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MS management Flashcards

1
Q

MS usually begins

A

begin the ages of 20-40

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2
Q

early course of MS is usually

A

relapsing/remitting

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3
Q

what is the Prevalence of MS in vancouver compared to malta

A

vancouver 91/100,000

Malta 4/100,000

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4
Q

what is the comparative risk for developing MS based on race in USA

A

White males 1.0
Black males 0.43
Other males. 0.22

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5
Q

what are the ratios of male to female cases of MS?

A

early onset 3 females :1 male

normal range 2 F: 1 M
Late onset 2.4 F: 1 M

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6
Q

MS prevalence can be altered by..

A

a change in environment

age of migration is critical for risk retention

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7
Q

according to Sadovnick et al 1993 what are the rates of concordance for MZ, DZ and siblings?

A

31% MZ, 5% DZ, 5% siblings

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8
Q

what components of the Immune system are thought to play a role in MS pathogeneis?

A

Lymphocytes (B&T)

Monocytes/macrophages

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9
Q

what qualities do remyelinating neurons axons have?

A

uniformly thin, short internodes

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10
Q

plaque distribution in the cerebral hemispheres relates to what symptoms

A

large variety of symptoms but also many silent lesions

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11
Q

plaque distribution in the spinal cord leads to what symptoms?

A

weakness, paraplegia, spasticity, tingling, numbness, lhermitte’s sign, bladder and sexual dysfunction

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12
Q

plaque distribution in the optic nerves leads to what symptoms?

A

impaired vision, eye pain

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13
Q

plaque distribution in the medulla and pons leads to what symptoms?

A

dysarthria, double vision, vertigo, nystagmus

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14
Q

plaque distribution in the cerebellar white matter leads to what symptoms?

A

Dysarthria, nystagmus, intention temor, ataxia

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15
Q

what are 6 typical symptoms/signs of MS

A

optic neuritis

spasticity and other pyramical signs

sensory signs and symptoms

lhermitte’s sign

nystagmus, double vision and vertigo

bladder and sexual dysfunction

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16
Q

what are the symptoms of optic neuritis?

A

impaired vision and eye pain

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17
Q

what are 5 atypical symptoms or signs of MS?

A

aphasia
hemianopia

extrapyramidal movement disturbance
severe muscle wasting
muscle fasiculation

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18
Q

what is the outcome when lesions affect the cranial nerves?

A

optic neuritis and other cranial nerve symptoms

diplopia and uhthoff’s phenomenon

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19
Q

what is the outcome when MS lesions affect the motor systems?

A

spasticity, weakness,temor and ataxia

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20
Q

what is the outcome when lesions affect the sensory systems?

A

many symptoms including lhermitte’s sign

21
Q

what is the outcome when lesions affect autonomic systems

A

bladder, bowel and sexual dysfunction

22
Q

what are the symptoms when the neurobehavioral systems are affected

A

cognitive problems and depression

23
Q

what qualities are seen on the CSF electrophoresis in MS?

