OA Flashcards

(21 cards)

1
Q

Front

A

Back

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2
Q

Define osteoarthritis (OA).

A

Degenerative joint disease characterised by progressive loss of articular cartilage, subchondral bone remodelling, osteophyte formation, and synovial inflammation leading to pain and functional limitation.

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3
Q

Which joints are most commonly affected in OA?

A

Weight-bearing joints (knees, hips, spine), hands (DIP, PIP, 1st CMC), and feet (1st MTP). MCP joints are spared.

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4
Q

Pathophysiology of OA?

A

Mechanical stress + biochemical degradation → chondrocyte injury → ↑ matrix metalloproteinases (MMPs), ↓ type II collagen synthesis → cartilage loss + bone sclerosis + osteophytes.

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5
Q

List modifiable and non-modifiable risk factors for OA.

A

Modifiable: obesity, joint injury, occupational stress. Non-modifiable: age, female sex, genetics, congenital malalignment.

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6
Q

Describe radiographic features of OA.

A

Joint space narrowing (asymmetric), osteophyte formation, subchondral sclerosis, subchondral cysts. No periarticular osteopenia (cf. RA).

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7
Q

Clinical features of OA.

A

Pain worse with activity, relieved by rest; morning stiffness <30 min; bony swelling; crepitus; restricted ROM; Heberden (DIP) and Bouchard (PIP) nodes.

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8
Q

Differentiate OA from rheumatoid arthritis (RA).

A

OA: asymmetric, non-inflammatory, <30 min stiffness, DIP involved, negative RF/CCP. RA: symmetric, inflammatory, >60 min stiffness, MCP/PIP involved.

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9
Q

Role of MRI in OA.

A

Not routinely required. Used for differential diagnosis (AVN, meniscal tear, stress fracture) or early OA detection before radiographic changes.

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10
Q

Initial management of OA.

A

Education, weight loss, exercise (quad strengthening, aerobic), physiotherapy, simple analgesia (paracetamol), topical NSAIDs, heat/cold therapy.

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11
Q

Second-line pharmacologic therapy.

A

Oral NSAIDs ± PPI cover, intra-articular corticosteroids for flare, duloxetine (chronic pain), topical capsaicin. Avoid opioids long-term.

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12
Q

Surgical indications in OA.

A

Severe pain/disability despite maximal therapy, significant functional limitation, radiographic evidence of joint destruction.

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13
Q

Describe the role of joint replacement in OA.

A

Total joint arthroplasty relieves pain and restores function. Most effective for end-stage knee and hip OA; lifespan ~15–20 years.

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14
Q

Which pharmacologic agents are NOT recommended for OA?

A

Glucosamine/chondroitin (no consistent evidence), hyaluronic acid injections (minimal benefit), systemic steroids (no role).

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15
Q

What is erosive OA?

A

Inflammatory subset of hand OA affecting DIP/PIP joints with central erosions (‘gull-wing’ deformities). Middle-aged women; may respond to hydroxychloroquine.

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16
Q

Biochemical findings in OA.

A

Normal inflammatory markers (ESR, CRP). Synovial fluid: non-inflammatory (WCC <2000/mm³).

17
Q

OA vs CPPD (pseudogout) overlap.

A

CPPD can mimic OA but often involves atypical joints (MCP, wrist). Radiograph: chondrocalcinosis. Synovial fluid: rhomboid, weakly positive birefringent crystals.

18
Q

Explain knee OA subtypes.

A

Medial compartment → varus deformity; Lateral → valgus deformity; Patellofemoral → anterior knee pain, worse on stairs.

19
Q

Practice-changing evidence for exercise therapy in OA.

A

2023 Cochrane review: structured exercise (≥12 weeks) improves pain/function equivalent to oral NSAIDs; cornerstone of long-term management.

20
Q

Australian PBS nuance for OA pharmacotherapy.

A

No PBS subsidy for duloxetine unless major depressive disorder; intra-articular corticosteroids PBS-listed for large joints; biologics not indicated.

21
Q

Key exam pearls.

A

Morning stiffness <30 min; asymmetrical; absence of systemic symptoms; no synovitis; DIP involvement; bony-hard swellings; x-ray features mnemonic: LOSS (Loss of space, Osteophytes, Sclerosis, Subchondral cysts).