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Bal (PPP1) > Clinical Case Studies Week 4 (Parkinsons, Anxiety Disorders, Bipolar and Mania) > Flashcards

Clinical Case Studies Week 4 (Parkinsons, Anxiety Disorders, Bipolar and Mania) Flashcards

1
Q

What is parkinson’s disease?

A

Parkinson’s disease results from the degeneration of dopaminergic neurons that arise in the substantia nigra and project to other structures in the basal ganglia.

> imbalance between dopamine and Acetylcholine

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2
Q

What happens if there is not enough dopamine?

A

The excitatory influence of ACh goes unopposed ⇒ excessive stimulation of neurons that release GABA

  • Overactivity of the GABAminergic neurons contributes to the motor Sx that characterise PD
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3
Q

What are the principles of treatment?

A
  • Maintain function as long as possible with minimum medication
  • Individualise therapy according to disease stage and main symptoms
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4
Q

What examples DDI and COMT inhibitors that are used with levodopa for therapy of PD?

A

DDI: carbidopa and benserazide

COMT-I: entecapone

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5
Q

What is preferred 1st line therapy for parkinsons? What is it given with?

A

Levodopa

  • Always with DDI (>75 mg benserazide or carbidopa daily)
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6
Q

Why is levodopa/DDI 1st line therapy? What is the AE?

A

Greatest benefit with the least adverse effects

  • especially in elderly and cognitive decline

> improves bradykinesia and rigidity, reduces mortality; less effective for tremor

> ADRs: orthostatic hypotension, neuropsychiatric effects, hallucinations and confusion, impulse control disorders, dopamine dysregulation syndrome (compulsive overuse)

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7
Q

Long term levodopa syndrome develops within 5 years of starting LD, what are the two major complications of this? Who is more likely to occur in?

A

1. Motor fluctuations

> Wearing OFF, delayed ON and ON-OFF swings

2. Drug-induced chorea/dyskinesias

> involuntary erratic, writhing motions usually affecting face, arms, legs or trunk

Especially in patients with earlier onset PD, more severe disease, higher LD dose, longer duration of disease

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8
Q

What happens with increased duration with levodopa therapy?

A

Therapeutic index window narrows

  • Spend more time ‘off’ and experiencing dyskinesias than their ‘on’ state

> on: On’ time is when levodopa is working well and your symptoms are controlled

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9
Q

Examples of ergot and non-ergot dopamine agonists?

A

Ergot: bromocriptine, cabergoline

Non-ergot: pramipexole, rotigotine (patch), apomorphine (inje)

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10
Q

Examples of MAO-B inhibitors?

A

Selegiline, rasagiline, safinamide

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11
Q

Describe the “Wearing OFF” stage of LD. How to manage?

A

> End of dose failure = earliest and most common motor complication

> Re-emergence of sx before next LD dose is due

  • related to the progressive loss of neuronal storage capacity and short half life of LD

First sign: early morning tremor and immobility = improves after 1st morning dose

Management

  • Smaller, more frequent doses (upto 5-6) doses per day
  • Add a dopamine agonist (or switch)
  • Use CR product –> bedtime dose at first, then during the day
  • Take on an empty stomach, reduce protein intake
  • Add a COMT inhibitor
  • Add rasgiline or selegiline
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12
Q

When does ON-OFF swings occur when using LD? How to manage?

A

Occur in advanced PD, after extended therapy with LD

Rapid and sudden motor fluctuations unrelated to timing of last LD dose

> exact emchanism unclear; therapeutic challenge

Management

  • DBS (deep brain stimulation)
  • Continuous dopaminergic therapy –> continous infusion + boluses

> SC apomorphine

> Dudodenal levodopa continous infusion

  • LD/CD gel given via percutaneous endoscopic gastronomy (PEG) tube into duodenum or jejunum

–> Reduces the fluctuations in concentrations due to erratic or delayed gastric emptying

–> Used only for uncontrolled advance disease with severe motor fluctuations, very expensive :(

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13
Q

What is meant by ‘freezing’ in PD? How to manage?

> motor complication

A
  • Sudden freezing of gait
  • Feet are stuck, difficulty initiating steps or turning
  • Exacerabted by stress or when obstacles are encountered
  • Symptom of disease or drug-related event

Management

  • Increase dopaminergic needs
  • Physiotherapy
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14
Q

What are dyskinesias/peak dose dyskinesias? How to manage?

