rheumatoid arthritis Flashcards
what are the risk factors for RA
genetic predisposition
- variations in HLA-DR4/ HLA-DR1
- FMHx rheumatoid factor positivity
what is the pathophysiology of RA
genetic predisposition + immunologic trigger
-> T-cell mediated immune response
-> inflammatory response and release of pro-inflamm cytokines (IL17, TNF, IL1, IL6)
-> release of proteases and prostaglandins
–> destruction of articular cartilage and underlying bone
what is the presentation of RA
- polyarthritis
- symmetrical
- pain (worse on rest, relieved with activity, nocturnal pain, worse in morning)
- associated sx ( systemic sx of general aching, malaise, fever, stiffness; morning stiffness >30mins, joint swelling and erythema)
- deformities (fingers = swanneck/ boutenneire; elbows = rheumatoid nodules; toes = MTP subluxation; back of knees = popliteal cysts)
- diagnostics (pos RF, pos anti-CCP, increased CRP, increased ESR, decreased Ht, increased WBC, increased PLT)
what are the goals of therapy for RA
- main goal is to achieve remission or low disease activity
- achieve maximal functional improvement
- stop disease progression
- prevent joint damage
- control pain
what is defined as achieving remission/ low disease activity for RA
for boolean
at least 6m of
- TJC 1 or less
- SJC 1 or less
- CRP 1mg/dL or less
- PGA using 10cm VAS is 2cm or less
what is the pharmacological management for RA
*NSAIDs unlikely helpful
- short term bridging therapy with GC (PO Prednisolone <7.5mg/d for up to 3m or IA GC q3m but max 2-3x/yr due to risk of tendon atrophy and accelerated joint destruction)
- csDMARDs (MTX, hydroxychloroquine, sulfasalazine, leflunomide)
- bDMARDs (TNF blocker - infliximab, etanercept; IL6 RA - tocilizumab; anti-CD20 B cell depletion mAb - rituximab)
- tsDMARDs (JAKi - tofacitinib)
what is the non-pharmacological management of RA
- rest inflammed and painful joints
- exercise when able to, to maintain joint range of motion and increase muscle strength, and to improve sleep
- psychosocial interventions like CBT
what are the dosing regimens for csDMARDs
MTX: initiate at 7.5mg q1w, titrate up 2.5-5mg/w q4-12w to target dose 15mg/w
+ folic acid 5mg/w
+ short-term PO Prednisolone <7.5mg/d for up to 3m
sulfasalazine: initiate at 500mg OD/BD, titrate up 500mg/w until MD of 1g BD
hydroxychloroquine: initiate at 200-400mg in one or two divided doses
what are the considerations when deciding to add bDMARDs or tsDMARDs
bDMARDs have lower risk of CV and malignancy adverse effects for patients with risk factors
what are the steps to take prior to initiating bDMARDs or tsDMARDs
- screen for latent or active TB, hep B and hep C
- obtain vaccinations for pneumococcal, influenza, hepB, varicella zoster
- obtain baseline labs for CBC w differential WBC and PLT, LFT, lipid, SCr
when to decide to switch or add bDMARD or tsDMARD in relation to monitoring in active diseases
monitor q1-3m in active disease, adjust therapy if no improvements by 3m mark or not at target at 6m mark
what are the c/i for each of the csDMARD
MTX: pregnancy, preexisting liver disease, immunodeficiency, blood dyscrasias, CrCl <30
sulfasalazine: sulfonamide allergies, caution in G6PD
hydroxychloroquine: preexisting retinopathy, caution in G6PD
leflunomide: pregnancy, ALT >2xULN
what are the significant s/e of csDMARDs
MTX: elevated transaminases, myelosuppression, SJS/TEN
hydroxychloroquine: retinopathy
leflunomide: elevated transaminases, alopecia, myelosuppression
what are the concerns with tofacitnib
tofacitinib is a JAKi with safety concerns esp regarding GI perforation and thrombosis, and higher risk of CV and malignancy adverse events in patients with risk factors
risk factors for CV are >65yo, past/ current smoking, obesity, PMHx of HTN/ DM
risk factors for malignancy are hx for past/ current malignancy
