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ANTIDEPRESSANTS & MOOD STABILISERS MEDICATION EXAM| 2025-2026|QS & AS|A+ VERIFIED, Exams of Nursing

ANTIDEPRESSANTS & MOOD STABILISERS MEDICATION EXAM| 2025-2026|QS & AS|A+ VERIFIED

Typology: Exams

2024/2025

Available from 07/03/2025

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carol-gakii ๐Ÿ‡บ๐Ÿ‡ธ

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ANTIDEPRESSANTS & MOOD STABILISERS
MEDICATION EXAM| 2025-2026|QS & AS|A+
VERIFIED
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
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Download ANTIDEPRESSANTS & MOOD STABILISERS MEDICATION EXAM| 2025-2026|QS & AS|A+ VERIFIED and more Exams Nursing in PDF only on Docsity!

ANTIDEPRESSANTS & MOOD STABILISERS

MEDICATION EXAM| 2025-2026|QS & AS|A+

VERIFIED

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

  • genetics
  • decreased prefrontal cortex activity
  • decreased reward pathway
  • fewer serotonin receptors Psychological factors
  • learned helplesness
  • cognitive distortions
  • attribution (think everything bad that happens is because of you) Sociocultural
  • Co rumination (having pal with depression increases your likelyhood)

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

PTSD

ED

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

  1. serotonin reuptake blockage
  2. NE reuptake blockage
  3. histamine receptor antagonist
  1. muscarinic and a adrenergic receptor antagonist
  2. Na and Ca channel blocker TCA side effects antihistamine effects
  • sedation, wt gain, confusion anticholinergic effects
  • dry mouth
  • blurred vision ( dilation)
  • urinary retention
  • constipation antiadrenergic effects