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Pharmacology and Therapeutics 2 Y2 > Anti-Depressants > Flashcards

Anti-Depressants Flashcards

1
Q

2 forms of psychoses?

A

Schizophrenia and affective disorders

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2
Q

2 forms of affective disorders?

A

Depression and mania

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3
Q

Emotional/psychological symptoms of depression?

A
  • Misery, apathy, pessimism
  • Low self-esteem
  • Loss of motivation
  • Anhedonia – inability to enjoy daily activities
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4
Q

Biological/somatic symptoms of depression?

A
  • Slowing of thought & action
  • Loss of libido
  • Loss of appetite, sleep disturbance
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5
Q

2 types of depression?

A

UNIPOLAR depression (also called depressive disorder)

and

BIPOLAR depression (also called manic depression)

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6
Q

Types of unipolar depression?

A
  • Reactive depression (more common) In response to stressful life events, appears to be non-familial (not genetically linked)
  • Endogenous depression unrelated to external stresses, shows a familial pattern
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7
Q

Onset of unipolar depression?

A

Relatively late

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8
Q

Onset of bipolar depression?

A

Early adult

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9
Q

Frontline treatment of bipolar depression?

A

Lithium

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10
Q

Which depressions show hereditary link?

A

Bipolar and endogenous

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11
Q

What are monoamines

A

NA and serotonin

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12
Q

What provides evidence for the monoamine theory of depression?

A

Pharmacology, when NA and 5-HT is increased via drugs, mood tends to go up

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13
Q

What provides evidence against the monoamine theory of depression? (2)

A
  • Biochemical evidence for the theory is inconsistent urine monoamine metabolites aren’t hugely different to normal
  • There is a delayed onset of clinical effect of drugs (despite the neurochemical effect being quick)
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14
Q

Explain the delayed onset of the clinical effect of antidepressants

A

Anti-depressants cause down-regulation of α2, β and 5-HT receptors, so for the receptors to go and effects of the receptors going to be seen it’ll take a while

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15
Q

3 main anti-depressant drug families?

A

Tri-cyclic antidepressants (TCAs)

Monoamine oxidase inhibitors

Selective serotonin reuptake inhibitors

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16
Q

2 types of MAO? What is each of their selectivities?

A

MAO-A Has preference for NA and 5-HT

MAO-B Has preference for DA (MAOBI used for Parkinsons)

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17
Q

What are MAOBi used for?

A

Parkinsons

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18
Q

What do monoamine oxidase enzymes do?

A

Metabolise monoamines in the cytoplasm

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19
Q

Where do MAO enzymes act?

A

Cytoplasm

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20
Q

What does MAO-A have a selectivity for?

A

NA and 5-HT

21
Q

What does MAO-B have a selectivity for?

A

Dopamine

22
Q

Majority of MAOi’s are selective or non-selective?

A

Non-Selective

23
Q

MAOI are reversible or irreversible?

A

Irreversible

24
Q

What are the rapid onset effects of MAOI

A

increase cytoplasmic NA and 5-HT

25
Q

What are the delayed onset effects of MAOI

A

clinical response and down-regulation of beta-adrenoceptors and 5-HT receptors

26
Q

Unwanted effects of MAOI? (5)

A
  • Atropine-like effects (less than those seen with the TCAs)
  • Postural hypotension (common)
  • Sedation (Seizures in overdose)
  • Weight gain associated with increased appetite (possibly excessive)
  • Hepatotoxicity (mainly with the hydrazines, but it’s rare)
27
Q

Drug interactions of MAOI? (3)

A
  • ‘Cheese reaction’ Tyramine-containing foods (indirectly acting sympathomimetic)+ MAOI  can cause hypertensive crisis (throbbing headache, increased BP, intracranial haemorrhage)
  • MAOIs + TCAs  hypertensive episodes (avoid)
  • MAOIs + pethidine  hyperpyrexia (high temperature), restlessness, coma and hypotension. MAOI’s inhibit the normal metaboliser of pethidine, meaning they’re metabolised by a different enzyme that leads to the toxic products
28
Q

Way to recognise TCAs?

A

3 ring structure

29
Q

MOA of MAOI

A

Inhibit MAO which breaks down monoamines (NA, 5-HT, DA)

30
Q

Main MOA of TCAs?

A

Neuronal monoamine reuptake inhibitors.

They combine with protein transporters on presynaptic nerve terminals and slow them down so Cause enhanced synaptic level of NA/5-HT

31
Q

What are TCA’s selective for?

A

NA = 5-HT > DA

32
Q

Delayed onset effects of TCAs?

A

They cause a delayed down-regulation of beta-adrenoceptors and 5-HT2 receptors, when the receptors appear to have been downregulated there is correlation to the anti-depressant activity

33
Q

Other receptors TCAs effect? (4)

A
  1. alpha2 receptors (alpha2 antagonists on presynaptic membrane - block negative feedback and allow greater increase of NA in the synaptic cleft)
  2. mAChRs
  3. Histamine receptors
  4. 5-HT receptors
34
Q

When do problems occur with TCAs?

A

when they interact with other protein bound drugs in the blood.

If another drug is administered that binds to plasma proteins, then TCA serum level increases which can lead to problems

35
Q

% of TCAs plasma protein bound?

A

90-95%, a lot

36
Q

Plasma half life of TCAs?

A

10-20 hours

37
Q

Side effects of TCAs at therapeutic dose? (3)

A
  • Atropine-like effects as they can interact with muscarinic receptors (mostly amitriptyline) Dry mouth, constipation etc.
  • Postural hypotension (mediated by the vasomotor centre in the brainstem)
  • Sedation (due to the H1 antagonism) – this can be useful in depressive insomnia
38
Q

Side effects of TCAs at toxic dose? (3)

A
  • CNS Excitement, delirium, seizures  can lead to coma, respiratory depression
  • CVS Cardiac dysrhythmias - ventricular fibrillation/sudden death
  • Care - attempted suicide
39
Q

TCAs interactions with hepatic microsomal enzymes? Consideration when giving drugs that are metabolised by hepatic microsomal enzymes?

A

These metabolise them, so if another drug is administered that is also metabolised by hepatic microsomal enzymes then TCA effects increase

40
Q

What metabolises TCAs

A

Hepatic microsomal enzymes

41
Q

What drugs do TCA’s interact with (4)

A

Hepatic microsomal enzyme using drugs (neuroleptics)
Antihypertensives
CNS depressants (e.g. alcohol)
Plasma protein bound drugs (aspirin)

42
Q

MOA of SSRIs?

A
  • Selective 5-HT re-uptake inhibition
43
Q

Effectiveness of SSRI’s

A

Good but less effective in severe depression

44
Q

Plasma 1/2 life of SSRIs?

A

18-24 hours

45
Q

Time for Onset of action for SSRIs?

A

2-4 weeks

46
Q

Side effects of SSRIs? (4)

A
  • Nausea, diarrhoea, insomnia & loss of libido

- Interact with MAOIs (avoid co-administration)

47
Q

Drug interactions of SSRIs?

A

MAOIS, avoid co-administration

48
Q

MOA of venlaxafine?

A

dose-dependent reuptake inhibition

49
Q

MOA mirtazapine?

A

A2 receptor antagonist (increases NA and 5-HT release)

Pharmacology and Therapeutics 2 Y2 (24 decks)

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