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Year 2 Collin > Pharm 23 - Antidepressants > Flashcards

Pharm 23 - Antidepressants Flashcards

1
Q

Psychoses can be split into schizophrenia and affective disorders. What are the types of affective disorders

A

Mania and depression

affective disorders = feelings, behaviour, mood

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2
Q

What is schizophrenia

A

Disorder of thought process

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3
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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4
Q

What are the features of unipolar depression/depressive disorder

A
  1. Mood swings in same direction
  2. Late onset (more common)
  3. 2 types: reactive depression (75% - stressful life events, non-hereditary) and endogenous depression (25% - unrelated to external stresses, familial pattern)
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5
Q

What are the features of bipolar depression/manic depression?

A
  1. Oscillation between depression and mania (hyper excitability)
  2. Early adult onset (less common)
  3. Strong hereditary tendency
  4. Different treatment unipolar depression - Li = mood stabiliser
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6
Q

Describe the monoamine theory of depression

MA = NA / 5-HT

Pharm evidence supports but not biochemical

A

Depression = functional deficit of central MA transmission

Mania = functional excess of central MA transmission

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7
Q

What is usually the response to antidepressants

A
  1. Downregulation of a2, B, 5-HT receptors
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8
Q

What are the classes of antidepressants

A
  1. TCAs
  2. MAO inhibitors (MAOI)
  3. SSRIs
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9
Q

Give an example of a TCA

A

Amitriptyline

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10
Q

How do TCAs work

A
  1. Inhibit neuronal monoamine reuptake (NA and 5-HT more than Dopamine) - so more NA/5-HT in synapses for longer —> potentiates effects of neurotransmitters
  2. TCA also antagonise a2 receptors
  3. TCA also have effects on mAChR, histamine-Rs, 5-HT-Rs
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11
Q

TCAs cause delayed downregulation of which receptors?

A

B-adrenoreceptors and 5-HT2 receptors

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12
Q

Describe the pharmacokinetics of TCAs

A
  1. Rapid oral absorption
  2. Highly PPB (90-95%)
  3. Hepatic metabolism produces active metabolites
  4. Quite long t1/2 - 10-20 hours
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13
Q

How are the active TCA metabolites excreted

A

Excreted via the kidney as glucuronide conjugates

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14
Q

At therapeutic dose, what are the side effects of TCAs?

A
  1. Atropine-like effects (dry mouth, constipation, bladder dysfunction)
  2. Postural hypotension
  3. Sedation/drowsy (H1 antagonism)
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15
Q

What are the symptoms of acute toxicity due to OD on TCA (TCA commonly used for suicide)

A

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

CVS - cardiac dysrhythmias —> ventricular fibrillation/sudden death

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16
Q

Give 4 drug interactions of TCAs

A
  1. Aspirin - aspirin displaces TCAs from plasma proteins - free TCA rises into toxic ranges
  2. If TCAs given alongside drugs (neuroleptics, oral contraceptives) that are metabolised by same hepatic metabolic enzymes -TCA conc rises as less TCA metabolism
  3. TCA can potentiate CNS depressants
  4. TCA may affect antihypertensives
17
Q

Give an example of a MAOI

A

Phenelzine

18
Q

What does MAO-A break down

A

NA and 5-HT

19
Q

What does MAO-B break down

A

Dopamine

20
Q

Why do most MAOIs have a long duration of action

A

Irreversible, Non selective inhibition

MAOIs also inhibit other enzymes

21
Q

Describe the structure of MAOIs

A

Single-ring structure

22
Q

What are the 2 main groups of TCAs

A

Dibenzazepines and dibenzocycloheptenes (3 tings w/ 2 benzene rings)

23
Q

What are the rapid effects of MAOIs

A

Increased cytoplasmic NA and 5-HT (in nerve terminals)

24
Q

What are the delayed effects of MAOIs

A

Clinical response and down regulation of B-adrenoreceptors and 5-HT2-Rs

25
Q

Describe the pharmacokinetics of MAOIs

A
  1. Rapid oral absorption
  2. Short t1/2 - BUT longer DOA due to irreversible inhibition
  3. Metabolised in liver and excreted in urine
26
Q

What are the side effects of MAOIs

A
  1. Atropine like effects (less than TCAs)
  2. Postural hypotension
  3. Sedation (seizures in OD)
  4. Weight gain (linked w increased appetite)
  5. Hepatotoxicity
27
Q

What are the serious drug reactions

A
  1. Cheese reaction - Tyramine containing foods + MAOI causes less tyramine broken down by MAO-A/B = more plasma tyramine which can cause a hypertensive crisis
  2. MAOIs and TCAs –> hypertensive episodes
  3. MAOIs and pethidine –> hyperpyrexia, restlessness, coma and hypotension
28
Q

What does tyramine do?

A

Indirectly activates SNS by inducing NA release from terminals

29
Q

Give an example of a reversible MAOI

A

Moclobemide - used for depression as fewer drug interactions but reduced DOA

30
Q

Give an example of a SSRI

A

Fluoxetine (Prozac) - most prescribed current antidepressant

31
Q

What is the mechanism of Prozac (SSRI)

A

Selective 5-HT reuptake inhibitor - but less effective against severe depression

32
Q

Describe the pharmacokinetics of SSRIs

A
  1. Oral administration
  2. Long plasma t1/2 - 18-24 hrs
  3. Delayed onset of action (2-4 weeks)
  4. Fluoxetine competes w/ TCAs for hepatic enzymes (avoid co-administration)
33
Q

What are the side effects of SSRIs

A
  1. Fewer than TCAs/MAOI –> less troublesome SEs and safer in OD
  2. Nausea, diarrhoea, insomnia and loss of libido
  3. Interact w/ MAOIs so avoid coadmin
34
Q

Name 2 other antidepressants

A
  1. Venlafaxine - Dose dependent reuptake inhibitor (SNRI - Serotinin and NA reuptake inhibitor)
  2. Mirtazapine - a2 receptor antagonist - inhibit negative feedback - causing increased NA and 5-HT release. Also reacts w/ histamines etc causing a sedative effect
35
Q

When is mirtazapine useful

A

In patients who are intolerant to SSRI

Year 2 Collin (114 decks)

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