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
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
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
4
Q
4 pillars of inflammation
A
Red (rubor)
Painful (dolor)
Hot (calor)
Swollen (tumour)
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)
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
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)
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
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)
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
11
Q
which gender does osteoarthritis affect more
A
female
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
13
Q
differential diagnoses for osteoarthritis
A
Fibromyalgia
Rheumatoid arthritis
Gout and pseudogout
14
Q
investigations for osteoarthritis
A
Radiographs show LOSS;
- Loss of joint space
- Osteophytes
- Subarticular sclerosis
- Subchondral cysts
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
16
Q
pharmacological management of osteoarthritis
A
Analgesia;
Topical – NSAIDs/ capsaicin
Oral – paracetamol/ NSAIDs/ opioids
Transdermal patches
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)
18
Q
what is RA
A
multisystem autoimmune disease in which the brunt of disease activity falls upon the synovial joints
19
Q
causes of RA
A
- not known
- once inflammation begins it becomes self-perpetuating
- auto-antibodies = RF, anti-CCP
20
Q
pathology of RA
A
- Infiltration of synovium by CD4+ T-cells, B-cells (lymphocytes), plasma cells and macrophages
- Chronic inflammation reaction
21
Q
clinical presentation of RA
A
- worse in morning
- symmetrical, swollen, painful, stiff, small joints of hands and feet
- systemic illness
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
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
24
Q
extra articular eyes (RA)
A
- episcleritis, scleritis and necrotising scleritis
25
rheumatoid nodule
- on pressure points (olecranon)
- RF positive
- palisading ring of macrophages and fibroblasts with central fibrinoid necrosis and cuff of connective tissue on the outside
26
investigations of RA
- 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)
27
management of RA
- DMARDs (methotrexate) and biological agents
- steroids for short term use
- NSAIDs = symptom relief
- physio, OT
- surgery
- manage CV risk factors
28
bone fracture patterns
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)
29
risk factors for bone fracture
Osteoporosis
Metabolic bone disease – Osteomalacia and rickets
Paget’s disease
Bone infiltrated by malignant tumours
30
management of fractures
```
Analgesia
Examination – neurovascular
Reduce
Immobilise
Rehabilitate
```
31
fracture healing
- 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.
32
what is osteoporosis
- metabolic bone disease
| - reduction in bone mass, increased bone fragility and predisposition to fracture
33
primary causes of osteoporosis
post-menopausal
| age (>70)
34
secondary causes of osteoporosis
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
35
mechanism of post-menopausal osteoporosis
- loss of restraining effect of oestrogen
- high bone turnover (resorption> formation)
- cancellous bone loss with microarchitectural disruption
36
mechanism of ageing related osteoporosis
- decrease in trabecular thickness, horizontal trabeculae and decrease in connections between them
- decrease in trabecular strength (Eular Buckling Theory)
37
classic sites for fragility fractures
- vertebrae, distal radius, neck of femur
| - vertebral fractures lead to loss of height and kyphosis
38
what kind of fracture is most likely with trabecular bone osteoporosis
- crush fractures of vertebrae
39
what kind of fracture is most likely with cortical bone osteoporosis
long bone fractures
40
investigations for osteoporosis
- 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
>
41
what is the FRAX questionnaire
- gives a 10 year probability of fracture
42
lifestyle measures for osteoporosis management
- stop smoking / alcohol
- weight bearing exercise
- balance exercises
- calcium and vit D rich diet
43
pharmacological management of osteoporosis
- 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
44
systemic sclerosis
- Features scleroderma (skin fibrosis), internal organ fibrosis (lung, cardiac, GI and renal) and microvascular abnormalities
- 90% are ANA positive
45
what is limited scleroderma (systemic sclerosis)
- face, hands and feet.
- anticentromere antibodies.
