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Pharmacology and Therapeutics > 22. Anti-depressants > Flashcards

22. Anti-depressants Flashcards

1
Q

What 2 types can psychoses be split into?

A
  • Schizophrenia (disorder of thought processes)

* Affective disorders (disorders of mood - mania + depression)

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2
Q

What is the most common affective disorder?

A

Depression

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3
Q

What are the emotional symptoms of depression?

A
  • Misery
  • Apathy
  • Pessimism
  • Loss of motivation
  • Anhedonia (inability to feel pleasure)
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4
Q

What are the biological symptoms of depression?

A
  • Slowing of thought and action
  • Loss of libido
  • Loss of appetite
  • Sleep disturbance
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5
Q

What are the 2 main groups of depression?

A

Unipolar (depressive disorder) and bipolar (manic depression)

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6
Q

Describe unipolar depression

A
  • Mood swings in the same direction
  • Late onset (adulthood)
  • Can be reactive (75%) or endogenous (25%)
  • Reactive: in response to stressful life events (non-familial)
  • Endogenous: unrelated to external stresses (familial pattern)
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7
Q

Describe bipolar depression

A
  • Oscillating depression and mania
  • Less common than unipolar depression
  • Early adult onset
  • Strong hereditary tendency
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8
Q

What is the drug treatment for bipolar depression?

A

Lithium - not conventional antidepressant, more mood-stabilising

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9
Q

Summarise the monoamine theory of depression

A
  • Depression - functional deficit of central monoamine transmission
  • Mania - functional excess of central monoamine transmission
  • NA + 5-HT (serotonin) are the two monoamines involved
  • Based on pharmacological evidence - biochemical evidence in inconsistant
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10
Q

How quickly is an effect seen in the use of anti-depressant drugs?

A
  • Changes in the monoamines is rapid
  • However, the clinical effects can take weeks
  • Dissociation between the neurochemical change and antidepressant effect
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11
Q

What receptors change in response to anti-depressants and how quickly does the change occur?

A

Down-regulation of α2, β and 5HT receptors
• Correlates with the onset of clinical drug effectiveness
• Therefore, this may be responsible for the clinical drug effects

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12
Q

How is the HPA (hypothalamic-pituitary-adrenal) axis involved in depression?

A
  • CRH (corticotropin-releasing hormone) levels increased in depressed patients
  • CRH stimulates the pituitary synthesis of ACTH
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13
Q

What is seen in the hippocampus in chronic depression?

A

Hippocampal neurodegeneration

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14
Q

What are the 2 main chemical groups of tri-cyclic antidepressants?

A

Dibenzazepines and dibenzocycloheptenes

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15
Q

How do tri-cyclic antidepressants work?

A
  • Neuronal monoamine re-uptake inhibitors
  • Prevent reuptake of NA and 5-HT more than dopamine
  • Also act on α2 receptors, muscarinic AChRs, histamine receptors and 5-HT receptors - some of these actions are important but some contribute to the side-effects

(3 ringed structures)

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16
Q

What happens if TCAs bind to and antagonise alpha 2 receptors?

A
  • Block inhibitory control over NA

* Enhance release of NA into synaptic cleft

17
Q

What effect do TCAs have on β-adrenoceptors and 5-HT receptors?

A
  • Down-regulation

* Could cause the delayed onset of the anti-depressant

18
Q

Describe the absorption and protein binding of TCAs?

A
  • Rapid oral absorption

* Highly protein bound (90-95%)

19
Q

How are TCAs metabolised and what is the half life?

A
  • Hepatic metabolism - generates active metabolites
  • Renal excretion as glucuronide conjugates
  • Half-life: 10-20 hours
20
Q

What are the unwanted effects of TCAs at a therapeutic dosage?

A
  • Atropine-like effects - dry mouth, blurred vision, constipation, urinary retention (TCAs have muscarinic antagonist activities)
  • Postural hypotension - central effect
  • Sedation - due to H1 antagonism
21
Q

What are the unwanted effects of TCAs at acute toxicity?

