Rheumatology Flashcards
Back pain red flags
<20 or >55, acute onset in elderly, constant/progressive pain, nocturnal pain, worse pain on being supine, fever/night sweats/ weight loss, malignancy, abdo mass, thoracic back pain, morning stiffness, bilateral/alternating leg pain, neurological disturbance, sphincter disturbance, current or recent infection, immunosuppression, leg claudication or exercise-related leg weakness/numbness
Causes of back pain based on age
15-30
30-50
>50
15-30: prolapsed disc, trauma, fractuer, ank spon, spondylolisthesis, pregnancy
30-50: degenerative spinal disease, prolapsed disc, malignancy (primary, or secondary from lung/ breast/ prostate/ thyroid/ kidney
>50: degenerative, osteoporotic vertebral collapse, pagets, malignancy, myeloma, spinal stenosis
Other (rare) causes: cauda equina, psoas abscess, spinal infection (TB, Staph, E coli)
Investigations for back pain
FBC, ESR and CRP (myeloma, infection, tumour), U+E, ALP (pagets), serum/urine electrophroesis (myeloma), PSA
X-Ray
MRI IS THE IMAGE OF CHOICE
L2 Nerve root lesion
- where the pain is
- where the weakness is
- reflex affected
Pain across upper thigh
Weakness in hip flexion and adduction
No reflex affected
L3 Nerve root lesion
- where the pain is
- where the weakness is
- reflex affected
Pain across lower thigh
Weakness in hip adduction and knee extension
Knee jerk affected
L4 Nerve root lesion
- where the pain is
- where the weakness is
- reflex affected
Pain across knee to medial malleolus
Weakness in knee extension, foot inversion and dorsiflexion
Knee jerk affected
L5 Nerve root lesion
- where the pain is
- where the weakness is
- reflex affected
Pain across lateral shin to dorsum of foot and great toe
Weakness in hip extension and abduction, knee flexion, foot and great toe dorsiflexion
Great toe jerk affected
S1 Nerve root lesion
- where the pain is
- where the weakness is
- reflex affected
Pain across posterior calf to lateral foot and little toe
Weakness in knee flexion, foot and toe plantar flexion and foot eversion
Ankle jerk affected
What causes osteoarthritis?
Mechanical (wear and tear): localised loss of cartilage, remodelling of adjacent bone, associated inflammation
What joints are affected in OA?
Large weight bearing joints (hip, knee), carpometacarpal joint, DIP, PIP joints
Signs and symptoms of OA
Pain and crepitus with movement, improves with rest, joints may feel unstable, unilateral symptoms, no systemic upset
Signs: joint tenderness, derangement and bony swelling (Heberdens at DIP and Bouchards at PIP), reduced range of movement, crepitus on movement, mild synovitis
Investigations for OA
X-Rays: (LOSS) loss of joint space, osteophytes at joint margin, subchondral sclerosis, subchondral cysts
CRP may be raised
Management of OA
Exercise, weight loss
Analgesia: regular paracetamol (+ topical NSAIDs if knee or hand) are first line.
