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Year 5 Psych > 22: Anti-Depressants > Flashcards

22: Anti-Depressants Flashcards

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1
Q

Explain the differnet types of Psychosis

A

Psychosis is a mental health problem that causes people to perceive or interpret things differently from those around them

Can be split into

  • Schizophrenia (thought disorders) and
  • Affective disorders (mood disorders)
    • Maina
    • Depression
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2
Q

What are the symptoms of depression?

A

Emotional symptoms

  • Misery, apathy, pessimism
  • Low self-esteem
  • Loss of motivation
  • Anhedonia (lack of enjoying things)

Biological symptoms

  • Slowing of thought & action
  • Loss of libido
  • Loss of appetite, sleep disturbance
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3
Q

What are the two different types of depression?

What is their characterisitcs?

A

Depression can be

  1. Unipolar
    • Mood swings in same direction
    • Relatively late onset
    • (reactive or endogenous)
    • Drug treatment for both is the same (TCAs, MAO, SSRIs)
  2. Bipolar
    • early onset (adolescence)
    • oscillating episodes of depression and mania
    • Strong hereditary tendency
    • Treated with lithium (mood stabelising)
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4
Q

What are the different types of unipolar depression?

A

Reactive depression (75%)

  • as reaction to stressful life events
  • non-familial pattern

Endogenous depression (25%)

  • unrelated to external stresses
  • familial pattern
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5
Q

Explain the therapeutic use of lithium

A

Can be used a mood-stablising agent in the treatment of Bipolar disorders

  • MOA unclear but thought to affect downstream mechanism of NA and 5HT release
  • Narrow therapeutic window and many side effects
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6
Q

Explain the Monoamine theory of depression

A

It is an attempt to explain the cause of depression

it says that

  1. Depression = is due to functional deficit of central MA transmission
  2. Mania = functional excess of Monoamines

MonoAmines= NA & 5-HT

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7
Q

Evaluate the validity of the monoamine theory of depression

A

There is some evidence for it but it is not 100% consistet (but best we have at the moment)

  1. There is strong pharmocological evidence
    • Drugs that Increase/decrease central MA levels cause increase in mood/depression respectively
    • BUT: though administration of drugs lead to a direct increase in neurotransmitters but only have a delayed onset (possibly due to adaptive changes -> α2 –> less negative feedback in cell (normally inhibits Noradrenaline release) –> if downregulatied: less NA binding –> more release) , β, 5HT receptors)
  2. Some but limited biochemical evidence
    1. e.g. cocaine inhibitss reuptake but does not have anti-depressant effect
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8
Q

Explain the possible reasons for the delayed onset of action of anti-depressant drugs

A

Possible due to adaptive changes in receptors e.g.

  • a2 receptors
    • normally decrease NA release when binding
    • if downregulated: more NA release is possible
  • ß receptors
  • 5HT receptors
  • treatment leading to ? upregulation of cAMP?
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9
Q

What is another name for Serotonin?

A

5-Hydroxytryptamin (5-HT)

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10
Q

What are TCAs?

Explain thir MOA

A

TCA=Tricyclic antidepressant

  • Mainly: Neuronal monoamine re-uptake inhibitors (Noradrenaline and Serotonin NA = 5-HT)
    • increase the levels of MA in synaptic cleft
  • But also: Other receptor actions?
    • α2 antagonists –> more NA release
    • mAChRs
    • histamine
    • 5-HT
  • Delayed down-regulation of β-adrenoceptors & 5-HT2 receptors –> delayed onset
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11
Q

Name an example of a TCA

A

Amitriptyline

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12
Q

What kind of drug is Amitriptyline?

A

A TCA (tricyclic antidepressant)

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13
Q

Summarise the pharmacokinetics of TCAs

A
  • Rapid oral absorption
  • Highly PPB (plasma protein bound) (90 - 95%)
  • Hepatic metabolism forms active metabolites
  • renal excretion (glucuronide conjugates)
  • Plasma t1/2 (10-20 hrs) –> OD administration enough
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14
Q

What are the side effects of TCAs at a therapeutic dose?

A

Some side-effects in use (but very dangerous in overdose)

  • Atropine - like effects (amitriptyline)
    • Amitripyline inhibiting mAChR
  • Postural hypotension (vasomotor centre)
    • a2 receptors in vasomotor centre?
  • Sedation (H1 antagonism)
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15
Q

What are the side effects of TCAs at a toxic dose?

A

Acute toxicity (o.d)

  • CNS:
    • excitement, delirium, seizures, coma, respiratory depression
  • CVS: –> increased SNS activity (increased NA release)
    • cardiac dysrhythmias, ventricular fibrillation/sudden death

Are often used to attempted suicide

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16
Q

Explain the drug-drug interactions of TCAs

A

Many drug-drug interactions

  • Many due to the fact that TCAs are highly Plasma Protein bound (e.g. asperin)
  • If other drugs are also PPB –> they displace TCAs from proteins and might cause toxicity
  • Also increase the effects of CNS depressant drugs (e.g. alcohol)
  • Monitor patients with antihypertensive drugs closely
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17
Q

What are MAOIs?

