Musculoskeletal Flashcards
What are degenerative MSK disorders
disorders involving progressive impairment of both the structure and function of part of the body.
3 examples of Degenerative disorders
Degenerative arthritis (osteoarthritis), disc disease and degenerative scoliosis.
What are inflammatory MSK disorders
disorders involving a local response to cellular injury that is marked by redness, heat, pain, swelling and often loss of function.
4 examples of inflammatory MSK disorders
Rheumatoid arthritis, gout, vasculitis, spondyloarthropathies, infection.
pain profile of inflammatory joint disorders
pain eases with use
stiffness profile of inflammatory joint disorders
significant (longer than 60mins) in the morning/at rest
swelling profile of inflammatory joint disorder
synovial +/- bony
patient demographics of inflammatory joint disorders
young, psoriasis, family history
joint distribution for inflammatory joint disorders
hands and feet
response to NSAIDs of inflammatory joint disorders
Yes
pain profile of degenerative joint disorders
increases with use
clicks/clunks
stiffness profile of degenerative joint disorders
not prolonged (<30mins)
morning/evening
swelling profile for degenerative joint disorders
none or bony
patient demographics of degenerative joint disorders
older, prior occupation/sport
joint distribution of degenerative joint disorders
1st CMC, DIP, knees
response to NSAIDs for degenerative joint disorders
not convincing
4 pillars of inflammation
rubor- red
dolor- painful
calor- hot
tumour- swollen
ESR
erythrocyte sedimentation rate
Rises with inflammation/ infection
Increased fibrinogen makes RBCs stick together, so the number of RBCs falls faster
When ESR rises, rate of fall is quicker
ESR rises and falls slowly (days to weeks)
What causes ESR false postives
Age, female, obesity, racial difference, hypercholesterolaemia, high immunoglobulins, anaemia
CRP
C-reactive protein
Acute phase protein – pentameric peptide
Released in inflammation/ infection
Produced by liver in response to IL-6
Rises and falls rapidly (high at 6 hours and peaks at 48 hours)
Osteoarthritis
A group of diseases characterised by joint degeneration. It is an age-related, dynamic reaction pattern of a joint in response to insult or injury.
features of osteoarthitis
Affects synovial joints
All tissues of the joint are involved
Articular cartilage is the most affected
Changes in underlying bone at the joint margins
causes of osteoarthritis
Primary osteoarthritis: most common with no clear cause
Secondary osteoarthritis: brought about by conditions causing damage to joints e.g. rheumatoid arthritis (RA), gout, trauma
pathology of OA
Insult to joint tissue initiating a cycle of cellular events, including low-grade chronic inflammation of the synovium, release of metalloproteinases, and degradation of articular cartilage matrix.
Originally considered to be an inevitable consequence of ageing and trauma
Main pathological features:
Loss of cartilage
Disordered bone repair
Risk factors for OA
Age
Female
OA hip less common in Afro-Caribbean and Asian populations
Obesity
Occupation
Local trauma
Inflammatory arthritis e.g. RA
abnormal biomechanics
3 examples of occupations causing OA
Manual labour associated with OA of small joints of hands
Farming associated with OA of hips
Football associated with OA of knees
3 examples of abnormal biomechanics causing OA
Joint hypermobility
Congenital hip dysplasia
Neuropathic conditions
clinical presentations of OA
Joint pain
Tenderness
Swelling (small joints)
Synovitis
Stiffness
Symptoms typically worsen during the day with activity
Alteration in gait
Heberden’s nodes
Bouchard’s nodes
principal joints affected by OA
hip, knee, spine, and small joints of the hands
location of heberdens and bouchards nodes
Heberden’s nodes – DIP joint
Bouchard’s nodes – PIP joint
differential diagnosis for OA
Fibromyalgia
Rheumatoid arthritis
Gout and pseudogout
Xray findings for OA
LOSS;
Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts
non-medical management of OA
Activity and exercise – improve local muscle strength and general aerobic fitness.
Weight loss if overweight
Physiotherapy
Occupational therapy
Walking aids – sticks/frames
Pharmalogical management of OA
Analgesia;
Topical – NSAIDs/ capsaicin
Oral – paracetamol/ NSAIDs/ opioids
Transdermal patches
Surgical management of OA
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)
rheumatoid arthritis
A multisystem autoimmune disease in which the brunt of disease activity falls upon the synovial joints.
causes of RA
The initial trigger remains unknown
Once inflammation begins, it appears to become self-perpetuating
Which auto-antibodies are found for RA
rheumatoid factor, anti-CCP
pathology of RA
Infiltration of synovium by CD4+ T-cells, B-cells (lymphocytes), plasma cells and macrophages
Chronic inflammation reaction
clinical presentations of RA
Symmetrical, swollen, painful, stiff, small joints of hands and feet
Symptoms are typically worse in the morning
Systemic illness e.g. fatigue, weight loss, pericarditis and pleurisy
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
differential diagnosis for RA
Osteoarthritis
Fibromyalgia
SLE
first line investigations for RA
Serology: anti CCP positive, rheumatoid factor positive
Bloods: anaemia, CRP/ESR raised
x-ray: less lost joint space, erosion, soft tissue swelling, soft bone
Gold standard investigations for RA
Clinical diagnosis, serology, inflammatory markers
Management for RA
1st line – DMARDs (disease modifying anti-rheumatic drugs) e.g., methotrexate, leflunomide, sulfasalazine
2nd – Add biological agent (infliximab, adalimumab, etanercept, rituximab)
3rd – corticosteroid (prednisolone), NSAIDs (ibuprofen)
management for pregnant RA patients
prednisolone, sulfasalazine, hydroxychloroquine
pathological bonefractures
A fracture is a soft tissue injury in which there is also a break in the continuity of a surface or substructure of bone.
