Musculoskeletal Flashcards
Definition of ankylosing spondylitis:
Ankylosing spondylitis is a seronegative inflammatory arthritis, primarily involving the axial skeleton. It is a type of axial spondyloarthritis known as radiographic axial spondyloarthritis, meaning that there are X-ray changes such as sacroiliitis (versus non-radiographic axial spondyloarthritis, where there may be changes visualised on MRI but not on X-ray.
What is the most important genetic factor for ankylosing spondylitis?
HLA-B27
What is an important modifiable risk factor for ankylosing spondylitis?
Smoking is an important modifiable risk factor
What are the musculoskeletal symptoms of ankylosing spondylitis
Lower back and buttock pain - alternating buttock pain
Pain elsewhere in the spine may also occur
Stiffness that is worse in the morning and with rest, and improves with activity
Patients may wake in the second half of the night with pain
Pain and stiffness respond to NSAIDs
Peripheral enthesitis (pain, stiffness and/or swelling of the Achilles, quadriceps or patellar tendons, as well as plantar fasciitis)
Peripheral arthritis occurs in up to a third of patients, commonly affecting the ankles, knees and hips
What are the extra-articular involvements of ankylosing spondylitis?
Anterior uveitis (eye pain, redness and blurred vision)
Inflammatory bowel disease (e.g. diarrhoea, abdominal pain, rectal bleeding)
Osteoporosis (increased risk of fragility fractures)
Aortitis which may lead to aortic regurgitation (shortness of breath, fatigue, chest pain)
Upper lobe pulmonary fibrosis (shortness of breath, exercise intolerance, dry cough)
IgA nephropathy (haematuria, fatigue)
Systemic symptoms of weight loss and fatigue
Triple A: anterior uveitis (most common), aortic insuffiencies and apical pulmonary fibrosis.
Signs on examination of ankylosing spondylitis
Restricted movement in the lumbar spine
Schober’s test can be used to assess this as follows:
Mark two points on the back (one at the level of the L5 spinous process and one 10 cm above this)
On forward flexion, the distance between the two points should increase by 5cm or more
If the increase in distance is <5 cm, this indicates restricted forward flexion
Hyperkyphosis of the thoracic spine may develop as the disease progresses
Reduced C-spine movements and fixed flexion deformities may be seen
This can be measured by asking the patient to stand with their back to the wall
A distance of > 2 cm between their occiput and the wall is abnormal
“Question mark posture” refers to the combination of thoracic hyperkyphosis, loss of the lumbar lordosis and flexion deformities of the neck and hips (seen in advanced disease)
Reduced chest expansion may be seen
Affected joints may be tender and swollen
Affected tendons may be tender, stiff or swollen
What would you expect to see on a blood test of ankylosing spondylitis?
FBC which may show anaemia of chronic disease
ESR and CRP are often raised due to inflammation
HLA-B27 positivity supports a diagnosis but a negative result shoudl not rule out ankylosing spondylitis
What are the image investigations for ankylosing spondylitis?
Pelvic X-rays looking for sacroiliitis
This is usually bilateral and symmetrical
In early disease, sclerosis or erosion of the sacroiliac joints may be difficult to visualise
In advanced disease, there is ankylosis or fusion of the joint
Lumbar X-rays may show squaring of the vertebral bodies
In late disease, there is ossification of spinal ligaments (“dagger sign”)
Fusion of the vertebral column by syndesmophytes may be seen (“bamboo spine”)
MRI may be required if X-rays are normal - MRI is the gold standard
Sensitivity for sacroiliitis is higher especially in early disease
Ultrasound or X-rays of other sites of pain may be indicated e.g. for enthesitis or peripheral arthritis
DEXA scans may be used to assess bone density
Signs of osteopenia or osteoporosis may be seen on other imaging also
DEXA imaging of the spine may be inaccurate due to syndesmophytes and calcification of ligaments (hip measurements tend to be more reliable)
Conservative management for ankylosing spondylitis?
