Rheumatology Flashcards
ANA
Anti-Nuclear Antibodies
ANCA
Anti-Neutrophilic Cytoplasmic Antibodies
Anti-CCP
Anti-Cyclic Citrullinated Peptide
CTS
Carpal Tunnel Syndrome
DXA
Dual Energy X-Ray Absorptiometry
GPA
Granulomatosis with PolyAngiitis
PV
Plasma Viscosity
RF
Rheumatoid Factor
Causes of acute monoarthritis
Septic arthritis until proven otherwise - streptococcal most common Crystal-induced - gout - often men - pseudogout - often elderly women with severe OA Trauma - haemarthrosis
Causes of chronic monoarthritis
Infections - TB Inflammatory - Psoriatic arthritis - Reactive arthritis - Foreign body Non-inflammatory - OA - Traumatic - meniscal tear - Osteonecrosis - a/w prednisolone use - Neuropathic - Charcot's joint Tumours - rare
Causes of acute polyarthritis
Inflammatory arthritis - RA - PsA - Reactive arthritis Autoimmune arthritis - SLE - vaculitis Viral infection - HIV - Chikungunya - Parovirus Crystal arthritis - Uncontrolled gout
Caues of chronic polyarthritis
Inflammatory arthritis - RA - PsA - Reactive arthrits Autoimmune arthritis - SLE - vasculitis Crystal arthritis - Uncontrolled gout
Causes of arthritis of DIPJs
PsA
- nail dystrophy on affected digit
OA - common
- Heberden’s nodes
Features to ask for rheumatology history
Pain - location, duration, pattern, relief/exacerbation Stiffness Joint swelling and deformity Fatigue Weakness
Features of inflammatory disease
Morning stiffness - > 1 hour Better on activity Worse on resting Significant fatigue Systemic involvement
Features of mechanical disease
Morning stiffness < 30 mins Worse on activity Better on rest Minimal fatigue Non systemic involvement
Features of GALS assessment
Gait, Arms, Legs, Spine
- quick screening assessment for MSK disorders
Stages of Arms of GALS assessment
Inspect hands - palmar and dorsal
Assess pincer-grip and power-grip
Squeezes across 2nd-5th MCPJs - tenderness
Assess active elbow flexion/extension and pronation/supination
Assess active shoulder external rotation
Stages of Legs of GALS assessment
Inspects the legs - deformities, leg length, inequality, swellings or muscle wasting
Knee joint effusion
Passive knee flexion and extension
Hip flexion and internal rotation
Inspects feet for deformities and callosites
MTPJ squeeze - tenderness
Stages of Spine of GALS assessment
Inspect spine from behind and sides
Palpates supraspinatus
Tests cervical spine lateral flexion
Tests hip and lumbar spine flexion
Features of antalgic gait
Pain causes patient to reduce time spent on the affected side
Features of Trendelenberg gait
Due to poor hip abduction (weak gluteus medialis)
- pelvis drops to opposite side when standing on affected leg
Features of sensory ataxia gait
Wide-based stamping
- stamping attempt to compensate for lack of sensory input
- worse when eyes shut
Features of cerebellar ataxia gait
Wide-based staggering
- arms often flung out to try to improve balance
Features of hemiplegic gait
Narrow-based
- leg swung forwards
- toes scrap ground
Features of festinant of projectile gait
Difficulty initiating walking
- shuffling run
- reduced arm swing
Features of waddling gait
Duck-like
- due to bilateral hip muscle weakness
Features of psychogenic gait
Variable
- worse under observation
Define varus
Bow-legged
Define valgus
Knock-kneed
Sensory nerve supply to hand of median nerve
Skin over thenar eminence
Lateral 2/3 palm of hand
Palmar aspect of lateral 3.5 fingers
