CNS Flashcards
(151 cards)
1
Q
What is the main treatment of VaD?
A
Prevention is the best treatment
Good management of BP, diabetes, heart disease, cholesterol, smoking
2
Q
Describe the extensor plantar response:
A
Sharp object is stroked up patients foot, big toe bend backwards in VaD
In healthy adults, big toe and all toes bend forwards
3
Q
Name the investigations used in primary care for establishing the cause of dementia and differential diagnosis:
A
FBC
U&Es
LFTs
CRP
Calcium and phosphate
TFTs
Vit b12 and folate
Urine dipstick
BG
Temperature
4
Q
Name the investigations used in secondary care for establishing the cause of dementia and differential diagnosis:
A
MRI and CAT scan
Urinalysis
HIV status
Neuropsychological assessment
ECG
5
Q
Name and describe the MMSE score:
A
27-30 Normal
25-27 Mild cognitive impairment
21-26 Mild AD (5%)- treatment commence
10-20 Moderate AD (32.1%)
10-14 Moderately severe AD
<10 Severe AD (12.5%)
6
Q
Name the different classes and give examples of different types of dementia medication:
A
AchEi e.g donepezil, rivastigmine, galantamine
NMDA antagonists e.g memantine
Antioxidants e.g ginkgo
Anit-inflammatories e.g ibuprofen
Neurotrophic factors e.g oestrogen
Antiamyloid agents e.g tramiprosate
7
Q
Name anti-amyloid antibodies used in early AD:
A
Aducanumab
Lecanemab
8
Q
Describe the dosing of donepezil as a drug in dementia:
A
Aricept
Start at 5mg OD ON then increase to 10mg OD ON
4 week interval between dose increase
Taken at night as some patients may feel dizzy/ cause bradycardia
orodisperisble available
9
Q
Describe the dosing of rivastigmine as a drug in dementia:
A
Exelon
1.5-6mg BD
Liquid (2 wk gap between dose increase)
Patch available (4 wk gap between dose increase):
9.5mg in 24 hr patch
10
Q
Describe the features of rivastigmine:
A
Non-selective reversible AchEi (non-competitive)
License: mild to moderate dementia in AD and PD (capsule)
11
Q
What would be the outcomes if the AchEi doesn’t work for the dementia patient?
A
Failure to benefit from one AchEi doesn’t necessarily mean that they won’t respond to another
Also poor tolerance to one AchEi doesn’t rule out good tolerance to another
12
Q
Describe the NICE 2018 guidelines for dementia treatment:
A
Use the least expensive one first- donepezil 70-80% of patients first line
Alternative AchEi could be prescribed if it is considered appropriate when taking into account adverse event profile, expectations about adherence, medical co-morbidity, possibility of drug interactions
13
Q
What are the adverse effects of AchEi?
A
When they start to work, they can cause cholinergic stimulation (procholinergic effect) of the body to:
Common SEs: N&V, diarrhoea, loss of appetite, sleep disturbance, abnormal dreams, incontinence, headache, fatigue
14
Q
What are the dangerous SEs of AchEi?
A
Bradycardia
Dangerous in certain heart diseases or if taking heart slowing drugs e.g digoxin, BBs, CCBs
15
Q
Name drugs that are associated with an increase in anticholingeric burden and therefore cognitive impariement:
A
Antihistamines
Tricyclic antidepressants
Antipsychotics e.g quetiapine
Drugs used in urinary incontinence e.g solfenacin
Hyoscine
Pain killers e.g morphine
Some asthma and COPD meds
16
Q
How would you optimise taking donepezil?
A
It can cause sleep disturbances/ nightmares so give dose in the morning
It has a long half life do doesn’t matter as much if missed a dose
17
Q
How would you optimise taking Rivastigmine?
A
Patches can cause rash
If mild then use an emollient cream
If severe then prescriber should be informed, rotation at the application site helps
It has a short half life so may need dose titration if doses missed
18
Q
Describe the features of memantine:
A
NMDAr antagonist that may be neuroprotective and thus disease modifying
License: moderate to severe dementia in AD
Monotherapy is recommended for managing moderate AD who are intolerant of or have CI to AchEi or severe AD
19
Q
What are the SEs of memantine?
