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Sem 2 Pharmacology > Week 4 - Antidepressants & mood stabilisers > Flashcards

Week 4 - Antidepressants & mood stabilisers Flashcards

1
Q

What characterises depression? Give examples

A

Emotional and biological symptoms including:

Emotional
Misery/apathy
Guilt
Low SE
Loss of motivation

Biological
Disturbances in appetite, energy, sleep, libido and psychomotor function

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2
Q

What are some causes of depression?

A 
Genes
Abuse/neglect
Prolonged excessive stress/trauma
Adverse social circumstances
General medical conditions - hypothyroidism
Substances

Postnatal is a thing

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3
Q

What is life time incidence of depression?

A

20%

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4
Q

What’s the rate of recurrence following a single episode?

A

50%

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5
Q

WHat is the suicidal behaviour incidence in patients with depression?

A

10-15%

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6
Q

What is bipolar disorder characterised by?

A

Destabilisation of mood - depressive and manic episodes

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7
Q

WHat is mania?

A

Episodes of pathologically elevated or irritable mood of at least a week
Symptoms include:
Increased sustained elation and energy, less need to sleep, reduced judgement

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8
Q

WHat are some monoamines that affect mood?

A

Serotonin (5-HT), noradrenaline, dopamine, ,acetylcholine, glutamate and GABA

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9
Q

What are the main pharamcological targets for depression?

A

Serotonin and noradrenaline

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10
Q

What are first line AD drugs?

A

SSRIs, including paroxetine and fluoxetine

Noradrenaline reuptake inhibitors - reboxetine

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11
Q

Which two drugs are reserved for psychiatrists?

A

Tricyclic antidepressants

Monoamine oxidase inhibitors

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12
Q

What does NA alpha2 signalling mechanism?

A

Lowering cAMP

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13
Q

What is 5-HT1A,B signalling mechanisms?

A

Reduces cAMP

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14
Q

What is the action of TCAs of monoamine transporters?

A

Act as reversible negative allosteric modulators on axon nerve terminals and dendrites, reducing monoamine transporter affinity for monoamine neurotransmitters - AKA NA and serotonin

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15
Q

Elevation of what leads to alleviation of depression?

A

Elevation of brain derived neurotrophic factor

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16
Q

How do you elevate brain derived neurotrophic factor

A

This is delayed from taking antidepressants, but increases transcription factor for BDNF via upregulation of cAMP pathway

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17
Q

What are the antidep drugs that increase CREB and BDNF?

A
  • SNRIs (NA + Serotonin)
  • SSRIs
  • NRIs
  • NDRI
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18
Q

What is a major theory of Mirtazapine success in depression?

A

Causes an immediate increase in synaptic levels of serotonin and noradrenaline by inhibiting inhibitory mechanisms on NA and serotonin nerve terminals

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19
Q

What does CREB do?

A

Increases BDNF gene expression

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20
Q

How does environment cause depression?

A

Trauma/abuse reduces neuronal plasticity in key areas of the brain –> antidepressants can restore this

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21
Q

What are TCAs and MAOIs reserved for?

A

Severe depression and now response to newer and safer antidepressants

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22
Q

What do you have to avoid in MAOIs?

A

HAve to avoid certain foods with tyramine i.e. soft cheeses, or sympathomimetic drugs because the MAOIs prevent tyramine from being inactivated in the gut –> hypertensive crisis

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23
Q

why are SSRIs safer than TCAs?

A

They have higher therapeutic indices because they lack the affinity for muscarinic receptors and don’t impair cardiac conduction like TCAs do

24
Q

WHat should SSRIs never be combined with? WHy?

A

MAOI or RIMA

–> leads to serotonin syndrome, which can lead to fatalities

25
Q

What are SSRI side effects?

A
  • GIT - nausea, anorexia, diarrhoea
  • CNS - insomnia, anxiety, restlessness
  • Sexual - decreased libido and sexual enjoyment
  • Increased suicidal ideation can occur at the start
26
Q

What is the main cause of SSRI side effects?

