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2A revision > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

what does seronegative and seropositive mean

A
  • seronegative = rheumatoid factor not present in blood serum
  • seropositive = RF present in blood serum
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2
Q

characteristics of inflammatory joint disease

A
  • pain eases with use
  • stiffness >60 mins in morning
  • synovial +/- bony swelling
  • hot and red
  • demographics = usually young, psoriasis, family history
  • mostly hands and feet
  • responds to NSAIDs
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3
Q

characteristics of degenerative joint disease

A
  • pain increases with use
  • clicks/ clunks
  • no or bony swelling
  • not clinically inflamed
  • demographics = older, occupation / sport
  • 1st CMCJ, DIPJ, knees
  • less response to NSAIDs
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4
Q

4 pillars of inflammation

A

Red (rubor)
Painful (dolor)
Hot (calor)
Swollen (tumour)

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5
Q

what can inflammation do to the bone

A
  • inflammatory exudate in bone marrow increases medullary pressure - into the bone cortex then ruptures through the periosteum
  • interruption of periosteal blood supply = necrosis
  • separated dead bone (sequestra)
  • new bone forms there (involucrum)
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6
Q

what is ESR

A
  • erythrocyte sedimentation rate
  • rises and falls over days/weeks
  • inflammation leads to increased fibrinogen which makes RBCs stick together so they fall faster
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7
Q

what is CRP

A
  • c-reactive protein
  • acute phase protein = pentametric peptide
  • rises and falls rapidly (peaks at 48h)
  • produced by liver in response to IL-6 (released in inflammation)
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8
Q

what is osteoarthritis

A
  • joint degeneration
  • age related, dynamic reaction pattern of a joint in response to insult or injury
  • Affects synovial joints
  • All tissues of the joint are involved
  • Articular cartilage is the most affected
  • Changes in underlying bone at the joint margins
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9
Q

what are the causes of osteoarthritis (primary and secondary)

A
  • primary = no clear cause

- secondary = caused by conditions causing joint damage (RA, gout, trauma)

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10
Q

pathology of osteoarthritis

A
  • low-grade chronic inflammation of the synovium, release of metalloproteinases, and degradation of articular cartilage matrix
  • metabolically active and dynamic process
  • loss of cartilage and disordered bone repair
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11
Q

which gender does osteoarthritis affect more

A

female

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12
Q

clinical presentation of osteoarthritis

A
  • joint pain, tenderness, swelling (synovitis), stiffness
  • worsen during day
  • hip, knee, spine, small joints of hands
  • gait alteration
  • Heberden’s nodes - DIP joint
  • Bouchard’s nodes - PIP joint
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13
Q

differential diagnoses for osteoarthritis

A

Fibromyalgia
Rheumatoid arthritis
Gout and pseudogout

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14
Q

investigations for osteoarthritis

A

Radiographs show LOSS;

  • Loss of joint space
  • Osteophytes
  • Subarticular sclerosis
  • Subchondral cysts
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15
Q

non medical management of osteoarthritis

A 
Activity and exercise – improve local muscle strength and general aerobic fitness. 
Weight loss if overweight 
Physiotherapy 
Occupational therapy
Walking aids – sticks/frames
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16
Q

pharmacological management of osteoarthritis

A

Analgesia;
Topical – NSAIDs/ capsaicin
Oral – paracetamol/ NSAIDs/ opioids
Transdermal patches

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17
Q

surgical management of osteoarthritis

A 
Joint replacement (hips or knees)
Arthroplasty (surgical reconstruction or a replacement of a joint)– if uncontrolled pain and significant limitation of function
Arthroscopy (keyhole surgery on a joint)
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18
Q

what is RA

A

multisystem autoimmune disease in which the brunt of disease activity falls upon the synovial joints

