Anti-depressant Flashcards

(37 cards)

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
What is the reaction between phenelzine and tyramine containing foods (cheese reaction) and why
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
what is the reaction between MAOIs and TCAs
Hypertensive crisis
27
What is the reaction between MAOIs and pethidine
Hyperpyrexia, restlessness, coma, hypotension
28
What does meclobemide do?
It is a reversible, selective MAO-A inhibitor (RIMA - reversible inhibitor of MAO-A) leading to reduced drug interactions and reduced DoA
29
Give an example of an SSRI
Fluoxetine
30
What is the mechanism of action of SSRIs
5HT reuptake inhibitor
31
when are SSRIs a better choice than other anti depressants and when is it not and why
It has less bad side effects so is safer in ODs but is less effective vs severe depression
32
Describe the administration, half life, onset of action and metabolism of SSRIs
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
What are unwanted effects of SSRIs?
Nausea Diarrhoea Insomnia Loss of libido
34
What is the effect of SSRIs on suicidality
It increases suicidality in <18s but due to less side effects than others, it is the currently most prescribed antidepressant
35
Give 2 antidepressant drugs that aren't SSRI, TCA or MAOIs
Venlafaxine and mertazapine
36
What does venlafaxine do? When is it used
dose dependant reuptake inhibitor leading to 5HT>NA>DA | Is 2nd line in severe depression
37
What does mertazapine do? When is it useful
alpha 2 receptor antagonist that inhibits negative inhibition of NA release and increases NA and 5-HT release. Useful in SSRI intolerant patients