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YR2 LCRS Pharm > Anti-depressants > Flashcards

Anti-depressants Flashcards

1
Q

What are the 2 classes of affective disorders?

A

Depression

Mania

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2
Q

List 4 4 emotional (psychological) symptoms of depression

A

Misery, Apathy, Pessimism
Low self-esteem
Loss of motivation
Anhedonia

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3
Q

List 3 biological (somatic) symptoms of depression

A

Slowing of thoughts + actions
Loss of libido
Loss of appetite + sleep disturbances

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4
Q

What characterises unipolar depression?

A

Mood swings in same direction

Relatively late adult onset

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5
Q

What are the 2 types of unipolar depression and how are they treated?

A

Reactive: inappropriate/ distorted reaction to stressful life event. Non-hereditary
Endogenous: Unrelated to external stresses. Familial pattern.
Drug treatment is similar for both

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6
Q

Describe the characteristics of bipolar depression

A 
Oscillating depression/ mania
Less common
Early adult onset
Strong hereditary tendency
Lithium used in drug treatment
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7
Q

What is the monoamine theory of depression?

A

Depression is due to a functional defect of central MA transmission
Mania is due to functional excess of MA transmission in the brain

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8
Q

What is not functioning optimally in clinical depression?

A

Central transmission of NA + 5-HT

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9
Q

Which drugs interfere with the reuptake of NA yet have unexpected consequence?

A

Cocaine + Amphetamine
Slow reuptake of NA, enhance NA in synaptic cleft
No antidepressant effect

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10
Q

How do levels of monoamine metabolites differ in the urine or a clinically depressed patient? What does this suggest? Are levels indicative of anything?

A

Reduced levels of monoamine metabolites in urine, suggesting reduced turnover of monoamines in the brain (reduced turnover of NA + 5-HT)
No correlation in reduction of turnover in mild, moderate + severe depression

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11
Q

Describe the onset of action of antidepressants

A

Pharmacological effects on NA + 5-HT are rapid

Antidepressant effects not seen for 2-3 weeks after commencement

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12
Q

Why do antidepressants have a delayed onset of action?

A

Original changes in NA + 5-HT cause adaptive changes in brain
Adaptive changes give rise to antidepressant effects e.g. by down regulating monoamine receptors e.g. A2, B + 5-HT

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13
Q

What is the MOA of Electroconvulsive therapy?

A

Increases CNS responses to NA + 5-HT

Elevates mood

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14
Q

Give an example of a Tricyclic antidepressant and explain its MOA

A

Amitriptyline
Neuronal monoamine re-uptake inhibitors- inhibit NA + 5-HT re-uptake
Prolongs presence of NA + 5-HT in cleft, enhancing signal

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15
Q

Which other receptor do TCAs interact with and what effect may this cause?

A

Alpha 2 antagonist action
Alpha 2 provides negative feedback on NA + 5-HT release; thus by blocking this, more NA + 5-HT is released, contributing to antidepressant effect

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16
Q

What causes the delay in onset of TCAs?

A

Delayed down regulation of B-adrenoceptors + 5-HT2 receptors

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17
Q

Give 4 pharmacokinetic features of TCAs

A

Rapid oral absorption
Highly plasma protein bound (~95%)
Hepatic metabolism; generate active metabolites, eventually excreted in urine
10-20 hour half life: taken once daily

18
Q

List 3 unwanted effects of TCAs seen at a therapeutic dose

A

Atropine-like effects: Dry mouth + Skin, due to inhibition of muscarinic receptors
Postural hypotension
Sedation

19
Q

List 2 unwanted effects of TCAs seen in an OD

A

CNS: excitement, delirium, seizures, coma, respiratory depression
CVS: cardiac dysrhythmias, ventricular fibrillation, sudden death

20
Q

Why do TCAs have many drug interactions?

A

TCAs are highly PPB, so other drugs can displace them, increasing free conc. of TCA, increasing their effects
Drugs that use same metabolic enzymes compete with TCAs, slowing TCA metabolism + increasing conc.

21
Q

List 5 drugs that should be prescribed with caution/ not prescribed to someone on TCAs

A 
Aspirin (Highly PPB)
Phenytoin (Highly PPB)
Warfarin (Highly PPB)
Neuroleptics (same metabolism)
Oral contraceptives (same metabolism)
22
Q

How do TCAs interact with CNS depressants e.g. alcohol??

A

Potentiates CNS depressants

23
Q

What varies in bi-directionally with TCAs, and thus must be monitored?

A

BP

Monitor use of antihypertensives

24
Q

Give an example of a monoamine oxidase inhibitor and briefly describe the MOA

A

Phenelzine

Irreversibly inhibit monoamine oxidases, thus preventing breakdown of NA + 5-HT

25
Q

What are the 2 types of monoamine oxidase?

A

A: Preferentially breaks down NA + 5-HT
B: Preferentially breaks down DA

26
Q

Describe the MOA of MAOIs

A

Lipid soluble, gain access to NA terminals
Inhibits MAO in NA + 5-HT terminals
Increases cytoplasmic conc. of NA + 5-HT, thus enhances release, synaptic conc. + effect

27
Q

Describe the duration of action of MAOs

A

Long due to irreversible inhibition

28
Q

Describe the onset of action of MAOs

A

Rapid effect in increasing cytoplasmic NA + 5-HT

Delayed anti-depressant effects due to down regulation of B-adrenoceptors + 5-H2 receptors

29
Q

Give 3 pharmacokinetic features of MAOis

A

Rapid oral absorption
Few hours half life but longer DOA- taken once/ twice daily
Hepatic metabolism, urinary excretion

30
Q

List 5 unwanted effects of MAOIs

A 
Atropine-like effects due to muscarinic receptor antagonism 
Postural hypotension
Sedation/ Seizures
Weight gain due to increase in appetite 
Hepatotoxicity
31
Q

What drug interaction of MAOIs has a serious consequence?

A

“Cheese reaction”
Tyramine from diet not broken down by MAO
High plasma levels cause sympathetic like effects due to pushing NA out of nerve terminals
Leads to hypertensive crisis (increased BP, headache, intracranial haemorrhage)

32
Q

What is the consequence of simultaneous use of MAOIs and TCAs? Thus what do we do?

A

Hypertensive episodes

Avoid coadministration

33
Q

What is the consequence of simultaneous use of MAOIs and pethidine?

A

Hyperpyrexia
Restlessness
Coma
Hypotension

34
Q

State a new MAOI which reversibly inhibits MAO-A? What is the advantage of using this? What is the disadvantage of using this?

A

Moclobemide
Has less drug interactions
Has shorter duration of action so needs multiple doses per day

35
Q

Give an example of a selective serotonin reuptake inhibitor and briefly describe the MOA

A

Fluoxetine

Selectively inhibits re-uptake of 5-HT

36
Q

What are the advantages and disadvantages of SSRIs?

A

A: Effective, less side effects, safer in OD
D: Less effective for severe depression

37
Q

Give 4 pharmacokinetic features of SSRIs

A

Oral administration
18-24 hour half life
Delayed onset of action
Hepatic metabolism

38
Q

What must be drug must not be used in conjunction with SSRIs?

A

TCAs as they compete for hepatic enzymes

MAOIs as the have complementary MOA

39
Q

List 4 unwanted effects of SSRIs

A

Nausea
Diarrhoea
Insomnia
Loss of libido

40
Q

Name 2 other antidepressant drugs

A

Venlafaxine: dose dependent re-uptake inhibitor
Mirtazapine: A2 receptor antagonist- increases NA + 5-HT release

YR2 LCRS Pharm (34 decks)

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