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2nd year > Multiple sclerosis > Flashcards

Multiple sclerosis Flashcards

1
Q

What are the cells involved in MS?

A

B and T lymphocytes

natural killer cells

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2
Q

pathogenesis of MS

A

immune cells pass through BBB
B and T cells attack oligodendrocytes
oligodendrocytes turn on the apoptotic pathway which activates microglia
microglia attack myelin exposing the axon
axon can degenerate - cerebral atrophy

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3
Q

cerebral atrophy

A

when the axon degenerates

occurs in progressive MS

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4
Q

pathogenesis of MS remissions

A

remyelination on some occasions

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5
Q

what areas of the CNS are affected by MS?

A
  • corpus callosum
  • cerebellum
  • pons
  • medulla
  • midbrain
  • spinal cord
  • optic nerve which is heavily myelinated
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6
Q

sclerosis

A

plaque formation

these cause the symptoms

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7
Q

for a diagnosis of MS to be made what has to be apparent?

A

lesions dispersed in time and space - multiple lesions and symptoms occurring at more than 1 time

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8
Q

what are the classifications of MS?

A

benign MS
relapsing remitting MS
secondary chronic progressive MS
primary progressive MS

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9
Q

what are the causes of MS?

A

genes

environmental triggers

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10
Q

Genetics of MS

A

IL-7 gene associated with MS
disease susceptibility genes
increased susceptibility when certain genes are triggered by environmental factors
polygenic
increased frequency of particular alleles within the MHC region of chromosome 6

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11
Q

environmental causes of MS

A 
further from equator increases risk 
lack of sun exposure/ vitamin D
pathogens - EBV
chemicals
smoking 
diet 
trauma
obesity
female
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12
Q

diagnosis of MS

A

history
dissemination in time and place
examination - reflexes and fundoscopy to check for optic neuritis
clinical tests

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13
Q

what clinical tests are involved in MS diagnosis?

A

MRI of brain and spine - gadolinium enhancement
lumbar puncture - get info on inflammation
visual evoked potentials - VEP

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14
Q

optic neuritis

A

inflammation of optic nerve

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15
Q

lumbar puncture for MS

A

carry out electrophoresis
compare proteins in CSF with serum
check for oligoclonal bands

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16
Q

oligoclonal bands

A

presence in CSF but not serum = inflammation of CNS and strongly indicates MS

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17
Q

VEP

A

used to identify inflammation of optic nerve
sends radiation through optic nerve and picked up by electrodes placed on back of the head - occipital lobe
P100 wave determines delay in optic nerve transmission suggesting demyelination

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18
Q

what is the diagnostic criteria for MS called?

A

McDonald’s diagnostic criteria

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19
Q

McDonald’s diagnostic criteria

A

clinical attacks
MRI scan
oligoclonal bands

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20
Q

1 episode of MS attack

A

clinically isolated syndrome

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21
Q

Clinically isolated syndrome

A

evidence of inflammation at 1 point in time but not disseminated across multiple time periods
can go on to develop/ become MS when other episodes occur

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22
Q

what are the differential diagnoses of MS?

A 
SLE
sarcoidosis
primary sjogren's syndrome
lyme borreliosis
cerebrovascular disease
meningovascular syphilis 
AIDs 
transverse myelitis 
spinal cord stroke 
optic atrophy 
vasculitis 
Devic's disease
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23
Q

Devic’s disease

A

neuromyelitis optica
affects optic nerve and spinal cord
blood and CSF tests to diagnose these specifically

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24
Q

other tests to exclude differential diagnoses

A 
CXR
ANA
ANCA
ENA
dsDNA
vitamin B12 
folate 
anti-aquaporin 4 
anti-mog antibodies 
TPHA/ VDRL
bone profile 
serum ACE
serology for borrelia burgdorferi
HIV
HTLV-1 serology 
genetic tests for hereditary ataxia
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25
Q

treatments for MS

A 
steroids 
beta interferons 
copaxone - disease modifying drugs 
tablets 
depleters 
B cell therapy 
stem cell transplants 
monoclonal antibodies
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26
Q

