Musculoskeletal Flashcards
what does seronegative and seropositive mean
- seronegative = rheumatoid factor not present in blood serum
- seropositive = RF present in blood serum
characteristics of inflammatory joint disease
- 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
characteristics of degenerative joint disease
- 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 pillars of inflammation
Red (rubor)
Painful (dolor)
Hot (calor)
Swollen (tumour)
what can inflammation do to the bone
- 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)
what is ESR
- erythrocyte sedimentation rate
- rises and falls over days/weeks
- inflammation leads to increased fibrinogen which makes RBCs stick together so they fall faster
what is CRP
- 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)
what is osteoarthritis
- 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
what are the causes of osteoarthritis (primary and secondary)
- primary = no clear cause
- secondary = caused by conditions causing joint damage (RA, gout, trauma)
pathology of osteoarthritis
- 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
which gender does osteoarthritis affect more
female
clinical presentation of osteoarthritis
- 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
differential diagnoses for osteoarthritis
Fibromyalgia
Rheumatoid arthritis
Gout and pseudogout
investigations for osteoarthritis
Radiographs show LOSS;
- Loss of joint space
- Osteophytes
- Subarticular sclerosis
- Subchondral cysts
non medical management of osteoarthritis
Activity and exercise – improve local muscle strength and general aerobic fitness. Weight loss if overweight Physiotherapy Occupational therapy Walking aids – sticks/frames
pharmacological management of osteoarthritis
Analgesia;
Topical – NSAIDs/ capsaicin
Oral – paracetamol/ NSAIDs/ opioids
Transdermal patches
surgical management of osteoarthritis
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)
what is RA
multisystem autoimmune disease in which the brunt of disease activity falls upon the synovial joints
causes of RA
- not known
- once inflammation begins it becomes self-perpetuating
- auto-antibodies = RF, anti-CCP
pathology of RA
- Infiltration of synovium by CD4+ T-cells, B-cells (lymphocytes), plasma cells and macrophages
- Chronic inflammation reaction
clinical presentation of RA
- worse in morning
- symmetrical, swollen, painful, stiff, small joints of hands and feet
- systemic illness
extra-articular manifestations of RA
- 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
later signs of RA
- Ulnar deviation and subluxation of the wrist and fingers
- Boutonniere and swan-neck deformities of fingers
- Z thumbs
extra articular eyes (RA)
- episcleritis, scleritis and necrotising scleritis
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
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)
management of RA
- DMARDs (methotrexate) and biological agents
- steroids for short term use
- NSAIDs = symptom relief
- physio, OT
- surgery
- manage CV risk factors
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)
risk factors for bone fracture
Osteoporosis
Metabolic bone disease – Osteomalacia and rickets
Paget’s disease
Bone infiltrated by malignant tumours
management of fractures
Analgesia Examination – neurovascular Reduce Immobilise Rehabilitate
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.
what is osteoporosis
- metabolic bone disease
- reduction in bone mass, increased bone fragility and predisposition to fracture
primary causes of osteoporosis
post-menopausal
age (>70)
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
mechanism of post-menopausal osteoporosis
- loss of restraining effect of oestrogen
- high bone turnover (resorption> formation)
- cancellous bone loss with microarchitectural disruption
mechanism of ageing related osteoporosis
- decrease in trabecular thickness, horizontal trabeculae and decrease in connections between them
- decrease in trabecular strength (Eular Buckling Theory)
classic sites for fragility fractures
- vertebrae, distal radius, neck of femur
- vertebral fractures lead to loss of height and kyphosis
what kind of fracture is most likely with trabecular bone osteoporosis
- crush fractures of vertebrae
what kind of fracture is most likely with cortical bone osteoporosis
long bone fractures
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
>
what is the FRAX questionnaire
- gives a 10 year probability of fracture
lifestyle measures for osteoporosis management
- stop smoking / alcohol
- weight bearing exercise
- balance exercises
- calcium and vit D rich diet
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
systemic sclerosis
- Features scleroderma (skin fibrosis), internal organ fibrosis (lung, cardiac, GI and renal) and microvascular abnormalities
- 90% are ANA positive
what is limited scleroderma (systemic sclerosis)
- face, hands and feet.
- anticentromere antibodies.