Referral to rheumatology for confirmation of the diagnosis and ongoing management
Involvement of other specialties may be required for extra-articular manifestations e.g. emergency ophthalmology assessment for suspected anterior uveitis
Smoking cessation counselling
Physiotherapy referral for a structured exercise programme to optimise mobility
Occupational therapy, orthotics or podiatry input may be required to help maximise function
Monitor bone density and consider bone protection for osteoporosis
Assess cardiovascular risk and consider initiating treatment (e.g. statins)
What is the medical management for ankylosing spondylitis?
NSAIDs as the first-line treatment
These should be used at the lowest effective dose
Symptoms should improve in 2-4 weeks
Switching to a different NSAID should be considered before escalating treatment
Consider co-prescribing a PPI to prevent peptic ulceration
Paracetamol +/- codeine may be trialled if NSAIDs are contraindicated
Adjuncts for analgesia include local steroid injections
Biological DMARDs are the next step in treatment of severe disease if response to NSAIDs is inadequate
Anti-TNF agents such as infliximab or adalimumab are the treatment of choice
Secukinumab (an anti-IL17A biologic) is another option
Regular monitoring is required for patients on these medications
They are usually highly effective
Conventional disease-modifying antirheumatic drugs (DMARDs) such as sulfasalazine and methotrexate are not effective for axial arthritis but may be used for peripheral involvement
Topical cyclopentolate for the anterior uveitis
What is the surgical management for ankylosing spondylitis?
Referral to spinal surgery for patients with complications such as suspected spinal fractures or cauda equina syndrome
Surgery to correct spinal deformities may be indicated in some patients with severe disease significantly affecting quality of life
Total hip replacement may be considered in patients with structural damage leading to refractory hip pain and/or difficulty mobilising
What are the complications for ankylosing spondylitis?
Spinal deformities including fusion of the axial skeleton in severe cases
Limited mobility
Deterioration in mental health due to chronic pain and limitations in function
Sleep difficulties due to pain and stiffness
Osteoporosis and spinal fractures
Increased cardiovascular risk
Heart failure
Aortic regurgitation and other valvular disorders
Restrictive lung disease
Apical pulmonary fibrosis
IgA nephropathy
Anterior uveitis
Side effects from treatment e.g. immunosuppression with DMARDs, peptic ulcers with NSAIDs
What is the prognosis for ankylosing spondylitis?
Ankylosing spondylitis tends to be a progressive disease involving irreversible damage - however the course of the disease is variable and effective and prompt treatment minimises disability.
Good prognostic factors include:
Low functional impairment at diagnosis
Young age at disease onset
Short disease duration
High inflammatory markers at diagnosis
Key signs and symptoms of crystal arthropathies?
joint pain and swelling, often affecting one joint at a time
What is the most important investigation to confirm a crystal arthropathy?
Joint aspiration with subsequent polarised-light microscopy, culture and sensitivity is the gold standard:
The fluid may appear milky
On microscopy, a raised white cell count may be seen (typically <50 × 109/l – values above this are more indicative of septic arthritis)
Crucially, the presence of crystals on polarised light microscopy confirms the diagnosis
Note: It is important to send the fluid for Gram stain and culture to exclude the diagnosis of septic arthritis.
What is gout caused by?
Caused by monosodium urate crystals
What do you see on light microscopy of gout?
negatively birefringent and needle-shaped on light microscopy
Gout has Negatively birefringent, Needle-shaped crystals
What is pseudogout caused by?
Caused by calcium pyrophosphate dihydrate crystals
What do you see on light microscopy of pseudogout?
Pseudogout has Positively birefringent, rhomboid-shaped crystals
What blood tests do we do for gout?
Uric acid (gout only) – It is important to monitor uric acid levels in recurrent gout (A serum urate of 360 micromol/L or more confirms the diagnosis) and urate-lowering therapies reduce the risk of further attacks note: urate levels often fall during an acute episode of gout so are not often useful in the diagnosis of acute gout
There is no equivalent test for pseudogout
Renal function (gout only) – Renal impairment is a risk factor for gout
Inflammatory markers – These may be raised as in any inflammatory arthritis
What would you see in an X-ray for gout?
Gout – may be useful as a baseline
X-ray changes (aside from soft-tissue swelling) are usually not seen until multiple attacks of gout have occurred, and can then include:
Tophi
“rat bite” Erosions
Subchondral sclerosis
What would you see in an x-ray for pseudogout?