7 fracture patterns
Transverse
Oblique
Spiral – generated from twisting injury
Butterfly
Comminution – generate from high energy impact
Segmental
Greenstick
features of greenstick fractures
Specific to children
Unicortical fracture in which the bone bends and breaks due to thick periosteum
Bones not completely broken, easy to treat
risk factors for pathological fractures
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 steps when not touching
Immediately after the fracture there will be a haemorrhage within the bone from ruptured vessels in the marrow cavity and also around the bone.
A haematoma at the fracture site facilitates repair by providing a foundation for the growth of cells.
There will also be devitalised fragments of bone and soft tissue damage nearby. So the initial phases of repair involve removal of necrotic tissue and organisation of the haematoma.
The capillaries in the haematoma are accompanied by fibroblasts and osteoblasts, which deposit bone in an irregularly woven pattern; a callus.
Woven bone is subsequently replaced by more orderly, lamellar bone, which in turn is gradually remodelled according to the direction of mechanical stress.
what delays fracture healing
if bone ends are mobile, infected very badly, misaligned or avascular.
osteoporosis
A metabolic bone disease characterised by a generalised reduction in bone mass, increased bone fragility, and predisposition to fracture.
primary causes of osteoporosis
post-menopausal and age-related (>70y)
7 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
risk factors for osteoporosis
SHATTERED
Steroid use (>5mg/d prednisolone)
Hyperthyroidism, hyperparathyroidism, hypercalciuria
Alcohol and tobacco use
Thin (BMI <18.5)
Testosterone levels low
Early menopause
Renal or liver failure
Erosive/ Inflammatory bone disease e.g. RA
Dietary low calcium/ malabsorption
what is bone mass in later life determined by
the peak bone mass attained in early adulthood and the subsequent rate of bone loss
what is peak bone mass determined by
largely genetically determined but is modified by factors such as nutrition, physical activity and health early in life
What causes bone loss with age
decreasing bone turnover, decreasing physical activity, reduced sex hormones and reduced calcium absorption from the gut
what causes women to be more susceptible to osteoporosis
oestrogen deficiency after the menopause markedly accelerates bone loss
affect of glucocorticoids in osteoporosis
decrease osteoblastic activity and lifespan, reduce calcium absorption from the gut, and increase renal calcium loss.
characterisation of post-menopausal osteoporosis
High bone turnover
(resorption>formation)
Predominantly cancellous bone loss
Microarchitectural disruption
osteoporosis of ageing
there are changes to the trabecular architecture.
Decreases in trabecular thickness, more pronounced for non-load bearing horizontal trabeculae
Decrease in connections between horizontal trabeculae
Decrease in trabecular strength and increased susceptibility to fracture
clinical presentations of osteoporosis
Most cases are clinically silent until fragility fractures occur
Vertebral fractures lead to loss of height and kyphosis. May occur spontaneously and after lifting, coughing, and bending down.
If trabecular bone is affected, crush fractures of vertebrae are common
If cortical bone is affected, long bone fractures are more likely e.g. femoral neck (big cause of death and orthopaedic expense)
classic sites of involvement for osteoporotic fractures
vertebrae, distal radius, neck of femur following a fall
differential diagnosis for osteoporosis
Paget Disease
Hyperparathyroidism
Scurvy
first line investigations for osteoporosis
Bone mineral density with DEXA bone scan, FRAX score, Calcium, phosphate, ALP normal
FRAX score
10-year probability of major osteoporotic fracture or hip fracture
Ranges for DEXA scan
(normal = T > -1, osteopenia = -2.5 < T < -1, osteoporosis = T < -2.5)
Gold standard investigations for osteoporosis
DEXA bone scan – dual energy x-ray absorptiometry yields T score
lifestyle changes for osteoporosis
Quit smoking and reduce alcohol consumption
Weight-bearing exercise may increase bone mineral density
Balance exercises such as tai chi reduce risk of falls
Calcium and vitamin D rich diet
First line pharmalogical management for osteoporosis
Bisphosphonates: alendronic acid (alendronate)
Anti-resorptive: decreases osteoclast activity and bone turnover
benefits of HRT
reduce risk of fractures by 50%, stop bone loss, reduce risk of colon cancer
risks of HRT
breast cancer, stroke, CVD, venous thrombo-embolic disease
4 alternative pharmological managements for osteoporosis
Teriparatide: increases bone density, improves trabecular structure
Anabolic drugs: increases osteoblast activity and bone formation
Calcium and vitamin D: offer if evidence of deficiency
Calcitonin: pain management after a vertebral fracture
Testosterone: may help in hypogonadal men by promoting trabecular connectivity
pathological changes in systemic sclerosis
scleroderma (skin fibrosis), internal organ fibrosis and microvascular abnormalities.
