Treatment of RA Flashcards
1
Q
What are goals ?
A
- reduce pain + DA - ideally remission ASAP
- protect articular structure + func
- control systemic complications
- improve QOL
2
Q
DMARDs
A
- 1/more initiated
- modify underlying cause + symptomatic relief
- trad/syntethic + biologic
- synthetic dmards - MXT, Chloroquine sulphate, leflunomide, sulphasalazine
- take weeks - months to work
AVOID COMBO TREATMENT BIOLOGIC DMARDS ESTABLISHED RA > 6M due to increased risk of infec
3
Q
Non-pharmacological therapy
A
- occupational + physical therapy - preserve jt func , extend jt rom , streghten jts + muscles
- joint deformities - minimize disability
- counsel stress management
4
Q
Bridge therapy / symptomatic relief
A
- NSAIDs
- analgesic, anti-inflamm = joitn pain + swelling
- depends on CV risk, GI ADR + adherence - Glucocortioids
- low-dose G < prednisons 1-mg/day
- reduce inflamm = inhibit cytokines + inflamm mediators
- duration < 3m
> prednisone 2/5mg/day lead to osteoperosis / bone loss
- intraarticular adm into joints
- cause cushing syndrome, peptic ulcer, HPT, weight gain, infection, mood changes, cataracts, dyslipidemia, hyperglyceamia
5
Q
Methotrexate = MTX
A
- synthetic
- monotherapy/ combo
- anti-inflamm
- inhibits DHF-R - inhibit purines + thymidylic acid + inhibit production certain cytokines
- ONCE week dosing not daily - myelosuppression - infection + bleeding
- swithc to MTX sc -off-lable - intolerant to git s/e
++ folic acid - reduce folate depleting rxns - stomatitis, d, alopecia, myelopsuppression, elvated LFT
6
Q
chloroquine
A
- MOA unkown
- well tolerated
- slow OA - given atleast 6m before treatment failure
= option if patient c/i to other DMARDs
= not associated renal, hepatic/ BM suppression
7
Q
sulfasalazine
A
- MOA unknown
- minimize nausea + abdominal discomfort = start low doses + titrate slowly
- sulfa allergy - NOT be given
8
Q
Leflunomide
A
- inhibits dihydroorotate DH - enzyme in mitochondria supplies T- lympoh with cytokine stimulation
- inhibits T-lymp + halt cell cycle
- similar MTX/ sulfa
- extended t1/2 - begin with LD
- MTX = hepatoxicity
- abrupt discontinuation - adm cholestyramine - accelerate removal lef from body
9
Q
Biologic DMARDs
A
- failed treatment synthetic DMARDS
- added monotherapy
- replace ineffective synthetic DMARD
- considered intiial therpay
biosimilars and ref product
- used caution ‘
- lymphorpoliferative disease
hepatitis
history malig
HF
10
Q
TNF antagonist
Etanercept
A
- recombinant form human T-recep
- bind to soluble TNF = prevent binding to TNF-R
- alone / combo synthetic
11
Q
TNF antang
Adaliumumab
A
- recombinant human IgG1 monoclonal antibody
- specific human TNF
- binds soluble + bound TNF-alpha
- adm with MTX / other Dmards
12
Q
TNF antag
Infliximab
A
- chimeric IgG1 monoclonal antibody
- binds soluble + bound TNF-alpha
- given with MTX = suppress antibody production against nouse-derived portion mol
- infusion related rxts - rash urticaria etc
1. discontinue infusion
2. slow infusion rate
3. adm corticosteroid / antihistamine
13
Q
TNF antag
Golimumab
A
- human monoclonal antibody
- binds membrane-bound + soluble TNF
- given MTX = moderate - severe RA
- once-monthly SC/ every other month IV dosing
14
Q
Abatacept
co-stimulation modulator
A
- interfer T cell signaling
- block t-cell activation
- cause anergy - lack response to antigen
- monotherapy / combo synthetic
15
Q
Rituximab
generically engineered chimeric anti-CD20 monoclonal antiboy
A
- B-lympho depletion in BM + synovial tissue
- patients moderate-severe RA
-history inadequate response 1/more TNF antagonists - RF +favour rit
ADR - fatal infusion rxns , severe mucocutaneous rxns, heaptitis B reactivation, progressive multifocal leukoencephalopathy