- Pulmonary hypertension is often present
46
what is diffuse scleroderma (systemic sclerosis)
- whole body
- poor prognosis
- control BP meticulously
- annual echocardiogram and spirometry
47
management of systemic sclerosis
- no cure
- immunosuppression (IV cyclophosphamide)
- monitor BP and renal function
48
what is polymyositis and dermatomyositis
- 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
49
presentation of dermatomyositis
- myositis + (macular rash, lilac-purple rash on eyelids, nailfold erythema, Gottron's papules over knuckles)
50
extra- muscular signs of myositis
```
Fever
Arthralgia
Raynaud’s
Interstitial lung fibrosis
Myocardial involvement (myocarditis, arrhythmias)
```
51
tests for myositis
- Muscle enzymes increased in plasma
- EMG (fibrillation potentials)
- Muscle biopsy confirms diagnosis
- MRI shows muscle oedema
52
management of myositis
- prednisolone
| - +/- immunosuppressives and cytotoxics
53
what is systemic lupus erythematous (SLE)
multisystem autoimmune disease characterised by autoantibody production against a number of nuclear and cytoplasmic autoantigens
54
causes of SLE
- unknown
| theory = defective phagocytosis of apoptotic bodies leads to immune response against intra-cellular self antigens
55
pathology of SLE
- 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
56
clinical presentation of SLE
- 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
57
immunology of SLE
- >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)
58
differential diagnoses for SLE
- RA
- fibromyalgia
- Sjogren syndrome
59
investigations for SLE
- 4+ criteria or biopsy proven lupus nephritis with positive ANA or anti-DNA
60
some criteria for SLE
-malar rash, discoid rash, alopecia, synovitis, serositis, proteinuria, neuro features, haemolytic anaemia, leucopenia, thrombocytopenia
61
management of SLE
- prednisolone for flares
- NSAIDs and methotrexate or hydroxychloroquine
- sun cream
- monoclonal Ab (Belimumab)
62
management of lupus nephritis
- intensive immunosuppression with steroids
63
what is Sjogren's syndrome
- 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)
64
features of Sjogren's syndrome
- 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)
65
investigations for Sjogren's
- 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
66
treatment for Sjogren's
- hypromellose (artificial tears) and frequent drinks
| - NSAIDs and hydroxychloroquine for arthralgia
67
what is Raynaud's phenomenon
Peripheral digital ischaemia due to paroxysmal vasospasm, precipitated by cold or emotion
68
what causes the colour changes in Raynaud's
Pale -> ischaemia
Blue -> deoxygenation
Red -> reactive hyperaemia
69
what causes Raynaud's phenomenon
- 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
treatment for Raynaud's
- keep warm
- stop smoking
- chemical or surgical sympathectomy
71
what are seronegative spondyloarthropathies
- 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
what is the allele linked to seronegative spondyloarthropathies
HLA-B27
73
pathology of seronegative spondyloarthropathies
- 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
shared clinical features of seronegative spondyloarthropathies
- 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
name 3 seronegative spondyloarthropathies
- ankylosing spondylitis
- psoriatic arthritis
- reactive arthritis
76
what is ankylosing spondylitis
- chronic inflammatory disease of spine and sacroiliac joints
- aetiology unknown
77
typical patient presentation for ankylosing spondylitis
- man <30
- gradual onset lower back pain worse during night
- morning stiffness relieved by exercise
- pain radiates to hip/ buttocks
78
management of ankylosing spondylitis
- exercise
- NSAIDs
- local steroid injections (temporary pain relief)
- surgery = hip replacement
79
pattern of psoriatic arthritis
1. Symmetrical polyarthritis (like RA)
2. DIP joints
3. Asymmetrical oligoarthritis
4. Spinal (similar to AS)
5. Psoriatic arthritis mutilans (severe deformation)
80
investigations for psoriatic arthritis
- radiology = pencil in cup erosion of phalangeals
| - nail changes, synovitis, acneiform rashes and palmo-plantar pustulosis
81
management of psoriatic arthritis
- NSAIDs 1st line
- methotrexate
- anti-TNF agents
82
what is reactive arthritis
- 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
clinical presentation of reactive arthritis
- 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
investigations for reactive arthritis
- Increased ESR and CRP
- Culture stool if diarrhoea
- Infectious serology
- Sexual health review
- X-ray may show enthesitis with periosteal reaction
85
management of reactive arthritis
- no cure
- NSAIDs
- methotrexate if >6 months
86
pathology of crystal arthropathies
- crystals deposited in joints
| - Neutrophils ingest the crystals and degranulate, releasing enzymes that damage the joint
87
pathology of gout
- deposition of monosodium urate crystals
88
clinical manifestations of gout
- acute, painful, swollen, red joint (1st metatarsophalangeal most common)
- Individuals with high urate levels may develop chronic tophaceous gout
89
what is tophaceous gout
large deposits of urate (tophi – chalky white material) occur in the skin and around joints
90
risk factors for gout - reduced urate excretion
Elderly, men, post-menopausal women, impaired renal function, hypertension, metabolic syndrome, diuretics, antihypertensives, aspirin
91
risk factors for gout - excess urate production
Dietary (alcohol, sweeteners, red meat, seafood), genetic disorders, myelo- and lymphoproliferative disorders, psoriasis, tumour-lysis syndrome, drugs
92
investigations for gout
- 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
management of gout
- Allopurinol – long term treatment
- High-dose NSAID or colchicine (effective but slower to work)
- Steroids may also be used
- Rest and elevate joint
94
prevention of gout
Lose weight, avoid prolonged fasts, alcohol excess, purine-rich meats and low-dose aspirin
95
what is pseudogout (CPPD)
- calcium pyrophosphate deposition into a joint causes an acute arthritis that mimics gout
96
acute CPPD crystal arthritis
- acute monoarthropathy usually of larger joints in elderly.
