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MSRA Content > BASIC - NEUROLOGY > Flashcards

BASIC - NEUROLOGY Flashcards

1
Q

Indications of carbamazepines?

A
  • Epilepsy – 1st line for focal seizures and primary generalised tonic-clonic seizures
  • Trigeminal neuralgia - 1st line to control pain and reduce frequency/severity
  • Bipolar disorder - option
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2
Q

Mechanism of carbamazepines?

A
  • Inhibit neuronal sodium channels, stabilising resting membranes potentials and reducing neuronal excitability
  • Inhibit spread of seizure activity in epilepsy
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3
Q

Side effects of carbamazepines?

A
  • N&V
  • Dizziness and ataxia
  • Oedema & hyponatraemia
  • Bone marrow suppression (agranulocytosis)
  • Hypersensitivity – 10% (Mild maculopapular skin rash)
  • Antiepileptic hypersensitivity syndrome – 1 in 5000, mortality 10%
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4
Q

Contraindications of carbamazepines?

A
  • AV conduction abnormalities (unless paced)
  • History of bone marrow depression
  • Prior antiepileptic hypersensitivity syndrome
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5
Q

Cautions of carbamazepines?

A
  • Pregnancy – need high dose folic acid

- Cardiac, hepatic and renal disease

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6
Q

Interactions of carbamazepines?

A
  • Induces CYP450 enzymes
  • Metabolised by CYP450 enzymes
  • Efficacy reduced by drugs that lower seizure threshold
    o SSRIs, TCAs, antipsychotics and tramadol
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7
Q

Dosing of carbamazepines?

A
  • Oral or rectal only
  • Started at low dose (100-200mg OD/BD) and increased gradually to maximum of 1.6g/day
  • Treatment must be withdrawn gradually over at least 4 weeks – seizure recurrence risk
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8
Q

Communication to patient of carbamazepines?

A
  • Must not drive until seizure free for 12 months

- Cannot drive 6 months after changing or stopping treatment

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9
Q

Monitoring of carbamazepines?

A
  • Report any unusual symptoms
  • Plasma concentration for response (4-12mg/litre) measured after 2 weeks
  • FBC, U&Es, LFTS may be beneficial
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10
Q

Indications of phenytoin?

A
  • Control seizures in status epilepticus when benzodiazepines are ineffective
  • Reduce frequency of focal or generalised seizures in epilepsy (if other drugs not suitable)
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11
Q

Mechanism of phenytoin?

A
  • Bind to neuronal sodium channels in inactive state, prolonging inactivity and preventing Na influx
  • Prevents drift of membrane potential from resting to threshold value
  • Reducing neuronal excitability
  • Inhibit spread of seizure activity in epilepsy
  • Similar effect seen in Purkinje fibres – account for antiarrhythmic and cardiotoxic effects
  • Low therapeutic index
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12
Q

Side effects of phenytoin?

A
  • Long-term – skin coarsening, acne, hirsutism and gum hypertrophy
  • Cerebellar toxcitiy (ataxia, nystagmus, discoordination), impaired cognition
  • Haematological disorders (folic acid metabolism)
  • Osteomalacia (vitamin D metabolism)
  • Hypersensitivity and Antiepileptic hypersensitivity syndrome – 1 in 5000, mortality 10%
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13
Q

Contraindications of phenytoin?

A
  • 2nd and 3rd degree heart block

- Sinus bradycardia

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14
Q

Cautions of phenytoin?

A
  • Dose reduction in hepatic impairment

- Pregnancy – need high dose folic acid (foetal hydantoin syndrome – craniofacial abnormalities and reduced IQ)

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15
Q

Interactions of phenytoin?

A
  • Induces CYP450 enzymes
  • Metabolised by CYP450 enzymes
  • Efficacy reduced by drugs that lower seizure threshold
    o SSRIs, TCAs, antipsychotics and tramadol
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16
Q

Dosing of phenytoin?

A
  • Status epilepticus – IV loading dose 20mg/kg (max 2g), followed by maintenance dose 100mg 6-8 hourly
  • Chronic epilepsy – 150-300mg daily
  • Treatment must be withdrawn gradually
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17
Q

Communication to patient of phenytoin?

A
  • Must not drive until seizure free for 12 months

- Cannot drive 6 months after changing or stopping treatment

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18
Q

Monitoring of phenytoin?

A
  • Recommends FBC before treatment
  • Plasma phenytoin concentrations measured immediately before next dose (10-20mg/L) – if needed, make small change to dose
  • After dose change, wait 7 days before repeating blood tests
  • Monitor BP, ECG during IV treatment
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19
Q

Indications of sodium valproate?

A
  • Epilepsy – 1st choice in generalised or absence seizures and option in focal
  • Bipolar disorder – Option for acute treatment of manic episodes and prophylaxis against recurrence
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20
Q

MEchanism of sodium valproate?

A
  • Weak inhibitor of neuronal Na channels, stabilising resting membrane potentials and reducing neuronal excitability
  • Increases content of GABA, principal inhibitory neurotransmitter
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21
Q

Side effects of sodium valproate?

A
  • Nausea, gastric irritation and diarrhoea
  • Tremor, ataxia
  • Behavioural disturbances
  • Thrombocytopenia
  • Transient rise in liver enzymes
  • Hypersensitivity reactions
    o Hair loss – regrowth curlier than original hair
  • Rare – pancreatitis, hepatic dysfnction, bone marrow failure, antiepileptic hypersensitivity syndrome
22
Q

Contraindications of sodium valproate?

A

o Suspected mitochondrial disorder

o Personal or family history of hepatic dysfunction

23
Q

Cautions of sodium valproate?

