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IBI Test 2 > B3.024 Rheumatoid Arthritis Therapy > Flashcards

B3.024 Rheumatoid Arthritis Therapy Flashcards

1
Q

DMARDs

A

disease modifying anti-rhuematic drug
immunosuppressive agents with goal of inducing/maintaining remission
older, oral

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2
Q

methotrexate mechanism

A

inhibition of dihydrofolate reductase-decreases synthesis of purines and pyrimidines thus interfering with DNA synthesis, repair, and cellular replication
increases adenosine release from cells which can dampen inflammation

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3
Q

what is given along with methotrexate

A

folic acid

prevent side effects

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4
Q

methotrexate administration

A

oral or subQ
weekly dose
low: 15-25 mg per week

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5
Q

methotrexate side effects

A 
oral ulcers
GI
nausea
cytopenias
liver tox
teratogen
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6
Q

leflunomide (Arava) mechanism

A

inhibits dihydroorotate dehydrogenase inhibiting pyrimidine synthesis leading to reduction of lymphocytes

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7
Q

leflunomide half life

A

prodrug; enterohepatocyte circulation leads to long half life

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8
Q

luflunomide administration

A

oral

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9
Q

leflunomide side effects

A

diarrhea
cytopenias
liver tox
teratogen

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10
Q

hydroxychloroquine mechanism

A

multiple
inhibits activity of TLRs
inhibits acidification of lysosomes ultimately interfering with antigen processing

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11
Q

hydroxychloroquine administration

A

oral

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12
Q

hydroxychloroquine side effects

A

rare retinal tox

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13
Q

sulfasalazine mechanism

A

sulfapyridine is active moiety but mechanism not identified

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14
Q

sulfasalazine administration

A

oral

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15
Q

sulfasalazine side effects

A

rash
GI
hepatotoxicity
cytopenias

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16
Q

azathioprine mechanism

A

protein synthesis inhibitor

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17
Q

azathioprine administration

A

oral

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18
Q

azathioprine side effects

A

cytopenias
rash
GI
pancreatitis

19
Q

list all conventional DMARDs

A 
methotrexate
leflunomide
hydroxychloroquine
sulfasalazine
azathioprine
20
Q

what are biologics

A

newer medications that are made by molecular biologic techniques

21
Q

what do biologics target

A

cytokines
T cell activation
deplete B cells

22
Q

what is the main goal of TNF inhibitors

A

reduce joint inflammation and damage to joints

23
Q

what are the different TNH inhibitors?

A 
etanercept
adalimumab
certolizumab
golimumuab
infliximab
24
Q

etanercept mechanism (subq)

A

fusion protein of TNF receptor linked to Fc portion of IgG

etanercept binds TNF and blocks its interaction with cell surface receptors

25
Q

adalimumab &golimumab mechanism (subq)

A

human monoclonal antibodies directed against TNF

26
Q

certolizumab mechanism (subq)

A

Fab fragment of a humanized monoclonal antibody directed against TNF

27
Q

infliximab mechanism (infusion)

A

chimeric monoclonal antibody directed against TNF

28
Q

tocilizumab mechanism

A

human monoclonal antibody targeting IL-6 receptor

reduces inflammation and joint damage

29
Q

tocilizumab administration

A

subq or IV

30
Q

ankinra mechanism

A

antagonist of IL-1 receptor

FDA approved for RA but not very effective

31
Q

abatacept mechanism

A

binds CD80/86 on APCs, blocking the interaction of CD28 between APCs and T cells
results in T cells than cannot be activated fully

32
Q

abatacept administration

A

subq or IV

33
Q

rituximab mechanism

A

monoclonal antibody directed against CD20 antigen on B lymphocytes
result is depletion of B cells (but not existing plasma cells without CD20)

34
Q

rituximab administration

A

IV

35
Q

why is rituximab’s success surprising?

A

current understanding does not place B cells as most prominent player (T cells more prominent)

36
Q

tofacitinib mechanism

A

inhibits JAK enzymes

prevents cytokine/growth factor mediated gene expression and intracellular activity of immune cells

37
Q

what type of drug is tofacitinib?

A

targeting synthetic DMARD

one of the most effective

38
Q

tofacitinib administration

A

oral

39
Q

1st line approach to RA therapy

A

methotrexate

40
Q

2nd line approach to RA therapy

A

either: sulfasalazide + hydroxychloroquine + methotrexate (triple therapy)
OR
TNF inhibitors + methotrexate

41
Q

3rd line approach to RA therapy

A 
abatacept
rituximab
tocilizumab
anakinra
tofacitinib
42
Q

what are the combining factors that create “pre-arthritis”

A

susceptibility genes (MHC shared epitope, PAD, PTPN)
environmental factors
epigenetic modifications
post translational modifications (acetylation, carbanylation, citrullination…etc.)

43
Q

what happens after pre-arthritis?

A 
production of autoantibodies and loss of tolerance
asymptomatic synovitis (cellular infiltrate)
symptomatic arthritis
44
Q

which RA drugs are teratogenic?

A 
methotrexate
leflunomide
tocilizumab
abatacept
rituximab
tofacitinib

IBI Test 2 (10 decks)

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