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
Q

describe the prognosis of MS

A

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
Q

name 6 clinical indicators of poor prognosis

A
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
Q

name 4 paraclinical indicators of poor prognosis in MS

A

Significant MRI disease burden at onset
Evidence of MRI disease activity
Positive cerebrospinal fluid analysis for OCB
Positive evoked potential examination

28
Q

what treatment modalities exist for MS?

A
IMMUNOMODULATORY THERAPY 
Acute repulses
Frequent relapses 
Aggressive illness 
Progressive illness 

MANAGEMENT OF SYMPTOMS

NON PHARMACOLOGICAL TREATMENTS
physiotherapy
occupational therapy

29
Q

what can be useful to hasten recover from acute exacerbations?

A

Oral or intravenous Methylprednisolone (steroids)

no evidence that this changes the overall disease progression

does not affect outcome but may shorten relapse

30
Q

when should plasma apheresis be used to treat MS?

A

short term for severe attacks if steroids are contraindicated of ineffective

2011 AAN guidelines (“probably effective”) as a second line treatment

31
Q

symptoms management can be used to treat which symptoms

A

can be pharmacological or non pharma

Fatigue
Spasticity
Bladder problems
Bowel problems
Cognitive dysfunction
Pain
Paroxysmal symptoms
Sexual dysfunction
Tremor
32
Q

patients with MS may benefit from referral to who?

A

Patients with MS may benefit from referral to
Physiotherapists
Occupational therapist
Speech therapists

33
Q

what should you do when patients have bad prognostic markers?

A

Treat early

Treat aggressively

34
Q

what is the prevalence of MS?

A

120-180/100,000 in britain depending on location

35
Q

what do Disease Modifying Therapies (DMTs) aim to do?

A

reduce the frequency and severity of relapses

36
Q

what is urthoffs phenonomenon?

A

worsening of neurological symptoms of demyelinating diseases such as MS from overheating

37
Q

what is the definition of a relapse in MS?

A

24 hours 1 month apart

- where infection is ruled out

38
Q

what are the 2008 sheffield definitions of a clinically significant relapse in MS?

A

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
Q

what is the sheffield 2008 definition of a disabline relapse in MS?

A

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
Q

do Disease Modifying Therapies have an effect on disease progression?

A

no but can reduce relapses and relapse related disability

41
Q

how to disease modifying therapies work?

A

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
Q

describe the evidence from trials for disease modifying therapies

A

evidence from BENEFIT (betaferon) and PRECISE (copaxone) that they delay time to conversion after clinically isolated syndrome (teriflunomide too)

43
Q

describe the four common first line DMTs in MS and how their effect

A

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
Q

what are some potential side effects of interferons?

A
skin site reactions
flu like symptoms 
leucopenia
anaemia
thrombocytopeinia
liver dysfunction
potentially teratogenic
can cause depression ( and suicide)
45
Q

what some of the newer DMDs?

A

ORALS
teriflunomide
dimethylfumarate

NON ORAL
fingolimod
natalizumab
alemtuzumab

46
Q

what sort of stem cell treatments are already used to tream MS?

A

autologous (self) bone marrow transplants

47
Q

how can vitamin d be used as a DMT?

A

diet supplementation

may act altering DRBI*1501

study in 132 hispanic people found that lower vitamin d experienced more relapses

48
Q

in terms of efficacy which drug is weakest and which is strongest?

A

laquinimod weakest

mitoxantrome strongest

49
Q

which DMTs are least and most convenient?

A

vitamins , anticonvulsants, and drugs such as teriflunomide are the most convenient (oral)

IV are least convenient such as natalizumab and mitoxantrone