Osteoarthritis

  • Created by: Paul
  • Created on: 08-12-12 11:16
Epidemiology - OA
Nearly half of all with radiological findings half no symptoms - vice versa, Is not reversible and prevalence increases with age, Woman more than men 2:1, 25-75, Top 10 disabling diseases in developed countries
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Aetiology - OA - Modifiable
Body mass, previous injury, Occupation, Footwear, Bio mechanics, Weakness
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Aetiology - OA - Non - Modifiable
Gender, Age, Race, Genetic prediposition
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Aetiology - OA - Others
Oestrogen deficiency (ERT may reduce risk of knee/hip OA), C-reactive protein, Lack of CED vitamins,
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Pathophysiology - OA - (1)
Although once considered a non-inflammatory arthritis increasing evidence has shown that inflammation occurs as cytokines and metalloproteinase are released into the joints
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Pathophysiology - OA - (2)
These agents are involved in the excessive matrix degradation that characterises cartilage degeneration in OA, In early OA swelling of the cartilage usually occurs due to synthesis of proteoglycans,
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Pathophysiology - OA - (3)
This reflects an effort by the chondrocytes to repair the cartilage damage, This stage may last for years or decades and is characterised by hypertrophic repair of the articular cartilage
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Pathophysiology - OA - (4)
As OA progresses the level of proteoglycans lowers and this causes the cartilage to soften and lose elasticity thereby further compromising joint integrity
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Pathophysiology - Rheumatoid Arthritis - (3)
These cells secrete a variety of pro inflammatory mediators such as TNF-a, IL-1 and other cytokines such as IL-6, resulting in the underlying joint destruction that is seen in patients with long standing RA
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Pathophysiology - Rheumatoid Arthritis - (2)
Infiltration by macrophage like cells occurs and the synovial membrane is thickened by these chronic inflammatory cells, This thickening is made up of a variety of cells including T and B cells as well as macrophages
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Pathophysiology - Rheumatoid Arthritis - (5)
The pathological changes are not confined to joints, The synovial lining of tendon sheaths may be similarly inflamed and thickened, both in hands and feet
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Pathophysiology - Rheumatoid Arthritis - (1)
Immune system is activated by an unknown antigen, antigen presenting cells take this antigen to the T-cells and stimulate them, The T-cells then proliferate and secrete a variety of pro inflammatory cytokines and migrate to the synovial tissue
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Pathophysiology - Rheumatoid Arthritis - (4)
As RA progresses the articular cartilage is softened and eroded the subchondral bone may also become eroded also, The eroded surfaces become covered by a soft membrane of inflammatory tissue known as pannus
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Pathophysiology - Rheumatoid Arthritis - (6)
The contained tendons may become softened and may rupture, This may aggravate any existing deformity, Inflammatory nodules may form in the soft tissue
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Pathophysiology - Rheumatoid Arthritis - (7)
After years of activity the disease tends to become less active usually leaving permanant damage, instability and deformity
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Pathophysiology - OA - (5)
Flaking and fibrillations develop along normally smooth articular cartilage surfaces, Over time the joint space will reduce
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Pathophysiology - OA - (6)
Erosion of the damaged cartilage in OA progresses until the underlying bone is exposed, Bone denuded of its protective cartilage continues to articulate, Biomechanical yeild strength, Vascular invasion and becomes thickened and dense (Eburnation)
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Pathophysiology - OA - (7)
Cystic degeneration may occur (geodes), Due to osseous necrosis from chronic impaction, Or due to synovial fluid intrusion, Osteophytes may form - Ligament damage + NM
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Clinical Manifestations - OA
Pain in affected joint on repeated movement, Morning stiffness usually brief and self limiting, Tenderness over joint, Warmth over joint, Crepitus on movement, Bony enlargements at joint margin
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Clinical Manifestations - OA
Dependant on joint involved, Radiographic changes, Arthrocentesis to detect WBC <1000 mm3 indicates OA higher than this consider inflammatory arthritis
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Clinical Manifestations - OA
Heberdens nodes + Bouchards nodes fingers, May be painful often associated with limitation in movement
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Clinical Manifestations - OA
Symptoms may be intermittent, Erythrocyte sedimentation rate should be normal for age, Not systemic so doesn't affect other organs, Can be unilateral does not usually affect the MTP joints, Can affect the whole spine unlike RA
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Rx - OA
No current cure, Rx usually focuses on relieving symptoms and improving function, Includes a combination of patient education, PT, weight control and medications
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Rx - OA
For persistant OA that does not respond to these Hyaluronic acid can be used especially if surgery is not being considered, Osteotomy, Arthrodesis, TJR and Arthroscopy may be used as a last resort
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Other cards in this set

Card 2

Front

Aetiology - OA - Modifiable

Back

Body mass, previous injury, Occupation, Footwear, Bio mechanics, Weakness

Card 3

Front

Aetiology - OA - Non - Modifiable

Back

Preview of the front of card 3

Card 4

Front

Aetiology - OA - Others

Back

Preview of the front of card 4

Card 5

Front

Pathophysiology - OA - (1)

Back

Preview of the front of card 5
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