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Year 3 Pharmacology > Pharmacology of Anti-Depressants and Mood Stabilisers > Flashcards

Pharmacology of Anti-Depressants and Mood Stabilisers Flashcards

1
Q

Which drugs easily cross the BBB?

A

Lipophilic drugs

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2
Q

Uses of anti-depressants?

A

Moderate to severe depression

Dysthymia (AKA persistent depressive disorder, a less severe but more chronic form of depression)

Generalised anxiety disorder

Panic disorder, OCD, PTSD

Premenstrual dysphoric disorder

Bulimia nervosa

Neuropathic pain

i.e: used for more than just depression

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3
Q

Classifications of anti-depressant drugs?

A

Monoamine oxidase inhibitors

Monoamine reuptake inhibitors:
• Tricyclics (TCAs)
• Other non-selective reuptake
• Selective serotonin reuptake inhibitors (SSRIs)

Atypical drugs (with post-synaptic receptor effects)

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4
Q

What are the monoamine neurotransmitters?

A
  1. Noradrenaline
  2. 5-HT
  3. Dopamine

NOTE - these share similar structures

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5
Q

What is the monoamine hypothesis?

A

Depression results from a functional deficit of monoamine transmitters, part. serotonin (5-HT) and noradrenaline

Drugs that deplete monoamine stores, e.g: reserpine, can induce low mood

This is because the CNS of a depressed patient has reduced monoamine (and metabolite) levels; also, most drugs that treat depression act to increase monoaminergic transmission

NOTE - this is too simplistic and the true mechanism of unknown

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6
Q

Serotonin projection pathways?

A

Rostral pathway is IMPORTANT for mood, sleep, feeding behaviour and sensory perception

Caudal raphe is important for analgesia

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7
Q

Describe transmission at the serotonergic synapse

A

Tryptophan (an amino acid) is converted to 5-OH-tryptophan, by tryptophan hydroxylase; this is then converted to 5-HT by L-AA decarboxylase

5-HT is stored in a vesicle and then released into the synapse, where it can bind to post-synaptic receptors

5-HT is then reabsorbed from the synaptic cleft, via a specific transporter, into the pre-synaptic neurone; MAO (monoamine oxidase) metabolises 5-HT to 5-HIAA

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8
Q

Noradrenaline projection pathway?

A

Locus coeruleus is important from arousal and emotion

Lateral tegmental area

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9
Q

Describe transmission at the noradrenergic synapse

A

Tyrosine (an amino acid) is converted to DOPA, by tyrosine hydroxylase; this is then converted to dopamine, by L-AA decarboxylase

Dopamine is converted to noradrenaline, by DA β-hydroxylase, which is then stored in a vesicle and released into the synapse

Noradrenaline is reabsorbed into the pre-synaptic neurone, via a specific transporter, and is metabolised by MAO into MHPG

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10
Q

Examples of MAO inhibitors?

A

Phenelzine

Moclobemide

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11
Q

Mechanism of action of MAO inhibitors?

A

Inhibit MAO-A and B and thus increase the conc. of NT in the pre-synaptic neurone, synaptic cleft and vesicles

MAO inhibition is:
• Irreversible - phenelzine
• Reversible - moclobemide

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12
Q

Side effects of MAO inhibitors?

A
  • ‘Cheese reaction’ and hypertensive crisis
  • Potentiates effects of other drugs, like barbiturates, by decreasing their metabolism
  • Insomnia
  • Postural hypotension
  • Peripheral oedema
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13
Q

What is the ‘cheese reaction’?

A

‘Cheese reaction’ - eating too much cheese / gravy can result in inhibition of gut & liver MAO, due to irreversible inhibitors; this prevents breakdown of dietary tyramine

When combined with multiple drugs that potentiate amine transmission, e.g: pseudoephedrine and other anti-depressants, this leads to HYPERTENSIVE CRISIS

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14
Q

Examples of TCAs?

A
  • Imipramine
  • Dosulepin
  • Amitriptyline
  • Lofepramine
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15
Q

Mechanism of action of TCAs?

A

Block the pre-synaptic transporter, preventing reuptake of monoamines (mainly noradrenaline and 5-HT) non-selectively

This increases NT in the synaptic cleft

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16
Q

Side effects of TCAs?

A 
Anti-cholinergic:
• Blurred vision
• Dry mouth
• Constipation
• Urinary retention

Sedation

Weight gain

CV:
• Postural hypotension
• Tachycardia
• Arrhythmias

If overdose, cardiotoxic

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17
Q

Examples of Selective serotonin reuptake inhibitors (SSRIs)?

A
  • Fluoxetine
  • Citalopram / escitalopram
  • Sertraline
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18
Q

Mechanism of action of SSRIs?

