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Pharmacology Y2 > Depression > Flashcards

Depression Flashcards

1
Q

What is the function of monoamine oxidase?

A

Metabolises dopamine, noradrenaline, serotonin in the synaptic cleft to remove it

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1
Q

What is the function of monoamine oxidase?

A

Metabolises dopamine, noradrenaline, serotonin in the synaptic cleft to remove it

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2
Q

What are the 2 main ways that antidepressants work?

A

1 - blocks metabolism of the neurotransmitter so it is not removed from the synapse
2 - blocks reuptake of noradrenaline and serotonin into the presynaptic membrane

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3
Q

What are the 4 categories of reuptake inhibitors?

A

1- Tricyclic antidepressants
2- Selective serotonin reuptake inhibitors
3- Noradrenaline reuptake inhibitors
4- Serotonin and noradrenaline reuptake inhibitors

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4
Q

What is the mechanism of action of 3rd generation antidepressants?

A

They are antagonists of the negative feedback mechanism for pre synaptic neurotransmitter release - means pre synaptic receptors will keep releasing neurotransmitter

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5
Q

Name some psychological symptoms of depression

A

Pessimism
Poor concentration
Low self esteem
Indecisiveness
Suicidal thoughts
Hypochondria

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6
Q

Name some biological symptoms of depression

A

Retardation of thoughts and action
Fatigue
Loss of appetite
Loss of libido
Aches and pains

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7
Q

Name some behavioural symptoms of dperession

A

Psychomotor agitation/retardation
Self neglect

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8
Q

What are thymoleptics?

A

Drugs that re elevate the mood

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9
Q

What is an example of a thymoleptic drug?

A

Tricyclic antidepressants

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10
Q

What are thymeretics?

A

Drugs that activate the psychomotor drive

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11
Q

What is an example of a thymeretic drug?

A

Monoamine Inhibitors

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12
Q

Why should a thymoleptic and thymeretic drug always be given together?

A

If there is a thymeretic drug without the mood elevation from the thymoleptic drug, it will increase suicide risk

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13
Q

Define bipolar depression

A

Depression that alternates with mania over periods of weeks

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14
Q

What is the monoamine hypothesis?

A

This states that lack of monoamine transmitter in the synapse (noradrenaline, dopamine, serotonin) can cause depression

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15
Q

Reserpine is an old antihypertensive drug. It removes pre synaptic catecholamines from the vesicles. Based on monoamine hypothesis what would this effective be?

A

Less monoamine neurotransmitter in the synapse = depressive symptoms

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16
Q

The action of which drug gives evidence for the monoamine hypothesis?

A

Iproniazid

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17
Q

What happened when patients took Iproniazid that gives evidence for the monoamine hypothesis?

A

Iproniazid prevents monoamine metabolism. Patients taking this drug felt euphoric.

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18
Q

What is the mechanism of alpha 2 receptors on the presynaptic membrane?

A

If the receptor is bound to its substrate, it will decrease release of neurotransmitter as it detects that enough is in the synaptic cleft

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19
Q

What would an alpha 2 antagonist result in?

A

Increased neurotransmitter release as the receptor does not know that there is enough neurotransmitter in the synapse due to the antagonism

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20
Q

Name an irreversible monoamine oxidase inhibitor

A

Clorgyline

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21
Q

List 5 reversible monoamine oxidase inhibitors

A

Moclobemide
Brofaromine
Pirlindole
Toloxatone
Befloxatone

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22
Q

List 4 non selective monamine oxidase inhibitors

A

Iproniazid
Isocarboxazid
Phenelzine
Tranylcypromine

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23
Q

How do monoamine oxidase inhibitors affect the body systemically?

A

Stimulates alpha 1 -> hypertension
Stimulates beta 1 -> tachycardia

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24
Q

What is the function of monoamine oxidase in the intestines and liver?

A

Metabolises dietary amines to prevent them passing into systemic circulation

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25
Q

Name the amine that increases in plasma concentration when there are monoamine oxidase inhibitors

A

Tyramine

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26
Q

What are fatal problems with monoamine oxidase inhibitors?

A

Fatal respiratory depression with overdose
Postural hypotension
Increased motor excitability

27
Q

How do tricyclic antidepressants work?

A

They inhibit the reuptake of serotonin and noradrenaline

27
Q

How do tricyclic antidepressants work?

A

They inhibit the reuptake of serotonin and noradrenaline

28
Q

What are the problems with TCAs?

A

Alpha 1 antagonist -> postural hypotension
H1 antagonist -> sedation
Muscarinic antagonism -> Dry mouth, blurred vision, constipation

29
Q

Name 3 TCAs that target serotonin reuptake

A

Imipramine
Amitriptyline
Clomipramine

30
Q

Name a TCA that targets noradrenaline reuptake

A

Desipramine

31
Q

What is the mechanism of action of selective serotonin reuptake inhibitors (SSRIs)?