A
Common: headache, constipation, dizziness, HTN, dyspnoea
Caution in using it with pts with history of epilepsy/ seizures
20
Q
What is the unlicensed use of dementia medications in Lewy body dementia?
A
Offer donepezil or rivastigmine to patients with mild to moderate dementia
Only consider galantamine for patients with mild to moderate dementia with LB if donepezil and rivastigmine are not tolerated
Consider donepezil or rivastigmine for people with severe dementia with LB
21
Q
What is the unlicensed use of dementia medications in vascular dementia?
A
Only consider AchEi or memantine for patients with VaD if they have suspected co-morbidities with ADs, PD dementia or dementia with LB
22
Q
What is the unlicensed use of dementia medications in frontotemporal dementia?
A
Do not offer AchEi or memantine to these patients
23
Q
What are the BPSD symptoms in mild dementia?
A
Anxiety/ depression
24
Q
What are the BPSD symptoms in moderate dementia?
A
Physical aggression
Wandering, sexual inhibition- disappear in the severe stages
Screaming
Swearing
Delusions
Hallucinations
25
What are the BPSD symptoms in severe dementia?
Depression
Screaming
Suspiciousness
Paranoia
Delusions
26
What is the first line treatment for BPSD?
Non-drug intervention
Modification of the carer may:
-decrease the occurrence of BPSD
-remove the need to treat the BPSD
Many symptoms naturally resolve themselves within 4-6 weeks
Other non-pharmacological depending on preference e.g music therapy
27
What are the monitoring steps in psychiatric medications?
Review all psychotropics at least every 3 months
Review all antipsychotics at least every 6 weeks
Time-limit Rx when possible
Review symptoms and behaviour
Review SEs
Decrease drug dosages
Discontinue when possible
28
Describe the use of combination medications in BPSD:
Use medicines that address several different symptoms to avoid unnecessary polyprescribing
e.g sedating antidepressants for:
-agitation
-depression
-sleep disturbance
29
Describe the use of Risperidone for BPSD:
Short term treatment of up to 6 weeks for persistent aggression on moderate to severe AD unresponsive to psychosis in dementia and risk to themselves and others
30
Which antipsychotics would you not use in BPSD and why?
Others are ineffective or have harmful SEs
Greater cognitive decline with quetiapine when compared to placebo- as has anti-cholinergic effect
Benzodiazepines can increase the risk of falls/ fractures by 8 fold
Haloperidol
31
Describe the discontinuation of Risperidone (antipsychotics) in BPSD:
Many patients can stop anti-psychotics for BPSD safetly without worsening of symptoms
Continue antipsychotic if patient relapses
Do NOT stop antipsychotic if it is treatment for schizophrenia (typical dose is 2mg daily)
32
What is early onset PD?
1 in 20 patients diagnosed before 40 years old
33
Name the motor symptoms of PD:
Bradykinesia
Muscle rigidity
Tremor
34
What is Parkinsonism?
All of the motor symptoms
PD is a type of Parkinsonism but there are other causes e.g drug induced Parkinsonism, stroke
35
Name the non-motor symptoms of PD:
Depression/anxiety
Fatigue
Cognitive impairment/ dementia
Sleep disturbance
Constipation
Dysphagia
Weight loss
Hyposmia (decrease sense of smell)
Sialorrhoea (drooling/ excessive salivation)
Excessive sweating
Urinary/bladder problems
Pain
Hypotension
36
Define bradykinesia:
Slowness of voluntary movement
This can be asymmetrical and unpredictable
37
Describe what rigidity is:
Increase in muscle tension
Characteristic of stooping posture
Rigidity affects balance, increased risk of falls (harmful as slow reactions due to bradykinesia)
Associated with muscle pain
38
Describe the symptoms of a tremor in PD:
Not all PD patients will have a tremor
Resting tremor, normally in one or both hands, stops with voluntary movement or mental concentration
'Pill rolling', fingers roll in a circular movement as in rolling fingers between thumb
39
Name common drugs that can cause a SE of tremor:
Antipsychotics normally in first 10 weeks of taking and more common in 1st gen e.g haloperidol, chlorpromazine- generally dose related and reversible
B agonists e.g salbutamol/ salmeterol
Antiemetics e.g prochlorperazine, metoclopramide
Co-trimoxazole, SSRIs, lithium, valporic acid, medroxyprogesterone
40
What is the first line treatment in PD with motor symptoms?
