drugs - MH and overdose Flashcards
(98 cards)
what is the monoamine theory in depression
depression results from functionally deficient monoaminergic (NA and/or 5HT) transmission in the CNS
what are the emotional symptoms of depression
- misery, apathy, pessimism
- low self esteem
- indecisiveness
- loss of motivation
what are the biological symptoms of depression
- retardation of thought and action
- loss of libido
- sleep disturbance
- change in weight and appetitie
how to tricyclic antidepressants work on 5HT and NA
inhibit the reuptake of 5HT and NA in the synaptic cleft - meaning there is more interaction with the receptors so increases the activity as there are more enzymes present to react
how do tricyclic antidepressants work on a1 and a2
- they act to antagonise alpha-cholinergic
- alpha 1 causes vasoconstriction which leads to orthostatic hypotension
how do tricyclic antidepressants work on muscarinic
- they block the muscarinic receptors
- causes mouth dryness and constipation
how do tricyclic antidepressants work on H1 receptors
they block the histamine receptors - causes sedation and weight gain
how do tricyclic antidepressants work on sodium chloride
block the sodium channels which causes ECG changes
what do TCAs work on
- 5HT
- NA
- sodium channels
- H1 receptors
- alpha cholinergic receptors (a1,a2)
- muscarinic receptors
examples of TCAs
- imipramine
- amitriptyline
- desipramine
- nortriptyline
- clomipramine
what are TCAs also used to treat
- neuropathic pain in adults
- enuresis in children
- insomina
why are TCAs not the first line of treatment
- have a low threshold for overdose
- less well tolerated than SSRIs
- varying degrees of antimuscarinic and anticholinergic side effects
what are side effects of TCAs cause from muscarinic receptor blockages
- dry mouth
- urine retention
- constipation
- blurred vision
- tachycardia
- pupil dialtion
what are the side effects of TCAs caused from H1 receptor blockages
- sedation
- weight gaine
what are the side effects from TCA caused a1 receptor blockages
orthostatic hypotension
why are SSRIs used as a first line defence
- they don’t target other receptors
- so don’t cause as many side effects
- they are relatively safe in an overdose
how do SSRIs work
- decrease serotonin deficiency
- inhibit reuptake of synaptic serotonin by the presynaptic neuron
- serotonin can then stay in the synapse for linger
- serotonin then repeatedly stimulated the postsynaptic receptors (increases activity)
what are examples of SSRIs
- fluoxetine
- fluvoxamine
- paroxetine
- sertraline
- citalopram
- escitalopram
what are the side effects of SSRIs
- insomnia
- sexual dysfunction
- prominent GI disturbances
- significant weight loss or anorexia
- suicidal ideation
how do SNRIs work
- same mechanism as TCAs
- block the reuptake of 5HT and NA
what are examples of SNRIs
- venlafaxine
- duloxetine
- reboxetine
what are side effects of SNRIs
- insomnia
- sexual dysfunction
- nausea
- dry mouth
- hypertension
how do serotonin antagonist and reuptake inhibitor (SARI) work
- inhibit the reuptake of 5HT - works as an agonist at 5HT1A and antagonist at 5HT3
- blocking 5HT3 - post synaptic effect, needed for depression management
- 5HT1a are pre-synaptic and are autoinhibitory, meaning thay block the slef release of serotonin. An agonistic affect, down regulates the receptor, if they are not present it mores that there is mrore serotonin to be released
what are the side effects of SARIs
- nausea
- diarrhoea
- constipation