Degenerative disorders I Flashcards
normal aging of articular cartilage
begins early adult life and progresses throughout life
smooth glistening surface to granular dull surface
regeneration is limited
biochemically- gradual loss of proteoglycan, collagen fibrils lose support and cartilage become shredded, artic cart less effect shock absorber, vulnerable to repeated friction
premature or excessive leads to arthritis and/or DJD
DJD synonyms
OA
Osteoarthritis
Degenerative arthritis
Senescent arthritis
Hypertrophic arthritis
DJD definition
initiated by local deterioration of artic cartilage and is characterized by-
progress degeneration of cartilage, hypertrophy, remodeling of subchondral bone, secondary inflamm of synovial membrane
DJD incidence
most common type of arthritis
after age 60… 25% women and 15% men have symptoms
after age 75, more than 80% of men and women are affected
Primary or idiopathic type
no known cause or no known pre-exisiting abnormality
can be accelerated in some indiv on a genetic basis
more common in women
obesity aggravates in wt bearing jts
Secondary type
more common than primary
develops at any age due to- injury, deformity, disease
wear and tear aggravates pathological process
more common in hip, knee, IV discs of lumbar (wt bearing jts)
Articular cartilage
earliest biochemical change in degenerative jt
cartilage softens and loss of elastic resilience (dec shock absorption)
breakdown can continue because jt not moving correctly
Articular cartilage-central area
exposed to most friction,
gradually abraded down to subchondral bone,
becomes smooth as polished ivory,
radiographs show narrowing of cartilage space
Articular cartilage- peripheral area
cartilage responds to hypertrophy and hyperplasia
forming thickened rim of cartilage around jt margin
endochondral ossification occurs of the outgrowth forming bone spurs/osetophytes
if becomes large enough causes decreased function
Subchondral bone
serves as a shock absorber
central area hypertrophies (becomes more dense)-can see on xray
peripheral area atrophy (becomes more osteoporotic)
cystic lesions develop in bone marrow- pain prodiced
remodeling occurs
synovial membrane and fibrous caspule
small fragments of dead cartilage may float in synovial fluid and becomes incorporated in synovial membrane
causes hypertrophy and synovial effusion
synovial fluid has inc viscosity
fibrous capsule become greatly thicken and fibrotic-decreased jt motion
Muscles
spasms occur-spasms in response to pain
contractures can develop- jt deformity and restricted motion
Decreased ROM causes increased stress to smaller area-centralized area of breakdown
spasms as protective mechanism
Clinical features and Dx
pain, jt crepitus, articular gelling, swelling of jt, restricted rom and arom, radiograph changes, NO increased warmth of overlying skin
ache more when whether change
pain not related to severity
Treatment
No cure
aims of tx- educate pt, psych support, pain mgmt, suppress inflamm response, correct existing deformities, strengthen improve function
physiological considerations
reassure patients of the local condition of joints vs generalized disease such as RA
education to overweight patients