A

SELECTIVELY inhibit reuptake of serotonin (5-HT), increasing conc. in the synaptic cleft

19
Q

Common side effects of SSRIs?

A

Nausea and headaches (usually improve after the 1st week)

Sweating

Vivid dreams

Worsening of anxiety (initially)

Sexual dysfunction

Hyponatraemia (in the elderly)

Transient increase in self-harm / suicidal ideation in those <25 YEARS

20
Q

Other issues with SSRIs?

A

Discontinuation effects

21
Q

Other monoamine reuptake inhibitors?

A

SNRIs (serotonin & noradrenaline reuptake inhibitors), e.g: venlafaxine, duloxetine

22
Q

Mechanism of action of SNRIs?

A

Block reuptake of monoamines (noradrenaline and 5-HT) into pre-synaptic terminals

23
Q

Side effects of SNRIs?

A

Similar to SSRIs

NOTE - they lack major receptor-blocking action so fewer side effects than TCAs, i.e: less anti-cholinergic and less anti-histaminergic

24
Q

Anti-depressant drugs that are noradrenaline selective?

A

Reboxetine

Maprotiline

Desipramine

Protriptyline

Nortriptyline

25
Q

Anti-depressant drugs that are 5-HT selective?

A

Venlafaxine

Paroxefine

Fluvoxamine

Sertraline

Fluoxetine

Citalopram

26
Q

Anti-depressant drugs that are non-selective?

A

Amitriptyline

Imipramine

Clomipramine

27
Q

Atypical anti-depressants?

A

Those with mixed receptor effects:
• Mirtazapine (blocks α2, 5-HT2 & 5-HT3)

Dopamine uptake inhibitors:
• Bupropion

28
Q

Side effects of mirtazapine?

A

WEIGHT GAIN AND SEDATION

NOTE - if given with SSRIs, serotenergic side effects can be blocked

29
Q

Efficacy of anti-depressants?

A

Most classes have a similar efficacy and most have delayed onset of action (several weeks)

30
Q

When are anti-depressants most useful?

A

Clearer evidence for benefit in severe depression, i.e: there is a large placebo response in mild depression

31
Q

Cautions in young adults / teenagers with anti-depressants?

A

Caution due to transient increase in suicide ideation / aggressive ideas

32
Q

Levels of treatment in BPAD?

A

Acute treatment of symptoms:
• To reduce mood in episodes of mania
• To raise mood in episodes of depression

Long-term treatment:
• To stabilise mood and prevent recurrence of both mania and depression, i.e: for prophylaxis

33
Q

Forms of lithium?

A

Normally given as lithium carbonate

NOTE - different forms have different bioavailability, so be careful with doses if the type of lithium salt is changed, i.e: 600mg of lithium carbonate will have a different effect compared to 600mg of lithium citrate

34
Q

Mechanism of action of lithium?

A

May block phosphatidylinositol pathway (2nd messenger system) OR inhibit glycogen synthase kinase 3β, i.e: uncertain

35
Q

Cautions with lithium?

A

12 hour post-dose blood levels must be monitored, due to narrow therapeutic index

36
Q

Common side effects of lithium?

A

Dry mouth / strange taste

Polydipsia and polyuria

Tremor

Hypothyroidism

Long-term reduced renal function

Nephrogenic diabetes insipidus

Weight gain

37
Q

Toxic effects of lithium?

A

Vomiting and diarrhoea (this is a big issue, as this dehydrates the patients and makes the Li more toxic)

Ataxia and coarse tremor

Drowsiness

Convulsions

Coma

38
Q

Uses of lithium?

A

Mood stabiliser

39
Q

Which anti-convulsants are often used as mood stabilisers?

A

Valproid acid

Lamotrigine

Carbamazapine

40
Q

Mechanism of action of anti-convulsants as mood stabilisers?

A

Unclear (perhaps they block overactive pathways)

41
Q

Side effects of anti-convulsants?

A 
Carbamazapine:
• Drowsiness
• Ataxia
• CV effects
• Induces liver enzymes

Volproate - TERATOGENICITY (neural tube defects); AVOID IN WOMEN OF CHILD-BEARING AGE

42
Q

Which anti-psychotics are often used as mood stabilisers?

A

Quentiapine, aripiprazole, olanzapine, lurasidone

43
Q

Mechanism of action of anti-psychotics?

A

Dopamine and 5-HT antagonism

44
Q

Side effects of anti-psychotics?

A

Sedation

Weight gain and metabolic syndrome

Extra-pyramidal side effects, esp. with aripiprazole

Year 3 Pharmacology (5 decks)

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