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Y2 Pharm (LCRS1) > Anti depressants > Flashcards

Anti depressants Flashcards

1
Q

What are the symptoms of depression?

A
  1. Emotional (Psycho-logical)
    * Misery, apathy, pessimism
    * Low self-esteem
    * Loss of motivation
    * Anhedonia (inability to feel pleasure)
  2. Biological (Somatic)
    * Slowing of thought & action
    * Loss of libido
    * Loss of appetite, sleep disturbance
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2
Q

What are the 2 types of depression?

A
  • Unipolar depression
  • Bipolar depression
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3
Q

What is the difference between the 2 different types of depression?

A
  1. Unipolar
  • Mood swings in the same direction
  • Relatively late onset
  1. Bipolar
  • Oscillating depression/mania
  • Less common
  • Early adult onset
  • Strong hereditary tendency
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4
Q

What are the 2 subsets of unipolar depression?

A
  1. Reactive depression
  • stressful life events
  • non-familial
  1. Endogenous depression
  • unrelated to external stresses
  • familial pattern
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5
Q

What is the monoamine theory of depression and mania?

A

Depression = Functional deficit in central monoamine transmission (NA and 5-HT)

Minia = functional excess

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6
Q

What’s the evidence for and against the monoamine theory of depression?

A
  • Pharmacological evidence is supportive
  • Biochemical evidence is inconsistant
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7
Q

What happens when antidepressant drugs are taken?

A
  • Delayed onset of action - 1 week
  • Down-regulation of alpha 2, beta and some subsets of 5HT receptors
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8
Q

What are other theories for depression?

A
  • Increased CRH levels play a role
  • Hippocampal neurodegeneration
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9
Q

What is the principal action of the main classes of antidepressant drugs?

A
  1. Tricyclic antidepressants
    * Block NA & 5-HT reuptake
  2. MAO inhibitors
    * Increase stores of NA & 5-HT by preventing metabolism
  3. SSRIs
    * Block 5-HT reuptake
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10
Q

What is the mechanism of action of TCAs?

A
  • Neuronal monoamine re-uptake inhibitors
  • Delayed down-regulation of β-adrenoceptors & 5-HT2 receptors
  • Possible other receptor actions -α2, mAChRs, histamine, 5-HT
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11
Q

What are the pharmacokinetics of TCAs?

A
  • Rapid oral absorption
  • Highly PPB (90 - 95%)
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12
Q

What’s the half life of TCAs?

A

10-20 hours

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13
Q

How are TCAs metabolised?

A
  • Hepatic metabolism - active metabolites
  • Renal excretion (glucuronide conjugates)
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14
Q

What are the unwanted effects of theraptuic doses of TCAs?

A
  • Atropine - like effects (amitriptyline)
  • Postural hypotension (vasomotor centre)
  • Sedation (H1 antagonism)
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15
Q

What are the effects of TCA acute toxicity?

A
  1. CNS:
    * excitement, delirium, seizures -> coma, respiratory depression
  2. CVS:
    * cardiac dysrhythmias -> ventricular fibrillation/sudden death
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16
Q

What are the drug interactions of TCAs?

A
  1. PPB: ­

Displace TCA effects (aspirin, phenytoin, warfrin)

  1. Hepatic microsomal enzymes: ­
    * Competition for enzymes (neuroleptics, oral contraceptives)
  2. Potentiation of CNS depressants (alcohol)
  3. Antihypertensive drugs (monitor closely)
    * Unpredictable rise or fall
17
Q

What is an example of a TCA?

A

Amitriptyline

18
Q

What is an example of a MAO inhibitor?

A

Phenelzine

19
Q

What do the MAO preferentially metabolise?

A
  • MAO-A : NA & 5-HT
  • MAO-B : DA
20
Q

What is the mechanism of MAO inhibitors?

A
  • Most are non-selective MAOIs
  • Irreversible inhibition -> long d.o.a.
21
Q

What are the rapid and delayed effects of MAO inhibitors?

A

Rapid effects : ­

  • increase in cytoplasmic NA & 5-HT

Delayed effects :

  • down-regulation of β-adrenoceptors & 5-HT2 receptors
22
Q

What are the pharmacokinetics of MAO inhibitors?

A
  • Rapid oral absorption
  • Short plasma t1/2 (few hrs) but longer d.o.a.
  • Metabolised in liver; excreted in urine

​

23
Q

What are the unwanted effects of the MAO inhibitors?

A
  • Atropine - like effects (< TCAs)
  • Postural hypotension (common)
  • Sedation (Seizures in o.d.)
  • Weight gain (possibly excessive)
  • Hepatotoxicity (hydrazines; rare)​
24
Q

What are the other drug interactions of MAO inhibitors?

A

MAOIs + TCAs = hypertensive episodes (avoid)

MAOIs + pethidine = hyperpyrexia, restlessness, coma & hypotension.

​

25
Q

What is the cheese reaction?

A

Tyramine

  • Tyramine is found in food
  • Tyramine is a sympathomimmetic drug
  • Gains access to the brain and enters NA neurones
  • Forces NA out of the pre synaptic terminal

Tyramine + MAOi

  • Excessive SNS activation as MAO breaks down tyramine
  • Hypertensive crisis - throbbing headaches, increase bp, inracranial haemorrhage
26
Q

What is Moclobemide?

A
  • reversible MAO-A inhibitor
  • ↓ Drug interactions
  • ↓ doa.
27
Q

What are SSRIs? Give an example

A
  • Selective serotonin reuptake inhibitors
  • Fluoxetine
28
Q

What is the mechanism of action of SSRIs?

A

Selective 5-HT re-uptake inhibition

29
Q

What are the advantages and disadvantages of SSRIs?

A

Advantage:

  • Less troublesome side-effects; safer in o.d.

Disadvantage:

  • Less effective vs severe depression

​

30
Q

What are the Pharmacokinetics of SSRIs?

A
  • p.o. administration
  • Plasma t1/2 (18-24 hrs)
  • Delayed onset of action (2-4 weeks)
  • Fluoxetine competes with TCAs for hepatic enzymes (avoid co-administration)

​

31
Q

What are the unwanted effects of SSRIs?

A
  • •Fewer than TCAs/MAOIs
  • Nausea, diarrhoea, insomnia & loss of libido
  • Interact with MAOIs (avoid co-administration)

​

32
Q

What is venlafaxine?

A
  • Anti-depressant drug
  • Dose-dependent Reuptake inhibitor
  • 5HT > NA >> DA (SNRI)
  • 2nd Line treatment for severe depression
33
Q

What is mirtazapine?

A
  • Anti-depressant
  • α2 Receptor antagonist
  • ↑ NA & 5HT release
  • Other R interactions (sedative)
  • Useful in SSRI-intolerant patients
34
Q

Why might fluoxetine be used over velafaxine?

A
  • Velafaxine can target serotonin > NA > dopamine
  • As the more selective drug, the side effect profile of fluoxetine is expected to be lower (a better risk-benefit ratio).
  • It is also the most cost-effective solution (i.e. cheapest).

Y2 Pharm (LCRS1) (34 decks)

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