Rheumatology Flashcards
Clinical Features of SLE (+subsequent investigations)
(SOAP BRAIN)
Skin/Serositis
Oral Ulcers
Arthritis
Photosensitivity
Blood Disorders
Renal Involvement
Autoantibodies
Immunological Tests
Neurological Disorders
1.) Skin/Serositis - Raynaud’s, digital ulcers, alopecia, abnormal nail folds, livedo reticularis
- serositis: pleurisy, pericarditis (chest pain or SOB)
- can present as chest pain or SOB
2.) Oral Ulcers - often painless, the palate is most specific
- can also have digital ulcers
3.) Arthritis - non-erosive, affects small joints
- acute or chronic polyarthritis w/ insidious onset
4.) Photosensitivity - butterfly/malar or discoid rash
- subacute cutaneous rash, bullous rash
- skin biopsy can be diagnostic
5.) Blood Disorders - haemolytic anaemia, leukopenia, thrombocytopenia, lymphopenia, Raynaud’s syndrome
- FBC: ↓Hb, ↓WCC, ↓Plts, ↓lymphocytes
- others: ↑ESR/↑plasma viscosity, normal CRP
6.) Renal Involvement - glomerulonephritis (nephritic)
- urinalysis: haematuria +/- proteinuria, U+Es
- renal biopsy can be diagnostic for SLE
7.) Autoantibodies - anti-dsDNA and ANA main ones
- Anti-dsDNA rises w/ disease activity
- Anti-Ro, Anti-La are common
- anti-histone antibodies raised in drug-induced lupus
- CLOT syndrome: anti-cardiolipin and lupus anticoagulant, signs are: Coagulation defect (↑APTT), Livedo reticularis, Obstetric complications (miscarriages), Thrombocytopenia
- treated w/ low dose aspirin or warfarin (INR 2-3)
8.) Immunological Tests - low complements
- C3 and C4 fall w/ ↑ disease activity
9.) Neurological - headaches, seizures, psychosis,
- visual disturbance caused by retinal vasculitis
- TIA, CVA
Systemic Lupus Erythematosis (SLE)
Pathophysiology
Triggers
Demographics
History Taking
Treatment
1.) Pathophysiology - multisystem autoimmune disease due to anti-nuclear antibodies (ANA), binding to dsDNA
- type 3 hypersensitivity reaction
2.) Triggers - UV light, drugs (CHIMP)
- UV light: alters DNA structure –> ↑immungenicity
- C: carbamazepine, chlorpromazine
- H: hydralazine
- I: isoniazid, infliximab (also causes renal damage)
- M: minocycline, minoxidil
- P: pencillamine, procainamide, pyrazinamide
- drug incuded lupus often has pulmonary involvement and is ANA +ve, anti-dsDNA -ve and anti-histone antibodies positive
3.) Demographics - young women
- 9x more common in women, often also have FH
- peak age of onset is in early adulthood
4.) History Taking - gloves and sweater approach
- gloves: raynauds, joint pain/swelling, hand rash
- sweater: hair loss, mouth ulcers, facial/truncal rash
proximal myalgia, pleuritic/pericardial chest pain
- systemic: fever, malaise, night sweats, weight loss,
5.) Treatment
- advice: healthy lifestyle (↑CVD risk), sun protection, vitD (deficiency from sun protection)
- hydroxychloroquine for rash and joint pains
- mycophenolate mofetil, azathioprine, rituximab
- prednisolone for flares
Raynaud’s Phenomenon
What is it?
