Week 7 - Osteoarthritis and related conditions Flashcards

1
Q

What is osteoarthritis?

A

A degenerative, non-inflammatory joint disease.

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2
Q

What is the most common articular disease worldwide?

A

Osteoarthritis

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3
Q

What parts of the joint does osteoarthritis affect?

A

Articular cartilage
Joint surface
Subchondral bone
Synovium

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4
Q

What are the primary joints affected by osteoarthritis?

A

Weight-bearing joints

DIP and PIP joints of hands

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5
Q

What are the risk factors of osteoarthritis?

A
Increasing age
Obesity
Female
Trauma
Infection
Repetitive occupational trauma
Genetic factors
History of inflammatory arthritis
Neuromuscular disorder
Metabolic disorder
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6
Q

What does osteoarthritis do to the joint?

A

It causes focal areas of damage to the articular cartilage
Remodels the underlying bone
Osteophytes form
Mild synovitis (swelling of the synovial membrane)

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7
Q

How does cartilage degradation in OA occur?

A
  1. Synovial cells overproduce enzymes which break up the cartilage matrix
  2. Cartilage becomes softer, allowing deformation and splitting called fibrillation.
  3. As the degradation progresses, these splits become deeper (fissures) reaching down to the bone
  4. Areas of full thickness loss of cartilage develop
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8
Q

What is periarticular bone growth?

A

Bone spur caused by cartilage transforming to bone in attempts to regrow cartilage.

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9
Q

What are the symptoms of OA?

A
Pain
Joint stiffness in morning
joint instability
joint mal-alignment
decreased ROM
muscle atrophy
joint effusion
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10
Q

How is OA diagnosed?

A

Radiographs

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11
Q

What are the impacts of OA?

A

Pain and functioning
Activity restrictions
Psychological distress
Effects of environmental and personal factors

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12
Q

How is OA managed?

A
Patient education
Heat/ice
Exercise
Weight loss
PT
OT
SP
Joint unloading principles
Analgesics
Surgical intervention as last resort
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13
Q

What is Paget’s Disease?

A

A localised disorder of bone remodelling that typically begins with excessive borne resorption followed by an increase in bone formation. This forms structurally disorganised “woven bone” which is mechanically weaker, larger, less compact, more vascular and more susceptible to fracture than normal bone.

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14
Q

Where are common sites for paget’s disease?

A

The axial skeleton
Pelvis
Long bones like tibia and fibula

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15
Q

What are the 3 phases of paget’s disease?

A
  1. Lytic phase
  2. Mixed phase
  3. Sclerotic phase
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16
Q

What is the lytic phase of paget’s disease?

A

Increase in bone resorption resulting in a bone turnover rate up to 20 times faster than normal

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17
Q

What is the mixed phase of paget’s disease?

A

Second phase of rapid increase in bone formation with the newly formed collagen fibres being deposited in an unorganised fashion

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18
Q

What is the sclerotic phase of paget’s disease?

A

Bone formation dominates with the new bone having a woven pattern, resulting in weaker, highly vascularised bone.

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19
Q

What are the cuases of paget’s disease?

A

Unknown, however suspected genetic and environmental contributors

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20
Q

Does paget’s affect more men or women?

A

Men, 3:2

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21
Q

Why is there increased morbidity in people with paget’s disease?

A

Bone pain, OA and fractures

22
Q

Why is there increased mortality in people with paget’s disease?

A

Likely to suffer fracture or tumour.

23
Q

What age group are most cases of paget’s reported?

A

Incidence increases with age, most cases reported in the 50+ age group

24
Q

How does paget’s present clinically?

A

Usually monostotic (affects 1 bone) but can be polyostotic
Many patients are asymptomatic and are diagnosed incidentally
Most common complaint is bone pain
May also present with pathological fractures, congestive heart failure, hearing loss, sensory disturbances and weakness due to nerve root compression.

25
Q

What is the aim of medical management for paget’s?

A

Control disease activity in short term and prevent disease progression and long term complications.

26
Q

How is paget’s treated?

A
Bisphosphonate and calcitonin therapy
NSAIDs for pain
Mobility aids
Regular monitoring for development of tumours and subsequent chemotherapy/radiotherapy
Surgery when indicated
27
Q

What is rickets?