- Usually spontaneous but can be provoked by illness, surgery or trauma
97
chronic CPPD crystal arthritis
inflammatory RA-like (symmetrical) polyarthritis and synovitis
98
clinical presentation of pseudogout/ CPPD
- 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
risk factors for pseudogout
old age, hyperparathyroidism, haemochromatosis, hypophosphatemia
100
investigations for pseudogout
- Polarised light microscopy of synovial fluid shows weakly positively birefringent rhomboid-shaped crystals.
- soft tissue calcium deposition on x-ray.
101
management of pseudogout
- Acute attacks: Cool packs, rest, aspiration, intra-articular steroids.
- Colchicine
- NSAIDs may prevent acute attacks
- Methotrexate and hydroxychloroquine ( for chronic)
102
what is vasculitis
- 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
what is large, medium and small vessel vasculitis
-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
tests for vasculitis
- Raised ESR/ CRP
- ANCA may be positive
- Raised creatinine if renal failure
- Urine: proteinuria, haematuria, casts on microscopy
- Angiography/ biopsy may be diagnostic
105
ANCA (anti-neutrophil cytoplasmic antibodies)
- small/medium vessel vasculitis
- Specific antibodies for antigens in cytoplasmic granules of neutrophils and monocyte lysosomes
- detect with indirect immunofluorescence microscopy
106
cytoplasmic (cANCA)
- Granular cytoplasmic staining
| - Major antigen – proteinase 3 (PR3)
107
peri-nuclear (pANCA)
- Homogenous perinuclear staining
| - Major antigen – myeloperoxidase (MPO)
108
management of vasculitis
- large vessel = steroids
| - small/medium vessel = immunosuppression with steroids +/- cyclophosphamide/methotrexate
109
giant cell (cranial or temporal) arteritis
- 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
diagnosis of giant cell arteritis
- 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
management of giant cell arteritis
- prednisolone or IV methylprednisolone
112
polyarteritis nodosa (PAN)
- 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
Granulomatosis with polyangiitis (GPA) – Wegener’s granulomatosis
- 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
diagnosis of Granulomatosis with polyangiitis (GPA) – Wegener’s granulomatosis
- 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
microscopic polyangiitis
- 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
staging of soft tissue tumours
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
staging of bone tumours
- pT1: tumour 8cm or less in greatest dimension
- pT2: tumour >8cm in greatest dimension
- pT3: discontinuous tumour in the primary bone site
118
what MSK tumours are treated with radiotherapy
Ewing’s, myeloma, lymphoma, STS, metastasis
119
4 different surgical margins in oncologic surgery
- 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
osteochondroma
- 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
osteoid osteoma
- 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
osteoblastoma
- 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
chondromas
- 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
chondroblastoma
- benign cartilage forming tumour of bone
- epiphyses of long bones in skeletally immature patients
- rare
- distal femur
125
metastases to bone
- majority of malignant bone tumours
- lung, breast, kidney, thyroid, prostate
- most osteolytic but prostate is osteoblastic (induce bone formation)
126
myeloma
- 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
pathology of myeloma
- 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
presentation of myeloma
- bone pain, fractures, infections
| - Anaemia, increased ESR, hypercalcaemia and renal impairment
129
conventional osteosarcoma
- 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
conventional chondrosarcoma
- malignant cartilage forming tumour
- pelvic bones
- atypical chondrocytes in cartilage matrix
131
benign fibrous dysplasia
- 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
benign non-ossifying fibroma
- variants of normal growth
- more diaphyseal as child grows
- on one side of bone, sclerotic rim, thinned cortex
133
unicameral bone cysts