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19
Q

causes of RA

A
  • not known
  • once inflammation begins it becomes self-perpetuating
  • auto-antibodies = RF, anti-CCP
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20
Q

pathology of RA

A
  • Infiltration of synovium by CD4+ T-cells, B-cells (lymphocytes), plasma cells and macrophages
  • Chronic inflammation reaction
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21
Q

clinical presentation of RA

A
  • worse in morning
  • symmetrical, swollen, painful, stiff, small joints of hands and feet
  • systemic illness
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22
Q

extra-articular manifestations of RA

A
  • Cardiac disease: ischaemic heart disease, pericarditis
  • Vascular disease: accelerated atherosclerosis, vasculitis
  • Haematological disease: anaemia, splenomegaly
  • Pulmonary disease: pulmonary fibrosis, pleuritis
  • Skin: rheumatoid nodules, erythema nodosum
  • Neurological: peripheral neuropathy, stroke
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23
Q

later signs of RA

A
  • Ulnar deviation and subluxation of the wrist and fingers
  • Boutonniere and swan-neck deformities of fingers
  • Z thumbs
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24
Q

extra articular eyes (RA)

A
  • episcleritis, scleritis and necrotising scleritis
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25
Q

rheumatoid nodule

A
  • on pressure points (olecranon)
  • RF positive
  • palisading ring of macrophages and fibroblasts with central fibrinoid necrosis and cuff of connective tissue on the outside
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26
Q

investigations of RA

A
  • RF in 70% (Ab against Fc portion of IgG
  • anti-CCP = Anticyclic citrullinated peptide antibodies are highly specific
  • X-rays = soft tissue swelling, juxta-articular osteopenia and decrease joint space.
  • Ultrasound and MRI (synovitis)
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27
Q

management of RA

A
  • DMARDs (methotrexate) and biological agents
  • steroids for short term use
  • NSAIDs = symptom relief
  • physio, OT
  • surgery
  • manage CV risk factors
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28
Q

bone fracture patterns

A

Transverse
Oblique
Spiral – generated from twisting injury
Butterfly
Comminution – generate from high energy impact
Segmental
Greenstick (children, bone bends and one side breaks sue to thick periosteum)

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29
Q

risk factors for bone fracture

A

Osteoporosis
Metabolic bone disease – Osteomalacia and rickets
Paget’s disease
Bone infiltrated by malignant tumours

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30
Q

management of fractures

A 
Analgesia 
Examination – neurovascular 
Reduce 
Immobilise 
Rehabilitate
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31
Q

fracture healing

A
  • Haematoma organised and dead bone removed
  • Callus formed, then replaced by trabecular bone
  • Finally remodelled into lamellar bone
  • Fracture healing delayed if bone ends are mobile, infected very badly, misaligned or avascular.
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32
Q

what is osteoporosis

A
  • metabolic bone disease

- reduction in bone mass, increased bone fragility and predisposition to fracture

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33
Q

primary causes of osteoporosis

A

post-menopausal

age (>70)

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34
Q

secondary causes of osteoporosis

A

Therapeutic agents; glucocorticoid therapy, anti-androgens and anti-oestrogens
Cushing’s syndrome
Hyperparathyroidism, hyperthyroidism
Hypogonadism (low levels of testosterone)
Coeliac disease
IBD
Alcohol, poor nutrition, immobilisation

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35
Q

mechanism of post-menopausal osteoporosis

A
  • loss of restraining effect of oestrogen
  • high bone turnover (resorption> formation)
  • cancellous bone loss with microarchitectural disruption
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36
Q

mechanism of ageing related osteoporosis

A
  • decrease in trabecular thickness, horizontal trabeculae and decrease in connections between them
  • decrease in trabecular strength (Eular Buckling Theory)
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37
Q

classic sites for fragility fractures

A
  • vertebrae, distal radius, neck of femur

- vertebral fractures lead to loss of height and kyphosis

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38
Q

what kind of fracture is most likely with trabecular bone osteoporosis

A
  • crush fractures of vertebrae
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39
Q

what kind of fracture is most likely with cortical bone osteoporosis

A

long bone fractures

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40
Q

investigations for osteoporosis

A
  • x-ray
  • bloods (Ca, K, ALP)
  • bone densitometry scan (DEXA) = bone mineral density compared to young healthy adults
    > T-score is number of SDs from the youthful average
    >
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41
Q

what is the FRAX questionnaire

A
  • gives a 10 year probability of fracture
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42
Q

lifestyle measures for osteoporosis management

A
  • stop smoking / alcohol
  • weight bearing exercise
  • balance exercises
  • calcium and vit D rich diet
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43
Q

pharmacological management of osteoporosis

A
  • bisphosphonates (alendronic acid= alendronate) decreases osteoclast activity
  • HRT = reduce fracture risk by 50%, anti-resorptive
  • teriparatide = increases osteoblast (anabolic), improves trabecular structure
  • calcium and vit D
  • calcitonin for pain management after vertebral fracture
  • testosterone
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44
Q

systemic sclerosis

A
  • Features scleroderma (skin fibrosis), internal organ fibrosis (lung, cardiac, GI and renal) and microvascular abnormalities
  • 90% are ANA positive
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45
Q

what is limited scleroderma (systemic sclerosis)

