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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
What is Codman triangle in relation to osteosarcoma?
Tumour spreads very quickly through the cortex of a bone, so forms a new cortex
26
Describe the management of osteosarcoma
8/52 chemo Surgery - endoprosthetic replacement Further chemo
27
Describe Paget's disease
Disorder of excessive bone turnover Infection of osteoclasts - resorb too much bone Activation of osteoblasts - structurally weak bone
28
What are the clinical signs of Paget's disease?
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
29
Describe Paget's sarcoma
``` Second osteosarcoma peak in elderly Usually lytic Long bones>spine Very poor prognosis Metastases to lung early ```
30
Describe enchondroma
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
31
Describe osteocartilaginous exostosis
Benign outgrowth of cartilage with endo-chondral ossification
32
Describe chondrosarcoma
Most commonly occurs in middle-aged/elderly Low grade tumours, less aggressive Requires surgery
33
Describe Ewing's sarcoma
``` Peak 5-15y Long bones Flat bones of limb girdles Early metastases to lung, bone marrow and bone Aggressive - 5y survival 50-60% ```
34
Define compartment syndrome
Elevated interstitial pressure within a closed fascial compartment resulting in microvascular compromise
35
Give some potential causes of compartment syndrome
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
Describe the pathophysiology of compartment syndrome
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
What are the signs of end-stage of compartment syndrome?
Stiff fibrotic muscle compartments Impaired nerve function Clawing of limbs (forearms flexed wrist and fingers; equine contracture in legs) Loss of function
38
Describe the clinical signs attributed to compartment syndrome
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
What is the normal intracompartment pressure?
0-4mmHg (10mmHg with exercise)
40
What Compartment Pressures are diagnostic of ICP?
DBP-CP <30mmHg | CP >30mmHg
41
Describe the management of compartment syndrome
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
What are the compartments of the forearm?
Flexor Extensor Mobile Wad of Three
43
What are the compartments of the leg?
Anterior Lateral Deep Posterior Superficial Posterior
44
What are the compartments of the thigh?
Anterior Adductor Posterior
45
Describe aspects of the preoperative management of compartment syndrome
``` Adequate fluid manage Measure fluid losses Monitor and regulate electrolytes - esp K Correct acidosis Monitor renal function/mygobulinuria ```
46
Describe the management of late presentation of compartment syndrome
Debride/amputate | Consider conservative management - splint in position of function
47
What are the clinical features of tendinopathy?
``` Loss of function Pain Swelling Thickening Tenderness ```
48
Describe the pathogenesis of tendinopathy
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
What are the risk factors for developing tendinopathy?
``` 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
What are some of the common tendinopathies?
``` Achilles tendinopathy Rotator cuff tendonitis Tennis elbow (lateral epicondylitis) Golfers elbow (medial epicondylitis) ```
51
How are tendinopathies diagnosed?
XR - calcification in tendon, bone deposits around tendon US - doppler to assess for neovascularisation MRI - T1 (thickening of tendon); T2 (accumulation of fluid)
52
Describe non-operative management of tendinopathies
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
Describe operative management of tendinopathies
Debridement - remove up to 50% of tendon before strength is affected Tendon transfers
54
Define reactive arthritis
Sterile synovitis which occurs after a distal mucosal infection
55
What HLA gene is associated with reactive arthritis?
HLA-B27
56
What organisms can cause reactive arthritis?
Chlamydia trochomatis Yersinia Salmonella Shigella
57
What are the clinical feature features of reactive arthritis?
Acute asymmetrical arthritis affecting the lower limb More common in males Occurs days-weeks post infection Can cause dactylitis - entire digit is swollen
58
What is Reuter's syndrome?
Post-infective arthritis Non-gonorrhoeal urethritis Conjunctivitis
59
How is reactive arthritis managed?
Treat underlying infection NSAIDs Intra-articular steroids
60
What is the prognosis of reactive arthritis like?
Usually self-limiting but can take up to 6/12 May be chronic May have cardiac complications (aortic regurgitation, aortitis, amyloidosis)
61
What is enteropathic arthritis?
Reactive arthritis seen in association with Crohn's disease/ulcerative colitis
62
How is enteropathic arthritis managed?
Treat underlying inflammatory bowel disease | NSAIDs
63
What are the clinical features of septic arthritis?
Pain Fever Swollen joint Loss of function
64
What are the most common causative organisms of septic arthritis?
S.aureus | S.pyogenes
65
What organism most commonly causes septic arthritis in people who are sexually active?
N.gonnorhoea
66
What organism is most likely to cause septic arthritis in children?
H.influenzae
67
What is the most commonly used Abx regimen for the management of septic arthritis?
Flucloxacillin + gentamicin | IV for 2/52 then oral for 4/52
68
Define gout
Inflammatory arthritis that results due to the deposition of urate crystals in and around joints
69
What is the clinical presentation of gout?
Podagra (very painful monoarthritis of 1st MTJ) | Pain
70
Describe the pathogenesis of acute gout
Deposition of urate crystals in joint --> acute inflammatory process --> joint destruction (increased CVA risk)
71
Describe the pathogenesis of chronic gout
Deposition of urate --> tophi formation (may develop renal disease)
72
What investigations are needed for suspected gout?
Aspirate - negatively birefringent needle shaped crystals on polarised microscopy Serum urate levels U&Es
73
What is a primary cause of gout?
Lesch-Nyhan Syndrome Rare inherited disorder Gout + poor muscle control + self-mutilating behaviours
74
What are some secondary causes of gout?
High uric acid due to myeloproliferative disorders Leukaemia treated with chemotherapy Thiazide diuretics Chronic renal disease
75
What are risk factors for developing high urate levels?
Older people Metabolic syndrome Alcohol excess Red meat, shellfish, anchovies
76
Describe the management of gout
NSAIDs - high dose needed to reduce pain/swelling Colchicine Corticosteroids
77
What can Colchicine interact with?
Statins, cyclosporin, clarithromycin
78
What medications can be used to prevent repeated attacks of gout?
``` Allopurinol (inhibits xanthine oxidase) Uricosuric agent (probenecid) - increase secretion of uric acid into urine ```
79
Define pseudo-gout
Calcium pyrophosphate crystals deposition in the synovium
80
Define Chrondrocalcinosis
Calcium pyrophosphate crystals deposited into cartilage and extra-articular tissue
81
What are potential secondary causes of pseudo-gout?
Haemochromatosis | Hyperparathyroidism
82
What is the classic feature of joint aspirate in pseudo-gout?
Positively birefringent rhomboid shaped crystals
83
How is pseudo-gout managed?
Aspiration - reduces pain and swelling NSAIDs Colchocine

MBChB (14 decks)

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