Offer Levodopa to patients with early PD whose motor symptoms affect their QoL
Consider a choice of dopamine agonists, L dopa, or MAO-B inhibitors with early PD whose motor symotms don't affect QoL
41
What is the adjuvant therapy in PD with motor symptoms?
Offer a choice of dopamine agonists, MAO-Bi or COMTi as an adjunct to L dopa
If dyskinesia is not adequately managed by modifying existing therapy, consider amantadine
42
When should you start L-dopa?
Different for every patient
e.g older patient may want to start asap but younger may want to start it later
43
What are the unwanted SEs of L-dopa?
Dyskinesia (involuntary movements)
Fluctuations in clincal state
Acute SEs
44
Describe the dyskinesia SE for L-dopa:
From 2 years of starting (50% of patients by year 5)
Affects face, arm and trunk (limbs)
45
Describe the fluctuations in clinical state SE for L-dopa:
'On-off' phenomena (bradykinesia/ rigidity suddenly worsen then better)
Wearing off effect (end of dose deterioration)
Freezing
46
What are possible solutions for PD patients when they get symptoms due to wearing off their medication?
Mainly long term
Night and first thing in the morning as its the longest time without medication
Using SR or COMTi (entacapone) can help stop this
47
Describe the acute SEs for L-dopa:
Nausea and anorexia
Hypotension
Sleep disturbances including sudden onset of sleep implications for driving
Psychological effects- anxiety/ depression, schizophrenia symptoms
48
Name inhibitors that is given with L-dopa to inhibit the metabolism and why?
Dopadecarboxylase inhibitors:
-carbidopa
-benserazide
L-dopa is always given in combo with one
These decrease peripheral metabolism of L-dopa and improve absorption of L-dopa which decreases peripheral SEs
They don't cross the BBB
49
Name the brands of the dopadecarboxylase inhibitors:
Carbidopa+ L-dopa= Co-careldopa (Sinemet®)
Benserazide+ L-dopa= Co-beneldopa (Madopar®)
50
Name 2 COMTi:
Entacapone
Tolcapone- rarely used due to risk of liver toxicity
51
Describe the SEs of entacapone:
Colours urine bright red/orange but this is harmless
Worsens SEs of L-dopa
52
What is the function of COMTi?
Potentiates the effects of levodopa
Helps counteract fluctuations in plasma conc of L-dopa
53
When are COMTi given?
Add on therapy in combo- not useful on their own
54
What is a dosing schedule to help with fluctuation SEs of L-dopa but a negative of this too?
Small doses of L-dopa at increased frequency to decrease 'peaks and troughs' and dyskinesia but high tablet burden
55
What are the counselling points for L-dopa?
Proteins inhibit the absorption, wait 30-60 mins after medication before eating- can eat a low protein snack like a cracker if nauseous
Brand specific
Manage underlying issues that affect absorption, iron supplements wait 2-3 hours as chelates form in GIT
56
Describe the benefits of dopamine receptor agonists as monotherapy compared to L-dopa:
Reduced (+increased time to) motor complications (less dyskinesia)
Can delay intro of L-dopa
Short plasma t1/2= 6-8 hours so TDS dosing
57
Describe the disadvantages of dopamine receptor agonists as monotherapy compared to L-dopa:
Slightly poorer improvement in motor function
Possible greater neuro-psychiatric SEs
Older ergot derived are limited by SEs e.g N&V, thunderlance, fibrotic reactions of lung, heart valves= dangerous
Only be used if inadequate response to non-ergot derived options
58
What are the SEs of non-ergot dopamine receptor agonists?
Better tolerated
Can sometimes cause thunderlance, compulsive behaviours e.g gambling, sex, eating
59
Name non-ergot derived dopamine receptor agonists:
Ropinirole
Rotigotine- transdermal patch, useful when patients not able to take oral
Pramipexole
60
Name ergot derived dopamine receptor agonists:
Bromocriptine
Cabergoline
Lisuride
Pergolide
61
What should be the action if a PD patient is suspected of having ICD?