A

IgG oligoclonal bonds

24
Q

what is one feature of a preclinical phases of MS

A

radiologically isolated sydrome

25
describe the prognosis of MS
less than 5-10% will have a mild phenotype with no significant disability More than 30% of patients will develop significant disability within 20-25 years after onset Life expectancy is shortened only slightly in persons with MS Survival rate is linked to disability Death usually results from secondary complications (pulmonary or renal) Marburg variant is an acute and clinically fulminant form of the disease that can lead to coma or death within days
26
name 6 clinical indicators of poor prognosis
``` Male gender Late age at onset Early motor, cerebellar, and sphincter symptoms Short inter-attack interval High number of early attacks Early residual disability ```
27
name 4 paraclinical indicators of poor prognosis in MS
Significant MRI disease burden at onset Evidence of MRI disease activity Positive cerebrospinal fluid analysis for OCB Positive evoked potential examination
28
what treatment modalities exist for MS?
``` IMMUNOMODULATORY THERAPY Acute repulses Frequent relapses Aggressive illness Progressive illness ``` MANAGEMENT OF SYMPTOMS NON PHARMACOLOGICAL TREATMENTS physiotherapy occupational therapy
29
what can be useful to hasten recover from acute exacerbations?
Oral or intravenous Methylprednisolone (steroids) no evidence that this changes the overall disease progression does not affect outcome but may shorten relapse
30
when should plasma apheresis be used to treat MS?
short term for severe attacks if steroids are contraindicated of ineffective 2011 AAN guidelines ("probably effective") as a second line treatment
31
symptoms management can be used to treat which symptoms
can be pharmacological or non pharma ``` Fatigue Spasticity Bladder problems Bowel problems Cognitive dysfunction Pain Paroxysmal symptoms Sexual dysfunction Tremor ```
32
patients with MS may benefit from referral to who?
Patients with MS may benefit from referral to Physiotherapists Occupational therapist Speech therapists
33
what should you do when patients have bad prognostic markers?
Treat early | Treat aggressively
34
what is the prevalence of MS?
120-180/100,000 in britain depending on location
35
what do Disease Modifying Therapies (DMTs) aim to do?
reduce the frequency and severity of relapses
36
what is urthoffs phenonomenon?
worsening of neurological symptoms of demyelinating diseases such as MS from overheating
37
what is the definition of a relapse in MS?
24 hours 1 month apart | - where infection is ruled out
38
what are the 2008 sheffield definitions of a clinically significant relapse in MS?
1) Any Motor relapse 2) Any Brainstem relapse 3) A Sensory relapse leading to functional impairment 4) Sphincter dysfunction 5) Optic Neuritis 6) Intrusive pain
39
what is the sheffield 2008 definition of a disabline relapse in MS?
1) Affects the patient’s ability to work 2) Affects the patient’s activities of daily living 3) Affects motor or sensory function sufficiently to impair the capacity or reserve to care for themselves or others 4) Requires treatment/hospital admission
40
do Disease Modifying Therapies have an effect on disease progression?
no but can reduce relapses and relapse related disability
41
how to disease modifying therapies work?
by altering various mechanisms in the immune system to prevent an inflammatory response ie immune modulators preventing cells crossing blood brain barrieer ( natalizumab) keep lymphocytes in the lymph tissue reduce lymphocyte formation (teriflunomide, azothiprine) reboot immune system (bone marrow transplant)
42
describe the evidence from trials for disease modifying therapies
evidence from BENEFIT (betaferon) and PRECISE (copaxone) that they delay time to conversion after clinically isolated syndrome (teriflunomide too)
43
describe the four common first line DMTs in MS and how their effect
interferon beta 1a IM interferen beta 1b SC interferon beta 1a SC Capaxone (galtimarmer acetate) all 4 reduce relapses by about a third make relapses milder interferons may have some effect on slightly slowing disease progression
44
what are some potential side effects of interferons?
``` skin site reactions flu like symptoms leucopenia anaemia thrombocytopeinia liver dysfunction potentially teratogenic can cause depression ( and suicide) ```
45
what some of the newer DMDs?
ORALS teriflunomide dimethylfumarate NON ORAL fingolimod natalizumab alemtuzumab
46
what sort of stem cell treatments are already used to tream MS?
autologous (self) bone marrow transplants
47
how can vitamin d be used as a DMT?
diet supplementation may act altering DRBI*1501 study in 132 hispanic people found that lower vitamin d experienced more relapses
48
in terms of efficacy which drug is weakest and which is strongest?
laquinimod weakest mitoxantrome strongest
49
which DMTs are least and most convenient?
vitamins , anticonvulsants, and drugs such as teriflunomide are the most convenient (oral) IV are least convenient such as natalizumab and mitoxantrone

neuroinflammation (14 decks)

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