investigations for Systemic sclerosis
90% are ANA positive
anti-SCL70 present
limited systemic scleroderma
involves face, hands and feet. Associated with anticentromere antibodies. Pulmonary hypertension is often present sub-clinically.
diffuse scleroderma
can involve the whole body, prognosis is poor. Control BP meticulously. Perform annual echocardiogram and spirometry.
potential complications for systemic sclerosis
organ fibrosis: lung, cardiac, GI and renal.
management of systemic sclerosis
No cure. Immunosuppressive regimens, including IV cyclophosphamide.
Monitor BP and renal function
polymyositis and dermatomyositis
Rare conditions characterised by insidious onset of progressive symmetrical proximal muscle weakness and autoimmune-mediated striated muscle inflammation.
complications of muscle weakness in polymyositis and dermatomyositis
may cause dysphagia, dysphonia, or respiratory weakness
skin signs of dermatomyositis
Macular rash
Lilac-purple rash on eyelids often with oedema
Nailfold erythema (dilated capillary loops)
Gottron’s papules: roughened red papules over the knuckles
extramuscular signs of polymyositis and dermatomyositis
Fever
Arthralgia
Raynaud’s
Interstitial lung fibrosis
Myocardial involvement (myocarditis, arrhythmias)
1st line investigations for polymyositis and dermatomyositis
Lactate dehydrogenase raised, AST and ALT raised, myoglobin raised, creatinine kinase raised (>1000 U/L. Normal = <300.)
Serology: anti-Jo-1 (polymyositis), anti Mi2 (dermatomyositis), anti-nuclear antibodies (dermatomyositis). Electromyograph
gold standard investigations for polymyositis and dermatomyositis
Muscle fibre biopsy – inflammation, necrosis
management of polymyositis and dermatositis
Start prednisolone
Immunosuppressives and cytotoxics are used in early resistant cases.
systemic lupus erythematosus
A multisystem autoimmune disease characterised by autoantibody production against a number of nuclear and cytoplasmic autoantigens.
pathophysiology of SLE
Anti-nuclear antibodies are antibodies which attack proteins in the person’s cell nucleus. This generates an inflammatory response and damage.
key presentations of SLE
Photosensitive red malar butterfly rash, glomerulonephritis (nephritic), arthralgia, fatigue, fever, hair loss, mouth ulcers, lymphadenopathy
signs of SLE
Butterfly rash, ulnar deviation, mouth ulcers, anaemia, Raynaud’s, lymphadenopathy and splenomegaly, pleuritic chest pain, hair loss, seizures and psychosis
symptoms of SLE
Weight loss, fever, fever, joint pain, myalgia, shortness of breath
1st line investigations for SLE
FBC (anaemia, leukopenia, thrombocytopenia), Normal CRP, raised ESR, raised urea and creatinine, urine protein:creatinine (proteinuria)
urine dipstick (haematuria, proteinuria)
anti-nuclear (ANA) and anti-double-stranded DNA (aDsDNA) antibodies present
gold standard investigations for SLE
Antinuclear antibodies (ANA)and clinical diagnosis
differential diagnosis for SLE
Rheumatoid arthritis, antiphospholipid syndrome, HIV, glomerulonephritis
management of SLE
1st line – Hydroxychloroquine
Consider: NSAIDs, corticosteroid, immunosuppressant (methotrexate), biologics (rituximab)
complications of SLE
Cardiovascular disease, infection, pericarditis, pleuritis, interstitial lung disease, anaemia
Sjorgens syndrome
A chronic inflammatory autoimmune disorder, which may be primary or secondary, associated with connective tissue disease.
what can sjorgens syndrome be secondary to
SLE, rheumatoid arthritis, scleroderma, primary biliary cirrhosis
key presentations of Sjorgens syndrome
Dry mucous membranes – dry mouth (xerostomia), dry eyes (keratoconjunctivitis sicca), dry vagina
1st line investigations for Sjorgens
Anti-Ro and anti-La antibodies. Schirmer test – tears travelling <10mm (>15mm is normal)
gold standard test for sjorgens
Anti-Ro and anti-La antibodies
Differential diagnosis for Sjorgens
Systemic lupus erythematosus, systemic sclerosis, rheumatoid arthritis
management of sjorgens
1st line – artificial tears, artificial saliva, vaginal lubricant.
Hydroxychloroquine used to halt progression
complications of sjorgens
Eye infections (conjunctivitis, corneal ulcers), oral problems (candida infection, dental cavities), vaginal problems (candidiasis, sexual dysfunction). Lymphomas
Raynauds phenomenon
Peripheral digital ischaemia due to paroxysmal vasospasm, precipitated by cold or emotion
features of raynauds
Fingers or toes ache and change colour.
