Flashcards in Osteoarthritis - Postlethwaite/Gupta Deck (29):
Osteoarthritis (OA) definition?
Progressive degeneration of articular cartilage
OA classified as inflammatory or noninflammatory?
Common sites affected by primary OA (5)? BE SPECIFIC
Hands (DIP & PIP joints, 1st MCP joint, CMC Joint)
spine (usually cervical and lumbar vertebrae)
feet (1st MTP Joint)
What is the most common disabling joint disease?
You guessed it. Osteoarthritis.
Greatest risk factor for developing OA? Others?
Age = 75% of persons over age 70 have OA
Others include obesity, trauma, hereditary, female sex, neuromuscular dysfunction, metabolic disorders
Instead of being systemic and inflammatory, OA is considered to be?
Localized and degenerative. Only involves certain joints, not associated with warmth of skin or erythema (signs of inflammation)
Normal articular cartilage has what 2 important components? Purpose of each?
Normal articular cartilage has:
1) Proteoglycans - provide elasticity
2) Type II Collagen - provides tensile strength
In OA, what is the importance of cytokines? List 1 cytokine Dr. Gupta mentioned
- Cytokines active metalloproteinases (MMPs)
- MMPs degrade proteoglycans and collagen
Dr. Gupta mentioned IL-1 that could potentially mediate these effects (she also said they didn't make "men" like Tyler anymore)
Early OA, what is going on in the cartilage?
Fibrillation and cracking of the matrix of articular cartilage.
Washout of proteoglycans.
Colonies "clones" of regenerating cartilage cells to try and replace the damaged chondrocytes
Within joint margins of OA patients, what can occur?
Osteophyte formation = reactive bone formation (can cause a slight increase in Alk Phos)
In advanced stage OA, what 2 important features occur?
1. Development of subchondral bone cysts = fibrous lines "cysts" under the exposed subchondral bone
2. Eburnation = highly polished appearance of exposed subchondral bone
What are joint mice?
fragments of articular cartilage that break free into the joint space
Joint stiffness and OA, what about it?
Minimal morning stiffness (
Joint pain and duration in OA?
Pain gets worse throughout the day (as a result of increased use)
As opposed to RA, pain gets better throughout the day
What physical exam finding can be observed in patients with OA? (vague question, just look at answer)
Range of motion in OA?
Enlargement of DIP joints results in?
Heberden nodes (osteophyte formation)
Enlargement of PIP joints results in?
Bouchard nodes (osteophyte formation)
Laboratory Tests to diagnose OA?
No specific tests, ESR and CRP are both usually normal
Most common location in hand affected by OA?
If a patient has OA in "wrong" joint, i.e. the ankle, would should you be thinking?
Must consider secondary causes of OA
List some common secondary causes of OA?
- Trauma and/or overuse of joint (in younger patients)
- Neuromuscular disease, especially diabetic or other neuropathies
- Metabolic disorders (esp pseudogout aka CPPD aka Calcium pyrophosphate deposition disease)
Secondary OA as a result of Diabetic Neuropathy. List clinical findings that could indicate this
- MTPs (metatarsophalangeal joint) 2-5 involved in addition to 1st bilaterally
- Destructive changes on Xray much worse than primary OA
- Midfoot involvement is common
Patient has hemochromatosis and OA. What are you thinking?
CPPD Disease (calcium pyrophosphate deposition disease aka pseudogout)
1st line therapy for OA?
2nd line therapy for OA?
- NSAIDs if acetaminophen fails
- Intra-articular agents or lavage
3rd line therapy for OA?
Total Joint replacement
2 types of intra-articular therapy for OA?
1. Intra-articular steroids
2. Hyaluronate injections