Pathophysiology of Osteoarthritis Exam 1 Flashcards

1
Q

What is the most common form of arthritis?

A

OA

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2
Q

What are the most common cause of long-term, lower extremity limitations?

A
  • hip OA

- knee OA

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3
Q

T/F; OA is among the 5 leading causes of physical disability in non-institutionalized elderly

A

T

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4
Q

What are risk factors for developing OA?

A
  • 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
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5
Q

How is genetics a risk factor for developing OA?

A

Heberden’s nodes (OA of DIP joints) are more frequent in mothers and sisters of affected women

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6
Q

What happens when you get older that contributes to a risk factor for OA?

A
  • 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)
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7
Q

What is the normal physiology of the articular cartilage (cartilage of the joint)?

A

Thin, avascular (without blood vessels) and aneural (without nerves) covering of bone (subchondral plate) in joints

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8
Q

What is cartilage composed of?

A
  • water
  • type II collagen
  • proteoglycans
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9
Q

What is the role of collagen?

A

provides structure, strength, and shape

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10
Q

What are proteoglycans composed of?

A

protein cores with attached glycosaminoglycans (GAGs)

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11
Q

What is the role of the GAGs?

A

draw in water which provides cartilage with resiliency, elasticity, and lubrication

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12
Q

What are chondrocytes?

A

cells that control the synthesis and degradation of cartilage

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13
Q

Alterations that occur in OA

A
  • 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
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14
Q

secondary causes of OA

A
  • Trauma
  • Abnormalities of the joint
  • Genetic abnormalities of the cartilage
  • Metabolic or endocrine abnormalities
  • Crystal deposition
  • Inflammatory conditions of joints
  • Avascular necrosis
  • Neuropathic
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15
Q

symptoms of OA

A
  • Pain
  • Stiffness
  • Impairment of motion
  • Very gradual progression
  • Functional impairment
  • Numbness, tingling, pain, weakness
  • Other neurological symptoms which results from nerve compression
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16
Q

physical manifestations of OA

A
  • Joint enlargement and other deformities
  • Crepitus
  • May have tenderness or get effusions (fluid)
  • Usually no clinical signs of inflammation
  • Decreased range of motion
  • Instability
  • Xray changes