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
what is fibromyalgia?
it is a syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites.
what are the features of fibromyalgia?
chronic pain - at multiple sites, sometimes pain all over lethargy cognitive impairment - fibro fog sleep disturbances headaches dizziness
on examination there may be diffuse tenderness
what are risk factors for fibromyalgia?
family history rheumatological conditions age between 20 and 60 female sex associated conditions - IBS, tension headaches, chronic fatigue syndrome, temporomandibular joint disorder
what are some differentials for fibromyalgia?
RA osteoarthritis SLE chronic fatigue syndrome ankylosing spondylitis polymyalgia rheumatica
What investigations are performed for fibromyalgia?
diagnosis is usually clinical
- you would do investigations to rule out differential diagnosis
What criteria is used to diagnose fibromyalgia?
American College of Rheumatology (ACR) criteria for fibromyalgia syndrome
The criteria include:
> Generalised pain, defined as pain in at least 4 of 5 regions.
Symptoms have been present at a similar level for at least 3 months.
Widespread Pain Index (WPI) ≥7 and symptom severity scale (SSS) score ≥ 5 or WPI 4-6 and SSS score ≥ 9.
A diagnosis of fibromyalgia is valid irrespective of other diagnosis. A diagnosis of fibromyalgia does not exclude the presence of other clinically important illnesses.
how is fibromyalgia managed?
management is often difficult and needs to be tailored to individual patients
explanation
aerobic exercise - good evidence to help symptoms
CBT
Medication
1st line = amitriptyline or cyclobenzaprine
2nd line - pregabalin, duloxetine or gabapentin
Analgesia such as naproxen or tramadol can be added
what is osteomyelitis?
infection in the bone
how can osteomyelitis be classified?
haematogenous osteomyelitis
- results from bacteraemia
- is usually monomicrobial
- most common form in children
- vertebral osteomyelitis is the most common form of haematogenous osteomyelitis in adults
- risk factors include: sickle cell anaemia, intravenous drug user, immunosuppression due to either medication or HIV, infective endocarditis
non-haematogenous osteomyelitis:
- results from the contiguous spread of infection from adjacent soft tissues to the bone or from direct injury/trauma to bone
- is often polymicrobial
- most common form in adults
- risk factors include: diabetic foot ulcers/pressure sores, diabetes mellitus, peripheral arterial disease
what bacteria causes osteomyelitis?
S-aureus = most common
in children other causes - GBS, aerobic gram -ve bacilli, strep pyogenes, H influenzae
drug users - pseudomonas aeruginosa
sickle cell disease - salmonella species
how does osteomyelitis present?
- non-specific pain at the site of infection
- malaise and fatigue
- local inflammation, erythema or swelling
- low grade fever
what investigations would you perform for osteomyelitis?
WBC count ESR CRP plain x-ray - in acute disease - osteopenia appears and evidence of bone destruction and cortical breaches and periosteal reaction follow qucikly MRI
how is osteomyelitis managed?
antibiotics
usually flucloxacillin for 6 weeks
clindamycin if penicillin allergy
what is septic arthritis?
it is where infection occurs in a joint
it can be in a native joint but is also a common and important complication of joint replacement
how does septic arthritis present?
usually just one single joint (most commonly in the knee)
Hot, red, swollen and painful joint
Stiffness and reduced range of motion
Systemic symptoms such as fever, lethargy and sepsis
what are the common causes of septic arthritis?
Staphylococcus aureus is the most common causative organism.
Other bacteria:
Neisseria gonorrhoea (gonococcus) in sexually active individuals
Group A Streptococcus (most commonly Streptococcus pyogenes)
Haemophilus influenza
Escherichia coli (E. coli)
what are differentials of septic arthritis?
Gout (fluid shows urate crystals that are negatively birefringent of polarised light)
Pseudogout (fluid shows calcium pyrophosphate crystals that are rod-shaped intracellular crystals positively birefringent of polarised light)
Reactive arthritis typically triggered by urethritis or gastroenteritis and associated with conjunctivitis
Haemarthrosis (bleeding into the joint)
what investigations would you perform for septic arthritis?
synovial fluid microscopy, gram stain and polarising microscopy synovial fluid culture and sensitivities synovial fluid WCC blood cultures and sensitivities WCC ESR and CRP U&E LFTs plain X-ray USS
how is septic arthritis managed?
Empirical IV antibiotics should be given until the sensitivities are known. Antibiotics are usually continued for 3 – 6 weeks in total. Choice of antibiotic depends on the local guidelines. Example regimes are:
Flucloxacillin plus rifampicin is often first line
Vancomycin plus rifampicin for penicillin allergy, MRSA or prosthetic joint
Clindamycin is an alternative
what are the complications of septic arthritis?
osteomyelitis
joint destruction
what is behcet’s syndrome?
Behcet’s syndrome is a complex multisystem disorder associated with presumed autoimmune-mediated inflammation of the arteries and veins.
what is the classic triad of symptoms in behcet’s syndrome?
what are other features
triad - oral ulcers, genital ulcers, anterior uveitis
other features
- thrombophlebitis and DVT
- arthritis
- aseptic meningitis
- abdo pain, diarrhoea, colitis
- erythema nodosum
- retinal haemorrhage
- headaches and migraines
- memory impairment
what investigations are done for Behcet’s disease?
