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Nayla Pharm > 3- MS > Flashcards

3- MS Flashcards

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
Q

How long does it take for first line therapies to have effect

A

1-2 years, not immediately efficacious!

They are self injected meds that decrease relapse and new white matter lesions

26
Q

How do IFN Beta 1a work

A

alter expression and response to surface antigen= enhanced (good) immune cell activity

27
Q

How does IFN Beta 1b work (immunomodulator)

A

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
Q

What do you have to monitor for if your pt is on IFN

A

Depression! (big S/E)

Electrolytes, CBC, LFT, Thyroid, LVEF

29
Q

What is Glatiramir acetate

A

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
Q

What can glatiramir acetate be used for

A

PREGNANCY!! and CIS and RRMS

but S/E are chest tightening and flushing

31
Q

What are your second line therapies (if 1st line don’t work)

A 
Mitoxantrone 
Natalizumab
Alemtuzumab
Ocrelizumab 
Fingolimod
32
Q

What is Mitoxantrone

A

inhibits RNA and DNA synthesis
BUT has a lifetime dose of 140 (because it can cause PML)
*pregnancy category D

33
Q

What is Mitoxantrone indicated for

A

SPMS
PRMS
worsening RRMS

34
Q

What is Natilizumab

A

attaches to VLA-1 and blocks it’s interaction with VCAM so activated lymphocytes can’t cross the BBB

35
Q

What is Alemtuzumab

A

Depletes CD52 expressing T cells, B cells, NK cells and monocytes

36
Q

What is Ocrelizumab

A

recombinant human anti-CD20 Ab that deletes B cells by modifying Fc region= enhanced Ab dependent cytotoxicity and reduced complement dependent cytotoxicity

37
Q

What is Fingolimod

A

Sequesters circulating lymphocytes into 2-ary lymph organs

Reduces T cell and macrophage infiltration into CNS

38
Q

Who should NOT take Fingolimod

A

Its on Class 1/3 anti-arrhythmics
recent cardiac disease
w/ 2/3 degree AV block
*If on Ketoconazole, fingolimod concentration will increase

39
Q

What are common MS symptoms

A

Spasticity
Bladder Sx
Sensory Sx
Fatigue

40
Q

What is the bottom line with MS

A

Don’t stop Tx, Tx is indefinite

No FDA approved drugs are approved for pregnant women, trying to become pregnant, or nursing

41
Q

No response to IFN Beta or Glatiramir acetate, give

A

Natilizumab

42
Q

If Sx worsen or pt with SPMS give

A

Mitoxantrone

43
Q

Only FDA approved drugs are

A

IFN-B
Glatiramir acetate
Mitoxantrone
Natalizumab

Nayla Pharm (12 decks)

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