L15 Multiple Sclerosis Flashcards

1
Q

What is Multiple Sclerosis

A

Auto-immune disorder

Immune Sytem attacks the myelinated axons in the CNS

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2
Q

What system does MS affect

A

Central Nervous System

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3
Q

When does the onset of MS begin

A

Ages of 20-50

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4
Q

Frequency of MS in society

A

Twice as common in women
1-1000 people in ireland diagnosed
2.8 globally affected

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5
Q

What does growing evidence show about the geography of MS

A

More frequent in areas further from equator
Studies linking the Vitamin D

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6
Q

3 Characteristics of MS

A

Destruction of Myelin Sheaths around neurons

Formation of lesions in CNS

Chronic Inflammation (activated microglia cells)

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7
Q

What do areas of myelin loss show in images

A

plaques/lesions

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8
Q

What is myelin

A

Insulating layer, or sheath that forms around nerves (brain and spinal cord)

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9
Q

Function of Myelin Sheath

A

Propogation of electrical impulses along axons is highly accelerated by myelin sheath

Produces saltating or jumping action potentials across internodes, from one node of ranvier to the next

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10
Q

Myelination in CNS and PNS

A

Oligodendrocytes (CNS)

Schwann Cells (PNS)

Both types of glia (non-neuronal cells in nervous system )

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11
Q

Glia Cells in the CNS (Brain, Spinal Cord)

A

Astrocytes: support immune function

Oligodendrocytes: insulation, myelination

Microglia: immune function, phagocytes

Ependymal Cells: create CSF

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12
Q

Glia Cells in PNS

A

Schwann Cells: insulation, myelination

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13
Q

Oligodendrocytes

A

Location: CNS
Function: Myelinating Axons
Disease Associated: MS

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14
Q

Schwann Cells

A

Location: PNS (myelinate the nerve cells that project to and from muscles, internal organs)

Function: responsible for myelinating a small portion of an axon

Disease Associated: Guillain- Barre syndrome

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15
Q

What is a multi-factorIal disease?

A

No single cause has been found, but a number of risk factors have been identified

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16
Q

Risk factors that may cause MS

A

Exposure to certain Viruses (Epstein-Barr = Glandular Fever)

Genetic Susceptibility

Environmental Factors: lack of sunlight, smoking, teenage obesity, pollutants, gut microbiota, stress and exercise

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17
Q

What causes demyelination resulting in MS

A

Risk factors together cause abnormal immune response against self antigen Myelin, leads to demyelination of axons

18
Q

Pathophysiology of MS

A

Activated T & B lymphocytes

Cross the Blood Brain Barrier

Infiltrate brain and spinal cord

Activate Microglia

Release Cytokines

Macrophages attack myelin and phagocytes large chunks of the myelin sheath

Loss of Myelin

Plaques of demyelination in white matter, demyelinating lesions in grey matter

Disappearance of oligodendrocytes and proliferation of astrocytes

Axonal loss and degeneration

Loss of signal conduction

19
Q

Symptoms of MS

A

Often unpredictable
Differ greatly between people
May be mild or severe, short term or long term

> > this dependent on the location of the affected nerve fibres

20
Q

Symptoms of Multiple Sclerosis

A

Vision Problems: such as optic neurotis (blurriness and pain in one eye) are often one of the first signs of MS

Changes in gait
Fatigue
Loss of Balance
Muscle Spasms
Muscle Weakness
Tingling pr numbness, especially in arms or legs

21
Q

Course of MS

A

Most people with MS have a relapsing- remitting disease course

  • experience periods of new symptoms or relapse that develop over days or weeks and usually improve partially or completely

these relapses are followed by quiet periods or remission that can last months to years

22
Q
A
23
Q

Types of MS

A

Relapsing- Remitting MS (RRMS)
Secondary Progressive MS (SPMS)
Primary Progressive MS (PPMS)
Progression Relapsing MS (PRMS)

24
Q

Relapsing Remitting MS

A

Flare ups and periods of remission

25
Q

Secondary Progressive MS

A

Starts like RRMS but there is stable progression of the disease and symptoms between relapses

26
Q

Primary Progressive MS

A

Symptoms that slowly and gradually worsen without any periods of relapse or remission

27
Q

Progressive Relapsing MS

A

Steadily worsens from the onset of the first symptoms, regardless of relapses or periods of remission

28
Q

What are complications of MS

A

If MS progresses, worsening symptoms may lead to complications such as :

  • Difficulty walking
    -Loss of bowel or bladder control
  • Memory problems
  • Speech Difficulties
  • Increase risk of life - threatening conditions
29
Q

How is MS diagnosed

A

1) Detailed Neurological examination - shows whether nerve pathways are damaged

2) Lumbar Puncture- reveals if there has been a breakdown of antibodies and oligoclonal bands which are suggestive of MS

3) MRI scans of the brain and spinal cord- to look for characteristic lesions of MS

4) Evoked potential tests -

30
Q

What shows in MRI if MS is present

A

white spots correspond to demyelinating lesions

31
Q

Treatment of MS

A

No cure

Treatment focuses on
-speedy recovery from attacks
reducing new clinical relapses
slowing the progression of the disease
managing MS symptoms

32
Q

Treatment for an MS attack

A

Corticosteroids

Oral Prednisone

Intravenous Methlyprednisolone

> > inhibit the synthesis of inflammatory proteins, through the suppression of the

Plasma exchange

> > the liquid portion of blood is removed and seperated from the blood cells. Mixed with protein solution and put back into body

33
Q

Treatment to modify disease progression

A

Injectable :
- Interferon beta medications
- Glatiramer
-Monoclonal

> > Lowere relapse rater
slow the formation of new lesions
potentially reduce risk of brain atrophy and disability accumation

34
Q

Interferon Beta Medication

A

Balances the expression of pro and anti- inflammatory agents in the brain, and reduces the number of inflammatory cells that cross the BBB

Increase the production of nerve growth factors

-Avonex
-Betaseron
-Rebif

35
Q

Glatiramer Acetate

A

Modifiy the immune processes that are believed to be responsible for the pathogenesis of MS

Inhibit the secretion of proinflammatory cytokines

Inducing the T-cells to cross the BBB and produce anti-inflammatory cytokines

Examples
- copaxine
- glatopa

36
Q

Monoclonal Antibodies

A

Reduces the level of B cells which contribute to the development and progression of MS

Binds to and blocks the action of CD-20, a molecule expressed on the surface of both healthy and leukimic B Lymphocytes

Eg.
- Kesimpta
-Arzerra

37
Q

Oral Medications for MS Progression

A

Teriflunomide

Fingolimid

Dimethyl Fumarate

> > reduces the relapse rate

38
Q

Teriflunomide

A

ORAL

Reduces the proliferation of activated T and B lymphocytes

eg. aubagio

39
Q

Fingolimid

A

Shifts macrophages to an anti-inflammatory phenotype. It modulated their proliferation

Eg. gilenya

40
Q

Dimethyl Fumarate

A

Lower levels of B lymphocytes
Blocks pro-inflammatory cytokine productiong. Tecfidera

41
Q

Cannabis

A

No cannagis based FDA approved medications for MS

Clinical Trials have shown it improves pain and spasticity, bladder issues in people with MS

42
Q
A