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Year 2 Pharma > Anti-depressant > Flashcards

Anti-depressant Flashcards

1
Q

What are emotional/psychological symptoms of depression

A

Misery, apathy, pessimism, low self esteem, loss of motivation, anhedonia (loss of enjoyment from activities)

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2
Q

What are biological symptoms of depression

A

Slowing of action/thoughts, loss of libido, loss of appetite, sleep disturbances

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3
Q

What are the two types of depression

A

Unipolar depression

Bipolar depression

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4
Q

Describe unipolar depression

A

A depressive disorder with mood swings that only swing in one direction:

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5
Q

What are different types of unipolar depression

A

reactive depression

endogenous depression

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6
Q

Describe bipolar depression

A

Manic depression with oscillations between depression and mania

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7
Q

What is a drug treatment for bipolar depression but what is the fault with it

A

Lithium - can stabilise the swings between mania and depression but has a narrow therapeutic window

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8
Q

When are the different types of depression onset

A

Unipolar depression is relatively late onset but bipolar, although less common, has an early adult onset

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9
Q

What is the monoamine theory of depression

A

Depression is a functional deficit of central MA transmission; mania is a functional excess of MA transmission - this is related to NA and serotonin deficits/excesses

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10
Q

What is biological evidence that counteracts the monoamine theory of depression

A
  • A reduction in NA metabolites is not concurrent with a worse depression
  • Delayed onset of clinical effect of drugs (a few weeks sometimes) - possibly due to an adaptive change and not MA theory (downregulation of alpha2, beta and serotonin receptors)
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11
Q

What is another name for serotonin

A

5 HT

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12
Q

What is the mechanims of action of TCAs

A

They are monoamine reuptake inhibitors that also act on alpha2, mAChR, histmine receptors, serotonin receptors.
They down regulate beta adrenoceptors and 5-HT2 receptors

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13
Q

Administation, metabolism, half life of amitriptyline

A

Oral,
Hepatic metabolism to active metabolites that are secreted in urine,
Plasma t1/2 10-20 hrs

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14
Q

What are unwanted effects to therapeutic doses of amitriptyline

A

Atropine like effects - anti PNS effects eg dry mouth, constipation
Postural hypotension - effect vasomotor
Sedation - effect on H1 antagonism

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15
Q

What are effects of acute toxicity of amitriptyline?

A

CNS - excitement, delirium, seizures -> coma, respiratory depression
CVS - cardiac dysrhythmias -> VF and sudden death (often used to commit suicide)

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16
Q

What are the drug interaction of amitriptyline with plasma protein binding

A

As it is very plasma protein binding, there can be a massive increase in bioavailability if co-administered with something that displaces it from plasma proteins eg aspirin, phenytoin

17
Q

What are the interactions of amitriptyline with hepatic enzymes

A

The drugs compete with the metabolising hepatic enzymes

18
Q

What are drugs that can potentiate the effects of CNS depression from amitriptyline

A

Alcohol for example

19
Q

What is the mechanism of action of MAOI (monoamine oxidase inhibitors)

A

MAO enzymes: MAO-A breaks down NA and 5HT, and MAO-B breaks down DA eg selegiline

20
Q

What are the rapid effects of MAOI

A

increase cytoplasmic (not enhanced release but more leakage) NA and serotonin

21
Q

What are the delayed effects of MAOI due to

A

Delayed clinical response due to down regulation of beta adrenoceptors and 5HT2 receptors

22
Q

What leads to the side effects of MAOI

A

It inhibits other enzymes

23
Q

Describe the administration, half life and metabolism of MAOI - phenelzine

A

Oral administration
Short plasma half life but longer duration of action
Metabolised in liver, excreted in urine

24
Q

What are unwanted effects of phenelzine

A 
Atropine like effects - anti PNS but less than tCA
Postural hypotension
Sedation
Weight gain
Hepatotoxicity
25
Q

What is the reaction between phenelzine and tyramine containing foods (cheese reaction) and why

A

Tyramine containing foods + MAOI -> hypertensive crisis
Tyramine is metabolised by MAO so high leves of tyramine compete with NA and so higher levels of NA leading to a hypertensive crisis

26
Q

what is the reaction between MAOIs and TCAs

A

Hypertensive crisis

27
Q

What is the reaction between MAOIs and pethidine

A

Hyperpyrexia, restlessness, coma, hypotension

28
Q

What does meclobemide do?

A

It is a reversible, selective MAO-A inhibitor (RIMA - reversible inhibitor of MAO-A) leading to reduced drug interactions and reduced DoA

29
Q

Give an example of an SSRI

A

Fluoxetine

30
Q

What is the mechanism of action of SSRIs

A

5HT reuptake inhibitor

31
Q

when are SSRIs a better choice than other anti depressants and when is it not and why

A

It has less bad side effects so is safer in ODs but is less effective vs severe depression

32
Q

Describe the administration, half life, onset of action and metabolism of SSRIs

A

Oral administration
Half life 18-24 hrs
Delayed onset of action 2-4 weeks
Fluoxetine competes with TCAs for hepatic enzymes so avoid co-adminstration

33
Q

What are unwanted effects of SSRIs?

A

Nausea
Diarrhoea
Insomnia
Loss of libido

34
Q

What is the effect of SSRIs on suicidality

A

It increases suicidality in <18s but due to less side effects than others, it is the currently most prescribed antidepressant

35
Q

Give 2 antidepressant drugs that aren’t SSRI, TCA or MAOIs

A

Venlafaxine and mertazapine

36
Q

What does venlafaxine do? When is it used

A

dose dependant reuptake inhibitor leading to 5HT>NA>DA

Is 2nd line in severe depression

37
Q

What does mertazapine do? When is it useful

A

alpha 2 receptor antagonist that inhibits negative inhibition of NA release and increases NA and 5-HT release.
Useful in SSRI intolerant patients

Year 2 Pharma (34 decks)

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