Second line: codeine, short-term oral NSAID (+ PPI), intra-articular steroids, topical capsicain
Heat or cold packs at the site of pain, walking aids, stretching/manipulation, TENS
Surgery: joint replacement
NSAID risks
GI bleed (ulcers, perforation) - prescribe with PPI if >45 and those with increased risk of GI bleeding. Avoid concomitant prescribing of anticoags, antiplatelets, SSRIs, spironolactone, steroids and bisphosphonates -> increased risk of bleeding
Cardiovascular (MI, stroke) - diclofenac is CI if history of MI/PVD/stroke/HF, naproxen has lowest cardiovascular risk
Renal injury - higher if already on diuretics, ACEI/ARB. Risk also higher if elderly/HTN/DM
Septic arthritis causative organisms and most common joint affected
Most common is Staphylococcus aureus
Young sexually active adults - Neisseria gonorrhoeae should be considered
Most common location in adult = knee
Kocher criteria for septic arthritis diagnosis
fever >38.5
non-weight bearing
Raised ESR
Raised WCC
Management of septic arthritis
IV abx which cover gram pos cocci (flucloxacillin, clindamycin if pen allergic)
Abx for 6-12 weeks
Needle aspirate to decompress joint
May require arthroscopic lavage
Investigations for septic arthritis
Bloods: ESR (raised), FBC (raised WCC), blood culture
Urgent joint aspiration for synovial fluid microscopy and culture
X-ray
Aetiology of rheumatoid arthritis
Which gender is most affected
Autoimmune
most commonly seen in females
Which joints are typically affected in RA
MCP, PIP
Typical signs and symptoms of RA
Morning stiffness (>30m), improves with use, bilateral symptoms Systemic upset (fatigue, fever, weight loss) Extra-articular manifestations Signs: bilateral symmetrical swollen painful and stiff small joints, ulnar deviation and subluxation of the wrist and fingers Boutonnière and swan neck deformities of the fingers, z-deformity of the thumbs, hand extensor tendons may rupture Positive squeeze test - pain on squeezing across metacarpal or metatarsal joints
Extra-articular manifestations of RA
Nodules: elbows, lungs, cardiac, CNS, lymphadenopathy, vasculitis
Lungs: pleural disease, interstitial fibrosis, bronchiolitis obliterans, oragnizing pneumonia
Cardiac: IHD, pericarditis, pericardial effusion
Eyes: episcleritis, scleritis, keratoconjunctivitis sicca
Peripheral neuropathy, splenomegaly, carpal tunnel syndrome
Felty’s syndrome: RA + Splenomegaly + Neutropenia
X-ray findings for RA
Loss of joint space, juxta-articular osteoporosis, periarticular erosions, subluxation
Antibodies involved in RA
Anti-cyclic citrullinated peptide antibody (Anti-CCP) - may be detected up to 10 years before development of RA, has a high specificity compared to RhF
Rheumatoid factor (IgM circulating ab) - seen in 70-80% of patients. High levels are associated with severe progressive disease, but not a marker of disease activity
Conditions which cause positive RhF
Sjögrens (around 100%), Felty’s (around 100%), RA, infective endocarditis, SLE, systemic sclerosis, general population
TB, HBV, EBV, leprosy
RA investigations
Anti-CCP (anti-cyclic citrullinated peptide antibody)
RhF
FBC (anaemia of chronic disease, raised platelets)
Raised ESR
Raised CRP
X-rays
USS and MRI can identify synovitis
RA drug side effects:
methotrexate
mucositis myelosuppression pneumonitis pulmonary fibrosis liver fibrosis
RA drug side effects: sulfasalazine
rashes, oligospermia, Heinz body anaemia, interstitial lung disease, myelosuppresion, lung fibrosis
RA drug side effects: hydroxychloroquine
Retinopathy, corneal deposits
RA drug side effects: leflunomide
Liver impairment, interstitial lung disease, HTN
RA drug side effects: prednisolone
Cushingoid features, osteoporosis, DM, HTN, cataracts
Management of RA
- Initial therapy: DMARD monotherapy +/- short-course of bridging prednisolone
- Combination DMARDs if monotherapy is ineffective
- TNF inhibitors if unresponsive to at least two DMARDs
Manage RA flares with oral or IM corticosteroids
Other important treatment options: analgesia, physiotherapy, surgery
Types of DMARDs
Methotrexate (most common, monitor FBC and LFTs)
Sulfasalazine
Leflunomide
Hydroxychloroquine
TNF-inhibitors
- indications in RA
- Examples
Used in RA if inadequate response to 2+ DMARDs
Etanercept (can cause demyelination and reactivation of TB)
Infliximab (monoclonal ab, can cause reactivation of TB)
2010 American College of Rheumatology diagnostic criteria for RA
Used for patients who: Have at least one joint with definite clinical synovitie, and with the synovitis not better explained by another disease
Add score of categories A-D -> a score of 6/10 is a definite diagnosis of RA
A. Joint involvement: 1 large joint (0), 2-10 large joints (1), 1-3 small joints (2), 4-10 small joints with or without large joint involvement (3), 10 joints with at least 1 small (5)
B. Serology: RhF-ve ACPA -ve (0), low positive RF or low positive ACPA (2), high positive RF or high positive ACPA (3)
C. Acute phase reactants: normal CRP and normal ESR (0), abnormal CRP or abnormal ESR (1)
D. Duration: <6w (0), >6w (1)
Gout features
- symptoms during flares
- which joints are affected
Inflammatory arthritis
Typically presents with an acute monoarthropathy with severe joint inflammation.