Behçet’s disease is a clinical diagnosis based on the features of the condition. The only particular investigation to be aware of is the pathergy test.
The pathergy test involves using a sterile needle to create a subcutaneous abrasion on the forearm. This is then reviewed 24 – 48 hours later to look for a weal 5mm or more in size. It tests for non-specific hypersensitive in the skin. It is positive in Behçet’s disease, Sweet’s syndrome and pyoderma gangrenosum.
how is Behcet’s disease managed?
Management involves a combination of:
Topical steroids to mouth ulcers (e.g. soluble betamethasone tablets)
Systemic steroids (i.e. oral prednisolone)
Colchicine is usually effective as an anti-inflammatory to treat symptoms
Topical anaesthetics for genital ulcers (e.g. lidocaine ointment)
Immunosuppressants such as azathioprine
Biologic therapy such as infliximab
what is discoid lupus erythematosus?
Discoid lupus erythematosus is a non-cancerous chronic skin condition. It is more common in women and usually presents in young adults between ages 20 to 40. It is more common in darker-skinned patients and smokers.
It is associated with an increased risk of developing systemic lupus erythematosus, however this risk is still below 5%. Rarely the lesions can progress to squamous cell carcinoma (SCC) of the skin.
how does discoid lupus erythematous present?
The lesions typically occur on the face, ears and scalp. They are photosensitive, meaning that they are made worse by exposure to sunlight. They are associated with scarring alopecia (hair loss in affected areas that does not grow back) and hyper-pigmented or hypo-pigmented scars.
The appearance of the lesions are: Inflamed Dry Erythematous Patchy Crusty and scaling
how is discoid lupus erythematous managed?
Skin biopsy can be used to confirm the diagnosis.
Treatment is with
Sun protection
Topical steroids
Intralesional steroid injections
Hydroxychloroquine
what is antisynthetase syndrome characterised by?
Antisynthetase syndrome is caused by autoantibodies against aminoacyl-tRNA synthetase e.g. anti-Jo1.
It is characterised by myositis interstitial lung disease thickened and cracked skin of the hands (mechanic's hands) Raynaud's phenomenon
what are bisphosphonates used for?
They inhibit osteoclasts by reducing recruitment and promoting apoptosis. Clinical uses prevention and treatment of osteoporosis hypercalcaemia Paget's disease pain from bone metatases
what are the adverse effects of bisphosphonates?
oesophageal reactions: oesophagitis, oesophageal ulcers (especially alendronate)
osteonecrosis of the jaw
increased risk of atypical stress fractures of the proximal femoral shaft in patients taking alendronate
acute phase response: fever, myalgia and arthralgia may occur following administration
hypocalcaemia: due to reduced calcium efflux from bone. Usually clinically unimportant
what is dermatomyositis?
an inflammatory disorder causing symmetrical, proximal muscle weakness and characteristic skin lesions
may be idiopathic or associated with connective tissue disorders or underlying malignancy (typically ovarian, breast and lung cancer, found in 20-25% - more if patient older). Screening for an underlying malignancy is usually performed following a diagnosis of dermatomyositis
polymyositis is a variant of the disease where skin manifestations are not prominent
**usually ANA positive
what are the features of dermatomyositis?
Skin features
photosensitive
macular rash over back and shoulder
heliotrope rash in the periorbital region
Gottron’s papules - roughened red papules over extensor surfaces of fingers
‘mechanic’s hands’: extremely dry and scaly hands with linear ‘cracks’ on the palmar and lateral aspects of the fingers
nail fold capillary dilatation
Other features proximal muscle weakness +/- tenderness Raynaud's respiratory muscle weakness interstitial lung disease: e.g. Fibrosing alveolitis or organising pneumonia dysphagia, dysphonia
what drugs can cause drug induced lupus erythematous?
Most common causes
procainamide
hydralazine
Less common causes
isoniazid
minocycline
phenytoin
what is Ehler-danlos syndrome?
an autosomal dominant connective tissue disorder that mostly affects type III collagen. This results in the tissue being more elastic than normal leading to joint hypermobility and increased elasticity of the skin.
Features and complications
elastic, fragile skin
joint hypermobility: recurrent joint dislocation
easy bruising
aortic regurgitation, mitral valve prolapse and aortic dissection
subarachnoid haemorrhage
angioid retinal streaks
what is McArdle’s disease?
autosomal recessive type V glycogen storage disease
caused by myophosphorylase deficiency
this causes decreased muscle glycogenolysis
Features muscle pain and stiffness following exercise muscle cramps myoglobinuria low lactate levels during exercise
what is lateral epicondylitis?
Lateral epicondylitis typically follows unaccustomed activity such as house painting or playing tennis (‘tennis elbow’). It is most common in people aged 45-55 years and typically affects the dominant arm.
what are the features of lateral epicondylitis?
pain and tenderness localised to the lateral epicondyle
pain worse on wrist extension against resistance with the elbow extended or supination of the forearm with the elbow extended
episodes typically last between 6 months and 2 years. Patients tend to have acute pain for 6-12 weeks
how is lateral epicondylitis managed?
advice on avoiding muscle overload
simple analgesia
steroid injection
physiotherapy
what are the rotator cuff muscles and what do they do?
Supraspinatus - abducts the arm before deltoid
Infraspinatus - rotates arm laterally
teres minor - adducts and rotates arm laterally
Subscapularis - adducts and rotates arm medially
