Cox: Arthritis CIS Flashcards
What kind of nodes would we find in OA
- Herberden’s
- the ones in the DIPs
What would we find in the synovial fluid if there we had a gouty joint?
-Urate crystals
RA
- morning joint stiffness, RF, Elevated ESR and CRP
- Antibody to CCP
- Lon standing RA may develop secondary OA
-Psoriatic Arthritis
-May taget 1 DIP, nail changes
Crystalline Arthritis
- Syovial fluid
- urate crystals, gout
Hemochromatosis
- FE overload
- MCP, wrists
Infectious
- Leukocytosis
- synovial or blood culture
OA
- degenerative joint disease (DJD)
- Most common joint disease
- Characteristically non-inflammatory
- Lack of systemic symptoms
- pain releived by rest, if present- morning joint stiffness is brief
- Oligoarticular
- Generalized
- Aging phenomenon
OA/DJD characteristics
- Bony changes in joint shape
- crepitus
- malalignment/instability
- Limited ROM
- Joint line tenderness
- Cool effusions
- Spasm or atrophy of adjacent muscles
Which regions are commonly affected by OA?
- Cervical spine
- lumbar spine
- PIP
- DIP
- hip
- knee
- 1st MTP
What would a patient’s hip look like with OA on an xray?
-sclerosis of femoral head
OA radiographic findings
- joint space narrowing
- osteophytes and marginal lipping
- subchondral thickening
- bone cysts
- joint mice
do radiographic findings always directly correlate to degree of symptoms?
-no
What causes the breakdown of cartilage in OA?
- Damage from physical forces
- so chondrocytes react and release degradative enzymes and there is an inadequate repair response
- drop-out, cartilage loss, bone changes, loose bodies (joint mice)
- Fundamental defective cartilage fails under normal joint loading
- Type 2 collagen gene defect
What is the new articular surface in OA?
- subchondral bone
- friction, bone eburnation
- sclerosis, small fracture, synovial fluid contating cyst
- altered bone contour, lipping
- osteophyte at margin as fibrocartilage and hyaline cartilage ossify
OA heredity
- risk of OA= sum of multiple genes
- genetically heterogeneous
- Heritable component…. particularly at hip
- generalized osteoarthritis characterized by osteophytes of the HIP (Heberden’s nodes) and PIP joints (bouchard’s nodes)
Primary OA
- Aging or idiopathic
- genetic: nodal OA
Secondary OA
-disorders that damage joint surfaces
OA characteristics
- Altered chondrocyte function
- loss of cartilage: thinning
- Subchondral bone thickening: sclerosis
- Remodeling of bone
- Marginal spurs: osteophytes
- Subchondral bone: cystic changes
- Mild reactive synovitis
Main distinguishing factors between OA and RA
- OA has:
- DIP and carpometacarpal joints affected
- heberden’s nodes
- hard and bony joints
- worse after effort
- not as much morning stiffness
- RF and Anti CCP negative
- Normal ESR and CRP
Hyperostosis
- Diffuse idiopathic skeletal hyperostosis (DISH)
- old ppl
- frequently but not always asymptomatic
- cervical spine=dysphagia
- Osteophytosis of spine… spans >3-4 segments
- Paraspinous ligaments= calcifications/ossification
- preservation of disc space
- some association with DM
What is the characteristic finding for hyperostosis
- flowing wax appearance on anterior vertebral bodies
- remember that the joint spaces are relatively normal
Management of OA
- no cure
- pain control
- minimize disability
- Improve quality of life
- education
- surgery
- nonpharmacologic: OMT to address compensatory changes, exercise, PT, OT, wt loss, acupuncture
What is the first pharmacologic action we would take in someone with OA?
-Acetaminophen
What other pharm things could we do for an OA patient
- Acetaminophen
- NSAID
- Capsaicin
- Intraarticular glucocorticoids
If symptomatic relief is inadequate, what else should we consider?
- intraarticular hyaluronic acid
- platelet rich plasma
- glucosamine and chondroitin
- opioid analgesics