…issa motor complication

A

Inability to control muscles giving rise to uncoordinated flailing of the arms or legs, or chorea, rapid repetitive movment of the limbs, face, tongue, mouth and neck

> not painful but very distressing

Management

  • Decrease LD dose (even though may worsen PD)
  • Smaller and more frequent LD doses
  • Add amantadine
  • Add dopamine agonists or increase dose
  • Switch dopamine agonists
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15
Q

What are examples of dopamine agonists used to treat advanced PD? Are they used on its own?

A

Rarely use as 1st line monotherapy (rotigotine (patch) for NBM patient, pramipexole for once-daily dosing); otherwise add on.

  • Pramipexole (preferred oral agent)
  • Rotigotine (transdermal patch)
  • Apomorphine SC injection prn or continuous infusion

> rescue medication for severe fluctuations refractory to conventional therapy

> effective within 5-10 minutes

> requires admission to specialised clinic or hosptial for intiation of therapy

> VERY emotgenic –> domeperidone required

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16
Q

AE of dopamine agonists? Which patients to avoid in? What to warn patients about?

> AE of dopamine agonists are 15% worse than levodopa

A

Hallucinations and confusion common, impulse control disorder (ICD), sudden sleep onset, dopamine dysregulation syndrome

  • ICD: problem gambling, hypersexuality, overspending, binge eating, inappropriate internet use, punding

> Avoid in patients with history of ICDs or similar, warn patients and carers, monitor behaviour

> If ICD develop, stop DA, taper gradually to avoid withdrawal syndrome

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17
Q

What COMT inhibitor is used to treat advanced PD? What is it given with? AE? Entacapone with each LD dose

A

Entacapone with each LD dose

> Take with each LD dose to prolong clinical response

> reduce LD dose by 10-30%

AE

  • Worsens dopaminergic ADRs; also bright yellow/organge urine, increased LFTs

> taper slowly due to NMS-like withdrawal syndrome

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18
Q

What MAO-B inhibitors are used to treat advanced PD? Advantage of using them? What are they used with? AE?

A

Adjunct to LD –> increase efficacy by 20% –> reduce “off” time

> may increase dopaminergic ADRs/dyskinesias

  • Rasagiline
  • Selegiline
  • Safinamide

AE

  • Insomnia, neuro-psychiatric ADRs common
  • Associated with serotonin toxicity; C/I with serotonergic agents
  • Tyramine reaction rare; follow dietary restrictions if taken with moclobemide
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19
Q

What is amantadine used with to treat advanced PD? When does it effectiveness reduce? What CNS side effects?

A

Adjunct therapy; useful for controlling LD-induced dyskinesias

CNS side effects

nervousness, depression, nightmares, hallucinations, insomnia, dizziness; also livedo reticularis

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20
Q

Why may anticholinergics be used to treat advanced PD? What areexamples of this? Why poorly tolerated?

A

Effective against tremor, may reduce sialorrhoea (hypersalivation)

  • Benzatropine
  • Biperiden
  • Trihexyphenidyl (benzhexol)

> poorly tolerated: blurred vision, cognitive impairment, constipation, dry mouth, urinary retention

  • avoid in elderly, cognitive impairment
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21
Q

What drugs may worsen PD?

A

Antipsychotics (esp typical antipsychotics)

Dopamine antagnoist antiemetics (droperidol, metoclopramide, prochlorperazine)

Methyldopa

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22
Q

What drugs not to use with MAO-B (+DDI) for PD?

A

Non selective MAOIs (phenelzine, tranylcypromine)

Moclobemide

Serotonergic drugs

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23
Q

What are some non-pharmacological therapies in PD?