Depleters

A

cladribine

alemtuzumab

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27
Q

B cell therapy

A

ocreluzumab

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28
Q

Stem cell transplants

A

haematopoietic stem cells

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29
Q

holistic approach to MS treatment

A 
physio
speech and language therapist 
MS specialist nurse 
occupational therapist
doctor 
MS administrator 
social services
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30
Q

symptom management of MS

A 
self-treatment 
bladder and bowel dysfunction 
relationship difficulties 
mood/ anger difficulties 
frustration 
spasticity 
fatigue 
pain
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31
Q

bladder and bowel dysfunction

A

catheter and bowel irrigation

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32
Q

relationship difficulties

A

high divorce

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33
Q

mood/ anger difficulties

A

counsellors
psychologists
anti-depressants

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34
Q

treatment of fatigue

A

education

sleep service

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35
Q

when are steroids used

A

during relapse to aid recovery

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36
Q

steroid treatment

A

short course
oral or IV if very severe
not very effective long-term and too many risks/ side effects

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37
Q

Oral steroid treatment

A

100mg methyprednisolone 5 times a day for 5 days

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38
Q

IV steroid treatment

A

3-5 days 1g of methyprednisolone per day

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39
Q

when should steroids be avoided?

A

when there is an infection that has precipitated the relapse due to the immunosuppressive effect of steroids
deal with infection first and then administer steroids if needed

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40
Q

risks associated with steroids

A

can cause osteoporosis which has an even higher fracture risk in MS due to ataxia increasing risk of falls

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41
Q

disease modifying drugs

A

interferons and copaxone

copaxone is safe in pregnancy

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42
Q

how do disease modifying drugs work?

A

manipulate immune system

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43
Q

administration and doses of disease modifying drugs

A

long-term
injection admin
baseline treatment

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44
Q

side effects of disease modifying drugs

A

flu-like symptoms

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45
Q

efficacy of disease modifying drugs

A

reduce rate of relapse by 50%

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46
Q

oral drugs

A

terifluonimide
techfidera
fingolimod
cladribine

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47
Q

terifluonimide

A

good long-term treatment

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48
Q

techfidera

A

higher efficacy

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49
Q

fingolimod

A

traps lymphocytes in peripheral lymph nodes so they cannot enter CNS, but can still respond to infection

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50
Q

cladribine

A

wipes out T cell population

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51
Q

monoclonal antibodies

A

targeted

the more humanised the more tolerated they are

52
Q

examples of monoclonal antibodies used for MS

A

Tysabri

campath/ alemtuzumab

53
Q

Tysabri

A

blocks migration of T cells into CNS - reduces relapse rate by 70-80%

54
Q

campath/ alemtuzumab

A

binds to CD8 receptor on T cells and kills this line of T cells

55
Q

Depleters examples

A

cladribine
campath/ alemtuzumab
tysabri
ocreluzumab

56
Q

how does Ocreluzumab work?

A

targets B cells

57
Q

treatment programme

A 
start treatment ASAP
aim to slow and reduce progression 
very expensive 
bluetec system used to determine who can be treated under NHS 
need to consider financial implications as treatments are long term 
benign phenotype may not need treatment
discussions with patient are essential 
risk stratification needed
58
Q

risks of treatments

A

thyroid disease
increased susceptibility to infections
potentially need to stop therapy if causing more harm than good
there is decreased immune surveillance

59
Q

issue with stem cell therapy

A

cannot just replace oligodendrocytes as MS is widespread

60
Q

which stem cells can be used?

A

embryonic
those from developing brain tissue
haematological stem cells

61
Q

how does the stem cell therapy work?

A

wipe out all bone marrow using chemotherapy and transplant stem cells into bone marrow to remove the self-attacking lymphocytes and the new cells differentiate into neurones and oligodendrocytes

62
Q

when can stem cell therapy be used?

A

for rapidly progressing aggressive MS - autologous haematopoietic stem cell transplant will be funded by NHS

63
Q

risks of autologous haematopoietic stem cell transplant

A

while immune cells regrow and develop there is a 2% risk of mortality from superimposed infections

64
Q

other treatments

A

cannabinoids - improvement of spasticity but not disease modifying
lifestyle changes to improve symptoms

65
Q

what lifestyle changes can be made to improve symptoms?

