anti-depressants Flashcards
what can psychoses be classified into
Schizophrenia
OR
Affective disorders
further divide affective disorders into different classes
Mania
Depression
what can the symptoms of depression be split into
Emotional
(Psycho-
logical)
Biological
(Somatic)
what are the emotional symptoms of depression
Misery, apathy, pessimism
Low self-esteem
Loss of motivation
Anhedonia
what are the biological symptoms of depression
Slowing of thought & action
Loss of libido
Loss of appetite, sleep disturbance
describe onset and key characteristic of unipolar depression
Mood swings in same direction
Relatively late onset
state some causes of unipolar depression
Reactive depression
endogenous depression
what can cause reactive depression
stressful life events
non-familial
what can cause endogenous depression
unrelated to external
stresses
familial pattern
Describe key feature and onset of bipolar depression
Oscillating depression/mania
Less common; Early adult onset
what increases likelihood of bipolar depression
Strong hereditary tendency
how is bipolar depression treated
lithium carbonate – decrease cAMP
what is the 1 theory of depression and mania
Monoamine theory of depression
Depression = functional deficit of central MA transmission (NA & 5-HT)
Mania = functional excess
what are strengths and weaknesses of this theory
Supportive Evidence:
Strong pharmacological
evidence
Inconsistency:
Delayed onset of clinical effect of drugs
Adaptive changes → down regulation of α2, β, 5HT receptors
what is the pharmacological evidence of this theory
look at table from lecture
drugs which increase NA and 5-HT levels increase mood
drugs which decrease NA/ 5-HT levels decrease mood
give an example of a TCA
Amitriptyline
what is the MOA of TCAs
Neuronal monoamine re-uptake inhibitors
Bind to NA & 5HT
carriers to slow
down reuptake
describe the pharmacokinetics of TCAs
Rapid oral
T1/2 (10-20hrs)
Highly PPB
Hepatic Met – active
metabolites
describe the unwanted effects of TCAs
Atropine like
Postural hypotension
Sedation (blocks H1)
Acute toxicity :
CNS
(excitement, resp depression)
CVS (v fib) (sudden death)
drug interactions of TCAs
PPB: increase TCA effects (aspirin, phenytoin)
Hepatic microsomal enzymes: increase TCA effects (neuroleptics; oral contraceptives)
Potentiation of CNS depressants (alcohol)
Antihypertensive drugs (monitor closely)
what are 3 commonly used antidepressants
TCAs
selective serotonin reuptake inhibitors
Monamine oxidase inhibitors
name a MAOIs
Phenelzine
what is the MOA of MAOIs
inhibits:
MAO-A : NA & 5-HT
MAO-B : DA
non selective and irreversible
Delayed effects : clinical response of MAOIs
down-regulation of β-adrenoceptors & 5-HT2 receptors
Pharmacokinetics of MAOIs
Rapid oral
Short T1/2
Metabolised in liver, excrete
in urine
unwanted effects of MAOIs
Atropine like, postural
hypotension, weight gain,
sedation, hepatotoxicity.
Avoid if liver problems.
MAOIs drug reactions
MAOIs + Tyramine containing foods → hypertensive crisis
MAOIs + TCAs → hypertensive crisis could = intracranial haemorrhage
MAOIs + pethidine→ hyperpyrexia, restlessness, coma
what is the clinical significan of moclobomide
reversible MAO-A inhibitor (RIMA).
↓ Drug interactions ↓ doa.
give an example of a SSRI
Fluoxetine
MOA of SSRIs
Selective 5-HT re-uptake inhibition
pharmacokinetics of SSRIs
Oral
T1/2 = 18-24hrs
Delayed onset action
(2-4wks)
Avoid coadmin with TCAs (hepatic enzyme competition)
grade the effects of SSRIs compared to other antidepressants
less effective in severe depression
unwanted effects of SSRIs
Less than TCAs/MAOIs
Nausea, diarrhoea, insomnia
1/10). Loss libido (1/3
