Study with the several resources on Docsity
Earn points by helping other students or get them with a premium plan
Prepare for your exams
Study with the several resources on Docsity
Earn points to download
Earn points by helping other students or get them with a premium plan
Community
Ask the community for help and clear up your study doubts
Discover the best universities in your country according to Docsity users
Free resources
Download our free guides on studying techniques, anxiety management strategies, and thesis advice from Docsity tutors
ANTIDEPRESSANTS & MOOD STABILISERS MEDICATION EXAM| 2025-2026|QS & AS|A+ VERIFIED
Typology: Exams
1 / 29
This page cannot be seen from the preview
Don't miss anything!
major depressive disorder traditionally considered to have neurochemical basis recent studies conclusion on major depressive disorders regional reductions in CNS volume decreased no of neurons in discrete brain areas with impairment of cellular resilience and neuroplasticity are the neuronal changes in depression reversible? yes biopsychosocial model of depression
Biological factors
they modify negative mood states by increasing intra synaptic concentrations of neurotransmitters they also interfere with signally pathways that regulate neuronal survival and resilience Neuroplasticity the ability of the nervous system to change in response to experience or the environment stress leads to synaptic loss in cortical and limbic areas decreases formation of new neurons in the hippocampus where emotion, mood, cognition controlled also have hypertrophied neurons in the nucleus accumbens and amygdala where we have motivation, reward and emotion chronic administration of anti depressants
enhances synaptic plasticity blocks synaptic deficiets caused by stress Mono-amines in depression predicts underlying pathophysiologic basis of depression is a depletion in the levels of serotonin, norepinephrine, dopamine in the CNS 5 neurotransmitters produced at cell body dopamine, noradrenaline, serotonin, histamine, adrenaline released at synapses to transmit signal to post synaptic neuron dopaminergic system coordination of movements & motivation nor adrenaline
classes of antidepressants Selective serotonin reuptake inhibitors (SSRIs) serotonin norepinephrine reuptake inhibitors (SNRIs) noradrenaline and serotonin ( non selctive monoamine) re uptake inhibitors (NSRI) monoamine oxidase inhibitors ( MAOI) tricyclic antidepressants (TCAs) atypical antidepressants SSRI moa inhibit serotonin reuptake how long does full therapeutic effect take to appear with SSRI 3-8 weeks
SSRI examples fluoxetine setraline paroxetine citalopram escitalopram fluvoxamine SSRI absorption absorbed in GI tract, binds to proteins and crosses the BBB SSRI peak plasma levels 1-8 hrs SSRI metabolism in liver
pre menstrual syndrome what % of patients fail to respond to SSRI 28-55% SSRI best for severe depression = efficacy increased compared to a placeabo which polymorphisms affect SSRI efficacy and safety CYP CYP2C SSRI side effects GI sx dizziness headache
sexual issues drowsy wt gain/loss insomnia SIADH hyponatraemia movement disorders QT prolongation increased risk diabetes, bleeding, bone loss? which SSRI is QT prolongation most common in citalopram dose dependant effect what may be increased <25 in SSRI suicide and self harm behaviour discontinuation syndrome SSRI
Reboxetine regime safe in combo therapy as few drug to drug interactions side effects of reboxetine Insomnia Dizziness Dry mouth Constipation Nausea Sweating SNRI examples Duloxetine Venlafaxine SNRI uses similar to SSRI and also chronic pain syndromes
give if dont respond to SSRI pharmacokinetics of SNRI improved potency and onset shorter 1/2 life than SSRI ( 5hrs) moderately potent CYP2D6 inhibitor side effects of SNRI HTN appetite loss hepatic failure & same side effects of SSRIs which SNRI doesnt cause HTN duloxetine
diet and MAOI avoid tyrosine, can get high levels selegiline also used for parkisnons- selective MOAI at low doses given as a transdermal patch cannot prescribe MAOI with SSRI = risk of serotonin syndrome side effects of MAOI hypotension dry mouth headache GI upset myoclonic jerks
serotonin syndrome cause by interaction between multiple medications that increase serotenergic neurotransmission e,g SSRI started earlier than 2 weeks after MAOI been stopped serotonin syndrome presents within 6 hours ( up to 24) from intiating or increasing the dose of a drug or an SSRI OD serotonin syndrome sx agitation tachycardia HTN tremor rigidity and clonus hyperthermia dilated pupils
also safe to combine with SSRI or MAOI TCA uses depression anxiety bulimia nervosa neuropathic pain smoking cessation TCA 1/2 life 1 day TCAs different mechanism of actions
