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Anti-depressants Flashcards

1
Q

Categorise psychosis

A

Schizophrenia (disorder of thought process)

Affective disorders (disorder of mood)

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2
Q

Categorise affective disorders

A

Mania

Depression

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3
Q

Symptoms of clinical depression

A

Emotional
(Psycho-logical):

  • Misery, apathy, pessimism
  • Low self-esteem
  • Loss of motivation
  • Anhedonia (inability to enjoy activities)
Biological
(Somatic): 
-Slowing of thought & action
-Loss of libido
-Loss of appetite, sleep disturbance
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4
Q

2 main types of depression

A

1) Unipolar depression/depressive disorder

2) Bipolar depression /manic depression

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5
Q

Outline unipolar depression

Categorise it in terms of cause

A

Mood swings in same direction

Reactive (75%):

  • Stressful life events
  • Non-familial

Endogenous:

  • Unrelated to external stress
  • Familial
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6
Q

What is the onset of unipolar

A

Relatively late onset

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7
Q

Differentiate treatment for reactive and endogenous depression

A

Same drugs

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8
Q

Outline bipolar/manic depression

A

Oscillating depression/mania

Strong hereditary tendency

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9
Q

What is the onset of bipolar depression

A

Less common; Early adult onset

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10
Q

Drug treatment for bipolar

Action of what drug can affect drug used in treatment of bipolar disorder

A

Lithium…. mood stabiliser
Orally (lithium carbonate)

Change in intracellular second messanger:

Involves change in IP3 (reduced) and cAMP

Small therapeutic window (like digoxin)- check plasma levels

Diuretics increase the action

Acute overodose–> confusion and convulsions and arrhythmia

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11
Q

Outline the monoamine theory of depression

A

Depression = functional deficit of central MA transmission;

Mania = functional excess

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12
Q

What are the mono-amines

A

NA & 5-HT

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13
Q

What is pharmacological evidence of the monoamine theory of depression

A

That various compounds which increase or decrease monoamine concentration in the synapse improve and worsen mood respectively

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14
Q

Outline the action of tricyclic antidepressants overall, and the effect on mood

This is pharmacological evidence of the monoamine theory of depression

A

Block NA & 5-HT reuptake and enhance synaptic levels of these

Improve mood

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15
Q

Outline the action of MAO inhibitors overall, and the effect on mood

This is pharmacological evidence of the monoamine theory of depression

A

Increase stores of NA & 5-HT in the cytoplasm of the presynaptic terminal (less in vesicles)

Increases synaptic level of NA and 5-HT

Improves mood

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16
Q

Outline the action of reserpine overall, and the effect on mood

This is pharmacological evidence of the monoamine theory of depression

A

Inhibits NA & 5-HT storage in the presynaptic terminals

Was used as antihypertenstive (but patients taking it got depressed) because they reduced NA in the SNS

Worsens mood (used in lots of animal studies of depression)

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17
Q

Outline the action of a-methyltyrosine overall, and the effect on mood

This is pharmacological evidence of the monoamine theory of depression

A

Inhibits NA synthesis

Mood ↓ Calming of manic patients

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18
Q

Outline the action of methyldopa overall, and the effect on mood

This is pharmacological evidence of the monoamine theory of depression

A

Inhibits NA synthesis

Worsens mood

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19
Q

Outline the action of ECT overall, and the effect on mood

This is pharmacological evidence of the monoamine theory of depression

A

Increases CNS responses to NA and 5-HT

Improves mood

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20
Q

Give an example of a TCA

A

Amitriptyline

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21
Q

Give e piece of pharmacological evidence that might count against the monoamine theory of depression

Give a possible explanation

A

Amphetamines normally gets taken up into the presynaptic nerve terminal and causes NA release

Should be mood enhancing according to theory, but they are not so aren’t used as antidepressants

Might be because in cinically depressed patients there are dysfunctional pre-synaptic nerve terminals (i.e. the amphetamine cannot bind to its target sites within the nerve terminal and cause NA release)

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22
Q

T/F amphetamine supports the monoamine theory of depression

A

Not really

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23
Q

Give biochemical evidence of the monoamine theory of depression

A

That clinically depressed patients have lower levels of NA and 5-HT metabolites in their urine implying they don’t have as much monoamine

But the severity of depression is not linked to how monoamine levels ar

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24
Q

T/F the onset of the clinical effects antidepressant drugs is delayed because the effects on NA and 5-HT take a while

