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Pre-reg exam > Anxiety > Flashcards

Anxiety Flashcards

1
Q

SSRI (Antidepressant)

Common indications

A
  1. Moderate-to-severe depression and in mild depression if psychological treatment fails
  2. Pain disorder
  3. OCD
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2
Q

SSRI (Antidepressant)

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 relieve symptoms of panic and OCD
  • SSRIs differ from TCA in that they do not inhibit NA uptake and cause less blockade of other receptors
  • The efficacy of the 2 drug classes in the treatment of depression is similar
  • However, SSRIs are generally preferred as they have fewer adverse effects and are less dangerous in overdose
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3
Q

SSRI (Antidepressant)

Adverse effects

A
  • Common adverse effects include: GI upset, appetite and weight disturbance (loss or gain) and hypersensitivity reactions, including skin rash
  • Hyponatraemia is an important adverse effect, particularly in the elderly, and may present with confusion and reduced consciousness
  • Suicidal thoughts and behaviour may be increased in patients on SSRIs
  • SSRI lower the seizure threshold and some (e.g. citalopram) prolong QT interval and can predispose to arrhythmias
  • SSRIs also increase the risk of bleeding
  • At high doses, in overdose, or in combination with other antidepressant classes, SSRI cause serotonin syndrome
  • This triad of autonomic hyperactivity, altered mental state and neuromuscular excitation, which usually responds to treatment withdrawal and supportive therapy
  • Sudden withdrawal of SSRI can cause GI, neurological, influenza-like symptoms and sleep disturbance
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4
Q

SSRI (Antidepressant)

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 by a specialists
  • As SSRIs are metabolised by the liver, dose reduction may be required in people with hepatic impairment
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5
Q

SSRI (Antidepressant)

Important interactions

A
  • SSRIs should not be given with MAOI as they both increase synaptic serotonin levels and together may precipitate serotonin syndrome
  • Gastroprotection should be prescribed for patients taking SSRIs with aspirin and NSAIDs due to an increased risk of GI bleeds
  • Bleeding risk is also increased where SSRIs are co-prescribed with anticoagulants
  • They should not be combined with other drugs that prolong the QT interval, such as antipsychotics
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6
Q

SSRI (Antidepressant)

Communication

A
  • Advise patients that treatment should improve symptoms over a few weeks, particularly sleep and appetite
  • Discuss referring them for psychomotor therapy, which may offer more long-term benefits than 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 (2 years for recurrent depression)
  • Warn them not to stop treatment suddenly as this may cause GI upset, flu-like symptoms and withdrawal symptoms and sleeplessness
  • When the time comes to stop treatment, they should reduce the dose slowly over 4 weeks
  • While patients may find some of the more common side effects unpleasant, they may tolerate them in favour of relieving depressive symptoms
  • Discussing at an early stage what side effects are expected may encourage patients to persist with treatment, at least until the full antidepressant effects are realised
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7
Q

Venlafaxine and mirtazapine

Common indications

A
  1. As an option for treatment of major depression where the first-line SSRI are ineffective or not tolerated
  2. Generalised Anxiety disorder
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8
Q

Venlafaxine and mirtazapine

MOA

A
  • Venlafaxine is a serotonin and NA reuptake inhibitor (SNRI), interfering with the uptake of these neurotransmitters from the synaptic cleft
  • Mirtazapine is an antagonist of inhibitory pre-synaptic a2-adrenoreceptor
  • 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 receptors than TCA, whereas mirtazapine is a potent antagonist of histamine (H1) but not muscarinic receptors
  • They therefore have fewer antimuscarinic side effects than TCA although mirtazapine is sedating
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9
Q

Venlafaxine and mirtazapine

Adverse effects

A
  • Common adverse effects of both drugs include GI upset (dry mouth, nausea, change in weight and diarrhoea or constipation) and central nervous system effects (e.g. headache, ab dreams, insomnia, confusion and convulsions)
  • Less common but serious adverse effects include hyponatraemia and serotonin syndrome
  • Suicidal thoughts and behaviour may increase
  • Venlafaxine prolongs the QT interval and can increase the risk of ventricular arrhythmias
  • Sudden drug withdrawal can cause GI upset, neurological and influenza-like symptoms and sleep disturbance
  • Venlafaxine is associated with a greater risk of withdrawal effects than other antidepressants
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10
Q

Venlafaxine and mirtazapine

Warnings

A
  • As with many centrally-acting medications, the elderly are at particular risk of adverse effects
  • A dose reduction should be considered in people with hepatic or renal impairment
  • Venlafaxine should be used with caution (if at all) in patients with CVD associated with an increased risk of arrhythmias
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11
Q

Venlafaxine and mirtazapine

Important interactions

A
  • The combination of these drugs with drugs from other antidepressant classes can increase the risk of adverse effects (including serotonin syndrome)
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12
Q