A
  • face, hands and feet.
  • anticentromere antibodies.
  • Pulmonary hypertension is often present
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46
Q

what is diffuse scleroderma (systemic sclerosis)

A
  • whole body
  • poor prognosis
  • control BP meticulously
  • annual echocardiogram and spirometry
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47
Q

management of systemic sclerosis

A
  • no cure
  • immunosuppression (IV cyclophosphamide)
  • monitor BP and renal function
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48
Q

what is polymyositis and dermatomyositis

A
  • rare conditions
  • insidious onset of progressive symmetrical proximal muscle weakness and autoimmune-mediated striated muscle inflammation
  • Muscle weakness may cause dysphagia, dysphonia, or respiratory weakness
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49
Q

presentation of dermatomyositis

A
  • myositis + (macular rash, lilac-purple rash on eyelids, nailfold erythema, Gottron’s papules over knuckles)
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50
Q

extra- muscular signs of myositis

A 
Fever 
Arthralgia 
Raynaud’s
Interstitial lung fibrosis
Myocardial involvement (myocarditis, arrhythmias)
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51
Q

tests for myositis

A
  • Muscle enzymes increased in plasma
  • EMG (fibrillation potentials)
  • Muscle biopsy confirms diagnosis
  • MRI shows muscle oedema
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52
Q

management of myositis

A
  • prednisolone

- +/- immunosuppressives and cytotoxics

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53
Q

what is systemic lupus erythematous (SLE)

A

multisystem autoimmune disease characterised by autoantibody production against a number of nuclear and cytoplasmic autoantigens

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54
Q

causes of SLE

A
  • unknown

theory = defective phagocytosis of apoptotic bodies leads to immune response against intra-cellular self antigens

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55
Q

pathology of SLE

A
  • Activation of autoreactive B- and T-cells = immune complexes between autoantibodies and self-antigens
  • Inadequate clearance
  • deposited in tissues (skin, joints and kidneys) = inflammation and tissue damage
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56
Q

clinical presentation of SLE

A
  • Fatigue, weight loss, and low-grade fever
  • Joint involvement = arthralgia
  • Skin = scaly red lesions on sun-exposed sites
  • Pulmonary = pleuritis and pleural effusion, pneumonitis (pulmonary fibrosis)
  • Renal = glomerulonephritis (lupus nephritis), leading to CKD
  • Haematological = anaemia, lymphopenia, and thrombocytopenia
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57
Q

immunology of SLE

A
  • > 95% have anti-nuclear antibodies
  • 60% have anti-double-stranded DNA antibodies
  • 20-30% have anti-Smith antigen antibodies
  • 20-30% have antiphospholipid antibodies (cause a hypercoagulable state)
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58
Q

differential diagnoses for SLE

A
  • RA
  • fibromyalgia
  • Sjogren syndrome
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59
Q

investigations for SLE

A
  • 4+ criteria or biopsy proven lupus nephritis with positive ANA or anti-DNA
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60
Q

some criteria for SLE

A

-malar rash, discoid rash, alopecia, synovitis, serositis, proteinuria, neuro features, haemolytic anaemia, leucopenia, thrombocytopenia

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61
Q

management of SLE

A
  • prednisolone for flares
  • NSAIDs and methotrexate or hydroxychloroquine
  • sun cream
  • monoclonal Ab (Belimumab)
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62
Q

management of lupus nephritis

A
  • intensive immunosuppression with steroids
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63
Q

what is Sjogren’s syndrome

A
  • chronic inflammatory autoimmune disorder (primary or secondary) associated with connective tissue disease.
  • Secondary to: SLE, rheumatoid arthritis, scleroderma, primary biliary cirrhosis
  • lymphocytic infiltration and fibrosis of exocrine glands (lacrimal and salivary)
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64
Q