Gradually decrease any dopamine agonists
Monitor whether impulse control disorder improved and whether the person has any symptoms of dopamine receptor agonist withdrawal
Offer specialist cognitive behavioural therapy targeted at ICD behaviours if modification of dapaminergic therapy isn't effective
62
Name the monoamine oxidase B inhibitors (MAO-B):
Selegeline
Rasagiline
63
What is the problem with selegeline?
Metabolised to amphetamine so causes excitement, anxiety and insomnia
64
When are MAO-Bi given?
Alone or as an adjunct
65
What are the SEs for MAO-Bi?
Nausea
Postural hypotension
Dyskinesia
Confusion (elderly)
66
When is amantadine given?
Only used as an adjuvant
67
What is the problem and resolution of amantadine?
Efficacy diminishes within a few months of continuous treatment- slowly withdrawing and reintroducing the drug may prolong effectiveness
68
Which initial treatment for PD offers the most improvement for motor symptoms?
Levodopa
69
Which initial treatment for PD offers the most improvement for ADLs?
Levodopa
70
Which initial treatment for PD offers the least motor complications?
Dopamine receptor agonists
MAO-Bi
71
Which initial treatment for PD offers the least adverse events?
L-dopa
MAO-Bi
72
Name the initial treatments in PD:
Ldopa
Dopamine r agonists
MAO-Bi
73
Name the adjuvant therapies in PD:
Dopamine r agonists
MAO-Bi
COMTi
Amantadine
74
Describe the adjuvant therapies affect on motor symptoms:
Dopamine r agonists- improvement
MAO-Bi- improvement
COMTi- improvement
Amantadine- no evidence of improvement
75
Describe the adjuvant therapies affect on ADLs:
Dopamine r agonists- improvement
MAO-Bi- improvement
COMTi- improvement
Amantadine- no evidence of improvement
76
Describe the adjuvant therapies affect on off time:
Dopamine r agonists- more off time
MAO-Bi- off time decreases
COMTi- off time decreases
Amantadine- no evidence report this
77
Describe the adjuvant therapies affect on adverse events:
Dopamine r agonists- intermediate risk
MAO-Bi- fewer SEs
COMTi- more SEs
Amantadine- no studies report this
78
Describe the adjuvant therapies on hallucinations:
Dopamine r agonists- more risk
MAO-Bi- lower risk
COMTi- lower risk
Amantadine- no studies report this
79
Describe the significance of missing a dose of Parkinson's medication:
Acute akinesia (inability to initiate movement)
Unable to communicate- more physically dependent on others
Loss of the ability to swallow, which increases risk of aspiration
Increase risk of falls, fractures
Neuroleptic- like malignant syndrome (very rare)
80
Describe the symptoms of neuroleptic-like malignant syndrome:
Fever, marked rigidity (increase respiratory causing hypoventilation), altered consciousness, leucocytosis and elevated creatine kinase
81
What is neuroleptic-like malignant syndrome caused by?
Caused by a sudden marked reduction in dopamine activity, either from withdrawal of dopaminergic agents or from blockage of dopamine receptors
More common in those with more severe PD symptoms or on high doses of Ldopa
82
Name non-motor symptoms that can be treated in PD:
Mental health
Autonomic dysfunction
N&V
Pain
Sleep disturbance and daytime sleepiness
Pressure sores
83
What is the first line treatment to treat depression in PD?
SSRIs
84
What is the treatment to help with dementia in PD?
Consider rivastigmine (licensed) or off label donepezil/ galantamine
Memantine last resort if these not tolerated
85
What is the treatment for confusion/ hallucinations in PD?
Quetiapine (1st line)
Clozapine (2nd line)- high risk drug specialist initiation, regular monitoring
86
What is the treatment for consitpation in PD?
Stimulant+ softener
87
What is the treatment for postural hypotension in PD?
Midodrine (1st line)
Fludrocortisone
88
What is the treatment for dysphagia in PD?
Medicines optimisation e.g dispersible tabs/ patches, build up drinks/ fluid thickener
89
What is the treatment for salivation/ drooling in PD?
Glycopyrronium
Hyoscine
90
What is the treatment for bladder dysfunction in PD?