Pale -> ischaemia
Blue -> deoxygenation
Red -> reactive hyperaemia
causative conditions for raynauds
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 of raynauds
Keep warm e.g. hand warmers
Stop smoking
Chemical or surgical (lumbar or digital) sympathectomy may help in those with severe disease
seronegative spondyloarthropathies
A group of inflammatory joint diseases characterised by arthritis affecting the spinal column and peripheral joints, and enthesitis (inflammation at the insertion site of tendons and ligament to bone).
Seronegative = rheumatoid factor is negative.
genetic factor for spondyloarthopathies
Strong association with possession of HLA-B27 allele.
pathology of seronegative spondyloarthropathies
Traditional theories proposed than an unidentified ‘arthritogenic peptide’ is present by HLA-B27 to CD8+ cytotoxic T cells, leading to joint inflammation.
clinical features of spondyloarthropathies
Seronegativity (-ve rheumatoid factor)
HLA B27 association
Axial arthritis: pathology in spine and sacroiliac joints
Asymmetrical large-joint oligioarthritis or monoarthritis
Enthesitis: inflammation of the site of insertion of a tendon or ligament into bone
Dactylitis: inflammation of an entire digit due to soft tissue oedema and tenosynovial and joint inflammation
Extra-articular manifestations: iritis, psoriaform rashes, oral ulcers, IBD
ankylosing spondylitis
A chronic inflammatory disease of the spine and sacroiliac joints, of unknown aetiology.
clinical presentations of ankylosing spondylitis
Lower back pain due to sacroiliitis
Typical patient: man <30yrs with gradual onset of low back pain, worse during the night with morning stiffness relieved by exercise.
Pain radiates from sacroiliac joints to hips/buttocks, usually improves later in the day.
Progressive loss of spinal movement in all directions
Extra-articular manifestations include;
Iritis
Pulmonary fibrosis
Aortitis
1st line investigations for ankylosing spondylitis
Pelvic x-ray, CRP and ESR raised, HLA B27 genetic test, MRI spine (bone marrow oedema in early disease before x-ray changes)
gold standard investigation for ankylosing spondylitis
X-ray of spine and sacrum:
* Bamboo spine (fusion of vertebral bodies)
* Sacroiliitis
* Squaring of vertebral bodies
* Subchondral sclerosis and erosions
* Syndesmophytes (bony outgrowths in spinal ligament)
* Ossification of ligaments, discs and joints
* Fusion of facet, sacroiliac and costovertebral joints
management of ankylosing spondylitis
Exercise for backache, including intense exercise regimens to maintain posture and mobility
NSAIDs relieve symptoms within 48h, may slow radiographic progression
Local steroid injections provide temporary pain relief
Surgery: hip replacement to improve pain and mobility. Rarely spinal surgery.
presentation of psoriatic arthitis
Symmetrical polyarthritis (like RA)
DIP joints
Asymmetrical oligoarthritis
Spinal (similar to AS)
Psoriatic arthritis mutilans
Mostly affects the interphalangeal joints and may lead to severe deformation
1st line investigations for psoriatic arthritis
CRP/ESR raised, joint x-ray, rheumatoid factor -ve, anti-CCP negative, joint aspiration negative for crystals or bacteria
gold standard investigation for psoriatic arthritis
Joint X-ray:
* erosion in distal interphalangeal joint and periarticular new bone formation.
* Osteolysis.
* Pencil-in-cup deformity (central erosions of bone beside the joints causing one to look hollow like a cup, and one to sit in the cup)
* Periostitis (periosteum inflammation causing thickened, irregular outline of bone)
* Ankylosis (joints fuse causing stiffness)
* Dactylitis (finger inflammation appears as soft tissue swelling)
management for psoriatic arthritis
1st line – NSAIDs for pain (naproxen, ibuprofen, indomethacin), intra-articular corticosteroid injection if severe
DMARDs (methotrexate, sulfasalazine, leflunomide), TNF inhibitor or monoclonal Ab (etanercept, adalimumab, infliximab), last resort – ustekinumab (Mab targeting IL 12 and 23)
reactive arthritis
A condition in which arthritis and other clinical manifestations occur as an autoimmune response to infection elsewhere in the body – typically GI or GU, although preceding infection may have resolved or be asymptomatic by the time arthritis presents.
pathophysiology of reactive arthritis
Occurs within 1 month of an infection elsewhere in the body. Usually related to a genitourinary infection with chlamydia or a GI infection with shigella, salmonella or campylobacter.
clinical presentations of reactive arthritis
Pain and stiffness in lower back, knees, ankles and feet.
Enthesitis (inflammation at the insertion site of tendons and ligament to bone).
Keratoderma blenorrhagica (brown, raised plaques on soles and palms).
Patients may present with a triad of urethritis, arthritis and conjunctivitis.
1st line investigation for reactive arthritis
ESR and CRP raised, antinuclear antibodies negative, rheumatoid factor negative, x-ray (sacroiliitis or enthesopathy), joint aspiration negative (exclude septic arthritis and gout), stool cultures, urine dipstick
goldstandard investigation for reactive arthritis
No GS. Joint aspiration MC+S to rule out organism in synovial fluid. Polarised light microscopy rules out crystal arthropathy
management of reactive arthritis
No cure.
