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eLCRS - 팜 > Pharm 23: antidepressant drugs > Flashcards

Pharm 23: antidepressant drugs Flashcards

1
Q

Definitions & classification

Monoamine theory of depression

Types of antidepressant drugs
Tricyclic antidepressants (TCAs)
Monoamine oxidase inhibitors (MAOIs)
Selective 5-HT re-uptake inhibitors (SSRIs)
Other drugs

Lithium - mood stabilizing drug

Electroconvulsive therapy (ECT)

A

-

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2
Q

What are the 2 classifications of psychoses?

A
  • schizophrenia

- affective disorders

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3
Q

What are the 2 classifications of affective disorders?

A

mania

depression

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4
Q

What are emotional symptoms of depression ?

A

Misery, apathy, pessimism

Low self-esteem

Loss of motivation

Anhedonia

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5
Q

What are biological symptoms of depression?

A

Slowing of thought & action

Loss of libido

Loss of appetite, sleep disturbance

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6
Q

what is Unipolar depression/depressive disorder?

onset =

A
  • Mood swings are in same direction

- Relatively late onset

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7
Q

What are the 2 types of unipolar depression?

how do they differ?

do drug treatments differ between these 2 or not?

A

Reactive depression (75%)

  • stressful life events (eg grief, divorce etc)
  • non-familial

Endogenous depression (25%)

  • unrelated to external stresses
  • familial pattern

–> drug treatment is same for both

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8
Q

What is Bipolar depression /manic depression

onset =

what treatments are available for patients ?

A
  • Oscillating depression/mania
  • Less common
  • Early adult onset
  • Strong hereditary tendency

–> drug treatment = lithium (mood stabilizer, restricts oscillation of manic + depression)

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9
Q

What is Bipolar depression /manic depression

onset =

what treatments are available for patients ?

A
  • Oscillating depression/mania
  • Less common
  • Early adult onset
  • Strong hereditary tendency

–> drug treatment = lithium (mood stabilizer, restricts oscillation of manic + depression)
(IP3 is reduced with use of lithium)
- narrow therapeutic window
- monitored through plasma level of lithium

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10
Q

Monoamine theory of depression

A
  • biochemical theory of depression:
  • depression = results from functional deficit of central (monoamine) MA transmission
  • Mania = functional excess of central (monoamine) MA transmission
  • depression = decrease in NA + 5HT in the brain
  • delayed onset of clinical effects of antidepressant drugs –> time correlates with down regulation of a2, B, 5HT receptors

other theories:
suggests involvement of HPA axis / hippocampal neurodegeneration in etiology of depression

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11
Q

depression is linked with a lack of ____ + ____ in the brain

A

NA + 5HT in the brain

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12
Q

Describe the MOA of tricyclic antidepressants (TCA) for depression?

A
  • e.g amitriptyline
  • neuronal monoamine re-uptake inhibitors
  • Block NA & 5-HT reuptake (central)
  • reduce rate of reuptake of NA/5HT –> enhances synaptic levels of NA / 5HT
  • can also act on other receipts e.g a2 receptors, histamine, 5HT receptors, mAChRs etc.
  • TCA inhibit a2 receptors –> reduce negative feedback –> increase release of NA into synapse
  • There is also Delayed down-regulation of β-adrenoceptors & 5-HT2 receptors
  • improves mood
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13
Q

Describe the MOA of Reserpine for depression?

A
  • not used now
  • inhibits NA storage in presynaptic terminals
  • decreases mood
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14
Q

Describe the MOA of MAO inhibitors for depression?

A
  • e.g Phenelzine
  • MAO-A : NA & 5-HT
    MAO-B : DA
  • mostly = non selective
  • irreversible inhibition –> so has long duration of action (due to presence of hydrazine - binds covalently to MAO)
  • Increase stores of NA & 5-HT
  • delayed effects –> correlates with down-regulation of β-adrenoceptors & 5-HT2 receptors
  • also inhibitors other enzymes
  • Mood ↑
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15
Q

Describe the MAO of a-methyl tyrosine for depression?

A

Inhibits NA synthesis
Mood ↓
–> Calms manic patients

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16
Q

Describe the MAO of methyldopa for depression?

A

Inhibits NA synthesis

Mood ↓

17
Q

Describe the MAO of ECT for depression?

