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Flashcards in MS Deck (40):
1

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

inflammation of optic vision
(causes pain and loss of vision)

2

does optic neuritis have a good prognosis

Yes

3

what drug is used to treat optic neuritis

steroid- predenisole.

4

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

50%
2-3 leisons

5

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

shows inflammation of the spinal cord

6

how do patients with optic neuritis present

pain and blurred vision

7

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

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.

8

does optic neuritis have a good prognosis

Yes

9

does transverse myelitis have a good prognosis

Yes

10

define Lhermites phenomenon.

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

11

how to patients with transverse myelitis present.

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

12

what investigations are used to diagnose MS

CT- shows inflammation of the spine.

13

how many people with transverse myelitis go on to develop MS

50% go on to develop multiple sclerosis
brain scan- 2-3 lesions

14

what is a key criteria for MS diagnosis

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

15

what are the symptoms of clinical definite MS

Optic neuritis and transverse myelitis at different times

16

what are the symptoms of non definite MS

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

17

why is a Lumbar puncture used to determine MS

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

18

treatment for MS

intravenous methylprednisolone 1g daily for 3 days.
beta-interferon 1a injections- 5-10 year treatment with subcutaneous injections.

19

Is MS autoimmune

Yes

20

define MS

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

which sex is MS more common in

females.

22

what is the pathogenesis of MS

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

how does interferon beta help is MS

reduced the number of relapses by 1/3.

24

what are the disease modyfying treatments of MS

• 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.