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Therapeutics 358 Final > Multiple Sclerosis > Flashcards

Multiple Sclerosis Flashcards

1
Q

What type of disease is MS?

A

Chronic disease of the CNS
- Effects the brain and the spinal cord

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2
Q

Describe the prevalence of MS?

A

2.8 million people affected worldwide

  • Not the most prevalent disease but arguably one of the most vtraumatic diseases
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3
Q

When is MS commonly diagnosed? Why is this a concern?

A

Commonly diagnosed between the ages of 20-40 years old

Diagnosed when 20 years old - Live many years with it and be disabling

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4
Q

What is the concern of MS in younger adults?

A

Most common form of non-traumatic disability in young adults

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5
Q

Describe the difference in MS between males and females? Severity differences?

A

Women are affected approx. 3:1

Males tend to have a more severe disease course than females

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6
Q

Describe the pathophtsiology of MS?

A

Myselin sheath gets damaged

Axon gets exposed and open for damage –> get damage and see complications of MS

Something in the immune system that causes the body to attck the myelin

Something that happens to the myelin and myselin calls in immune system –> Immune system attacks the myelin sheath

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7
Q

Describe the distribution of MS? Therapy?

A

High in North America –> Canada and the USA, western side of Europe

MS incidence higher in northern climates; speculated that vit D deficiency may contribute

Individuals often supplemented higher with vitamin D - likely no benefit

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8
Q

What are two hypothesis that can describe the variation in distribution of MS?

A

Due to vitamin D levels –> Due to the lack of vitamin D (nothing found definitively)

Do not have acess to diagnostics; not picking it up to diagnose in those areas –> More prominent worries

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9
Q

Describe the etyiology of MS. Examples?

A

Immunological:
- Myelin sheath is attcking itself do know their is an immune component

Genetic
- First degree relative with MS - Higher risk but not purely genetic

Environmental
- Sunlight, gestation time (born in May higher risk of MS), agriculture (pesticides, gas wells, agriculture)

Infectious
-Infectious: Epstein Barr Virus
- Followed veterans for decades, 32x more likely to develop MS if you had the Epstein

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10
Q

Describe the overall summary of the etyiology of MS

A

Something you have in genetic makeup and something you are exposed too –> Leads to MS

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11
Q

What are some symptoms of MS? Most common side effects?

A

Lhermitte’s Sign
-Uhtohoff’s Phenomena
-“MS Hug”

Big Ones –> Nu8mbness, tingling, fatigue, and pain, vision problems, weakness

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12
Q

Describe the cognitive sx that may occur in MS?

A

Brain fog, difficulty thinking

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13
Q

What is the most common early symptom of MS?

A

Vision problems common early on

Can’t see out of one eye or both eyes

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14
Q

What is a common commorbidity in MS that makes symptom presentation complicated?

A

Wheelchair is common; a lot of these sx are invisble

Do not present with outward sx

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15
Q

Are the symptoms an individual experiences with MS the same in primary disease and in a relapse? Prognosis?

A

Sx can change in different relapses

Someone presents with first clinical sx as(optic neuritis) –> Better prognosis

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16
Q

Define the following:
-Lhermitte’s Sign
-Uhtohoff’s Phenomena
-“MS Hug”

A

Lhermittes –> Tuck head down –> Shooting pain downwards

Uhtohoffs –> Heat intolerance – sx get worse and cannot handle the heat

MS Hug –> Tightness around mid-section, sensation around mid-section

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17
Q

What is an issue with the symptoms of MS?

A

Can write off these sx – Do not always think of MS

Not uncommon to see someone get a diagnosis and say they have had these sx for a long time until a sx ike vision loss makes them go to ER

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18
Q

Describe the different types of MS

A
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19
Q

Describe relapses of MS in regards to symptoms and timing

A

Cannot predict when relapses will occur

Cannot predict what will happen in a relapse

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20
Q

Define Relapsing-Remitting MS. Prognosis?

A

Patients have discrete attacks over days to weeks with some recovery over weeks to months

Function us relatively stable between attacks

  • 30% of cases will will convert to Secondary progressive MS (SPMS) after 10 yrs
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21
Q

Define secondary progressive MS.Medications?

A

Progression of disability may occur in the abscence of active MS or with continued active MS (after 10 years, 30% of RRMS convert to SPMS)

  • Medications can delay/possibly prevent the conversion of RRMS to SPMS
  • Clinicians may treat SPMS with DMT’s
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22
Q

Define primary progressive MS. Therapy?

A
  • Around 10% of cases

Characterized by steady deterioration of fucntion from onset

  • Ocrelizumab is the only officially indicated PPMS medication
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23
Q

Define clinically isolated syndrome (CIS). Medications?