Splint affected joints acutely; treat with NSAIDs or local steroid injections
Consider methotrexate if symptoms >6 months.
Treating the original infection may make little difference to the arthritis
crystal arthropathies
A group of joint diseases caused by deposition of crystals in joints.
pathology of crystal arthropathies
Crystals are deposited in joints
Neutrophils ingest the crystals and degranulate, releasing enzymes that damage the joint
pathology of Gout
caused by deposition of monosodium urate crystals in joint
Most cases are related to hyperuricaemia due to impaired excretion of urate by the kidneys.
clinical manifestations of gout
Acute, painful, swollen, red joint
Any joint may be involved, but the first metatarsophalangeal joint is typical
Individuals with high urate levels may develop chronic tophaceous gout, in which large deposits of urate (tophi – chalky white material) occur in the skin and around joints.
differential diagnoses for gout
Reactive arthritis
Hemarthrosis
CPPD
Palindromic RA
risk factors for gout related to reduced urate excretion
Elderly, men, post-menopausal women, impaired renal function, hypertension, metabolic syndrome, diuretics, antihypertensives, aspirin.
Gout risk factors relating to excess urate production
Dietary (alcohol, sweeteners, red meat, seafood), genetic disorders, myelo- and lymphoproliferative disorders, psoriasis, tumour-lysis syndrome, drugs.
1st line investigations for gout
Joint aspiration, Increased serum uric acid
gold standard investigations for gout
joint aspiration and polarised light microscopy (needle-like crystals, negative birefringent of polarised light, monosodium urate crystals)
differential diagnoses for gout
Septic arthritis, pseudogout, trauma, rheumatoid arthritis, psoriatic arthritis
management of Gout
Lifestyle changes (decreased purines, more diary – antigout)
Acute flare: NSAIDs, Colchicine, corticosteroids
Prevention: allopurinol (xanthine oxidase inhibitor > reduces uric acid
Pseudogout
(Calcium Pyrophosphate Deposition-CPPD)
caused by deposition of calcium pyrophosphate crystals in a joint
Shedding of crystals into a joint precipitates an acute arthritis which 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
inflammatory RA-like (symmetrical) polyarthritis and synovitis
key presentations of psuedogout
Often polyarticular with knee commonly involved. Hot swollen painful red joint. Other joints commonly affected: shoulder, wrist, hips
1st line investigations for pseudogout
Joint aspiration, x-ray: chondrocalcinosis (thin white line in the middle of joint space caused by calcium deposition), serum calcium/PTH/iron elevated
gold standard investigation for pseudogout
Joint aspiration and polarised light microscopy (rhomboid shaped crystals, positive birefringent of polarised light, calcium pyrophosphate crystals)
differential diagnoses for psuedogout
Septic arthritis, osteoarthritis, gout, rheumatoid arthritis, psoriatic arthritis
management for psuedogout
1st line – NSAIDs, colchicine, corticosteroids/intra-articular steroid injection
risk factors for psuedogout
Old age
Hyperparathyroidism
Haemochromatosis
Hypophosphatemia
Giant cell arteritis
A vasculitis of medium and large vessels which preferentially affects head and neck arteries
presentation of Giant cell arteritis
Presents over weeks or months with;
Fever
Anorexia
Weight loss
Involvement of the temporal artery causes headache, scalp tenderness, and jaw claudication
Involvement of ocular vessels can cause blindness
Aortic involvement may lead to thoracic or abdominal aortic aneurysm formation
1st line investigations for giant cell arteritis
Raised CRP, Raised ESR >50mm/hr. FBC (anaemia), LFT/RFT may be abnormal
Halo sign (wall thickening) on vascular ultrasonography of temporal and axillary artery
Gold standard investigations for giant cell arteritis
Temporal artery biopsy (shows giant cells, granulomatous inflammation – patchy lesions therefore take big sample)
differential diagnoses for giant cell arteritis
Polymyalgia rheumatica, rheumatic arthritis, Takayasu’s arteritis
management for giant cell arteritis
1st line – high dose corticosteroid (e.g., prednisolone 40-60mg)
Consider: tocilizumab, methotrexate. Amaurosis fugax – high dose IV methylprednisolone.
POLYARTERITIS NODOSA
Polyarteritis nodosa affects medium blood vessels
key presentations of polyarteritis nodosa
Peripheral neuropathy (mononeuritis multiplex – ischaemia of vasa nervorum), cutaneous/SC nodules, abdominal pain, unilateral orchitis (testicle inflammation), livedo reticularis (mottled, purple lace rash), AKI/CKD, hypertension
1st line investigations for polyarteritis nodosa
Raised ESR, raised CRP, HBsAg (Hep B antigen), CT angiogram (beaded appearance – aneurysms)
gold standard investigation for polyarteritis nodosa
Biopsy e.g., kidney (transmural fibrinoid necrosis)
management of polyarteritis nodosa
Hep B negative: corticosteroids and cyclophosphamide (DMARDs)
Hep B positive: antiviral agent, plasma exchange and corticosteroids
Granulomatosis with polyangiitis (GPA)
A systemic ANCA-associated vasculitis characterised by dominant upper respiratory tract, lung, and renal involvement and cANCA positivity.
presentation of GPA
Nasal symptoms
Acute renal failure
Pulmonary symptoms
diagnosis of GPA
Renal biopsies show a focal segmental necrotizing glomerulonephritis with crescent formation (identical to microscopic polyangiitis).
