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Clinical pharmacology and therapeutics > S12: antiepileptics & neuropharmacology > Flashcards

S12: antiepileptics & neuropharmacology Flashcards

1
Q

Define seizure

A

Transient occurrence of signs or symptoms due to abnormal electrical activity in the brain
Leads to a disturbance of consciousness, behaviour, emotion, motor function/sensation

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2
Q

Outline the most important excitatory and inhibitory neurotransmitters

A 
Glutamate + NMDA receptor: cation channel – lets in Na+ and Ca2+ and lets K+ out
-depolarises membrane 
-more likely to fire action potential 
GABA and GABAa receptor: Cl- channel 
-hyperpolarise membrane 
-less likely to fire action potential
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3
Q

Explain the pathology of seizures

A

Seizure = clinical manifestation of abnormal and excessive excitation & synchronisation of a group of neurones within the brain
Loss of inhibitory signals OR too strong an excitatory one
Imbalance can happen in any point in the brain & local changes can lead to generalised effects

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4
Q

What causes an imbalance in signals in a seizure?

A

Genetic differences in brain chemistry/receptor structure = genetic epilepsy syndromes
By exogenous activation of receptors = drugs
Acquired changes in brain chemistry = drug withdrawal, metabolic changes
Damage to any of these networks = strokes, tumours

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5
Q

Outline the symptoms and signs of seizures

A

Generalised seizures: loss of consciousness often with changes in muscle tone, tongue biting
Tonic-clonic seizures: initial hypertonic phase, followed by rapid clonus (shaking/jerking) of the limbs
Post-ictal period present (can last minutes up to hours)
Often an aura prior to seizure
May be more varied or subtle depending on type of seizure

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6
Q

Define epilepsy

A

Tendency toward recurrent seizures unprovoked by a systemic/neurological insult

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7
Q

Describe the diagnosis of an epilepsy syndrome

A

At least two unprovoked seizures occurring more than 24 hours apart
One unprovoked seizure & a probability of further seizures similar to the general recurrence risk after two unprovoked seizures

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8
Q

List different stimuli that can bring on seizures

A 
Photogenic 
Musicogenic 
Thinking
Eating
Hot water immersion 
Reading 
Orgasm 
Movement
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9
Q

Compare generalised seizures and focal seizures

A

Generalised seizures: originate at some point within and rapidly engage both hemispheres
Focal seizures: originate within networks limited to one hemisphere, may be discretely localised or more widely distributed

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10
Q

Describe provoked seizures

A

Seizure as a result of another medical condition
Examples include:
-drug use or withdrawal
-alcohol withdrawal
-head trauma & intracranial bleeding
-metabolic disturbances
Key is to treat both the seizure & underlying condition

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11
Q

List different diagnoses of seizures

A

Syncopal episodes
Cardiac issues (reflex anoxic seizures, arrythmias)
Movement disorders (Parkinson’s, Huntington’s)
TIAs
Migraines
Non-epileptic attack disorders

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12
Q

Describe the initial management of a seizure

A

A to E assessment
Look at a clock/start a timer (majority will self terminate without the use of drugs, wait 5 minutes)
Get some help

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13
Q

Define status epilepticus

A 
A seizure (of any variety) lasting 5 minutes or more, or multiple seizures without a complete recovery between them 
Medical emergency
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14
Q

Outline the pharmacological treatment for status epilepticus

A

0-5 minutes: full dose benzodiazepine
0-15 minutes: 2nd full dose benzodiazepine
15-45 minutes: 2nd line anti-epileptic = phenytoin, levetiracetam (consider IV thiamine if alcohol use)
45+ minutes: thiopentone/anaesthesia (with support)

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15
Q

Describe benzodiazepines

A

GABAa agonists
Increased Cl- conductance = more negative resting potential, less likely to fire
Work best when membrane positive (in seizures), no firing neurones = no more seizure
Be aware: addiction, cardiovascular collapse & airway issues
Other indications: anxiolytics, sleep aids & alcohol withdrawal