- Pulmonary hypertension is often present
what is diffuse scleroderma (systemic sclerosis)
- whole body
- poor prognosis
- control BP meticulously
- annual echocardiogram and spirometry
management of systemic sclerosis
- no cure
- immunosuppression (IV cyclophosphamide)
- monitor BP and renal function
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
presentation of dermatomyositis
- myositis + (macular rash, lilac-purple rash on eyelids, nailfold erythema, Gottron’s papules over knuckles)
extra- muscular signs of myositis
Fever Arthralgia Raynaud’s Interstitial lung fibrosis Myocardial involvement (myocarditis, arrhythmias)
tests for myositis
- Muscle enzymes increased in plasma
- EMG (fibrillation potentials)
- Muscle biopsy confirms diagnosis
- MRI shows muscle oedema
management of myositis
- prednisolone
- +/- immunosuppressives and cytotoxics
what is systemic lupus erythematous (SLE)
multisystem autoimmune disease characterised by autoantibody production against a number of nuclear and cytoplasmic autoantigens
causes of SLE
- unknown
theory = defective phagocytosis of apoptotic bodies leads to immune response against intra-cellular self antigens
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
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
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)
differential diagnoses for SLE
- RA
- fibromyalgia
- Sjogren syndrome
investigations for SLE
- 4+ criteria or biopsy proven lupus nephritis with positive ANA or anti-DNA
some criteria for SLE
-malar rash, discoid rash, alopecia, synovitis, serositis, proteinuria, neuro features, haemolytic anaemia, leucopenia, thrombocytopenia
management of SLE
- prednisolone for flares
- NSAIDs and methotrexate or hydroxychloroquine
- sun cream
- monoclonal Ab (Belimumab)
management of lupus nephritis
- intensive immunosuppression with steroids
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)
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)
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
treatment for Sjogren’s
- hypromellose (artificial tears) and frequent drinks
- NSAIDs and hydroxychloroquine for arthralgia
what is Raynaud’s phenomenon
Peripheral digital ischaemia due to paroxysmal vasospasm, precipitated by cold or emotion
what causes the colour changes in Raynaud’s
Pale -> ischaemia
Blue -> deoxygenation
Red -> reactive hyperaemia
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
treatment for Raynaud’s
- keep warm
- stop smoking
- chemical or surgical sympathectomy
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.
what is the allele linked to seronegative spondyloarthropathies
HLA-B27
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
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
name 3 seronegative spondyloarthropathies
- ankylosing spondylitis
- psoriatic arthritis
- reactive arthritis
what is ankylosing spondylitis
- chronic inflammatory disease of spine and sacroiliac joints
- aetiology unknown
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
management of ankylosing spondylitis
- exercise
- NSAIDs
- local steroid injections (temporary pain relief)
- surgery = hip replacement
pattern of psoriatic arthritis
- Symmetrical polyarthritis (like RA)
- DIP joints
- Asymmetrical oligoarthritis
- Spinal (similar to AS)
- Psoriatic arthritis mutilans (severe deformation)
investigations for psoriatic arthritis
- radiology = pencil in cup erosion of phalangeals
- nail changes, synovitis, acneiform rashes and palmo-plantar pustulosis
management of psoriatic arthritis
- NSAIDs 1st line
- methotrexate
- anti-TNF agents
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)
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
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
management of reactive arthritis
- no cure
- NSAIDs
- methotrexate if >6 months
pathology of crystal arthropathies
- crystals deposited in joints
- Neutrophils ingest the crystals and degranulate, releasing enzymes that damage the joint
pathology of gout
- deposition of monosodium urate crystals
clinical manifestations of gout
- acute, painful, swollen, red joint (1st metatarsophalangeal most common)
- Individuals with high urate levels may develop chronic tophaceous gout
what is tophaceous gout
large deposits of urate (tophi – chalky white material) occur in the skin and around joints
risk factors for gout - reduced urate excretion
Elderly, men, post-menopausal women, impaired renal function, hypertension, metabolic syndrome, diuretics, antihypertensives, aspirin
risk factors for gout - excess urate production
Dietary (alcohol, sweeteners, red meat, seafood), genetic disorders, myelo- and lymphoproliferative disorders, psoriasis, tumour-lysis syndrome, drugs
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)
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
prevention of gout
Lose weight, avoid prolonged fasts, alcohol excess, purine-rich meats and low-dose aspirin
what is pseudogout (CPPD)
- calcium pyrophosphate deposition into a joint causes an acute arthritis that mimics gout
acute CPPD crystal arthritis
- acute monoarthropathy usually of larger joints in elderly.
- Usually spontaneous but can be provoked by illness, surgery or trauma
chronic CPPD crystal arthritis
inflammatory RA-like (symmetrical) polyarthritis and synovitis
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
risk factors for pseudogout
old age, hyperparathyroidism, haemochromatosis, hypophosphatemia
investigations for pseudogout
- Polarised light microscopy of synovial fluid shows weakly positively birefringent rhomboid-shaped crystals.
