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Year 2 - LCRS - Pharmacology > Antidepressants (20.02.2020) > Flashcards

Antidepressants (20.02.2020) Flashcards

1
Q

What are the symptoms of depression?

A

Emotional/Psychological

  • Misery, apathy, pessimism
  • Low self-esteem
  • Loss of motivation
  • difficulty making decisions
  • Anhedonia (don’t enjoy activities)

Biological/somatic

  • Slowing of thought & action (psychomotor retardation)
  • Loss of libido
  • Loss of appetite
  • sleep disturbance
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2
Q

What are the main types of antidepressant drugs?

A
  • Tricyclic antidepressants (TCAs)
  • Monoamine oxidase inhibitors (MAOIs)
  • Selective 5-HT re-uptake inhibitors (SSRIs)
  • Other drugs
    • incl. lithium (not really an antidepressaant)
    • electroconvulsive therapy (ECT) -> currents pass through temporal lobes, give them suxamethonium before, acts for 5-6 minutes
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3
Q

What is another term for serotonin?

A

5HT

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4
Q

What is depression? (classification)

A

affective disorder (a subclass of psychoses)

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5
Q

What are psychoses separated into?

A
  • schizophrenia

- affective disorders (main and depression)

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6
Q

What are the two main types of depression?

A

Unipolar = depressive disorder

Bipolar depression = maniac depression

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7
Q

Unipolar depression

A

= depressive disorder

  • Mood swings in same direction
  • Relatively late onset
  1. Reactive depression
    - stressful life events
    - non-familial
  2. Endogenous depression
    - unrelated to external stresses
    - familial pattern
  • Drug treatment is the same for both types
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8
Q

What are the 2 subtypes of unipolar depression?

A
  1. Reactive depression

2. Endogenous depression

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9
Q

Bipolar depression

A

= maniac depression

  • Oscillating depression/mania
  • Less common;
  • Early adult onset
  • Strong hereditary tendency
  • Drug treatment (Lithium = mood stabiliser, MoA action not fully understood but known that it changes second messenger systems, narrow therapeutic window)
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10
Q

Monoamine theory of depression

A
  • biochemical theory, stood the test of time
  • Schildkraut (1965)
  • Depression = functional deficit of central MA transmission; - Mania = functional excess
  • NA & 5-HT
  • Based on pharmacological evidence -> drugs changing levels of monoamines make depression better/worse
  • Biochemical evidence inconsistent (e.g. changes in urine, changes in receptors (post-mortem))
  • Delayed onset of clinical effect of drugs (adaptive changes?) -> about 2-3 weeks until you have the antidepressant effect.
  • adaptive changes: Down-regulation: α2, β, 5HT receptors => maybe these adaptive changes are responsible for the antidepressant effect.
  • General conclusions remain firm
  • HPA axis (↑ CRH levels)?
  • Hippocampal neurodegeneration?
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11
Q

Cocaine and depression

A

Cocaine does not have an antidepressant effect

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12
Q

TCAs

A

= tricyclic antidepressants

  • e.g. Amitriptyline
  • three ring structure with different R groups on them
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13
Q

Pharmacokinetic of TCAs

A
  • Rapid oral absorption
  • Highly PPB (90 - 95%)
  • Hepatic metabolism - active metabolites - renal excretion (glucuronide conjugates)
  • Plasma t1/2 (10-20 hrs)
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14
Q

What are the unwanted effects of TCAs?

A
  • Atropine - like effects e.g. constipation (amitriptyline)
  • Postural hypotension (vasomotor centre)
  • Sedation (H1 antagonism) -> this can also be used to assist the patients in falling asleep
  • they can also develop drowsiness during the day, however patients can develop tolerant to it.
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15
Q

MoA of TCAs

A

MoA

  • Neuronal monoamine re-uptake inhibitors
  • same effect on NA and 5-HT
  • Other receptor actions?
    • α2
    • mAChRs
    • histamine
    • 5-HT
  • Delayed down-regulation of β-adrenoceptors & 5-HT2 receptors
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16
Q

What is seen in acute toxicity / overdose of TCAs?

A
  • CNS: excitement, delirium, seizures-> coma, respiratory depression
  • CVS: cardiac dysrhythmias -> ventricular fibrillation/sudden death (NA antagonism and muscarinic effects)
  • Care - attempted suicide (one of the most common drugs used to commit suicide)
17
Q

What are the drug interactions of TCAs?

A

MANY!!

  • PPB: increased TCA effects (aspirin, phenytoin, warfarin) - displacement due to taking other PPB drugs can cause higher TCA concentration and stronger effects and even a toxic level!!
  • Hepatic microsomal enzymes: increased TCA effects if other drugs are using these enzymes to be metabolised and then less TCAs can be metabolised and TCA actions will be enhanced (neuroleptics; oral contraceptives)
  • Potentiation of CNS depressants (alcohol) -> both are depressants, it will have a sedating effect
  • Antihypertensive drugs (monitor closely!!) - less predictable, BP can go both down and up;
18
Q

MAOIs

A

= monoamine oxidase inhibitors

  • e.g. Phenelzine
  • structure: ring with chain / single cyclical molecule with chain
19
Q

MoA of MAOIs

A
  • MAO-A : NA & 5-HT
  • MAO-B : DA (relevant to treatment of PD)
  • Most are non-selective MAOIs
  • Irreversible inhibition -> long duration of action (d.o.a.)
  • Structures: ring with chain
  • Rapid effects : increased cytoplasmic NA & 5-HT (enhanced NA release, increased synaptic concentration, same with 5HT)
  • Delayed effects :
    • clinical response
    • down-regulation of β-adrenoceptors & 5-HT2 receptors
  • Inhibition of other enzymes
20
Q

What are the two MAOs?

