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MRCS Part B > T&O > Flashcards

T&O Flashcards

1
Q

What structures are cut through during the posterior approach to the hip joint?

A

Skin, subcut fat, gluteal fascia, glut max, short external rotators, hip joint capsule

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2
Q

What nerves are at risk during a posterior approach to the hip joint?

A

Sciatic and superior gluteal

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3
Q

What is the surface marking of the lateral cutaneous nerve of the thigh as used for nerve blocks?

A

It passes beneath the inguinal ligament approximately 2cm inferior and medial to the ASIS

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4
Q

Describe some of the approaches to the hip joint.

A

Lateral: over the GT through the skin, adipose, fascia lata, trochanteric bursa, glut med and min and the hip capsule.

Posterior: skin adipose, fascia lata, glut max, short hip rotators, hip capsule

Anterior: incision between the sartorius and the TFL

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5
Q

How long should you give thromboprophylaxis after a hip replacement?

A

28 days

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6
Q

How long should you give VTE prophylaxis after a knee replacement?

A

14 days

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7
Q

Explain the garden classification of hip fracture.

A
  1. undisplaced, incomplete #
  2. undisplaced, complete #
  3. partially displaced, complete #
  4. completely displaced, complete #
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8
Q

What are the signs of a serious ligament injury?

A

Rapid swelling over 1-2 hours
Haemoarthrosis
Large effusions that cause limited movement
Bony avulsions
Localised tenderness

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9
Q

What is the typical mechanism of a meniscal injury?

A

Rotation of the tibia in a flexed, weight bearing knee.
Medial is 20x more common due to the laxity, typically causes a vertical tear in the anterior or posterior horn.

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10
Q

What are the features of a meniscal injury?

A

Locked knee
Haemarthrosis
Joint line tenderness
Clicking of the joint

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11
Q

What are the features of an extensor apparatus tear of the leg?

A

Unable to SLR or extend knee
Swelling or bruising
Palpable gap

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12
Q

What is the management of an injury to the extensor apparatus of the leg?

A

Muscle tear = conservative
Tendon rupture = surgical repair
Vertical patella fracture = conservative
Transverse patella fracture = ORIF with tension wiring.

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13
Q

What is the gustillo-anderson classification used for?

A

Open fractures.

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14
Q

Describe the levels of a gustillo-anderson score.

A

Type 1: wound <1cm with minimal contamination or muscle damage

Type 2: wound 1-10cm with moderate soft tissue injury

Type 3a: wound >10cm with adequate tissue for flap coverage. Contaminated/

Type 3b: required rotational/free flap coverage. May have periosteal stripping.

Type 3c: has a vascular injury

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15
Q

Weakness of what muscle causes claw toes?

A

Interosseous and lumbrical muscles (which normally extend the interphalangeal joints).

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16
Q

What joint deformity do you see in Hammer toes?

A

Hyperextension of MTP
Flexion of PIP.

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17
Q

What is Morton’s neuroma?

A

Plantar or digital neuroma affecting the plantar nerve between the 3rd and 4th metatarsal.

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18
Q

What are the functions of the bone?

A

Supports the body and facilitates locomotion.
Protects organs.
Produces blood cells and immune cells
Regulates calcium

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19
Q

What hormones act upon the bone?

A

Calcitonin: causes increase osteoblast function and increased bony uptake of calcium.

Vitamin D: causes increased osteoclast function and release of Ca

PTH: causes increased osteoclast function and release of Ca

Growth hormone: stimulates bone growth

Gluco-corticoids: reduce bony matrix

Thyroid hormone: cause increase osteoclast function

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20
Q

What is the main constituent of bone?

A

35% organic matrix
65% inorganic matrix which is mainly made up of calcium hydroxyapatite.

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21
Q

What are the cells of the bony matrix?

A

Osteoprogenitor cells: derived from mesenchymal stem cells and form osteoblasts.

