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LCRS Pharm > Anti-depressants > Flashcards

Anti-depressants Flashcards

1
Q

How are psychoses classified and subclassified?

A 
Schizophrenia
Affective disorders (mania and depression)
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2
Q

What are the two classifications of depression?

A

Unipolar

Bipolar

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3
Q

How is unipolar depression further subdivided? Give some facts about these.

A 
Endogenous 
- familial pattern 
- unrelated to external stresses
Reactive 
- Non familial 
- reactive to stressful life events
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4
Q

Describe the biological symptoms of depression

A 
Slowing of thought 
Slowing of action 
Loss of libido 
Loss of appetite 
Sleep disturbance
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5
Q

List the psychological symptoms of depression

A 
Misery
Apathy
Pessimism
Low self-esteem
Loss of motivation
Anhedonia
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6
Q

Compare the onset of unipolar vs bipolar depression

A

Unipolar - late onset

Bipolar - early adult onset

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7
Q

Describe the monoamine theory of depression

A

Schildkraut’s theory
Depression = functional deficit of central monoamine transmission (NA + 5HT)
Mania = functional excess

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8
Q

State two bits of evidence which disagree with the theory

A

Lower levels of MAO metabolites in urine, however no correlation with severity

Clinical effects are delayed, suggesting body may be ADAPTING to the drug by downregulating a2, beta or 5HT receptors instead of this being pathological

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9
Q

Give three examples of pharmacological interventions which increase mood and support the theory

A

Increased mood seen after:
TCAs which block MA reuptake
MAOi which increase MA stores
ECT which increases response to NA&5HT

note: MA = NA+ 5HT

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10
Q

Give three examples of pharmacological interventions which decrease mood and therefore support the theory

A

Decreased mood seen after:
Reserpine - inhibits NA + 5HT storage
Alpha methyl tyrosine - inhibits NA synthesis + calms manic patients
Methyldopa - inhibits NA synthesis

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11
Q

What are the emerging theories of depression?

A

Increase in CRH/HPA activity

Hippocampal neurodegeneration

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12
Q

How do TCAs work?

A

Inhibit reuptake of monoamines

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13
Q

Describe the efficacy of action of TCAs on NA, 5HT and dopamine

A

Equal effects on NA + 5HT
Less effect on dopamine

NA=5HT>DA

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14
Q

Describe the chemical structure of TCAs

A

3 rings (tri-cyclic!)

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15
Q

Give an example of a TCA

A

Amitriptyline

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16
Q

Where else do TCAs work? List some examples

A

On other receptors:

  • α2 antagonism
  • mAChRs antagonism
  • histamine
  • 5-HT

MASH

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17
Q

TCAs result in delayed downregulation of what?

A

Beta adrenoceptors

5HT2 receptors

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18
Q

Describe the plasma protein binding of TCAs

A

Heavily PPB

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19
Q

Describe the metabolism and excretion of TCAs

A

Active metabolites produced by liver

Glucoronide conjugation, excreted via kidneys

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20
Q

What is the half life of TCAs?

A

10-20hrs

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21
Q

What are the side effects of TCAs at therapeutic doses? Link these to TCAs’ actions on other receptors

A

mAchR antagonism - atropine like anti-PNS effects
H1 antagonism - sedation/drowsiness
Postural hypotension - direct effects via vasomotor centre

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22
Q

What are the side effects of TCAs at toxic doses?

A

Attempted suicide
CNS - excitement, delirium, seizures, coma, respiratory depression
CVS - VF, dysrhythmias, sudden death

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23
Q

List some drugs which should not be given with TCAs/monitored closely?

A

Aspirin
Warfarin
Phenytoin
Neuroleptics e.g. antipsychotics

Oral contraceptives
Antihypertensives (monitor closely)
SSRIs

Alcohol

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24
Q

Why should oral contraceptives, antipsychotics and SSRIs be avoided when giving TCAs?

A

These drugs will compete with TCAs for hepatic microsomal enzymes and therefore increase plasma TCA

25
Q

Why should aspirin, warfarin and phenytoin not be given with TCAs?

