osteoarthritis Flashcards
what are the investigations that can be done to differential diagnose joint pain
- hematological tests
- rheumatoid factor (RF)
- anticitriullinated protein antibody (anti-CCP)
- c-reactive protein (CRP)
- erythrocyte sedimentation rate (ESR)
- joint aspiration
- xray/MRI
what is the presentation of osteoarthritis
- polyarthritis
- asymmetrical
- pain characteristics: gradual onset, pain on movement, worse at end of day, no nocturnal pain, relieved with rest
- assoc sx: potential joint swelling and erythema, early morning stiffness <30mins, crepitus
- deformitis: enlarged joints (due to osteophytes), heberden’s/ bouchard’s node in fingers
what are the risk factors for OA
- genetic predispostion (rare mutations in collagen types)
- anatomical factors (varus: bow legged, valgus: knocked knee)
- aging (ECM changes - thinning, decreased hydration, increased brittleness)
- joint injury
- obesity
- gender
- occupation
what is the pathophysiology of OA
- articular cartilage damage leading to cartilage degradation due to production of improperly mineralized collagen
- weakened collagen matrix leads to thickening of subchondral bone and sclerosis and formation of bone spurs called osteophytes
- synovial inflamm as weakened collagen matrix undergo degradation and flakes off as shards causing recruitment of lymphocytes and macrophages to remove debris, producing pro-inflammatory factors like cytokines, chemokines and matrix degrading enzymes like MMPs that promote joint tissue destruction
how does pain arise in OA
pain arises when there is
- activation of nociceptive nerve endings within the joint by mechanical or chemical irritants
- distension of synovial capsule from increased joint fluid, microfracture, periosteal irritation or damage to ligament, synovium or meniscus
what are the goals of therapy for management of OA
- relieve pain
- improve or preserve range of motion and joint function
- improve QoL
*note that surgical intervention has a “lifespan”
what are the non-pharmacological management for OA
- exercises to relieve pain and improve functioning (low-impact, strengthening and neuromuscular training)
- consider referral to PT for supervised exercise and training
- weight management to reduce load on joints
- patient education on should not rely on analgesics but on exercise to strengthen joint and prevent further deterioration
- surgical intervention (total joint arthroplasty) with postoperative rehabilitation
what are the pharmacological management of OA
*start with least systemic exposure or toxicity, and also lowest effective dose for shortest period of time
- topical NSAIDs
- PO NSAIDs/ coxibs
- PO paracetamol/ tramadol (only if c/i to NSAIDs)
- IA GC (but effects shortlived for 6m to a few months and max 3-4inj a year)
what are the significant considerations when choosing PO NSAIDs or coxibs
GI (N, dyspepsia, abdominal pain)
- risk factors include >65yo, hx of ulcer, use of high dose NSAID, concurrent GC/ anticoagulants
CVS (MI, stroke, vascular death)
- related to cox 2 inhibition, use celecoxib at <400mg/d and use of high dose systemic diclofenac of 150mg/d for >4w is c/i in established CVD or uncontrolled HTN
renal (AKI)
- risk factors include volume depletion, severe hypercalcemia, renal artery stenosis, concom AG/ amphotericin B/ radioconstrast material/ diuretics/ ACEi/ ARB/ hyper K/ hypo Na, >65yo
add-on PPI prophylaxis
what are other safety concerns of PO NSAIDs
- allergic rxn
- pseudoallergic rxn
which special populations should PO NSAIDs and coxibs be avoided in
- asthma (caution for coxib)
- third trimester pf pregnancy (24-40w)
- concurrent use of anticoagulant
- active GI bleed/PUB (caution for coxib)
- severe kidney impairment
- HF, IHD, PAD, uncontrolled HTN
- hypersensitivity esp anaphylaxis to aspirin, NSAIDs, coxibs (and sulphonamides for celecoxib)
what are the usual dosing of PO NSAIDs
diclofenac 50mg BD/TDS (max 150mg/d)
indomethacin 25-50mg BD/TDS (max 150mg/d)
*more associated with CNS effects (HA, altered mental status)
mefenamic acid 250mg TDS (max 1000mg/d)
*more often used for dysmenorrhea
ibuprofen 400mg TDS/QDS (max 3200mg for acute, 2400mg for chronic)
naproxen sodium 275-550mg BD (max 1375mg for acute. 1100mg for chronic)
what are the usual dosings for PO coxibs
celecoxib 200mg OD (max 400mg/d)
etoricoxib 30-60mg OD (max 60mg for chronic, 120mg up to 8d for acute)
compare and contrast the GI, CVS and renal concerns between NSAIDs and coxibs
coxibs like celecoxib and etoricoxib have lesser risk of GI toxicity relative to NSAIDs, no effect on PLT function, CV and kidney risks are dose related and similar to NSAIDs