A

Over stimulation of some serotonin receptors

Tolerance ends up reducing side effects

27
Q

When do the antidep and anti-anx effects of SSRIs kick in?

A

2-4 weeks

28
Q

What are SSRI indications?

A 
Depression
OCDs
Social phobia
Panic disorders
GAD
ADD
PTSD
Eating disorders
29
Q

What are the most commonly prescribed AD drugs?

A

SSRIs

30
Q

What is Venlafaxine?

A

An SNRI - serotonin and noradrenaline reuptake inhibtors

31
Q

How does Venlafaxine activity change with dose?

A

At lower doses, blocks more serotonin reuptake.

At higher doses, mostly NA

32
Q

What are side effects of Venlafaxine?

A

Nausea, anorexia, constipation, secual dysfunction, hypertension

33
Q

WHat is Venlafaxine very good for?

A

Depressed patients with anxiety

May be good for chronic pain

34
Q

What does Mirtazapine do?

A

It’s an NaSSA - antagonises alpha a adrenoceptors, histamine 1 receptors and serotonin receptors

35
Q

What would you use Mirtazapine?

A

Depressed individuals requiring sedation

Alternative to SSRIs if insomnia or seual dysfunction are problematic

36
Q

What are Mirtazapine side effects?

A

Dizziness, weight gain, drowsiness, dry mouth, constipation

37
Q

What is Bupropion used for and why?

A

Smoking cessation
It’s a weak NA and dopamine reuptake inhibitor - good for smoking cessation because blocks dopamine reuptake at the dopamine transporters, which mitigates some cravings in a minimal way to avoid addiction

38
Q

Which patients would bupropion be good for with depression?

A

It’s activation - godo for patients with low energy and who are prone to fatigue

39
Q

What’s the main problem with bupropion?

A

Seizures

–> less likely with slow release bupropion

40
Q

What are contraindications of bupropion?

A

Seizure history
Anorexia
Bipolar
Insomnia

41
Q

What does lithium do?

A

Neuro-protective action - promotes neuroplasticity
Mood stabilising
Significant anti-suicide action

42
Q

What’s the main 2 problems with lithium?

A

Low therapeutic index for toxicity

Big weight gain

43
Q

What are SEs of lithium?

A

Nausea, thirst, polyuria, hypothyroidism, weight gain, diarrhoea, tremor, weakness and mental confusion

44
Q

Which organ does lithium effect?

A

Kidney function - prolongued lithium treatment may cayse serious tubular damage

45
Q

WHat would you use for bipolar after lithium?

A

Anti-convulsant mood stabilisers

Atypical antipsychotics

46
Q

What are first line treatment for acute mania?

A

Lithium, valproate, atypical antipsychotics

47
Q

What’s first line treatment for bipolar depression?

A

Lithium, sodium valproate, quetiapine and lamotrigine

48
Q

What do you need to be aware of in pregnancy with bipolar treatment?

A

Lithium and anticonvulsant mood stabilisers can increase the chance of foetal malformation

49
Q

WHen can you conclude antidep isn’t working?

A

4-6 weeks

50
Q

When do you discontinue antidepressant medications?

A

After 4-9 months, gradually
If on multiple episodes, can consider 2-5 ears
Severe = rest of lives

51
Q

What are 1st line ADs for MDD?

A

SSRIs - sertraline
SNRIs - venlafaxine
Mirtazapine - NaSSa

52
Q

What are 2nd line ASs for MDD?

A

Moclobemide
Reboxetine
Agomelatine

53
Q

What is last resort in MDD treatment?

A

Electroconvulsive therapy - who are resistant to antidep medications

54
Q

Which medication combination is really good for bipolar depression?

A

Fluoxetine - olanzapine

55
Q

WHat should you try for mild-moderate depression?

A

Psychotherapy, exercise and lifestyle modifications

56
Q

What should you monitor after AD initiation in patients under 25 particularly?

A

Anxiety
Agitation
Suicidal ideation

Sem 2 Pharmacology (4 decks)

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