Chondrocalcinosis (calcification of cartilage)
The changes that are seen in osteoarthritis include:
Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts
What would you see in a ultrasound of gout?
The double-contour sign is the most sensitive ultrasound finding of gout
A hyperechoic irregular band over the superficial margin of the articular cartilage
Gouty tophi and erosions may be seen
Define gout:
Gout is a form of arthritis that occurs when monosodium urate crystals deposit in joints. This causes both acute inflammation (gout flares) and in the longer-term, a chronic gouty arthritis with tophi (hard deposits of monosodium urate crystals in soft tissues).
What is the main risk factor for gout?
Hyperuricaemia (high urate) is the main risk factor (although most patients with a high urate do not develop gout, and some patients develop gout with a normal urate)
What are some factors that contribute to gout?
Older age - typically patients are above the age of 40
Male sex (post-menopausal women are also at increased risk)
Comorbidities including chronic kidney disease (CKD), diabetes, osteoarthritis, hypertension
Excess alcohol consumption
Dietary excess of meat, seafood and sugary drinks
Overweight or obesity
Medications such as thiazide diuretics and ciclosporin (diuretics (furosemide) and salicylates (aspirin) are risk factors)
Anti-tuberculosis medications such as pyrazinamide and ethambutol can significantly decrease uric acid excretion, increasing the risk of acute gout attacks.
Family history of hyperuricaemia and gout
Genetic disorders associated with hyperuricaemia such as Lesch-Nyhan or glycogen storage disorders
Organ transplant recipients
Acute attacks may be triggered by stressors including:
Trauma and surgery
Intercurrent illness
Alcohol excess
Sudden excess of protein in the diet
Chemotherapy (due to cell breakdown)
Urate-lowering medications can cause a flare (as crystals are shed into the joint space)
Signs and symptoms of acute gout?
Commonly presents with a monoarthritis
Pain is severe and rapid in onset, reaching a peak within 24 hours
Affected joints become swollen, erythematous and tender
The first metatarsophalangeal (MTP) joint is the most commonly affected (70% of first attacks)
Other common sites include the knees, ankles, midtarsal joints, wrists, elbows and small joints of the hands
Systemic features such as fever and malaise may be seen
Patients may be tachycardic due to pain
For the medication for gout which screening tests need to be done first?
Liver function tests are needed prior to starting febuxostat
Patients from Han Chinese, Thai and Korean backgrounds should be screened for HLA-B5801 prior to starting allopurinol (as this increases the risk of severe cutaneous adverse reactions if present)
What are the first three treatments for gout?
NSAIDs e.g. naproxen
Give at maximum dose
Continue until 1-2 days after resolution of symptoms
Consider giving with a PPI for gastric protection
Avoid in peptic ulcer
Avoid in heart failure, patients at high risk of gastrointestinal bleeding and severe renal failure
Colchicine
Dosing is 500 mcg 2-4 times per day
Continue until pain resolves
Dose-dependent side effects include diarrhoea, nausea and vomiting
Oral corticosteroids
e.g. prednisolone 30mg once a day for 3-5 days
Useful in patients with contraindications to both NSAIDs and colchicine
An injection of intramuscular, intravenous or intra-articular steroids can also be considered
Alongside this, consider other analgesia (e.g. paracetamol) and other non-pharmacological pain relief such as ice packs
A combination of the above may be tried if a single agent is ineffective
Patients should be advised to keep the affected joint cool and exposed and to rest and elevate the affected limb
Patients already on urate lowering treatment should continue this throughout the acute flare
In patients with chronic kidney disease on haemodialysis and an eGFR less than 10ml/minute/1.73m2, low dose steroids may be appropriate for managing gout attacks due to the need to avoid NSAIDs and Colchicine.
What is the prevention of acute gout?
Reducing alcohol consumption
Maintaining a balanced diet and healthy weight
Investigate and treat for comorbidities such as hypertension or CKD
Review medications and consider switching medications such as thiazides that cause hyperuricaemia
Where possible, switch antihypertensive medications to losartan or amlodipine, which have modest urate-lowering effects
Initiating urate-lowering therapy (see below)
When should someone with acute gout be sent to prompt referral to or discussion?