features of Sjogren’s syndrome

A
  • Decreased tears (dry eyes, keratoconjunctivitis sicca)
  • Decreased salivation
  • Parotid swelling
  • vaginal dryness, dyspareunia, dry cough and dysphagia.
  • Systemic signs (polyarthritis/arthralgia, Raynaud’s, lymphadenopathy, vasculitis, lung, liver and kidney involvement, peripheral neuropathy and fatigue)
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65
Q

investigations for Sjogren’s

A
  • Schirmer’s test (conjunctival dryness <5mm in 5 min)
  • Rose bengal staining = keratitis
  • anti-RO and anti-LA Abs
  • ANA usually positive
  • biopsy = focal lymphocytic aggregation
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66
Q

treatment for Sjogren’s

A
  • hypromellose (artificial tears) and frequent drinks

- NSAIDs and hydroxychloroquine for arthralgia

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67
Q

what is Raynaud’s phenomenon

A

Peripheral digital ischaemia due to paroxysmal vasospasm, precipitated by cold or emotion

68
Q

what causes the colour changes in Raynaud’s

A

Pale -> ischaemia
Blue -> deoxygenation
Red -> reactive hyperaemia

69
Q

what causes Raynaud’s phenomenon

A
  • Connective tissue disorders e.g. systemic sclerosis, SLE
  • Occupational e.g. using vibrating tools
  • Obstructive e.g. thoracic outlet obstruction, atheroma
  • Blood e.g. thrombocytosis, cold agglutinin disease, polycythaemia rubra vera
  • Drugs - β-blockers
  • Others – hypothyroidism
70
Q

treatment for Raynaud’s

A
  • keep warm
  • stop smoking
  • chemical or surgical sympathectomy
71
Q

what are seronegative spondyloarthropathies

A
  • group of inflammatory joint diseases characterised by arthritis (spinal column and peripheral joints) and enthesitis (inflammation at the insertion site of tendons and ligament to bone).
  • Seronegative = rheumatoid factor is negative.
72
Q

what is the allele linked to seronegative spondyloarthropathies

A

HLA-B27

73
Q

pathology of seronegative spondyloarthropathies

A
  • misfolded HLA-B27 causes endoplasmic reticulum stress and production of IL-23 via the T-helper 17 axis
  • HLA heavy chain homodimer hypothesis = heavy chain dimers accumulate in endoplasmic reticulum then initiate inflammation and bind to regulatory immune receptors
74
Q

shared clinical features of seronegative spondyloarthropathies

A
  • Seronegativity
  • HLA B27 association
  • Axial arthritis
  • Asymmetrical large-joint arthritis
  • Enthesitis
  • Dactylitis: inflammation of an entire digit
  • Extra-articular manifestations: iritis, psoriaform rashes, oral ulcers, IBD
75
Q

name 3 seronegative spondyloarthropathies

A
  • ankylosing spondylitis
  • psoriatic arthritis
  • reactive arthritis
76
Q

what is ankylosing spondylitis

A
  • chronic inflammatory disease of spine and sacroiliac joints
  • aetiology unknown
77
Q

typical patient presentation for ankylosing spondylitis

A
  • man <30
  • gradual onset lower back pain worse during night
  • morning stiffness relieved by exercise
  • pain radiates to hip/ buttocks
78
Q

management of ankylosing spondylitis

A
  • exercise
  • NSAIDs
  • local steroid injections (temporary pain relief)
  • surgery = hip replacement
79
Q

pattern of psoriatic arthritis

A
  1. Symmetrical polyarthritis (like RA)
  2. DIP joints
  3. Asymmetrical oligoarthritis
  4. Spinal (similar to AS)
  5. Psoriatic arthritis mutilans (severe deformation)
80
Q

investigations for psoriatic arthritis

A
  • radiology = pencil in cup erosion of phalangeals

- nail changes, synovitis, acneiform rashes and palmo-plantar pustulosis

81
Q

management of psoriatic arthritis

A
  • NSAIDs 1st line
  • methotrexate
  • anti-TNF agents
82
Q

what is reactive arthritis

A
  • arthritis and other clinical manifestations as autoimmune response
  • within 1 month of an infection elsewhere
  • Usually related to a genitourinary infection (chlamydia) or a GI (shigella, salmonella or campylobacter)
83
Q

clinical presentation of reactive arthritis

A
  • Pain and stiffness in lower back, knees, ankles and feet.
  • Enthesitis
  • Keratoderma blenorrhagica (brown, raised plaques on soles and palms).
  • urethritis, arthritis and conjunctivitis
84
Q

investigations for reactive arthritis

A
  • Increased ESR and CRP
  • Culture stool if diarrhoea
  • Infectious serology
  • Sexual health review
  • X-ray may show enthesitis with periosteal reaction
85
Q

management of reactive arthritis

A
  • no cure
  • NSAIDs
  • methotrexate if >6 months
86
Q

pathology of crystal arthropathies

A
  • crystals deposited in joints

- Neutrophils ingest the crystals and degranulate, releasing enzymes that damage the joint