A

A single dymylenating event event and not fully diagnostic criteria of MS

Starting meds can delay, but NOT likely prevent, conversion to MS

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24
Q

Describe the prevalence of the different types of MS

A

85%-90% will have relapsing-remitting and then eventually leads to secondary progressive (hard to predict but on average 15-20 years)
–> Cannot predict what the disease will do

Body can repair the myselin a bit, cannot repair the axon

10-15% are primary progressive –> Right from the start have progressive
- Continual increasing disability over time
- Men tend to have the progressive phenotype

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25
What is a clinically isolated syndrome example?
Clinically Isolated Syndrome E.g. loss vision but never had a second attack or waiting for clinical attack
26
What use to be required for a diagnosis of MS? Is this still the recommendation?
Use to need a second clinically attack in 2 years to be diagnosed with MS Now: - If have MS will send them to imaging right away to start Disease modifiable therapy
27
Regarding diagnosis of MS, what are some critical points?
Lesions that corespond to the sx you are having Example: Lesion on the optic nerve Enhancing Lesion --> Active inflammation --> Often have clinical sx but not always identifying MS earlier now rather than later MRI earlier now
28
Describe the natural history of MS (IMPORTANT) Issue?
Over time, see axonal loss Remitiiing-Relapsing course turns into secondary progressive Brain volume shrinking Relapses --> Inflammation is high - Over time as the dx progressqes and moves into the more progressive state,inflammation decreases over time Majority of drugs available are doing something to limit the inflammation - Drugs do not work as no inflammation there to work on Progresisve phase --> less inflammation than relapsing-remitting - limited drug options as the drugs work on inflammation
29
How can the progression of MS be measured?
Expanded Disability Status Scale
30
What is the purpose of the EDSS? Relavence as pharamcists?
A way of trying to classify and cetagorize the level of disability someone has 6 is the threshold: Dx has progressed to a level to where they can cannot mobilize (walk independtly over 100 metres) Only know how the drugs work in those who are in 6 or 5.5 or less
31
Is MS a major cause of death in individuals with the disease?
Majority of people do not die from MS Often not the cause of death in the majority of people
32
What are some limitations of the EDSS?
Only know how the drugs work in those who are in 6 or 5.5 or less Limits what we have for people - RCT’s only with EDSS of less than 6, drug coverage only lists those drugs for those with that score Focuses on mobility; a lot of other sx in MS - Does not capture cognition or even upper limb mobility - If in wheel chair and lower limbs affected, may have strong upper body strength
33
What are some non-pharamcological strategies for the management of MS?
Exercise (major one) Diet Complementary / alternative medicine: a) Hyper-baric chambers b) Bee-sting therapy c) Liberation Therapy (CSSVI)
34
Describe exercise as a non-pharmacological management strategy of MS
Exercise is a major one Not the case to just rest, exercise Not high intensity: Just something to get moving
35
Describe diet as a non-pharamcological strategy for the management of MS
Diets : No evidence to suggest one diet over another Eat a well balanced diet
36
Describe Liberation Therapy ? Efficacy?
Lberation therapy (CSSVI) MS is due to buildup of iron in the brain and due to the vein running down the brain is occluded Stent or open the vein up Pt’s supposebly did well People travelled to oyher countries Stents often only seen in arteries; stents in veins likely to move and some people died RCT’s --> No benefit to this therapy; even inventor turned back Could have been placebo effect; expensive - Risk > Benefit
37
What are some of the pharmacological strategies for the management of MS?
Treat acute relapses Treat / manage symptoms (Can treat them the same way as we would in someone who does not have MS ) Prevent disease activity and progression
38
Define a relapse in MS
New or worsening symptoms Last ≥24 hrs in length Absence of fever (infection) or other causes, Seperated from previous relapse by ≥30 days
39
Describe the therapy for relapse management in MS
High-dose corticosteroids Methylprednisolone 500mg – 1000mg IV x 3-5 days May or may not have oral taper Oral options 1250mg prednisone = 1000mg IVMP Non-responders – may consider plasma exchange Not all relapses are treated
40
What is the most common therapy for a relapse of MS? Is IV more effective than oral?
Treat with high dose corticosteroids Usually IV methylprednisone 3 to 5 days - May see a taper (physician preference) and may not see a taper done Oral works just as well and just as effective --> No more adverse effects
41
When treating a relapse of MS with corticosteroids, when are certain routes of administration used?