- metaphyseal
- lytic
- expand bone symmetrically
- border growth plate
- trabeculations in them once fractured
- conservative therapy
134
aneurysmal bone cyst
- biopsy
- metaphyseal and eccentric (to one side)
- MRI = look for fluid levels
- simple curettage
135
Giant cell tumour
- 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
Ewing's sarcoma
- 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
adamantinoma
- rare tumour of long bones
- pain
- x-ray = radiolucent zones interlaced with sclerosis
- metastasise to lungs
- wide surgical excision and reconstruction
138
what is fibromyalgia
- 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
risk factors for fibromyalgia
```
Female
Middle age
Low household income
Divorced
Low educational status
Psychosocial factors
```
140
clinical presentation of fibromyalgia
- allodynia (pain without painful stimulus)
- hyperaesthesia (exaggerated perception of pain)
- chronic >3 months, widespread
- fatigue
- unrefreshing sleep
141
investigations for fibromyalgia
- all normal
| - diagnosis is clinical
142
management of fibromyalgia
- encourage to remain active
- review new symptoms
- relaxation, physio
- CBT
- low-dose amitriptyline
143
red flags for sinister causes of back pain
- <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
management of back pain
- 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
what is septic arthritis
- infection within a joint
146
pathology of septic arthritis
- relative inability of phagocytes to enter the joint space
- haematogenous spread or after penetrating trauma
- infection spreads quick, rapid and irreversible joint destruction
147
clinical presentation of septic arthritis
- extremely painful, hot, red, swollen joint
- Fever
- Knee > hip > shoulder
148
investigations for septic arthritis
- microbiology (most are staph. aureus)
- joint aspiration for fluid microscopy (neutrophils but no crystals)
- culture joint fluid and blood
149
management of septic arthritis
- empirical IV Abx until sensitivities are known
- flucloxacillin
- 2 weeks IV
- analgesia
150
what is osteomyelitis
infection of a bone
151
pathology of osteomyelitis
- infection = influx of acute inflammatory cells = suppurative inflammation
- necrotic bone = sequestrum
- failure to eradicate infection = chronic osteomyelitis = areas of new bone formation (involucrum)
152
clinical presentation of osteomyelitis
- 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
investigations for osteomyelitis
- microbiology = staph. aureus, salmonella in sick-cell disease patients
- bloods = high WCC, raised ESR and CRP
154
management of osteomyelitis
- IV Abx and surgical debridement
- antimicrobial therapy
- hardware replacement or removal
155
what is Osteomalacia
a metabolic bone disease characterised by inadequate mineralisation of bone in the mature skeleton
156
what is Rickets
a metabolic bone disease characterised by inadequate mineralisation of bone and epiphyseal cartilage in the growing skeleton of children
157
aetiology of osteomalacia and rickets
- 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
pathology of osteomalacia and rickets
- 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
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clinical presentation of rickets
- Growth retardation, hypotonia, apathy in infants
| - Once walking – knock-kneed, bow-legged
160
clinical presentation of osteomalacia
Bone pain and tenderness, fractures, proximal myopathy (waddling gait)
161
investigations for osteomalacia and rickets
- Bone biopsies: incomplete mineralisation
- Plasma: mildly reduced calcium levels
- X-ray: loss of cortical bone
- Imaging: osteopenia
162
management of osteomalacia and rickets
- vit D supplements = rapid remineralisation
| - if renal disease/ vit D resistance give alfacalcidol
163
what is Paget's disease
A metabolic bone disease characterised by excessive chaotic bone turnover in localised parts of the skeleton
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pathology of Paget's disease
- 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
treatment of Paget's disease
- bisphosphonates
| - analgesia