Antimuscarinics e.g tolteradine, solefacin, oxybutinin
91
What is the treatment for ED in PD?
PDE5i e.g sildenafil
92
What is the treatment for N&V in PD?
Domperidone (1st line)
Consider cyclizine and ondansetron
NEVER metoclopramide/ prochlorperazine
Protein free snacks with L-dopa to decrease SEs e.g crackers
93
What is the treatment for pain in PD?
Follow pain ladder
Consider SEs e.g drowsiness consitpation, PPIs with NSAIDs- PPI can increase fracture risk
Physiotherpay
94
What is the treatment for sleep disturbances and daytime sleepiness in PD?
Sedatives- short term/occasional
Daytime sleepiness- modafinil- specialist use
95
What is the treatment for pressure sores in PD?
Barrier creams
Change position every 2 hours
Pressure relieving mattresses and cushions
96
What are some medicines management aspects for patients with PD:
Review all aspects of their care every 6-12 months
Prioritise med rec for parkinsons patients
Print medication timings on pharmacy labels
Avoid meds which worsen symptoms
97
Name some OTC and POM meds which can worsen PD symptoms:
Sympathomimetics (e.g pseudoephedrine) with MAO-B inhibitors
OTC antihistamines
CCBs- occasional extrapyrimindal SEs, frequency unknown so need to monitor patients
98
What are other considerations for patients with PD?
DVLA must be informed
Awareness of communications difficulties e.g quiet voice, slurred speech, decrease facial expressions
Encourage self admin and independence
Recommend cholecalciferol (vit D) as increase risk of osteoporosis
99
What is convulsive status epilepticus?
The prolonged convulsive seizure lasting 5 mins or longer or recurrent seizures one after the other without recovery in between
100
What is SUDEP?
Sudden Unexpected Death in Epilepsy
Most cases are thought to occur after a seizure
Normally happens unwitnessed at night whilst asleep
101
What are the risk factors for SUDEP?
Tonic seizures
Night time seizures
Not being on anti-epileptic drugs
102
What are the investigations carried out when diagnosing epilepsy?
EEG (electroencephalogram)- to support diagnosis
Blood tests, U&E, ECG
Neuroimaging (MRI,CT)
Genetic testing (informed consent)
Antibody testing- new onset epilepsy if AI encephalitis suspected
Neurophysiological assessment- evaluate learning disabilities
103
What are the different seizure types?
Focal
Generalised
Unknown
104
What are the different epilepsy types?
Focal
Generalised
Combo
Unknown
105
What are focal seizures?
Increase in neuronal activity originating and remaining in one hemisphere of the brain
These are then subdivided into level of awareness:
-simple focal seizures (no loss of consciousness)
-complex or focal dyscognitive seizures (impaired awareness)
106
What are the aware+ impaired motor symptoms of focal seizures?
Automatisms (repeated/automatic movement)
Atonic (loss of muscle tone)
Clonic (jerking)
Epileptic spasms (extending of muscles in trunk/ close to trunk)
Hyperkinetic (irregular big movements)
Myoclonic
Tonic (stiffness)
107
What are the aware+ impaired non-motor symptoms of focal seizures?
Autonomic (changes in HR, breathing, colour)
Behaviour arrest (blank stare, stop talking/moving)
Cognitive (confusion, slowed thinking, problems talking)
Emotional (sudden fear, dread, anxiety, pleasure)
Sensory (change in vision, taste, tingling, pain)
108
What is the name of seizures have a focal onset but spread to other areas of the brain?
Focal to bilateral tonic clonic seizures
109
What is the difference between generalised and focal seizures?
Level of awareness isn't looked into as much as with generalised the majority (not all) of these seizures have impaired awareness
110
What are the motor symptoms in generalised seizures?
Tonic
Myoclonus
Atonic
Clonic
Tonic-clonic (ONLY IN GENERALISED)
111
What is tonic movement?
Sustained increase in muscle contraction (tense and rigid muscles)
112
What is myoclonus movement?
Muscle twitching (can involve single or multiple muscle groups)
113
What is atonic movement?
Muscle becoming limp (opposite to tonic)
114
What is clonic movement?
Jerking, rhythmic twitching movements
115
What is tonic-clonic movement?