Oral: More convenience, cheaper IV over oral: Can’t swallow, a lot of tablets for someone, comes down to convenience
42
Describe two critical factors regarding steroid usage in the management of a MS relapse
1) May speed recovery but does not alter the course of the disease 2) Oral steroids have similar efficacy to IV
43
Are all relapses of MS treated? If not, when do we treat MS relapses?
No If involving optic nerves, will often treat that If numbness in hands and legs, may not look at treating that
44
What can be done for the management of an MS relapse if an individual does not respond to high dose corticosteroids?
If hit with high dose CS’s and no/minimal response: Plasma exchange --> Swap out the plasma and reintroduction of plasma with replacement fluid - Removal of natibodies from the blood Very rarely done
45
What are some comorbidities that can occur in MS? How are they treated?
Bladder dysfunction -Constipation, Diarrhea, Bowel dysfunction - Urgency Depression Fatigue Pain Sexual dysfunction Spasticity Tremor Vertigo / dizziness Walking / gait Individuals who have comorbidities and need to look at these separately and address them - Do not treat them any differently than a person without MS
46
Describe the fatigue of MS
Not just super tired Fatigue is severe enough to disrupt function and cannot be in the work force anymore > 90% of patients experience
47
Describe the causes of fatigue in the different forms of MS
48
What are some non-pharamcological strategies for management of fatigue in MS?
OT / PT Sleep hygiene Avoid excessive heat Exercise and diet
49
Describe the role of occupational therapy in MS
Occupational therapy has a huge role to play in people with MS managing daily activities - Fatigue and cognition issues: How can they manage the activities of daily living
50
Describe the pharmacological therapies for fatigue in MS
Amantadine Modafinil Methylphenidate
51
Describe the pharmacological options for management of fatigue in MS and its dose, adverse effects and efficiacy
Do not work well Try them but may not have success Medications not superior to placebo with more adverse effects and not recommended
52
Describe the prevalence of gait disturbances in MS
> 90% of patients
53
Non-pharmacological Management of Gait Disturbances in MS
OT / PT Bracing / walking aids Exercise
54
What are some pharamcological option(s) for the managemnt of gait disturbances in MS? Dose, risks, coverage?
Fampridine - Indication for MS to increase walking speed --> increased speed of 25 foot walk This drug allowed people to walk faster People want to walk better and not faster EDS criteria --> if really wanna try something
55
Describe the prevalence of spasticity in MS
Up to 70% of patients wille xperience
56
Describe non-pharamcological treatment of spasticity in MS
Exercise Stretching Phsyio-therapists are able to provide exercise to work at home
57
Describe the pharamcological options for muscle spasticity in MS
Botox can help with spasticity --> 1-2 weeks to have effect Baclofen is the most common for this one
58
What is anotehr pharamcologicla agent that can. be used for pain and spasticity management in MS?
Indicated as an add on treatment --> Baclofen and not working
59
What are the potential adverse drug reactions from Sativex? Most common?
60
Describe the efficacy/evidence for cannabis use in MS
Lack of evidence for use in any other MS symptoms Poor quality studies (or none)
61
What are some challenges regarding determining efficacy of cannabis in MS?
Dosage/ratio unknown Type of cannabinoid(s) to use Varying quality/quantity if street cannabis Finding cannabis “naïve” study participants
62
What is the main therapy for disease managemnt in MS?
Disease-modifying therapies (DMT)
63
Describe the efficacy/effects of DMT's in MS
Attempt to slow the inflammatory process Decrease frequency and severity of relapses Decrease lesions on MRI Reduce accumulation of neurological impairment and disability over time (?)
64
When should DMT be initiated in MS?
Earlier Treatment is better Older --> Unlikely to see a reduction in long term progression of disability - Earlier is better --> Time is brain
65
What do DMT's attempt to do overall in MS?
Slow down the inflammatory process and stop the dmage from occurring
66
First DMT
Very first drug for MS Betaseron --> Canada in 1996 Could only do tx with CS for the acute things occurring
67
Describe the indication of DMT for the types of MS? Exception?
All for relapsing and remitting Ocrelizumab --> Relapse-remitting and primary progressive Siponimod - Secondary Progressive MS
68
Describe the available DMT agents
69
Describe the mechanism of action of DMT
Immunomodulators: Tinker with the immune system; make changes to it Immunosuprresnats --> Not same as chemotx or anti-rejection drugs - Suppresses the immune system but not completely wiping it out - No need for isolation
70
Describe the DMT, WHO classification and effect on immune system
71
What is PML?
Progressive multifocal leukoencephalopathy
72
Describe what PML is?