Osteoblasts: build bone

Osteoclasts: derived from hemopoietic progenitor cells which then act to reabsorb bone. They have multiple nuclei.

Osteocytes: mature bone cells, derived from osteoblasts. Control fluctuations of Ca and Phosphate.

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22
Q

What is the periosteum?

A

This is a layer of fibrous tissue that is attached to the bone by Sharpey’s fibres.
It contains the blood vessels via its cambral layer and also acts as attachment for muscles and ligaments.

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23
Q

What are the two types of bone?

A

Woven (immature, irregular and disorganised bone)

Lamellar (regular, orderly arrangement of collagen fibres in weight bearing forces that gradually replace woven bone).

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24
Q

How do bones develop?

A
  1. Via direct ossification (such as ribs and clavicle)
  2. Chondrocytes produce hyaline cartilage which forms a template for endochondral ossification.
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25
Q

What are the zones of the physis?

A
  1. resting zone (on epiphyseal side)
  2. proliferative zone
  3. Hypertrophic zone of maturation
  4. Provisional calcification (on the metaphyseal side)
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26
Q

What are the two methods of bone healing?

A

Primary: healing by direct union with no callus formation. In this osteoblastic bone formation occurs directly between the fragments.

Secondary: healing via callus formation when the bone ends are not well aligned.

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27
Q

What are the steps of secondary bone healing?

A
  1. Haematoma formation: this seals off the fracture site.
  2. Inflammation: haematoma provides a framework for the influx of inflammatory cells which activate the osteoprogenitor cells. This occurs during the first 1-7 days.
  3. Soft callus stage: lasts 2-3 weeks. Uncalcified tissue provides anchorage of the bone ends but no structural support.
  4. Hard callus stage: lasts 3-4 months. The activated progenitor cells deposit subperiosteal woven bone and chondroblasts deposit cartilage which undergoes endochondral ossification.
  5. Remodelling: woven hone is replaced by Lamella bone.
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28
Q

What is Wolff’s law?

A

The lamellar bony canals form in the direction of mechanical stress.

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29
Q

What is malunion?

A

This is bone healing in a sub-optimal position causing a deformity.

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30
Q

What is non-union?

A

This is failure to reach bony union by 9 months or no evidence of any healing for 3 months.

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31
Q

What is delayed union?

A

This is no union by 6 months.

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32
Q

What factors may delay bone healing?

A

Patient factors:
- Smoking
- Alcohol
- Obesity
- Malnutrition
- Immunosuppression
- PVD
- Anaemia
- Diabetes
- Age

Injury Factors:
- Infected wound
- Soft tissue damage
- Local ischaemia
- Instability
- Poor technique
- Pathological #

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33
Q

Why should you be cautious when giving NSAIDs in a post-operative fracture fixation?

A

NSAIDs are COX inhibitors and therefore they may interfere with the inflammatory stages of bone healing.

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34
Q

What are the different types of joints?

A

Fibrous: no cavity. The bones are joined by fibrous tissue. (examples - cranial sutures, syndesmosis, gomphosis).

Cartilaginous:
Primary (Synchondroses): bone meets hyaline cartilage: immovable.
Secondary (symphysis): Bones have an articular surface covered with fibrocartilage (slightly movable).

Synovoal: fluid filled capsule allowing movement.

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35
Q

What are the differences between rheumatoid and osteoarthritis clinically?

A

Rheumatoid is an inflammatory arthritis, worse on waking, relieved by NSAIDs, may have systemic signs or symptoms, can have a familial element. Get soft tissue swelling. warm and red joints, with raised ESR, raised CRP, low Hb, and +ve antibodies.

Osteoarthritis is a mechanical condition, worse on exercise, and relieved by simple analgesia.
There will be no systemic symptoms. They get bony swellings with normal inflammatory markers, normal Hb, negative antibodies.

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36
Q

What are the differences between RA and Osteoarthritis on imaging?

