MS Flashcards

1
Q

One of the clinical presentations of MS is optic neuritis. What is optic neuritis

A

inflammation of optic vision

causes pain and loss of vision

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2
Q

does optic neuritis have a good prognosis

A

Yes

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3
Q

what drug is used to treat optic neuritis

A

steroid- predenisole.

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4
Q

what percentage of those who have optic neuritis develop MS within 10 years and what will be seen on a brain scan

A

50%

2-3 leisons

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5
Q

transverse myelitis is one of the clinical presentations of MS what is it

A

shows inflammation of the spinal cord

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6
Q

how do patients with optic neuritis present

A

pain and blurred vision

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7
Q

what investigations are used to determine where a patient has optic neuritis or not

A

Reduced colour vision (Ishihara chart),
Reduced pupillary light response (no constriction) (RAPD),
Hole in visual field (scotoma)- due to enlarged blind spot.
Fundoscopy- used to see if there is anything behind the eye, which may be causing the symptoms- everything, was normal.

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8
Q

does optic neuritis have a good prognosis

A

Yes

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9
Q

does transverse myelitis have a good prognosis

A

Yes

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10
Q

define Lhermites phenomenon.

A

shock like sensation from the midline at the neck down the arms.

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11
Q

how to patients with transverse myelitis present.

A

tingling numbness starting in both feet and ascending to the level of the chest “like a tight band”
Felt unsteady walking and fatigued easily.
Hyperreflexia.
Electric shock sensations running down the body whenever she bent her head

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12
Q

what investigations are used to diagnose MS

A

CT- shows inflammation of the spine.

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13
Q

how many people with transverse myelitis go on to develop MS

A

50% go on to develop multiple sclerosis

brain scan- 2-3 lesions

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14
Q

what is a key criteria for MS diagnosis

A

dissemination in time and place- 2 different parts of the body must be affected over a period of time

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15
Q

what are the symptoms of clinical definite MS

A

Optic neuritis and transverse myelitis at different times

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16
Q

what are the symptoms of non definite MS

A

Clinically isolated syndrome (CIS)
Myelitis and optic neuritis at the same time
Recurrent myelitis
Recurrent or sequential optic neuritis

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17
Q

why is a Lumbar puncture used to determine MS

A

– Check for OCB (oligo-clonal band) in CSF. These are immunoglobulins, which indicate inflammation in the CNS.

18
Q

treatment for MS

A

intravenous methylprednisolone 1g daily for 3 days.

beta-interferon 1a injections- 5-10 year treatment with subcutaneous injections.

19
Q

Is MS autoimmune

20
Q

define MS

A

disease of the central nervous system.
inflammatory reaction in the CNS causes loss of myelin and slowing of nerve conduction- Areas of demyelination, loss of axons

21
Q

which sex is MS more common in

22
Q

what is the pathogenesis of MS

A

both antibody and immune mediated.
Certain components of complement (e.g. lymphocytes), sit on the axon and breakdown myelin which slows down nerve transmission.
oligodendrocytes form myelin- destroyed by T cells.

23
Q

how does interferon beta help is MS

A

reduced the number of relapses by 1/3.

24
Q

what are the disease modyfying treatments of MS

A
  • Interferon beta 1-b
  • Interferon beta 1-a
  • Glatiramer acetate
  • Teriflunamide
  • Dimethyl Fumarate
  • Fingolimod
  • Natalizumab (Tysabri)
  • Alemtuzumab (Lemtrada)
  • Mitoxantrone
25
what does gadolinium enhancement of MS mean
it has crossed the blood brain barrier.
26
how is gadolinium diagnosed
MRI
27
Tysabri is new drug, what type of drug is it and how does it work.
first humanized monoclonal antibody. Prevents immune cells from migrating from the bloodstream into the brain where they can cause inflammation and potentially damage nerve fibers and their insulation.
28
what are the side effects of TYSABRI
predisposes patient to getting JC virus which results in Progressive Multifocal Leukoencephalopathy (PML)
29
What is the mechanism of action of Natalizumab
interaction of the adhesion molecules, α4-integrin on the activated leukocyte with VCAM-1 on the blood-brain barrier is the key components involved in immune cell adhesion and migration. Natalizumab blocks the α4-integrin so leukocyte cannot cross the BBB and cause demyelination.
30
Initial treatments foe MS were IV/SC, new drugs are now oral these include
Fingolimod Teriflunomide Dimethyl Fumarate
31
what is the mechanism of action of fingolimod
internalisation of the receptor S1P1 | This blocks lymphocyte egress from lymph nodes while sparing immune surveillance by circulating memory T cells
32
what are the main side effects of the fingolimod drug
fatal herpes virus infection and bradycardia
33
what are the 4 types of MS
Relapsing remitting MS Secondary progressive MS Primary progressive MS Progressive relapsing MS.
34
Spastic paraparesis (rogressive weakness and spasticity (stiffness) of the legs.) suggests a problem in which part of the body
spinal cord
35
what neurological problems does MS cause
forgetfullness.
36
The different types of treatment for MS
Symptomatic treatments- management of acute relapse- Corticotherapy- treatment for symptoms. Modifying course treatments.
37
what are the potential targets in therapy MS
1. Inflammatory mechanisms 2. Excitotoxic mechanisms: 3. Energy depletion: 4. Genetic determination: 5. Apoptotic mechanisms: 6. Depletion of growth factor 7. Demyelination induced:
38
what use can stem cell be in MS
Stimulate oligodendrocytes to make myelin | stimulate new oligodendrocyte production
39
what is the name of the pathway involved in apoptotic mechanism
caspase pathway
40
what growth factor depletion is devastating to MS
stem cell.