Rheumatology Flashcards
Give examples of alarm features in an individual presenting with back pain.
Aged over 50, constant pain, nocturnal pain, worse when lying flat, loss of sensation, weight loss, night sweats, fever, active/previous cancer, weakness and immunosuppression.
What are the five most common causes of back pain in those aged 15-30 years?
Mechanical back pain. Vertebral prolapse. Trauma. Ankylosing spondylitis. Pregnancy.
What are the three most common causes of back pain in those aged 30-50 years?
Degenerative disease.
Vertebral prolapse.
Malignancy.
What are the six most common causes of back pain in those aged over 50 years?
Degenerative disease. Osteoporosis. Pagets. Malignancy. Myeloma. Spinal stenosis.
What is the general management of back pain?
NSAIDs, paracetamol, physiotherapy, movement techniques and low-dose amitriptyline.
What is the pathophysiology of simple lower back pain?
Muscle strain causes spasms and temporary paralysis of the spinal area which results in pain.
What is osteoarthritis?
A degenerative condition characterised by the loss of cartilage at the synovial joints.
What is the most common type of arthritis?
Osteoarthritis.
What are risk factors for the development of osteoarthritis?
Obesity, increasing age, occupation (e.g. manual intense labour), female and family history.
What joints are typically affected in osteoarthritis?
Large, weight-bearing joints (hip, knee). Carpometacarpal joints (in the palm). Distal and proximal interphalangeal joints. Cervical spine.
What is the characteristic presentation of osteoarthritis?
Unilateral joint pain (ache) and stiffness without systemic upset.
Describe the stiffness associated with osteoarthritis.
Transient morning stiffness that lasts a few minutes.
What are the signs of osteoarthritis?
Joint line tenderness, limited range of movement, bony swelling, Heberden’s nodes and Bouchard’s nodes.
What radiological signs are found in patients with osteoarthritis?
Loss of joint space (narrowing). Osteophytes. Subchondral sclerosis. Subchondral cysts. (Remember: LOSS)
How is osteoarthritis managed?
Encourage weight loss and muscle strengthening exercises. Give paracetamol and topical NSAIDs first-line. Consider oral NSAIDs second-line - give with proton-pump inhibitor.
Intrarticular steroid injections if symptoms aren’t well managed and arthroplasty.
How is joint pain in osteoarthritis associated with activity?
Pain is provoked by movement and relieved by rest.
What is rheumatoid arthritis?
A long-term autoimmune disorder that causes chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa.
What is the characteristic presentation of rheumatoid arthritis?
Symmetrical distal polyarthropathy (painful, warm, swollen, stiff joints).
How is the joint pain of rheumatoid arthritis associated with rest/activity?
Pain is often worse after rest but improves with activity.
Describe the joint stiffness of rheumatoid arthritis.
Morning stiffness lasting at least thirty minutes.
What systemic features are associated with rheumatoid arthritis?
Fever and low energy.
What joints are most commonly affected in rheumatoid arthritis?
Proximal interphalangeal joints.
Metacarpophalangeal joints.
What signs of rheumatoid arthritis are found in the hands?
Z shaped deformity of the thumb.
Swan neck deformity.
Boutonnieres deformity.
Ulnar deviation of the fingers.
Give four examples of extra-articular manifestations of rheumatoid arthritis (excluding the eyes).
Pulmonary fibrosis.
Bronchiolitis obliterans.
Felty’s syndrome.
Secondary Sjogren’s syndrome.
Give three examples of ocular manifestations of rheumatoid arthritis.
Keratoconjunctivitis sicca (dry eyes).
Episcleritis (painless, red).
Scleritis (severe pain, photophobia).
The presence of which two antibodies are used in the diagnosis of rheumatoid arthritis?
Rheumatoid factor.
Anti-cyclic citrullinated peptide antibody.
Rheumatoid arthritis: what is the difference in utility of investigations of rheumatoid factor and anti-CCP antibody?
Anti-CCP antibody are more sensitive and specific than RF and can be detected up to ten years before the development of RA.
Other than rheumatoid arthritis, give examples of three conditions in which rheumatoid factor may be raised.
Sjogren’s syndrome.
SLE.
Infective endocarditis.
What is first-line treatment of rheumatoid arthritis?
