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MSK Flashcards

1
Q

What are the 5 adult cancers that commonly metastases to bone?

A 
Bronchus/lung
Breast
Prostate
Kidney
Thyroid (follicular thyroid)
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2
Q

What are the two paediatric cancers that commonly metastases to bone?

A

Rhabdomyosarcoma

Neuroblastoma

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3
Q

What bones are most commonly the site of metastases?

A

Long bones
Vertebrae

(good blood supply)

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4
Q

What is the most common primary bone tumour?

A

Myeloma

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5
Q

Describe some of the effects of bone metastases

A

Bone pain/destruction
Pathological fractures of long bones
Hypercalcaemia

Spinal metastases:
Vertebral collapse –> spinal cord compression –> nerve root compression –> back pain/paralysis (oncological emergency –> emergency radiotherapy)

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6
Q

What are the majority of bone mets? (Lytic/sclerotic?

A

Lytic

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7
Q

Describe lytic bone mets

A

Destroys the bone
Release of cytokines from tumour cells which activate osteoclasts to resorb bone

Can be inhibited by bisphosphonates

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8
Q

Describe sclerotic bone mets

A

Production of new woven bone

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9
Q

What types of cancer are sclerotic bone mets most commonly seen?

A

Prostate
Breast
Carcinoid tumours

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10
Q

What cancers most commonly cause a solitary bone met?

A

Renal and thyroid cancer

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11
Q

What are the orthopaedic consequences of a myeloma?

A

Punched out lytic foci

Generalised osteopenia - bone pain, tendency to fracture

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12
Q

What are the medical consequences of a myeloma?

A

Pancytopenia

Anaemia, thrombocytopenia, infections due to leucopenia

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13
Q

What are the immunological signs associated with a myeloma?

A

ESR >100
Serum electrophoresis: monoclonal bands
Bence Jones Protein in urine (immunological light chains)

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14
Q

What are the renal impairments associated with myeloma?

A 
Myeloma kidneys (precipitated light chains in renal tubules)
Hypercalcaemia
Amyloidosis
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15
Q

Give three benign primary bone tumours

A

Osteoid osteoma
Chondroma
Giant Cell Tumour

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16
Q

Give three malignant primary bone tumours

A

Osteosarcoma
Chondrosarcoma
Ewing’s tumour

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17
Q

Describe osteoid osteoma

A

Small benign osteoblastic proliferation
(osteoblasts –> osteoid - woven bone)

Esp. common in adolescents

M:F 2:!

Can occur in any bone esp long bones, spine

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18
Q

What is the classical history of an osteoid osteoma?

A

Pain - worse at night
Relieved by NSAIDs
(+ scoliosis)

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19
Q

What is the management of osteoid osteoma?

A

Radiofrequency ablation

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20
Q

Describe osteosarcoma

A

A malignant tumour who’s cells form osteoid/bone

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21
Q

What is the peak incidence of osteosarcoma?

A

10-25y

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22
Q

What is the typical site of an osteosarcoma?

A

Metaphysis of long bones (50% around knee)

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23
Q

What clinical features are associated with osteosarcoma?

A

Pain, swelling, inability to move the joint

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24
Q

What is the natural history of osteosarcoma?

A

Highly malignant
Aggressive
Early lung metastases
5y survival 50-60%

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25
Q

What is Codman triangle in relation to osteosarcoma?

A

Tumour spreads very quickly through the cortex of a bone, so forms a new cortex

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26
Q

Describe the management of osteosarcoma

A

8/52 chemo
Surgery - endoprosthetic replacement
Further chemo

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27
Q

Describe Paget’s disease

A

Disorder of excessive bone turnover
Infection of osteoclasts - resorb too much bone
Activation of osteoblasts - structurally weak bone

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28
Q

What are the clinical signs of Paget’s disease?

