Multiple sclerosis Flashcards

1
Q

Definition

A

Potentially disabling myelinating disease of the CNS

where the immune system attacks the myelin that surrounds your neurons

Oligodendorcytes are cells that make up the myelin

This disease can eventually lead to complete permenant damage of the myelin and lead to serious communication problems between the brain and the body

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2
Q

How it occurs

A

The brain and the neurons within the brain are seperated by a blood brain barrier that only allows certain T and B cells through if they have the right ligand/surface molecule

When a T cell with the right ligand gets in, it can be activated by something it encounters, in the case of MS its the myelin

Once it is activated it changes the blood brain barrier so now it has more receptors on so more immune cells can get in

MS is a type 4 hypersensitivity (cell mediated hypersensitivity):
– meaning that when it is activated as well as increasing the amount of receptors on the BBB, it also releases cytokines like (IL-1, IL-6, TNF alpha, Interferon-gamma)
– these together will dilate the blood vessels, allowing more immune cells to get in
– while causing direct damage to the oligodendrocytes

The cytokines also attract B-cells and macrophages as part of the inflammatory response
– these will together destroy the oligodendrocytes leaving scar tissue

The attacks happen in bouts:
– due to the cytokines also attracting Regulatory t-cells which can calm down the immune cells reducing the inflammation

Over time the damage can be irreversible, at first the oligodendrocytes can recover and regrow

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3
Q

Aetiology

A

Cause is unknown like most autoimmune disease

Can be influenced by genetic and environmental factors

Genetic:
– women
– HLA-DR2 gene

Environmental:
– infections
– vitamin D deficiency (higher rates in less sunny areas)

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4
Q

Epidemiology

A

Affects 20-40

Women 2-3x more likely than men to get RRMS

Family history

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5
Q

Types of multiple sclerosis

A

Relapsing-remitting MS (most common, least serious):
– attacks happening in bouts months or years apart, causing an increase in the disability in these bouts
– remyalination occurs in between bouts, over time the damage can however become reversible

Secondary progressive MS (SPMS):
– starts off like RRMS but then become progressive and has a constant worsening of the disease no longer happening in bouts

Primary progressive MS (PPMS):
– one constant attack on the myelin, steady progression of the disease over someones life

Progressive relapsing MS (PRMS):
– one constant attack, with bouts that make it even worse and progression goes even faster in these periods

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6
Q

Clinical presentation

A

Varies from person to person

Symptoms during bouts can get worse, and linger for months without proper treatment

– Charcot’s neurologic triad:
—- dysarthria (due to plaques in the brain stem)

—- nystagmus (due to plaques in the nerves of the eyes or optic neuritis)

—- intention tremor (due to plaques along the motor pathways)
—— muscle weakness
—— muscle spasms
—— ataxia
—— paralysis in serious cases

Numbness and pins and needles, parasthesia (due to plaques in the sensory pathways from the skin)
– may present with L’hermittes sign

– Bowel and bladder symptoms
– sexual dysfunction
—– due to plaques in the autonomic nervous system

– poor concentration and critical thinking
– depression
– anxiety

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7
Q

Prognosis

A

Can treat symptoms but disease cant be cured as its autoimmune

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