A

CAMs

  • No evidence, vitamin E/vitamin C, CoQ10 that signficantly delay PD progression

Multidisciplinary approach

  • Physiotherapy, speech therapy, occupational therapy, dietetics
  • Physical therapies (active music therapy, treadmill training, balance training) can improve function

Surgery (deep brain stimulation)

  • high frequency DBS with an inserted electrode
  • Most succeful in patients with motor fluctuations and dyskinesias
  • does not alleviate cognitive deficits, NMS (non-motor symptoms) and some motor effects

C/I in major psychatric/medical illness, cognitive impairment, PPM, levodopa-resistant parkinsonism, +/- advanced age

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24
Q

How to manage the following non-motor smyptoms (NMS) in PD (lifestlye advice and also medications used):

A) orthostatic hypotension (20 mmHg fall in SBP, 10mmg Hg in DBP; risk of falls, injuries)

B) constipation

C) sleep problems

D) psychosis

E) depression and anxiety

F) dementia

A

A)

review medications (antiparkinsons drug, antiHTN drugs)

avoid heat, alcohol, large meals, straining, standing up rapdily

increase sodium and water intake

smaller, more frequent meals

exercise in horizontal position (swimming)

compression sotckings

sleep with head of the bed raised

drug treatment:

> fludrocortisone 0.1 mg daily, increasing to 0.2 mg daily if needed

> alternatives: pyridostigimine, ephedrine

B)

Increase fluids, dietary fibre

Remove anticholinergics

Osmotic laxatives –> PEG, macrogol

C)

Insomnia, RLS, hypersomnia

Parasomnia (REM sleep behaviour disorders) –> clonazepam 0.25mg nocte (monitor for decline in cognition and symptom control)

Sleep hygiene

D)

  • common in PD, eldely have cognitive disturbance and anticholinergic drugs wihich worsen cogntive function
  • often drug induced –> reduce LD dose, simplify regimen

> withdraw anticholinergics and DAs

  • Antipsychotic therapy (low dose second gen antipsychotics)

> clozapine most effective but difficult to use, needs regular blood monitoring

> quetiapine useful and often used empirically

> avoid other second gen and first gen antispychotics

E)

  • Treat with standard pharmacotherapy
  • Common and often undertreated

F)

  • 2-6x increased risk with PD –> increases with time
  • cholinesterase inhibitors have mild-mod benefit

> donepezil, rivastigmine –> fewer ADRs –> can exacerbate motor symptoms in PD e.g. tremor

> Trial for 2-3 months; taper slowly if no benefit

check if patient on anticholinergic as it worsens cognitive function

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25
Q

Anxiety from this card onwards…

A
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26
Q

What are the THREE steps to general principles of management of anxiety disorders?

A

Step 1: Confirm diagnosis

  • History assessment
  • Physical examination to exclude underlying medical cause
  • Identify features to define specific anxiety disorder (&/or co-existing psychiatric disorders)
  • Assess degree of distress

Step 2: Identify and address factors that may exccerbate the disorder

  • Psychological factors
  • Lifestyle factors

Step 3: Initiate therapy –> if required

Psychoeducation

Psychological treatments

Pharmacological management

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27
Q

What TWO types of exacerbating agents to avoid? Provide examples

A

1. Psychological factors

  • Financial difficulties
  • Relationship difficulties

2. Lifestyle factors

  • Alcohol, nicotine and illicit drug use
  • Excessive caffeine intake
  • Excessive work
  • Inadequate sleep
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28
Q

What is psychoeducation about? What treatment options does it lead into?

A

The nature of the anxiety

It’s purpose

How it can present

  • leads into relaxation techniques, yoga, exercise, CBT
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29
Q

Psychological interventions are the most appropriate initial treatment choice in most cases. What do psychological interventions include?

A

Cognitive behavioural therapy (CBT)

Exposure therapy

& many others

  • Many treatments are available as self-help therapies on-line and are referred to as e-therapy
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30
Q

For Cognitive Behavioural Therapy (CBT) –> most effective therapy for anxiety 1st line intervention

​A) What is the focus on?

B) Based on what 2 key principles

C) How many sessions are there

D) What interferes with the effectiveness

A

A)

Focus is on changing maladaptive thinking patterns and behaviour

B)

Cognitions may control feelings and behaviour

Behaviours may affect thought patterns and emotions

C)

Acute treatment 12 – 20 weekly sessions

  • Individual, group therapy or selfdirected formats
  • Follow-up booster sessions after 3 or 6 months useful

D)

Benzodiazepine

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31
Q

What is exposure therapy? What anxiety conditions is it useful for?

