Rheumatoid Arthritis Flashcards Preview

Musculoskeletal > Rheumatoid Arthritis > Flashcards

Flashcards in Rheumatoid Arthritis Deck (23):
1

Epidemiology of RA

•Most common type of polyarthritis. 3x more common in women. 1% total population.
•Peak onset in 3rd to 5th decade

2

2 risk factors for RA

Tobacco and HLA-DRB1 (shared epitope)

3

Pathogenesis of RA

Synovial membrane cells proliferate into a pannus rich w/ macrophages, fibroblasts, PMNs, B cells, plasma cells, and T cells. Vascular proliferation permits increased cell trafficking. Cytokines are released, MMPs break down bone / cartilage

4

5 diagnostic criteria for RA

•Must have synovitis w/o other cause
•Multiple joints
•RF / CCP (more specific). High titer is >3xULN.
•Increased ESR / CRP
•>6 weeks

5

What joints are usually involved in RA? Which are not involved?

Usually involves PIPs, MCP, wrist, and MTP.
Usually does NOT involve hips, DIPs, and lumbar spine.

6

ESR vs CRP

ESR reflects 1 month, CRP reflects days.

7

Extra-articular / systemic manifestations of RA
Mild
Moderate / severe

•Mild: rheumatoid nodules, nail fold infarcts, iron deficiency anemia, Raynauds, Sjogrens
•Moderate / severe: scleritis, interstitial lung disease, pericarditis, pleuritis, vasculitis (may cause ulcers), Felty syndrome (neutropenia + splenomegaly), nerve impingement from cervical spine disease, premature CVD (due to systemic inflammation)

8

Treating acute RA (3)

•NSAIDs – naproxen is good to start with.
•Prednisone – use while DMARDs kick in. Good for flares. Extra-articular disease requires higher dose.
•Steroid injections if only a few joints are involved.

9

4 DMARDs
What does DMARDs stand for?

Disease modifying anti rheumatic drugs
Methotrexate, leflunomide, Sulfasalazine, and hydroxchloroquine.

10

Methotrexate
Mechanism
Toxicity
Requirements

•Mechanism – inhibition of dihydrofolate reductase blocks purine synthesis. Blocks cells w/ high turnover.
•Toxicity – TERATOGEN, CIRRHOSIS (esp w/ ETOH), oral ulcers, GI, cytopenias, cough / SOB (lung hypersensitivity), infection
•Requires daily folic acid. Monitor CBC, liver, kidney. Get baseline LFTs, Hep B / C, and CXR.

11

Leflunomide
Mechanism
Toxicity
Requirements
How is drug eliminated quickly?

•Mechanism – inhibits dihydroorotate dehydrogenase → stops pyrimidine / purine synthesis → stops proliferation of T cells.
•Toxicity – Teratogen, GI, alopecia, HTN, cytopenias, liver toxicity (esp w/ alcohol), infection
•Requirements: Monitor CBC, liver, kidney. Get baseline Hep B / C and CXR.
•Give cholestyramine in hospital for px w/ infection to get rid of drug quickly

12

Sulfasalazine
Mechanism
Toxicity
Safe with what?
Requirements

•Mechanism – AB and anti-inflammatory
•Toxicity – GI, liver toxicity, aplastic anemia, nephritis syndrome, pancreatitis, headache. Contraindicated w/ sulfa allergy.
•Safe w/ pregnancy and alcohol.
•Monitor CBC, liver, and screen for G6PDH

13

Hydroxychloroquine
Use
Mechanism
Toxicity
Requirement

•Use – Mainstay for lupus. Used for very mild RA.
•Mechanism – mild antimalarial that stablizes lysosomes, inhibits DNA polymerase, decreases fibronectin / platelet aggregation / histamine / IL1 cellular inflammation and destruction. Does NOT cause immunosuppression.
•Toxicity – retinal toxicity, pigment, neuromyopathy
•Monitor visual field testing every 1-5 years

14

Triple therapy
Works as well as what?

Mtx, Ssz, Hcq.
Works as well as TNF-inhibitor

15

TNFa Inhibitors
4 monoclonal Abs
1 soluble receptor drug

•Monoclonal Abs: infliximab, adalimumab, golimumab, certolizumab
•Etancercept is soluble receptor

16

4 risks of TNFa Inhibitors

•Infection – may not mount high fever, atypical / fungal infection, disseminated TB (TB test should be done before starting anti-TNF)
•Heart failure
•Demyelination
•Malignancy – nonmelanoma skin cancer, lymphoma

17

4 non-TNF biologics

Abatacept, rituximab, tocilizumab, tofacitinib

18

Abatacept
Mechanism
Pro / con

CTLA4 blocks T cell co-stimulation.
Lower infection risk than anti-TNF, but takes 4 months to work

19

Rituximab
Mechanism
Risk factors

Anti-CD20 Ab depletes naïve B cells.
Risk of Hep B reactivation and progressive multifocal leukoencephalopathy (PML, brain infection)

20

Tocilizumab mechanism

Anti-IL6, which normally triggers cartilage destruction

21

Tofacitinib
Mechanism
Risk

JAK kinase inhibitor.
Risk of EBV-related malignancy

22

4 general risks of biologics

•Injection / infusion rxns due to being foreign molecules
•Predisposition to infection. Avoid live vaccinations. Evaluate fever / monoarthritis.
•Non-melanoma skin cancer
•Biologics should not be combined. May be used w/ DMARDs.

23

Fibromyalgia
Gender / age
Sxs
Management

•2x more common in women. Mean onset is 45 y/o. 2-5% of adults.
•Sxs: Diffuse chronic pain is hallmark. May have migrating burning, tender skin, flares, fatigue / sleep disruption, cognitive problems (“fibro fog”), headache, IBS, TMJ
•Management – sleep regulation, gentle exercise, non-narcotic pain meds; NO steroids b/c not inflammatory.