Multiple Sclerosis Flashcards

1
Q

What is MS?

A

An inflammatory demyelinating disorder of the CNS with plaques disseminated in time and space

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2
Q

What is the gender ratio of MS?

A

F:M 3:1

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3
Q

When does MS usually present?

A

30s and 40s

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4
Q

What are the clinical courses of MS?

A

Relapsing remitting
Secondary progressive
Progressive relapsing
Primary progressive

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5
Q

What are the clinical features of MS?

A
Pyramidal dysfunction
Optic neuritis
Sensory symptoms
Lower urinary tract dysfunction
Cerebellar & brain stem features
Cognitive impairment
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6
Q

What does pyramidal dysfunction in MS cause?

A

Increased tone, spasticity, weakness, effects extensors of upper limbs and flexors of lower limbs

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7
Q

Describe optic neuritis in MS

A

Painful visual loss for 1-2wks. Most improve in time.

RAPD present

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8
Q

What sensory symptoms occur in MS?

A
Pain
Paraesthesia
Dorsal column loss (proprioception & vibration)
Numbness
Trigeminal neuralgia
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9
Q

What occurs due to cerebellar dysfunction in MS?

A
Ataxia
Intention tremor
Nystagmus
Past pointing
Pendular reflexes
Dysdiadokinesis
Dysarthria
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10
Q

What palsys occur due to brain stem dysfunction in MS?

A

R VI palsy-diplopia

R VII palsy- facial weakness

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11
Q

What lateral gaze disorder occurs due to MS?

A

Internuclear ophthalmoplegia

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12
Q

What occurs in internuclear ophthalmoplegia in MS?

A
Demyelination of medial longitudinal fasciculus
Distortion of binocular vision
Failure of adduction-diplopia
Nystagmus in abducting eye
Lag
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13
Q

What urinary tract problems occur due to MS?

A
Frequency
Nocturia
Urgency
Urge Incontinence
Retention
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14
Q

How is fatigue treated in MS?

A

Amantadine
Modafinil if sleepy
Hyperbaric oxygen

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15
Q

What is the diagnostic criteria for MS?

A

At least 2 episodes suggestive of demyelination
Dissemination in time and space
McDonald criteria

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16
Q

What should be on the DDx in suspected MS?

A
Vasculitis
Granulomatous disorder
Vascular disease 
Structural lesion
Infection
Metabolic disorder
17
Q

How is MS diagnosed?

A
Clinical
MRI
CSF
Neurophysiology
Blood tests
18
Q

Which blood tests should be done and come back as -ve to aid in a MS diagnosis?

A
PV, FBC, CRP
Renal liver bone profile
Auto-ab screen
Borellia, HIV, syphilis serology
B12 and folate
19
Q

Will oligoclonal bands be present or absent in CSF?

A

Present, but caution when absent

20
Q

How is a mild acute exacerbation of MS treated?

A

Symptomatic treatment

21
Q

How is a moderate acute exacerbation of MS treated?

A

Oral steroids

22
Q

How is a severe acute exacerbation of MS treated?

A

Admit/IV steroids

23
Q

What is the symptomatic treatment for pyramidal dysfunction?

A

Physiotherapy
OT
Anti-spasmodic agent: baclofen, tizanidine, botulinum toxin, intrathecal baclofen/phenol

24
Q

How are sensory symptoms treated in MS?

A
Anti-convulsant e.g. gabapentin
Anti-depressant e.g. amitriptyline
Tens machine
Acupuncture
Lignocaine infusion
25
Q

How is lower urinary tract dysfunction treated in MS?

A

Bladder drill
Anti-cholinergics e.g. oxybutynin
Desmopressin
Catheterisation

26
Q

What pathologies occur in urinary tract dysfunction in MS?

A

Increased tone at bladder neck
Detrusor hypersensitivity
Detrusor sphyncteric dyssenergia

27
Q

What is the first line therapy in MS?

A

Interferon Beta – Avonex, Rebif, Betaseron, Extavia
Glitiramer Acetate (Copaxone)
Tecfedira

28
Q

What is the second line therapy in MS?

A

Monoclonal antibody- Tysabri, Lemtrada

Fingolimod

29
Q

What is the third line therapy in MS?

A

Mitoxantrone

30
Q

Describe Interferon beta and copaxone

A
Injectable agents-SC,IM
Decrease relapse rate by 1/3
Decrease severity of relapses by 50%
Effect on disability
All comparable re efficacy
31
Q

Describe Tecfidera

A

Oral agent
First line in RR MS
44% reduction in relapse rate

32
Q

Describe Fingolimod

A

Oral agent
Sphingosine 1-phosphate (S1P) modulator
>50% reduction in relapse rate
Significant effect on disease progression

33
Q

What is the role of alpha4beta1 integrins in MS?

A

Trans-endothelial migration of activated T-cells across BBB in EAE mediated by integrins

34
Q

What is the inflammatory cascade in MS?

A

Immune cells pass through BBB
Cells may re-activate and produce cytokines
Cells mount AI attack against myelin

35
Q

What is the MOA of Tysabri?

A

Leucocyte migration from blood to tissue
Leucocyte priming and activation
Modulation of leucocyte apoptosis

36
Q

What virus are MS sufferers at risk of contracting if they take Tysabri?

A

Progressive multifocal leukoencephalopathy (PML) caused by JC virus

37
Q

Describe mitoxantrone

A

For relapsing progressive MS
12 infusions over 2 years
Cardiac toxicity dose related