A

Based on the principle of respondent conditioning

> Can be useful for PTSD, OCD and specific phobias

> sometimes used together with CBT

  • When people are fearful of something they often avoid what they fear however in the long term this can make fears worse
  • Exposure therapy = “Face fears” and challenge them in a controlled way

> can be done using virtual reality

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32
Q

Generally CBT-based treatment approach

> Can be as effective as face-to-face therapies

A
  • Mood gym
  • Mindsport courses
  • E-couch programmes
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33
Q

For pharmacotherapy for anxiety (used when psychological interventions are ineffective or not available):

A) What is first line?

B) What is used in exceptional circumstances?

C) What are other drugs used in anxiety?

A

A)

  • SSRIs for all anxiety disorders
  • SNRIs for some disorders

B)

  • Benzodiazepines

C)

  • TCAs
  • MAOIs
  • Buspirone
  • Anticonvulsants
  • Antipyschotics
  • Beta blockers
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34
Q

For the follwowing anxiety disorders;

A) What drugs are used for GAD

B) What drugs are used for SAD

C) What drugs are used for panic disorder

D) What drugs are used for specific phobias

E) what drugs are used for OCD

F) What drugs are used for PTSD

A

A)

  1. An SSRI or duloxetine or venlafaxine
  2. imipramine or buspirone

B)

  1. An SSRI or venlafaxine

C)
1. An SSRI or venlafaxine

  1. clomipramine or imipramine

D)

No ongoing pharmacotherapy recommended

E)

  1. An SSRI
  2. clomipramine

F)

  1. An SSRI
  2. mirtazepine or amitriptyline
35
Q

How to dose SSRIs in patients who have anxiety? What is seen when starting SSRIS? What is the onset of action?

A

Start patients on half the minimum strength tablet available –> continue at that dose for a few days to a week until patient feels confident enough to increase dose

  • Increased anxiety when starting SSRIs
  • Onset of action is slower for anxiety (4-6 weeks)
36
Q

Precautions of SSRIs in anxiety?

A

Most patients with anxiety are highly sensitive to the physiological effects of SSRIs

Patients with anxiety disorders may experience suicidal ideation and risks with medication should be assessed

37
Q

Which BZDs are used for the following and why:

A) For anxiety

B) For insomnia

C) For controlled drugs

A

A)

  • Diazepam, lorazepam, oxazepam

> rapid onset of action and long half life –> less withdrawal symptoms

B)

  • Temazepam

> rapid onset of action but short half life

C)

  • Alprazolam
  • Flunitrazepam
38
Q

What are the indications for BZDs? Provide THREEE answers.

A

Can provide rapid symptomatic relief

Reserved for short-term (2 to 4 weeks) use or intermittent use as part of a broader treatment plan

Occasionally used short term (up to 2 weeks) to manage agitation or insomnia when starting antidepressants

39
Q

What conditions is there evidence of benefit/no benefit in for the use of BDZs?

A

Benzodiazepines have evidence of benefit in GAD, SAD and panic disorder, but not OCD or PSTD

40
Q

For BDZs use:

A) What is used in GAD? Why is it used? How long to use for?

B) What is used in SAD? Why is it used?

C) What is used in Panic Disorder?

D) What is used in specific phobias?

A

A)

Diazepam 2mg to 5mg as a single dose repeated up to twice daily

Short term measure only during a crisis for severe or disabling anxiety

Up to 2 weeks treatment then reduce dose to zero by 6 weeks

Long term use only in rare instances where other therapies have failed.

B)

A short-acting BDZ can be used just before a performance in instances of specific performance anxiety

However, side effects may inhibit the performance

C)

Role of BZDs replaced by antidepressants

Most effective are high-potency BDZs (alprazolam and lorazepam) but these are also the most addictive

D)

Diazepam can be used as a single dose prior to a necessary exposure to control anxiety (e.g. claustrophobia and MRI)

41
Q

What are the concerns with BZDs? What to consider if prescribing

A

Can lead to physical and psychological dependence, tolerance and misuse –> drug seeking behaviour, craving, disturbed work and personal functioning

If considering prescribing BZDs:

  • Always check for a history of problem alcohol or drug use
  • Be wary of prescribing to unfamiliar patients, especially if asking for a particular drug by name (may indicate drug-seeking behaviour)
  • Carefully discuss the potential for addiction with the patient
  • Avoid using short-acting drugs as they are the most highly addictive
  • Only prescribe small quantities of medication at a time
  • Use only as short-term treatment
  • Ensure regular review of the patient and continuity of care.
42
Q

What are the common AE of BZDs?