Patients with complications of gout
Atypical presentations (e.g. aged under 30) or uncertain diagnosis
Pregnant patients
Stage 3b to 5 CKD
Organ transplant recipients
Those at risk of adverse effects with standard medical treatment, or if treatment is ineffective or not tolerated
Indications for urate - lowering therapy?
Multiple or troublesome gout flares
Chronic gouty arthritis or tophi
Patients taking diuretics
CKD stage 3 to 5
How do you monitor urate levels?
ULT should be started at least 2-4 weeks after an acute flare if possible as medications can precipitate further attacks
Colchicine should be given whilst starting ULT to reduce the risk of a flare (NSAIDs or steroids are second-line)
Doses should be uptitrated with monthly monitoring of serum urate levels, aiming for a target of 360 micromol/L
A target urate level of 300 micromol/L may be helpful in patients with tophi or chronic arthritis due to gout, or those who continue to have flares despite ULT
First-line options are either allopurinol or febuxostat which are both xanthine oxidase inhibitors (so reduce uric acid production)
It is advised to start allopurinol after an acute flare of gout has completely settled. If started before this it can paradoxically cause symptoms to worsen.
Allopurinol is preferred in patients with significant cardiovascular disease
Allopurinol can cause serious side effect of Steven Johnson Syndrome
Second line options include uricosuric medications (e.g. probenecid) - these can promote stone formation so should be avoided if there is nephrolithiasis
Complications of gout:
Chronic gouty arthritis and permanent joint damage
Tophi, which may become inflamed or infected
Nephrolithiasis due to uric acid precipitation - these are responsible for 8% of renal calculi and are radiolucent
Chronic urate nephropathy - urate deposition in the renal interstitium causes inflammation and fibrosis
Both allopurinol and febuxostat can cause rashes, which in rare cases may be severe (e.g. Stevens Johnson syndrome or toxic epidermal necrolysis)
Increased risk of cardiovascular disease and mortality
Define pseudogout:
Articular and periarticular calcium pyrophosphate deposition (CPPD) causes a spectrum of disease, ranging from asymptomatic radiographic changes, to acute arthritis (also known as “pseudogout”) as well as a chronic inflammatory arthritis.
What are the risk factors for psuedogout?
Previous joint injury or surgery
Hyperparathyroidism and Haemochromatosis are specific for pseudogout!
Hypomagnesaemia
Hypothyroidism
Family history (ANK human gene mutations may be present)
What are the acute symptoms of CPP crystal arthritis?
Typically presents with an acute monoarthritis (rarely, an oligoarthritis)
The knee, wrist, shoulder and elbow are the most commonly affected joints
The affected joint is swollen, erythematous, warm and tender with an effusion on examination
Systemic symptoms include fever and malaise
What are the chronic CPP crystal inflammatory arthritis symptoms?
Usually a polyarticular arthritis affecting the small joints of the upper and lower limbs
May present similarly to osteoarthritis with knee involvement, but inflammatory flares and severe articular damage can differentiate
May resemble rheumatoid arthritis with wrists and metacarpophalangeal joint involvement
Symptoms and signs are of chronic intermittent swelling and pain of affected joints
What is the management for CPPD arthritis?
There are no treatments that eliminate CPP crystals or reduce articular deposition and so management is symptomatic
Non-pharmacological treatment includes resting the joint and using ice packs for pain
Joint aspiration may help to relieve symptoms as well as being important for diagnosis
As for an acute gout flare, options include a short course of NSAIDs, colchicine or steroids (either systemic or an intra-articular injection)
Long-term low dose colchicine may be used in chronic CPP arthritis to reduce flares
Long-term NSAIDs or steroids may also be considered however have a higher burden of adverse effects
Causes of secondary CPPD (as above) should be investigated for and treated e.g. with magnesium supplementation for hypomagnesaemia
What is the prognosis for CPP arthritis?
