Rheumatology/musculoskeletal Flashcards
What is bone made up of?
Bone is made of type 1 collagen,calcium, and phosphate (that become hydroxyapatite).
What is the difference between trabecular and cortical bone?
Cortical bone is made up of haversian systems, with concentric lamellar of bone tissue surrounding a central canal that contains blood vessels. Cortical bone is dense and forms the hard envelope around the long bones.
Trabecular or cancellous bone fills the centre of the bone and consists of interconnecting meshwork or trabeculae separated by spaces filled with bone marrow.
What happens if there is an abnormally high turnover of bone? What happens if there is over mineralisation of bone?
High turnover leads to the formation of weak woven bone such as in pagets or hyperparathyroidism. Over mineralisation leads to brittle bones, such as in osteogenesis imperfecta.
What are the three different types of joints?
Joints can be fibrous, fibrocartilagenous, and synovial. Fibrous joint is the sutures of the skulls. A fibrocartilagenous joint is the pubic symphysis or costochondral joints.. Synovial joints are the joints that move.
What is the difference between irate crystals and calcium pyrophosphate crystals?
Urate crystals (gout) are long and needle shaped and show a strong light intensity with a negative bifringence. Calcium pyrophosphate crystals (pseudo gout ) are rhomboid in shape, have a weak intensity, and a positive bifringence.
When do you use synovial fluid analysis?
Synovial fluid analysis should be used for any monoarthritis, or for anyone suspected of septic arthritis, crystal associated arthritis, or intra-articular bleeding. If sepsis is suspected, synovial fluid should be sent for an urgent gram stain in and culture in a sterile container. Crystals are detected by a polarised light microscopy of unrefridgerated SF (refrigeration causes crystal dissolution and post aspiration crystallisation).
What are the cardinal signs of OA on X-ray?
Narrowing of the joint space, osteophytes, subchondral sclerosis (focused areas of increased bone density), cysts, and osteochondral ‘loose’ bodies are also features.
What is rheumatoid factor?
Rheumatoid factor is an antibody directed against the Fc fragment of IgG. RF may be of any antibody class, but is most commonly IgM. RF has a low diagnostic sensitivity and specificity. 30% of people with RA won’t have RF. however, a high RF has a poorer prognosis. RF is also associated with sjorgenssyndrome, primary biliary cirrhosis, subacute bacterial endocarditis, SLE tubercolusis, old age and can be found in healthy people.
What are anti CCP antibodies?
Antibodies to citric citrullinated peptides. Inflamed synovium is high in the enzyme peptidylarginine delaminase. Peptidylarginine deaminase converts arginine in peptides into citrulline. Anti CCP antibodies will bind to tissue with citrulline in it. Anti CCP have a low sensitivity but a high specificity. So if someone doesn’t have anti CCP they may or may not have RA, but if they do then they definitely have it. Anti CCP are also associated with severe disease.
What are antinuclear antibodies (ANAs) ?
ANAs are antibodies directed against the nucleus. Healthy people will have a low titre of ANAs, the higher the ANAs are, the more likely that thee is illness. A negative ANA titre will rule out SLE, but a high ANA titre does not necessarily confirm it. A high ANA is not associated with a worse prognosis. Whilst ANAs are mostly used in systemic sclerosis, sjorgenssyndrome, scleroderma, dermatomyositis, or poly myosotis, mixed connective tissue disease or autoimmune hepatitis.
DS DNA abs and SM abs ( smiths antibodies) are very specific for lupus.
Anti histone abs are very specific for drug induced lupus.
What are ANCAs?
ANCAs are anti neutrophil cytoplasmic antibodies. They are useful in the diagnosis of vasculitis. ANCAs are antibodies against the cytoplasm of granulocytes (neutrophils). When looked at under immunoflourescence there are two common patterns. There may be cytoplasmic fluorescence (c ANCA) or peri nuclear fluorescence (p ANCA).
What are c ANCA?
C ANCAs are associated with antibodies to proteinase 3 (PR3) and occur in >90% of patients with Wegeners granulomatosus with renal involvement.
What is a p ANCA?
A p ANCA finding is fairly non specific, but if it is due to anti MPO antibodies it may be due to churn Strauss vasculitis or microscopic polyartheritis. Atypical p ANCA are found in people with ulcerative colitis or autoimmune liver disease.
What are the most likely causes of an acute onset monoarthritis?
