3- MS Flashcards

(43 cards)

1
Q

What is Multiple Sclerosis

A

CNS demyelination and axial damage

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2
Q

What is the key to MS diagnosis

A

dissemination of plaques

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3
Q

What is the pathophys of MS

A

PMN infiltrate space between A&V and pia mater and demyelinate axons. Immune reactions form plaques in multiple areas of CNS

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4
Q

What gets MS

A

genetically susceptible people exposed to random environmental effects that trigger immune mediated CNS damage

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5
Q

What are th most common MS triggers

A
Vitamin D deficiency
CMV 
EBV
HHV6
Smoking
High dietary sodium 
Circadian Disruption
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6
Q

What is the “theory” behind MS

A

T helper cells stick to vessels and create openings allowing them to cross BBB
In the CNS, T helper cells produce cytokines
Cytokines call other inflammatory cells and they all form an immune attack causing plaques

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7
Q

What are the cytokines involved in MS

A

Th1 and Th2: pro-inflammatory
Th17 anti-inflammatory
Treg regulatory

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8
Q

Name the most favorable prognosis patient with MS

A
<40
female
presenting Sx of option neuritis or sensory Sx
RRMS
Low T1/T2
single lesions
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9
Q

What is unique about Th17 and Treg

A

They can change and become Th1 and Th2

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10
Q

What are indications for Treatment of MS exacerbation

A

Relapses localize to optic nerve, spinal cord, or brainstem
Sx affect daily living
Sx worsen over 2 weeks

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11
Q

What is your med tx of choice for exacerbations of MS

A

Corticosteroids; high dose IV Methylprednisone w/in 2 days of Sx
(improvement w/in 3-5 days)

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12
Q

How does Methylprednisone work

A

Improves recovery by decreasing edema around demyelination

BUT doesn’t affect disease progression

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13
Q

What are S/E of Methylprednisone

A

Sleep disturbance
Metallic taste
Increase BG in Diabetics
Long term: acne, fungal infections, mood changes

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14
Q

What should your RRMS treatment regimen be (steps)

A
Interferon
Glatarimir acetate
Fingolimode 
Teriflunomide
Dimethyl fumarate
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15
Q

What is Terifluronimide

A

Oral DMT that (inhibits dihydroorotate dehydrogenase) prevents proliferation of peripheral T/B lymphocytes= lower inflammation and demyelination
Pregnancy X**

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16
Q

S/E of Teriflunomide include

A

Steven-Johnson syndrome (flu sx, then painful red and purple rash and blisters, then top layer of skin dies and sheds)

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17
Q

What is Leflunomide

A

active metabolite of Teriflunomide

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18
Q

What is Dimethyl Fumarate

A

Nicotinic receptor agonist
Nuclear factor pathway activator
-Involved in response to oxidative stress

19
Q

What are S/E of Dimethyl fumarate

A

Flushing (give w/ food)
Lymphocyopenia
rash, pruritus, GI discomfort

20
Q

What do you need to monitor if patient is taking Teriflunomide or Dimethyl fumarate

A
Pregnancy 
TB test
LFT
CBC
BP (may increase)
21
Q

When would you add Teriflunomide or Dimethyl fumarate

A

If Symptoms continue to worsen when already on corticosteroids

22
Q

What are your First Line DMT

A

Interferons (IFN Beta 1a/1b) and Glatiramir acetate

23
Q

What are the IFN Beta 1a

A

Avonex (low potency)

Rebif (high potency)

24
Q

What are the IFN Beta 1b

A

Betaseron (high potency)

Extavia (high potency)

25
How long does it take for first line therapies to have effect
1-2 years, not immediately efficacious! | They are self injected meds that decrease relapse and new white matter lesions
26
How do IFN Beta 1a work
alter expression and response to surface antigen= enhanced (good) immune cell activity
27
How does IFN Beta 1b work (immunomodulator)
Increase suppressor cell fxn and reduce IFN-y secretion Activates Macrophages Surpasses T cell proliferation (less BBB permeability) Increases CD56 NK cells and Treg
28
What do you have to monitor for if your pt is on IFN
Depression! (big S/E) | Electrolytes, CBC, LFT, Thyroid, LVEF
29
What is Glatiramir acetate
4 AA (Ala, Glut acid, Lys, Tyr) that mimic myelin basic protein (MBP)= No binding of MBP to T receptor cells = reduced inflammation, demyelination, and axon damage *Suppresses T cell activation *Neuroprotective effect
30
What can glatiramir acetate be used for
PREGNANCY!! and CIS and RRMS | but S/E are chest tightening and flushing
31
What are your second line therapies (if 1st line don't work)
``` Mitoxantrone Natalizumab Alemtuzumab Ocrelizumab Fingolimod ```
32
What is Mitoxantrone
inhibits RNA and DNA synthesis BUT has a lifetime dose of 140 (because it can cause PML) *pregnancy category D
33
What is Mitoxantrone indicated for
SPMS PRMS worsening RRMS
34
What is Natilizumab
attaches to VLA-1 and blocks it's interaction with VCAM so activated lymphocytes can't cross the BBB
35
What is Alemtuzumab
Depletes CD52 expressing T cells, B cells, NK cells and monocytes
36
What is Ocrelizumab
recombinant human anti-CD20 Ab that deletes B cells by modifying Fc region= enhanced Ab dependent cytotoxicity and reduced complement dependent cytotoxicity
37
What is Fingolimod
Sequesters circulating lymphocytes into 2-ary lymph organs | Reduces T cell and macrophage infiltration into CNS
38
Who should NOT take Fingolimod
Its on Class 1/3 anti-arrhythmics recent cardiac disease w/ 2/3 degree AV block *If on Ketoconazole, fingolimod concentration will increase
39
What are common MS symptoms
Spasticity Bladder Sx Sensory Sx Fatigue
40
What is the bottom line with MS
Don't stop Tx, Tx is indefinite | No FDA approved drugs are approved for pregnant women, trying to become pregnant, or nursing
41
No response to IFN Beta or Glatiramir acetate, give
Natilizumab
42
If Sx worsen or pt with SPMS give
Mitoxantrone
43
Only FDA approved drugs are
IFN-B Glatiramir acetate Mitoxantrone Natalizumab