Osteoathritis Flashcards

1
Q

Which joints are affected in OA

A
  • Mainly weight-bearing joints (SC, AC, hip, knee) as well as DIPs. Also PIPs and MCPs, interphalangeal joint of big toe
  • Joints spared: GH, elbow, wrist, ankle, toe joints
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2
Q
  1. Briefly describe the pathological joint changes which are seen in early and late osteoarthritis
A

Early
Occurs in the articular cartilage
1. Biochemical changes appear in cartilage
- Increased water content of cartilage matrix
- Proteoglycans decrease in molecular size and increase in rate of synthesis
2. Chondrocytes compensate with increased wear
- Increase metabolic activity and turnover
- Causes release of proteolytic enzymes which cause further damage
3. Cartilage degeneration occurs as loss exceeds replacement
- Abnormalities gradually appear in articular cartilage, especially in weight bearing joints
- Discrete areas of full thickness cartilage loss, not symmetrical throughout the joint
- Continued thinning and degeneration of articular cartilage
- Exposed subchondral bone appears as shiny foci on articular surface (eburnation)
- Note areas of reactive cartilage growth

Late
Occurs in the subchondral bone
1. loss of articular cartilage results in
- stimulation of reactive proliferation of the plate leading to sclerosis
- osteophyte formation about joint margins
- dense bone cannot act as a shock absorber, resulting in damage to remaining cartilage
2. cystic lesions (lytic in nature) appear from
deformation of articular cartilage surface
- loss of normal molecular structure
3. fibrosis of the joint (capsular fibrosis)

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3
Q

Write brief notes on Osteophytes

A

Osteophytes are reactive bone growth occurring at joint sites due to increased mechanical stress
They are usually asymptomatic but can
- project into areas causing irrigation and reduction of ROM
- cause pain
- rare but cause ankylosis
- nerve impingement
- deformity = bouchard and haberdens nodes in DIPs and PIPs

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4
Q

Clinical features of OA

A
Pain
better with rest
insidious onset
local or referred
worse at end rom
worse with extension
relief becomes less complete with time
worse in bed at night
local tenderness

Stiffness
common
occurs after inactivity
may become constant and aggressive

Swelling
may be intermittent
may be continuous (capsular)
potential for synovitis

Deformity
via capsular contraction
joint instability
osteophytes (eg. Herberdens or bouchards)

Loss of function
via damage and pain
via muscle wasting

Crepitus
grating sound produced via friction between areas of increased wear

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5
Q

Radiological features of OA

A
plain x-ray is very characteristic of OA
observe the 4 cardinal signs 
LOSS
L - loss of joint space (asymmetrical narrowing)
O - osteophytic growth at joint margins 
S - subchondral bone sclerosis 
S - subchondral bone cysts 
Others:
haberden's and bouchard's nodes in fingers (DIPs, PIPs)
vertebral joints show:
- facet narrowing 
- foraminal stenosis 
- stenosis of spinal cord 
- osteophyte formation
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6
Q

Hypertrophic Osteoarthropathy

A

3 cardinal features:

  • clubbing
  • arthralgia of adjacent joints
  • periosteal new bone formation

Common aetiologies:

  • bronchogenic carcinoma (+ other lung/mediastinal diseases i.e. mediastinal hodgkins lymphoma, adenocarcinomas)
  • lung infections, chronic lung diseases
  • chronic liver disease
common causes of clubbing:
- 	Cyanotic heart disease
-	Infective endocarditis/aortitis
-	Crohn’s disease
-	Ulcerative colitis
-	Cancer of the oesophagus/colon 

and those above
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