Dorsal fingertips of lateral 3.5 fingers
Motor supply of median nerve to hand
All muscles of anterior compartment except - flexor carpi ulnaris - medical parts of flexor digitorum profundus Intrinsic mucles of hand - LOAF - lateral two lumbricals - opponens pollicis - abductor pollicis brevis - flexor pollicis brevis
Features of median nerve palsy
Numbness of hand in median nerve distribution
- sparing of palm due to intact palmar cuaneous branch
Weakness of thumb opposition and abduction
Thenar eminance wasting
Sensory supply of ulnar nerve to hand
Skin over hypothenar eminence Medial 1/3 palm of hand Palmar aspect of lateral 1.5 fingers Medial 1/3 dorsum of hand Dorsal aspect of medial 1.5 fingers
Motor nerve supply of ulnar nerve to hand
Two muscles of forearm
- flexor carpi ulnaris
- flex ring and little fingers at DIPJs
Most intrinsic muscles of hand
Clinical features of ulnar nerve palsy
Numbness over hypothenar eminence and in ulnar nerve distribution of hand
Paralysis of flexor carpi ulnaris
- weak wrist flexion and adduction
Paralysis of medial two parts of flexor digitorum profundus
- weakness of flexion of ring and little finger DIPJs
Paralysis of most intrinsic mucles of hand
- weak MCPJ flexion and IPJ extension of ring and litter finger, loss of finger abduction and adduction, loss of opposition of little finger
Claw hand deformity
- fixed flexion of IPJs and hyperextension of MCPJs of ring and little fingers due to unopposed median nerve function
Interpreting blood tests in rheumatic disease
Hb - anaemia of chronic disease - RA - NSAIDs Platelets - rise in inflammation or bleeding - fall in SLE Neutrophils - rise in inflammation, sepsis and prednisolone usage - fall in SLE or with DMARD toxicity Lymphocytes - fall in SLE or DMARD incuded U&E - rise in NSAIDs, renal disease in lupus/vasculitis or gout Uric acid - elevated in gout - falls in inflammation LFTs - hepatic rise due to DMARD toxicity CK, ALT, LDH - rise in myositis
What does ESR test reflect the presence of?
Fibrinogen
Immunoglobulins
Advantages of ESR test
Widely understood
Well established in diagnosis and monitoring of GCA
Disadvantages of ESR test
No technique for calibration to test for accuracy
Poor reproducibility
Test takes 1 hour
Must be carried out within 4 hours of blood sampling
What does PV test reflect the presence of
Fibrinogen
Immunoglobulins
Advantages of PV test
Automatable
Sensitive
No affected by haemocrit
Measurement can be made on stored blood samples
Disadvantages of PV test
Not widely used - lack of familiarity with interpretation
What does CRP test reflect the presence of
C-Reactive Protein
Advantages of CRP test
Automatable
Very sensitive
Not affected by haematocrit
Measurement can be made on stored blood samples
Disadvantages of CRP test
Short lived indicator
Good at monitoring sepsis as rises and falls quickly
Autoantibodies in RA
Rheumatoid factor (RF)
- antibody directed against Fc fragment in human immunoglobulin G
- seropositive patients tend to have more severe disease
Anti-cyclic citrullinated peptide antibody (ACPA)
- more specific for RA for RF
Neither rise in disease flares
Antinuclear antibodies (ANA) and their disease associations
Anti-dsDNA = SLE - rises with disease activity Anti-RO and anti-LA = SLE, Sjogren's Anti-centromere and anti-Scl70 = Systemic Sclerosis Anti-Jo-1 = Polymyositis
What are anti-neutrophil cytoplasmic antibodies directed against?
