Osteoarthritis Flashcards
1
Q
Osteoarthritis (OA)
A
- Degenerative joint disease of the elderly, characterized by progressive cartilage loss, subchondral bone thickening, and marginal osteophytes
- NO inflammation in OA
- After age 75 80% of people have OA
2
Q
Normal articular cartilage
A
- Normal articular cartilage (type 2 collagen) provides an almost frictionless articulation and serves to absorb and dissipate load
- The cartilage is made by chondrocytes, which also secrete nzs to degrade the ECM
- Healthy collagen matrix is a balance btwn anabolic (production of collagen) and catabolic (destruction of collagen) processes
3
Q
Pathogenesis of OA (!)
A
- A combination of things, mostly decreased articular cartilage matrix synthesis and increased matrix breakdown by the chondrocytes
- Biomechanical factors also contribute to loss of cartilage and matrix integrity
- Genetic and metabolic factors both play a role
4
Q
Primary vs secondary OA
A
- Primary OA: no identifiable cause, often involves the spine, hip, and knee (weight bearing joints)
- Secondary OA: identifiable cause and can involve any joint
- Must consider secondary OA if arthritis is present in unusual locations or below age of 50
5
Q
Ochronosis
A
- Connective tissue manifestation of alkaptonuria (recessive metabolic d/o)
- Buildup of homogentisic acid in joints/tissues
- Results in pigmentation, calcification, and inflammation of joints and tissue
- Can be a cause of secondary OA
6
Q
Gout
A
- Recurrent attacks of inflammatory arthritis
- Caused by elevated levels of uric acid in blood
- Uric acid crystallizes and the crystals (monosodium urate) are deposited into joints, tendons, tissue
- Can be a cause of secondary OA
7
Q
Physical exam features of OA
A
- Bony enlargement: new bone formed due to worn down cartilage
- Effusions: swelling of the joints
- Heberden’s and bouchard’s nodes (OA of the hand)
- Heberden’s: nodes of the DIPs (HeDIPs)
- Bouchard’s: nodes of the PIPs (BoPIPs)
- Crepitus: crackling/popping sounds when the joint is passively moved
8
Q
Strongest risk factors for OA
A
- Age and obesity
- Others: female, previous injury, genetics
- Previous injuries: old fractures, abnormalities of the meniscus, ligament tears
- Running is NOT a risk factor
- Gene that is associate w/ OA: type 2 collagen gene COL2A1
9
Q
OA vs inflammatory arthritis
A
- OA is mechanically driven and not inflammatory
- Inflammatory arthritis can be due to autoimmune illness, crystalline arthropathy, infections, or malignancy
- Key differences: OA is always progressive (inflammatory can be acute or progressive), OA is mostly >50, morning stiffness lasts 30 min (1hr w/ IA), activity makes OA worse (makes IA better), rest makes OA better (makes IA worse), no heberden/bouchard nodes in IA, no osteophytes in IA
10
Q
Rx of OA
A
- Mild-moderate pain: acetaminophen, topical agents
- Moderate-severe pain: joint aspirations if there are effusions, intra-articular injections of glucocorticoids and hyaluronan, COX-2 specific inhibitors, NSAIDs, tramadol, opioids
- If overweight, weight loss is key