A

Drowsiness, over-sedation, light-headedness, hypersalivation, ataxia, slurred speech, dependence, effects on vision,

43
Q

How to do dose reduction for BZDs? What are the peak effects at weak 2 of withdrawal?

A

Dose reduction at a rate of 15% per week is usually tolerated

  • Higher dose preparations – stabilise on equivalent dose (ddd) of diazepam before reducing dose (not > 80mg/day)

> may need to withdraw in inpatient setting

Peak effects at week 2

anxiety, panic, insomnia, muscle spasms, vomitting, diarrhoea, seizures

44
Q

For other drugs used for anxiety, whhen should TCAS be avoided?

A

Need to be avoided with any patient at risk of suicide or those with underlying cardiac disease

  • lomipramine, imipramine, amitriptyline
  • risk of anxiety increases when started like SSRIs

> second line after SSRIs (prolong QT interval and increase arrythmias)

> cardiotxocitiy in overdosage

> Efficacious but more side effects than SSRIs – anticholinergic effects, hypotension and weight gain

45
Q

For other drugs used for anxiety, MAOIs, explain why they may be used?

A

(phenelzine = irreversible, moclobemide = reversible)

  • Occasionally used by specialists in social phobia following failure of SSRI. Phenelzine also used rarely in PTSD

> orthostatic hypertension common dose limiting factor with both of these drugs

46
Q

When may mirtazapine be used for anxiety? Side effects?

A

An option in PTSD

Less nausea vomiting and sexual dysfunction than SSRIs but more weight gain and sedation

47
Q

Which antipsychotics are used for anxiety? Why are they used?

A

Antipsychotics (risperidone*, quetiapine*, olanzapine)

> evidence limited and side effects risk high

  • Most evidence of effect* in OCD when used in combination with an SSRI
  • Olanzapine with SSRI has been used for PTSD and social phobia
48
Q

When may buspirone used for anxiety? MOA and when is it appropriate to use?

A

Partial agonist of serotonin 5HT1A receptors

  • May be preferable to BDZs for management of GAD in patients with a history of substance misuse – less potential for dependence
  • May take 2 weeks for optimal benefit
49
Q

When is pregabalin used for anxiety? What is the MOA? AE?

A

Pre-synaptic inhibitor of the release of excitatory neurotransmitters

  • Effective for GAD (not licensed in Aust)
  • Commonly causes somnolence, nausea, dizziness, dry mouth and also expensive
  • No rebound anxiety when discontinued but need to withdraw slowly to avoid precipitating a seizure
50
Q

when are beta blockers used for anxiety? Which patient is not appropriate in?

A

Used for physical symptoms (manifestations of sympathetic overactivity) including tremor, palpitations and sweating which can be distressing and unpleasant

  • Does not relieve the mental aspects of social phobia

> propranolol 10 to 40mg, 30-60 minutes before the social event or performance

> caution in patients with diabetes

> Avoid use in patients with asthma, severe peripheral vascular disease and some patients with heart failure

51
Q

Summary for Anxiety

A
  • Use key symptoms to differentiate between types of anxiety disorders and determine effective treatment
  • Trial non-drug therapy including psychological therapy as first line
  • Consider an antidepressant for those who do not respond to non-drug therapy, selecting on the basis of evidence of efficacy in the diagnosed anxiety disorder
  • Reserve benzodiazepines for short term use in selected circumstances
52
Q

Bipolar from this card onwards…

A
53
Q

How is medication treatment for bipolar disorder split into 2 parts?

A

Treating a current episode (acute) of mania, hypomania or depression

Preventing the long term recurrence of mania, hypomania and depression (prophylaxis) –> mood stabiliser

54
Q

What are the management aims for BPAD?

A
  • Resolution of acute symptoms
  • Prevention of relapse (Individualise treatment)
  • Minimise ADRs
  • Encourage adherence
  • Patient education
  • Non-pharmacological interventions
55
Q

Why do relapses often occur in BPAD that leads to acute mania?

A

Relapses often due to poor medication compliance, substance abuse, antidepressants or stressful life events.