A

stop smoking
reduce salt intake
weight loss
sun exposure increase - vitamin D

66
Q

future treatments of progressive MS

A

current drugs - simvastatin, phenytoin, amiloride, riluzole
don’t require extensive trialling
potential for combo therapies

67
Q

where is MS most and lead common?

A

most = North america and europe
least = sub-saharan africa and east asia
higher rates in colder climates and lower rates in hotter climates

68
Q

moving during early childhood

A

adopt incidence rate of country they moved to

69
Q

moving in late childhood/ early adulthood

A

retain incidence rate of country moved from

70
Q

peak incidence of onset

A

late 20s, early 30s

71
Q

prognosis of MS

A

reduces life expectancy by 5-10 years

72
Q

average age at diagnosis

A

30

73
Q

symptoms of MS

A 
upper motor neurone symptoms 
fatigue 
cognitive impairment 
depression 
unstable mood 
nystagmus 
optic neuritis 
diplopia 
dysarthria 
dysphagia 
weakness
mood changes 
memory changes 
spasticity 
spasms
ataxia
disease of cerebellum 
pain
hypoethesias 
paraesthesias 
incontinence of faeces or urine 
sexual dysfunction 
diarrhoea 
constipation
urinary frequency
urinary retention
transverse myelitis
74
Q

what are the different types of MS?

A

clinically isolated syndrome - may develop into MS
relapsing remitting MS
secondary progressive MS
primary progressive MS

75
Q

neuropathic pain

A 
burning 
nerve pain 
tingling 
tight cramp
very different to MSK
different drugs to treat than MSK
76
Q

general management

A 
lifestyle modifications 
exercises and stretching 
strengthening exercises 
balance training 
energy conservation training 
environmental adaptations
equipment 
medications
77
Q

drugs for MS

A

symptom management
slowing progression using disease modifying therapies
for RRMS and PPMS

78
Q

disease modifying therapies

A

9
aim to reduce number of relapses
expensive
significant side effects

79
Q

what is the treatment for spasticity and muscle spasms

A

intrathercal baclofen

uses an implant pump

80
Q

what do microglia do in MS

A

macrophages of CNS
cytokine release
phagocytosis
antigen-presentation

81
Q

MS plaques

A

formed from continued immune damage to oligodendrocytes

82
Q

what make up plaques?

A

myelin reactive T cells, B cells and macrophages

83
Q

what is gliosis

A

scarring of CNS

84
Q

where can plaques be found?

A

optic nerve
spinal cord
brainstem
cerebellum
juxtacortical white matter - near cerebral cortex
periventricular white matter - near ventricular system

85
Q

most common age of presentation for MS

A

20-40

86
Q

risk factors for MS

A 
genetics
viral infections - EBV
geographical latitude - further from the equator increases risk 
sunlight exposure
obesity in adolescence 
smoking 
gender
87
Q

what is lhermitte phenomenon?

A

uncomfortable electric-shock feeling triggered by neck flexion
common clinical manifestation of MS

88
Q

visual symptoms of MS

A 
visual loss
blurred vision
pain behind eye on movement
scotoma 
poor colour differentiation 
relative afferent pupillary defect 
optic nerve swelling on fundoscopy
89
Q

what is transverse myelitis

A

focal inflammation within the spine

90
Q

supporting lab tests for MS diagnosis

A 
FBC
CRP
LFTs
U&Es
bone profile -calcium 
glucose
HBA1c
TFTs - thyroid
haematinics
HIV test
91
Q

how does teriflunomide work?

A

inhibits pyrimidine synthesis

antiproliferative and anti-inflammatory

92
Q

how does alemtuzumab work?

A

monoclonal antibody targeting CD52 found on many immune cells

93
Q

how does cladribine work?

A

purine nucleoside analogue
has cytotoxic effects of B and T lymphocytes
prevents DNA synthesis

94
Q

how does Natalizumab work?