DMARD monotherapy (methotrexate or sulfasalazine or hydroxychloroquine).
Rheumatoid arthritis: What monitoring is required for individuals taking DMARDs?
FBC and LFT monitoring due to risk of myelosuppression and liver cirrhosis.
What is second-line treatment of rheumatoid arthritis?
Two DMARDs.
What is the pharmacological management of rheumatoid arthritis following a failure to respond to two DMARDs?
Biologics - TNF-inhibitors such as etanercept, infliximab and adalimumab.
Describe the action of methotrexate.
Interferes with metabolism of folate and suppresses certain components of the immune system.
How often is methotrexate taken in the treatment of rheumatoid arthritis?
Once weekly.
What should be prescribed alongside methotrexate?
5mg folic acid taken on a different day to the methotrexate.
How should methotrexate use be managed during pregnancy?
Highly teratogenic - stop six months before conception in men and women.
What is psoriatic arthritis?
An inflammatory arthritis associated with psoriasis.
What % of patients with psoriasis develop psoriatic arthritis?
10-20%.
Give examples of patterns of psoriatic arthritis.
Symmetrical polyarthritis.
Asymmetrical pauciarthritis.
Spondylitic pattern.
What are the presenting features of psoriatic arthritis?
Psoriasis plaques on skin, pitting of the nails, onycholysis (separation of nail from nail bed), dactylics (inflammation of finger), enthesisitis.
What are extra-articular features of psoriatic arthritis?
Conjuncitivitis, anterior uveitis, aortitis, amyloidosis.
What does x-ray reveal in psoriatic arthritis?
Periostitis, ankylosis, osteolysis, dactylitis and pencil-in-cup appearance.
What is the management of psoriatic arthritis?
NSAIDs for pain.
DMARDs (methotrexate, sulfasalazine).
Anti-TNF (etanercept, infliximab).
What is reactive arthritis?
A condition of synovitis in the joints in reaction to a recent infection trigger.
Reactive arthritis: What is the typical pattern of disease?
Acute monoarthritis typically affecting the lower limb and most often the knee.
What clinical features are associated with reactive arthritis?
Warm, swollen, painful joint.
Give examples of possible triggers of reactive arthritis
Gastroenteritis.
Sexually transmitted infections (chlamydia, gonorrhoea).
Give examples of extra-articular features associated with reactive arthritis.
Conjunctivits, anterior uveitis, urethritis, circinate balantitis.
Remember: can’t see, can’t pee, can’t climb a tree.
Reactive arthritis: What is circinate balantitis?
Dermatitis of the head of the penis.
What important differential diagnosis for reactive arthritis must be excluded in the management of this condition?
Septic arthritis.
How is reactive arthritis managed while investigations are pending?
Antibiotics given to treat potential septic arthritis.
How is reactive arthritis investigated // septic arthritis excluded?
Joint aspirate followed by gram-staining, cultures and sensitivities. Crystal examination can also be performed for investigation of gout/pseudogout.
What is the management of reactive arthritis after septic arthritis has been excluded?
NSAIDs.
Intrarticular steroid injections.
Systemic steroids may be required.
Name three conditions within the seronegative group of spondyloarthropathies.
Ankylosing spondylitis.
Reactive arthritis.
Psoriatic arthritis.
The seronegative spondylorthropathy group of conditions are associated with what gene?
HLA B27.
What is ankylosing spondylitis?
Inflammatory condition affecting the spine.
What joints are most often affected in ankylosing spondylitis?
Sacroiliac joints.
Vertebral column joints.
Ankylosing spondylitis typically affects what group of people?
Young males.
What is the characteristic presentation of ankylosing spondylitis?
Pain and stiffness in the lower back and sacroiliac pain in the buttock. Pain is worse at night and can wake from sleep.
How does rest/activity affect the pain associated with ankylosing spondylitis?
Pain improves with movement and worsens with rest.
Describe the joint stiffness associated with ankylosing spondylitis.
Morning stiffness lasting at least 30 minutes.
Describe how joint inflammation can progress in ankylosing spondylitis.
Progresses to fusion of the vertebral and sacroiliac joints.
What is the characteristic finding on spinal x-ray of someone with later stage ankylosing spondylitis?
Bamboo spine.
