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2nd Year: Drugs and the Mind > Depression > Flashcards

Depression Flashcards

1
Q

What proportion of people will have a depressive episode at some point during their life?

A

1/4.

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2
Q

There are 2 classes of depression. What are they?

A
  1. Natural: after a life event

2. Clinical: a chronic relapsing disorder

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3
Q

Clinical depression can cause premature death. What proportion of those who suffer from it attempt suicide?

A

1/5.

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4
Q

In which age group is suicide the biggest killer?

A

17-34 year olds.

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5
Q

Methods of suicide are becoming more violent, particularly in women. True or false?

A

True.

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6
Q

Approximately how many people per year OD on antidepressants?

A

~400.

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7
Q

There are 3 categories of symptoms for depression. What are they?

A
  1. Psychological
  2. Somatic
  3. Behavioural
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8
Q

List some psychological symptoms.

A
  1. Anhedonia
  2. Low mood
  3. Low self-esteem
  4. Poor concentration
  5. Guilt
  6. Hopelessness
  7. Hypochondria
  8. Suicidal thoughts
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9
Q

List some somatic symptoms.

A

Changes to the drives, e.g. sleep, sex and appetite. Appetite changes can cause weight changes.

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10
Q

List some behavioural symptoms.

A

Self-neglect, motor retardation (lethargy), withdrawal etc.

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11
Q

What is the ‘rule of thirds’ in terms of ADs?

A

1/3 of patients respond immediately. 1/3 of patients respond later on in treatment. 1/3 of patients never respond.

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12
Q

In the patients that do not respond to ADs, ECT is recommended. What is this?

A

Electroconvulsive therapy. Electric currents are sent through the brain to try and induce an epileptic fit.

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13
Q

How long is the treatment for ECT?

A

4-5 weeks.

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14
Q

Is ECT successful?

A

It has a very high remission rate.

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15
Q

Are there any side effects to ECT?

A

It initially causes retrograde amnesia.

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16
Q

Failure to respond to ADs increases with each depressive episode in those that are clinically depressed. By the 4th bout, their depression is said to be untreatable. True or false?

A

True.

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17
Q

By the 3rd bout of depression in a clinically depressed patient, it is recommended they stay on ADs for life. True or false?

A

False: by the 2nd bout they should stay on ADs for life.

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18
Q

“Anti-depression is not the opposite of depression”. What does this mean?

A

Anti-depression does not cure the cause of depression, it only treats the symptoms.

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19
Q

In the 1960s amphetamines were given as ADs. What effects did these have on patients?

A

They were hugely addictive and only treated motor retardation as amphetamine affects dopaminergic and noradrenergic (motor and arousal) systems. There was no positive effect on mood as amphetamine does not affect 5HT systems.

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20
Q

What are monoamines?

A

Chemicals with a single amine group.

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21
Q

What are the monoamine NTs?

A

Dopamine, noradrenaline and 5HT.

22
Q

What is the monoamine theory of depression?

A

Depression is caused by a decrease in monoamine transmission, in the sense that not enough monoamine NTs are produced.

23
Q

Reserpine gave basis for the monoamine theory of depression. How?

A

Reserpine is a naturally occurring alkaloid used to treat high blood pressure. It made users suicidal as it stripped neurons of monoamine NTs.

24
Q

Isoniazid gave basis for the monoamine theory of depression. How?

A

Isoniazid is an anti-TB drug. It induced euphoria in euthymic patients. Isoniazid inhibits MAO so monoamine NTs accumulated in the synapse, increasing transmission.

25
Q

What is MAO?

A

Monoamine oxidase, an enzyme that metabolises monoamine NTs.

26
Q

MAO-A specifically metabolises which NTs?

A

Noradrenaline and 5HT.

27
Q

MAO-B specifically metabolises which NT?

A

Dopamine.

28
Q

Most ADs seek to increase monoamine NT transmission. How can this be achieved?

A

By increasing NT release or blocking re-uptake.

29
Q

What is moclobemide?

A

A reversible MAO-A inhibitor. Thus it prevents the metabolism of noradrenaline and 5HT, allowing them to accumulate in the synapse.

30
Q

Why can MAO inhibitors like moclobemide be extremely dangerous?

A

Due the amino acid tyramine. Tyramine is naturally absorbed by the gut and metabolised by MAOs. In the presence of MAO inhibitors it is instead absorbed by neurons and stored in NT vesicles. The NTs then leak out via a pump and into the synapse via a transporter.

31
Q

Tyramine causes high levels of a) 5HT and b) noradrenaline in the synapse. Why is this dangerous?

