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Drugs and the Brain > Antidepression drugs > Flashcards

Antidepression drugs Flashcards

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The Brain flashcards
1
Q

Iproniazid mechanism

A

MOA inhibitor

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2
Q

Iproniazid use

A

AD (no longer used clinically)
Tuberculosis drug - patients aborally happy - evidence for monoamine hypothesis

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3
Q

List MOA inhibitors used in depression

A

Phenelzine
Tranylcypromine
Isocarboxazid
Moclobemide

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4
Q

MAOI mechanism

A

Inhibit MOA in presynaptic mt outer membrane
Increases releasable pool of MAs
Immediate action

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5
Q

Name older MOAI drugs

A

Phenelzine
Tranylcypromine
Isocarboxazid

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6
Q

Describe the use of older MOAI drugs

A

Very effective
Not prescribed much due to lots of interactions (dietary) e.g. cheese reaction

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7
Q

What is the cheese reaction and what drug is it found in

A

Tyramine (dietary MA) cannot be metabolised in the liver by MOA-A as normal when it is inhibited my MOAIs
Tyramine does not cross the BBB but in periphery acts as a false substrate for:
NET (gets taken into presynaptic sympathetic terminals)
VMAT (gets put into vesicles)
It is then released (non-vesicularly) and causes massive activation of sympathetic ns
Hypertensive crisis - stroke and death

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8
Q

Newer MAOI

A

Moclobomide

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9
Q

New MAOI mechanism of action

A

Selective for MAO A
Reversible inhibitor

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10
Q

Why are the dietary interactions seen with old MAOIs not seen in new MAOIs

A

New MAOIs are reversible - tyramine can compete with drug so does get broken down in liver

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11
Q

Use of moclobemide

A

AD
Newer MAOI
Still under prescribed due to prejudice of MAOIs caused by older class MAOIs

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12
Q

What is serotonin syndrome and what is is caused by

A

Interaction of old class MAOIs with SSRIs or tricyclic ADs
Causes huge increase in synaptic serotonin ]Can cause confusion, muscles twitching, seizure, coma, death

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13
Q

what are SSRIs

A

Selective seretonin reuptake inhibitors

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14
Q

What are SNRIs

A

Serotonin/noradrenaline reuptake inhibitors

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15
Q

What are NRIs

A

NA reuptake inhibitors

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16
Q

What is the most widely used class of AD

A

SSRIs

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17
Q

Name 4 SSRIs

A

Citalopram
Paroxetine (Paxil)
Sertraline
Fluoxetine (Prozac)

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18
Q

What is citalopram

A

An SSRI

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19
Q

What is Paroxetine/Paxil

A

An SSRI

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20
Q

What is Sertraline

A

An SSRI

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21
Q

What is Fluoxetine/Prozac

A

AN SSRI

22
Q

Name 2 SNRIs

A

Venlafaxine
Duloxetine

23
Q

What is venlafaxine

A

An SNRI

24
Q

What is Duloxetine

A

An SNRI

25
Q

Name 2 NRIs

A

Reboxetine
Atomoxetine

26
Q

What is reboxetine

A

An NRI

27
Q

What is atomoxetine

A

An NRI

28
Q

Other uses of SSRIs/SNRIs/NRIs

A

anxiety disorders
premature ejaculation

29
Q

What are 1st generation ADs

A

MAOIs
Tricyclic ADs

30
Q

What are 2nd generation ADs

A

SSRIs
Some people include SNRIs and NRIs

31
Q

What are 3rd generation ADs

A

SNRIs
NRIs
Only some people recognise these as their own generation

32
Q

First SSRI produced

A

Fluoxetine/Prozac

33
Q

What is the side effect profile of 2nd/3rd generation ADs like and why is it important

A

Quite benign, low overdose suicide risk (compared to 1st gen)
Important as med overdose is common method of suicide attempt

34
Q

Name 3 tricycles ADs

A

Amitriptyline
Nortriptyline
Imipramine

35
Q

Tricyclic ADs mechanism

A

Similar to SNRIs
Inhibit SERT and NET
Increase synaptic concentration of MAs

36
Q

Why are tricyclic ADs only used for treatment resistant MDD

A

They have a high suicide mortality on overdose

37
Q

Other uses of tricyclic ADs

A

Pain
Migraine
(At lower doses)

38
Q

What is the difference between SNRIs and tricyclic

A

Side effect profiles
Tricyclics have hard to deal with side effects and very dangerous in overdose

39
Q

What is discontinuation syndrome

A

flu like symptoms when suddenly stop taking
Insomnia
Motor and cog problems
last 1-4 weeks

40
Q

Name newer treatments for depression

A

Ketamine/esketamine
Psychedelics - LSD, psylocibin
Agomelatine

41
Q

How is esketamine administered

A

Nasal spray - sickened in UK

42
Q

How long do AD effects of ketamine/eskatamine take to occur after administration

A

4 hours

43
Q

Possible risks of ketamine (based on ketamine abuse)

A

bladder dysfunction and personal lesions - unsure

44
Q

How is discontinuation syndrome combatted

A

ween off meds rather than cold turkey

45
Q

Which drugs give discontinuation syndrome (worst)

A

Duloxetine
Venlafaxie
Also SSRIs citalopram and paroxetine, MAOIs and NaSSAs

46
Q

Name an NaSSA

A

Mirtazapine

47
Q

Where does Mirtazapine act

A

Antagonist at alpha 2 adrenoceptors and 5HT2 A and C
Antagonist at histamine H1

48
Q

Which receptors doe mirtazapine have highest affinity for/cause most side effects

A

H1 histamine receptor

49
Q

Benefits of mirtazapine

A

Generally effective and well tolerated (does not cause sexual dysfunction or nausea
Faster onset than others

50
Q

Mirtazapine mechanism

A

Alpha 2 adrenoceptors for NA - presynaptic autoreceptors (feedback inhibition for nt release) - antagonise so increase release of 5HT or NA
5HT2A/C receptors involved in mood (overactivity = depression and maybe anxiety) - antagonise
5HT3 receptors - antiemetic

51
Q

How do psychedelics act

A

MA based
Act faster than normal ADs

52
Q

How does Agomelatine act

A

moderately potent antagonist of 5HT2 receptor (influence mood - overactivity of these milked to depression)
Melatonin receptor
Equivalent effect to SSRIs but may be better tolerated
Approved

Drugs and the Brain (5 decks)

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