What are the features of a bamboo spine on x-ray?
Squaring of the vertebral bodies. Subchondral sclerosis. Subchondral erosions. Syndesmophytes. Ossification.
What investigations are performed in ankylosing spondylitis?
Inflammatory markers (CRP and ESR).
HLA B27 genetic testing.
Spinal and sacral x-ray.
Spinal MRI.
What extra-articular features are associated with ankylosing spondylitis?
Chest pain (costovertebral and costosternal joint inflammation). Plantart fasciitis (due to enthesitis). Dactylitis. Anaemia. Anterior uveitis. Aortitis. Heart block. Restrictive lung disease (restricted chest wall movement). Inflammatory bowel disease.
What is the management of ankylosing spondylitis?
NSAIDs for pain, steroids to control flares, anti-TNF medication (etanercept) to suppress disease activity. Physiotherapy, exercise, smoking avoidance, bisphosphonates.
What is systemic lupus erythematosus?
An inflammatory autoimmune connective tissue disease.
What is the presentation of SLE?
Non-specific features: Fatigue, hair loss, arthralgia, myalgia, fever, weight loss, photosensitive malar rash, lymphadenopathy, splenomegaly, shortness of breath, pleuritic chest pain, mouth ulcers and Raynaud’s phenomenon.
SLE: The disease is characterised by the presence of which autoantibody?
Anti-nuclear antibody.
What % of people with SLE are positive for anti-nuclear antibody?
85%.
How specific is anti-nuclear antibody for SLE?
Also present in healthy individuals and other autoimmune conditions (such as autoimmune hepatitis).
Give an example of an autoantibody that is more specific for SLE than anti-nuclear antibody.
anti-dsDNA antibody.
What is anti-dsDNA antibody?
Anti-double stranded DNA antibody is a subtype of anti-nuclear antibody that is specific for SLE. Levels vary with disease activity so can be used for monitoring.
What syndrome of hypercoagulation is associated with SLE?
Antiphospholipid syndrome.
Give examples of complications of SLE.
Cardiovascular disease, infection, anaemia of chronic disease, pericarditis, pleuritis lupus nephritis, neuropsychiatric SLE and recurrent miscarriage.
What is first-line management for mild SLE?
NSAIDs, prednisolone, suncream/sunavoidance, hydroxychloroquine.
What is management of moderate-severe SLE?
Immunosuppressants (methotrexate, mycophenolate mofetil, azathioprine).
What is the management of SLE that fails to respond to immunosuppressants?
Biologics - rituximab, belimumab.
What is systemic sclerosis?
An autoimmune inflammatory and fibrotic connective tissue disease that affects the skin (most notably) and internal organs.
What are the two main patterns of systemic sclerosis?
Limited cutaneous systemic sclerosis (CREST syndrome).
Diffuse cutaneous systemic sclerosis.
What autoantibody is positive in most patients with systemic sclerosis?
Anti-nuclear antibody.
What are the features of limited cutaneous systemic sclerosis?
Calcinosis. Raynaud's phenomenon. oEsophageal dysmotility. Sclerodactyly. Telangiectasia.
Remember CREST.
What autoantibody is most associated with limited cutaneous systemic sclerosis?
Anti-centromere antibody.
What are the features of diffuse cutaneous systemic sclerosis?
CREST features + Cardiovascular disease (hypertension, coronary artery disease. Lung disease (pulmonary hypertension and pulmonary fibrosis). Renal disease (glomerulonephritis, scleroderma renal crisis).
What autoantibody is most associated with diffused cutaneous systemic sclerosis?
Anti-Scl-70 antibody.
Other than autoantibodies, what investigation can be performed in the diagnosis of systemic sclerosis?
Nailfold capillaroscopy (inspection of base of capillary to assess health of peripheral capillaries).
What is the non-medical management of systemic sclerosis?
Stop smoking, gentle skin stretching, avoiding cold triggers, physiotherapy and occupational therapy.
What is the medical management of systemic sclerosis?
Treat directly with steroids and immunosuppressants. Treat complications with emollients, nifedipine (Raynaud’s), omeprazole (gastro sx), analgesia (joint pain), antibiotics (skin infections) and antihypertensives.
What is polymyalgia rheumatica?
Relatively common inflammatory condition.