A

Both cause joint space narrowing.
Osteoarthritis causes: osteophytes, subchondral sclerosis, subchondral cysts
Rheumatoid causes: marginal erosions, periarticular osteoporosis, soft tissue changes, normally symmetrical and may get subluxation deformity.

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37
Q

What is the pathophysiology of oestoarthritis?

A

Affects the synovial joints due to the reduction in proteoglycans, causing a reduced binding capacity for H20 which causes a thinner and stiffer cartilage.
The breakdown products activate the immune system and cause inflammation and tissue destruction and attempts at repair (resulting in osteophytes and subchondral sclerosis).

38
Q

How can you grade cartilage damage?

A
  1. softening
  2. fissure
  3. partial thickness loss/flap
  4. full thickness loss with exposed bone
39
Q

How would you manage osteoarthritis?

A

Conservative: physio, splints
Medical: analgesia or steroids
Surgical: arthroplasty or arthrodesis.

40
Q

What is the pathophysiology of Rheumatoid Arthritis?

A

This is a symmetrical polyarthropathy affecting the synovial joints by causing chronic synovitis. This occurs due to invasion of macrophages and T lymphocytes.
The inflamed synovium of pannus impinges the joint, which causes an inflammatory response causing bony erosions.

41
Q

What is a rheumatoid nodule?

A

These are subcutaneous lesions with central necrosis surrounded by macrophages and fibroblasts.

42
Q

How would you manage rheumatoidarthritis?

A

Medical: NSAIDs, methotrexate, sulfasalazine, azothioprine, TNF-alpha blockers (etanercept and infliximab)
Surgical: synovectomy/arthodesis and arthoplasty

43
Q

What is gout?

A

Acute arthritis secondary to crystallisation of monosodium urate in the joint.

44
Q

What are the extra-articular features of gout?

A

Gouty tophi: urate deposits in the periarticular tissue.
Kidney disease: uric acid nephropathy/stones

45
Q

What are the causes of hyperuricaemia?

A

Increased production: high purine diet (cheese, alcohol, meat), tumour lysis syndrome, organ transplant.

Decreased secretion: renal failure, dehydration, diuretics, salicylates and ciclosporin.

46
Q

What causes pseudogout?

A

Positively bifringent rhomboid shaped crystals of calcium pyrophosphate.

47
Q

What is the classical radiographic feature of pseudogout?

A

Chondrocalcinosis.

48
Q

What are the risk factors for pseudogout?

A

Hyperparathyroidism
Hypothyroidism
Low phosphate
Hemochromatosis
Acromegaly
Wilsons disease

49
Q

What is the definition of osteoporosis?

A

This is bone density below 2.5SD of the normal range, due to porosity of the mineralised bony matrix.

50
Q

What are the risk factors for osteoporosis?

A

Reduced physical activity, reduced oestrogen levels, smoking and malnutrition

51
Q

How should osteoporosis be managed?

A

Calcium and Vitamin D supplements and bisphosphonates.

52
Q

How do bisphosphonates work?

A

Inhibit bony reabsorption by inhibiting osteoclast activity and binding to calcium phosphate crystals to prevent breakdown.

53
Q

What is osteomalacia?

A

This is a metabolic bone disorder characterised by deranged vitamin D metabolism due to inadequate synthesis or reduced absorption.

Inadequate synthesis: reduced sunlight exposure, malnutrition, cholestatic liver disease, pancreatitis, coeliac

Reduced absorption: phenytoin, rifampicin, kidney disease, low phosphate.

54
Q

What would be the picture on blood tests in osteomalacia?

A

Reduced phosphate, reduced calcium and increased ALP.

55
Q

What is Rickets?

A

This is inadequate calcification of epiphyseal cartilage which causes overgrowth with irregular pattern. Occurs due to low Vitamin D.

56
Q

What are the features of Rickets?

A

Scoliosis or biconcave vertebral body
Bowing of the diaphysis
Soft thin skull
Cupping at the metaphysis
Bony spurs in the growth plate
Wide growth plate

57
Q

What is Pagets diease of the bone?

