhibitors work
block the reuptake of monoamines noradrenaline and 5HT into presynaptic terminals
43
when are dual reuptake inhibitors taken
in the morning - insomnia
44
what other use does duloxetine have
neuropathic pain and bladder instability (stres incontinence)
45
when are dual reuptake inhibitors usually used
if SSRI hasnt worked excellent in combination with mirtazapine
46
in which cases may mirtazapine be considered first line
if patient has insomnia and or poor appetite
47
does mirtazapine have a faster or slower onset than others
faster
48
what substance should mirtazapine not be combined with
alcohol - can cause GI upset
49
trazodone
monoamine receptor antagonist
50
which drug can cause priapism
trazodone, MARA
51