Joint pathology Flashcards
Primary/ idipathic osteoarthritis?
aging phenomenon
appears insidiously without cause
oligoartiuclar (few joints affected)
Secondary osteoarthritis?
younger individuals
history of predisposing conditions
-previous injury, congenital deformity, systemic disease
usually affect the predisposed joint
Clinical course osteoarthritis?
insidious deep, achy pain morning stiff crepitus limit ROM impingment on spinal foramina causing radiular pina, muscle spasm, muscle atrophy, and neuro deficits
Commonly seen with/ joints of osteoarthritis?
hips, knees, cervical and lumbar vertebrae, PIP, DIP
herberden nodes common in women
no preventive treatment, cannot halt progression
Genetic factors osteoarthritis?
genes involved with prostaglandin metabolism and WNT signaling
Environmental factors osteoarthritis?
Aging, 80-90% have evidence of OA by 65 yo Biochemical stress (joint stability, muscle strength)
Path mechanism of OA?
chondrocyte injury cause proliferation and form clusters
water content increases and concentration of proteoglycans decreases
Cracking of the matrix occurs as the supporing catilage and type II collage are degraded
Gross morphology of OA?
exposed subchonral surface
subchondral cyst
residual cartilage (destruction of)
Eburnation?
dectructive process of cartialge that exposes the bone
Rheumatoid arthritis?
chronic, systemic, inflammatory disorder
affects many tissues and organs
women more than men
nonsuppurative, profilerative and inflammatory synovitis
clinical course Rheumatoid arthritis?
slow and insidious
maliase, fatigue, generalized MSK pain
joint involvement ensuses after several weeks to months, small before large/symmetrical
(joints swollen, warm, painful, stiff from inactivity)
Lab indicators of Rheumatoid arthritis?
Rheumatoid factor- may appear in other conditions
Anti-CCP antibody (both tests together are sensitive)
synovial fluid shows:
neutrophils, high protein content, low mucin content
Diagnose Rheumatoid arthritis? (four of following)
morning stiffness arthritis in 3 or more joints arthritis of hang joints symmetric arthritis rheumatoid nodules serum rheumatoid factor typical radiographic changes
Pathogenesis Rheumatoid arthritis?
genetic susceptibilty associated with HLA-DRB1
Environment arthritogen microbial agents: EBV, retrovirus, mycobaterium citrullinated proteins
autoimmunity
What causes bone/cartilage destruction?
antigen is picked up by MHC class II, present to CD4+ T cell, release cytokines activate macrophages, B cells, and recruit leukocytes
leads to pannus formation, destroy bone, catilage
fibrosis, ankylosis
Histology of Rheumatoid arthritis?
formaiton of villi
proliferative synovium
dense lymphoid aggregate
Rheumatoid nodule?
most common cutaneous lesion
usually in areas subjected to pressure (elbows, forearm)
less common in lungs, spleen, heart
What is a Rheumatoid nodule?
central zone of fibrinoid necrosis surrounded by palisading granuloma and numerous lymphocytes and plasma cells
Herberden’s nodes?
at the DIP