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Missed Lectures > Anti Depressants > Flashcards

Anti Depressants Flashcards

1
Q

Types of Antidepressant drugs

A 
TCAs
MAOI
SSRI
Lithium
Electroconvulsive
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2
Q

What are the two classes of psychoses

A

Schizophrenia and affective disorders

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3
Q

Whats are the two classes of affective disorder

A

Mania and Depression

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4
Q

Symptoms of Depression

A 
(emotional)
Misery/Pessimism
Low Self-esteem
Loss of Motivation
Anhedonia
(biological)
Slowing of thought & action
Loss of Libido
Loss of Appetite
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5
Q

Describe Reactive Depression

A

Unipolar, relatively late onset, caused by stressful life events, non-familial

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6
Q

Describe endogenous Depression

A

Unipolar, unrelated to external stress, shows familial pattern

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7
Q

Describe bipolar depression

A

Oscillating depression, less common, early adult onset, strong hereditary tendency, drug treatment Lithium

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8
Q

Monoamine Theory of Depression

A

Depression is a functional deficit of monoamines, mania is a functional excess

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9
Q

How does reserpine act to reduce mania

A

inhibits NA and 5-HT (serotonin) storage

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10
Q

How does ECT work

A

Increases CNS response to NA and 5-HT

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11
Q

How is cocaine an exception to the Monoamine Theory

A

Cocaine reduces NA re-uptake in the synapse, but has no anti-depressive effects

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12
Q

What is a biochemical inconsisteny with the monoamine theory?

A

reduction in monoamine metabolites in the urine in and delay of onset for treatment

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13
Q

How do TCAs work eg Amitriptyline

A

Neuronal monoamine re-uptake inhibitors. Actions on NA and 5-HT is equal. Act on a2, histamine and mAChR receptors.Causes delayed down-regulation of b-adrenoceptors and 5-HT2 receptors

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14
Q

How are TCAs taken

A

Orally, and highly PPB

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15
Q

How are TCAs metabolised

A

Hepatic metabolism -> activated, and renal excretion

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16
Q

What is the TCA H1/2

A

10-20 hrs

17
Q

What are the unwanted effects?

A

Atropine like effects, postural hypotension, sedation (H1 antagonism)

18
Q

Describe the Acute Toxicity of TCA

A

CNS: Excitement, delirium, seizures, coma, respiratory depression.
CVS: Cardiac dysrhythmias and ventricular fibrillation

19
Q

What are the drug interactions with TCAs

A

Other highly PPB drugs such as Aspirin
Hepatic microsomal enzymes eg. oral contraceptives
Potentiate other CNS depressants eg. alcohol
Antihypertensive drugs (monitor BP)

20
Q

How do MAOIs such as Phenelzine work

A

non-selective MAOI

21
Q

What do MAO-A an B correlate to?

A

A: NA and 5-HT
B: DA

22
Q

Why do MAOIs have long duration of action

A

Irreversible inhibitions

23
Q

What are the rapid effects of penelzine

A

increased cytoplasmic NA and 5-HT

24
Q

What are the delayed effects of Phenelzine

A

Down-regulation of 5-HT and b-adrenoceptors

25
Q

Describe the pharmacokinetics of pnelezine

A

Rapid oral absorption, short plasma t1/2, metabolised in liver, excreted in kidneys

26
Q

What are the unwanted effects of MAO

A

Atropine like effects, postural hypotension, sedation, weight gain, hepatotoxicity

27
Q

What are the drug interactions of MAOIs

A

Cheese reaction- tyramine containing foods + MAOI -> hypertensive crisis

MAO + TCA = hypertensive crisis
MAOI + pethidine -> hyperpyrexia, restlesness, coma and hypotenstion

28
Q

How do SSRIs like Fluoxetine work?

A

selective 5-HT reuptake inhibition
less troublesome side effects
Less effective vs severe depression

29
Q

What are the pharmacokinetics of SSRIs

A

Oral administration, 18-24hrs working, delayed onset of action (2-4 weeks), competes with TCA for hepatic enzymes therefore toxix

30
Q

Unwanted effects of SSRI

A

Nausea, diarrhoea, insomnia, loss of libido
Interact with MAOI
Prozac = Fluoxetine

31
Q

What are uses of Venlafaxine

A

Dose dependent reuptake inhibitor
5HT>NA>DA
2nd line treatment of depression

32
Q

What are the uses of Mirtazapine

A

a2 receptor antagonist
increases NA and 5HT release
Useful in SSRI intolerant patients

Missed Lectures (5 decks)

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