A

Inhibits SERT, the serotonin transporter, thereby preventing the reuptake of serotonin from the synapse

32
Q

List some examples of SSRIs

A

Zimelidine
Fluoxetine
Citalopram
Paroxetine
Vortioxetine
Fluvoxamine
Sertraline

33
Q

What are the adverse effects of SSRIs?

A

Constipation, diarrhoea -> there are serotonergic neurones in the gut so these can be overactivated
Rashes and tremors
Loss of libido

34
Q

What is the mechanism of action of NRIs?

A

Inhibits NET, noradrenaline reuptake transporter, so noradrenaline remains in the synapse

35
Q

Give an example of an NRI?

A

Maprotiline

36
Q

What is the mechanism of action of SNRIs?

A

Inhibits SERT and NET transporters, serotonin and noradrenaline remain in the synapse

37
Q

Give an example of an SNRI?

A

Venlafaxine

38
Q

Which 2 receptors are targeted as monoamine antagonist antidepressants?

A

Alpha 2 adrenoreceptors
Presynaptic 5HT1a receptors

39
Q

What is the effect of the monoamine antagonists?

A

Increased release of neurotransmitter from the presynaptic membrane

40
Q

Name 3 monoamine antagonists

A

Mirtazapine
Mianserin
Trazodone

41
Q

Which receptors does monoamine antagonist mirtazapine antagonise?

A

Alpha 2 receptors

42
Q

Which receptors does monoamine antagonist mianserin antagonise?

A

Alpha 2 receptors
Presynaptic 5HT receptors

42
Q

Which receptors does monoamine antagonist mianserin antagonise?

A

Alpha 2 receptors
Presynaptic 5HT receptors

43
Q

Which receptors does monoamine antagonist trazadone antagonise?

A

Presynaptic 5HT receptors

43
Q

Which receptors does monoamine antagonist trazadone antagonise?

A

Presynaptic 5HT receptors

44
Q

Does mirtazapine antogonise alpha 1 receptors aswell?

A

No

45
Q

Does trazadone antagonise alpha 1 receptors aswell?

A

Yes

46
Q

What systemic side effect could occur when antagonising alpha 1 receptors?

A

Orthostatic hypotension

47
Q

Do monoamine antagonists block H1 receptors aswell?

A

Yes !

48
Q

What is the systemic effect of blocking H1 receptors?

A

Sedation

49
Q

Name a drug that targets intracellular messengers that can be used as an antidepressant

A

Rolipram

50
Q

What is the mechanism of action of rolipram?

A

It is a phosphodiesterase inhibitor, so prevents the breakdown of cAMP

51
Q

Why is rolipram not widely used?

A

It has a lot of side effects - involved in anti inflammatory pathways

52
Q

What therapy is used on severely depressed and manic patients that are non responsive to medication?

A

Electro convulsive therapy, increases patients sensitivity to noradrenaline and serotonin

53
Q

What evidence is there to support the monoamine hypothesis of depression?

A

1- Inhibition of storage and synthesis of monoamines, results in a low mood.
2- Whereas preventing reuptake and metabolism of monoamines results in a good mood.

54
Q

What evidence is there to counter the monoamine hypothesis of depression?

A

1- Some drugs such as cocaine, amphetamines, increase noradrenaline transmission but do not have antidepressant action.
2- There is delayed therpeutic action of all drugs.
3- Not all antidepressants increase monoaminergic transmission.

55
Q

What is the difference between short term and long term use of SSRIs?

A

Short term - Increased serotonin activates 5HT1a + 5HT1b (a is inhibitory) so has an inhibitory effect
Long term - 5HT1a receptors are desensitised, so increased serotonin activates 5HT1b only, which gives an excitatory effect

56
Q

Describe what happens in bipolar 1

A

Manic episodes with psychotic element requiring hospitalisation, in a cycle with major depression

57
Q

Describe what happens in bipolar 2

A

Chronic hypomaniac episodes

58
Q

What is given to bipolar patients to prevent mood switching?

A

Lithium - reduces GPCR activity

59
Q

Name 3 anticonvulsants given to patients with bipolar 1

A

Lamotrigine
Carbemazepine
Valproate

60
Q

Name Name 3 antipsychotics given to patients with bipolar 2

A

Quetiapine
Olanzapine
Risperidone

61
Q

Why would ketamine theoretically be an effective antidepressant?

A

It works acutely and rapidly in people with major depressive disorders

62
Q

What is the mechanism of action of ketamine?

A

1- Blocks NMDA receptors
2- Increases AMPA receptors activation
3- DIsinhibits glutamate release (inhibits GABA)
4- Activates protein translation
5- Upregulates BDNF pathway

Pharmacology Y2 (9 decks)

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