What group of people are classically affected by polymyalgia rheumatica?
White females > 50 years.
What is the clinical presentation of polymyalgia rheumatica?
Two week history of bilateral shoulder pain and pelvic girdle pain (making rising from chair and overhead activities painful). Mild fever, weight loss, low mood and malaise.
Polymyalgia rheumatica is associated with what vascular disease (and what are the features)?
Giant cell arteritis - unilateral headache, jaw claudication and visual disturbance.
How is pain associated with rest/activity in polymyalgia rheumatica?
Worse with movement and interferes with sleep.
Describe the stiffness associated with polymyalgia rheumatica.
Morning stiffness for at least 45 minutes.
What investigations are performed in polymyalgia rheumatica?
ESR, CRP, TFTs, CK, rheumatoid factor and serum protein electrophoresis.
What is the treatment of polymyalgia rheumatica?
High dose (15mg) prednisolone followed by steroid reducing regime.
What should be given alongside steroids in management of polymyalgia rheumatica?
Bisphosphonates, calcium supplements, vitamin D supplements, proton pump inhibitor.
What is temporal arteritis?
A vasculitis that affects the temporal artery.
What is the clinical presentation of temporal arteritis?
Unilateral headache, jaw claudication, visual disturbances, tender + palpable temporal artery.
Temporal arteritis is associated with which inflammatory condition?
Polymyalgia rheumatica (shoulder pain, pelvic girdle pain, morning stiffness).
What investigations are performed in temporal arteritis (with results)?
ESR (raised).
Temporal artery biopsy (skip lesions of multinucleated giant cells).
Why should temporal arteritis be treated urgently?
Visual loss is often irreversible.
What is the management of temporal arteritis?
High-dose prednisolone followed by reducing-regime.
What is Sjogren’s syndrome?
An autoimmune condition that affects the exocrine glands.
What are the clinical features of Sjogren’s syndrome?
Dry mucous membranes (dry eyes, dry mouth, dry vagina).
What is the difference between primary and secondary Sjogren’s syndrome?
Primary occurs in isolation.
Secondary is associated with SLE and rheumatoid arthritis.
Sjogren’s syndrome is associated with which autoantibodies?
Anti-Ro.
Anti-La.
What special test is performed in Sjogren’s syndrome?
Schirmer test.
Sjogren’s: Describe the Schirmer test.
Filter paper placed under lower eyelid with strip hanging over eyelid for five minutes and tear travel distance is measured.
What is the result of Schirmer test in a person with Sjogren’s?
< 10mm travel.
What is the management of Sjogren’s?
Artificial tears, artificial saliva, vaginal lubricants.
Hydroxychloroquine given to halt disease progression.
What are complications of Sjogren’s?
Eye problems (conjunctivitis, corneal ulcers). Mouth problems (dental cavities, candida infections). Vaginal problems (sexual dysfunction, candidiasis).
What is gout?
Crystal arthropathy (a form of inflammatory arthritis) associated with chronically high blood uric acid levels.
What is the presentation of gout?
Hot, painful, swelling and erythema of joints.
What is the most commonly affected joint in gout?
Metatarsophalangeal joint (base of the big toe).
What is the pathophysiology of gout?
Deposition of monosodium rate crystals in the synovial as a result of chronic hyperuricaemia.
What are three causes of decreased uric acid excretion?
Diuretics.
CKD.
Lead toxicity.
What are three causes of increased production of uric acid?
Cytotoxic drugs.
Severe psoriasis.
Myeloprolifrative / lymphoproliferative disorders
Gout: What are gouty tophi?
Subcutaneous deposits of uric acid in the small joints and connective tissues (of the hands, elbow and ears).
What differential should be considered when diagnosing gout?
Septic arthritis.
How is gout diagnosed?
Clinically.
Joint aspiration.
Imaging.
What are the findings of joint aspiration in gout?
No bacterial growth.
Monosodium urate crystals.
Negatively birefringent of polarised light.
Needle shaped crystals.
What are the findings on radiological imaging in gout?
Preservation of joint space.
Joint effusion.
Punched-out erosions.
Eccentric erosions.
What is the acute management of gout?
1st line: Naproxen (NSAID) + lansoprazole.
2nd line: Colchicine.
What can be given for gout prophylaxis?
