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Pharmacology > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

What are the two classes of psychoses?

A

Schizophrenia

Affective disorders

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2
Q

What are the two main classes of affective disorders?

A

Mania

Depression

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3
Q

List emotional (psychological) symptoms of depression.

A

Misery

Apathy

Pessimism

Low self-esteem

Loss of motivation

Anhedonia

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4
Q

List biological (somatic) symptoms of depression.

A

Slowing of thought and action

Loss of libido

Loss of appetite

Sleep disturbance

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5
Q

What are the two main classifications of depression?

A

Unipolar depression/depressive disorder

Bipolar depression/ manic depression

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6
Q

What are the features of unipolar depression/depressive disorder?

A

Mood swings in same direction

Relatively late onset

Reactive (stressful life events, non-familial) or endogenous (unrelated to external stresses, familial pattern)

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7
Q

What are the features of bipolar depression/ manic depression?

A

Oscillating depression/mania

Less common

Early adult onset

Strong hereditary tendency

Treated with lithium- mood stabiliser

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8
Q

What is the monoamine theory of depression?

A

Depression results from a functional deficit of central monoamine transmission in the brain; mania results from functional excess.

Original hypothesis was based on noradrenaline and 5-HT: overactive in clincal depression.

Based on pharmacological evidence.

Biochemical evidence inconsistent.

Delayed onset of clinical effect of drugs (adaptive changes?).

Down-regulation: alpha-2, beta, 5-HT receptors.

General conclusions remain firm.

HPA axis (increased CRH levels)?

Hippocampal neurodegeneration?

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9
Q

What is the principal action and effect in depressed patients of tricyclic antidepressants?

A

Block NA and 5-HT reuptake

Improved mood

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10
Q

What is the principal action and effect in depressed patients of MAO inhibitors?

A

Increase stores of NA and 5-HT

Improve mood

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11
Q

What is the principal action and effect in depressed patients of reserpine?

A

Inhibits NA and 5-HT storage

Lower mood

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12
Q

What is the principal action and effect in depressed patients of alpha-methyltyrosine?

A

Inhibits NA synthesis

Lower mood, calming of manic patients

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13
Q

What is the principal action and effect in depressed patients of methyldopa?

A

Inhibits NA synthesis

Lower mood

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14
Q

What is the principal action and effect in depressed patients of ECT?

A

Increases CNS responses to NA and 5-HT

Improved mood

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15
Q

What are the main types of antidepressant drugs?

A

Tricyclic antidepressants (TCAs)

Monoamine oxidase inhibitors (MAOIs)

Serotonin selective reuptake inhibitors (SSRIs)

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16
Q

What is the mechanism of action of tricyclic antidepressant drugs?

A

Neuronal monoamine reuptake inhibitors.

NA = 5-HT > DA

Other receptor actions?

  • alpha-2: presynaptic receptor, TCAs act as antagonists, noradrenaline release affects postsynaptic neuron, alpha-2 provides negative feedback system, slows down release of noradrenaline, more in synaptic cleft
  • mAChRs
  • histamine
  • 5-HT

Delayed down-regulation of beta-adrenoceptors and 5-HT2 receptors.

17
Q

Describe the pharmacokinetics of tricyclic antidepressants.

A

Rapid oral absorption

Highly plasma protein bound (90-95%)

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

Plasma half-life: 10-20 hrs

18
Q

What are the unwanted effects of tricyclic antidepressants at therapeutic dosage?

A

Atropine-like effects (amitriptyline)

Postural hypotension (vasomotor centre)

Sedation (H1 antagonism)

19
Q

What are the unwanted effects of tricyclic antidepressants through acute toxicity (overdose)?

A

CNS: excitement, delirium, seizures → coma, respiratory depression

CVS: cardiac dysrhythmias → ventricular fibrillation/sudden death

Care- attempted suicide

20
Q

Give an example of a tricyclic antidepressant drug.

A

Amitriptyline.

21
Q

What are the drug interactions of tricyclic antidepressants?

A

Plasma protein bound: increased TCA effects with coadministration of aspirin, phenytoin, etc.

Hepatic microsomal enzymes: increased TCA effects with coadministration of neuroleptics, oral contraceptives.

Potentiation of CNS depressants (alcohol).

Antihypertensive drugs (monitor closely).

22
Q

Give an example of a monoamine oxidase inhibitor.

A

Phenelzine.

23
Q

What is the mechanism of action of monoamine oxidase inhibitors?

A

MAO-A: NA & 5-HT

MAO-B: DA

Most are non-selective MAOIs.

Irreversible inhibition → long duration of action.

Rapid effects: increased cytoplasmic NA & 5-HT- breakdown of both is blocked- increased concentration in the synapse.

Delayed effects: clinical response; down-regulation of beta-adrenoceptors and 5-HT2 receptors.

Inhibition of other enzymes.

24
Q

Describe the pharmacokinetics of monoamine oxidase inhibitors.

A

Rapid oral absorption

Short plasma half-life: few hours, but longer duration of action because it is irreversible inhibition

Metabolised in liver, excreted in urine

25
Q

What are the unwanted effects of monoamine oxidase inhibitors?

A

Atropine-like effects (<tcas></tcas>

<p>Postural hypotension (common)</p>

<p>Sedation (seizures in overdose)</p>

<p>Weight gain (possibly excessive)</p>

<p>Hepatotoxicity (hydrazines; rare)</p>

</tcas>

26
Q

What are the drug interactions of monoamine oxidase inhibitors?

A

Serious problem.

‘Cheese reaction’: tyramine-containing foods + MAOI → hypertensive crisis (throbbing headache, increased blood pressure, intracranial haemorrhage).

MAOIs + TCAs → hypertensive episodes (avoid).

MAOIs + pethidine → hyperpyrexia, restlessness, coma and hypotension.

27
Q

What is moclobemide?

A

Reversible MAO-A inhibitor (RIMA)

Decreased drug interaction

Decreased duration of action

28
Q

Give two examples of selective serotonin reuptake inhibitors.

A

Fluoxetine

Citalopram

29
Q

What is the mechanism of action of selective serotonin reuptake inhibitors?

A

Selective 5-HT reuptake inhibition.

Less troublesome side effects.

Safer in overdose.

Less effective vs. severe depression.

30
Q

Describe the pharmacokinetics of selective serotonin reuptake inhibitors.

A

Oral administration.

Plasma half-life: 18-24 hours.

Delayed onset of action (2-4 weeks).

Fluoxetine competes with TCAs for hepatic enzymes (avoid coadministration).

31
Q

What are the unwanted effects of selective serotonin reuptake inhibitors?

A

Fewer than TCAs/MAOIs

Nausea, diarrhoea, insomnia and loss of libido

Interact with MAOIs (avoid coadministration)

32
Q

What is currently the most prescribed antidepressant drug?

A

Fluoxetine (‘Prozac’).

33
Q

What is venlafaxine?

A

Dose-dependent reuptake inhibitor

5HT > NA (SNRI)

2nd line treatment for severe depression

34
Q

What is mirtazapine?

A

Alpha-2 receptor antagonist

Increased NA & 5-HT release

Other receptor interactions (sedative)

Useful in SSRI-intolerant patients

Pharmacology (21 decks)

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