A

F…

THERE IS DELAYED ONSET

But not because of the NA and 5-HT

The levels of these are increased quickly,

it’s because the benefits of these drugs is linked to another mechanism

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25
What is thought to be the mechanism of action of anti-depressant drugs which icnrease 5-HT and NA inthe synapse
The delayed clinical onset with these drugs coincides with the downregulation of a2, b and 5HT receptors This might be the clinical effect rather than just increased levels of the chemicals
26
As well as monoamine theory, what else might be related to cause of depression
HPA axis increase in CRH Hippocampal degeneration in chronic severe depression (which can be reduced with the current antidepressant drugs!)
27
Give an example of a TCA
Amitryptiline
28
Structures of TCAs
Dibenzazepines Dibenzcycloheptenes
29
What type of molecule is amitryptiline
Dibenzcycloheptenes with aliphatic side chain on the central ring
30
Mechanism of action of TCAs
NA = 5-HT NA is inactivaated mainly by reuptake 1 The TCAs get into the brain and then they block the carrier molecules which move 5HT and NA back into the presynaptic nerve terminal This enhances the levels of these monoamines in the synapse There are different carriers for each monoamine and on different nerve terminals, but they are both blocked equally by TCAs
31
T/F TCAs bind to NA receptors on the presynaptic membrane to prevent NA reuptake equally to 5-HT receptors
FALSE FALSE FALSE THEY BIND TO REUPTAKE PROTEINS ON THE PRESYNAPTIC MEMBRANE, THESE ARE NOT RECEPTORS THESE ARE CARRIER MOLECULES (however they do also inhibit a2 receptors which does increase NA release due to loss of negative feedback)
32
What could be other mechanism of action of TCAs
Action on receptors (i.e. not just the reuptake CARRIER MOLECULES that they block, but possibly also receptors, presynaptic and post synaptic) Antaganonism of: - α2 and various actions on - mAChRs - histamine - 5-HT Might be cause of side effects
33
What is the effect of TCAs on a2 receptors
They are a2 antagonists a2 present on presynaptic nerve terminal and negatively feedsback for NA release, reduces release So TCA reduces the negative feedback and increases NA release
34
Outline the adaptive changes TCAs cause
Delayed down-regulation of β-adrenoceptors & 5-HT2 receptors This may coincide with the delayed onset of action of these drugs
35
Where is the absorption of TCAs
Rapid oral absorption
36
How are TCAs foud in the plasma
90-95% plasma protein bound
37
Outline metabolism of TCAs
Hepatic 1st pass metabolism Active metabolites that are more weakly active but can act on the NA and 5-HT reuptake proteins
38
Outlinee excretion of TCAs
renal excretion (glucuronide conjugates)
39
What is the plasma half time of TCAs
Plasma t1/2 (10-20 hrs)
40
Unwanted effects of TCAs at therapeutic dose
Atropine - like effects e.g. dry mouth, constipation, blurry vision (amitriptyline, Musc. antagonism) Postural hypotension (central- vasomotor centre) Sedation (H1 antagonism)... leads to potentiation of alcohol depressive effect
41
Why to TCAs give atropine like side effects
Because they have antagonistic effects on muscarinic acetycholine receptors
42
What are atropine like effects
Blurred vision Dry mouth Urinary retention Constipation
43
Why could the histamine receptor related side effects of TCAs be useful
H1 antagonists (drowsy, so sedative) This can help if you get patients to take last thing at night before they go to sleep helps with the insomnia symptom of depression (but some sedation might carry on)
44
Unwanted effects of TCAs at toxic dose
CNS: excitement, delirium, convulsive seizures --> coma, respiratory depression CVS: cardiac dysrhythmias --> ventricular fibrillation/sudden death Patients on these drugs can attempt suicude due to these toxicity
45
Drug interactions of TCAs
Many PPB: TCA effects can be increased to toxic levels by drugs which compete for PPB Hepatic microsomal enzymes metabolise lots of drugs and if taking another drug metabolised by this system it can slow metabolism of TCAs and increase to toxic dose in plasma Potentiation of CNS depressants - ALCOHOL Antihypertensives
46
State drugs which compete with TCAs for PPB
Aspirin and phenytoin and warfarin so can push TCA level to toxic free level
47
State drugs which compete with TCAs for hepatic microsomal enzyme
Microsome is referring to the rER Neuroleptics Oral contraceptives Steroids So have to be careful when prescriping anti-pschotics with antidepressants
48
What is the problem with alcohol and TCAs
Both causing CNS depression (TCA through droswiness due to H1 antagonism) problems with suicide cos they might be drunk first
49
How could TCAs affect BP with antihypertensives
Could increase or decrease BP
50
Give an example of monoamine oxidase inhibitors
Phenelzine
51
What are the two types of MAO
MAO A: preferentially breaks down NA and 5-HT MAO B: preferentially breaks down DA Both break down both