Venlafaxine and mirtazapine

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 than 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 (2 years for recurrent depression)
  • Warn them not to stop treatment suddenly as this may cause withdrawal symptoms and sleeplessness
  • When the time comes to stop treatment, they should reduce the dose slowly over 4 weeks
  • warn patients taking mirtazapine to seek medical advice for symptoms of infection such as sore throat, blood tests for disorders
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13
Q

Venlafaxine and mirtazapine

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
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14
Q

SEE alcohol withdrawal for BZ

A
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15
Q

Gabapentin and Pregabalin

Common indications

A
  1. Both drugs are used for focal epilepsies (with or without secondary generalisation), usually, as an add-on treatment .when other anti-epileptic drugs (e.g. CBZ) provide inadequate control
  2. Both drugs are used for neuropathic pain; pregabalin , in particular, is recommended as a 2nd-line option in painful diabetic neuropathy (after duloxetine) and as a first-line option in other painful neuropathies
  3. Gabapentin is used in migraine prophylaxis
  4. Pregabalin is used in GAD
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16
Q

Gabapentin and Pregabalin

MOA

A
  • From a structural point of view, gabapentin is closely related to GABA, the major inhibitory neurotransmitter in the brain
  • However, its mechanism of action, although not completely understood appears largely unrelated to GABA
  • It binds with voltage sensitive calcium (Ca2+) channels, where it presumably prevents inflow of Ca2+ and in doing so, inhibits neurotransmitter release
  • This interferes with synaptic transmission and reduces neuronal excitability
  • Pregabalin is a structural analogue of gabapentin that probably has a similar MOA
17
Q

Gabapentin and Pregabalin

Adverse effects

A
  • Gabapentin and pregabalin are generally better tolerated than other anti-epileptic drugs
  • Their main side effects are drowsiness, dizziness and ataxia, which usually improves over the first few weeks
18
Q

Gabapentin and Pregabalin

Warnings

A
  • Both drugs depend on the kidneys for their elimination, so their doses should be reduced in renal impairment
19
Q

Gabapentin and Pregabalin

Interactions

A
  • The sedative effects of gabapentin and pregabalin may be enhanced when combined with other sedating drugs (e.g. BZ)
  • Other than this, Gabapentin and Pregabalin are notable in having few interactions- compared to most other anti-epileptic drugs
  • This makes it useful in combination therapies
20
Q

Gabapentin and Pregabalin

Communication

A
  • Explain that you are offering a medicine which you anticipate will reduce the severity of their symptoms (e.g. the frequency of their fits)
  • Explain that medicine commonly causes some drowsiness or dizziness
  • For this, reason, you will prescribe a low dose initially, then increase this gradually (make sure they are clear on the dosing instructions)
  • Explain that these side effects should improve over the first few weeks
  • They should avoid driving or operating machines until they are confident that the symptoms have settled
21
Q

Gabapentin and Pregabalin

Monitoring

A
  • The best guide to clinical effectiveness is to enquire about symptoms and side effects
  • There is no need to monitor serum plasma concentrations of Gabapentin and Pregabalin
22
Q

Buspirone

Indications

A
  • Anxiety disorder (Short term use only)
23
Q

Buspirone

MOA

A
  • Member of azapirone class of drugs
  • It has anxiolytic activity but is largely lacking in sedative and muscle relaxant effects and anticonvulsant activity.
  • Based on 5-HT receptors, it acts as an agonist of the pre-synaptic and partial agonist of the post-synaptic 5-HT1A receptors.
  • It is thought to initiate long-term changes in central 5-HT neurotransmission, producing efficacy in anxiety.
  • It is also thought to have activity at D2 receptors, still unclear though
  • Some evidence suggests buspirone has some GABA antagonist-like action
24
Q

Buspirone

Warnings

A
  • Contraindicated in- epilepsy
  • Cautioned in
    • Angle-closure glaucoma
    • Does not alleviate symptoms of BZ withdrawal
    • Myasthenia gravis
25
Q

Buspirone

Adverse effects

A
  • Psychiatric disorders- Insomnia, confusion
  • CNS- Dizziness, somnolence, headache
    *
26
Q

Buspirone

Interactions

A
  • MOAI- may cause an increase in BP
  • CYP inhibitors- cause a dramatic increase in buspirone concentration- reduce from 5mg (BD-TDS) to 2.5mg BD when on CYP inhibitor
  • CYP inducers
  • Antidepressants- the occurrence of elevated BP in patients
  • May get the synergistic effect with other sedative medications
  • SSRIs- rare cases of seizures
  • Serotonergic medications- always a risk of serotonin syndrome.
    *
27
Q
A

Pre-reg exam (113 decks)

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