56
Q

What is used for primary treatment of elevated mood in acute mania?

A

Lithium

Sodium valproate

Atypical antispychotic

> mood stabiliser with/without antipsychotic

57
Q

What is used for short-term management of associated behavioural disturbance in acute mania?

A

Benzodiazepines

Atypical antipsychotics

Classical antipsychotics (only if other options have failed)

  • Withdraw once settled
58
Q

What combination of drugs is used for acutely manic patients?

A

Mood stabilsier + antipsychotic

59
Q

What are the 2 steps in treating acute mania?

A

Stop antidepressant (if taking)

Commence mood stabiliser

> If already on mood stabiliser:

  • check level
  • increase the dose
  • switch agents
60
Q

Mood stabilisers have delayed of onset of action of around 1 week. What medication is used to calm/sedate the patient as an interim measure?

A

Use an antipsychotic and/or benzodiazapine for short term treatment

  • Antipsychotics used for up to 6 months. May also be used as mood stabiliser
  • Benzodiazepines used for days-weeks
61
Q

What are the 2 options of treatment of acute depression in BPAD? What is a precaution?

A

Antidepressants –> DONT USE ANTIDEPRESSANTS ALONE IN TREATMENT OF BPAD

  • SSRIs. SNRIs, Mirtazapine = 1st line
    • mood stabiliser/atypical antipsychotic = lithium, olanzapine, quietapine, lamotrigine good choices

Quietapine 300-600mg/day

  • monotherapy less commonly used than antidepressant/mood stabiliser combination
62
Q

What is a mood stabiliser? What does it decreases the chances of? How long does it take to work?

A

A medication that has anti-depressant and anti-manic properties, that is effective for the acute treatment of mania and/or bipolar depression.

Decreases the chances of having further episodes of mania or depression

Delay in onset of 1 week+

Goal is to obtain and maintain remission

63
Q

What is the therapeutic range of lithium dosing for

A) acute mania

B) prophylaxis

A

A)

  • Therapeutic range = 0.5-1.2 mmol/L

B)

  • Therapeutic range = 0.4-1.0 mmol/L

> small therapeutic window

> toxicity experience at levels just outside therapeutic range

> many drug interactions which can increase/decrease level

64
Q

What are the precautions of lithium?

A

Acute hyponatraemia - increased risk of toxicity

Dehydration - increased risk of toxicity

Renal impairment - increased risk of toxicity

Elderly patients - age-related renal function decline and more sensitive to toxic effects

Psoriasis, acne - can be worsened

65
Q

Common, infrequent and rare adverse effects of lithium

A

Common

Headache, Fatigue, Vertigo, Acne, Psoriasis, Hypothyroidism, weight gain, thirst, polyuria, metallic taste, gi upset

Infrequent

Diabetes insipidus, memory impairment, hair loss, hyperparathyroidism

Rare

Cardiac arrythmias

Hyperthyroidism

66
Q

For lithium drug interactions, what increases lithium levels?

A

Loop diuretics §

Thiazide diuretics §

NSAIDs §

ACE inhibitors §

Sartans §

Theophylline §

Topiramate (high doses)

67
Q

What are some considerations for preventing lithium toxicity?

A
  • Avoid dehydration – regular salt and fluid intake. Take care with major dietary changes
  • Do not change sodium intake
  • Avoid drinking large amounts of caffeinated drinks
  • Take extra care in hot weather and during activities causing you to sweat heavily ie. hot baths, saunas & exercise
  • Infection or illness that causes heavy sweating, vomiting or diarrhoea
  • Some patients experience toxic symptoms within normal range
68
Q

How to monitor effects of lithium toxicity? What tests needs to be done when lithium is commenced? What other tests are required?

A

Patients should be aware that regular blood tests are important during treatment with lithium

  • Patients commencing lithium - U+E, TFT,PTH, ECG and pregnancy test

Li can cause hypothyroidism. If this occurs, often treated with Levothyroxine

> Monitor serum lithium levels 5 to 7 days after starting or changing dose

> Monitor lithium levels, U+E and TFT every 3-6 months and when clinically indicated

> Blood samples for lithium serum levels should be taken 12 hours post dose (withhold morning dose of lithium if any until blood taken)

69
Q

What is some counselling information for lithium?