A

a) Serotonin sickness: causes elevated body temp. and muscle degradation
b) Noradrenaline increases blood pressure and vasoconstriction, which can lead to angiorrhexis (blood vessel rupture) and stroke.

32
Q

Why are MAO inhibitors like moclobemide not instantly effective?

A

MAO is not present in the synapse - it is found within cells attached to the mitochondria. Thus they must first be uptaken by cells.

33
Q

Why is the monoamine theory of depression contested?

A

Due to the AD time-lag.

34
Q

What is the AD time-lag?

A

ADs that increase monoamine transmission act almost immediately. If there is an immediate increase in MA transmission, which is supposed to be the problem, then why does it take weeks for a patient to begin remission?

35
Q

What is a contrasting theory for the cause for depression?

A

The receptor sensitivity theory.

36
Q

Explain the receptor sensitivity theory.

A

The pre-synaptic receptors (autoreceptors) responsible for re-uptake of NTs in feedback mechanisms are too sensitive, meaning they reuptake NTs before they have a chance to act on the post-synaptic neuron. Thus there is a decrease in stimulation of the post-synaptic neuron.

37
Q

Under the receptor sensitivity theory, how do ADs work?

A

ADs increase synaptic levels of NTs. Initially the autoreceptors compensate for this and induce re-uptake. However after several weeks of bombardment they begin to lose sensitivity to the NTs in down-regulation. This results in higher levels of NT in the synapse which thus increases transmission. This explains the AD time-lag.

38
Q

So what actually is the difference between the monoamine theory and the receptor sensitivity theories of depression?

A

They both involve monoamine transmission: the monoamine theory states that depression is due to low levels of monoamines being produced which reduces transmission. The receptor sensitivity theory states that adequate levels are produced but pre-synaptic receptors are too sensitive, causing re-uptake which reduces transmission.

39
Q

Another class of ADs are the tricyclic ADs. How do these work?

A

They disrupt noradrenaline transporters, meaning noradrenaline is not re-uptaken by the pre-synaptic neuron and remains in the synapse, causing increased transmission.

40
Q

List some effects of noradrenaline.

A

It increases heart rate, mobilises glucose stores, increases blood pressure and causes the redirection of blood flow to skeletal muscles.

41
Q

Tricyclic ADs are dangerous for the body (due to the physiological effects of noradrenaline) but hugely effective in treating depression. Give an example of a tricyclic AD.

A

Imipramine is considered the ‘bench mark’ for new antidepressants, although it is not used anymore for its adverse effects on the heart.

42
Q

Another class of ADs are SSRIs. What are these?

A

Selective serotonin re-uptake inhibitors.

43
Q

How do SSRIs work?

A

They bind to 5HT transporters and prevent re-uptake, meaning 5HT remains in the synapse, causing increased transmission.

44
Q

What is Prozac?

A

A cult-status SSRI from the 1990s. Glorified by Peter Kramer in his book “Listening to Prozac” where he said ‘it makes euthymics feel better than well and cures depressives’.

45
Q

What are the side effects of Prozac?

A

Confusion, nausea, loss of libido etc.

46
Q

Which is safer to OD on, SSRIs like Prozac or tricyclic ADs?

A

SSRIs.

47
Q

Another theory for the AD time-lag (other than the desensitisation of autoreceptors on the pre-synaptic neuron) is that ADs affect the brain in a lasting mechanism. Which mechanism is this?

A

That ADs cause phosphorylation, activating gene transcription which leads to neurogenesis. 5HT and noradrenaline are essential for neurogenesis, thus drugs like SSRIs and tricyclic ADs may actually cause nervous growth, which takes time. Neurogenesis would increase monoamine transmission.

48
Q

Each class of AD target monoamines. What monoamine NT do a) MAO inhibitors, b) tricyclic ADs and c) SSRIs target?

A

a) Depends which MAO is inhibited: if MAO-A then noradrenaline and 5HT, if MAO-B then dopamine.
b) Noradrenaline
c) 5HT

49
Q

Previously it was thought that more selective ADs were better. Why is this not the case?

A

The same receptor is found with multiple roles throughout the body. If the drug effects are more specific, so will the side effects be.

50
Q

Atypical drugs are now favoured. Why? Give an example.

A

There is more benefit in one molecule. Venofaxine blocks noradrenaline and 5HT re-uptake.

51
Q

Is CBT effective in patients with both natural and clinical depression?

A

Yes, although it is far more effective in natural depression. It is rarely successful in suicidal patients when used alone.

52
Q

Low levels of opioid activity can affect dopaminergic transmission True or false?

A

True.

2nd Year: Drugs and the Mind (12 decks)

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