52
What are MAOIs | What is their MOA
Monoamine oxidase inhibitors non-selective MAO inhibitors i.e. not selective for MAO A or B Inhibiting ENZYMES unlike TCAs which were inhibiting CARRIER PROTEINS These enzymes are present in the cytoplasm of the presynaptic nerve terminal of 5-HT neurons and NA neurons Inhibiting them increases MA in the cytoplasm, and then this causes leakage into the synaptic cleft
53
What type of enzyme inhibiors are MAOIs
IRREVERSIBLE --> long d.o.a
54
Structures of MAOIS
Single ring structure with aliphatic side chain
55
Why does phenelzine bind irreversibly
It has hydrazine NN group whcih is highly reactive and binds covalently to MAO enzymes A and B
56
What are the rapid and delayed effects of MAOIs
Rapid effects : increased cytoplasmic NA & 5-HT Delayed effect: down-regulation of beta adrenoceptors and 5-HT2 receptors
57
Differentiate MOA of MAOIs and TCAs
Both increase MA in the synapse. TCAs by MA reuptake inhibition MAOIs by inhibiting enzyme which breaks down MAs Both have their clinical effects by downregulatin of beta adrenoceptros and 5-HT receptors though
58
Outline absorption of MAOIs
Rapid oral absorption
59
Half life of MAOIs
few hours
60
T/F MAOIs need to be taken quite regularly because their t1/2 is only a few hours
F... because they irreversibly bind enzymes, they have long d.o.a despite their relatively short plasma half life THIS IS A KEY POINT
61
Where are MAOIs metabolised and excfreted
Metabolised in liver; excreted in urine
62
What are the unwanted effects of MAOIs
Atropine - like effects (< TCAs) Postural hypotension (common) Sedation (Seizures in o.d.) Weight gain (possibly excessive) Think MAObeseI Hepatotoxicity (reactive hydrazine group; rare)
63
T.F the atropine like effects of MAOIs are caused by the same thing as TCAs but they arent as bad
T... both caused by antagonism action on mAChR But worse with TCA
64
Compare severity of side effects vs drug interactions with MAOIs and TCAs
MAOI side effects not as bad but the drug interactions worse
65
Drug interaction with MAOIs
Cheese reaction Tyramine (=sympathomimetic drug like amphetamine) containing foods+MAOI can lead to hypertensive crisis (throbbing headache, increasing bp, intracranial haemorrahage) MAOI + TCAs leads to HTN epidodes MAOIs + pethidine (=opioid) --> hyperpyrexia, restelessness, coma and hypotension
66
Why can cheese reaction occur with MAOIs but not in notmal people
MAO is present in gut wall too and breaks down any tyramine Tyramine basically acts like amphetamine and causes release of NA into the synaptic cleft Normally all tyramine is broken down completely by the MAO and doesn't get into blood If taking MAOI for depresion it won't be broken down, can get into blood and into CNS and have sympathomimejtc effect
67
What is the cause of the hyperprexia,restlessness, coma & hypotension that comes with co-administering MAOI and pethidine
MAOIs also block the enzyme which breaks down this opioid Thereore the opioid gets broken down by different enzyme which causes metabolites that have these effects
68
What is moclobemide. Benefit and cost
reversible MAO-A inhibitor (RIMA). ↓ Drug interactions BUT ↓ doa so need to give 2-3 times per day Less cheese reacton too (think of be mid(n)e and rima)
69
Give example of SSRI
e.g. Fluoxetine and citalopram
70
What is SSRI mecahnism of action
Selective 5-HT re-uptake inhibition not on NA
71
What is the structure of SSRI
Not significant
72
What is the benefit of SSRI compare to TCA and MAOIs But what is the problem
Less troublesome side effects (no cheese reaction(although strictly this is interaction), less atropine like side effects); safer in o.d. But less effective vs severe depression
73
Administration of SSRIs
Oral
74
What is the plasma t1/2
Plasma t1/2 (18-24 hrs)
75
Onset of action of SSRIs
Delayed onset of action (2-4 weeks)
76
Why is coadministration of fluoexetne and TCA avoided vs why is coadministration of MAOI and TCA acoided
Fluoxetine competes with TCAs for hepatic enzymes (avoid co-administration) TCA and MAOI avoided due to hypertension
77
Side effects of SSRI
Nausea (10%), diarrhoea, insomnia & loss of libido (30%)
78
Drug interactions of SSRI
Interact with MAOIs (avoid co-administration).. due to additive effect And TCA for hepatic enzymes
79
What is most prescrbed antidepressant drug
Fluoxetine (‘Prozac’): currently most prescribed antidepressant drug
80
Atypical antidepressants
Venlafaxine and mirtazapine
81
How does venlafaxine work
Dose-dependent Reuptake inhibitors With increasing dose, reduces uptake of: 5HT > NA >> DA (SNRI) 2nd Line treatment for severe depression
82
What are the SNRIs
Seratonin and NA reuptake inhibitor venlafaxine
83
How does mirtazapin work
α2 Receptor antagonist ↑ NA & 5HT release Other R interactions (sedative) Useful in SSRI-intolerant patients

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