Associated Diseases
Clinical Features
Management
1.) What is it? - condition due to vasospasm of the digits characterised by a typical sequence of colour changes
- precipitated by the cold stimulus as well as stress
- common in young women, may be familial
- complications: digital ischaemia/ulcers/infections
2.) Underlying Pathophysiology - esp if in >30s
- associated diseases: SLE, dermatomyositis, polymyositis, scleroderma, Sjogren’s syndrome
- rheumatic cause: abnormal nail-fold capillaries or puffy fingers or photosensitive rash
- physical causes: use of heavy vibrating tools, cervical rib, cryoglobulinaemia (‘sticky blood’)
- drug-induced: ß-blockers
3.) Clinical Features - painful, colour changes:
- triphasic: white (inadequate blood flow) –> blue (venous stasis) –> red (re-warming hyperaemia, causing pain)
- symmetrical, bilateral pattern, episodes last minutes
- in underlying disease, may last hours and often asymmetrical, only affecting a few digits
4.) Management
- keep warm (wear gloves), avoid smoking
- Rx: CCBs (nifedipine), phosphodiesterase-5i, prostacyclins
- avoid beta-blockers as can worsen the condition
Rheumatoid Arthritis
Pathophysiology
Risk Factors
Clinical Features
Examinations
1.) Pathophysiology - autoantibodies to Fc portion of IgG (RF) and citrullinated cyclic peptide (CCP)
- ↑inflammatory cells (T/B cells) –> ↑TNF-a –> ↑IL-6 leads to synovitis and joint destruction
- type 3/4 hypersensitivity reaction
2.) Risk Factors
- 30-50 yrs, female (3:1), smoking, FH
3.) Clinical Features - symmetrical polyarthritis w/ insidious onset
- >6wks, morning stiffness >30m, better w/ activity
- affects mainly MCPs and PIPs (often spares DIPJs)
- other joints: MTPJs, wrist, elbow, shoulder, knee
- systemic sx: fatigue, lethargy, pyrexia, weight loss
4.) Examinations
- soft tissue swelling, warmth, tenderness
- ulnar deviation and palmar subluxation of MCPJs
- Swans Neck and Boutonniere’s deformities
- rheumatoid nodules common in elbows, Achilles’ tendon, fingers
- often associated w/ carpal tunnel syndrome
- muscle wasting
Diagnosing and Managing Rheumatoid Arthritis
Investigations
EULAR Classification
Management
1.) Investigations
- routine bloods: ↑CRP, ↑ESR, ↓Hb (anaemia of CD)
- RF and anti-CCP/ACPA (more specific)
- X-ray (LESS): loss of joint space, erosions (periarticular), subluxations, soft tissue swelling
- ultrasound or MRI in early stages
2.) EULAR Classification - diagnostic criteria for RA using 4 categories, score >6/10 definitive for RA
- joint distribution (0-5): ↑no and smaller joints ↑score
- serology (0-3): RF and ACPA, the more +ve, ↑score
- duration (0-1): <6wks = 0, >6wks = 1 point
- acute phase reactants: abnormal CRP/ESR = 1 point
3.) Management - DMARDs, NSAIDs, biologics
- NSAIDs w/ PPI cover for symptom (pain) management
- DMARDs: methotrexate (weekly), can combine w/ sulfasalazine, hydroxychloroquine, leflunomide
- biologics: anti-TNFs, (etanercept), CD20i (rituximab), IL-6i (tociluzumab), JAKi
- steroids for flare-ups: IM methylprednisolone or PO prednisolone or intra-articular injections, IV steroids ARE NOT used in flares of RA
- non-pharmacological: OT/PT, podiatry, psychological
Extra-articular Manifestations of RA (CAPS)
3Cs
3As
3Ps
3Ss
1.) 3Cs
- Carpal tunnel syndrome,
- ↑CVD risk
- (spinal) Cord compression: atlanto-axial subluxation
2.) 3As
- Anaemia: anaemia of chronic disease, normocytic
- Amyloidosis (v. rare), can –> CKD and nephrotic syn..
- Arteritis (now rare) can –> vasculitis, mononeuritis
3.) 3Ps
- Pleural Disease: pleural effusion, pleurisy
- Pulmonary Disease: bronchiectasis, fibrosis, alveolitis
- Pericarditis
4.) 3Ss
- Sjogren’s Syndrome
- Scleritis
- Splenic enlargement (w/ neutropenia = Felty’s syn…)
Spondyloarthropathies
What are They?