87
Q

pathology of gout

A
  • deposition of monosodium urate crystals
88
Q

clinical manifestations of gout

A
  • acute, painful, swollen, red joint (1st metatarsophalangeal most common)
  • Individuals with high urate levels may develop chronic tophaceous gout
89
Q

what is tophaceous gout

A

large deposits of urate (tophi – chalky white material) occur in the skin and around joints

90
Q

risk factors for gout - reduced urate excretion

A

Elderly, men, post-menopausal women, impaired renal function, hypertension, metabolic syndrome, diuretics, antihypertensives, aspirin

91
Q

risk factors for gout - excess urate production

A

Dietary (alcohol, sweeteners, red meat, seafood), genetic disorders, myelo- and lymphoproliferative disorders, psoriasis, tumour-lysis syndrome, drugs

92
Q

investigations for gout

A
  • Polarised light microscopy of synovial fluid shows negatively birefringent needle-shaped urate crystals.
  • Serum urate is usually raised
  • Radiographs show only soft-tissue swelling (punched out erosions in later stages)
93
Q

management of gout

A
  • Allopurinol – long term treatment
  • High-dose NSAID or colchicine (effective but slower to work)
  • Steroids may also be used
  • Rest and elevate joint
94
Q

prevention of gout

A

Lose weight, avoid prolonged fasts, alcohol excess, purine-rich meats and low-dose aspirin

95
Q

what is pseudogout (CPPD)

A
  • calcium pyrophosphate deposition into a joint causes an acute arthritis that mimics gout
96
Q

acute CPPD crystal arthritis

A
  • acute monoarthropathy usually of larger joints in elderly.
  • Usually spontaneous but can be provoked by illness, surgery or trauma
97
Q

chronic CPPD crystal arthritis

A

inflammatory RA-like (symmetrical) polyarthritis and synovitis

98
Q

clinical presentation of pseudogout/ CPPD

A
  • gout attack= crystals break loose and move into joint space
  • sudden, severe pain with reddness, warmth, inflammation, low grade fever
  • pain worsens with movement
  • knee or wrist
99
Q

risk factors for pseudogout

A

old age, hyperparathyroidism, haemochromatosis, hypophosphatemia

100
Q

investigations for pseudogout

A
  • Polarised light microscopy of synovial fluid shows weakly positively birefringent rhomboid-shaped crystals.
  • soft tissue calcium deposition on x-ray.
101
Q

management of pseudogout

A
  • Acute attacks: Cool packs, rest, aspiration, intra-articular steroids.
  • Colchicine
  • NSAIDs may prevent acute attacks
  • Methotrexate and hydroxychloroquine ( for chronic)
102
Q

what is vasculitis

A
  • group of conditions in with inflammation and damage to blood vessels
  • can be primary or secondary to other diseases (SLE, RA, hep B/C , HIV)
103
Q

what is large, medium and small vessel vasculitis

A

-Large: giant cell arteritis, Takayasu’s arteritis
-Medium: polyarteritis nodosa, Kawasaki disease
-Small:
>ANCA-associated: microscopic polyangiitis, granulomatosis with polyangiitis
>Immune complex vasculitis: Goodpasture’s disease, cryoglobulinaemic vasculitis, IgA vasculitis
-Variable vessel vasculitis: Behçet’s and Cogan’s syndrome.

