Pathophysiology of Osteoarthritis Exam 1 Flashcards
What is the most common form of arthritis?
OA
What are the most common cause of long-term, lower extremity limitations?
- hip OA
- knee OA
T/F; OA is among the 5 leading causes of physical disability in non-institutionalized elderly
T
What are risk factors for developing OA?
- older age
- sex; under 45 -> male more prevalent; above 55, women more prevalent
- genetics
- obesity
- occupation
- sports
- any existing factors that can increase susceptibility of OA
How is genetics a risk factor for developing OA?
Heberden’s nodes (OA of DIP joints) are more frequent in mothers and sisters of affected women
What happens when you get older that contributes to a risk factor for OA?
- Reduced repair of cartilage
- Ligament laxity (less stable, susceptible to injury)
- Muscle weakness (less shock absorption, protection)
- INT-6, Neurologic slowing (reduced protection)
- Reduced non-calcified cartilage (increased shear stress)
What is the normal physiology of the articular cartilage (cartilage of the joint)?
Thin, avascular (without blood vessels) and aneural (without nerves) covering of bone (subchondral plate) in joints
What is cartilage composed of?
- water
- type II collagen
- proteoglycans
What is the role of collagen?
provides structure, strength, and shape
What are proteoglycans composed of?
protein cores with attached glycosaminoglycans (GAGs)
What is the role of the GAGs?
draw in water which provides cartilage with resiliency, elasticity, and lubrication
What are chondrocytes?
cells that control the synthesis and degradation of cartilage
Alterations that occur in OA
- loss of extracell. matrix
- loss of chondrocytes
- decrease proteoglycan; aggregation -> cartilage softening, etc
- synovial membranes can become inflamed
- cartilage fails to repair itself
- cartilage degeneration
- new bone growth at joint margins - osteophytes
- sclerosis of subchondral bone
- microfractures and formation of bone cysts
secondary causes of OA
- Trauma
- Abnormalities of the joint
- Genetic abnormalities of the cartilage
- Metabolic or endocrine abnormalities
- Crystal deposition
- Inflammatory conditions of joints
- Avascular necrosis
- Neuropathic
symptoms of OA
- Pain
- Stiffness
- Impairment of motion
- Very gradual progression
- Functional impairment
- Numbness, tingling, pain, weakness
- Other neurological symptoms which results from nerve compression