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16
Q

List benzodiazepine options for status epilepticus

A

Intravenous lorazepam
Diazepam rectally
Buccal/intranasal midazolam

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17
Q

Describe investigations for epilepsy

A

Electroencephalography:

  • record of electrical pattern of activity in brain
  • can be very useful, especially if an attack is caught whilst being recorded
  • many people without epilepsy have an abnormal EEG
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18
Q

Describe the role of imaging for epilepsy

A

MRI is the imaging of choice
May detect vascular or structural abnormalities that can account for epilepsy
Generally not required when there is a degree of confidence that there is a generalised epilepsy syndrome

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19
Q

List types of anti-epileptic drugs

A 
Carbamazepine 
Phenytoin 
Valproate 
Lamotrigine 
Levetiracetam 
Benzodiazepines for seizure termination
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20
Q

What is SUDEP?

A

Sudden unexplained death in epilepsy

More frequent in people with poor seizure control

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21
Q

Describe sodium channel blockade (in AEDs)

A

Blocking of Na+ channels in central neurones
Slows recovery of neurones from inactive to closed state
Reduces neuronal transmission

22
Q

Describe carbamazepine

A

Sodium channel blocker
Other indications: bipolar & sometimes chronic pain
Side effects: suicidal thoughts, joint pain & bone marrow failure

23
Q

Describe phenytoin

A

Sodium channel blocker
Exhibits zero order kinetics
Side effects: bone marrow suppression, hypotension & arrythmias (IV use)

24
Q

Describe sodium valproate

A

A mix of GABAa effects & sodium channel blockade

Specific side effects: liver failure, pancreatitis & lethargy

25
Q

Describe lamotrigine

A

Primarily a sodium channel blocker, may also affect calcium channels
Good for focal epilepsy
Used often when valproate contraindicated in generalised epilepsy

26
Q

Describe levetiracetam

A

Synaptic vesicle glycoprotein binder – stops the release of neurotransmitters into synapse and reduces neuronal activity
Option for focal seizures and generalised seizures
Safe in pregnancy

27
Q

List side effects of anti-epileptic drugs

A

Tiredness/drowsiness
Nausea and vomiting
Mood changes and suicidal ideation
Osteoporosis
Rashes, including steven johnson syndrome; most likely in carbamazepine or phenytoin
Many cause anaemia, thrombocytopenia or bone marrow failure

28
Q

Describe common DDIs of AEDs

A

Patients on AEDs and warfarin require close monitoring
Patients should not consume alcohol
Carbamazepine & phenytoin may decrease effectiveness of oral contraceptive pills & some antibiotics
Valproate can increase plasma concentration of other AEDs

29
Q

Describe the link between AEDs and CYP enzymes

A

AEDs can be both inducers and inhibitors of CYP enzymes
Therefore, interact with a wide variety of drugs, including each other
Inducers: phenytoin, carbamazepine & barbiturates
Inhibitors: valproate

30
Q

Describe the importance of family planning when female is on an AED

A

Some risk of congenital malformations with all AEDs
Valproate should not be prescribed to any woman of childbearing age unless they meet the conditions of a pregnancy prevention programme
Lamotrigine and levetiracetam are the safest

31
Q

Describe epilepsy and driving

A

Need to ask all patients with seizures about driving
Temporarily lose license and needed to be seizure free for one year before reapplying
Patients responsibility to inform DVLA

32
Q

Outline the basic classification of seizures

A

Focal onset seizures:
1) Aware – motor, somatosensory/psychic symptoms, consciousness not impaired
2) Impaired awareness – consciousness affected and may be confused
Generalised onset seizures:
1) Tonic-clonic – jerking and shaking as muscles relax and contract
2) Myoclonic – muscle jerking
3) Absence – abrupt loss of awareness
4) Atonic – loss of muscle tone, often collapse