Rare, but often fatal Opportunistic infection by JC virus (john Cunningham) 40-90% of population is JCV+ --> Doesn’t cause sx usually and many have had it Infection in the brain and now immune system cannot get into the brain Destroys the cells that produce myelin -->Clumsiness, weakness, changes to vision and speech (similar to MS relapse, concern with natalizumab)
73
Describe the treatment for PML?
No cure – “fix” reason for immune suppression Stop meds (plasma exchange if needed) Symptomatic care, stop the drug they are one, wait and see
74
What drugs is PML associated with? Risk factors?
Seen with natalizumab (major), dimethyl fumarate, fingolimod, ocrelizumab Increased risk: JCV+, prior immunosuppressant, >2 years use (natalizumab) (risk increased)
75
Is JCV + a contraindication to use of these agents?
Can stay on drug if they are JCV + - Can pick up PML on an MRI early on - More monitoring required - Can stay on after 2 years and know they are JCV+ If risk is higher not an automatic reason to come off of it
76
Describe Interferon beat-1B
Injectable
77
Describe interferon beta-1a
Injectable
78
Describe peginteferon beta-1a
79
Describe glatiramer acetate
Injectable
80
Describe ofatatunumab
Injectable
81
Describe teriflunomaide
Oral
82
Describe dimethyl fumurate
Oral
83
Describe fingolimod
Oral
84
Describe siponomod
Oral
85
Describe ozanimod and ponesimod
Oral
86
Describe cladbridine
Oral Disappointment – did not have long term effect that was expected Infections with this one are critical
87
Describe natalizumab
Infusion
88
Describe ocrelizumab
Infusion
89
Describe alemtuzumab
Infusion
90
Define immune reconstitution therapy. Which DMT's are immune reconstitution therapies?
Immune reconstitution therapy (IRT) is a treatment that involves temporarily suppressing the immune system to allow it to renew itself e.g. Alemtuzumab, Cladibrine
91
Describe rituximab
Used off-label in MS Indicated in non-Hodgkin’s lymphomas, RA Anti-CD20 MAB Potential for PML SK dosing: 500-1000mg at Week 0, 2, and then q 6/12 Listed on SK formulary as of Nov 1, 2022 Saskatchewan drug plan put it on formulary even though its off label Significantly cheaper and works just as well without a lot of side effects Dosed every 6 months Can be used in children --> Fongolimid is the only drug with an indication in children (10 and up) Similar adverse effects to ocrelizumab Used for secondary progressive, persistent progressive, relapsing-remitting
92
Describe the efficcay of the available DMT therapies. Is this how we select a DMT for a patient based solely on efficacy?
Alemtuzumab --> Most efficacy Line of no difference: 1.0 Comparable to placebo – all better than placebo Way less relapses of alemtuzumab Some drugs work way better than another – do not pick drugs just on how well they work, other factors to be considered
93
How a DMT be chosen for a patient?
94
describe induction vs escalation techniques in the intiation of a DMT in MS
Induction – Hit them with that high efficacy drugs, then put them on lower efficacy to maintain Escalation – Start at least effective then move upwards NOW --> Offered the higher efficacy ones now and maintained on them
95
Describe the risk of preganancy and MS?
Genetic component but not an absolute risk to pass it on to children Risk of symptomatic treatments in pregnancy not affected by MS – condition you are treated
96
Describe the DMT therapies and usage in preganncy
97
Which DMT"s are teratogens?
Teriflunomide Fingolimod Siponimod Ozanimod/Ponesimod Clabridine Ocrelizumab
98
Describe tx of MS in preganncy
ANti-CD20 therapies can be used in women wishing to get pregnant Current evidence suggests that women can safely start trying to concieve without delay following ant--CD20 therapy Women wil relapsing-remitting MS are at incr4eased risk in the post-partum period, and so prompt treatment post-partum is reocmmended Where women wish to breastfeedm they should be encourage to do so alongside therapy resumption where their tretament of choice is an anti-CD20 monoclonal antibody
99
Describe vaccinations and MS
Inactivated vaccines = generally safe (e.g. flu shot) Live and live-attenuated = generally not recommended (esp if taking DMT)
100
How long should be waited after a relapse for an individual to get a vaccine?
Wait until 4-6 weeks after relapse onset Complex patients on complex drugs…so consider referring If travelling as example and a vaccine not sur eof (yellow-fever as example) – REFER
101
If starting a new DMT, when should an indivdiual get a vaccination?
Need vaccination before starting medication --> 4-6 weeks before starting medication
102
Describe specific DMT agents and Covid Vaccines
COVID vaccines – “boosters” for anti-CD20 DMTs (Ocreluzamab, Rituximab, ateluminuzab) Immune system not building up enough of a response
103
Describe Saskatchewan coverage of DMT in MS
Pharmacists cannot apply for EDS for MS DMT Specific panel that meets and discusses the cases – specific criteria to start a new drug and maintain a new drug Mandate: Insuring that they meet the criteria for the drug

Therapeutics 358 Final (3 decks)

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