A

This is a metabolic bony disease characterised by disorganised bony turnover. It will have a normal calcium and phosphate but a high ALP.

Clinical features include:
- bony pain
- bowing of the tibia/femur
- craniofacial overgrowth
- distortion of the femoral head
- nerve root compression
- high OP cardiac failure

58
Q

What are the pathological stages of Paget’s disease of the bone?

A

1.Osteolytic (mediated by osteoclasts_
2.Reparative (rapid bone formation alongside osteoclast activity causing an overall increase in bone)
3.Inactive phase (burn out of the cells causing dense osteo-sclerotic lesions)

59
Q

How would you manage Paget’s disease of the bone?

A

Bisphosphonates, calcitonin
Surgery if there is a pathological fracture or a nerve root compression

60
Q

What tumours may be associated with Paget’s disease of the bone?

A

Benign: giant cell granuloma
Malignant: sarcoma, osteosarcoma (most common), chondrosarcoma, giant cell tumour, malignant fibrous histeocytoma.

61
Q

What is the most common organism of septic arthritis?

A

Staph A

62
Q

When should you be cautious doing a joint aspirate?

A

Coagulopathy
Fracture
Prosthesis
Bursitis or cellulitis

63
Q

What is a DAIR procedure?

A

This is a debridement, antibiotic, implant retention procedure.

64
Q

What would your differentials for a hot, swollen, painful knee be?

A

Septic arthritis, osteomyelitis, bursitis, cellulitis, gout, pseudogout, arthritis, hemarthrosis

65
Q

What is the definition of a sarcoma?

A

This is a tumour arising from the mesenchymal tissue (connective tissue), they can occur anywhere in the body.

66
Q

What is the most common primary bone tumour?

A

Osteosarcoma

67
Q

What is an osteosarcoma?

A

These are malignant osteoblast producing osteoid masses. They cause a “sub-burst” pattern on imaging due to the overlying periosteal reaction.
Present as a painful, enlarging mass.

68
Q

What is a chondrosacrcoma?

A

This is a malignant tumour of the cartilage. It causes a slow growing mass with endosteal scalloping and cortical thickening. Requires wide local excision and chemo.

69
Q

What is a Ewing’s sarcoma?

A

This is a bony tumour arising from poorly differentiated neuroectodermal cells. They cause a “moth eaten” appearance on an XR and periosteal reaction which looks like onion skin.
Needs resection and chemo.

70
Q

What are the macro- and microscopic features of Ewings Sarcoma?

A

Macro: moth eaten appearance with an “onion skin” reaction of periosteum.
Micro: small round cells

71
Q

What are the macro and microscopic features of Malignant fibrous histocytoma?

A

Macro: lytic lesions and bony destruction.
Micro: spindle cells, histiocytes, giant cells

72
Q

What is the pathophysiology of multiple myeloma?

A

This is a disease of the plasma cells causing uncontrolled replication and overproduction of immunoglobulins.
The cloned plasma cells accumulate in the bone marrow and cause a decrease in the normal healthy bone matrix which causes decreased production of blood clots causing anaemia, impaired immune function and low platelets.

The cloned plasma cells also activate osteoclasts which cause an increase in bony lesions leading to bone pain, high calcium and pathological fracture.

73
Q

How does multiple myeloma cause kidney failure?

A

The cloned plasma cells produce a paraprotein which forms protein casts in the renal tubules which damage the kidneys.

74
Q

What are the subtypes of multiple myeloma?

A

IgG (most common - approx 2/3)
IgA (approx 1/3)
IgD or IgM (very rare)

75
Q

What are the features of multiple myeloma?

A

Increased calcium
Renal failure
Anaemia
Bony lesions

Also become immunocompromised and may get amyloid deposits.

76
Q

What investigations would you do if you were suspicious of multiple myeloma?

