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Clinical symposium > MS > Flashcards

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

A

Yes

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

A

females.

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
Q

what does gadolinium enhancement of MS mean

A

it has crossed the blood brain barrier.

26
Q

how is gadolinium diagnosed

A

MRI

27
Q

Tysabri is new drug, what type of drug is it and how does it work.

A

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
Q

what are the side effects of TYSABRI

A

predisposes patient to getting JC virus which results in Progressive Multifocal Leukoencephalopathy (PML)

29
Q

What is the mechanism of action of Natalizumab

A

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
Q

Initial treatments foe MS were IV/SC, new drugs are now oral these include

A

Fingolimod
Teriflunomide
Dimethyl Fumarate

31
Q

what is the mechanism of action of fingolimod

A

internalisation of the receptor S1P1

This blocks lymphocyte egress from lymph nodes while sparing immune surveillance by circulating memory T cells

32
Q

what are the main side effects of the fingolimod drug

A

fatal herpes virus infection and bradycardia

33
Q

what are the 4 types of MS

A

Relapsing remitting MS
Secondary progressive MS
Primary progressive MS
Progressive relapsing MS.

34
Q

Spastic paraparesis (rogressive weakness and spasticity (stiffness) of the legs.) suggests a problem in which part of the body

A

spinal cord

35
Q

what neurological problems does MS cause

A

forgetfullness.

36
Q

The different types of treatment for MS

A

Symptomatic treatments- management of acute relapse- Corticotherapy- treatment for symptoms.
Modifying course treatments.

37
Q

what are the potential targets in therapy MS

A
  1. Inflammatory mechanisms
  2. Excitotoxic mechanisms:
  3. Energy depletion:
  4. Genetic determination:
  5. Apoptotic mechanisms:
  6. Depletion of growth factor
  7. Demyelination induced:
38
Q

what use can stem cell be in MS

A

Stimulate oligodendrocytes to make myelin

stimulate new oligodendrocyte production

39
Q

what is the name of the pathway involved in apoptotic mechanism

A

caspase pathway

40
Q

what growth factor depletion is devastating to MS

A

stem cell.

Clinical symposium (20 decks)

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