Directed against enzymes present in neutrophils
Anti-neutrophil cytoplasmic antibodies and their disease associations
C ANCA = GPA, infection, neoplasia
- antibody to proteinase-3
P ANAC = microscopic polyangiitis, infection, neoplasia
- antibody to myelopreoxidase
Features of Human Leukocyte Antigen B27 (HLA-B27)
Class 1 surface antigen - found in 10% of white people - present in 90% of white people with AS Strongly associated with - ankylosing spondylitis - iritis - juvenile arthritis
Features of synovial fluid analysis
Gram stain and culture - septic arthritis
Polarized light microscopy
- negatively birefringent needle shaped crystals = gout
- positively birefringenet rhomboid shaped crystals = pseudogout
Uses of biopsies in rheumatoid diseases
Temporal artery - vasculitis in GCA
Muscle - polymyositis or dermatomyositis
Skin - vasculitis, dermatomyositis and SLE
Lip/salivary gland - Sjogren’s
Lymph node - rule out lymphoma or TB in SLE
Synovial - rare tumours or infection
Sural nerve - vasculitis with monoeuritis multiplex / peripheral neuropathy
Renal - vasculitis, SLE
Use of NSAIDs
Initial therapy
Provide symptomatic relief
Side effects of NSAIDs
GI problems
Renal impairment
Caution in patients with cardiovascular risk and asthma
Uses of corticosteroids
For inflammatory arthritis - used initially for a few weeks till DMARDs kick in
PO, IV, IM or directly into joint or soft tissue
Mainstay of treatment for PMR and GCA
Uses of non-biological DMARDs
RA, PsA, SLE and vasculitis
Started asap
Life-long
Most common non-biological DMARDs for inflammatory arthritis
Methotrexate
Hydroxychoroquine
Sulfasalazine
Effects of non-biological DMARDs
Sustained reductions in pain, stiffness and fatigue and improvements in physical function
Make take up to 3 months
Uses of biological DMARDs
RA, PsA and AS
Psoriasis and IBD
Biological DMARDs used in RA
Rituximab - CD-20 inhibitor
Tocilizumab - IL-6 inhibitor
Adalimumab (Humira) - TNF-alpha inhibitors
JAK inhibitors
Biological DMARDs used in AS and PsA
IL-17 antagonists
Biological DMARDs used in Crohn’s disease and its enteropathic arthritis
IL-12/23 blocker
Long term effects of DMARDs
Increased infection risk - immunosuppressive
Malignancy
Ractivation of hepatitis B and TB
Regular flu and pneumococcal vaccination - no live vaccinations
Drug treatment for osteoporosis
Calcium and vitamin D
Oral bisphosphonates
How to take oral bisphosphonates
Taken on empty stomach
Avoid food, water or other drugs for 30 mins post - maximise gut absorption
Swallow whole with water and avoid bending for 30 mins - reduce chance of ingestion
Drugs for acute attacks for crystal arthritis
NSAIDs
Colchicine
- avoid in renal failure
Intra-articular steroid injections
Drugs for prophylaxis for crystal arthritis
Allopurinol - urate-lowering
- flares common in first 6th months so cover with NSAIDs, colchicine or prednisolone
- avoid in renal failure
Feboxostat - used if allopurinol not tolerated
Side effects of Methotrexate
Nausea Oral ulcers Hair thinning Hepatitis, cirrhosis Pneumonitis Bone marrow suppression
Side effects of Hydroxycholorquine
GI disturbance
Retinal pigmentation and loss of vision - annual eye tests
No blood tests needed
Side effects of Sulfasalazine
GI upset
Rash
Hepatitis
Bone marrow suppression
Side effects of Azathioprine
GI upset
Bone marrow suppression
Side effects of Cyclophosphamide
Bone marrow suppression
Infertility
Increased cancer risk
Side effects of Ciclosporin
Renal impairment
Hypertension
Side effects of Leflunomide
GI upset
Hypertension
Bone marrow suppression
Hepatitis
What is dermatomyositis and polymyositis
Rare idiopathic muscle diseases
Characterised by inflammation of striated muscles
Epidemiology of dermatomyositis and polymyositis
M:F = 1:1
Peak onset 40-50 years
Symptoms and signs of dermatomyositis and polymyositis
Insidious onset of muscle proximal weakness - often painless
SOB
Rash
Raynaud’s syndrome common
Diagnostic criteria of dermatomyositis and polymyositis
Symmetricial proximal muscle weakness
Raised serum muscle enzyme levels
Typical electromyographic changes
Biopsy evidence of myositis
PM if >3
DM if rash and >2
Investigations of dermatomyositis and polymyositis
Raised inflammatory markers
Raised ALT (from muscle) with liver enzymes normal
80% antinuclear antibody positive
- specific auto-antibodies include anti-Jo-1 and anti-Mi2
Myositis on MRI
Treatment for dermatomyositis and polymyositis
High dose corticosteriods - mainstay for first few weeks
Inflammatory markers and CK used to monitor disease
EMG studies/MRI
Long term control
- MTX or AZA
- IV immunoglobulin
- Rituximab
In DM sun-protection and HCQ may reduce rash
Complications of dermatomyositis and polymyositis
Aspiration pneumonia - upper oesophagus is striated muscle
Respiratory failure - diaphragmatic involvement
Inflammatory lung disease
Increased malignancy risk (DM)
Features of dermatomyositis rash
Photosensitive
Post inflammatory hyper or hypo pigmentation
Appears in light exposed areas such as scalp, face and neck
Linear plaques on dorsal aspects of hands - Gottron’s papules
Dilated nail-fold capillaries, dry cracked palms and fingers
Periorbital oedema
Violet rash to eyelids
What is fibromyalgia
Central pain processing characterised by chronic widespread pain in all 4 quadrants of the body
Allodynia is heightened and painful response to innocuous stimuli
Pathogenesis of fibromyalgia
Can be induced by deliberate sleep deprivation
Sleep disturbance likely trigger in most patients
- EEG studies show reduced REM sleep and delta sleep wave
Causes hyper-activation in response to noxious stimulation, and neural activation in brain regions associated with pain perception in response to non-painful stimuli
Symptoms and signs of fibromyalgia
Pain Joint/muscle stiffness Profound fatigue Unrefreshed sleep Numbness Headaches Irritable bowel/bladder syndrome Depression and anxiety Poor concentration and memory "fibrofog"
Risk factors for fibromyalgia
Affects 5% of population
F:M = 9:1
Peak age onset 40-50
Onset may have an obvious trigger - emotional or physical
Treatment for fibromyalgia
Education CBT Physical - sleep improvement Drugs - pregabalin - amitriptyline
What is Giant Cell Arteritis
Chronic vasculitis of large and medium sized vessels that occurs among individuals over 50 years of age
Most commonly causes inflammation of arteries originating from the arch of the aorta
Risk factors for giant cell arteritis
Age is greates risk
Increased prevalence in individuals in northern latitude
2-4 times for common than women
Strong association with polymyalgia rheumatica
Genetic predisposition: HLA-DR4
Symptoms of giant cell arteritis
Headache - localised, unilateral, boring or lancinating in quality over the temple Tongue or jaw claudication upon mastication Constitutional symptoms Visual findings - weeks to months - amaruosis fugax - blindness - diplopia - blurring Scalp tenderness
How is diagnosis made of giant cell arteritis
Presence of two or more of the following in patients over 50
- raised ESR, CRP or PV
- new onset of localised headache
- tenderness or decreased pulsation of temporal artery
- new visual symptoms
- biopsy revealing necrotising arteritis
Treatment of giant cell arteritis
Prednisolone 60-100mg PO per day for at least 2 weeks before tapering down slowly
For acute onset visual symptoms consider
- 1g methylprednisolone IV pulse therapy 1-3 days
Low dose aspirin therapy to reduce thrombotic risks
What is gout?
Inflammatory arthritis related to a hyperuricemia
Acute gout can affect > 1 joint - commonly 1st metatarsalphalangeal joint
Associated with high risk of CVD
What causes gout?
Deposition of monosodium urate (MSU) crystals that accumulate in joints and soft tissues
- acute and chronic arthritis
- tophi - soft tissue masses
- urate nephropathy
- uric acid nephrolithiasis
Risk factors for gout
Non-modifiable - age > 40 - male Modifiable - increased purine intake - meats and seafood - alcohol intake - high fructose intake - obesity - CCF - coronary artery disease - dyslipidemia - renal disease - organ transplant - hypertension - smoking - DM
Conservative management of gout
Maintain optimal weight Regular exercise Diet modification Reduce alcohol consumption Smoking cessation Maintain fluid intake and avoid dehydration
Medical management of gout
Acute
- NSAIDs
- oral/IM steriods
- colchicine
Chronic - urate lowering therapy
- allopurinol and febuxostat - xanthine oxidase inhibitors and reduce urate formation
- benzbromarone and sulfinpyrazone - increase renal excretion of uric acid
Features of urate crystals
Negatively birefringent needles
Cause of pseudogout
Calcium pyrophosphate crystals
What is hypermobility
Pain syndrome in people with joints that move beyond normal limits
- due to laxity of ligaments, capsules and tendons
- thought that pain originates from microtrauma
- may affect any number of joints
Epidemiology of hypermobility
10% of population - only few symptomatic
Often familial
More common in women and asian people
Usually presents in childhood or young adulthood
May feature recurrent subluxations or disclocations
Symptoms and signs of hypermobility
Pain - around joints - worse after activity Fatigue Soft tissue rheumatism - epicondylitis Abnormal ski - papyraceous scars - hyperextensible - thin striae Marfanoid habitus Arachnodactyly Drooping eyelids Hernias and uterine/rectal prolapse
Treatment aims for hypermobility
Improve pain and reduce disability
Treatment for hypermobility
Strengthening exercises to reduce joint subluxation Work on posture and balance Splinting and surgical interventions Advice on pacing and goal setting Specialist pain management Paracetamol mainstay of pain relief
Features of hypermobility scoring
One point for each feature (left and right)
- put hands flat on floor with knees straight
- bend elbows backwards
- bend knee backwards
- bend thumbs back to front of forearm
- bend little finger at 90° to back of hand
Heritable connective tissue disorders
HSD
Marfan syndrome
Ehlers Danlos syndrome
What is osteoarthritis
Degenerative joint disorder
- progressive loss of articular cartilage accompanied by new bone formation and capsular fibrosis
Aetiology of osteoarthritis
Failure of normal cartilage subject to abnormal or incongruous loading for long periods
Damaged or defective cartilage failing under normal conditions of loading
Break up of cartilage due to defective stiffened subchondral bone passing more load to it
Key features of osteoarthritis
Loss of elasticity with a reduced tensile strength
Cellularity and proteoglycan content are reduced
Risk factors for osteoarthritis
Increasing age
Female
Obesity
Trauma and joint malalignment through trauma or muscle weakness
Symptoms and signs of OA
Hip, knee and spine most commonly affecgted
Pain provoked by movement and weight bearing
- intermittent at first by later constant
Inactivity gelling and feeling of joint giving way
X-ray signs of OA
Joint space narrowing
Subarticular sclerosis
Bone cyts
Osteophytes
Treatment aims for OA
Improve pain and reduce disability
Treatment for OA
Non-drug - strengthening and ROM exercises - weight loss - laterally wedged insoles (medial compartment OA) or walking stick Pharmacological - paracetamol - NSAIDs short term - topical NSAIDs and rubefacients and capsaicin - intra-articular corticosteriods Surgery - joint replacement
Features of nodal OA
More common in women Affects PIPJs (Bouchard's nodes) and DIPJs (Herberden's nodes) and thumb CMCJ
What is polymalgia rheumatica (PMR)
Clinical syndrome characterised by pain and stiffness of shoulders, hip girdles and neck
Primarily impacts the elderly
Associated with morning stiffness and elevated inflammatory markers
Epidemiology of PMR
Increasing incidence with age
- average onset 70 years
Associated with GCA
Symptoms of PMR
New sudden onset proximal limb pain and stiffness
Difficulty rising from chair of combing hair - proximal muscle involvement
Night time pain
Systemic symptoms
Signs of PMR
Decreased ROM of shoulders, neck and hips
Muscle strength normal
Muscle tenderness
Treatment for PMR
Prednisolone
- 15mg then taper down
Methotrexate
- steriod-sparing in relapsing patients
What is Raynaud’s phenomenon
Due to vasospasm of the digits
Painful
Characterised by typical sequence of colour changes in response to cold stimuli
Often precipitated by stress
Colour change in Raynaud’s phenomenon
White - inadequate blood flow
Blue - venous stasis
Red - re-warming hyperaemia
What is Raynaud’s syndrome
Idiopathic Raynaud’s phenomenon
Treatment of Raynaud’s syndrome
Measures to keep warm
Avoid smoking
Diseases associated with Raynaud’s phenomenon
Scleroderma SLE Dermatomyositis and polymyositis Sjogren's syndrome Use of heavy vibrating tools Cervial rib Drug induced - beta blockers
Treament for Raynaud’s phenomenon
Keep warm and avoid smoking
CCB
Phosphodiesterase-5 inhibitors and prostacyclins
Complications of Raynaud’s phenomenon
Digital ulcers
Severe digital ischaemia
Infection
Gangrene
What is rehumatoid arthritis
Autoimmune disease associated with antibodies to Fc portion of IgG (rheumatoid factor) and anti citrullinated cycle peptide (anti-CCP)
Pathogenesis of RA
Citrullination of self-antigens which are recognised by T & B cells which can then produce antiboides (RF and anti-CCP)
Stimulated macrophages and fibroblasts release TNFalpha
Inflammatory cascade leads proliferation of synoviocytes -> grow over cartilage and restrict nutrients and cartilage damaged
Activated macrophages stimulate osteoclast differentiation -> bone damage
Epidemiology of RA
Female - 3:1
30-50 years old
Signs of RA
Usually MCPs/PIPs/MTPs - spares DIPs
Pain > 6 week history
Morning stiffness > 30 mins
Commonly fatigue and malaise
Symptoms of RA
Soft tissue swelling and tenderness first
Ulnar deviation/palmar subluxation of MCPs
Swan-neck and Boutonniere deformity
Rheumatoid nodules - elbow
Check median nerve - carpal tunnel association
Investigation for RA
RF and anti-CCP
FBC - normocytic anaemia
WCC - rule out sepsis
X-ray changes in establised disease - USS/MRI more sensitive in early disease
Treatment for RA
DMARD monotherapy - methotrexate Combintation DMARDs - lefluomide, hydroxychloroquine, sulfasalazine Steriods - acutely Symptom control with NSAIDs + PPI cover Biologics Supportive - OT, PT, podiatry, psychological
Extra-articular manifestations of RA
3Cs - carpal tunnel syndrome - elevated cardiac risk (CVD) - cord compression - atlanto-axial subluxation 3As - anaemia - amyloidosis -> CKD and nephrotic syndrome - arteritis 3Ps - pericarditis - pleural disease - pulmonary disease 3Ss - Sjogren's - scleritis - splenic enlargement
X-ray features of RA
Loss of joint space
Erosions
Soft tissue swelling
Subluxation
What is Sjogren’s syndrome
Chronic autoimmune inflammatory disorder
- characterised by diminished lacrimal and slaivary gland secretion
Symptoms of Sjogren’s syndrome
Myalgia Arthralgia Dry mouth Fatigue Raynaud's phenomenon Enlarged parotids Dry eyes
Investigations for Sjogren’s syndrome
Anti-Ro and anti-La antibodies
RF and anti ds-DNA antibodies
Schirmer’s test - measures tear volume
Salivary gland biopsy
Treatment for Sjogren’s syndrome
Symptomatic
- avoid dry or smoky atmospheres
- dry eyes = artificial tears
- dry mouth = artificial saliva, sugar free gum
- skin emolliens
- vaginal lubricants
Diseases associated with Sjogren’s syndrome
RA SLE Coeliac disease PBC Auto-immune thyroid disease
What are spondyloarthropathies?
Group of conditions that affect the spine and peripheral joints and associated with presence of HLA-B27
Conditions of spondyloarthopathies
Ankylosing spondylitis
Enteropathic arthritis
Psoriatic arthritis
Reactive arthritis
Common clinical features of spondyloarthropathies
Sacroiliac/axial disease - back/buttock pain
Inflammatory arthropathy of peripheral joints
Enthesitis - inflammation of tendon insertions
Extra-articular features - skin, gut, eye
Features of ankylosing spondylitis
Long term inflammation of joints of the spine
Usually young men (teens-mid-thirties)
Complications of AS
Osteoporosis Spinal fractures CVS Pneumonia Kidney disease
Signs and symptoms of AS
Bilateral buttock pain, chest wall and thoracic pain
Exam often normal early
Later - loss of lumbar lordosis, exaggerate thoracic kyphosis, reduced chest expansion
Raised CRP
MRI spine and SI joints - inflammation
Treatment for AS
NSAIDs
Physio
TNF inhibitors
IL-17 inhibitors
Epidemiology of psoriatic arthritis
10% of patients with psoriasis
M=F
Features of psoriatic arthritis
Oligo-arthritis
Dactylitis or “sausage” digit
Can be symmertrical or monoarthritis
Investigations for psoriatic arthritis
CRP often raised
Central joint erosions seen early on USS or MRI
- pencil in cup x-ray appearance
Treatment of psoriatic arthritis
NSAIDs DMARDs - TNF inhibitors - IL-17 inhibitors - IL12/23 inhibitors
What is reactive arthritis
Sterile synovitis developing after a distant infection
- post dysentery - Salmonella, Shigella, Campylobacter
- urethritis/cervicitis - Chlamydia trachomatis
Presentation of reactive arthritis
Few days - 2 weeks post infection Acute asymmetrical lower limb arthritis develops Other features incluce - circinate balanits - keratoderma blennorrhagica - conjunctivitis - uveitis - enthesitis
Investigations for reactive arthritis
Serology/microbiology
Inflammatory markers raised
Joint aspirate to rule out septic/crystal arthritis
Treatment for reactive arthritis
Treat infection
NSAIDs and joint injections
Most resolve within 2 years - if not may need DMARDs
What is enteropathic arthrits
Inflammatory condition affecting the spine and other joints
- associated with IBD
Types of peripheral disease of IBD
Type 1 - oligoarticular - asymmetric - correlation with IBD flares Type 2 - polyarticular - symmetrical - less correlation with IBD flares
Treatment of enteropathic arthritis
DMARDs
- TNF inhibitors treat both bowel and arthritis
NSAIDs can flare IBD
Extra-articular manifestations of ankylosing spondylitis
Anterior uveitis Aortic incompetence AV block Apical lung fibrosis Amyloidosis
Features of inflammatory back pain
Insidious onset Pain at night - improvement with getting up Age onset < 40 Improvement with exercise No improvement with rest
What is systemic lupus erythmatosus (SLE)?
Autoimmune disease
- inadequate T cell suppressor activity with increased B cell activity
- antibodies to certain cell nucleus components
Complex multisystem disease charactersied by remissions and flares
Common signs and symptoms of SLE
Serositis - pleurisy, pericarditis Oral ulcers - painless Arthritis - small joints, non-erosive Photosensitivity - malar/discoid rash Blood disorders - low WCC, lymphopenia, thrombocytopenia, haemolytic anaemia Renal involvement - glomerulonephritis Autoantibodies - ANA positive in 90% Immunologic tests - low complements Neurologic disorder - seizures or psychosis
Investigations for SLE
Raised ESR or plasma viscosity - normal CRP Anaemia and leukopenia common 95% antinuclear antibody positive - anti-Ro and anti-La common - anti-dsDNA rises with disease activity - anti-phospholipid antibodies C3 and C4 fall with disease activity Urinarlysis for renal disease Skin or renal biopsy can be diagnostic
Treatment for SLE
Sun protection
Advice on healthy lifestyle in view of CVS risk
Hydroxychloroquine for rash and arthralgia
Mycophenolate mofetil, azathioprine and rituximab common used
Short course prednisolone for flares
Epidemiology of SLE
9x more common in women
Peak onset in early adulthood
What is systemic sclerosis
Multisystem autoimmune disease
Increased fibroblast activity resulting in abnormal growth of connective tissue
-> vascular damage and fibrosis
Types of systemic sclerosis (SSc)
Limited
Diffuse
Features of limited SSc
Calcinosis cutis - calcium deposits in skin
Raynaud’s phenomenon
Oesophageal dysmotility
Sclerodactyly - thickening + tightness of skin of fingers/toes -> ulcers
Telangiectasia - widened venules -> threadlike red lines on skin
Features of diffuse SSc
Less common but higher mortality risk
Sudden onset skin involvement - proximal to elbows/knees
Investigations for SSc
Inflammatory markers normal
X-ray hands - calcinosis
CXR, HRCT, PFT - pulmonary disease
ECG + ECHO - PA hypertension, CCF, myocraditis and arrhythmias
Antibodies is SSc
Positive ANA in 90% patients Limitied SSc - anti-centromere Diffuse SSc - Scl-70 (topisomerase) - anti RNA polymerase III
Treatment for SSc
No cure
Psychological support
Calcium antagoinst / sildenafil / iloprost for Raynaud’s
Methotrexate and mycophenolae mofetil reduce skin thickening
ACEi prevent hypertensive crisis and reduce mortality from renal failure
Short course prednisolone for flares
PPI for GI symptomrs
What is vasculitis
Inflammatory blood vessel disorder
Features of vasculitis
Constitutional symptoms
Raynaud’s
MSK - arthralgia, myalgia, proximal muscle weakness
CNS/PNS - headaches, visual loss, tinnitus, stroke, seizure, encephalopathy
Nose bleeds
Heart/lung - pericarditis, cough, chest pain, haemoptysis, dyspneoa
Abdominal pain
Haematuria
Neuropahty, digital ulcers/ischaemia
Signs of vasculitis
Hypertension
Palpable purpura, livedo reticularis, nodules, digital ulcers, gangrene, nail bed capillary changes
Scleritis, uveitis, episcleritis
Crackles, pleural rub, murmurs, arrhythmias
Abdominal tenderness and organomegaly
Types of vasculitis
Small-vessel - microscopic polyangiitis (MPA) - granulomatosis with polyangiitis (GPA) - eosinophilc granulomatosis with polyangiitis (EGPA) - IgA vasculitis Medium-vessel - polyarteritis nodosa (PAN) - Kawasaki disease (KD) Large-vessel - Takayasu arteritis (TAK) - giant cell arteritis (GCA)
Causes of vasculitis
Primary Secondary - infections - drugs - malignancy - connective tissue diseases
Diagnostic tests for vasculitis
ANA, ANCA and RF antibodies Complement levels C3 and C4 Hep screen for B and C and HIV Cryoglobulins Serum and urine protein
Treatment of vasculitis
Rule out infection and stop offending drugs
Corticosteriods
DMARDs - cyclophosphamide, methotrexate, azathioprine, leflunomide, mycophenolate mofetil, rituximab