A

FBC (anaemia)
UE (renal failure)
ESR (inflammation)
Bone profile (high calcium)
Blood film (rouleaux formation due to stacking of RBC)
IgA and IgM measurements.
Protein electrophoresis (Bence Jones paraprotein)
Free light chain levels
Skeletal survey
Bone marrow biopsy and immunohistochemistry

77
Q

How would you manage multiple myeloma?

A

If <65: chemotherapy and stem cell transplant

If >65: chemotherapy alone

Maintenance chemotherapy at a low dose improves progression and survival.

78
Q

What is the prognosis of multiple myeloma?

A

Often patients get a relapse and therefore they need re-treatment.
They may become resistant to chemotherapy so need a new regime

Overall 5 year survival is about 35%.

79
Q

What are some example of benign bony tumours?

A

Osteochondroma: most common, normally around age 20. Causes a bony outgrowth capped in a layer of cartilage. They have a small chance of malignant transformation.

Enchondroma: well defined lesion of lobulated hyaline cartilage with some ossification.

Chondroblastoma: tumour of hyaline cartilage occurs at the epiphysis of long bones, has a chicken wire pattern.

Osteoid osteoma: benign bone forming tumour, causes night pain.

Giant cell tumour (osteoclastoma): these are found just below the subchondral plate in the epiphysis. They can be benign or malignant but are always locally aggressive. They cause a “soap bubble” lesion with multinucleated giant cells.
They require curratage and adjuvent phenol therapy

80
Q

What are common primary cancers causing skeletal mets?

A

Sclerotic: prostate and renal
Lytic: breast, thyroid and lung

81
Q

Explain the Mirrel score.

A

This is a score that predicts the risk of spontaneous fracture.

Site:
1 - Upper extremity
2- lower extremity
3- peri-trochanteric

Size:
1 - less then 1/3
2 - 1/3-2/3
3 - over 2/3

Radiology:
1 - sclerotic
2- mixed
3 - lytic

Pain:
1 - mild
2- moderate
3 - on movement

A score of below 7 gives a risk of approximately 4% and therefore conservative Mx

A score of over 9 is 33% risk and therefore prophylactic fixation should be undertaken

82
Q

What is compartment syndrome?

A

This is a surgical emergency.
It is caused by inadequate tissue perfusion or oxygenation in a compartment due to the raised pressures.

83
Q

What is the pathophysiology of compartment syndrome?

A

Swelling due to oedema, inflammation or haematoma cause a venous outflow obstruction which leads to further swelling which leads to reduced arterial inflow and therefore ischaemia. Which causes a negative cycle.

84
Q

What are the features of compartment syndrome?

A

Pain out of proportion
Tense compartment
Pain on passive stretch
Weakness, paraesthesia and pulselessness.

85
Q

How would you manage compartment syndrome of the lower extremity?

A

Urgent decompression with fasciotomy.
Lateral incision: 2 fingers lateral to the anterior border of the tibia.
Medial incision: behind the medial malleolus.

86
Q

What are the causes of compartment syndrome?

A

Intrinsic: bleeding, fractures, crush injury, reperfusion injury
Extrinsic: eschar formation, overly tight splints or casts.

87
Q

Can you name a complication of compartment syndrome?

A

Rhabdomyelysis may occur due to myoglobin release. This blocks the renal tubules.

88
Q

What are the causes of a fat embolus?

A

Blunt trauma, long bone injury, pancreatitis, severe burns, CP bypass, bone marrow biopsy, liposuction

89
Q

What are the features of fat embolus?

A

Rash, ARDS, Cerebral features.

90
Q

How do you manage fat embolus syndrome?

A

Supportive therapy: O2, renal support
Rule out PE

91
Q

Why would you choose to do a cemented hemiarthroplasty in an elderly patient with an intracapsular fracture?

A

ORIF not suitable as risk of avascular necrosis.
Less operative time, less blood loss than THR.
Reduced risk of dislocation compared to THF.
Cemented have a lower 30 day mortality than uncemented

92
Q
A

MRCS Part B (14 decks)

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