A

Bone pain
Deformity
Pathological fracture
Osteoarthritis
Deafness (compression of CNVIII due to thickened skull)
High cardiac output failure (very vascular bone –> takes blood away from heart)
Paget’s sarcoma

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29
Q

Describe Paget’s sarcoma

A 
Second osteosarcoma peak in elderly
Usually lytic
Long bones>spine
Very poor prognosis
Metastases to lung early
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30
Q

Describe enchondroma

A

Lobulated mass of cartilage within medulla
>50% hands, feet, long bones
Often asymptomatic in long bones
Hands - swelling, pathological fracture
Low cellularity - often surrounded by plates of lamellar bone

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31
Q

Describe osteocartilaginous exostosis

A

Benign outgrowth of cartilage with endo-chondral ossification

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32
Q

Describe chondrosarcoma

A

Most commonly occurs in middle-aged/elderly
Low grade tumours, less aggressive
Requires surgery

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33
Q

Describe Ewing’s sarcoma

A 
Peak 5-15y
Long bones
Flat bones of limb girdles
Early metastases to lung, bone marrow and bone 
Aggressive - 5y survival 50-60%
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34
Q

Define compartment syndrome

A

Elevated interstitial pressure within a closed fascial compartment resulting in microvascular compromise

35
Q

Give some potential causes of compartment syndrome

A

Increased internal pressure:
Trauma - fracture, bleeding, entrapment
Muscle oedema/myositis
Intracompartment administration of fluids/drugs

Increased external pressure:
Full thickness circumference burns
Impaired consciousness
Positioning in theatre - lithotomy
Bandages/casts
36
Q

Describe the pathophysiology of compartment syndrome

A

Pressure within the compartment > pressure within the capillaries
Microcirculatory collapse –> muscle becomes ischaemic
Oedema develops through increased endothelial perrmeability
Necrosis begins in the ischaemic tissue after 4 hours
Release of myoglobin –> kidney damage
Ischaemic nerves –> neurophraxic (irreversible after 4 hours)
Compromise of arterial supply –> absent pulse (late sign)

37
Q

What are the signs of end-stage of compartment syndrome?

A

Stiff fibrotic muscle compartments
Impaired nerve function
Clawing of limbs (forearms flexed wrist and fingers; equine contracture in legs)
Loss of function

38
Q

Describe the clinical signs attributed to compartment syndrome

A

Autonomic response - sweating, tachycardia
Swelling, shiny skin

6 P’s:
Pain out of proportion to be expected for level of injury
Pain on passive stretching of the compartment
Pallor
Parathesia
Paralysis
Pulseless (late sign)

39
Q

What is the normal intracompartment pressure?

A

0-4mmHg (10mmHg with exercise)

40
Q

What Compartment Pressures are diagnostic of ICP?

A

DBP-CP <30mmHg

CP >30mmHg

41
Q

Describe the management of compartment syndrome

A

Open any constricting bandages/dressings down to skin –> reassess

Surgical release: full length decomposition of all compartments, excise any dead tissue

Later wound closure (48hr) - repeat debridement until pressure is down and all dead muscle has been excised

Skin grafts/plastic surgery

42
Q

What are the compartments of the forearm?

A

Flexor
Extensor
Mobile Wad of Three

43
Q

What are the compartments of the leg?

A

Anterior
Lateral
Deep Posterior
Superficial Posterior

44
Q

What are the compartments of the thigh?

A

Anterior
Adductor
Posterior

45
Q

Describe aspects of the preoperative management of compartment syndrome

A 
Adequate fluid manage
Measure fluid losses 
Monitor and regulate electrolytes - esp K 
Correct acidosis 
Monitor renal function/mygobulinuria
46
Q

Describe the management of late presentation of compartment syndrome

A

Debride/amputate

Consider conservative management - splint in position of function

47
Q

What are the clinical features of tendinopathy?

A 
Loss of function
Pain
Swelling
Thickening
Tenderness
48
Q

Describe the pathogenesis of tendinopathy

A

Chronic tendon injury due to overuse
Deranged collagen fibres in tendon
Invasion of blood vessels to aid healing
Increased cellularity (myofibroblasts) but not much of an inflammatory response
Release of inflammatory mediators (IL-1, NO, PG) –> apoptosis, pain, provokes degeneration through release of matrix metalloproteinases

49
Q

What are the risk factors for developing tendinopathy?

A 
Age
Chronic disease (DM, RA)
Adverse biomechanics (tight calf muscle --> achilles tendon under higher tension --> more likely to be damaged)
Repetitive exercise
Recent increase in activity
Quinolone Abx
50
Q

What are some of the common tendinopathies?

A 
Achilles tendinopathy
Rotator cuff tendonitis
Tennis elbow (lateral epicondylitis)
Golfers elbow (medial epicondylitis)
51
Q

How are tendinopathies diagnosed?