- soft tissue calcium deposition on x-ray.
management of pseudogout
- Acute attacks: Cool packs, rest, aspiration, intra-articular steroids.
- Colchicine
- NSAIDs may prevent acute attacks
- Methotrexate and hydroxychloroquine ( for chronic)
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)
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.
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
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
cytoplasmic (cANCA)
- Granular cytoplasmic staining
- Major antigen – proteinase 3 (PR3)
peri-nuclear (pANCA)
- Homogenous perinuclear staining
- Major antigen – myeloperoxidase (MPO)
management of vasculitis
- large vessel = steroids
- small/medium vessel = immunosuppression with steroids +/- cyclophosphamide/methotrexate
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
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
management of giant cell arteritis
- prednisolone or IV methylprednisolone
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
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
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
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)
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
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
what MSK tumours are treated with radiotherapy
Ewing’s, myeloma, lymphoma, STS, metastasis
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
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
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
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
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
chondroblastoma
- benign cartilage forming tumour of bone
- epiphyses of long bones in skeletally immature patients
- rare
- distal femur
metastases to bone
- majority of malignant bone tumours
- lung, breast, kidney, thyroid, prostate
- most osteolytic but prostate is osteoblastic (induce bone formation)
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
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
presentation of myeloma
- bone pain, fractures, infections
- Anaemia, increased ESR, hypercalcaemia and renal impairment
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
conventional chondrosarcoma
- malignant cartilage forming tumour
- pelvic bones
- atypical chondrocytes in cartilage matrix
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
benign non-ossifying fibroma
- variants of normal growth
- more diaphyseal as child grows
- on one side of bone, sclerotic rim, thinned cortex
unicameral bone cysts
- metaphyseal
- lytic
- expand bone symmetrically
- border growth plate
- trabeculations in them once fractured
- conservative therapy
aneurysmal bone cyst
- biopsy
- metaphyseal and eccentric (to one side)
- MRI = look for fluid levels
- simple curettage
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
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
adamantinoma
- rare tumour of long bones
- pain
- x-ray = radiolucent zones interlaced with sclerosis
- metastasise to lungs
- wide surgical excision and reconstruction
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
risk factors for fibromyalgia
Female Middle age Low household income Divorced Low educational status Psychosocial factors
clinical presentation of fibromyalgia
- allodynia (pain without painful stimulus)
- hyperaesthesia (exaggerated perception of pain)
- chronic >3 months, widespread
- fatigue
- unrefreshing sleep
investigations for fibromyalgia
- all normal
- diagnosis is clinical
management of fibromyalgia
- encourage to remain active
- review new symptoms
- relaxation, physio
- CBT
- low-dose amitriptyline
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
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
what is septic arthritis
- infection within a joint
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
clinical presentation of septic arthritis
- extremely painful, hot, red, swollen joint
- Fever
- Knee > hip > shoulder
investigations for septic arthritis
- microbiology (most are staph. aureus)
- joint aspiration for fluid microscopy (neutrophils but no crystals)
- culture joint fluid and blood
management of septic arthritis
- empirical IV Abx until sensitivities are known
- flucloxacillin
- 2 weeks IV
- analgesia
what is osteomyelitis
infection of a bone
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)
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
investigations for osteomyelitis
- microbiology = staph. aureus, salmonella in sick-cell disease patients
- bloods = high WCC, raised ESR and CRP
management of osteomyelitis
- IV Abx and surgical debridement
- antimicrobial therapy
- hardware replacement or removal
what is Osteomalacia
a metabolic bone disease characterised by inadequate mineralisation of bone in the mature skeleton
what is Rickets
a metabolic bone disease characterised by inadequate mineralisation of bone and epiphyseal cartilage in the growing skeleton of children
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)
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
clinical presentation of rickets
- Growth retardation, hypotonia, apathy in infants
- Once walking – knock-kneed, bow-legged
clinical presentation of osteomalacia
Bone pain and tenderness, fractures, proximal myopathy (waddling gait)
investigations for osteomalacia and rickets
- Bone biopsies: incomplete mineralisation
- Plasma: mildly reduced calcium levels
- X-ray: loss of cortical bone
- Imaging: osteopenia
management of osteomalacia and rickets
- vit D supplements = rapid remineralisation
- if renal disease/ vit D resistance give alfacalcidol
what is Paget’s disease
A metabolic bone disease characterised by excessive chaotic bone turnover in localised parts of the skeleton
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
treatment of Paget’s disease
- bisphosphonates
- analgesia