Acute CPP arthritis usually resolves within days to short weeks, although some flares may last months
Chronic CPP arthritis can cause significant joint damage with subsequent disability
In some cases of refractory chronic disease, biologic agents have been trialled (e.g. anakinra)
A diagnosis of pseudogout in a patient with diabetes and signs of bronzed skin pigmentation and gynaecomastia should raise suspicion for ???, characterised by excessive iron deposition leading to potential joint complications, thus, checking serum iron levels is crucial.
hereditary haemochromatosis
expect elevated serum iron in a blood test
What are the side effects of colchicine?
the most common side effects are diarrhoea, nausea and vomiting
Define osteoarthritis?
Osteoarthritis (OA) is the commonest form of arthritis, which is characterised by degenerative changes affecting the entirety of joints affected. Cartilage is lost, the subchondral bone becomes sclerosed with formation of osteophytes and subchondral cysts and there is inflammation of the synovial membrane lining the joint capsule (synovitis).
Risk factors for osteoarthritis:
Older age
Female sex
Overweight or obesity
Family history of OA
Previous joint injury
Joint damage due to inflammation (e.g. in patients with inflammatory arthritis)
Physical inactivity and reduced muscle strength
Low bone density
Deformities such as development dysplasia of the hip or leg length discrepancy
Stresses on joints due to occupational factors (e.g. repetitive squatting or kneeling) or exercise
Key symptoms of osteoarthritis:
Pain in the affected joint exacerbated by use
Pain may radiate e.g to the thigh, knee and ankle in hip OA, or to the wrist in hand OA
Joints may feel stiff (although prolonged morning stiffness is suggestive of inflammatory arthritis)
Worse after activity related exercise
Functional limitations such as difficulty opening jars (hand OA) or mobilising (knee or hip OA)
Locking or giving way of the knee
Examination findings of osteoarthritis:
Restricted and painful range of motion (e.g. in hip OA internal rotation with the hip flexed is particularly painful)
Crepitus (friction between bone and cartilage)
Affected joints may appear swollen or enlarged
A small effusion may form, especially when the knee is affected
Synovitis may present with mild soft tissue swelling, tenderness and warmth
Muscle wasting and weakness can result from disuse atrophy
Joint instability
An antalgic gait (“limping”) in knee OA
Trendelenburg gait in hip OA (due to weak abductors patients lurch towards the affected hip)
Deformities, including:
DIP and thumb CMC
Heberden’s nodes (bony nodules over the distal interphalangeal joints)
Bouchard’s nodes (bony nodules over the proximal interphalangeal joints)
Fixed flexion of the first carpometacarpal joint with hyperextension of the distal joints
This may lead to squaring of the joint with subluxation and remodelling
Ulnar or radial deviation of joints in the hand may occur
In severe hip OA the leg may be shortened due to fixed flexion and external rotation
Varus (most commonly) or valgus deformities of the knees
When can diagnosis of osteoarthritis be made on clinical history alone?
Osteoarthritis can be diagnosed clinically if the following apply:
The patient is aged over 45 years AND
The patient has activity-related joint pain AND
The patient has no morning stiffness or the morning stiffness lasts less than 30 minutes
Typical findings of osteoarthritis on x-ray can be remembered using:
Loss or narrowing of joint space due to thinning of cartilage
Osteophytes i.e. formation of new bony spurs at the joint margins
Subchondral sclerosis i.e. increased bone density beneath the cartilage
Subchondral cysts which are fluid-filled sacs in the subchondral bone
What is the conservative management for osteoarthritis?
Patient education and advice on self-care e.g. appropriate footwear
Weight loss advice and signposting to services in patients with excess body weight
Exercise has many benefits including strengthening muscles, improving fitness, reducing pain and improving function
Options include online fitness programmes designed for people with arthritis, physiotherapy and supervised exercise sessions
Physiotherapy services may also be able to offer manual therapies and joint supports such as braces or splints to reduce load and improve instability
Occupational health input may be needed in patients with functional impairment to assess their working environment and suggest adaptations
Patients should be asked about psychosocial stressors and support offered e.g. for associated depression and anxiety
Occupational therapy input may be helpful to advise on aids and devices to assist with activities of daily living (e.g. walking sticks, sock aids, grab rails, tap turners)
Podiatry input may be useful to assess the biomechanics of joint pain and advise on orthotic devices such as insoles
Referral to a pain management service may be appropriate for patients who have not responded to maximal medical (and if appropriate, surgical) management of OA
Assess falls risk and consider referral to specialist services for patients at risk (e.g. those with abnormal gait or balance, or who have had a fall in the last year)
What is the medical management for osteoarthritis?