33
Q

Describe the pathophysiology of Parkinson’s disease

A

Loss of dopaminergic neurones in substantia nigra results in reduced inhibition in neostriatum
Loss of inhibition in neostriatum allows increased production of acetylcholine
Chain of abnormal signalling leads to impaired mobility

34
Q

List clinical features of Parkinson’s disease

A 
Tremor 
Rigidity 
Bradykinesia 
Postural instability
Non-motor manifestations: mood changes, hallucinations, pain, urinary symptoms & sweating
35
Q

List drug classes used to treat Parkinson’s disease

A 
Levodopa 
Levodopa with COMT inhibitor 
Dopamine receptor agonists 
MAOI type B inhibitors 
Anticholinergics 
Amantadine
36
Q

Describe levodopa (L-DOPA)

A

Dopamine precursor which allows it to cross BBB, must be taken up by dopaminergic cells in the SN to be converted to dopamine -> fewer remaining cells results in less reliable effect
Used in combination with a peripheral dopa decarboxylase inhibitor – reduced dose required, reduced side effects & increased levodopa reaching brain

37
Q

Describe levodopa pharmacokinetics

A

Oral administration
Absorbed by active transport (in competition with amino acids)
90% inactivated in intestinal wall

38
Q

List side effects and contraindications of levodopa

A

Side effects: N&V, anorexia, hypotension, psychosis, tachycardia
Contraindications: melanoma, diabetes, psychotic disorder, suicidal tendencies

39
Q

List DDIs of levodopa

A

Pyridoxine (vitamin B6) increases peripheral breakdown of levodopa
MAOIs risk hypertensive crisis
Many antipsychotic drugs block dopamine receptors & parkinsonism is a side effect

40
Q

Describe COMT inhibitors

A

Always use with levodopa
Reduces peripheral breakdown of levodopa
Prolongs to motor response to levodopa

41
Q

List examples of dopamine receptor agonists

A

Ropinirole
Amantadine
Rotigotine
Apomorphine – only for patients with severe motor fluctuations

42
Q

List side effects and contraindications of dopamine receptor agonists

A

Side effects: impulse control disorder, sedation, confusion, hallucination, hypotension, seizures
Contraindications: epilepsy, gastric ulcer

43
Q

Describe monoamine oxidase B inhibitors

A

Rasagaline, selegiline
Enhance dopamine
Prolong action of levodopa but can be used alone
Smooth out motor response

44
Q

Describe anticholinergics

A

Orphenadrine, procyclidine
Minor role in treatment of PD – effectiveness won’t decrease as lose dopaminergic neurones
Side effects: confusion, drowsy, bradykinesia, anticholinergic symptoms
Contraindications: acute porphyrias, GI obstruction

45
Q

Describe amantadine

A

Mainly effective for levodopa induced dyskinaesia

Few side effects: hallucinations, confusion

46
Q

Describe clinical features of myasthenia gravis

A

Fluctuating, fatigable, weak skeletal muscle

  • extraocular muscles
  • bulbar involvement: dysphagia, dysphonia & dysarthria
  • limb weakness: proximal symmetric
  • respiratory muscle involvement
47
Q

Outline the therapeutic management of myasthenia gravis

A 
Acetylcholinesterase inhibitors 
Corticosteroids – decrease immune response 
Steroid sparing – azathioprine 
IV immunoglobulin 
Plasmapheresis
48
Q

Describe acetylcholinesterase inhibitors

A 
Pyridostigmine, neostigmine 
Enhance neuromuscular transmission 
Skeletal & smooth muscle 
Excess dose can cause depolarising block
Muscarinic side effects – SSLUDGE
49
Q

List the muscarinic side effects

A 
Salivation 
Sweating
Lacrimation 
Urinary incontinence 
Diarrhoea
GI upset and hypermotility 
Emesis
50
Q

Name 4 types of generalised seizures

A

Absence
Myoclonic
Tonic-clonic
Atonic

Clinical pharmacology and therapeutics (14 decks)

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