A

Take with food to minimise gastric upset

Regular blood tests are required

Avoid dehydration. Drink extra fluids on hot days, after exercise (sweating), spa/sauna or after vomiting/diarrhoea

Educate patient on symptoms of toxicity. Advise doctor if symptoms of toxicity arise (e.g. tremor, increased nausea)

Many drug interactions. Always advise doctor/pharmacist you are taking lithium

70
Q

Why is sodium valproate given in BAD? What are some side effects?

A

Most commonly used mood stabiliser –> lithium has narrow TI and can be toxic. Also used to treat aggressive behaviours.

  • take with food to reduce stomach upset
  • weight gain can be problematic
71
Q

What is sodium valproate used as first line in?

A

Generally used first line in bipolar maintenance as more tolerable than lithium

  • Evidence for acute mania, maintenance, and acute depression in combination with antidepressant
72
Q

Which patients should sodium valproate be avoided in?

A

Avoid if possible in women of childbearing potential

  • Human teratogen
  • If necessary, active contraception must be used (i.e contraceptive pill, injection, implant or IUD)
73
Q

What are some precautions for sodium valproate?

A
  • Hepatic impairment - avoid use
  • Surgery - check platelet count and INR before having any surgery
  • Pregnancy – do not use. increased risk of congenital malformations.
  • Women of childbearing age must be on contraception
  • Lactation - safe to use at low dose
74
Q

Common, infrequent and rare adverse effects of sodium valproate

A

common

GI upset

Increased appetite

weight gain

tremor

numbness

drowsiness, ataxia

elevated liver enymes

infrequent

thinning or hair loss

rash

Menstrual Irregularities (polycystic ovaries)

Abnormal Bleeding Time

Rare

hepatic failure

pancreatitis

decreased white cells

decresed platelets

peripheral oedema

extrapyramidal sydnrome

75
Q

How to monitor for sodium valproate? What tests to do when commencing?

A

Patients commencing sodium valproate - FBC, LFT and pregnancy test

> a minimum of 6-monthly thereafter

> monitor serum levels 3-5 days after each dose increase

  • Blood samples for serum levels should be trough levels (withhold morning dose if any until blood taken)
76
Q

What is the therapeutic range of sodium valproate?

A

Therapeutic range 50-100mg/L

  • In BPAD generally aim for this level
  • Can be used to monitor compliance
  • Toxicity generally >125mg/L
77
Q

How does lamotrigine interact with sodium valproate?

A

Valproate increases lamotrigine levels, increasing the risk of potentially dangerous rashes

If currently on valproate, start lamotrigine even more slowly

78
Q

What decreases sodium valproate levels?

A

Carbamezepine and phenytoin

79
Q

What increases sodium valproate levels?

A

Aspirin increases­ valproate levels (doses <300mg do not interact);

  • Combination also increases risk of bleeding
80
Q

When is lamotrigine used?

A

One of the few agents effective for bipolar depression

  • Consider if depression a prominent feature
  • Used when there has been inadequate response to existing medications
81
Q

What is the AE of lamotrigine?

A
  • Including (rarely) Stevens-Johnson syndrome
  • Rashes minimised by very slow up-titration of dose
  • Risk of serious rash is associated with high initial doses and exceeding dose escalations
  • If a skin reaction occurs stop treatment immediately
82
Q

What to do when there is failure to respond to treatment?

A

Check blood level (if applicable)

Increase dose if required

Assess adherence with medication

Check for substance abuse

Implement psychological therapies

Combine treatments

83
Q

When is combination therapy done in BPAD?

A

May be beneficial when there is poor response to monotherapy n

Lithium + valproate more effective than either agent alone n

Sodium valproate and carbamazepine combination is associated with high rates of adverse effects n

Lithium/valproate + antipsychotic increasing in practice n

Limited clinical trial evidence

Halve dose of lamotrigine if combining with sodium valproate to reduce risk of rash

84
Q

What are the general principles in mood stabiliser therapy?

A

Everyone responds differently regarding efficacy and adverse effects

Not a cure

Monitor for side effects

Monitor for signs of toxicity, reminding patients how to avoid toxicity

Ongoing monitoring of blood levels/tests & signs of relapse

Bal (PPP1) (20 decks)

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