A

XR - calcification in tendon, bone deposits around tendon

US - doppler to assess for neovascularisation

MRI - T1 (thickening of tendon); T2 (accumulation of fluid)

52
Q

Describe non-operative management of tendinopathies

A

NSAIDs

Activity modification

Physio - eccentric exercises

GTN patches - increase local perfusion –> increase blood flow to tendon –> aids healing (takes 12/52 therefore compliance, headaches)

Platelet rich plasma - contains GF –> aids healing

53
Q

Describe operative management of tendinopathies

A

Debridement - remove up to 50% of tendon before strength is affected

Tendon transfers

54
Q

Define reactive arthritis

A

Sterile synovitis which occurs after a distal mucosal infection

55
Q

What HLA gene is associated with reactive arthritis?

A

HLA-B27

56
Q

What organisms can cause reactive arthritis?

A

Chlamydia trochomatis
Yersinia
Salmonella
Shigella

57
Q

What are the clinical feature features of reactive arthritis?

A

Acute asymmetrical arthritis affecting the lower limb
More common in males
Occurs days-weeks post infection
Can cause dactylitis - entire digit is swollen

58
Q

What is Reuter’s syndrome?

A

Post-infective arthritis
Non-gonorrhoeal urethritis
Conjunctivitis

59
Q

How is reactive arthritis managed?

A

Treat underlying infection
NSAIDs
Intra-articular steroids

60
Q

What is the prognosis of reactive arthritis like?

A

Usually self-limiting but can take up to 6/12
May be chronic
May have cardiac complications (aortic regurgitation, aortitis, amyloidosis)

61
Q

What is enteropathic arthritis?

A

Reactive arthritis seen in association with Crohn’s disease/ulcerative colitis

62
Q

How is enteropathic arthritis managed?

A

Treat underlying inflammatory bowel disease

NSAIDs

63
Q

What are the clinical features of septic arthritis?

A

Pain
Fever
Swollen joint
Loss of function

64
Q

What are the most common causative organisms of septic arthritis?

A

S.aureus

S.pyogenes

65
Q

What organism most commonly causes septic arthritis in people who are sexually active?

A

N.gonnorhoea

66
Q

What organism is most likely to cause septic arthritis in children?

A

H.influenzae

67
Q

What is the most commonly used Abx regimen for the management of septic arthritis?

A

Flucloxacillin + gentamicin

IV for 2/52 then oral for 4/52

68
Q

Define gout

A

Inflammatory arthritis that results due to the deposition of urate crystals in and around joints

69
Q

What is the clinical presentation of gout?

A

Podagra (very painful monoarthritis of 1st MTJ)

Pain

70
Q

Describe the pathogenesis of acute gout

A

Deposition of urate crystals in joint –> acute inflammatory process –> joint destruction (increased CVA risk)

71
Q

Describe the pathogenesis of chronic gout

A

Deposition of urate –> tophi formation (may develop renal disease)

72
Q

What investigations are needed for suspected gout?

A

Aspirate - negatively birefringent needle shaped crystals on polarised microscopy
Serum urate levels
U&Es

73
Q

What is a primary cause of gout?

A

Lesch-Nyhan Syndrome
Rare inherited disorder
Gout + poor muscle control + self-mutilating behaviours

74
Q

What are some secondary causes of gout?

A

High uric acid due to myeloproliferative disorders
Leukaemia treated with chemotherapy
Thiazide diuretics
Chronic renal disease

75
Q

What are risk factors for developing high urate levels?

A

Older people
Metabolic syndrome
Alcohol excess
Red meat, shellfish, anchovies

76
Q

Describe the management of gout

A

NSAIDs - high dose needed to reduce pain/swelling
Colchicine
Corticosteroids

77
Q

What can Colchicine interact with?

A

Statins, cyclosporin, clarithromycin

78
Q

What medications can be used to prevent repeated attacks of gout?

A 
Allopurinol (inhibits xanthine oxidase) 
Uricosuric agent (probenecid) - increase secretion of uric acid into urine
79
Q

Define pseudo-gout

A

Calcium pyrophosphate crystals deposition in the synovium

80
Q

Define Chrondrocalcinosis

A

Calcium pyrophosphate crystals deposited into cartilage and extra-articular tissue

81
Q

What are potential secondary causes of pseudo-gout?

A

Haemochromatosis

Hyperparathyroidism

82
Q

What is the classic feature of joint aspirate in pseudo-gout?

A

Positively birefringent rhomboid shaped crystals

83
Q

How is pseudo-gout managed?

A

Aspiration - reduces pain and swelling
NSAIDs
Colchocine

MBChB (14 decks)

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