Where the seizure starts off in tonic phase (muscle rigidity, loss of consciousness, rest stops, involuntary crying) into clonic phase where you have muscle twitching- relaxing and contracting with loss of control of bladder and/or bowels
After the seizure, some people will get a post ictal phase
116
What is a post ictal phase in seizures?
They have trouble remembering what has happened, feels tired, confused
117
What is absence in the non-motor symptoms?
Vacant starting, movement stops
118
What is status epilepticus?
A prolonged convulsive seizure lasting 5 mins or longer OR recurrent seizures one after the other without recovery in between or more than 3 in an hour
119
What should occur if a patient has a seizure lasting longer than 5 mins in the community?
Airways, respiratory and cardiac function must be secured
Buccal midazolam (first line) or rectal diazepam
This should only be administered by a trained personnel or specified individually agreed protocol draw up by specialist and family members
120
What should occur if a patient has a seizure in the hospital from 0-5 mins?
The seizure is timed from onset
Establish IV access
Airways must be secured and regular monitoring of cardiac and respiratory function set up
Give high conc oxygen
Give high potency thiamine (if suggestion of alcohol abuse) e.g pabrinex
Give glucose if patient is hypoglycaemic
121
What should occur if a patient has a seizure in the hospital from 5-20 mins?
Get a bit more info about the patient- if pre-hospital benzo given
Start setting up other investigations to help manage e.g chest x-ray, CT scan
Give IV lorazepam (0.1mg/kg, max 4mg) or IV diazepam if lorazepam not available, alternative to this is buccal midazolam if no IV access, max of 2 doses to be given including pre-hospital dose
122
What should occur if a patient has a seizure in the hospital from 20-40 mins?
Alert anaesthetist and ICU- if pt isn't responding to treatment more intervention and care is needed
Give 2nd line IV anti epileptic drug (AED)- this will depend on hospital protocols in place (in NICE guidance they mention use of phenytoin, fosphenytoin sodium and phenobarbital, however newer AEDs such as SV/ levetiracetam can be used)
123
What should occur if a patient has a seizure in the hospital from 40-60 mins?
Transfer to ICU and general anaesthesia would be administered:
-propofol
-midzolam
-thiopental sodium
EEG monitoring needs to be set up when giving the anaesthetic
Anaesthetic continued for 12-24 hrs after last clinical/ electrographic seizure
124
What should occur if a monotherpy of a first anti-epileptic drugs fails?
Treatment should be switched to another:
-this is done by adding the 2nd and titrating up, while 1st is titrated down
If the second AED fails, then combo therapy is considered:
-only considered when monotherapy has been tried and not resulted in seizure freedom
125
What other the major points to be aware of with AEDs?
Suicidal behaviour- seek medical advice immediately
Anti-epileptic hypersensitivity syndrome- fatal- occur within 1-8 weeks of exposure
Vit D supplementation- if immobile/ low sun exposure
126
What is the guidance for prescribing sodium valproate in accordance to the MRHA safety alert?
All products containing SV or valproic acid should not be started and prescribed to patients under 55 years old (male and female) unless 2 specialists independently consider and document that other treatments are ineffective or not tolerated or unless there is compelling reasons that reproductive risks do not apply
Girls and women need to have a pregnancy prevention programme
127
What are the different categorises AEDs are put into?
Category 1,2,3
128
What do category 1 AEDs mean?
Patients should be maintained on a specific manufacturer brand
Don't switch
129
Name examples of category 1 AEDs:
Carbamazepine
Phenobarbital
Phenytoin
Primidone
130
What do category 2 AEDs mean?
The need for continued supply of a particular manufacturers product should be based on clinical judgement and consultation with pt/carer taking into account clinical and non clinical factors
131
Name examples of category 2 AEDs:
Clobazam
Clonazepam
Zonisamide
Eslicarbazepine
Lamotrigine
Perampanel
Oxcarbazepine
Rufinamide
Topiramate
SV
132
What do category 3 AEDs mean?
Usually unnecessary for pts to be maintained on specific manufactures brand as therapeutic equivalent is assured
Non clinical factors should be considered
133
What are clinical factors relating to changing AEDs?