Flares: significant pain, swelling, erythema
Majority of patient’s first presentation affects the 1st metatarsophalangeal joint (big toe)
Other commonly affected joints = ankle, wrist, knee
Radiological features of gout
- Joint effusion is an early sign
- Well-defined punched out erosions with sclerotic margin in a juxta-articular distribution, often with overhanging edges
- Relative preservation of joint space until late disease
- Eccentric erosions
- No periarticular osteopenia (in contrast to RA)
- Soft tissue tophi
Causes and predisposing factors to gout
Caused by deposition of monosodium urate crystals in the synovium
Caused by chronic hyperuricaemia
Decreased excretion or uric acid: drugs (diuretics), CKD, lead toxicity
Increased production of uric acid: myeloproliferative/ lymphoproliferative disorder, cytotoxic drugs, severe psoriasis
Lesch-Nyhan syndrome: X-linked recessive syndrome causing gout, renal failure, neuro deficits and learning difficulties
Acute management of gout
First line: NSAID or colchicine
Continue max dose NSAID until 1-2 days after symptoms have settled
PPI may be indicated
Colchicine has slower onset of action than NSAID
Colchicine SE = diarrhoea
Consider oral steroids if NSAIDs and colchicine are contraindicated
If the person is already taking allopurinol it should be continued
Indications for urate-lowering therapy
Offered to all patients after their first attack of gout
Urate lowering therapy is particularly recommended if:
- > =2 attacks in 12m
- tophi
- renal disease
- uric acid renal stones
- prophylaxis if on cytotoxics or diuretics
Urate lowering therapy
Allopurinol is first line
Delay starting urate-lowering therapy until after acute attack
Consider starting colchicine when starting allopurinol
Lifestyle modifications for gout
Reduce alcohol intake Avoid alcohol during acute attack Lose weight if obese Avoid food high in purines (liver, kidney, sea food, oily fish, yeast products) Stop precipitating drugs Increase vit C
Differential diagnoses for monoarthritis
Septic arthritis Trauma Reactive arthritis (reiters) Haemarthrosis Psoriatic arthritis Gout Calcium pyrophosphate deposition (pseudogout)
Investigations for gout
Joint aspirate
Polarised light microscopy of synovial fluid shows negatively birefringent urate crystals
Serum urate is usually raised
X-rays
Pseudogout
- Cause
- Joints
- Risk factors
- Ix
- Mx
- Cause: Calcium pyrophosphate dihydrate crystal deposition in the synovium
- Joints: Usually occurs in larger joints compared to gout (eg. knee, wrist, shoulders)
- Risk factors: haemochromatosis, hyperparathyroidism, acromegaly, low magnesium, low phosphate, wilsons disease
-Ix: Joint aspiration shows weakly positive birefringent rhomboid-shaped crystals
X-ray shows chrondrocalcinosis
-management: joint fluid aspiration to exclude septic arthritis, NSAIDs or intra-articular/IM/PO steroids
Features of spondylarthropathies
- Seronegative (RhF ive)
- HLA B27
- Axial arthritis (pathology in spine and sacroiliac joints)
- Asymmetric large joint oligoarthritis (<5 joints) or monoarthritis
- Enthesitis (inflam of tendon/ligament insertion)
- Dactylitis (inflam of entire digit)
- Extra-articular: iritis, psoriaform rashes, oral ulcers, aortic valve incompetence, IBD
Types of spondylarthropathies
Ankylosing spondylitis
Psoriatic arthritis
Reiters syndrome
Enteropathic arthritis
Ankylosing spondylitis features
- typical presentation
- clinical examination
- the A’s
HLA-B27
More common in males, aged 20-30
‘young man who presents with lower back pain and stiffness of gradual onset, stiffness usually worse in the morning and improves with exercise, patient experiences pain at night which improves on getting up’
