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S3 Case 3 - Musculoskeletal > Pathophysiology of Bone + OA > Flashcards

Pathophysiology of Bone + OA Flashcards

1
Q

What are the functions of bone?

A

Structural = support, protection + movement
Mineral storage = calcium + phosphate
Lipid storage
Blood cell formation

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2
Q

What are the different types of bones?

A

Long bone
Short bone
Flat bone
Irregular bone

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3
Q

Describe a long bone

A

Long shaft + 2 distinct ends
Compact bone on exterior with spongey inner bone marrow

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4
Q

What is an example of a long bone?

A

Humerus, femur

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5
Q

Describe a short bone

A

Roughly cube-like
Thin compact bone layer surrounding spongy bone mass

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6
Q

What is an example of a short bone?

A

Carpal + tarsal bones

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7
Q

Describe a flat bone

A

Thin, flattened + usually curved
Parallel layer compact bone with spongy layer between

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8
Q

What is an example of a flat bone?

A

Sternum, skull, ribs

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9
Q

Describe an irregular bone

A

Complicated shapes
Consist of spongy bone with thin layer of compact

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10
Q

What are the 2 major types of bone?

A

Compact bone = stronger, dense, NOT porous
Cancellous bone = spongy

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11
Q

Describe a compact bone

A

Mechanical + protective
Dense bone tissue on outside of bone
Enclosed + covered by periosteum

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12
Q

Describe a cancellous bone

A

Interior = fibres + lamellae
Metabolic Ca regulation
Storage
Stem cells

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13
Q

LEARN long bone gross anatomy

A

LOOK AT LECTURE

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14
Q

What does red bone marrow do?

A

Supplies nutrients to osteoclasts
Forms red + white blood cells

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15
Q

What does yellow bone marrow do?

A

Stores fat

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16
Q

What are the 4 main types of bone cells?

A

Osteoprogenitor
Osteoblasts
Osteocytes
Osteoclasts

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17
Q

What is the function of osteoprogenitor?

A

Develop into osteoblasts

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18
Q

What is the function of osteoblasts?

A

Bone building
Differentiate into osteocytes

19
Q

What is the function of osteocytes?

A

Form osteoblasts

20
Q

What is the function of osteoclasts?

A

Bone crushing

21
Q

What is the mechanism of bone remodelling?

A

Response of osteocytes to microdamage
Signalled by growth hormones/cytokines
Bone surface populated with osteoclast precursors
Osteoclast + osteoblasts recruited
Osteoclasts mature + remove mineralised bone
Osteoclast numbers decline + replaced by osteoprogenitor cells
Osteoprogenitor = osteoblasts = collagen = mineralisation

22
Q

Describe the method of osteoclast resorption

A

Osteoclast adheres to bone = secretes HCl + proteases

23
Q

What is osteoarthritis?

A

Degenerative disorder of joints, causes significant pain + disability

24
Q

Where is osteoarthritis usually located?

A

Knee
Hip
Spine
Small joints of hand

25
Q

What are the risk factors for OA?

A

Obesity
Increasing age

26
Q

What is the cause of primary OA?

A

Idiopathic

27
Q

What is the cause of secondary OA?

A

Previous injury to joint
Inflammatory arthritis (gout/RA)

28
Q

What is the pathophysiology of OA?

A

Imbalance between joint repair + destruction
Joints subjected to large load/impact = cartilage + bone strain + damage
Rate of damage > rate of repair
Cartilage progressively destroyed
= narrowing of joint space + overgrowth of bone
= inflammation of synovial lining + swelling of joint

29
Q

What is OA characterised by?

A

Breakdown of articular cartilage + proliferative changes of surrounding bones

30
Q

What are the risk factors of OA?

A

> 50
Female
BMI >25
Previous injury
Laxity of joint ligaments
Occupational/recreational use of affected joint
Family history

31
Q

What happens with OA?

A

Thinned cartilage = bone ends rub together

32
Q

What is the diagnosis of OA?

A

No validated diagnostic tool
Pain symptoms with physical joint findings in patients with risk factors
OA features can be seen on a x-ray

33
Q

What OA features can be seen on a x-ray?

A

Space narrowing
Bone spurs
Subchondral sclerosis
Subchondral cysts

34
Q

What are Heberden’s nodes?

A

Hard bony swelling on distal interphalangeal joints at end of fingers

35
Q

What are Bouchard’s nodes?

A

Hard bony cysts occurring on proximal interphalangeal joints

36
Q

What is the most common location of OA?

A

Knee joint

37
Q

Describe the pain with OA in knee

A

Activity-related
Worse at end of day
Symptoms may be episodic + vary in severity

38
Q

What is the second most common location of OA?

A

Hip

39
Q

What are the risk factors for hip OA?

A

Obesity
Employment with lifting heavy objects
Physical work
Sport - eg. running

40
Q

What is common in patients with hip OA?

A

Difficulty moving hip joints
= putting shoes + socks on
= getting in + out of car
= going up + down stairs

41
Q

What is the molecular pathophysiology of OA?

A

Chondrocytes generate matrix degradation products + proinflammatory mediators for repair
= stimulate chondrocyte + proliferation
= increased vascularity + vascular invasion
= increased bone turnover + subchondral bone marrow lesions
Osteophytes form at joint margins

42
Q

Describe the symptoms of OA

A

Pain
Morning stiffness
Joint swelling
Reduced range of motion + muscle weakness
Crepitus of joints
Joint instability
Fatigue
Pain-related psychological stress

43
Q

Describe treatment of OA

A

1st line = paracetamol/topical NSAID
Adjuncts = capsaicin cream/intra-articular corticosteroids
Ineffective = add in OR substitute
Add in/substitute = NSAID + PPI

S3 Case 3 - Musculoskeletal (14 decks)

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