Management of orthopaedic conditions Flashcards

1
Q

What are osteogenic cells? What do they do?

A

Bone stem cells

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2
Q

What are osteoblasts? What do they do?

A

Bone forming cells
Secrete osteoid
Catalyse mineralisation of osteoid

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3
Q

What are osteocytes? What do they do?

A

Mature bone cells
Formed when an osteoblast gets embeded in its secretions
Sense mechanical strain to direct osteoblast and osteoclast activity

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4
Q

What are osteoclasts? What do they do? From where are they derived?

A

Bone breaking cells
Dissolve and resorb cells by phagocytosis
Derived from bone marrow

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5
Q

What is the fundamental unit of compact bone?

A

Osteon

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6
Q

How does having few spaces between osteons in compact bone contribute to function?

A

Provides protection, support and resists stresses produced by weight of movement

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7
Q

Describe the structure of osteons

A

concentric ‘Lamellae’ around a central ‘Haversian Canal’

‘Haversian Canal’ – contain blood vessels, nerves and lymphatics.

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8
Q

What are lacunae and what radiates from lacunae?

A

Lacunae – small spaces containing osteocytes
Tiny Canaliculi radiate from lacunae filled with extracellular fluid.

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9
Q

What are Volkmann’s canals?

A

Transverse perforating canals

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10
Q

Structure of long bones (layers)

A
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11
Q

Mechanisms of bone fracture

A
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12
Q

Pahtological causes of bone fracture

A
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13
Q

Classification of fracture patterns

A
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14
Q

Describe this radiograph

A

Mid/distal third tibia
Simple
Transverse
15%lateral translation- you describe translation based off distal fragment
Minimal angulation (distal part anteriorly tilted 10degrees)

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15
Q

Describe this fracture

A

Mid/distal third tibia/fibula
Immature skeleton- growth plate still open
Multifragmentary
Oblique (butterfly)
Valgus angulation (20 degrees)
Anterior?? tilt (20 degrees)
Minimal translation

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16
Q

Why are children’s bones more elastic than an adults and what can this lead to?

A

Increased density of haversian canals
Therefore you can get:
Plastic deformity
bends before breaks

Buckle fracture

Greenstick
– like the tree
One cortex fractures but does not break the other side

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17
Q

Fracture reduction classification

A
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18
Q

Holding a fracture: classification

A
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19
Q

Fixation classification

A
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20
Q

What is done in rehabilitation and what are the principles of rehabilitation?

A

Physiotherapy

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21
Q

Urgent fracture complications

A

Local visceral injury
Vascular injury
Nerve injury
Compartment syndrome
Haemarthrosis
Infection
Gas gangrene

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22
Q

Less urgent fracture complications

A

Fracture blisters
Plaster sores
Pressure sores
Nerve entrapment
Myositis ossificans
Algodystrophy
Joint stiffness
Tendon lesions
Ligament injury

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23
Q

Late fracture complications

A

Delayed union
Mal union
Non union
Avascular necrosis
Muscle contracture
Osteoarthritis
Joint instability

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24
Q

What do we mean when we say that the femoral head has a retrograde blood supply?

A

blood supply comes up through capsule, not down through heart

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25
Q

Describe the risk to blood supply and of AVN in the case of extracapsular, intracapsular undisplaced and intracapsular displaced fractures

A

Extracapsular: minimal risk to blood supply and AVN
Intracapsular: if undisplaced: less risk to blood supply
If displaced: 25-30% risk AVN

26
Q

How would we define fitness/ mobility in >65 when deciding whether to do total hip replacement or hemiarthroplasty in NoF fractures?

A

Fit and mobile:
Walks >mile day
Independent
Minimal comorbidities

Less fit:
Lower mobility
Multiple comorbities

27
Q

How do we classify joints?
Describe the mobility and give examples for each type

A

Fibrous (immoveable): sutures, syndesmosis, interosseous membrane
Cartilaginous (semi-moveable): Synchondroses (e.g. sine), symphyses (e.g. pubic)
Synovial (freely moveable): ball and socket, plane, pivot, hinge, saddle, condyloid

28
Q

Give examples for each type of synovial joint

A
29
Q

How are synovial joints stabilized?

A
30
Q

What is cartilage composed of and what is its blood supply?

