L21- Arthritis Flashcards
(39 cards)
Synovial Joints:
- (1) describe cells
- cells produce (2), which has (3) functions
1- Synovial cells- mesenchymal cells; cuboid or fibroblast like cells, 1-4mm thick
2- Synovial fluid into joint space, hyaluronic acid, proteins
3- lubrication and nourishment to joint / articular cartilage
Articular cartilage is made out of (1) which is produced by (2). (2) also has (3) functions. Articular cartilage has (4) thickness.
1- type II collagen, proteoglycans
2- chondrocytes
3- produces matrix degrading enzymes for turnover
4- 1-4mm thick
Articular cartilage:
- (1) function
- (2) are importantly absent
- (3) provides nourishment to cells
1- shock absorber, smooth / friction free movements — type II collagen disperses force across joint surface so bone absorbs most of the shock
2- BVs, nerves
3- synovial fluid
describe the arrangement of type II collagen in articular cartilage
Area closest to bone- vertical arrangements
Area furthest from bone (closest to joint)- horizontal arrangement
Functions: transmit vertical stress, resists tensile forces, disperse force across joint surface into bone
list the common types of arthritis
osteoarthritis rheumatoid arthritis seronegative arthritis crystal deposition- gouty arthritis infectious arthritis
(1) is the most common type of arthritis, describe as (2).
Osteoarthritis: progressive destruction of articular cartilage
Indicate primary or secondary OA:
- (1) older patients
- (2) affects more joints
- (3) more severe
1- primary, 80-95% are >65 y/o
2- secondary polyarticular (many joints)— primary oligoarticular (few joints)
3- secondary
(1) is the cause of primary OA.
(2) conditions have risks of developing secondary OA.
1- aging
2- DM, hemachromatosis, ochronosis, obesity, congenital deformity
list the three general changes seen to synovial joints in OA
- changes to Articular Cartilage components
- chondrocyte changes
-others: proinflammatory CKs –> inflammatory cells
describe the changes to articular cartilage in OA
- altered proteoglycans => water(inc)-PG(dec) imbalance = chondromalacia-softening
- diminished pliability of collagen due to orientation mismatch or defective structure
=> weaker articular cartilage
describe the changes to chondrocytes in OA
- IL-1, TNF-α release –> breakdown matrix
- inhibition of type II collagen synthesis
=> cartilage breakdown => reactive changes => inflammatory response
In OA there is decreased synthesis of (1) and increased activity of (2) in synovial joints. (2) occurs via (3) enzymes which regulated via (4) mediators, and (5) may be an additional factor contributing to (2).
1- articular cartilage
2- enzymatic breakdown
3- metalloproteins: proteoglycan breakdown, Stromelysins // collagen breakdown, Collagenases
4- IL-1, TNF-α
5- collagen gene mutations (genetic predisposition)
Primary OA:
- (1) prevalence
- (2) commonly affected joints
- affects (males/females) more
- (4) and (5) are major risk factors
- (6) are secondary risk factors
1- 75% of all people >70y/o
2- knee, hip, spine, fingers/toes (oligoarticular)
3- females
4- obesity
5- hereditary / genetic predisposition
6- trauma, neuromuscular dysfunction, metabolic disorders
list the commonly affected locations of primary OA and what deviations from these locations may indicate
knee, hip, spine, finger/toes
-if in other locations –> investigate for secondary causes of OA
list the many changes seen on X-Ray for OA
- dec joint space
- erosion of articular cartilage
- eburnation (smoothing of bone where cartilage should be via friction)
- sclerosis
- subchondral cysts
- osteophytes
describe the development of osteophytes in OA
- occurs due to reparative process occurring around articular cartilage
- fibrocartilage deposition –> bony spur
describe the major histological changes seen in OA
- horizontal oriented type II collagen fibers destroyed (the more superficial layer)
- vertical cracking in cartilage
- chondrocytic proliferation => hyperplasia, hypertrophy –> degeneration / removal exposes bone
describe the major gross changes seen in OA
- Erosion of articular cartilage, could be totally absent at joint apex and intact at periphery
- Eburnation: bone smooth due to friction
- Subchondral Cysts: synovial fluid –> pushed into bone –> creates cyst + sclerosis reaction (denser bone)
______ is arthritis due to an autoimmune condition
rheumatoid arthritis
RA:
- (1) general signs and symptoms (indicate common locations of arthritis)
- (2) are the main investigatory markers / indicators of RA
1- Symmetrical Polyarthritis: hands/feet + ankles, wrists, elbows, shoulders
-pain, inflammation, swelling, destruction of joints
2- rheumatoid factor, ACPA (anti-citrullinated protein antibody)
RA:
- affects (males/females) more
- (2) is the main risk factor
- (3) are the main triggers
1- females, 2.5:1
2- HLA-DRB1 polymorphisms
3- smoking, stress, infections: EBV, E. coli
RA:
- genetic predisposition leads to (1)
- environmental triggers lead to (2)
- (1) and (2) cause a type (3) sensitivity reaction
1- failure of tolerance to self and unregulated lymphocyte activity
2- enzymatic modification of self-protein
3- type II (B-cells), type IV (Th1, Th17) cells
In RA, the initiation of hypersensitivity reactions causes the proliferation of (1) cells. (1) cells will release (2) which causes (3), the main process causing RA directly. (1) cells will also release (4) in order to increase (5) activity to cause secondary osteoporosis.
1- fibroblasts, chondrocytes, synovial cells
2- collagenase, stromyelysin, elastase, PGE2 + other enzymes
3- Pannus formation: bone/cartilage destruction => fibrosis and ankylosis
4- IL-1 / TNF (macrophages) + RANK/RANKL (T-cells)
5- osteoclast activity
RA histology:
- (1) is the highlight change, describe
- (2) are the other important cellular changes
1- Pannus: granulation tissue infiltration = synovial cell hypertrophy
2:
- papillary synovial hyperplasia – multi-layered synovial cells
- lymphocyte, plasma cell invasion: perivascular lymphoid aggregates + vascular congestion