Lung biopsies show large geographical areas of necrotising granulomatous inflammation and a necrotising vasculitis.
management of GPA
Aggressive immunosuppression is needed to prevent mortality
pathological 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 in size
Regional lymph nodes (N)
N0: no regional lymph node metastasis
N1: regional lymph node metastasis
pathological staging of bone tumours
Primary tumour (T)
pT1: tumour 8cm or less in greatest dimension
pT2: tumour >8cm in greatest dimension
pT3: discontinuous tumour in the primary bone site
Regional lymph nodes (N)
N0: no regional lymph node metastasis
N1: regional lymph node metastasis
naming tumours- prefixes
Prefix will be the tissue of origin, for example:
Osteo = bone
Chondro = cartilage
Rhabdomyo = skeletal muscle
Lipo = fat
naming tumours- suffix
Suffix tells you whether it is benign or malignant
Oma = benign tumour
Sarcoma = malignant connective tissue tumour
Carcinoma = malignant epithelial/ endothelial tumour
Blastoma = malignant tumour of embryonic cells
management of MSK tumours
MDT management
Histological tests help to show sensitivity of tumour to chemotherapy agents and radiotherapy
Chemo/radiotherapy can be given:
Neo-adjuvant i.e. before surgery
Adjuvant
Radiotherapy: Ewing’s, myeloma, lymphoma, STS, metastasis
Surgery can either be limb-sparing or limb-sacrificing
Local recurrence vastly increases risk of future amplification
intralesional MSKoma surgery
the plane of surgery goes through the tumour
marginal MSKoma surgery
the plane of surgery goes through the reactive zone of the lesion (the reactive zone contains oedema, tumour cells, fibrous tissue, and inflammatory cells)
Wide MSKoma surgery
the plane of dissection goes through normal tissue
radical MSKoma surgery
the entire anatomic compartment of the lesion is removed
4 types of Bone cancer
benign-
osteoid osteoma
osteoblastoma
osteochondroma
malignant-
osteosarcoma
3 types of cartilage tumour
benign-
enchrondroma
chondroblastoma
malignant-
chondrosarcoma
3 types of fibrous tumours
benign-
fibrous dysplasia
non-ossifying fibroma
malignant-
fibrosarcoma
osteochondroma
A benign conventional cartilaginous-forming tumour of bone.
features of osteochondroma
Typically grows as a solitary metaphyseal exophytic tumour
Multiple osteochondromas: inherited in an autosomal dominant manner, Langer-Giedion syndrome and DEFECT-11 syndrome.
presentation of osteochondroma
Generally presents in young children with;
Reduction in skeletal growth
Bony deformity, restricted joint motion, and shortened stature
Painless lump – may have a narrow stalk or broad base
management of osteochondroma
Surgical excision if symptomatic
osteoid osteoma
A benign bone-forming tumour of bone
presentation of osteoid osteoma
Commonly arises in the cortex of a long bone of a child or young adult
Characteristically painful, especially at night
investigation of osteoid osteoma
Readily identified on plain radiographs as a small lucent nidus <1cm in size
Best appreciated on CT
management of osteoid osteoma
Pain relieved by NSAIDs
Surgical: radiofrequency ablation
osteoblastoma
A benign bone-forming tumour of bone
presentation of osteoblastoma
Most commonly arises in the medullar in the axial skeleton of a child or young adult but can present later in life
Pain, not self-limiting
Spine lesions can present with neurology
investigation for osteoblastoma
Radiographs: bone destruction surrounded by reactive new bone that can be misdiagnosed as a malignancy
Can be difficult to diagnose/ mistaken for osteosarcoma
management for osteoblastoma
Excision with at least a marginal line of excision
chondromas
A benign conventional cartilaginous-forming tumour of bone.
enchondroma site
arise in the medulla of the bone, most commonly in the hands and feet
periosteal chondroma site
arises on the bone surface, the proximal humerus being a characteristic site
endochondromas features
Tend to occur in small bones (hands, foot)
Can occur anywhere in the skeleton
Do not destroy bone
Hot on bone scan
chondroblastoma
A benign conventional cartilage-forming tumour of bone.
presentation of chondroblastoma
Typically involves the epiphyses of the long bones in skeletally immature patients but may present later in life
Usually distal femur
5 most common tumour to metastasise to bone
Lung
Breast
Kidney
Thyroid
Prostate
metastatic bone deposits interaction with bone
Most metastatic deposits are osteolytic (they destroy bone), but some are osteoblastic (induce bone formation) e.g. prostate.
myeloma
The most common tumour arising in bone. A disseminated bone marrow-based plasma cell neoplasm associated with a serum and/or urine paraprotein.
pathology of myelomas
The neoplastic plasma cells secrete cytokines which activate osteoclasts, causing lytic bone lesions
Circulating paraprotein depresses normal immunoglobulin production, increasing the risk of infections.
