MS Flashcards

1
Q

What is MS?

A

acute localised, and chronic diffuse, inflammation of the CNS and subsequent demyelination of neurone, following the infiltration of immune cells across the BBB

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2
Q

What is the pathophysiology of MS (as a generality)?

A
  • clonal expansion of immune cells (T and B cells) in peripheral compartment
  • ->Immune attack against oligodendrocytes leading to:
  • loss of nerve fibres (myelin sheaths): saltatory conduction altered
  • pockets of inflammation: local oedema
  • glial scarring or sclerosis
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3
Q

How can you tell between a new and old lesion in MS?

A
  • white around lesion is oedema (fried egg appearance): new

- if no oedema: old lesion

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4
Q

What is comprised of the BBB?

A

endothelial cell, basement membrane, pericytes, astrocyte, neuron

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5
Q

What is the pathophysiology of MS?

A
  1. infection by bacteria or virus
  2. antigen gets into the blood stream, digested by APC
  3. macrophage cell displays antigen with MHC molecule
  4. MHC-ag can be recognised by T cells
  5. activated T cell crosses BBB
  6. in CNS, Th cells encounter microglia (which are local APCs)
  7. APCs present a MHC-ag complex (containing myelin product) to T cells. Th cells are locally reactivated when they recognise ag on surface of local APCs (epitope-self protein of the MBP, MOG or MAG)
  8. activated Th cells secrete cytokines that:
    - stimulate microglia and astrocytes
    - recruit additional inflammatory cells from peripheral blood (macrophages, B cells)
    - induce antibody production (B cells)
    - complement system production
  9. demyelination, oligodendrocyte degeneration
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6
Q

What is the incidence of MS in the UK?

A

1:500

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7
Q

What is the female:male ratio for MS?

A

3:1

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8
Q

What is the genetic component in MS?

A
chromosome 6
colocalisation of genres involved in MS and MHC class 1, 2 and 3
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9
Q

What is
MBP
MOG
MAG?

A

myelin basic protein
myelin oligodendrocytes glycoprotein
Myelin associated glycoprotein

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10
Q

What are the difference molecular homology?

A
  • sequence homology: sequence of amino acids

- structural homology: protein shape

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11
Q

What are the different symptoms in MS?

A
  • optic neuritis (pain on eye movement, blurring of vision, red colour saturation) + Uhthoff’s phenomenon (if there has been optic neuritis in the past and you get fever, it can irritate the scar tissue and cause symptoms)
  • brainstem: vertigo slur speech, ataxia, incoordination, double vision
  • spinal cord:
  • > sensory: Lhermitte’s phenomenon: shock pain running gown spinal cord, irritation lesion)
  • ->motor: upper and lower limb weakness
  • ->autonomic: bowels, bladder, sexual dysfunction

MORE depends where they are

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12
Q

How can you tell the difference between an upper and lower motor neurone lesion?

A

upper: increased tone, exaggerated reflexes, present Babinaski’s sign

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13
Q

What are the different types of MS and how are they characterised?

A
  1. relapsing-remitting (85-90%)
    - attacks (relapses) with complete or partial recovery
    - no progression between attacks (remission)
  2. secondary progressing
    - initial relapse-remitting course followed by progression (usually 10-15 years)
    - with or without attacks
  3. Primary progressive (10-15%)
    - progressive from onset, no attacks
  4. progressive-relapsing (<5%)
    - progression from onset with attacks
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14
Q

How do you diagnose MS,

A

history
MRI
CSF (oligoclonal IgG)
evoked potentials

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15
Q

What is the 2017 McDonald Criteria for diagnosis of MS?

A

2 different attacks and 2 different times:

  • dissemination on space (dvlpt of lesions in distinct anatomical locations within the CNS: multifocal CNS process)
  • dissemination in Time (dvlpt or appearance of new CNS lesions over times + pos oligoclonal bands: bands take a while to appear so if they are there, they have been for a while)
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16
Q

What is the better prognosis for MS?

A
caucasian
monodical onset
females
onset with optic neuritis or isolated sensory symptoms
low relate rate first 2-5 years
long interval to second relapse
no or low disability at 5 years
abnormal MR with low lesion load
high vit D
17
Q

What is worse prognosis for MS?

A
afro-american or non white
multifocal onset
males
onset with motor cerebellar or bladder or bowel symptoms
high relapse rate 2-5 years
short inter attack latency
disability at 5 years
abnormal MR with 2 contrast lesions
habit: smoking, high salt intake
18
Q

How do you treat MS?

A

high dose corticosteroids (orally or IV) for relapse: reduce inflammatory activity/stabilises BBB
BUT
-no significant effect on MS disease progression

19
Q

What is a myelin sheath made out of?

A

-lipids: galactocerebroside
-glycoproteins:
MBP
MOG
MAG