An acute onset monoarthritis is most likely caused by sepsis or crystals (gout or pseudo gout). It may also be caused by trauma (heamoarthrosis), or a foreign body reaction, or a mono articular presentation of a poly or oligoarthritis.
Which joint does gout classically target?
Gout classically targets the first metotarsalphalangeal joint.
Which joint does reactive/psoriatic arthritis typically affect?
Reactive/psoriatic arthritis typically affects the big toe inter phalangeal joint.
Which joint does heamoarthrosis or seronegative spondyloarthritis commonly affect?
Seronegative spondyloarthritis will commonly affect the elbow or ankle.
What joint does pseudo gout affect?
Pseudo gout affects the elbow or ankle.
What are the seronegative spondyloarthropathies?
The seronegative spondyloarthropathies are reactive arthritis, psoriatic arthritis, ankylosing spondylitis, and enteropathic arthritis.
How does septic arthritis present?
Septic arthritis presents with acute or subacute monoarthritis and fever. The joint is red, swollen, and hot, and held in a loose pack position with an effusion, and rest pain and stress pain on movement. Any limb can be affected but it most commonly affects the knee or hip.
What is the most likely organism to cause septic arthritis?
In adults, the most likely organism is staph aureus. For sexually active young adults, consider untreated gonorrhoea.
What investigations are used in septic arthritis?
Joint aspiration (synovial fold is usually turbid and blood stained, should be sent for gram stain and culture)
Blood cultures
Obtain culture from genital tract to test for gonorrhoea
FBC may show a leukocytosis
ESR and CRP
What is giant cell arteritis and polymyalgia rheumatica ?
Giant cell arteritis and poly myalgia rheumatica are related diseases. They are both associated with granulomatous arteritis of the head and neck.PMR and GCA are sometimes considered as seperate diseases. The average age of onset is 70 and they are very rare under the age of 60. There is a female preponderance of 3:1. The clinical features of PMR and GCA result from occlusion of vessels and subsequent tissue ischeamia.
What are the clinical features of polymyalgia rheumatica?
Polymyalgia rheumatica presents with muscle soreness, particularly affecting the hip and shoulder girdles. There may be stiffness and painful restriction of active movements, but passive movements are preserved. Muscles are tender to palpation but weakness and muscle wasting are absent. Constitutional symtoms may be present, such as fevers, wasting, night sweats, fatigue and malaise.
What are the clinical features of giant cell arteritis?
Giant cell arteritis presents with a headache, localised to the temporal or occipital area. It may be accompanied by scalp tenderness. Jaw pain may develop in some patients, and is brought on by chewing or talking due to ischeamia of the massater muscles. Visual disturbances may occur, such as the emergency presentation with blindness in one eye due to pcclusion of the posterior ciliary artery. The optic disk may appear pale and swollen with haemorrhages on fundscopy. But this takes 24 to 36 hours to develop and initially fundoscopy will appear normal. Other visual symptoms may include loss of visual acuity, poor colour vision, or papillary defects. Rarely , neurological involvement may occur, with TIAs, brainstem infarcts, and hemiparesis.
How do you confirm a diagnosis of PMR or GCA? How do you treat it?
Confirm diagnosis with temporal artery biopsy (nb if negative you haven’t ruled out Dx, you may have just missed the affected parts). Treat with corticosteroids (eg prednisolone) straight away due to risk of vision loss for GCA. The response to treatment will be dramatic and symptoms will be resolved within 48-72hours. Start with a high dose and then bring it down to somehing acceptable. Also consider administering osteoporosis prophylaxis.
What is adhesive capsulitis? How does it present? How is it treated?
Adhesive capsulitis is a chronic fibrosing condition the presents over 4-10 weeks before subsiding over a similar time course. Glenohumoral restriction is present at onset,and continues to progress to its maximum as the pain settles. Early there is stress pain and capsular tenderness, later there is painless restriction of both active and passive movements.
Adhesive capsulitis may be treated with analgesics, capsular steroid injections, and regular pendulum arm exercises.
List the rotator cuff muscles
Supraspinatus, infraspinatus, subscapularis, and terres minor.
What is the typical presentation of a rotator cuff lesion?
Rotator cuff lesions produce pain on active movement.
Pain on abduction: supraspinatus
Pain on internal rotation: subscapularis
Pain on external rotation: infraspinatus and terres minor.