Explain their MAO

A

Monoamineoxidase Inhibitors

  • Irreversible block MAO –> that would normally break down NA; 5HT and Dopamine
  • Increase rapidly tha cytoplasmic NA+5HT levels
    • leading to increased release of MA
  • Delayed effects (weeks later) : clinical response down-regulation of β-adrenoceptors and 5-HT2 receptors
  • (also inhibit other enzymes)
18
Q

Name an example of a MAOI

A

Phenelzine

19
Q

What kind of drug is Phenelzine

A

A MOAI

20
Q

Explain the pharmacokinetics of MAOI

A
  • Rapid oral absorption
  • Short plasma t1/2 (few hrs) but longer duration of action
    • due to irreversible inhibition of MAOs
  • Metabolised in liver; excreted in urine
21
Q

What are the side effects of MAOI?

A
  • Atropine - like effects (but less than TCAs)
  • Postural hypotension (common)
  • Sedation (Seizures in overdose )
  • Weight gain (possibly excessive)
    • increase appetite
  • Hepatotoxicity (rare)
    • due to reactive hydrazine goups
  • Cheese reaction
22
Q

What is the “Cheese Reaction”?

Explain it in the context of MAOI

A

It is a reaction leading to

  • hypertensive crisis (throbbing headache, ­ b.p., intracranial haemorrhage

Due to

  • Tyramine rich foods lead to
  • increased tyramine levels in the brain
  • tyramine leads to increased release of Noradrenaline
  • Normally: boken down by MAO but in MAOI treatment: levels are too high leading to symtoms
23
Q

What are SSRIs?

What is their MOA?

A

Selective Serotonin Reuptake inhibitors

•Selective 5-HT re-uptake inhibition

–> increased serotonin levels in synaptiv cleft

24
Q

What are the advantages and disadvantages of the use of SSRI in comparison to TCA or MAOI

A
  • Less troublesome side-effects; safer in overdose.
  • But less effective in severe depression
25
Q

Summarise the pharmacokinetics of SSRI

A
  • p.o. administration
  • Plasma t1/2 (18-24 hrs) (OD perscription)
  • Delayed onset of action (2-4 weeks)
  • Fluoxetine competes with MAOIs for hepatic enzymes (avoid co-administration)
26
Q

Explain the side effects of SSRI

A
  • Fewer than TCAs/MAOIs
    • GI:
      • Nausea, diarrhoea,
    • insomnia
    • loss of libido
    • Interact with MAOIs (avoid co-administration)
27
Q

Name an exaple of a SSRI

A

Fluoxetine —> (Prozac)

28
Q

What kind of drug is Fluoxetine?

What is its trade name?

A

It is a SSRI

Fluoxetine (‘Prozac’): currently most prescribed antidepressant drug

29
Q

Differentiate between fluoxetine and venlafaxine

A
  • fluoxetine = SSRI, specific for the serotonin transporter
  • venlafaxine has variable effects on other monoamine transporters
    • low dose: it is more specific for serotonin transporters
    • high dose: blocks noradrenaline transporter
    • Also: mild effects on dopamine transporters
30
Q

Why would you prefere using fluoxetine and venlafaxine?

A

Not sure which one is more effective but NICE guidelines:

  • More selective–> fewer expected side-effects
  • cheaper
    • Might give the ablility to combine the drugs (if not working and make sure patient was adherent)
31
Q

What follow-ups does a patient started on lithium need?

A
  1. Must check plasma levels 1 week post starting
    1. Taken 12h post dose, therapeutic window 0.6-1mmol/L
  2. Weekly monitoring until steady therapeutic level
  3. Once steady level: every 3 month level monitoring
    1. Every 6 months: U&E, TFT and Calcium monitoring
32
Q

What are side effects of lithium?

A

Many

  • Tremor
  • GI upset/ Nausea/Vomiting
  • Fatigue
  • polyuria/polydipsia (nephrogenic DI)
  • Hypothyroidism
  • Hyperparathyroidism
  • Weight gain
  • Swollen ankles
  • Metallic taste
  • Teratogenetiy (Ebstein’s abnormality)
33
Q

What teratogentic effects do

  • Litium
  • Valporate
  • and Carpamazepine have?
A
  1. Lithium = Ebstein’s abnromality (tricuspid valve effect)
  2. Valporate and Carbamazepine: Spina bifida)
34
Q

What is the preferred medical treatment for women of child Bearing age with BPAD?

A

Second Generation antipsychotics

(due to teratogenic effects of other mood-stabelising medication)

If Carbamazepine and Valporate started, prescribe with Contraception and folic acid supplements

35
Q

Whare tre the side effects of Carbamazepine?

A
36
Q

What should a patient be councelled for when starting Carbamazepine?

A
37
Q

What are the side effect of Valporate?

A
38
Q

What should a patient be councelled for before starting Valporate?

A
39
Q

What are mood stabelisers used in the treatment of BPAD?

A
  1. Lithium (acute+prophylaxis)
  2. Valporate (acute mania + prophylaxis)
  3. Carbamazepine (only prophylaxis but fewer side effects)
  4. Lamotrigine (good for depressive symptoms and BPAD type II)
40
Q

What are side effects of Lamotrigine?

A
41
Q

What should a patient be councelled for before starting Lamotrigine?

A
42
Q

Which SSRIs are associated with prolonged QT-intervals?

Which one is the most commonly associated one?

A

Most commonly associated: Citalopram

But also
* Sertraline
* Fluoxetine
(although both less commonly)

Year 5 Psych (11 decks)

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