Exam 3: MS Flashcards
Treatment of acute attacks
methylprednisolone
prednisone
ACTH
Disease Modifying Therapies
reduce relapse rates, may slow the progression of disability (generally used to treat relapsing rather than progressive forms of MS)
First Line DMTs
interferon B1a (Avonex, Rebif)
interferon B1b (Betaseron, Extavia)
glatiramer acetate (Copaxone)
fingolimod (Gilenya)
Second Line DMTs
natalizumab (Tysabri)
mitoxantrone (Novantrone)
New Drug DMTs
teriflunomide (Aubagio)
dimethyl fumarate (Tecfidera)
cladribine (Mylinax)
Corticosteroids MOA
act by up-regulating anti-inflammatory genes, down regulating pro-inflammatory genes, and alleviating edema in demyelinated areas
Interferons MOA
act in the periphery and at the BBB
periphery: inhibition of auto-reactive lymphocytes
BBB: inhibition of BBB penetration by decreasing matrix metalloproteinase (MMP)
Interferons Clinical Feature
efficacy reduced by neutralizing antibodies
Glatiramer Acetate MOA
synthetic polypeptide, mimics antigenic properties of myelin basic protein
modulation of antigen-presenting cells such as dendritic cells, leading to decreased T cell activation
Fingolimod MOA
sphingosine-1-phosphate receptor agonist
stimulation of oligodendrocyte survival, remyelination (CNS)
interference with lymphocyte movement out of lymphoid organs (periphery)
Fingolimod Clinical Features
progressive multifocal leukoencephalopathy (PML), a potentially lethal brain infection
superior to INF-B
Natalizumab MOA
mab specific for alpha 4 integrin
alpha 4 integrin pairs with beta 1 integrin to produce very late antigen (VLA-4)
inhibition of VLA-4 binding to its ligand and interferes with B and T cell movement into the CNS