MSK 2 Flashcards
what is gout?
Gout is a type of crystal arthropathy associated with chronically high blood uric acid levels. Urate crystals are deposited in the joint causing acute inflammatory arthritis, trophi around the joints and possible joint destruction, renal glomerular, tubular and interstitial disease and uric acid urolithiasis
where does gout commonly affect?
the first toe (podagra), foot, ankle, knee, fingers, wrist, and elbow; however, it can affect any joint.
*it usually affects cool parts of the body
what causes gout?
There is a causal relationship between hyperuricaemia (high urate level) and gout
Hyperuricaemia is due to renal under-excretion of urate in 90% of cases and to over-production in 10%
what are risk factors for gout?
risk factors for hyperuricaemia:
- dietary - seafood, meat. alcohol, especially beer
- obesity
- insulin resistance
- hypertension
- diuretic can increase urate levels
- high cell turnover - haematological cancer and chemotherapy - leads to urate production
- ciclosporin or tacrolimus (lead to increased tubular re-absorption of urate and well as decrease GFR
- Pyrazinamide - increase re-absorption of urate
how does gout present?
rapid onset of severe pain joint stiffness - usually in morning swelling and joint effusion tenderness tophi - subcutaneous deposits of uric acid (typically in hands, elbows, ears, achilles tendon)
how is gout diagnosed?
joint aspiration - synovial fluid analysis - this will provide a definate diagnosis and exclude septic arthritis and differentiate from pseudogout (calcium pyrophosphate deposition disease)
- no bacterial growth
- needle shaped crystals
- strongly negative birefringent of polarised light
- monosodium urate crystals
you could also perform a Joint x-ray which would show:
- Typically the space between the joint is maintained
- Lytic lesions in the bone
- Punched out erosions
- Erosions can have sclerotic borders with overhanging edges
how would you manage gout?
what are the indicaitons for urate lowering therapies?
ACUTE GOUT
1st line - NSAIDs or colchicine
2nd line - corticosteroid - prednisolone
*colchicine has slower onset and can cause diarrhoea
RECURRENT GOUT - 2-3 weeks post acute episode
1st line - allopurinol plus naproxen
2nd line - febuxostat
lifestyle changes
** exam tip - do not start allopurinol until acute attack is settled
the British Society of Rheumatology Guidelines now advocate offering urate-lowering therapy to all patients after their first attack of gout
ULT is particularly recommended if:
>= 2 attacks in 12 months
tophi
renal disease
uric acid renal stones
prophylaxis if on cytotoxics or diuretics
what are the complications of gout?
acute uric acid nephropathy
nephrolithiasis
what is pseudogout?
Pseudogout is a crystal arthropathy caused by calcium pyrophosphate crystals. Calcium pyrophosphate crystals are deposited in the joint causing joint problems. It is also known as chondrocalcinosis.
can be both acute and chronic
how does pseudogout present?
tender painful joints
typically an older adult with a hot swollen, stiff, painful knee
other joint that may be affected: shoulders, wrists and hips
what are the risk factors of pseudogout?
advanced age (it is rare in people younger than 60) Injuries or previous joint surgeries hyperparathyroidism haemochromatosis family history hypomagnesaemia hypophosphatasia
what are the investigations for pseudogout?
joint aspiration with synovial fluid analysis - important for diagnosis, to exclude septic arthritis and differentiate from gout. It will show:
- calcium pyrophosphate crystals
- intracellular or extracelllular positively birefringent of polarised light
- rhomboid-shaped crystals under polarised light.
- no bacterial growth
X-ray - chondrocalcinosis is the classical xray change in pseudogout. It appears as a thin white line in the middle of the joint space by the calcium deposition - this is diagnostic of gout
other joint x-ray changes are similar to osteoarthritis - loss of joint space, osteophytes, subarticular sclerosis, subchondral cysts
serum calcium - exclude hyperparathyroidism
serum parathyroid hormone - exclude hyperparathyroidism
serum magnesium
serum alkaline phosphatase
what is the treatment for pseudogout?
intra-articular corticosteroids NSAIDs if injection declined or joint not accessible second line - colchicine 3rd line - joint aspiration add paracetamol for analgesia
for severe cases joint wash out - arthrocentesis
what is Paget’s disease?
a chronic bone disorder that is characterised by focal areas of increased bone remodelling, resulting in overgrowth of poorly organised bone
what areas are most commonly affected in paget’s disease?
skull
spine/pelvis
long bones of the lower extremities
what are the risk factors for Paget’s disease?
increasing age
male sex
family history
how does Paget’s disease present?
- only 5% of patients are symptomatic
- *the stereotypical presentation is an older male with bone pain and an isolated raised ALP
- bone pain - in the pelvis, lumbar spine, femur
- if untreated - bowing of tibia, bossing of skull
- raised ALP
- other markers of increased bone turnover - PINP, CTx, NTx and urinary hydroxyproline
what investigations would you perform for Paget’s disease?
plain XR - mostly lytic changes, V shaped lytic lesions in the long bones, occasional fractures, skull XR - may show thickening of the calvarium
Isotope bone scan - areas of dense uptake - may identify all areas involved and often picks up non-symptomatic regions
ALP - may be normal or raised
bone specific ALP - sensitive blood test for diagnosis
calcium will usually be normal
P1NP and CTX - will initially be elevated - markers of bone turnover
what is the management for Paget’s disease?
if asymptomatic - observation, regular follow up, patient education and preventive measurs. If there is highly active disease and high risk of complications - bisphosphonate or calcitonin
If they are symptomatic
- bisphosphonate (IV zoledronic acid or oral riseronate) or calcitonin
plus supportive therapies e.g. physiotherapy
what are the complications of Paget’s disease?
deafness (cranial nerve entrapment) bone sarcoma (1% if affected for > 10 years) fractures skull thickening high-output cardiac failure
what is osteomalacia?
Osteomalacia is a metabolic bone disease characterised by incomplete mineralisation of the underlying mature organic bone matrix (osteoid) following growth plate closure in adults.
what causes osteomalacia?
vitamin D deficiency (can be from lack of sun exposure, malabsorption or chronic kidney disease)
VD is essential in calcium and phosphate absorption from the intestine and kidneys.
Vitamin D is also responsible for regulating bone turnover and promoting bone bone reabsorption to boost the serum calcium level.
Inadequate VD leads to a lack of calcium and phosphate in the blood.
Low calcium causes a secondary hyperparathyroidism as the parathyroid gland tries to raise the calcium level by secreting parathyroid hormone. Parathyroid hormone stimulates increased reabsorption from the bones. This causes further problems with bone mineralisation.
how does osteomalacia present?
may be asymptomatic Fatigue Bone pain Muscle weakness Muscle aches Pathological or abnormal fractures
how is osteomalacia investigated?
Serum 25-hydroxyvitamin D
Serum calcium is low
Serum phosphate is low
Serum alkaline phosphatase may be high
Parathyroid hormone may be high (secondary hyperparathyroidism)
Xrays may show osteopenia (more radiolucent bones)
DEXA scan shows low bone mineral density
how is osteomalacia managed?
calcium plus vitamin D - ergocalciferol or colecalciferol and calcium carbonate or calcium citrate