A

Cartilage is composed of:
1) specialized cells (chondrocytes)
2) extracellular matrix: water, collagen and proteoglycans
(mainly aggrecan)

Cartilage is avascular – it has no blood supply

31
Q

What is aggrecan?

A

a proteoglycan that possesses many chondroitin sulfate and keratin sulfate chains
-characterized by its ability to interact with hyaluronan (HA) to form large proteoglycan aggregates

32
Q

Two major divisions of arthritis?

A
33
Q

Radiographic changes in Rheumatoid Arthritis vs. osteoarthritis

A
34
Q

What does joint space narrowing indicate and how does it differ between osteoarthritis and rheumatoid arthritis

A

Joint space narrowing indicates articular cartilage loss. This can occur in osteoarthritis (primary abnormality) and in Rheumatoid Arthritis (secondary damage due to synovitis)

35
Q

What are osteophytes at
a)DIP joints
b) PIP joints known as

A

a) Heberden’s nodes
b) Bouchard’s nodes

36
Q

Early radiographic sign of rheumatoid arthritis? What other types of inflammatory arthritis can this indicate?

A

Juxta-articular osteopenia is common early radiographic sign in inflammatory arthritis of any cause

37
Q

Where do bony erosions initially occur in rheumatoid arthritis?

A

Erosions occur initially at the margins of the joint where the synovium is in direct contact with bone (the ‘bare’ area)

38
Q

WHO definition of osteoarthritis?

A

chronic disease characterized by the deterioration of cartilage in joints which results in bones rubbing together and creating stiffness, pain, and impaired movement.

39
Q

OA is a degenerative disease of what type of cartilage?

A

Chondral cartilage

40
Q

What occurs in late stage OA?

A

Inflammation occurs late in disease cf. rheumatoid
Inflammatory mediators include proteinases, e.g., matrix metalloproteinases (MMPs) and aggrecanases, and inflammatory cytokines, including interleukin (IL)-1β and tumor necrosis factor α (TNFα), which enhance the synthesis of proteinases and other catabolic factors to degrade the articular cartilage membrane

41
Q

OA risk factors

A
42
Q

What are the key history points for suspected OA?

A

Pain (exertional/rest/night)
Disability: walking distance/stairs/giving way
Deformity
Previous history: trauma/infection
Treatments given (physio/injections/operations)
Other joints affected

43
Q

What is this deformity?

A

Valgus

44
Q

Likely reason for this scar?

A

ACL reconstruction surgery

45
Q
A
46
Q

What special tests can be used to look for ACL injury?

A

Anterior drawer test
Lachmanns (pictured)

47
Q

Radiographic changes seen in OA?

A

Joint space narrowing
Subchondral sclerosis
Subchondral cysts
Osteophytes

48
Q

OA management

A
49
Q

Which type of operation is this?

A

Total knee replacement

50
Q

What type of operation is this?

A

Ankle fusion

51
Q

Give examples for bone infection

A

Bone: osteomyelitis
Joint: septic arthritis

52
Q

How can osteomyelitis be classified

A

Acute or chronic
Primary or secondary

53
Q

Give examples for bone infection

A

Bone: osteomyelitis
Joint: septic arthritis

54
Q

Signs of osteomyelitis

A

Pain/swelling/discharge
Systemic signs:
Fevers, sweats wt loss

55
Q

Signs of septic arthritis

A

Pain
Joint swelling/stiffness
Fevers, sweats, wt loss

56
Q

Bone infection investigations

A

Radiology:
Plain films
MRI scans: bony architecture/collections
CT if MRI not available
Bone scans: multifocal disease
Labelled White cell scans

Bloods:
CRP (acute marker)
ESR slower response
WCC
TB culture/PCR

57
Q

Treatment of osteomyelitis

A

Antibiotics: iv weeks
Surgical drainage: especially collections/sequestrum
Chronic: antibiotic suppression/dressings
??amputation

58
Q

Treatment of septic arthritis

A

Surgery: joint washout and drainage (repeated if required)
Iv antibiotics (days/weeks)
Immobilise joint in acute phase
Physiotherapy once over acute phase

59
Q

Shoulder conditions by age

A
60
Q

Hip conditions by age

A
61
Q

Knee conditions by age

A