Reactive Arthritis
Psoriatic Arthritis
Ankylosing Spondylitis
Enteropathic Arthropathy
What are They? - group of seronegative inflammatory conditions associated with HLA-B27
- present with asymmetrical oligo/mono-arthritis
- axial arthritis, tendinopathy, dactylitis, extra-articular features
- enthesitis (worse prognosis): Achilles tendinitis, lateral/medial epicondylitis, plantar fasciitis
- more common in men and young adults
1.) Reactive Arthritis - often develops after infection, GI: (salmonella/shigella/campylobacter) or GU (chlamydia)
- presents few days - 6wks post-infection and often as acute asymmetrical lower limb arthritis
- others: eyes (conjunctivitis, uveitis), mouth ulcers, enthesitis, skin (keratoderma blennorrhagia)
- stool/urine sample, ↑CRP, joint aspirate (cloudy/yellow, culture negative, no crystals) to exclude septic arthritis
- Rx: NSAIDs, ?Abx, joint injections > oral prednisolone, DMARDs if chronic (sulfasalazine, methotrexate)
2.) Psoriatic Arthritis - in 10% of patients w/ psoriasis
- asymmetrical oligoarthritis w/ swelling + dactylitis,
mainly fingers and toes, other joints maybe affected
- nail lesions e.g. pitting, can lead to arthritis mutilans
- CRP should be raised
- X-ray: periarticular erosions and bone resorption, ‘pencil in cup’ appearance USS/MRI may also central joint erosions)
- Rx: NSAIDs, DMARDs, TNFi, IL-17/12/23 inhibitors
3.) Ankylosing Spondylitis - chronic inflammation of the spine and other parts of the body, affects young men
- bilateral buttock pain, chest wall and thoracic pain
- ↓chest expansion, ↓lordosis, ↑kyphosis, + Schober’s
- extra-articular (5As): anterior uveitis, AV block, aortic incompetence, apical lung fibrosis, amyloidosis
- X-ray: sacroiliitis on pelvic X-ray, ‘bamboo spine’ (subchondral erosions, vertebral body squaring, ligament calcification and syndesmophytes)
- MRI spine and scaroiliac joints
- Rx: NSAIDs, physio, TNFi, IL-17i (NO DMARDS)
4.) Enteropathic Arthropathy - in 10-20% of IBD patients
- 1/3 develop axial disease, 2/3 w/ peripheral arthritis:
- 1: asymmetrical oligoarthritis correlating to IBD flares
- 2: symmetrical polyarthritis w/o correlation to flares
- Rx: DMARDs, TNFi, avoid NSAIDs (cause flares)
Osteoarthritis
What is it?
Risk Factors
Clinical Features
Examination
Investigations
1.) What is it? - progressive loss of articular cartilage and remodelling of the underlying bone
- loss of articular cartilage due to inflammatory cells
- bone remodelling due to chondrocytes
2.) Risk Factors for Primary OA
- ↑age, obesity, female, manual labour, trauma, FH
3.) Clinical Features - distal, large joint pain/stiffness worsened by activity and relieved by rest
- pain worsens through the day, stiffness improves
- sx are insidious, chronic, and gradually worsening, starts off intermittent then can become constant
4.) Examination
- main joints: hip, knee, hands (DIP, PIP, 1st CMCJ),
spine (C-spine, lumbar), feet (1st TMTJ)
- bouchard’s (PIPJ) nodes and herbeden’s (DIPJ) nodes
- prolonged OA leads to deformity and reduced ROM
- hip/knee: wasting of vastus medialis –> bow legs
5.) Investigations - to exclude differentials
- bloods: rule out inflammatory or infective
- X-ray: confirm diagnosis, exclude fractures
- LOSS: loss of joint space, osteophytes, subchondral sclerosis, subchondral bony cysts
Gout (+Pseudogout)
Pathophysiology
Risk Factors
Clinical Features
Pseudogout
1.) Pathophysiology - inflammatory arthritis due to collection of monosodium urate crystals in a joint
- often due to hyperuricaemia, however, not all cases of gout will have high serum urate levels
2.) Risk Factors - similar to CVD (gout and CVD linked)
- age >40, male (oestrogen is protective),
- alcohol, smoking, obesity, dyslipidaemia, HTN, DM, HF
- ↑urate drugs: thiazide and loop diuretics, aspirin
3.) Clinical Features - acutely hot, red, swollen joint
- mainly 1st MTPJ, but also knee, elbow, wrist, fingers
- episodic, triggered by stress/illness/dehydration
- flare-ups can last from days to weeks
- gout tophi are nodular masses of crystals deposited in soft tissues, mainly occurs in fingers
4.) Pseudogout - mimics gout, deposits of calcium pyrophosphate crystals within the joint
- affects proximal joints, knee and wrist most common
- risk factors: older women w/ OA, hypercalcemia
- also treated with NSAIDs
Investigations and Management of Gout (+Pseudogout)
Investigations
Management
1.) Investigations
