Arthritis Flashcards
Pathology and pathogenesis of OA
- IL-1, TNF-1,PG,NO,Matrix Degradation Products
- Synovial Inflammation => Dediffererentiation of Chondrocytes (Inc in 1 and 2 type of collagen,shorter proteoglycans,dec. proteinases,inc. proteinases) => Inc collagen breakdown => Carillage loss => Fibrillations => subchondral bone remodelling =>osteophytosis
Gross Features of ARthritis
- End Stage bone disease
- Bone spurs,Exposed bone,Eroded cartillage and Meniscus
Consequence of Shorter proteoglycans
Cartillage are less hydrophillic, stiffer, and more to cracking/fracturing
Morphologic changes in OA
1 Shift to chondrocyte catabolic phenotype
2 mechanical stress as a relevant inducer of downstream inflammatory and catabolic events in cartillage
3 TLR2, TLR4 upregulation
4 Complement dysregulation
Classification OA
Idiopathic (localized and Primary) and Secondary (Trauma 40%)
Primary Non-modifiable Risk Factors for OA
Age
Race
Female Gender
GEnetic Factors (col 1 gene)
Responsible for Low-grade inflammatory State of obesity
adipokines
Secondary OA
ACl tear, repetitive stress, inflamamtory joint disease, Metabolic.endocrine disorders, congenital and dev defects, proprioceptive defects, Vitamin D and C deficiency
clinical features of oa
no systemic mx, slow evolution, age,one or few joints,non-inflamatory
Sx of OA (different from sign)
*Use related pain, relief with rest, gelling, loss of movement
Signs of OA
Coarse crepitus, Bony swelling, Mild inflammation, deformities, Tenderness around joint
First symptom of OA
first symptom is pain
Pip Swellings
bouchard’s nodes
DIP nodes
heberden’s nodes
PAthology of RA
Microvascular endothelial cell activation /injury => Synovial hyperplasia > Synovial hypertrophy and edema => Tissue ischemia and infarction = Pannus => Erosion of subchondral bone