Free light chains passing through the kidney contribute to renal failure.
The interaction between myeloma cells and bone marrow stromal cells increases myeloma cell growth and it is a target for new treatments.
presentation of myeloma
Bone pain, pathological fractures, recurrent infections
Anaemia, increased ESR, hypercalcaemia and renal impairment are common
management of myeloma
Myeloma is an incurable disease.
conventional osteosarcoma
A malignant bone-forming tumour
The most common malignant primary bone tumour
presentation of osteosarcomas
Persistent deep pain within a long bone.
A palpable mass may be present
management of osteosarcoma
If left untreated will be fatal
Multi-agent chemotherapy
Aims to kill tumour cells, reduce further spread, treat micro-metastases
chondrosarcoma features
A malignant cartilage forming tumour.
The most common site is the pelvic bones
Atypical chondrocytes distributed in a cartilage matrix
benign fibrous dysplasia
A benign intramedullary fibro-osseous lesion.
features of benign fibrous dysplasia
Presents in a wide age range, with peak incidence <30y
Not inherited – a mosaic disorder
Can occur in any bone, proximal femur is the most common
Progressive in children, non-progressive in adults
Can worsen during pregnancy
xray presentation of benign fibrous dysplasia
ground glass lesion with sclerotic margin
benign non-ossifying fibroma
Variants of normal growth
Become more diaphyseal as child grows
fibromyalgia
A long term condition that causes pain all over the body. Very similar to chronic fatigue syndrome.
risk factors for fibromyalgia
Female
Middle age
Low household income
Divorced
Low educational status
Psychosocial factors;
Sickness behaviours such as extended rest
Social withdrawal
Problems or dissatisfaction at work
Emotional problems such as low mood, anxiety or stress
clinical features of fibromyalgia
Allodynia: pain in response to a non-painful stimulus
Hyperaesthesia: exaggerated perception of pain in response to a mildly painful stimulus
Diagnosis depends on a pain that is chronic (>3 months), and widespread (involves left and right sides, above and below the waist, and the axial skeleton)
Profound fatigue
Complaint of unrefreshing sleep
Significant fatigue and pain with small increases in physical exertion
differential diagnoses for fibromyalgia
Rheumatoid arthritis
Vasculitis
Hypothyroidism
Myeloma
investigations for fibromyalgia
All normal. Diagnosis is clinical
Over-investigation can consolidate illness behaviour, but exclude other causes of pain and/or fatigue
management of fibromyalgia
Patient encouraged to remain as active as they feel able, and to continue to participate in the workforce.
New symptoms reviewed to exclude an alternative diagnosis
Graded exercise programmes – improve functional capacity
Relaxation, rehabilitation and physiotherapy may help
Cognitive-behavioural therapy aims to help patients develop coping strategies and set achievable goals.
pharmacotherapy for fibromyalgia
Low-dose amitriptyline has been shown to relieve pain and improve sleep.
Steroids or NSAIDs are not recommended because there is no inflammation.
mechanical lower back pain
Back pain is very common, and often self-limiting, but be alert to sinister causes i.e. malignancy, infection or inflammatory causes.
causes of mechanical back pain for those 15-30
Prolapsed disc, trauma, fractures, ankylosing spondylitis, spondylolisthesis, pregnancy
causes for mechanical back pain for those 30-50
Degenerative spinal disease, prolapsed disc, malignancy
causes for mechanical back pain for those >50
Degenerative, osteoporotic vertebral collapse, Paget’s, malignancy, myeloma, spinal stenosis
investigations for mechanical back pain
SOCRATES, clinical examination, x-ray if serious pathology suspected, e.g., myeloma, neuropathic pain. MRI
septic arthritis
Infection within a joint.
pathology of septic arthritis
Establishment of infection is favoured by the relative inability of phagocytes to enter the joint space
Acquisition of infection: infection is usually via haematogenous spread, occasionally may follow penetrating trauma
Infection spreads quickly, leading to rapid and irreversible joint destruction if antibiotic treatment is not started early.
risk factors for septic arthritis
Pre-existing joint disease (especially rheumatoid arthritis)
Diabetes mellitus
Immunosuppression
Chronic renal failure
Recent joint surgery/ prosthetic joints
clinical presentations for septic arthritis
An extremely painful, hot, red, swollen joint
Fever
Knee > hip > shoulder
differential diagnosis for septic arthritis
Crystal arthropathies
first line investigations for septic arthitis
Urgent aspirate joint for microscopy and culture (polarised light microscopy to identify organism), synovial fluid raised WCC, blood culture, raised CRP/ESR, FBC: raised WCC
gold standard investigation for septic arthitis
Joint aspiration MC+S (ID organism)
management of septic arthritis
Start empirical IV antibiotics (after aspiration) until sensitivities are known.
Common causative organisms are Staph. aureus, streptococci, Neisseria gonococcus, and gram -ve bacilli.