First-line analgesia is with topical NSAIDs (such as ibuprofen gel) - patients should be made aware that some systemic absorption may occur
If this is ineffective or unsuitable, oral NSAIDs should be considered (with a PPI for gastroprotection if there are risk factors for gastrointestinal side effects)
Paracetamol or weak opioids (e.g. codeine) may also be used in the short-term
Topical capsaicin is another option, especially for knee OA
Intra-articular steroid injections may be considered if other treatments are not effective, and/or to enable therapeutic exercise
What is the surgical management for osteoarthritis?
Patients with OA of the hip, knee or shoulder who have symptoms significantly impacting quality of life despite optimal medical management should be considered for orthopaedic referral
The usual operation offered is an arthroplasty (joint replacement)
Rehabilitation before and after surgery is key to optimising outcomes
Complications of osteoarthritis:
Joint deformities (as above)
Increased risk of falls
Functional limitations, e.g. hand OA may making writing, turning keys or fasting buttons challenging
Reduced mobility
Sleep difficulties
Low mood and anxiety
Chronic pain
What is the prognosis of osteoarthritis?
Not all cases of OA are progressive and the disease course is variable
OA of the hands generally has a good prognosis, especially interphalangeal joint involvement
Hip OA has a poorer prognosis with many patients requiring arthroplasty
Knee arthroplasties for OA are also common however many patients’ symptoms improve or remain stable with time
Intermittent flares of OA may occur, where symptoms increase in intensity suddenly
Flares tend to last for a few days before improving
Define osteomalacia?
Osteomalacia is a metabolic bone disease that occurs in adults (i.e. after growth plate fusion) and is characterised by insufficient osteoid mineralisation.
Known as rickets in children
Risk factors for vitamin D deficiency?
Older age (aged over 65)
Darker skin pigmentation (e.g. South Asian or African-Caribbean patients)
Obesity
Patients who cover their skin for cultural, religious or health reasons
Housebound patients or those living in care homes
Malabsorption due to a gastrointestinal disorder or previous weight-loss surgery
End-stage chronic kidney disease
Severe liver cirrhosis
Vegetarian or vegan diets
Medications increasing risk of vitamin D deficiency (e.g. orlistat, carbamazepine, antacids)
What causes Vit D deficiency in osteomalacia?
The commonest cause of osteomalacia is vitamin D deficiency, which may occur due to:
Inadequate dietary intake
Lack of exposure to sunlight
Decreased absorption e.g. in coeliac disease, post-gastrectomy or pancreatic insufficiency
Medications e.g. antiepileptic medications, corticosteroids, rifampicin and thiazide diuretics
Vitamin D metabolism may be defective, for example in chronic kidney disease or cirrhosis
Phosphate deficiency may also cause osteomalacia
Dietary deficiency or decreased absorption may be responsible
Renal phosphate wasting may occur in Fanconi syndrome or rarely due to malignancy
The pathophysiology of osteomalacia involves chronic vitamin D (or rarely phosphate) deficiency leads to osteoclastic destruction of bone to maintain serum calcium levels
Resorbed bone is replaced with unmineralised osteoid and bone mineral density declines as a result (causing or worsening osteopenia or osteoporosis)
Symptoms of osteomalacia?
Bony pain (e.g. lower back, pelvis, shoulders, legs or ribs)
Muscular weakness and pain
Difficulty walking
Malaise and lethargy
Persistent fatigue
Paraesthesias (late sign)
Signs of osteomalacia?
A waddling gait
Proximal muscle weakness
Generalised bone and joint tenderness
Signs of hypocalcaemia (e.g. tetany, carpopedal spasm)
Spinal deformities e.g. kyphoscoliosis
Bedside tests for osteomalacia?
Urinalysis may show proteinuria in chronic kidney disease
Urinary calcium will be reduced
24 hour urinary phosphate to screen for renal phosphate wasting
Blood tests for osteomalacia?