A

They can displace TCAs from the plasma proteins and therefore increase TCA bioavailability

26
Q

Describe the interaction between hypertensives and TCAs

A

Increase or decrease TCA bioavailability, therefore monitor closely

27
Q

Describe the mechanism of action of monoamine oxidase inhibitors, and give an example

A

Phenelzine (MOAi)

IRREVERSIBLY inhibits MOA non-selectively, thereby rapidly increasing cytoplasmic serotonin and dopamine levels

28
Q

Give the two subclasses of MAO and their preferences for binding

A

MAO-A - Noradrenaline + serotonin

MAO-B - Dopamine

29
Q

Describe the chemical structure of monoamine oxidase inhibitors, and given an example of a subgroup

A

Single ring structures
Carbon side chains and functional groups

Example: hydrazine

30
Q

Where else do MAOi act?

A

Inhibit other enzymes
Downregulate beta receptors
Downregulate 5HT2 receptors

31
Q

Describe the half life and duration of action of MAOi

A

Short plasma half life BUT:

Long duration of action (irreversible inhibition)

32
Q

Give the side effects of MAOi at therapeutic doses

A

SIMILAR TO TCAs:
Atropine like anti-PNS effects
Postural hypotension
Sedation

Other SE:
Weight gain

33
Q

Give the side effects of MAOi at toxic doses

A

Hepatotoxicity

Seizures

34
Q

In relation to diet, what should you advise patients who take MAO inhibitors?

A

AVOID FOODS WITH TYRAMINE e.g. cheese
Cheese reaction - tyramine increases NA levels. Monoamine oxidases normally break down the tyramine to decrease the noradrenaline levels.
Inhibiting the enzyme = increased tyramine = hypertensive crisis

35
Q

What would be the consequences of the cheese reaction?

A

Hypertensive crisis
Throbbing headache
Intracranial haemorrhage

36
Q

State and explain the consequence of giving MAOi with TCAs

A

Hypertensive episodes (noradrenaline overload)

37
Q

Which other drug should be avoided with MAOi?

A

Pethidine (opiod for child birth)

38
Q

What are the consequences of giving Pethidine with MAOi?

A

Hyperpyrexia
Restlessness
Hypotension
Coma

39
Q

Give the name and site of action of a newer drug which is selective for an MAO.

A

Moclobemide - reversible MAO-A inhibitor

40
Q

What class of drugs does moclobemide come under?

A

RIMA - reversible inhibitors of monoamine oxidase A

41
Q

Give an advantage of using RIMAs instead of conventional MAOi

A

RIMA interact less with other drugs

42
Q

Give two disadvantages of using RIMAs instead of conventional MAOi

A 
Shorter duration of action (due to being reversible)
Less efficacy (as it only works on MAO-A)
43
Q

Describe the structure of SSRIs and give an example

A

Ring structures
Aliphatic side chain

Example: Fluoxetine

44
Q

Why are SSRIs the most commonly prescribed antidepressant?

A

Less troublesome side effects

Safer in overdose

45
Q

What is the disadvantage of using SSRIs?

A

Less effective against severe depression

46
Q

What is the plasma half life of SSRIs?

A

18-24hrs

47
Q

When do SSRIs start working?

A

After 2-4 weeks

48
Q

What are the side effects of SSRIs?

A

Nausea
Diarrhoea
Insomnia
Loss of libido

49
Q

Out of all three classes of anti-depressants, which has the least side effects?

A

SSRIs

50
Q

Which two classes of drugs cause downregulation of beta and 5HT2 receptors?

A

TCAs and MAOi

51
Q

Which drugs should be avoided when taking SSRIs and why?

A

TCAs - competition for hepatic enzymes

52
Q

Why should you advise patients to avoid alcohol when taking TCAs?

A

To avoid CNS depression

53
Q

What is the second line treatment for severe depression and how does this work?

A

Venlafaxine - SNRI: serotonin and noradrenaline reuptake inhibition

54
Q

Describe the dose-dependent inhibition of Venlafaxine

A

At low doses - inhibits reuptake of serotonin
At high doses - inhibits reuptake of noadrenaline

5HT>NA>DA

55
Q

What drug is given to patients who are intolerant to SSRIs? How does this work?

A

Mirtazapine - alpha 2 receptor antagonist (therefore increases noradrenaline and serotonin levels)

56
Q

What other actions does mirtazapine have?

A

Other receptor actions including on histamine receptor:

Sedative effects

57
Q

Name a drug which decreases mood by inhibiting stores of noradrenaline and serotonin

A

Reserpine

58
Q

Name two drugs which inhibit NA synthesis and lowers mood/causes calming effects in manic patients

A

Alpha methyl tyrosine (calms manic patients)

Methyldopa

LCRS Pharm (6 decks)

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