A

monoclonal antibody against integrin preventing migration of leucocytes across BBB

95
Q

treatment for bladder dysfunction

A

anticholinergics - oxybutynon
botox
catheterisation

96
Q

treatment for bowel dysfunction

A

dietary changes
laxatives
enemas

97
Q

treatment for depression in MS

A

duloxetine if neuropathic pain or fatigue

SSRIs

98
Q

treatment for fatigue

A

non-pharmacological interventions, such as physical activity

modafinil - wakerfulness promoting agent

99
Q

treatment for gait impairment

A

occupation therapy and physio, walking aids, wheelchairs

100
Q

treatment for MS pain

A

amitriptyline
gabapentin
pregabalin

101
Q

treatment for spasticity

A

physiotherapy
baclofen
botox

102
Q

what are dawsons fingers

A

radiographic feature of demyelination
periventricular demyelinating plaques seen perpendicular to body of lateral ventricles
causes by inflammation

103
Q

causes of relative afferent pupil defect with visual loss

A

compression of optic nerve
retinal detachment
ischaemic optic neuropathy
central retinal artery occlusion

104
Q

causes of relative afferent pupil defect without visual loss

A 
glaucoma
severe retinal disease
MS
optic neuritis 
macular degeneration 
mass/ tumour causing compression
giant cell arteritis
105
Q

causes of cerebellar symptoms

A 
infarction 
TIA
head trauma
oedema
haemorrhage
infections
medications
toxins 
poisons
alcohol
intracranial tumours
vitamin deficiencies 
paraneoplastic cerebellar degeneration 
genetic conditions
MS
wilson's disease
106
Q

indications for self-catheterisation

A 
neurological bladder dysfunction 
urinary retention 
incontinence due to hypotonic bladder 
spina bifida 
spinal cord injury
spinal tumour diabetic neuropathy 
functional obstruction
detrusor hyperactivity 
urge incontinence
107
Q

what are the different types of catheterisation?

A

intermittent urinary
indwelling urinary
suprapubic

108
Q

intermittent urinary catheter

A

inserted several times a day
drains bladder then removed
can be done by patient themselves
via urethra

109
Q

indwelling urinary catheter

A

via urethra
foley catheter - held in place by a balloon
collection bag strapped to leg
need changing every 3 months

110
Q

suprapubic catheters

A

left in - changed every 4-12 weeks
surgical insertion directly to bladder
insertion under general, local or epidural anaesthetic
used when urethra blocked/ damaged and unable to use intermittent

111
Q

sizes of catheters

A

12 or 14Ch

rarely 16Ch

112
Q

tests for assessing bladder function

A 
cystometry
uroflowmetry
pressure-flow study
urethral pressure profile 
leak point pressure
postvoidal residual volume
electromyelogram
ultrasound
CT
renal scintigraphy 
voiding cystourethrogram
IV urography 
CT urography 
retrograde urethrogram
retrograde CT cystography 
cystoscopy
113
Q

TI weighted MRI

A

highlights fat

114
Q

what is black on a T1 MRI?

A

air
calcium
dense bone

115
Q

what is dark on T1 MRI?

A

CSF
oedema
most lesions

116
Q

what is grey on T1 MRI?

A

white matter

grey matter

117
Q

what is bright on T1 MRI?

A

fat
blood
gadolinium contrast
orbits

118
Q

uses for T1 MRI

A

borders between brain and CSF
not very sensitive for lesions
with contrast good for vascular changes or disruption to BBB

119
Q

T2 weight MRI

A

highlighted fat and water

120
Q

what is black on T2 MRI?

A 
air
calcium
dense bone 
flow
vessels
121
Q

what is dark on T2 MRI?

A

white matter

gray matter

122
Q

what is bright on T2 MRI?

A 
CSF
blood - except deoxyhaemoglobin 
oedema
most lesions
eyes
scalp
123
Q

uses for T2 MRI

A

brain anatomy
most lesions
cannot distinguish lesions from CSF

124
Q

FLAIR MRI

A

same as T2 but CSF is black/ suppressed
ventricles, cisterns and sulci are black
most pathology is bright
useful for lesions

125
Q

what are MRIs good for?

A 
circulation - blood 
spinal cord
brain 
bone infections
soft tissue and soft organ abnormalities
cancer
joint damage
spinal disc problems
nerve problems 
breasts
liver
kidneys
ovaries
pancreas
prostate
functional MRI maps brain activity
126
Q

contraindications for MRI

A 
1st trimester of pregnancy
contrast cannot be used in pregnancy or those with severe kidney damage 
allergy to contrast 
metal implants 
certain tattoos

2nd year (48 decks)

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