A
  • Avoid in women of child-bearing age (particularly first trimester and conception)
    o Teratogenic - risk of foetal abnormalities
    o Only used if on contraception and other treatment not suitable
  • Avoid in hepatic impairment
  • Dose reduction in severe renal impairment
24
Q

Interactions of sodium valproate?

A
  • Inhibits CYP450 enzymes
  • Metabolised by CYP450
  • Efficacy reduced by drugs that lower seizure threshold
    o SSRIs, TCAs, antipsychotics and tramadol
25
Q

Dosing of sodium valproate?

A
  • Sodium valproate – prescribed for epilepsy – 600mg
  • Valproic acid – used in bipolar disorders – 750mg
  • Withdraw over 4 weeks gradually
26
Q

Communication to patient of sodium valproate?

A
  • Must not drive until seizure free for 12 months
  • Cannot drive 6 months after changing or stopping treatment
  • Recognised symptoms of liver dysfunction and blood abnormalities and seek advice immediately
  • Contraception
    o Pregnancy excluded before starting treatment
    o Need effective contraception before use and during treatment
27
Q

Monitoring of sodium valproate?

A
  • LFT before and during 6 months of treatment
28
Q

Names of dopaminergic Parkinsons’ drugs?

A

Levodopa (co-careldopa, co-beneldopa), ropinirole, pramipexol
Co-careldopa = Levodopa + benserazide
Co-beneldopa = Levodopa + carbidopa

29
Q

Indications of Levodopa?

A
  • Early Parkinson’s disease when dopamine agonoists (ropinirole, pramipexol) preferred over levodopa
  • Later Parkinson’s disease – levodopa and add on option of dopamine agonists
  • Secondary Parkinsonism
30
Q

Mechanism of Levodopa?

A
  • In Parkinson’s disease, deficiency of dopamine in nigrostriatal pathway
    o Causes basal ganglia to exert greater inhibitory effects on thalamus which reduces excitatory input to motor cortex
    o Generates bradykinesia, rigidity
  • Treatment increases dopaminergic stimulation to striatum
    o Dopamine does not cross BBB so Levodopa is a precursor that enters brain
    o Ropinirole and pramipexol are selective agonists for D2 receptor in striatum
31
Q

Side effects of Levodopa?

A
  • Nausea, drowsiness, confusion, hallucinations and hypotension
  • Levodopa
    o Weaning off effect – patient’s symptoms worsen towards end of dose
     Gets worse over time – need to increase dose/frequency but may lead to dyskinesias at beginning – on-off effect
32
Q

Interactions of Levodopa?

A
  • Levodopa given with peripheral dopa-decarboxylase inhibitor to reduce conversion to dopamine outside brain
  • Do not combine with antipsychotics or metoclopramide – contradictory effects on dopamine receptors
33
Q

Prescription of Levodopa?

A
  • Take at times that produce best symptom control

- Never stop abruptly – risk of neuroleptic malignant syndrome

34
Q

Monitoring of Levodopa?

A
  • Blood pressure
35
Q

Names of anticholinergics used in neurology?

A

Procyclidine, trihexyphenidyl

36
Q

Indications of procyclidine?

A
  • Parkinsonism, extrapyramidal symptoms (not tardive dyskinesia)
  • Acute dystonia
37
Q

Mechanism of procyclidine?

A
  • Reducing effects of relative central cholinergic excess that occurs due to dopamine deficiency
38
Q

Side effects of procyclidine?

A
  • Constipation
  • Dry mouth
  • Urinary retention
  • Blurred vision
39
Q

Contraindications of procyclidine?

A
  • GI obstruction

- Myasthenia gravis

40
Q

Cautions of procyclidine?

A
  • CV disease
  • Hypertension
  • Prostatic hypertrophy
  • Renal and Hepatic impairment
41
Q

Interactions of procyclidine?

A
  • Additive effects to antimuscarinics
42
Q

Prescription of procyclidine?

A
  • 2.5mg TDS oral initially – Parkinsonism/Extrapyramidal symptoms
  • 5-10mg IM/IV – acute dystonia
  • Lower end of range of medication for elderly
43
Q

Names of triptans?

A

Sumatriptan, almotriptan, eletriptan, rizatriptan, zolmitriptan

44
Q

Indications of triptans?

A
  • Acute migraine

- Acute Cluster headache

45
Q

Mechanism of triptans?

A
  • Agonist of serotonin receptors (5-HT 1B&1D) in blood vessels (causing constriction) and never endings in brain
  • Inhibition of pro-inflammatory neuropeptides
46
Q

Side effects of triptans?

A
  • Recurrence of migraine
  • Dizziness, dyspnoea, flushing
  • Nausea, vomiting
  • Coronary artery spasm
47
Q

Contraindications of triptans?

A
  • Coronary vasospasm
  • Ischaemic heart disease
  • Moderate and severe hypertension
  • Previous CVA/MI/TIA
  • Prinzmetal angina
48
Q

Cautions of triptans?

A
  • Conditions predisposing to CAD

- History of seizures

49
Q

Interactions of triptans?

A
  • Risk of serotonin syndrome increased with SSRIs, lithium, NaSSA, methadone, tramadol
50
Q

Prescription of triptans?

A
  • Sumatriptan can be given OTC if evidence of prescribed before
  • Initially oral 50-100mg for 1 dose, followed by 50-100mg after at least 2 hours (if migraine recurs, not for same attack)
  • Either oral, intranasal
51
Q

Communication to patient in triptans?

A
  • Take as soon as migraine starts

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