A

Increases CNS responses to NA & 5-HT

Mood ↑

18
Q

Describe the pharmacokinetics of TCAs?

A

Rapid oral absorption

Highly PPB (90 - 95%)

Hepatic metabolism - active metabolites - renal excretion (glucuronide conjugates)

Plasma t1/2 (10-20 hrs)

19
Q

What are some unwanted effects of TCA as an anti-depressant?

A

at therapeutic dosage:
Atropine - like effects (amitriptyline)
–> blurred vision, dry mouth, constipation

Postural hypotension
–> TCA action on vasomotor centre

Sedation
–> TCA = H1 antagonism

at overdose:
CNS: excitement, delirium, seizures –> coma, resp depression

CVS: cardiac dysrhythmias –> ventricular fibrillation/sudden death

TCA –> can cause attempted suicide

20
Q

What drug interactions might occur for TCA?

A

if other drugs such as aspirin given, they compete for PPB –> increases TCA effects –> due to higher TCA bioavailability

(neuroleptics; oral contraceptives) –> compete with TCA for hepatic microsomal enzymes, less metabolism, increase in TCA bioavailability, Increase TCA EFFECTS

Potentiation of CNS depressants (e.g alcohol)
–> doubling of depressant effects

Antihypertensive drugs (monitor closely)

21
Q

Describe 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

22
Q

What are some unwanted effects of MAO inhibitors

A

Atropine - like effects (< TCAs)

Postural hypotension (common)

Sedation (Seizures in overdose)

Weight gain (possibly excessive)

Hepatotoxicity (due to –> hydrazine - rare)

23
Q

What drug interactions can occur from MAO inhibitors

what is possible alternative medication with less drug interactions?

A
  • cheese reaction –> tyramine = component of food –> indirect sympathomimetic drug
  • -> binds to NA transporter –> increases release of NA out out into synapse
  • -> can causes HYPERTENSIVE CRISIS (headache, Increase BP, intracranial hemorrhage)

–> avoid mature cheese, marmite etc .

  • interact with TCAs
  • -> can also cause hypertensive crisis
  • MAOIs + Pethidine –> can cause hyperpyrexia / restlessness / coma / hypotension

what is possible alternative medication with less drug interactions?

  • Moclobemide = reversible MAO - A inhibitor [RIMA]
    (decreases drug interactions + decreases duration of action)
24
Q

SSRI MAO

A
  • e.g fluoxetine
    Selective 5-HT re-uptake inhibition

Less troublesome side-effects
–> safer when over dosed

But less effective vs severe depression

25
Q

Describe the pharmacokinetics of SSRI

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)

26
Q

What are some unwanted effects of SSRIs?

A
  • generally Fewer SE than TCAs/MAOIs
  • Nausea, diarrhoea, insomnia & loss of libido
  • Interact with MAOIs (avoid co-administration)
  • Fluoxetine (‘Prozac’) = currently most prescribed antidepressant drug
27
Q

There are also other anti depressant drugs available such as venlafaxine + Mirtazapine.

How do these work?

a) venlafaxine
b) Mirtazapine

A

Venlafaxine:
- Dose-dependent Reuptake inhibitor
- initial dose 5HT reuptake inhibition
increase in dose –> shows NA reuptake inhibition
further increase –> shows Dopamine reuptwake inhibition

—> 2nd Line treatment for severe depression

Mirtazapine:

  • α2 Receptor antagonist –> less negative feedback
  • ↑ NA & 5HT release into synapse
  • Other R interactions (sedative)
  • Useful in SSRI-intolerant patients
28
Q

Tricyclic antidepressant drugs (TCAs) work largely by:

A: Antagonism at 5HT receptors
B: Inhibiting central DA reuptake
C: Blocking VSCCs
D: Inhibition of central NA &amp; 5HT reuptake 
E: Enhancement of the action of GABA
A

D

29
Q

The ‘cheese reaction’ is most likely to be caused by:

A: Tricyclic antidepressants (TCAs)
B: Selective serotonin reuptake inhibitors (SSRIs)
C: Monoamine oxidase inhibitors (MAOIs)
D: Reversible MAO-A inhibitors (RIMAs)
E: α2-Adrenoceptor antagonists
A

C

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