24. Drugs Used In Psychiatric Disease Flashcards
What factors can influence the expression of psychiatric disease?
- life events e.g. divorce, bereavement
- environment e.g. drugs, alcohol
- individuals personality, coping skills, social support
- genetics
- health, viruses, toxins
The bio psychosocial model can help identify therapeutic options
What are the core symptoms of depression?
Mnemonic: LAD
1) low mood
2) Anhedonia
3) decreased energy
2 of the 3 core symptoms are needed
Name some secondary symptoms of depression
- decreased appetite
- disturbed sleep
- hopelessness
- irritability
- reduced concentration
- suicidal thoughts/self harm
- reduced libido
- psychotic symptoms
What is the monoamine hypothesis do depression?
- the idea that a deficiency of monoamine neurotransmitters e.g. noradrenaline and serotonin lead to depression
- this can occur if certain drugs deplete these MA NT’s e.g. reserpine (mixed evidence )
- so thought that monoamine oxidase inhibitors can reduce breakdown of these NTs
What is the neurotransmitter receptor hypothesis and why is it generally refuted?
- the idea that there is an abnormality in the receptors for monoamine transmission leading to depression
However, there is no clear evidence that monoamine deficiency or receptor changes causes depression. Evidence shows that despite apparently normal levels of monoamines these systems do not respond normally.
Why don’t we use Monoamine oxidase inhibitors as much anymore?
- you have to avoid tyramine if on these drugs
- tyramine found in cheese and lots of food so potential danger
- now only used in those who have been on it for years or resistant to other treatment
- but in theory, MAOI lead to build up on NA and serotonin in the synaptic cleft which supports the treatment of depression
Which major class of drug do we use to treat depression?
Monoamine uptake inhibitors
- these can be classified as selective and non -selective noradrenaline and serotonin reuptake inhibitors
- selective: SSRIs, NARIs
- non selective: TCAs
How do SSRIs work? Give examples
- used for moderate to severe depression
- 1st line medication in conjunction with CBT
- inhibit reuptake of serotonin so greater amount in the synaptic cleft thereby treating depression
- examples include: fluoxetine, paroxetine, sertraline, citalopram
- metabolised by liver, can be taken once daily
Extra: fluoxetine long T1/2 will last for 2 weeks after discontinuing. Citalopram most selective and paroxetine most potent
What are the side effects of SSRIs?
- loss of appetite
- nausea and diarrhoea
- in bipolar patients can precipitate mania
- citalopram prolongs QTc interval
- increased suicidal ideation in some
- neurological side effects e.g. extra pyramidal side effects e.g. tremor
How do TCA’s work and give an example?
- not used first line
- example is amitriptyline (used a lot for neuropathic pain)
- inhibition of NA uptake
- reduces cholinergic transmission
- reduces noradrenergic transmission
Describe the pharmacokinetics of TCAs?
Same as SSRIs:
- absorbed in gut
- metabolised in liver
- long half lives
What are the side effects of TCAS?
- sedation
- lower seizure threshold
- constipation
- tachycardia
What are non selective monoamine uptake inhibitors (SNRIs)?
- inhibition of serotonin and noradrenaline
- e.g. venlafaxine and duloxetine
- 2nd/3rd line
- dose dependent - lower doses serotonin action and higher doses have a noradrenaline action
- higher doses antidepressant and anxiolytics effect
What are the side effects of SNRIs?
- same as SSRIs and additionally:
- sleep disturbance
- increased BP
- dry mouth
- hyponatraemia (if this is suspected do U and E’s)
May be withdrawal symptoms on discontinuation due to short half life.
What is psychosis?
When you have a lack of contact with reality