A
  • MAO-A : NA & 5-HT

- MAO-B : DA (relevant to treatment of PD)

21
Q

Pharmacokinetics of MAOIs?

A
  • Rapid oral absorption
  • Short plasma t1/2 + rapid absorption (few hrs) but longer d.o.a. -> can be given e.g. once or twice a day or maybe even not every day
  • Metabolised in liver; excreted in urine
22
Q

What are some unwanted effects of MAOIs?

A
  • Atropine - like effects (less than with TCAs)
  • Postural hypotension (common)
  • Sedation (Seizures in o.d.)
  • Weight gain (possibly excessive)
  • Hepatotoxicity (hydrazines; rare)
23
Q

Drug interactions of MAOIs?

A

SERIOUS PROBLEM!!

  • ‘Cheese reaction’: Tyramine-containing foods + MAOI -> hypertensive crisis (throbbing headache, increased b.p., intracranial haemorrhage); Reason: Tyramine not broken down because the MAOI is given for the depresssion! Dietary restrictions in patients takin MAOIS?
  • MAOIs + TCAs -> hypertensive episodes (avoid)
  • MAOIs + pethidine (synthetic opiod) -> together cause hyperpyrexia, restlessness, coma & hypotension (MAOIs may inhibit the metabolism of pethidine)

Moclobemide (new MAOI): reversible MAO-A inhibitor (RIMA). ↓ Drug interactions ↓ doa.

24
Q

Cheese reaction

A
  • many food contain tyramine
  • tyramine is a sympathomimetic compound
  • pushes NA out of vesicles -> higher cytoplasmic concentration -> higher release into synapse

An acute attack of hypertension that can occur in a person taking a monoamine oxidase inhibitor (MAOI) drug who eats cheese, caused by an interaction of the MAOI with tyramine, formed in ripe cheese when bacteria provide an enzyme that reacts with the amino acid tyrosine in the cheese. Other foods and drinks that produce the same effect include pickled herring, yeast extract, and certain red wines. Also called the cheese reaction.

25
Q

RIMA

A

= reversible MAO-A inhibitor
- e.g. Moclobemide

Advantages:
↓ Drug interactions

Disadvantages:

  • reduced DoA (might have to take it more frequently)
  • less efficacious?
26
Q

SSRIs

A
  • selective serotonin reuptake inhibitor

- e.g. fluoxetine

27
Q

SSRI MoA

A
  • Selective 5-HT re-uptake inhibition
  • Less troublesome side-effects e.g. no cheese reaction, safer in o.d.
  • But less effective vs severe depression
28
Q

Pharmacokinetics of SSRIs

A
  • oral administration
  • Plasma t1/2 (18-24 hrs) -> long acting, can be taken 1x daily
  • Delayed onset of action (2-4 weeks) until you see antidepressant activity
  • Fluoxetine competes with TCAs for hepatic enzymes (avoid co-administration) interact and enhance the effect, potentially toxic effects
29
Q

unwanted effects of SSRIs

A
  • Fewer than TCAs/MAOIs
  • Nausea, diarrhoea, insomnia & loss of libido (loss of libido is the most common SE of SSRIs)
  • Interact with MAOIs (avoid co-administration)
  • Fluoxetine (‘Prozac’): currently most prescribed antidepressant drug
30
Q

What are some ‘other’ antidepressant drugs? (not TCA, MAOI or SSRI)

A

Venlafaxine

Mirtazapine

31
Q

Venlaflaxine

A
  • Dose-dependent Reuptake inhibitor
  • 5HT > NA&raquo_space; DA (SNRI) => dose dependant effect (with a higher dose you have more effects)
  • 2nd Line treatment for severe depression
32
Q

Mirtazapine

A
  • α2 Receptor antagonist (blocks inhibition of NA release)
  • ↑ NA & 5HT release
  • Other R interactions (sedative)
  • effective antidepressant
  • Useful in SSRI-intolerant patients
33
Q

SBA 1: Tricyclic antidepressant drugs (TCAs) work largely by:

A: Antagonism at 5HT receptors
B: Inhibiting central DA reuptake
C: Blocking VSCCs
D: Inhibition of central NA & 5HT reuptake 
E: Enhancement of the action of GABA
A

D

Tricyclic antidepressant drugs (TCAs) work largely by inhibition of central NA & 5HT re-uptake

34
Q

SBA 2: The ‘cheese reaction’ is most likely to be caused by:

A: Tricyclic antidepressants (TCAs)
B: Selective serotonin reuptake inhibitors (SSRIs)
C: Monoamine oxidase inhibitors (MAOIs)
D: Reversible MAO-A inhibitors (RIMAs)
E: α2-Adrenoceptor antagonists
A

C

The ‘cheese reaction’ is most likely to be caused by Monoamine oxidase inhibitors (MAOIs)

Year 2 - LCRS - Pharmacology (34 decks)

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