104
Q

tests for vasculitis

A
  • Raised ESR/ CRP
  • ANCA may be positive
  • Raised creatinine if renal failure
  • Urine: proteinuria, haematuria, casts on microscopy
  • Angiography/ biopsy may be diagnostic
105
Q

ANCA (anti-neutrophil cytoplasmic antibodies)

A
  • small/medium vessel vasculitis
  • Specific antibodies for antigens in cytoplasmic granules of neutrophils and monocyte lysosomes
  • detect with indirect immunofluorescence microscopy
106
Q

cytoplasmic (cANCA)

A
  • Granular cytoplasmic staining

- Major antigen – proteinase 3 (PR3)

107
Q

peri-nuclear (pANCA)

A
  • Homogenous perinuclear staining

- Major antigen – myeloperoxidase (MPO)

108
Q

management of vasculitis

A
  • large vessel = steroids

- small/medium vessel = immunosuppression with steroids +/- cyclophosphamide/methotrexate

109
Q

giant cell (cranial or temporal) arteritis

A
  • medium/ large arteries of head and neck
  • presenation over weeks with fever, anorexia, weight loss.
  • temporal artery = headache, scalp tenderness, and jaw claudication
  • ocular vessels = blindness
  • Aortic = thoracic or abdominal aortic aneurysm formation
110
Q

diagnosis of giant cell arteritis

A
  • Positive temporal artery biopsies show a lymphohistiocytic infiltrate with disruption of the media = giant cell reaction
  • Raised ESR and CRP (significantly), raised platelets, ALP and low Hb
111
Q

management of giant cell arteritis

A
  • prednisolone or IV methylprednisolone
112
Q

polyarteritis nodosa (PAN)

A
  • systemic medium vessel vasculitis
  • aneurysm formation and narrowing causes infarction of organs
  • GI tract, nervous system and muscles
  • main cause of death = renal artery narrowing and glomerular ischaemia
  • imaging, necrosis of biopsy, raised WCC, mild eosinophilia, anaemia
  • control BP and steroids
113
Q

Granulomatosis with polyangiitis (GPA) – Wegener’s granulomatosis

A
  • A systemic ANCA-associated vasculitis
  • dominant upper respiratory tract, lung, and renal involvement and cANCA positivity
  • nasal symptoms, AKI, pulmonary symptoms
  • needs aggressive immunosupression
114
Q

diagnosis of Granulomatosis with polyangiitis (GPA) – Wegener’s granulomatosis

A
  • Renal biopsies show a focal segmental necrotizing glomerulonephritis with crescent formation
  • Lung biopsies show large geographical areas of necrotising granulomatous inflammation and a necrotising vasculitis
115
Q

microscopic polyangiitis

A
  • systemic ANCA-associated vasculitis
  • renal and lung involvement and pANCA positivity
  • small/medium vessels
  • AKI, pulmonary haemorrhage
  • focal segmental necrotising glomerulonephritis
  • alveolar haemorrhage with necrotising capillaries
  • aggressive immunosuppression (steroids+ methotrexate)
116
Q

staging of soft tissue tumours

A

Primary tumour (T)

  • pT1a: superficial tumour 5cm in size
  • pT1b: deep tumour 5cm in size
  • pT2a: superficial tumour >5cm in size
  • pT2b: deep tumour >5cm

nodal spread - N0 = non N1= regional metastasis

117
Q

staging of bone tumours

A
  • pT1: tumour 8cm or less in greatest dimension
  • pT2: tumour >8cm in greatest dimension
  • pT3: discontinuous tumour in the primary bone site
118
Q

what MSK tumours are treated with radiotherapy

A

Ewing’s, myeloma, lymphoma, STS, metastasis

119
Q

4 different surgical margins in oncologic surgery

A
  • Intralesional: through the tumour
  • Marginal: the plane of surgery goes through the reactive zone of the lesion
  • Wide: goes through normal tissue
  • Radical: entire anatomic compartment
120
Q

osteochondroma

A
  • benign cartilaginous-forming bone tumour
  • solitary metaphyseal exophytic tumour
  • multiple osteochondromas - AD- DEFECT-11 syndrome
  • presents in young children with short stature, deformity, painless lump
  • surgical excision
121
Q

osteoid osteoma

A
  • benign bone forming bone tumour
  • in cortex of long bone in children, painful especially at night
  • CT/ X-ray = small lucent nidus <1cm
  • NSAIDs for pain and radiofrequency ablation
122
Q

osteoblastoma

A
  • benign bone forming bone tumour
  • in medullar of axial skeleton of child (can present in later life)
  • pain, spine lesions = neuropathy
  • X-ray = bone destruction surrounded by reactive new bone
  • mistaken for osteosarcoma
  • excision with at least a marginal line
123
Q