- joint aspiration: thin needle-shaped urate crystals (pseudogout is polygonal crystals)
- polarisation microscopy: negatively birefringent (pseudogout is postively birefringent)
- X-rays: soft tissue swelling, bony erosions, (pseudogout shows chondrocalcinosis (↓joint space, cartilage calcification)
2.) Management
- treated acutely with NSAIDs, steroids, colchicine
- allopurinol (↓uric acid) if chronic, given after initial attack (worsens initially) to prevent remission
- reduce risk factors: ↓smoking, exercise etc…
Management of Osteoarthritis
Conservative
Medical
Surgical
1.) Conservative
- weight loss, joint protection (insoles, walking stick)
- heat/ice packs, joint supports,
- physiotherapy, strengthening and exercise
2.) Medical
- simple analgesics and topical NSAIDs
- intra-articular steroid injections
3.) Surgical - if others fail, options include:
- total joint arthroplasty is gold standard in patients with severe end-stage symptomatic osteoarthritis
- joint replacements last roughly 20 years
- others: osteotomy, arthrodesis
Giant Cell (Temporal) Arteritis
Pathophysiology
Diagnostic Features
Management
1.) Pathophysiology - chronic vasculitis of large and medium-sized vessels causing inflammation of arteries
- superficial temporal artery is most common
- can cause acute visual loss as occlusive arteritis –> anterior ischaemic optic neuropathy (AION)
- associated with HLA-DR4 gene
- risk factors: >50s, FH, caucasian, female, PMR
2.) Diagnostic Features - >50 w/ 2+ of following features:
- unilateral headache localised in the temporal region
- tenderness/↓pulsation of temporal artery
- visual sx: blurring, diplopia, blindness, amau.. fugax
- other sx: jaw claudication, tongue discomfort
- constitutional sx: fever, night sweats, weight loss
- bloods: ↑ESR, ↑CRP
- temporal artery biopsy: reveals necrotizing arteritis
3.) Management - steroids (don’t wait for biopsy)
- PO prednisolone (40mg, 60mg if visual sx) OD for 2wks then taper
- visual sx: IV methylpred (1g) pulse therapy (1-3d)
- low dose aspirin to reduce thrombotic risk
Polymyalgia Rheumatica
What is it?
Clinical Features
Investigations
Treatment
1.) What is it? - clinical syndrome characterised by pain and stiffness of the shoulder, neck, and hip girdles
- mainly affects the elderly, >50, avg onset is 70yrs
2.) Clinical Features
- sudden onset of proximal limb pain and stiffness
- difficulty rising from chair or combing hair
- pain at night, constitutional symptoms
- ↓ROM of shoulders, neck, and hips
- normal muscle strength (limited by pain/stiffness)
- muscle tenderness
3.) Investigations - ↑inflammatory markers (ESR/CRP)
- usually always raised
- CK is normal (raised in polymyositis)
4.) Treatment
- PO prednisolone (15mg) OD for around 18 months, produces rapid response, then tapered down slowly
- methotrexate in relapsing patients (steroid-sparing)
- often given with bisphosphonates and Ca/vitD
Fibromyalgia
What is it?
Clinical Features
Investigations
Management
1.) What is it? - disorder of central pain processing –>
widespread pain in all 4 quadrants of the body
- sleep disturbance is underlying pathophysiology
- affects mainly middle aged women (40-50s, 9:1)
2.) Clinical Features
- joint and muscle pain and stiffness, numbness
- headaches, fatigue, unrefreshed sleep, IBS/bladder
- depression, anxiety, poor concentration and memory
- normal MSK and neuro examinations, may have tender points on palpation e.g. over supraspinatus
3.) Investigations - bloods to exclude other pathology
- FBC, CRP, ESR, U+Es, LFTs, TFTs, Ca,
- will all be normal in fibromyalgia
4.) Management
- improve sleep and physical activity levels
- amitryptiline (low dose), pregabalin, no opiates
- education about condition, CBT
Hypermobility Spectrum Disorder
What is it?
Clinical Features
Management
1.) What is it? - pain syndrome in the ‘double-jointed’
- due to laxity of ligaments, capsules, and tendons
- can affect any number of joints
- common in women and Asians, often familial
- link to Marfan’s and Ehlers Danlos syndrome
2.) Clinical Features - joint pain worse after activity
- skin: thin, striae, hyperextensible, papyraceous scars
- epicondylitis, marfanoid habitus, drooping eyelids
- myopia, hernias, uterine/rectal prolapses
- Beighton scoring system
3.) Management
- strengthening exercises, work on posture/balance
- paracetamol, specialist pain management
- splinting, surgical intervention may be needed