Relating to seizure freq
Treatment history
Complications of having a breakthrough seizure e.g if driving as a job, could lose job
134
What are the non-clinical factors relating to changing AEDs?
Alternative medication could have a negative effect on pt/carer leading to anxiety, confusion, admin errors or changing adherence
135
Describe the withdrawal procedure for epilepsy patients on AEDs:
Aim for treatment to be discontinued in patients that have been seizure free for at least 2 years
The AED would be slowly withdrawn over 3 months, can be longer
Pts who are on barbiturates/ benzodiazepines, withdrawal must be much slower (6 months) due to withdrawal symptoms and potential seizure recurrence
If patients are on multiple AEDs one drug must be withdrawn at a time
136
Which 2 categories can AEDs be divided into?
Enzyme inducers
Non enzyme inducers
137
What are the contraceptives which are not effective in enzyme inducing AEDs?
Oral POP
Progesterone only implant
COC with less than 50mcg of ethinyestradiol
138
What should occur even after an enzyme inducing AED is withdrawn?
The enzyme induction persists for 4 weeks after and therefore contraception methods must be continued during this time
139
What is the guidance for emergency contraception with enzyme inducing AEDs?
1st- copper IUD (most effective)
2nd- Levonorgestrel 1.5 mg tabs- double dose should be taken to provide cover if copper IUD not suitable/ acceptable
3rd- ulipristal acetate 30mg tablet- effectiveness unknown
140
What are the contraceptives used in non-enzyme inducing AEDs?
Normal contraceptive methods can be used
Except for lamotrigine
141
Describe what measures need to be taken with contraception and lamotrigine?
COC can decrease the efficacy of lamotrigine (including glucornidation, decreases serum lamotrigine levels):
-increased risk of seizures 21 days
-increased risk of toxicity 7 day free period so continuous COC would be better
A POC desogestrel is also thought to potentially increase the exposure of lamotrigine
Additional barrier advised
142
What contraceptions are not thought to be affected by lamotrigine?
Levonorgestrel IUD
Copper IUD
Injection
Still need to monitor lamotrigine levels
143
What are the medications that should be monitored pre/during conception of AEDs?
Phenytoin
Oxcarbamazepine
Phenobarbital
Carbamazepine
Lamotrigine
Levetriacetam
144
What are the safest AEDs to use during pregnancy and why?
Lamotrigine and levetiracetam
They don't increase the risk of birth abnormalities compared to the general population
145
What are the AEDs that can affect babies during pregnancy and why?
Carbamazepine, phenobarbital, phenytoin or topiramate use during pregnancy increases the risk of physical birth abnormalities compared to the general population
Phenobarbital, topiramate or zonisamide during pregnancy increases the risk of baby born smaller than expected compared to general pop
146
What are the AEDs that can affect babies after pregnancy and why?
Phenytoin or phenobarbital taking during pregnancy can increase the risk of child having difficulty with learning and thinking ability (neurodevelopmental adverse effects)
147
What supplement does a pregnant women taking AED need to take and why?
5mg fold acid at least 1st trimester-often longer
To help prevent neural tube defects
148
What are the factors that should occur when a patient with epilepsy is pregnant?
Notify the UK Epilepsy and Pregnancy register- pt choice
Care of women with epilepsy when pregnant should be shared with the epilepsy specialist, 1º care team and obstetrician/midwife
Some patients need more frequent review based on certain factors
Detailed ultrasound at 18-20 weeks to scan for structural abnormality
149
What are the AEDs which can decrease bone health?
Enzyme inducers: carbamazepine, phenytoin, primidone
Non-enzyme inducers: SV
150
What is the NICE guidance for bone health with AEDs?
Monitor VitD levels of patients on these AEDs and supplementation to those at risk
Other tools such as DEXA/FRAX
Counselling on bone health important:
-healthy diet, healthy sun exposure, exercise, smoking and alcohol cessation
151
What are the rules when a patient has epilepsy and drives?
The patient must inform the DVLA if they have an epileptic seizure or blackout and stop driving immediately
-pts who fail to inform DVLA could face a fine of £1000 and be prosecuted
-informing DVLA can be done online or by filling in an FEP1 form
Tougher rules for bus, coach, lorry driving licenses
