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P317: Human Psychopharmacoragy > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

What was the original purpose of iproniazid?

A

Chemotherapy for tuberculosis-patients reported feelings of euphoria - it had a stimulant effect

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2
Q

Name 3 common side effects of iproniazid

A

Mood elevation, weight gain, increased sociability

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3
Q

Name 3 rarer side effects of iproniazid

A

Psychomotor agitation, hypersexuality and psychoses

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4
Q

What was iproniazid typically referred to as?

A

A psychic energiser

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5
Q

Who introduced the term antidepressant

A

Max lurie

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6
Q

What were tricyclics first used for

A

Do treat schizophrenics - but it had no effect

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7
Q

Name a tricyclic

A

Imipramine

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8
Q

How do tricyclics work

A

Block the reuptake of serotonin and noradrenaline into the presynaptic neuron

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9
Q

Which are safer: Mao inhibitors or tricyclics

A

Tricyclics

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10
Q

What evidence did Ashcroft and Eccleston (1960) contribute towards the monoamine hypothesis

A

Autopsy studies of suicide victims and CSF in depressed patients: low serotonin, 5ht, or metabolite 5-HIAA concentrations

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11
Q

Who discovered mono amine reap take was blocked by tricyclics

A

Axelrod

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12
Q

Who dismissed the role of serotonin, focusing on the noradrenaline hypothesis of depression

A

.Schildkraut

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13
Q

What does the monoamine hypothesis propose

A

Depression is associated with deficiency of monoamine neurotransmitters, particularly noradrenaline and serotonin

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14
Q

name some of the serious side effects of MAOi

  • why are there serious side effects associated
A

liver damage and blood control issues

  • because they are non-specific - can also act in the periphery as well as centrally.
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15
Q

people using MAOi need to make dietary changes, why?

A

dietary tyramine is an indirect noradrenaline agonist found in mature cheeses, red wines, pickled herring and yeast.

  • when MAO-A is inhibited as little as 10 mg of dietary tyramine can increase BP
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16
Q

what causes the associated side effects of tricyclic use

name 2 side effects

A

antagonist of muscarinic acetylcholine or cholinergic receptors in the PNS = dry mouth, impaired muscular control, tachycardia, constipation

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17
Q

name the two main enzymes responsible for the destruction of noradrenaline

A

monoamineoxidase
catechol-O-methyl-transferase (COMT)

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18
Q

it is important that appropriate antidepressants are prescribed for the right patient (each has specific effects), what is the specific effects of these:
- MAOIs
- trimipramine
- clomipramine

A

MAOIs = enhance drive
Trimipramine = sedative effects
clomipramine = mood and emotion

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19
Q

what was the name of the first SSRI

A

zelmid

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20
Q

what was later found about zelmid

A

found to cause Guillain-barre syndrome
= immediately removed from the market

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21
Q

name a well known SSRI

A

prozac

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22
Q

how do SSRIs work

A

they inhibit the reuptake of serotonin into the pre-synaptic neuron = more serotonin left in the synaptic cleft

23
Q

prozac has been praised for having less severe side effects, name two of them:

A

nausea
sexual dysfunction

24
Q

what are the main problems with the monoamine hypothesis

A
  1. time lag between administration and depressive symptom relief
  2. inconsistent findings regarding produced noradrenaline and serotonin in depressed patients = suggests the issue is at the receptor level.
25
Q

SNRIs are a new treatment, what is it?

A

serotonin-noradrenaline reuptake inhibitors

26
Q

name a SNRI

A

venflaxine

27
Q

what are SARIs (new treatment), name one

A

serotonin antagonist and reuptake inhibitors - such as trazodone.

28
Q

what are the main effects of trazodone, what does this mean when administering it to treat depression

A

hypnotic with sedative effects
- as it is hypnotic at low doses, to have an antidepressant effect it must be administered at high doses

29
Q

how does trazodone create a antidepressant effect

A

blocks the serotonin transporter.

30
Q

when patients do not respond to SSRIs, what are they given

A

Quetiapine

31
Q

what receptors does Quetiapine have an affinity to which make it useful in the treatment of schizophrenia, bi-polar depression and depression

A

D2
5-HT2A
H1
alpha 1
5-HT1A

32
Q

mirtazapine is known as Californian rocket fuel - how does it work

A

serotonergic and noradrenergic antidepressant with no MAO inhibiton

33
Q

explain the study ran by Tranter et al. 2002

A

healthy volunteers to compare the effects of sertraline (SSRI) and reboxetine (SNRI)

large individual differences in response to drugs - some healthy people developed suicidal ideation and emotional blunting.

34
Q

name 2 dangerous side effects of SSRIs

A

akathisia (agitation)
suicidal ideation

35
Q

how many more times are SSRIs selective for serotonin reuptake inhibition than for noradrenaline reuptake inhibition?

A

10 x

36
Q

why is it that SSRIs have multiple pharmacological actions - which explain the differences in efficacy between different patients

A

they bind to a large number of other receptors and enzymes that can contribute to their overall clinical effect

37
Q

what does sertraline do?

A

dopamine-re uptake inhibition

38
Q

how does sertraline work?

A

binds with high affinity to the sigma receptor - which is involved in multiple cellular functions, biological processes and diseases.

39
Q

how does paroxetine work?

A

muscarinic/ cholinergic antagonist
noradrenaline reuptake inhibition
cytochrome p450 enzymes: 2D6 and 3A4 inhibition

40
Q

what does cytochrome p450 do?

A

role in drug metabolism

41
Q

why is it important that paroxetine inhibits cytochrome p450 enzymes?

A

the drug will stay for longer in the system - as it inhibits the enzymes involved in metabolism

42
Q

when was it brought to attention that antidepressants may trigger suicide

A

1958

43
Q

which type of antidepressants is more likely to cause problems?

A

activating antidepressants more likely to cause problems over sedating antidepressants

44
Q

which class of drugs is most associated with suicide attempts

A

monoamine oxidase inhibitors

45
Q

which symptoms does desipramine and nortripytline clear up first, and before what

A

alleviates depressive psychomotor retardation before it clears up suicidal ideation

46
Q

which drug is the most drive enhancing

A

MAOis

47
Q

describe the case study finding high suicide rates in fluoxetine treatments

A

5 females and 1 male depressed patients free of recent suicidal ideation

developed intense violent suicidal preoccupation after 2-7 wks of fluoxetine treatment

48
Q

what are the 2 controversial side effects of SSRIs

A

akathisia
suicidal agitation

49
Q

which drug has received lots of negative press from the FDA

A

paroxetine (Paxil)

50
Q

what is an assessment of causality

A

challenge, de-challenge, and re-challenge

51
Q

what evidence is there for a dose response relationship between drugs and outcomes

A

akathisia and suicidal thinking disappeared upon the discontinuation of fluoxetine

52
Q

what is said to be the cause of suicidal ideation

A

the akathisia which is reported from drug use

53
Q

name 4 side effects of sertraline that stopped a trial within one week in Leeds in the 1980s

A

apprehension, insomnia, movement disorders, akathisia

54
Q

describe the neurotransmitter receptor sensitivity hypothesis for depression

A

depression is caused by abnormal upregulation of receptors. elevating neurotransmitter levels through the use of antidepressants leads to long term down regulation of receptors

this explains why there is a time lag between administration and clinical effects.

P317: Human Psychopharmacoragy (7 decks)

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