A

CNS - excitement, delirium, seizures, coma, respiratory depression

CVS - dysrhythmias, ventricular fibrillation, sudden death

22
Q

Outline the drug interactions of TCAs

A

Plasma protein binding
• Increased TCA effects when co-administered with aspirin and phenytoin
• Warfarin can displace TCAs from their binding sites - toxic levels of TCA

Hepatic microsomal enzymes
• These metabolise TCAs
• If drugs are metabolised by the same enzyme (e.g. oral contraceptives), TCA effect increases

  • Potentiation of CNS depressants (alcohol) with TCAs
  • Interaction with antihypertensives
23
Q

Describe the action of monoamine oxidase inhibitors

A
  • Most are non-selective - can inhibit MAO-A and MAO-B
  • May result in the inhibition of other enzymes
  • Inhibition is irreversible - long duration of action
  • Rapid increase in cytoplasmic NA and 5-HT
  • Down-regulation of β-adrenoreceptors and 5-HT receptors
24
Q

Which monoamines does MAO-A and MAO-B have a preference for?

A

MAO-A - NA and 5-HT

MAO-B - DA

25
Q

Describe the chemical structure of MAO inhibitors

A

• Single rings structure
• Phenelzine is a hydrazine - single ring with carbon side chain and a hydrazine functional group at the end
- this group is very reactive
- forms covalent bonds with the MAO enzyme

26
Q

Describe the absorption, metabolism and half life of MAOIs

A
  • Rapid oral absorption
  • Metabolised in liver and excreted in urine
  • Short plasma half-life (but long action due to irreversible inhibition)
27
Q

What are the unwanted effects of MAOIs

A
  • Atropine-like effects
  • Postural hypotension
  • Sedation with long-term usage
  • Weight gain
  • Hepatotoxicity
28
Q

Describe the drug/chemical interactions of MAOIs

A

Tyramine
• Indirectly acting sympathomimetic amine
• Metabolised by MAOs
• Tyramine-containing foods (e.g. cheese) + MAOI => hypertensive crisis
• Throbbing headache, increased BP, intracranial haemorrhage

Pethidine (opioid) - hyperperexia, restlessness, coma, HT

29
Q

Which MAOI has fewer drug interactions?

A
  • Moclobemide
  • Reversible MAO-A inhibitor
  • Selective
  • However, shorter duration of action
30
Q

How do selective serotonin reuptake inhibitors (SSRIs), e.g. fluoxetine, work?

A
  • Selective 5-HT re-uptake inhibition

* Increased plasma 5-HT

31
Q

How safe and effective are SSRIs?

A
  • Safe in case of overdose - less troublesome side-effects

* Less effective against severe depression - still need other classes of drugs

32
Q

What is the half-life of SSRIs and how often is it administered?

A
  • Half-life - 18-24 hours

* Given once a day, orally

33
Q

Describe the onset of action of SSRIs

A
  • Delayed

* 2-4 weeks before optimal anti-depressant action

34
Q

Why should co-administration of SSRIs with TCAs be avoided?

A

Competition for hepatic enzymes

35
Q

Briefly describe the chemical structure of SSRIs

A

Couple of ring structures with an aliphatic side chain

36
Q

What are the unwanted effects of SSRIs?

A
  • GI side effects e.g. nausea, diarrhoea
  • Insomnia
  • Loss of libido
37
Q

What is the most prescribe antidepressant drug?

A

Fluoxetine (Prozac) - SSRI

38
Q

How do SNRIs (e.g. venlafaxine) work and when are they used?

A
  • Dose-dependent re-uptake inhibition of 5-HT and NA
  • 5-HT > NA - so if you have a high dose, you can inhibit the dopamine transporter too
  • 2nd line treatment
39
Q

How do α2 receptor antagonist work and what patients are they used for?

A
  • Increases NA and 5-HT release in the brain
  • Other receptor interactions may contribute to antidepressant activity
  • Useful in SSRI-intolerant patients

Pharmacology and Therapeutics (33 decks)

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