Vitamin D - deficiency and osteomalacia occur at levels of under 25 nmol/L (levels of 25-50 may be insufficient; over 50 nmol/L is sufficient for most people)
Bone profile to check calcium and phosphate (which may be low or normal) and ALP (which will be raised)
Parathyroid hormone will be raised
U&Es to look for chronic kidney disease which may have associated renal osteodystrophy
LFTs looking for liver failure
Full blood count may show anaemia in patients with malabsorption
Ferritin, B12 and folate to identify other deficiencies
Thyroid function tests to rule out derangement as a cause of symptoms
Coliac serology if this is suspected as an underlying cause
Imaging for osteomalacia?
DEXA scanning shows low bone density
Bone X-rays may show insufficiency fractures
Looser zones (or pseudofractures) are transverse lucencies with sclerotic borders
These are often bilateral and symmetrical
Demineralisation of the bone may cause an “erased” or “fuzzy” appearance
Management for osteomalacia?
Underlying causes should be investigated for and managed (e.g. malabsorption)
Provide lifestyle advice on safe sun exposure and dietary intake of vitamin D and calcium
Loading dose vitamin D should be prescribed with approximately 300,000 IU given in total over 6-10 weeks (either weekly or daily)
After this is completed, maintenance vitamin D (800-2000 IU per day) should be continued
If calcium intake is insufficient and dietary measures are not possible, calcium supplements should be prescribed
Patients should be followed up to ensure symptoms resolve and vitamin D and calcium levels normalise
Patients with chronic kidney disease may require alfacalcidol rather than calciferol (due to reduced activity of 1-alpha hydroxylase which activates vitamin D)
Define osteomyelitis
Osteomyelitis is an infection of the bone that can manifest in both acute and chronic forms, caused by bacterial or fungal pathogens.
Acute infections of osteomyelitis are usually caused by a single or polymicrobial?
Single where as chronic are caused by polymicrobial
What are the most common causes of osteomyelitis?
The most common causative pathogens are Staphylococcus aureus and coagulase-negative staphylococci
What is the pathophysiology of osteomyelitis?
The pathophysiology of osteomyelitis involves:
Haematogenous seeding of the infection, which commonly occurs in children.
Spread from adjacent soft tissues or joints.
Direct inoculation of infection into the bone due to wound contamination during trauma or surgery.
What are the risk factors for osteomyelitis?
Diabetes mellitus
Peripheral vascular disease
Malnutrition
Immunosuppression
Malignancy
Extremes of age
Local factors such as chronic lymphedema, vasculitis, neuropathy etc.
Signs and symptoms of acute osteomyelitis?
Acute osteomyelitis is characterised by:
Fever
Pain at rest, worsening with weight-bearing
Swelling
Erythema of the affected site
Signs and symptoms of chronic osteomyelitis?
A lengthy history of pain
Persistently draining sinus tract or wound
Soft tissue damage
The presence of risk factors such as diabetes and peripheral vascular disease further supports the likelihood of chronic osteomyelitis
Investigations for osteomyelitis?
Blood inflammatory markers such as CRP, as well as routine markers checking for systemic upset
Blood cultures, which should always be obtained regardless of fever status.
Imaging:
X-ray: While it may initially present as negative, periosteal reactions become visible after around seven days, with bone necrosis detectable after ten. X-rays are useful for diagnosing chronic osteomyelitis, but cannot exclude the possibility of the condition.
MRI: This is the gold standard imaging for visualising both bone and soft tissue. Typical findings include bone marrow oedema secondary to inflammation.
CT: Effective in identifying necrotic bone and guiding a needle for biopsy.
Other tests:
Cultures from expressed pus. However, samples from sinus tracts are deemed unreliable.
Explain the ACR/EULAR 2010 criteria
Compare osteoarthritis and rheumatoid arthritis?
How does one classify systemic lupus erythematous?
patients need to have positive antinuclear antibodies (ANA) and score 10 or more with at least one clinical criterion:
What are the renal manifestations of systemic lupus erythematous?
The majority of patients develop renal disease, with approximately 4% progressing to end-stage renal disease
Lupus nephritis varies in severity and may be asymptomatic, or present with nephritic or nephrotic syndrome
Presenting features include hypertension, frothy urine and peripheral oedema
Renal involvement is classified based on histology as below:
