Rheum fifth yr Flashcards
What is polymyalgia rheumatica?
an inflammatory condition that causes pain and stiffness in the shoulders, pelvic girdle and neck
strong association with GCA
Demographics of PMR?
> 50
F>M
Caucasians
Features of PMR?
core features, present for at least 2 weeks:
Bilateral shoulder pain that may radiate to the elbow
Bilateral pelvic girdle pain
Worse with movement
Interferes with sleep
Stiffness for at least 45 minutes in the morning
Rapid onset
Other features:
Systemic symptoms such as weight loss, fatigue, low grade fever and low mood
Upper arm tenderness
Carpel tunnel syndrome
Pitting oedema
Ix of PMR?
Diagnosis is mainly based on the clinical presentation and the response to steroids
Need to exclude other conditions:
Full blood count
Urea and electrolytes
Liver function tests
Calcium can be raised in hyperparathyroidism or cancer or low in osteomalacia
Serum protein electrophoresis for myeloma and other protein disorders
Thyroid stimulating hormone for thyroid function
Creatine kinase for myositis
Rheumatoid factor for rheumatoid arthritis
Urine dipstick
Additional investigations to consider:
Anti-nuclear antibodies (ANA) for systemic lupus erythematosus
Anti-cyclic citrullinated peptide (anti-CCP) for rheumatoid arthritis
Urine Bence Jones protein for myeloma
Chest xray for lung and mediastinal abnormalities
EMG normal
Inflammatory markers (ESR, plasma viscosity and CRP) are usually raised however normal inflammatory markers do not exclude PMR
Differentials of PMR?
Osteoarthritis
Rheumatoid arhtirits
Systemic lupus erythematosus
Myositis (from conditions like polymyositis or medications like statins)
Cervical spondylosis
Adhesive capsulitis of both shoulders
Hyper or hypothyroidism
Osteomalacia
Fibromyalgia
Tx of PMR?
Steroid regime
Initially patients are started on 15mg of prednisolone per day.
Assess 1 week after starting steroids. If there is a poor response in symptoms it is probably not PMR and an alternative diagnosis needs to be considered. Stop the steroids.
Assess 3-4 weeks after starting steroids. You would expect a 70% improvement in symptoms and inflammatory markers to return to normal to make a working diagnosis of PMR.
If 3-4 weeks of steroids has given a good response then start a reducing regime with the aim of getting the patient off steroids:
15mg until symptoms are fully controlled then
12.5mg for 3 weeks then
10mg for 4-6 weeks then
Reduce by 1mg every 4-8 weeks
Additional measures for patients taking long term steroids?
Don’t STOP
DON’T – Make them aware that they will become steroid dependent after 3 weeks of treatment and should not stop taking the steroids due to the risk of adrenal crisis if steroids are abruptly withdrawn
S – Sick Day Rules: Discuss increasing the steroid dose if they become unwell (“sick day rules”)
T – Treatment Card: Provide a steroid treatment card to alert others that they are steroid dependent in case they become unresponsive
O – Osteoporosis prevention: Consider osteoporosis prophylaxis whilst on steroids with bisphosphonates and calcium and vitamin D supplements
P – Proton pump inhibitor: Consider gastric protection with a proton pump inhibitor (e.g. omeprazole)
What is SLE?
an inflammatory autoimmune connective tissue disease. It is “systemic” because it affects multiple organs and systems and “erythematosus” refers to the typical red malar rash that occurs across the face. It presents with varying and non-specific symptoms
often takes a relapsing-remitting course, with flares and periods where symptoms are improved. The result of chronic inflammation means patients with lupus often have shortened life expectancy. Cardiovascular disease and infection are leading causes of death.
Demographics of SLE?
more common in women and Asians + Afro-Caribbean, and usually presents in young to middle aged adults (20-40) but can present later in life.
Pathophysiology of SLE?
ANA
antibodies to proteins within the persons own cell nucleus. This causes the immune system to target theses proteins - causing inflammatory response
Type 3 hypersensitivity reaction - thought to be caused by immune system dysregulation leading to immune complex formation
Associated with HLA B8, DR2, DR3
Presentation of SLE?
Fatigue
Weight loss
Arthralgia (joint pain) and non-erosive arthritis
Myalgia (muscle pain)
Fever
Photosensitive malar rash. This is a “butterfly” shaped rash across the nose and cheek bones that gets worse with sunlight.
Lymphadenopathy and splenomegaly
Shortness of breath
Pleuritic chest pain
Mouth ulcers
Hair loss
Raynaud’s phenomenon
Ix of SLE?
Autoantibodies:
ANA - non specific
anti-dsDNA - specific to SLE
Full blood count (normocytic anaemia of chronic disease)
C3 and C4 levels (decreased in active disease)
CRP and ESR (raised with active inflammation)
Immunoglobulins (raised due to activation of B cells with inflammation)
Urinalysis and urine protein:creatinine ratio for proteinuria in lupus nephritis
Renal biopsy can be used to investigate for lupus nephritis
Diagnosis of SLE?
SLICC Criteria or the ACR Criteria
involves confirming the presence of antinuclear antibodies and establishing a certain number of clinical features suggestive of SLE
Complications of SLE?
Cardiovascular disease - HTN and CAD
Infection - as part of disease but also secondary to immunosuppressants
Anaemia of chronic disease - normocytic anaemia, due to bone marrow inflammation, can also get leucopenia, neutropenia, thrombocytopenia
Pericarditis
Pleuritis
Interstitial lung disease - leads to pulmonary fibrosis
Lupus nephritis - ssessed urine protein:creatinine ratio and renal biopsy. The renal biopsy is often repeated to assess response to treatment. Can lead to ESRF
Neuropsychiatric SLE - optic neuritis (inflammation of the optic nerve), transverse myelitis (inflammation of the spinal cord) or psychosis.
Recurrent miscarriage, intrauterine growth restriction, pre-eclampsia and pre-term labour.
VTE - antiphospholipid syndrome occurring secondary to SLE
Treatment of SLE?
anti-inflammatory and immunosuppression to reduce Sx and complications
First line treatments are:
NSAIDs
Steroids (prednisolone)
Hydroxychloroquine (first line for mild SLE)
Suncream and sun avoidance for the photosensitive malar rash
Other commonly used immunosuppressants in resistant or more severe lupus: Methotrexate, Mycophenolate mofetil, Azathioprine, Tacrolimus, Leflunomide, Ciclosporin
Biological therapies: Rituximab (MAB target CD20 on B cells), Belimumab (MAB target B-cell activating factor)
Drug-induced lupus features?
arthralgia
myalgia
skin (e.g. malar rash) and pulmonary involvement (e.g. pleurisy) are common
ANA positive in 100%, dsDNA negative
anti-histone antibodies are found in 80-90%
anti-Ro, anti-Smith positive in around 5%
renal and nervous system involvement being unusual
Causes of drug-induced lupus?
Most common causes
procainamide
hydralazine
Less common causes
isoniazid
minocycline
phenytoin
What is polymyositis?
inflammatory disorder causing symmetrical, proximal muscle weakness. thought to be a T-cell mediated cytotoxic process directed against muscle fibres. Associated with malignancy
Affects middle-aged, F:M 3:1
Features of polymyositis?
Proximal muscle weakness +/- tenderness
Raynaud’s
Respiratory muscle weakness
Interstitial lung disease - fibrosis alveoli, organising pneumonia - indicates poor prognosis
Dysphagia, dysphonia
Investigations and management for polymyositis?
Elevated CK - usually >1000
Other muscle enzymes (LDH, aldolase, AST and ALT)
EMG
Muscle biopsy
Anti-synthetase antibodies - anti-Jo-1
Tx - high-dose corticosteroids, azathioprine as steroid-sparing agent, IV immunoglobulins, biologics (infliximab/etanercept)
PT/OT to help muscle strength and function
What is dermatomyositis?
an inflammatory disorder causing symmetrical, proximal muscle weakness and characteristic skin lesions
can be idiopathic, associated with CTD or underlying malignancy (ovarian, breast, lung)
Features of dermatomyositis?
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
proximal muscle weakness +/- tenderness
Raynaud’s
respiratory muscle weakness
interstitial lung disease: e.g. Fibrosing alveolitis or organising pneumonia
dysphagia, dysphonia
Ix of dermatomyositis?
CK - usually >1000
Majority are ANA positive
Antibodies to aminoacyl-tRNA synthesase - anti-Jo-1, SRP, anti-Mi-2 antibodies
What is fibromyalgia?
syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites. The cause of fibromyalgia is unknown.
Women 5 times more affected
30-50 yrs old
Features of fibromyalgia
chronic pain: at multiple site, sometimes ‘pain all over’
lethargy
cognitive impairment: ‘fibro fog’
sleep disturbance, headaches, dizziness are common
Diagnosis and treatment of fibromyalgia?
Diagnosis is clinical and sometimes refers to the American College of Rheumatology
classification criteria which lists 9 pairs of tender points on the body. If a patient is tender in at least 11 of these 18 points it makes a diagnosis of fibromyalgia more likely
Management tailored to individual patient. Psychosocial and MDT approach.
Explanation
Aerobic exercise
CBT
Medication - pregabalin, duloxetine, amitriptyline
What is gout + features of gout?
type of crystal arthropathy and inflammatory arthritis. associated with chronically high blood uric acid levels. Urate crystals are deposited in the joint causing it to become hot, swollen and painful. Gout flares
Gouty tophi are subcutaneous deposits of uric acid typically affecting the small joints and connective tissues of the hands, elbows and ears. The DIP joints are most affected in the hands.
typically presents with a single acute hot, swollen and painful joint. Typical joints - metatarsophalangeal, wrists, carpometacarpal - also knee and ankle
Risk factors for gout?
Male
Obesity
High purine diet (e.g. meat and seafood)
Alcohol
Diuretics
Existing cardiovascular or kidney disease
Family history
increased production of uric acid - myeloproliferative, cytotoxic drugs, severe psoriasis
Lesch-Nyhan syndrome
Diagnosis of gout?
diagnosed clinically or by aspiration of fluid from the joint. Excluding septic arthritis is essential as this is a potential joint and life-threatening diagnosis.
uric acid - checked once acute episode settled down (2wks later)
Aspirated fluid - no bacterial growth, needle shaped, negatively birefringement of polarised light, monosodium urate crystals
X-ray - joint space maintained, lytic lesions in bone, punched out erosions with sclerotic borders and overhanging edges
Management of gout?
Acute:
NSAIDs, colchicine, steroids
colchicine - SE diarrhoea
Prophylaxis:
Allopurinol (xanthine oxidase inhibitor) - reduces uric acid levels
Lifestyle changes
What is pseudogout?
form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium
Cause hot, swollen, stiff, painful knee - or shoulder, wrist, hip
Associated with increasing age. If younger (<60) then usually have underlying risk factor (haemochromatosis, hyperparathyroidism, low Mg, low phosphate, acromegaly, Wilsons)
Ix of pseudogout?
joint aspiration: weakly-positively birefringent rhomboid-shaped crystals
x-ray: chondrocalcinosis
in the knee this can be seen as linear calcifications of the meniscus and articular cartilage
Management of pseudogout?
aspiration of joint fluid, to exclude septic arthritis
NSAIDs or intra-articular, intra-muscular or oral steroids as for gout
Joint washout in severe cases
What is osteoporosis?
Condition where there is reduction in the density of bones. Osteopenia is less severe reduction than osteoporosis. Means bone is less strong and more prone to fractures
Osteoporotic vertebral fracture - loss of height, kyphosis, localised tenderness on palpation of spinous processes at fracture site
Risk factors for osteoporosis?
Older age
Female
Reduced mobility and activity
Low BMI (<18.5 kg/m2)
Rheumatoid arthritis
Alcohol and smoking
Long term corticosteroids. NICE suggest the risk increases significantly with the equivalent of more than 7.5mg of prednisolone per day for more than 3 months)
Other medications such as SSRIs, PPIs, anti-epileptics and anti-oestrogens
Post menopausal - as oestrogen is protective against osteoporosis
Investigations for osteoporosis?
FRAX assessment on patients at risk: women >65, men >75, Younger patients with risk factors such as a previous fragility fracture, history of falls, low BMI, long term steroids, endocrine disorders and rheumatoid arthritis.
FRAX outcome without a BMD result will suggest one of three outcomes:
Low risk – reassure
Intermediate risk – offer DEXA scan and recalculate the risk with the results
High risk – offer treatment
FRAX outcome with a BMD result will suggest one of two outcomes:
Treat
Lifestyle advice and reassure
Lab values all normal (calcium, phosphate, ALP, PTH)
Management for osteoporosis?
Lifestyle - activity and exercise, healthy weight, adequate calcium and vitamin D, avoid falls, stop smoking, reduce alcohol consumption
calcium supplementation with vitamin D in patients at risk of fragility fractures with an inadequate intake of calcium - e.g., calcichew D3. If adequate calcium intake but lack sun exposure - vit D supplementation
Bisphosphonates - reduce osteoclast activity and preventing the reabsorption of bone. E.g., alendronate, risedronate, zoledronic acid. SE - reflux, oesophageal erosions, atypical fractures, osteonecrosis of jaw and external auditory canal
Denosumab is a monoclonal antibody that works by blocking the activity of osteoclasts.
Strontium ranelate is a similar element to calcium that stimulates osteoblasts and blocks osteoclasts but increases the risk of DVT, PE and myocardial infarction.
Raloxifene is used as secondary prevention only. It is a selective oestrogen receptor modulator that stimulates oestrogen receptors on bone but blocks them in the breasts and uterus.
Hormone replacement therapy should be considered in women that go through menopause early.
Follow up for low risk patients, and pt’s on bisphosphonates should have repeat FRAX and DEXA scan after 3-5 years. Consider treatment holiday if BMD improved and no fractures.
Summary of FRAX tool
Gives prediction of the risk of a fragility fracture over the next 10 hears
Input information (age, BMI, co-morbidities, smoking, alcohol, FHX, and also BMD if available). Gives percentage risk of 10 year probability of major osteoporotic fracture and hip fracture
in patients 40-90
QFracture tool - pts 30-90, larger group of RFs included
Summary of bone mineral density and DEXA
BMD measured using DEXA (dual energy X-ray absorptiometry)
Reading at hip used for classification and management of osteoporosis
Bone density can be represented as a Z score or T score. Z scores represent the number of standard deviations the patients bone density falls below the mean for their age. T scores represent the number of standard deviations below the mean for a healthy young adult their bone density is.
WHO classification - T score > -1 is normal, -1 to -2.5 is osteopenia, less than -25 is osteoporosis, less than -2.5 plus fracture is severe osteoporosis
Investigations for secondary causes of osteoporosis?
Blood cell count, sedimentation rate or C-reactive protein, serum calcium,
albumin, creatinine, phosphate, alkaline phosphatase and liver transaminases
Thyroid function tests
Bone densitometry ( DXA)
Other procedures, if indicated:
Lateral radiographs of lumbar and thoracic spine/DXA-based vertebral imaging
Protein immunoelectrophoresis and urinary Bence-Jones proteins
25OHD
PTH
Serum testosterone, SHBG, FSH, LH (in men),
Serum prolactin
24 hour urinary cortisol/dexamethasone suppression test
Endomysial and/or tissue transglutaminase antibodies (coeliac disease)
Isotope bone scan
Markers of bone turnover, when available
Urinary calcium excretion
What is osteomalacia?
a condition where there is defective bone mineralisation causing “soft” bones. Results from insufficient vitamin D.
Vitamin D is essential in calcium and phosphate absorption from the intestines and kidneys. Vitamin D is also responsible for regulating bone turnover and promoting bone reabsorption to boost the serum calcium level. Causes low Ca and phosphate and hence defective bone mineralisation.
Low Ca causes secondary hyperparathyroidism, so more PTH and increased reabsorption from bones.
Presentation of osteomalacia?
May be asymptomatic
Fatigue
Bone pain
Muscle weakness - proximal myopathy > waddling gait
Muscle aches
Pathological or abnormal fractures - especially femoral neck
Looser zones
Investigations of osteomalacia?
Serum 25-hydroxyvitamin D is the laboratory investigation for vitamin D. The interpretation of the results is as follows:
<25 nmol/L – vitamin D deficiency
25 – 50 nmol/L – vitamin D insufficiency
75 nmol/L or above is optimal
Low Ca, low phosphate, increased ALP, increased PTH
X-rays - osteopenia (more radiolucent)
DEXA - low BMD
Risk factors for osteomalacia?
Darker skin
Low exposure to sunlight
Live in colder climates
Spend a lot of time indoors
CKD
Drug induced - anticonvulsants
Inherited - hypophosphatemic rickets
Liver disease - cirrhosis
Coeliac disease
Treatment of osteomalacia?
supplementary vitamin D (colecalciferol) - several regimes 50,000 IU once weekly for 6 weeks, 20,000 IU twice weekly for 7 weeks, 4000 IU daily for 10 weeks
maintenance supplementary dose for of 800 IU or more per day should be continued for life after the initial treatment
What is psoriatic arthritis?
inflammatory arthritis associated with psoriasis that is within the seronegative spondyloarthropathy group.
Often precedes the development of skin lesions. It occurs in 10-20% of patients with psoriasis and usually occurs within 10 years of developing the skin changes. It typically affects people in middle age but can occur at any age.
Associations
Eye disease (conjunctivitis and anterior uveitis)
Aortitis (inflammation of the aorta)
Amyloidosis
Features of psoriatic arthritis?
Not a single pattern of affected joints:
symmetrical poly arthritis - similar to RA, more common in women, hands, wrists, ankles, DIP, MCP less commonly (unlike RA)
asymmetrical pauciarthritis - mainly digits and feet, only few joints
spondylitic pattern - more common in men, back stiffness, sacroilitis, atlanto-axial joint involvement
also: spine, achilles tendon, plantar fascia
Plaques of psoriasis
Pitting of nails
Onycholysis
Dactylitis
Enthesitis - points of insertion of tendon to bone
Arthritis mutilans - most severe form of psoriatic arthritis occurring in phalanxes - osteolysis (destruction) of the bones around the joints in the digits. This leads to progressive shortening of the digit. The skin then folds as the digit shortens giving an appearance that is often called a “telescopic finger”.
Investigations of psoriatic arthritis?
PEST tool - nvolves several questions asking about joint pain, swelling, a history of arthritis and nail pitting. A high score triggers a referral to a rheumatologist.
X-ray:
Periostitis is inflammation of the periosteum causing a thickened and irregular outline of the bone
Ankylosis is where bones joining together causing joint stiffening
Osteolysis is destruction of bone
Dactylitis is inflammation of the whole digit and appears on the xray as soft tissue swelling
Pencil-in-cup appearance - central erosions of the bone beside the joints
Management of psoriatic arthritis?
Similar to RA - coordinated between dermatologists and rheumatologists.
NSAIDs
DMARDs
Anti-TNF (etanercept, infliximab, adalimumab)
Ustekinumab - last line - monoclonal antibody that targets interleukin 12 and 23
Summary of Ehlers-Danlos syndrome?
AD CTD
Mostly affects type III collagen
Tissue more elastic than normal - causing joint hyper mobility and increased elasticity of the skin
Features -
elastic, fragile skin
joint hypermobility: recurrent joint dislocation
easy bruising
aortic regurgitation, mitral valve prolapse and aortic dissection
subarachnoid haemorrhage
angioid retinal streaks
mild can be managed in GP
MDT - PT, CBT, symptom relief, genetic counselling, celiprolol to prevent Aortic dissection, care with wound healing
Summary of Marfan’s syndrome?
AD CTD
Defect in FBN1 gene on chromosome 15 that codes for protein fibrillar-1
1 in 3000 people
Features
tall stature
high arched palate
arachnodactyly
Pectus excavatum
pes planus
scoliosis of >20 degrees
heart - dilation of aortic sinuses (aortic aneurysm, aortic dissection, aortic regurgitation), MV prolapse
lungs - repeated pneumothoraces
eyes - upwards lens dislocation, blue sclera, myopia
dural ectasia
Ghent criteria
Thumb and wrist sign
regular ECHO
beta-blocker and ACEi therapy
aortic dissection and CVD problems are leading cause of death
Summary of Raynauds phenomenon?
characterised by an exaggerated vasoconstrictive response of the digital arteries and cutaneous arteriole to the cold or emotional stress.
It may be primary (Raynaud’s disease) or secondary (Raynaud’s phenomenon). Raynaud’s disease typically presents in young women (e.g. 30 years old) with bilateral symptoms. Secondary causes = CTD (scleroderma, RA, SLE), leukaemia, type 1 cryoglobulinaemia, cold agglutinins, use of vibrating tools, drugs (OCP, ergot), cervical rib
Management
- if suspected secondary then referral to secondary care
first-line - calcium channel blocker (nifedipine)
IV prostacyclin (epoprostenol) infusions: effects may last several weeks/months
Summary of anti-phospholipid syndrome?
an acquired disorder characterised by a predisposition to both venous and arterial thromboses, recurrent fetal loss and thrombocytopenia.
Primary or secondary, commonly from SLE. Also other AI disorders, lymphoproliferative disorders, phenothiazines
Causes paradoxical rise in APTT - due to an ex-vivo reaction of the lupus anticoagulant autoantibodies with phospholipids involved in the coagulation cascade
Features of APS?
venous/arterial thrombosis
recurrent fetal loss
livedo reticularis
other features: pre-eclampsia, pulmonary hypertension
Libmann-Sacks endocarditis is a type of non-bacterial endocarditis where there are growths (vegetations) on the valves of the heart. The mitral valve is most commonly affected.
Ix for APS?
Antibodies = anticardiolipin, ant-beta2 glycoprotein, lupus anticoagulant
Thrombocytopenia
Prolonged APTT
Management for APS?
Primary thromboprophylaxis = low-dose aspirin
Secondary thromboprophylaxis = initial venous thromboembolic events: lifelong warfarin with a target INR of 2-3
recurrent venous thromboembolic events: lifelong warfarin; if occurred whilst taking warfarin then consider adding low-dose aspirin, increase target INR to 3-4
arterial thrombosis should be treated with lifelong warfarin with target INR 2-3
Pregnancy - LMWH plus aspirin. Warfarin CI’ed in pregnancy
What is Behcet’s disease?
complex inflammatory condition. presumed autoimmune-mediated inflammation of the arteries and veins
It characteristically presents with recurrent oral and genital ulcers.
It can also cause inflammation in a number of other areas such as the skin, gastrointestinal tract, lungs, blood vessels, musculoskeletal system and central nervous system.
There is a link with the HLA B51 gene. This is a prognostic indicator of severe disease.
relapsing remitting condition
more common in eastern Mediterranean (Turkey) and men
DDx for mouth ulcers?
Simple aphthous ulcers are very common
Inflammatory bowel disease (particularly Crohn’s disease)
Coeliac disease
Vitamin deficiency (B12, folate or iron)
Herpes simplex ulcers
Hand, foot and mouth disease (coxsackie A virus)
Squamous cell carcinoma
Features of Behcet’s disease?
Triad - mouth ulcers, genital ulcers, anterior uveitis
Mouth ulcers - at least 3 episodes, painful, red halo, oral mucosa, heal over 2-4 weeks
Genital ulcers - similar appearance to oral ulcers, ‘kissing ulcers’
Skin - Erythema nodosum, Papules and pustules (similar to acne), Vasculitic type rashes
Eyes - need emergency review by ophthalmology - Anterior or posterior uveitis, Retinal vasculitis, Retinal haemorrhage
MSK - morning stiffness, arthralgia, oligoarthritis (knee/ankle)
GI system - inflammation and ulceration
CNS - Memory impairment, Headaches and migraines, Aseptic meningitis, Meningoencephalitis
Veins - inflamed veins causing vein thrombosis - Budd Chiari, DVT, PE, cerebral venous sinus thrombosis
Lungs - pulmonary artery aneurysms
Ix and Tx for Behcet’s disease?
Clinical diagnosis
Pathergy test - abrasion on forearm, creates weal - positive in Behcets, Sweets syndrome and pyoderma gangrenosum
Tx:
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 ankylosing spondylitis?
HLA-B27 associated spondyloarthropathy
M>F (3:1)
aged 20-30
Features of ankylosing spondylitis?
Young man with lower back pain
Stiffness of insidious onset
Stiffness worse in AM - improves with exercise
Pain at night - improves on getting up
Features of ankylosing spondylitis on examination?
Reduced lateral flexion
Reduced forward flexion - Schober’s test
Reduced chest expansion
Other features of ankylosing spondylitis? (A’s)
Apical fibrosis
Anterior uveitis
Aortic regurgitation
Achilles tendonitis
AV node block
Amyloidosis
and cauda equina syndrome
peripheral arthritis (25%, more common if female)
Investigations for ankylosing spondylitis?
Inflammatory markers raised
HLA-B27 - little use in Dx
Plain X-ray of sacroiliac joints:
sacroilitis - subchondral erosions, sclerosis
squaring of lumbar vertebrae
bamboo spine - late, uncommon
syndesmophytes - due to ossification of outer fibres of annulus fibrosus
CXR - apical fibrosis
If still suspicion and -ve X-ray - MRI - shows bone marrow oedema
Spirometry - restrictive defect - pulmonary fibrosis, kyphosis and ankylosis of costovertebral joints
Management of ankylosing spondylitis?
Lifestyle - encourage regular exercise, NSAIDs, physiotherapy, avoid smoking, bisphosphonates if osteoporosis, treatment of complications
Steroids in flares
DMARDs - e.g., sulphasalazine - only useful if peripheral joint involvement
Anti-TNF therapy is persistently high disease activity despite conventional treatments - etanercept, MAB’s (infliximab, adalimumab)
Surgery - deformities of spine/joints
What is reactive arthritis?
Synovitis due to a recent infective trigger
Acute mono arthritis - usually knee. No infection in joint
Link with HLA B27
Part of seronegative spondyloarthropathy
Infections that trigger reactive arthritis?
Gastroenteritis - shigella, salmonella, campylobacter
STI - chlamydia
Features of reactive arthritis?
Acute mono arthritis - within 4 weeks of initial infection
Bilateral conjunctivitis
Anterior uveitis
Circinate balanitis
Keratoderma blenorrhagica
Management of reactive arthritis?
ABx until septic arthritis excluded
NSAIDs
Steroid injections
Systemic steroids - if multiple joints
Most resolve within 6 months and don’t recur. Recurrent cases may require DMARDs or anti-TNF medications
Ix of reactive arthritis?
Aspirate joint - gram staining, C&S, crystal examination
RFs for osteoarthritis?
Obesity
^ age
Occupation
Trauma
Female
FHx
Hypermobility
What is osteoarthritis?
Disease of ‘wear and tear’
Causes - genetic, overuse, injury
Synovial joints
Imbalance between cartilage being worn down and chondrocytes repairing it - causing structural issues in joint
Features of osteoarthritis?
CMC + DIP joint
Squaring of thumb base
Episodic joint pain - worse with movement, relieved by rest
Stiffness - few mins in AM
Painless nodes - Bouchards and Heberdens
Commonly affected joints - hips, knees, sacro-iliac joints, DIP, CMC, wrist, cervical spine
Ix for osteoarthritis?
If typical features = clinical Dx (over 45 and no stiffness)
Plain X-rays - LOSS
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts
X-ray changes don’t correlate with Sx
Oxford Hip score
Management of osteoarthritis?
Patient education
Lifestyle changes - WL, local muscle strenghening exercises, aerobic fitness
PT, OT, orthotics
Stepwise analgesia:
1 - paracetamol + topical NSAID (knee/hand)
2 - oral NSAID (+PPI)
3 - opiates (codeine/morphine)
Intra-articular steroid injections
Supports/braces
TENS
Shockin absorbing soles and shoes
Joint replacement - if severe
What is rheumatoid arthritis?
Autoimmune condition causing chronic inflammation of synovial lining of joints, tendon sheaths and bursa
Inflammatory and symmetrical polyarthritis
RFs for rheumatoid arthritis?
F>M
Middle age
FHx
Genetic associations - HLA DR4, HLA DR1
Features of rheumatoid arthritis?
Symmetrical distal polyarthropathy - PIP, MCP, wrist/ankle, MTP, cervical spine, large joints
Pain, swelling, stiffness (>1 in AM
Z-shaped thumb
Ulnar deviation of fingers at knuckle
+ve squeeze test
Swan neck + boutonniere
Systemic Sx - fatigue, WL, flu-like illness, muscle aches
Palindromic RA - self-limiting short episodes, affecting few joints
Atlantoaxial subluxation - can cause SCC - emergency
Extra-articular manifestations of RA?
Pulmonary fibrosis w/ pulmonary nodules (Caplan’s)
Bronchiolitis obliterans - small airway obstruction
Felty’s (RA, neutropenia, splenomegaly)
Secondary Sjogrens
Anaemia of chronic disease
CVD
Episcleritis + scleritis
Rheumatoid nodules
Lymphadenopathy
CTS
Amyloidosis
Dx of rheumatoid arthritis?
Clinical
American College of Rheum Criteria - joints involved, serology, inflammatory markers, duration
Ix of rheumatoid arthritis?
RF
Anti-CCP
Inflammatory markers
X-rays of hand:
Loss of joint space
Erosions (periarticular)
Subluxation
Soft tissue swelling
Juxta-articular osteoporosis
HAQ - functional ability of pt
NICE referral - persistent synovitis even if -ve serology, urgent if >3m
Management of rheumatoid arthritis?
Initial - DMARD +/- short course of bridging prednisolone
Flares - corticosteroids (oral + IM)
Surgery - if significant problems
DMARDS - methotrexate (monitor FBC + LFT), sulfasalazine, leflunomide, hydroxychloroquine
TNF-i - etanercept, infliximab, adalimumab - if inadequate response to 2 DMARDs
Abatacept - causes decreased T-cell proliferation and cytokine production
Monitoring Tx response - CRP and disease activity - DAS28
Poor prognostic features for RA?
RF +ve, anti-CCP +ve
Poor function at presentation
X-ray early erosions <2 years
HLA DR4
Insidious onset
Extra-articular features
Female