Consider flucloxacillin
For suspected gonococcus or meningococcus, consider ceftriaxone.
Antibiotics are required for a prolonged period, conventionally 2 weeks IV.
Analgesia
osteomyelitis
Infection of a bone.
acquisition of osteomyelitis
Haematogenous spread – this is typically the case in acute osteomyelitis in children
Penetrating trauma, e.g. open fracture
Iatrogenic e.g. following joint replacement or root canal treatment
Direct spread from an adjacent infection, e.g. as a complication of a foot ulcer in a diabetic
pathology of osteomyelitis
Infection leads to an influx of acute inflammatory cells into the bone and suppurative inflammation
Destruction of bone leads to necrotic bone known as sequestrum
Failure to eradicate infection may lead to chronic osteomyelitis with areas of infected necrotic bone surrounded by areas of new bone formation (involucrum)
clinical presentations 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
differential diagnosis of osteomyelitis
Avascular necrosis of bone
Fracture
Malignancy
1st line investigation for osteomyelitis
FBC – raised WCC, raised CRP/ESR, blood culture MC+S, x-ray (osteopenia - thinning, periosteal reaction – changes to bone surface, destruction of bone), MRI (bone marrow oedema)
gold standard investigation for osteomyelitis
Bone marrow biopsy and culture (identify organism)
management for osteomyelitis
Aggressive treatment is needed with intravenous antibiotics and surgical debridement of any necrotic bone if cure is to be achieved.
Surgical – hardware replacement or removal
Antimicrobial therapy
osteomalacia
a metabolic bone disease characterised by inadequate mineralisation of bone in the mature skeleton.
rickets
a metabolic bone disease characterised by inadequate mineralisation of bone and epiphyseal cartilage in the growing skeleton of children.
causes of calcium deficiency
Calcium deficiency which is usually due to vitamin D deficiency (source: sunlight)
Calcium deficiency is also caused by nutritional deficiency: diet, malabsorption of calcium due to chronic liver disease, CKD, GI bypass surgery, nutritional
hypophosphataemic rickets
characterised by low serum phosphate levels and resistance to treatment with UV radiation and vitamin D, mainly caused by genetic defects involving renal absorption of phosphate
pathology of osteomalacia/ 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)
1st line investigations for osteomalacia
X-ray (loss of cortical bone – defective mineralisation, looser zone), U&E (low calcium and phosphate), raised PTH, low serum 25-hydroxyvitamin D (<25 nmol/L = deficiency)
gold standard investigation for osteomalacia
bone biopsy (incomplete mineralisation)
management of osteomalacia/rickets
Vitamin D supplementation usually results in rapid mineralisation of bone and resolution of symptoms, though some deformity may remain.
If due to malabsorption give vitamin D2
If due to renal disease/ vit D resistance give alfacalcidol
pagets disease
A metabolic bone disease characterised by excessive chaotic bone turnover in localised parts of the skeleton.
pathology of pagets disease
The disease passes through a number of stages, all of which may be seen simultaneously within the same bone or in different bones
Initially, there is intense osteoclastic bone resorption
Osteoblastic activity then becomes exaggerated with laying down of grossly thickened, poorly organised weak bone which is prone to deformity and pathological fracture
presentation of pagets disease
The vast majority of patients are asymptomatic, the diagnosis being made incidentally on radiology
Symptomatic disease usually presents with bony pain and deformity
1st line investigation for pagets disease
x-ray (bone enlargement + deformity, osteoporosis circumscripta – well defined osteolytic lesions, cotton wool appearance of skull – poorly defined areas of sclerosis and lysis, V-shaped defects in long bones)
urinary hydroxyproline (protein constituent of collagen)
bloods: raised ALP, normal calcium and phosphate
gold standard investigation of pagets
X-ray of bones
management of pagets disease
Bisphosphinates to reduce bone turnover + NSAIDs
capsaicin
Symptomatic relief in osteoarthritis
side effects of capsaicin
Cough
Sneezing, watering eye
Asthma exacerbated
paracetamol side effects
Thrombocytopenia
Bronchospasm
Rash
Hepatic function abnormal
side effects of NSAIDs
Diarrhoea
Dizziness
GI discomfort / nausea
bisphosphonates action
Bisphosphonates are adsorbed onto hydroxyapatite crystals in bone, slowing both their rate of growth and dissolution, and therefore reducing the rate of bone turnover
e.g. alendronic acid
side effects of bisphosphonates
Alopecia
Anaemia
Constipation/ diarrhoea
Headache/ fever/ malaise
methotrexate action and use
Methotrexate inhibits the enzyme dihydrofolate reductase, essential for the synthesis of purines and pyrimidines.
Used to treat moderate to severe active rheumatoid arthritis by mouth, and severe RA by IM/SC injection.
DMARD
side effects of methotrexate
Fever/ headache/ nausea/ vomiting
Anaemia
Diarrhoea
Fatigue/ drowsiness
use of hydroxychloroquine
Active rheumatoid arthritis
DMARD
side effects of Hydroxychloroquine
Abdominal pain
Diarrhoea/ vomiting
Vision disorders
Headache