chondromas

A
  • benign cartilaginous forming tumour of bone
  • endochondroma= in medulla of the bone in hands and feet. Hot on bone scan
  • periosteal chondroma= on bone surface, proximal humerus
124
Q

chondroblastoma

A
  • benign cartilage forming tumour of bone
  • epiphyses of long bones in skeletally immature patients
  • rare
  • distal femur
125
Q

metastases to bone

A
  • majority of malignant bone tumours
  • lung, breast, kidney, thyroid, prostate
  • most osteolytic but prostate is osteoblastic (induce bone formation)
126
Q

myeloma

A
  • The most common tumour arising in bone.
  • A disseminated bone marrow-based plasma cell neoplasm associated with a serum and/or urine paraprotein.
  • incurable
127
Q

pathology of myeloma

A
  • neoplastic plasma cells secrete osteoclast activating cytokines
  • paraprotein depressed immune system
  • free light chains cause renal failure
  • interaction between myeloma cells and bone marrow stromal cells increases myeloma cell growth
128
Q

presentation of myeloma

A
  • bone pain, fractures, infections

- Anaemia, increased ESR, hypercalcaemia and renal impairment

129
Q

conventional osteosarcoma

A
  • malignant bone forming tumour
  • intramedullary (high grade), parosteal (low grade), periosteal (high), telangiectatic
  • secondary = from radiation, fibrous dysplasia
  • deep pain in long bone +/- palpable mass
  • multi agent chemo
130
Q

conventional chondrosarcoma

A
  • malignant cartilage forming tumour
  • pelvic bones
  • atypical chondrocytes in cartilage matrix
131
Q

benign fibrous dysplasia

A
  • benign intramedullary fibro-osseous lesion
  • <30 y
  • progressive in children, not in adults
  • proximal femur
  • Xray = ground glass lesion with sclerotic margin
  • bisphosphonates and curettage+ cortical autograft
132
Q

benign non-ossifying fibroma

A
  • variants of normal growth
  • more diaphyseal as child grows
  • on one side of bone, sclerotic rim, thinned cortex
133
Q

unicameral bone cysts

A
  • metaphyseal
  • lytic
  • expand bone symmetrically
  • border growth plate
  • trabeculations in them once fractured
  • conservative therapy
134
Q

aneurysmal bone cyst

A
  • biopsy
  • metaphyseal and eccentric (to one side)
  • MRI = look for fluid levels
  • simple curettage
135
Q

Giant cell tumour

A
  • benign, locally aggressive neoplasm of bone (intramedullary) that arises in the ends of long bones in mature skeleton
  • osteoclast rich, locally destructive
  • pain and sweling
  • calcium and phosphate levels elevated
  • biopsy = multinucleated cells
  • x-ray = destructive lesion with no sclerotic rim
  • bisphosphonates and surgical treatments
136
Q

Ewing’s sarcoma

A
  • malignant round cell tumour of bone of neuroectodermal origin (neural crest cells)
  • pain and mass in long bone/ pelvis/ rib
  • lytic or sclerotic diaphyseal mass, periosteum lifted off (onion skin)
  • biopsy = blue cell tumour, indistinct borders, no matrix
  • treatment = chemo, radiotherapy, surgical excision
137
Q

adamantinoma

A
  • rare tumour of long bones
  • pain
  • x-ray = radiolucent zones interlaced with sclerosis
  • metastasise to lungs
  • wide surgical excision and reconstruction
138
Q

what is fibromyalgia

A
  • long term condition that causes pain all over the body.
  • Very similar to chronic fatigue syndrome
  • Caused by aberrant peripheral and central pain processing
139
Q

risk factors for fibromyalgia

A 
Female 
Middle age
Low household income
Divorced 
Low educational status
Psychosocial factors
140
Q

clinical presentation of fibromyalgia

A
  • allodynia (pain without painful stimulus)
  • hyperaesthesia (exaggerated perception of pain)
  • chronic >3 months, widespread
  • fatigue
  • unrefreshing sleep
141
Q

investigations for fibromyalgia

A
  • all normal

- diagnosis is clinical

142
Q

management of fibromyalgia

A
  • encourage to remain active
  • review new symptoms
  • relaxation, physio
  • CBT
  • low-dose amitriptyline
143
Q