Clinical examination: reduced lateral flexion, reduced forward flexion (schober’s test), reduced chest expansion
The A’s: apical fibrosis, anterior uveitis, aortic regurgitation, achilles tendonitis, AV node block, amyloidosis, and cauda equina syndrome (peripheral arthritis, more common if female)
Schober’s test
A line is drawn 10cm above and 5cm below the back dimples, the distance between the two lines should increase by more than 5cm when the patient bends forward as far as possible
Ankylosing spondylitis = reduced forward flexion
Ankylosing spondylitis investigations
Inflam markers (ESR, CRP) typically raised
HLA-B27 is of little use in making diagnosis
Plain X-ray of sacroiliac joints is the most useful Ix for diagnosis
If the X-ray is negative but suspicion remains high -> MRI
Spirometry may show restrictive defect due to pulm fibrosis, kyphosis and ankylosis of costovertebral joints
Radiological features of ankylosing spondylitis
Plain radiograph of the sacroiliac joints
- sacroilitis: subchondral erosions and sclerosis
- Squaring of lumbar vertebrae
- bamboo spine
- syndesmophytes (ossification of outer fibres of annulus fibrosus)
Apical fibrosis on CXR
MRI may show bone marrow oedema as an early sign
Management of ankylosing spondylitis
Encourage regular exercise (swimming)
NSAIDs are first line
Physiotherapy
Anti-TNF for patients with persistently high disease activity despite conventional treatment
DMARDs if there is peripheral joint involvement
Enteric arthropathy
- associated diseases
- treatment
HLA-B27
Associated with IBD, GI bypass, coeliacs and whipples disease
Arthropathy usually improved with treatment of IBD
Beware of NSAIDs
Use DMARD if resistant
Psoriatic arthritis
- different types
- management
HLA-B27
Types: rheumatoid–like polyarthritis (most common), asymmetrical oligoarthritis (typically affects hands and feet), sacroillitis, DIP joint disease, arthritis mutilans)
Management: treat as RA (DMARDs), better prognosis than RA
Reactive arthritis
- what is it
- cause
- features
- management
- prognosis
-HLA-B27
-Arthritis that develops following an infection where the organism cannot be recovered from the joint
-Often develops post-STI or post-dysentry
-Chlamydia trachomatis
-Shigella, Slamonella, Campylobacter
-Features: typically develops within 4 weeks of infection, and usually lasts 4-6m. Asymmetrical oligoarthritis of lower limbs, dactylitis, urethritis, conjunctivitis, anterior uveitis, keratoderma blenorrhagica (raised brown plaques on soles and palms).
Reiter’s syndrome: can’t see, can’t wee, can’t climb a tree (conjunctivitis, urethritis, arthritis)
-Mx: analgesia, NSAIDs, intra-articular steroids
Sulfasalazine and methotrexate if persistent
-Symptoms rarely last beyond 12m
Systemic sclerosis
- gender
- what is it
- 3 types
- antibodies involved
- management
- Hardened, sclerotic skin and connective tissue, more common in females
- Limited cutaneous systemic sclerosis (face and distal limbs. Raynauds phenomenon, CREST syndrome)
- Diffuse cutaneous systemic sclerosis (trunk and proximal limbs. ILD, pulm HTN, renal disease)
- Scleroderma (tight fibrotic skin, plaques)
-Antibodies -
ANA in 90%, RhF in 30%, anti-scl07 (diffuse), anti-centromere antibodies (limited)
-manage with immunosuppressive therapy (cyclophosphamide)
Dermatomyositis features
Inflam disorder -> symmetrical proximal muscle weakness and skin lesions
Skin features:
- photosensitive
- macular rash over back/ shoulders
- heliotrope rash in periorbital region
- Gottron’s papules (rough red papules over extensor surfaces of fingers)
- dry scaly hands
- nail fold capillary dilatation
Other features:
- proximal muscle weakness +/- tenderness
- Raynauds
- Resp muscle weakness
- ILD
- Dysphagia/dysphonia
Investigations for dermatomyositis
