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PED2006 - Systems Pharmacology > Antidepressants [5] > Flashcards

Antidepressants [5] Flashcards

1
Q

Name as many affective disorders as possible

A

Major depressive disorder (MDD)
Unipolar / bipolar depression
Attention deficit hyperactivity disorder (ADHD)
Obsessive compulsive disorder (OCD)
Panic disorder
Post traumatic stress disorder (PTSD)
Seasonal affective disorder (SAD)

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2
Q

Emotional symptoms of depression

A

Misery
Apathy
Hopelessness
Low self esteem
Guilt
Inadequacy

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3
Q

Biological symptoms of depression

A

Retardation of thought
Loss of libido
Sleep disturbance
Loss of appetite

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4
Q

Difference between unipolar and bipolar depression

A

Unipolar - only negative moods & no evidence for genetic cause
Bipolar - depression + mania & evidence for genetic cause

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5
Q

What are the two types of unipolar depression

A

Reactive and endogenous

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6
Q

What is reactive depression

A

Response to distress
3-10% population
Women > men

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7
Q

What is endogenous depression

A

Biochemical cause
1% population
Women = men

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8
Q

What is the monoamine theory of depression and mania

A

Depression - deficient monoaminergic transmission
Mania - excessive NA & 5-HT transmission

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9
Q

What is 5-HT and what does it control

A

Serotonin
Mood , sleep , sexual behaviour , appetite , sensory perception

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10
Q

What are the noradrenaline receptors

A

Alpha and beta adrenergic receptors

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11
Q

What locus does NA bind

A

Locus coeruleus
Malfunctions cause depression / anxiety

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12
Q

How is dopamine made

A

From the precursor DOPA by DOPA decarboxylase

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13
Q

What does dopamine control

A

Motivation, reward, reinforcement

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14
Q

What dopamine receptors increase cAMP

A

D1 and D5

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15
Q

What dopamine receptors decrease cAMP

A

D2, D3 and D4

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16
Q

How are Parkinson’s disease and dopamine linked

A

Caused by death of dopamine

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17
Q

How are schizophrenia and dopamine linked

A

Caused by overactivity of dopamine levels in certain brain regions

18
Q

How does cocaine affect dopamine

A

It inhibits uptake
Increased conc of dopamine in synapse
Prolonges it’s action

19
Q

What is the pharmacological evidence for the monoamine theory

A

Reserpine (inhibits brain storage of NA and 5-HT) causes depression

20
Q

What is the pharmacological evidence against the monoamine theory

A

Amphetamine (release do NA & blocks reuptake) has no effect in depressed patients
Cocaine (inhibits NA reuptake) has no effect on depressed patients

21
Q

Biochemical evidence for the monoamine theory

A

Urinary & CSF conc of MOPEG (a NA metabolite) is reduced by 25% in depressed patients
CSF conc of 5-H1AA (5-HT metabolite) is reduced in some depressed patients

22
Q

Biochemical evidence against the monoamine theory

A

Urinary excretion of 5-H1AA does not change in depression
CSF conc of 5-1AA is not reduced in all patients

23
Q

What are the reuptake inhibitor antidepressant drugs

A

Serotonin reuptake inhibitors (SRI)
NA reuptake inhibitors (NRI)
Selective SRI (SSRI)
Selective NRI (SNRI)

24
Q

What are tricyclic antidepressants (TCA) structurally closely related to

A

Neuroleptics
TCA has extra atom in central ring

25
Q

Mechanism of TCAs

A

Blocks reuptake of amines by nerve terminals
Mainly effective on NA and 5-HT with little selectivity

26
Q

Why do TCAs cause side effects

A

They also bind to Muscarinic receptors
Cause dry mouth, blurred vision, constipation and urinary retention

27
Q

How are TCAs metabolised

A

By N-demethylation and ring hydroxylation (3° -> 2° amines)

28
Q

2 forms of MAO

A

MAO-A and MAO-B

29
Q

MAO-A has substrate preference for …

A

5-HT

30
Q

MAO-B has substrate preference for …

A

Phenylethylamine

31
Q

MAOIs have preference for …

A

MAO-A

32
Q

Monoamine oxidase regulates what

A

Concentrations of NA & dopamine

33
Q

Side effects of MAOIs

A

Hypotension
Excessive central stimulation
Weight gain
Hepatotoxicity

34
Q

Explain the cheese reactions

A

Caused by MAOIs
Tyramine found in mature cheese and marmite
Usually metabolised by MAO in gut wall
MAOIs cause tyramine to be absorbed and it’s sympathomimetic effect enhances
- acute hypertension
- severe headache
- intracranial bleeding

35
Q

Examples of SSRIs

A

Fluoxetine, sertraline, citalopram

36
Q

Do SSRIs or TCAs have fewer side effects

A

SSRI

37
Q

Theory behind the 2-3 weeks therapeutic effect of SSRI

A

Quick increase in serotonin inhibits serotonin firing
Desensitisation of autoreceptors after prolonged SSRI exposure
Feedback regulation requires chronic administration to sustain serotonin levels
Need to alter delta and beta adrenergic receptor expression

38
Q

4 advantages of SSRIs over TCAs & MAOI

A

Lack of anticholinergic & cardiovascular side effects
No weight gain
Low acute toxicity (low risk of overdose)
No food reaction

39
Q

Disadvantages of SSRIs

A

Nausea, anorexia, insomnia
Reported increase in aggression

40
Q

What happens when SSRIs is combined with MAOI

A

Serotonin syndrome

41
Q

Example of NRI

A

Reboxetine - most effective for social functioning

42
Q

Example of dopamine agonist

A

Bupropion - blocks reuptake of NA and dopamine

PED2006 - Systems Pharmacology (19 decks)

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