May30 M2-Osteoarthritis Flashcards
(45 cards)
charact of mechanical joint pain
- no pain when resting, lying or sitting
- morning stiffness <30 min
- pain with no swelling
- no systemic symptoms fatigue, anorexia, fever
- worse with use and mobility
OA typical history
pain that has been getting worse, no trauma, not clear when started, history very normal. old person
pathology of OA
- damage to articular cartilage
- osteophyte formation at joint margins
- subchondral bone sclerosis
- synovial joint and capsule thickening
consequence of OA pathology
- joint degeneration
- pain, stiffness and loss of function
- loss of tissue homeostasis
steps of articular damage in OA
- smooth to rough
- clefts become cracks
- cracks extend to middle
- get holes with bone exposed
steps of subchondral sclerosis in OA
-happens bc of increased remodelling
-eburnation (ivory=like) of bone
-bone cysts
-bone marrow edema
+osteophytes
structures with homeostasis affected in OA joint
- cartilage
- bone
- synovium
- ligaments
- muscle
changes in cartilage matrix in OA
- type II becomes type 1 cartilage
- less proteoglycans
- shorter glycosaminoglycans
- less water retention by ECM so changes in force distribution to subchondral bone
what causes cartilage damaged in OA
- MMPs upregulated and chew ECM proteins (inbalance, more catabolism than anabolism)
- ADAMTS (aggrecanases) cleave aggrecan (the major proteoglycan in cartilage)
- upregulated bc cytokines released or bc of mechanical stress
anabolic developmental pathways activated in OA lead to what
- TGF-beta (and Wnt and BMP) which have phgy role on cartilage
- in aging and OA, this leads to cartilage hypertrophy, osteophyte formation, synovial fibrosis
synovitis and pro-inflammatory molecules components in OA
- more synovial inflam. bc of cartilage breakdown
- inflamed synovoum makes pro-inflam mediators (IL-1, TNF-a)
- consequence is excess prod of proteolytic enzymes (back to MMPs and aggrecanases)
- systemic mediators too (adipokines) IMPORTANT***
inflammation in OA vs in RA (why still said to be non-inflammatory)
- local inflammation
- same as a blister and accum of a bit of fluid, not more
- inflammation is secondary, not primary
- bit of irritation
most important systemic mediators in OA
adipokines (like adipokinesare). obese people may get OA in non weight-bearing joints
OA prevalence
90% women and 80% men above 70 so is normal
OA predisposing (non modifiable) factors
age, female gender, ethnicity, genetics, joint deformity, laxity, acute injury, occupational factors
best description of type of disease OA is
chronic degenerative disease
modifiable risk factors in OA
- obesity
- muscle weakness
why obesity problem in OA
- higher bone mass
- more mechanical stress to weight bearing joints
- higher levels of IGF1 and visfatin
- hyperglycemia induces MMPs
- hypercholesterolemia assoc with OA
why muscle weakness problem in OA
OA of knee = quadriceps weakness, altered muscle activation patterns and proprioceptive defects
charact of hx in an inflammatory arthritis (not OA)
- pain acute or subacute
- wake up in 2nd half of night
- > 30 min morning stiffness
- better with mvmt
- fatigue
- all joints can be involved
charact of hx of mechanical joint problem like OA
- pain is chronic
- no night awakening
- <15 min stiffness in morning
- worse with mobility
- no fatigue and constitutional symptoms
- PIP, DIP, AC, spine, hip, knee, 1st MTP, CMC
joints NOT involved in OA
- ankles, wrists, shoulders, elbows
- no toes should be affected except 1st MTP
inspection in RA vs OA
- RA: redness (in acute arthritis) and swelling with synovitis
- OA: bony swelling but not joint swelling
palpation RA vs OA
- RA: pain, warmth, swelling
- OA: minor pain, minimal warmth, may palpate osteophytes, maybe joint swlling but no synovitis