Allopurinol.
What lifestyle modifications can be made to reduce the risk of gout?
Reduce alcohol intake.
Weight loss.
Avoiding foods high in purines (liver, kidney, seafood, oily fish).
What is pseudogout?
Crystal arthropathy the result of accumulation of calcium pyrophosphate dehydrate crystals within joint soft tissues.
What is the presentation of pseudogout?
Hot, swollen, stiff, painful knee. Other affected joints include shoulders, wrists and hips.
What investigations are performed in the diagnosis of pseudogout?
Joint aspiration.
X-ray.
What are the findings on joint aspiration in pseudogout?
No bacterial growth.
Rhomboid shaped crystals.
Positive birefringent of polarised light.
Calcium pyrophosphate crystals.
What is the pathognomic finding on X-ray in pseudogout?
Chondrocalcinosis.
What is osteoporosis?
A condition of reduced mineral bone density that increases the risk of fractures.
What are risk factors for the development of osteoporosis?
Increasing age, female sex, reduced mobility and activity, Low BMI, rheumatoid arthritis, smoking, alcohol and medications.
Give examples of medications that increase the risk of developing osteoporosis?
Long-term corticosteroids, SSRIs, PPIs, anti-epileptics and anti-oestrogens.
Which group of women are particularly at risk of osteoporosis (and why)?
Post-menopausal women as they have less oestrogen (unless on HRT).
What tool is used to predict bone fracture risk?
FRAX.
What does the FRAX tool specifically predict?
10-year-probability of major osteoporotic fracture or hip fracture.
What investigation is used in the assessment of osteoporosis?
DEXA scan.
What is a DEXA scan?
Dual-energy X-ray absorptiometry measures bone mineral density.
The measurement of bone mineral density at which area of the body is used in the classification and management of osteoporosis?
Hip.
DEXA scan: What is a T score?
The number of standard deviations below the mean bone mineral density of a healthy young adult.
DEXA scan: A T score of more than -1 means what?
BMD normal.
DEXA scan: A T score of -1 to -2.5 means what?
Osteopenia.
DEXA scan: A T score of less than -2.5 means what?
Osteoporosis.
DEXA scan: A T score of less than -2.5 plus a fracture means what?
Severe osteoporosis.
What lifestyle changes are advised in the management of osteoporosis?
Activity and exercise, maintain healthy weight, vitamin D supplements, calcium supplements, smoking cessation, alcohol consumption reduction.
What class of medications are used in the management of osteoporosis?
Bisphosphonates.
What is the function of bisphosphonates in the management of osteoporosis?
Interfere with osteoclasts and reduce their activity… preventing reabsorption of bone.
What instructions should be given to people taking bisphosphonates for the management of osteoporosis?
Take on an empty stomach, sit upright for at least 30 minutes.
Osteoporosis management: What are the potential risks of bisphosphonate use?
Oesophageal erosions.
Atypical fractures.
Osteonecrosis of the jaw.
Osteonecrosis of the external auditory canal.
What is osteomalacia?
A condition of defective bone mineralisation that leads to ‘soft’ bones.
What causes osteomalacia?
Vitamin D deficiency.
What is the presentation of osteomalacia?
Bone pain, muscle weakness/aches and fractures.
Describe the physiology of how vitamin D is produced.
Vit. D is a hormone produced from cholesterol by the skin in response to ultraviolet radiation. The kidneys metabolise vitamin D to its active form.
Give examples of two conditions that can result in vitamin D deficiency.
Malabsorption (inflammatory bowel disease).
Chronic kidney disease.
Describe why vitamin D is essential in normal physiology.
Vitamin D is essential for calcium and phosphate absorption from the intestines and kidneys. Inadequate vitamin D = lack of calcium and phosphate. which are both required for the construction of bone.
What endocrine disorder can result from low calcium as a result of vitamin D deficiency?
Secondary hyperparathyroidism.
What main investigation is performed in osteomalacia?
Serum 25-hydroxyvitamin D (< 25 mol/L indicates deficiency).
Other than serum vitamin D what investigations are performed in osteomalacia (with results).
Serum calcium (low). Serum phosphate (low). Parathyroid hormone (raised). Xray (osteopenia). DEXA scan (low bone mineral density).
