Depression Flashcards
1
Q
Selective serotonin reuptake inhibitors (SSRI)
Common indications
A
- First line treatment of depression
- Panic disorder
- OCD
2
Q
SSRI
MOA
A
- SSRI preferentially inhibit neuronal reuptake of serotonin (5-HT) from the synaptic cleft, thereby increasing its availability for neurotransmission
- This appears to be the mechanism by which SSRIs improve mood and physical symptoms in depression and releve symptoms of panic and OCD
- SSRI differ from tricyclic antidepressants in that they do no inhibit NA uptake and cause less blockade of other receptors
- The efficacy of the two drug classes in the treatment of depression is similar
- However SSRIs are generally preferred as they have fewer adverse efffects and are less dangerous in overdose
3
Q
SSRI
adverse effects
A
- Common adverse effects include GI upset, appetite and weight disturbance (loss of gain( and hypersensitivity reactions including skin rash
- Hyponatraemia is an important adverse effect, particularly in the elderly, may present with confusion and reduced consciousness
- Suicidal thought and behaviour may be increased in patients on SSRI’s
- SSRI lower the seizure threshold and some (particularly citalopram) extend QT interval and can dispose to arrhythmias
- SSRIs also increase the risk of bleeding
- At high doses in overdose or in combination with other antidepressants classes, SSRIs can cause serotonin syndrome
- This is a triad of autonomic hyperactivity, altered mental state and neuromuscular excitation, which usually responds to treatment withdrawal and supportive therapy
- Sudden withdrawal of SSRIs can cause GIT upset, neurological and influenza-like symptoms and sleep disturbance
4
Q
SSRI
warnings
A
- SSRIs should be prescribed with caution where there is a particular risk of adverse effects, including in epilepsy and peptic ulcer disease in young people
- SSRIs have poor efficacy and are associated with an increased risk of self-harm and suicidal thoughts, so should only be prescribed
- As SSRIs are metabolised by the liver, dose reduction may be required in people with hepatic impairment
5
Q
SSRI
Interactions
A
- SSRIs should not be given with Monoamine Oxidase Inhibitors (MOAI) as they both increase synaptic serotonin levels are together may precipitate serotonin syndrome
- Gastroprotection should be prescribed for patients taking SSRIs with Aspirin or NSAIDs due to an increased risk of GI bleeding
- Bleeding risk is also increase where SSRIs are co-prescribed with anticoagulants
- They should not be combined with other drugs that. rpolong the QT intervals such as antipsychotics
6
Q
SSRI
Communication
A
- Advise patients that treatment should improve symptoms over a few weeks, particularly sleep and appetite
- Discuss referring them for psychological therapy, which may offer more long-term benefits that drug treatment
- Explain that they should carry on with drug treatment for at least 6 months after they feel better to stop the depression from coming back
- Warn them not to stop treatment suddenly as this may cause a tummy upset, flu-like withdrawal symptoms and sleeplessness
- Withdrawal should be done slowly over 4 weeks
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7
Q
SSRI
Monitoring
A
- Symptoms should be reviewed 1-2 weeks after starting treatment and regularly thereafter. If no effect has been seen at 4 weeks, you should consider changing the dose or drug
- Otherwise, the dose should not be adjusted until after 6-8 weeks of therapy
8
Q
Tri-cyclic antidepressants
Common indications
A
- As a second-line treatment for moderate-to-severe depression
- Neuropathic pain, although they are not licensed for this indication
9
Q
Tri-cyclic antidepressants
MOA
A
- Tri-cyclic antidepressants inhibit neuronal reuptake of serotonin (5-HT) and NA from the synaptic cleft, thereby increasing their availability for neurotransmission
- This appears to be the mechanism by which they improve mood and physical symptoms in moderate-to-severe (but not mild) depression and probably accounts for their effect in modifying neuropathic pain
- Tri-cyclic antidepressants also block a wide array of receptors including muscarinic, histamine (H1), adrenergic (a1,2) and dopamine (D2) receptors
- This accounts for the extensive adverse effects profile that limits their clinical utility
10
Q
Tri-cyclic antidepressants
Adverse effects
A
- Blockade of antimuscarinic receptors causes dry mouth, constipation urinary retention and blurred vision
- Blockade of H1 and a1 receptors causes sedation and hypotension
- Cardiac adverse effects (multiple mechanisms) include arrhythmias and ECG changes (including prolongation of the QT and QRS duration). In the brain, more serious effects include convulsions, hallucinations and mania
- Blockade of dopamine receptors can cause breast changes and sexual dysfunction and rarely causes extrapyramidal symptoms (tremor and dyskinesia)
- Tricyclic antidepressents are extremely dangerous in overdose, causing severe hypotension, arrhythmias, convulsion, coma and respiratory failure
-
Sudden withdrawal- similar to SSRI
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11
Q
Tri-cyclic antidepressants
Warnings
A
- Elderly
- CVD
- Epilepsy
- Constipation
- Prostatic hypertrophy
- Raised intraocular pressure
12
Q
Tri-cyclic antidepressants
Interactions
A
- MAOI as both increase NA and 5-HT- they precipitate hypertension and hyperthermia or serotonin syndrome
- Tricyclic antidepressants can augment antimuscarinic, sedative or hypotensive effects of other drugs
13
Q
Tri-cyclic antidepressants
Communication
A
- Same as SSRI
14
Q
Venlafaxine and mirtazapine
Common indications
A
- As an option for treatment for major depression where the first-line SSRI is ineffective or not tolerated
- Generalised anxiety disorder (venlafaxine)
15
Q
Venlafaxine and mirtazapine
MOA
A
- Venlafaxine- is a 5-HT and NA reuptake inhibitor, interfering with the uptake of these neurotransmitters from the synaptic cleft
- Mirtazapine- is an antagonist of inhibitory pre-synaptic a2-adrenoreceptors
- Both drugs increase the availability of monoamines for neurotransmission, which appears to be the mechanism whereby they improve mood and physical symptoms in moderate-to-severe (but not mild) depression
- Venlafaxine is a weaker antagonist of muscarinic and histamine (H1) receptors than TCA, whereas mirtazapine is a potent antagonist of histamine but not muscarinic receptors
- They, therefore, have fewer antimuscarinic side effects than tricyclic antidepressants, although mirtazapine commonly causes sedations
