Pharmacology of Antidepressants and Mood Stabilisers Flashcards
How do monamine oxidase inhibitors work? Give an example of each of the types
Slow down breakdown of neurotransmitters by inhibiting MAO enzyme
Phenelzine (iireversible)
Moclobemide (reversible)
List some TCA’s
Amitriptyline
Clomipramine
Imipramine
Dosulepin
List some SSRI’s
Fluoxetine
Citalopram
Sertraline
Paroxetine
Whereabouts in the synapse do MAO inhibitors act? What is their action?
Presynaptic terminal
Inhibit MAO A and B enzyme to prevent breakdown of NT into metabolites
Whereabouts in the synapse do TCA’s act? What is their action?
Synaptic cleft
Block reuptake oof monoamines (NA and 5HT) into presynaptic terminals
Whereabouts in the synapse do SSRI’s act? What is their action?
Presynaptic terminal
Selectively inhibit reuptake of 5HT from the synaptic cleft
Which SSRI’s can inhibit CYP450 system?
Fluoxetine
Paroxetine
List some adverse effects of SSRI’s
Nausea, headache, sweating, vivid dreams
Sexual dysfunction
Hyponatraemia in elderly
Short-term anxiety
List some adverse effects of TCA’s
Anticholinergic - Constipation, dry mouth, blurred vision, urinary retension
Sedation
Weight gain
CV - postural hypotension, tachycardia, arrhythmias
Cardiotoxic overdose
List the clinical uses of antidepressants
Moderate-severe depression Dysthymia Generalised anxiety Panic disorder, OCD, PTSD Premenstrual dysphoric disorder Bulimia nervosa Neuropathic pain
List types of monoamine reuptake inhibitors
Tricyclics
Other non-selective reuptake inhibitors
Selective serotonin reuptake inhibitors
NA reuptake inhibitors
What is the ‘monamine hypothesis’ for depression. How do anti-depressants work to counteract this?
Depression results from a functional deficit of monoamine transmitters esp. serotonin, NA
Antidepressant act to increase monoaminergic transmission by increasing NT levels
List side effects of monoamine oxidase inhibitors
‘Cheese reaction’/hypertensive crisis - inhibiting MAOA enzyme prevents breakdown and transmission of amines
Potentiate effects of other drugs e.g. barbiturates by decreasing their metabolism
Postural hypotension
Insomnia
Peripheral oedema
Give examples of SNRIs, and state their of action
Venlafaxine
Duloxetine
Block reuptake of both monoamines into presynaptic terminals
Whereabouts in the synapse do atypical antidepressants act? Give some examples. List some side effects
Postsynaptic terminal (on the receptor) Mirtazapine (mixed receptor effects) Bupropion (dopamine uptake inhibitor) Weight gain, sedation, constipation, dizziness/ falls
What two antidepressants can be combined to reduce side effects?
SSRIs
Atypical antidepressant - mirtazapine
What group of the population should SSRIs be prescribed cautiously in? Why?
Young adults
Transient increased in suicidal/ aggressive/ self-harm ideas
What is the purpose of prescribing in bipolar disorder?
ACUTE: reduce mood in episodes of mania and increase in episodes of depression
LONG-TERM: stabilise mood and prevent recurrence of both mania and depression (prophylaxis)
List the three classes of drugs prescribed most commonly in bipolar disorder. Give examples.
Lithium
Anticonvulsants - valproic acid, lamotrigine, carbamazepine
Antipsychotics - quetiapine, ariprazole, alanzopine, lurasidone
What is the mechanism of action of lithium carbonate?
Block phosphotidylinosital pathway or inhibit glycogen synthase kinase 3B
List some side effects of lithium
Dry mouth/ strange taste, polydipsia, polyuria, tremor
Reduced renal function, nephrogenic diabetes insipidus
Weight gain, hypothyroidism