MDEMO - rheumatology and orthopaedics Flashcards
Give a quick summary of Polymyalgia rheumatica
A specific disease (autoimmune) causing early morning prolonged proximal muscle stiffness (shoulder and pelvic girdle), but not arthritis. It tends to occur in people over 60, and sometimes in association with temporal (or giant cell) arteritis (when younger people might be affected). Note that it is stiffness and not weakness.
Does creatine kinase tend to be raised in polymyalgia rheumatica?
No, CK levels tend to be normal, and this helps to distinguish it from myositis/ myopathies
What is the treatment for polymyalgia rheumatica?
Prednisolone 15mg / day = expect a dramatic response within 1 week and if not consider an alternative diagnosis (as steroids work amazingly for PMR). Provide bone protection. NSAIDS are not effective.
What is the difference between osteomalacia and osteoporosis
In osteomalacia, there is a normal amount of bone, but its mineral content is low (there is excess uncalcified osteoid and cartilage). In osteoporosis, the mineralisation is unchanged, but there is overall loss of bone.
List some causes of osteomalacia
Vitamin D deficiency/ resistance Renal osteodystrophy Liver disease Drug induced Tumour induced osteomalacia
What might you find on x-ray in a patient with osteomalacia?
Looser’s zones - since osteomalacia affects cortical bone you see apparent partial fractures without displacement, and these may typically be seen on the lateral border of the scapula, inferior femoral neck and medial femoral shaft
Recap the 4 radiographic features of OA
Loss of joint space (joint space narrowing)
Osteophytes
Subarticular sclerosis
Subchondral cysts
What are Heberden’s and Bouchard’s nodes?
Heberden’s nodes = DIP joints
Bouchard’s nodes = PIP joints
In OA what tissue type is primarily damaged?
Cartilage (focal loss in early OA), in end stage OA some parts total loss of cartilage. Patchy cartilage death and local bony overgrowth
What is the difference between primary and secondary OA?
Primary OA is degeneration of the articular cartilage and surfaces of a joint with no predisposing factors- in this sense the disease is idiopathic. In secondary OA, there is an underlying precipitation to the degenerative process e.g. post-traumatic, post-operative, post-infective etc.
What is the classic pattern of joint involvement in RA?
Classically a symmetrical distal small joint polyarthropathy, often affecting the hands and feet, but later stage can affect any joint. MCP joints predominantly affected. PIP joints also affected (sparing of DIP joints)
Roughly what percentage of RA patients will have a positive rheumatoid factor?
Around 70%
What are the two markers of RA that tend to be measured in the blood?
Rheumatoid factor and anti-CCP
What are the x-ray findings in RA?
Soft tissue swelling, juxta-articular osteopenia and decreased joint space. Later on, there may be bony erosions, subluxation or complete carpal destruction
What tool is used to measure disease activity in RA?
DAS-28
What is involved in the early inflammatory arthritis protocol?
Identify and treat early and aggressively
DMARDs- methotrexate is usually first line unless contraindicated
Biologics- e.g. anti-TNF alpha, anti-IL6 etc
Patients have to have tried at least 2 DMARDs before going onto biologics
What are the key clinical features of anti-phospholipid antibody syndrome?
Can be remembered as ‘CLOT’: Coagulation defects (arterial/venous), Livedo reticularis, Obstetric (recurrent miscarriage), Thrombocytopenia. Also, cerebral disease (e.g. migraine/seizure)
What is antiphospholipid syndrome also known as and with what other disease may it be associated?
Also known as Hughes’ syndrome. Was initially described in SLE and can be associated with SLE in 20-30% of cases
What are the autoantibodies associated with antiphospholipid syndrome?
Antiphospholipid antibodies (anticardiolipin, lupus anticoagulant, anti-Beta 2 glycoprotein 1)
In SLE, patients may rarely develop a symmetrical small joint polyarthropathy similar to that seen in rheumatoid arthritis. What is this called in the context of SLE and what is the main difference between it and RA?
It is called Jaccoud’s arthropathy and the difference is that it tends to be non-deforming
What is the typical epidemiology of SLE?
Prevalence of ~0.2%, F:M = 9:1, tends to affect women of child-bearing age, commoner in Afro-Caribbean and Asian populations. Associated genetic factors: HLA DR2, DR3 and B8
What are some key signs/ symptoms to ask about in a history if suspecting SLE?
Rashes, photosensitivity, alopecia, mucosal ulceration, Raynaud’s phenomenon
What are the three best ways of monitoring disease activity in SLE?
- anti-DNA antibody titres, 2. Complement (reduced C3 and C4 and increased C3d and C4d degradation products- as complement is used up), 3. ESR. Note that CRP tends to be normal
What are the key autoantibodies involved in SLE?
Anti-dsDNA, anti-Ro, anti-La.
As well as anti-Sm, anti-RNP.
40% are rheumatoid factor positive and antiphospholipid antibodies may also be positive.
What are the treatment principles for SLE?
Avoidance of sun exposure where possible and high factor suncream for photosensitive rashes. For skin flares, try topical steroids first. NSAIDs are useful for joint pains (caution in patients with renal disease). Hydroxychloroquine is used to alleviate symptoms mediate term. Immunosuppressants such as azathioprine, cyclophosphamide and methotrexate are sometimes used too. For severe flares urgent high-dose steroids, mycophenolate, Rituximab and cyclophosphamide
What are the shared features of the spondyloarthropathies?
Absence of rheumatoid factor (hence seronegative)
HLA-B27 association
‘Axial arthritis’ pathology in the spine and sacroiliac joints
Peripheral arthropathy- asymmetrical large joint oligoarthritis or monoarthritis
Enthesitis: e.g. plantar fasciitis, Achilles tendinitis
Extra-articular manifestations e.g. anterior uveitis
What tends to be the first line and the gold standard investigations for the spondyloarthropathies?
MRI tends to be gold standard, but x-rays tends to be first line
The ‘5A’s’ of ankylosing spondylitis is a way to remember some of the extra-articular manifestations. What are they?
Anterior uveitis, Achilles tendinitis, Apical lung fibrosis, Aortic regurgitation, amyloidosis
What tends to be the only radiological investigation required to assist in a diagnosis of ankylosing spondylitis?
A plain x-ray
What is the epidemiology of ankylosing spondylitis?
Prevalence 0.25-1%. Men present earlier : M:F 6:1 at 16 years, 2:1 at 30 years old. ~90% are HLA-B27 positive.
What is the typical presentation of a patient with ankylosing spondylitis?
A man <30 years old with gradual onset of low back pain, worse during the night with spinal morning stiffness relieved by exercise. Pain radiates from sacroiliac joints to hips/ buttocks and usually improves towards the end of the day. There is progressive loss of spinal movement in all directions.
What tends to be one of the first areas affected by inflammation in ankylosing spondylitis?
The sacroiliac joints. What initially starts as joint space widening eventually leads to sclerosis and joint fusion, visible on x-ray.
Briefly what is enteropathic arthritis and what is it’s epidemiology?
Enteropathic arthritis is acute-onset inflammatory oligoarthritis which is associated with IBD. Approximately 10% of those with UC, and twice as many with Crohn’s suffer from enteropathic arthritis. Men and women are affected equally. Exacerbations of arthritis tend to occur simultaneously with flare ups of bowel disease.