A

A softening and weakening of bones in children, usually due to inadequate vitamin D. It is a failure of osteoid to calcify in a growing person

28
Q

What is scurvy?

A

A condition of brittle bones caused by a severe lack of vitamin C in the diet.

29
Q

What causes rickets?

A

Environmental pollution
Low exposure to natural sunlight
Lack of vitamin D in diet or malabsorption of Vit D
Dietary deficiency of calcium or phosphorus

30
Q

What causes scurvy?

A

Vitamin C deficiency

31
Q

How does rickets present?

A
General muscular hypertonia
Skull thickening
Knobby deformities
Pit in chest deformity
Bowed legs
32
Q

How does scurvy present?

A

Haemorrhage
Hyperkeratosis
Hematologic abnormalities
Hypochondriasis

33
Q

How is rickets managed?

A

Vitamin D supplementation
Usually gradually over 2-3 months
Orthopaedic surgery to correct severe deformities
Allied health input

34
Q

How is scurvy managed?

A

Vitamin C supplementation
Orthopaedic surgery to correct severe deformities
Allied health input

35
Q

What is osteoporosis?

A

Osteoporosis is a bone disease that develops when bone mineral density and bone mass decreases, or when the quality or structure of bone changes. This can lead to a decrease in bone strength that can increase the risk of fractures (broken bones).

36
Q

What is primary osteoporosis?

A

Idiopathic osteoporosis

Juvenile Osteoporosis

37
Q

What is secondary osteoporosis?

A
Congenial
Toxic Endocrine/Hypogonadal
Deficiency/Malabsorption
Haematological/Neoplastic disorders
Medications
Weightlessness
38
Q

What is osteopaenia?

A

A condition that occurs when the body doesn’t make new bone as quickly as it reabsorbs old bone, making prone to fracture

39
Q

Where are the most common sites of Osteoporotic fracture?

A

Where cancellous bone predominates including:
Vertebral bodies
Neck of femur
Distal radius

40
Q

How does Osteoporosis clinically present?

A

Dull aching
Often in thoracic spine region
Posture
Often do not present until they have had a fracture

41
Q

How is osteoporosis managed?

A

Health promotion for prevention including:

  • promoting behaviours to improve bone health
  • Physical activity
  • adequate calcium and vit D
  • avoid smoking
  • Avoid excess alcohol
  • falls prevention strategies

Maintaining and improving bone health

42
Q

What is osteomyelitis?

A

Acute or chronic inflammation of bone or bone marrow caused by infection, generally in the legs, arm or spine.

43
Q

When does osteomyelitis occur?

A

Any time through the lifespan

44
Q

How is osteomyelitis treated?

A

IV Antibiotics
Orthopaedic review
Infectious diseases review
Allied health input

45
Q

What are the signs of long bone osteomyelitis?

A
Abrupt onset of high fever
Fatigue
Irritability
Malaise
Restriction of movement
Local oedema, erythema and tenderness
46
Q

What are the signs of vertebral osteomyelitis?

A

Insidious onset
History of an acute bacteraemia episode
May be associated with contagious vascular insufficiency
Local oedema, erythema, and tenderness
Failure of a young child to sit up normally

47
Q

What is chronic Osteomyelitis?

A

Non-healing ulcer
Sinus tract drainage
Chronic fatigue
Malaise

48
Q

What are osteosarcomas?

A

Most common form of malignant bone tumour

49
Q

Where does osteosarcoma appear in children?

A
Arise as solitary lesions in the growing areas of long bones in children including:
Distal femur
Proximal tibia
Proximal humerus
Also seen in skull (8% of cases)
50
Q

What are the risk factors of osteosarcoma?

A

Rapid bone growth
Environmental factors such as radiation exposure
Genetic predisposition

51
Q

How does osteosarcoma present clinically?

A
Pain especially with activity
Altered gait pattern with LL involvement
Palpable mass
Tenderness and increased warmth in the areas of the mass
Decreased ROM
52
Q

How is osteosarcoma managed?

A

Surgical resection
Pre and post operative chemotherapy
Allied health input to return to function