red flags for sinister causes of back pain

A
  • <20 or >55, constant or progressive, nocturnal, worst when supine, fever, weight loss, malignant history, abdo mass, thoracic, morning stiffness, leg pain, neuro disturbance, sphincter disturbance, infections, immunosuppression
144
Q

management of back pain

A
  • urgent neuro referral if any neurological deficit
    >acute cauda equina compression (bilateral root pain in legs)
    > acute cord compression (bilateral pain, LMN signs)
  • remain active
  • low dose amitriptyline
  • physio, acupuncture, exercise programme
145
Q

what is septic arthritis

A
  • infection within a joint
146
Q

pathology of septic arthritis

A
  • relative inability of phagocytes to enter the joint space
  • haematogenous spread or after penetrating trauma
  • infection spreads quick, rapid and irreversible joint destruction
147
Q

clinical presentation of septic arthritis

A
  • extremely painful, hot, red, swollen joint
  • Fever
  • Knee > hip > shoulder
148
Q

investigations for septic arthritis

A
  • microbiology (most are staph. aureus)
  • joint aspiration for fluid microscopy (neutrophils but no crystals)
  • culture joint fluid and blood
149
Q

management of septic arthritis

A
  • empirical IV Abx until sensitivities are known
  • flucloxacillin
  • 2 weeks IV
  • analgesia
150
Q

what is osteomyelitis

A

infection of a bone

151
Q

pathology of osteomyelitis

A
  • infection = influx of acute inflammatory cells = suppurative inflammation
  • necrotic bone = sequestrum
  • failure to eradicate infection = chronic osteomyelitis = areas of new bone formation (involucrum)
152
Q

clinical presentation of osteomyelitis

A
  • Fever and pain in the affected bone
  • Children may present with failure to weight-bear
  • May be aggravated by movement
  • Tenderness, warmth, erythema and swelling
153
Q

investigations for osteomyelitis

A
  • microbiology = staph. aureus, salmonella in sick-cell disease patients
  • bloods = high WCC, raised ESR and CRP
154
Q

management of osteomyelitis

A
  • IV Abx and surgical debridement
  • antimicrobial therapy
  • hardware replacement or removal
155
Q

what is Osteomalacia

A

a metabolic bone disease characterised by inadequate mineralisation of bone in the mature skeleton

156
Q

what is Rickets

A

a metabolic bone disease characterised by inadequate mineralisation of bone and epiphyseal cartilage in the growing skeleton of children

157
Q

aetiology of osteomalacia and rickets

A
  • Ca deficiency due to vit D deficiency or nutritional deficiency (diet, malabsorption due to chronic liver disease, CKD etc)
  • vit D resistance = hypophosphataemic rickets, low phosphate and resistance to vit D treatment
  • tumour induced osteomalacia (fibroblast growth factors)
158
Q

pathology of osteomalacia and rickets

A
  • Inadequate mineralisation of bone matrix (osteoid) due to lack of calcium and occasionally phosphate
  • Bones become abnormally soft and prone to deformity and fracture
  • In children, the soft bone formed at the epiphyseal plate results in skeletal deformity and short stature
159
Q

clinical presentation of rickets

A
  • Growth retardation, hypotonia, apathy in infants

- Once walking – knock-kneed, bow-legged

160
Q

clinical presentation of osteomalacia

A

Bone pain and tenderness, fractures, proximal myopathy (waddling gait)

161
Q

investigations for osteomalacia and rickets

A
  • Bone biopsies: incomplete mineralisation
  • Plasma: mildly reduced calcium levels
  • X-ray: loss of cortical bone
  • Imaging: osteopenia
162
Q

management of osteomalacia and rickets

A
  • vit D supplements = rapid remineralisation

- if renal disease/ vit D resistance give alfacalcidol

163
Q

what is Paget’s disease

A

A metabolic bone disease characterised by excessive chaotic bone turnover in localised parts of the skeleton

164
Q

pathology of Paget’s disease

A
  • number of stages, can be seen simultaneously in the same bone or different bones
  • intense osteoclastic bone resorption
  • Osteoblastic activity then becomes exaggerated with laying down of grossly thickened, poorly organised weak bone
  • bony pain and deformity
165
Q

treatment of Paget’s disease

A
  • bisphosphonates

- analgesia

2A revision (10 decks)

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