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Pharmacology and Therapeutics > Anti-depressants > Flashcards

Anti-depressants Flashcards

1
Q

Unipolar depression/depressive disorder

A
  • Mood swings in same direction
  • Relatively late onset
  • all types respond in the same way to the same drug treatments
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2
Q

Bipolar depression/manic depression

A
  • Oscillation between depression and mania
  • Early adult onset
  • Less common
  • Strong hereditary tendency
  • Drug treatment includes Lithium=stabilise swings between depression and mania but lithium has a narrow therapeutic window
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3
Q

Tricyclic antidepressants (TCAs)

A

Principal action: Blocks NA and 5-HT reuptake

  • IMPROVES mood in depressed patients
  • Example: Amitriptyline
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4
Q

MAO inhibitors

A

Principal action: Increases stores of NA and 5-HT

  • IMPROVES mood in depressed patients
  • Example: Phenelzine
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5
Q

Reserpine

A

Principal action: Inhibits NA and 5-HT storage

-WORSENS mood in depressed patients

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6
Q

Alpha-Methyltyrosine

A

Principal action: Inhibits NA synthesis

  • WORSENS mood in depressed patients
  • CALMING of maniac patients
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7
Q

Methyldopa

A

Principal action: Inhibits NA synthesis

-WORSENS mood in depressed patients

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8
Q

ECT (Electroconvulsive Therapy)

A

Principal action: Increases CNS responses to NA and 5-HT

-IMPROVES mood in depressed patients

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9
Q

Tricyclic antidepressants pharmacokinetics

A
  • Oral administration
  • Rapid absorption
  • highly plasma-protein bound (90%-95%)
  • hepatic metabolism gives active metabolites->renal excretion as glucuronide conjugates
  • 10-20 hour plasma half life
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10
Q

Tricyclic antidepressants side effects

A

At therapeutic doses:
-Atropine-like effects
-Postural hypotension (vasomotor centre)
-Sedation (H1 antagonism)
Overdose (acute toxicity):
-CNS: excitement, delirium, seizures leading to coma, respiratory depression
-CVS: cardiac dysrhythmias leading ventricular fibrillation/sudden death

-often used in suicide attempts

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11
Q

Tricyclic antidepressants drug interactions

A
  • PPB=increase TCA effects
  • hepatic microsomal enzymes=increase TCA effects
  • potentiation of CNS depressants (eg: alcohol)
  • antihypertensive drugs (close monitoring)
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12
Q

MAO inhibitors pharmacokinetics

A
  • Oral drug
  • Rapid absorption
  • few hour plasma half life
  • long duration of action
  • metabolised in liver -excreted in urine
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13
Q

MAO inhibitors side effects

A
  • Atropine-like effects (less so than TCAs)
  • Postural hypotension (common side effect)
  • Sedation (seizures in overdose)
  • Weight gain (possibly excessive)
  • Hepatotoxicity (hydrazines, rare)
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14
Q

MAO inhibitors drug interactions

A
  • ‘Cheese reaction’=tyramine-containing foods and MAO inhibitors leading to hypertensive crisis (throbbing headaches, increased blood pressure, intracranial haemorrhage)
  • MAO inhibitors and TCAs leading to hypertensive episodes
  • MAO inhibitors and pethidine leading to hyperpyrexia, restlessness, coma and hypotension
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15
Q

SSRIs pharmacokinetics

A
  • Oral administration
  • 18-24 hour plasma half life
  • delayed onset of action (2-4 weeks)
  • Fluoxetine competes with TCAs for hepatic enzymes (avoid co-administration)
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16
Q

SSRIs side effects

A

Fewer than TCAs and MAO inhibitors

  • Nausea, diarrhoea, insomnia and loss of libido
  • MAO inhibitor interaction so avoid co-administration
17
Q

Venlafaxine

A
  • Dose-dependent Reuptake inhibitor
  • Second line treatment for severe depression
  • serotonin> noradrenaline»dopamine
18
Q

Mirtazapine

A
  • Alpha-2 receptor antagonist
  • Increase NA and 5-HT release
  • Useful in SSRI-intolerant patients
19
Q

Depression symptoms

A 
Emotional/psychological:
-misery
-apathy
-pessimism
-low self-esteem
-loss of motivation
-anhedonia (loss of enjoyment from 
normally pleasurable activities)
Biological/somatic:
-slowing of thought and action
-loss of libido
-loss of appetite
-sleep disturbance
20
Q

Types of unipolar depression

A

Reactive depression=response to stressful life events, non-familial
Endogenous depression=unrelated to external stresses, familial pattern

21
Q

Monoamine theory of depression

A
  • depression is a functional deficit of central monoamine transmission
  • mania is a functional excess of monoamine transmission
  • relation to NA and 5-HT (serotonin) deficits/excesses
22
Q

Tricyclic antidepressants MOA

A
  • Example: Amitriptyline
  • neuronal monoamine re-uptake inhibitor
  • TCAs down-regulate beta-adrenoceptors and 5-HT2 receptors
23
Q

SSRIs MOA

A
  • Example: Fluoxetine (currently most prescribed antidepressant)
  • Selective 5-HT re-uptake inhibition
  • less troublesome side effects so safer in overdose situation
  • less effective vs severe depression
24
Q

Moclobemide

A
  • Reversible MAO-A inhibitor (RIMA)

- leads to reduced drug interactions and reduced duration of action

25
Q

MAOI’s MOA

A
  • Example: Phenelzine
  • MAO-A break down noradrenaline and serotonin
  • MAO-B break down dopamine
  • most are non-selective inhibitors
  • irreversible inhibition leads to long duration of action
  • rapid effects=increased cytoplasmic noradrenaline and serotonin
  • delayed effects=clinical response due to down-regulation of beta-adrenoceptors and 5-HT2 receptors
  • inhibition of other enzymes
26
Q

Meclobemide

A
  • reversible MAO-A inhibitor (RIMA)

- reduced drug interactions and reduced duration of action

Pharmacology and Therapeutics (30 decks)

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