- Muscle enzymes: ALT, AST, LDH, CK all raised in plasma
- EMG shows characteristic fibrillation potentials
- muscle biopsy confirms diagnosis and excludes differentials
- ANA positive (80%)
- Anti-synthetase antibodies (anti-Jo-1, anti-SRP, anti-Mi-2)
Management of dermatomyositis
Prednisolone
Immunosuppressives and cytotoxics
Hydroxychloroquine/topical tacrolimus for skin disease
Systemic Lupus Erythematosus at risk group
Females, afro-caribbeans/asian population, onset usually 20-40
Pathophysiology of SLE
Autoimmune, type 3 hypersensitivity reaction
Associated with HLA B8, DR2, DR3
Immune system dysregulation -> immune complex formation and deposition throughout organs
Features of SLE
General: fatigue, fever, mouth ulcers, lymphadenopathy
Skin: malar rash, discoid rash, photosensitivity, Raynauds, livedo reticularis, non-scarring alopecia
MSK: arthralgia, non-erosive arthritis
CVS: pericarditis, myocarditis
Resp: pleurisy, fibrosing alveolitis
Renal: proteinuria, glomerulonephritis
Neuro: anxiety, depression, psychosis, seizures
Antibodies in SLE
90% ANA positive
20% RhF positive
Anti-dsDNA highly specific but less sensitive (70%)
Anti-Smith most specific but very low sensitivity (30%)
Anti-Ro, Anti-La
diagnosis and monitoring for SLE
- Antibodies (Anti-dsDNA titre)
- Complement (low C3, low C4)
- ESR raised
Also: BP, urine for casts/protein, FBC, U+E, LFT, CRP (normal)
Skin or renal biopsies may be diagnostic
Management of SLE
- -Screen for comorbidities
- High factor SPF
- NSAIDs and hydroxychloroquine often used as maintenance
- Steroids are usually used for flares
- Azathioprine, methotrexate and MMF as steroid-sparing agents
- Monoclonal ab (belimumab) as an add on therapy for autoantibody positive disease
- mild flares (no organ involvement): hydroxychloroquine or low dose steroids
- moderate flares (orgna involvement): DMARDs or mycophenolate
- Severe flares (life/organ threatening): urgent high dose steroids, mycophenolate, rituximab, cyclophosphamide
Polyarteritis nodosa
- what is it
- what gender
- what age
- what infection is it associated with
Medium-sized necrotising vasculitis leading to aneurysm formation
More common in middle-aged men
Associated with hep B
Polyarteritis nodosa features
Fever, malaise, arthralgia weight loss HTN Mononeuritis multiplex, sensorimotor polyneuropathy Testicular pain Livedo reticularis Haematuria, renal failure p-ANCA (20%) Hep B positive (30%)
Takayasu’s arteritis
- what is it
- gender
- features
Inflammatory, obliterative arteritis affecting aorta and its branches
Affects females > males
Upper limb claudication, diminished/absent pulses
ESR affected during acute phase
Polymyalgia rheumatica
- pathophysiology
- features
- investigations
- treatment
- overlaps with temporal arteritis (giant cell vasculitis)
- typically >60yrs old
- Rapid onset (<1m)
- Aching, morning stiffness in proximal limb muscles, no weakness
- Polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats
- Investigations: ESR >40, CK and EMG normal
- Management: prednisolone
Fibromyalgia features and diagnosis
Chronic pain at multiple sites, lethargy, cognitive impairment (fibro fog), sleep disturbance, headache, dizziness
Clinical diagnosis (all results normal)
Fibromyalgia management
MDT
Aerobic/strength based exercise
CBT
Meds: pregabalin, duloxetine, amitriptyline
Steroids and NSAIDs not recommended as there is no inflammation
Sjögren’s syndrome features
dry eyes (keratoconjunctivitis sicca) dry mouth Vaginal dryness Arthralgia Raynauds Myalgia Sensory polyneuropathy Recurrent episodes of parotitis Renal tubular acidosis
Investigations for Sjögren’s syndrome
RhF in nearly 100% ANA in 70% Anti-Ro Anti-La Schirmer's test: filter paper near conjunctival sac to measure tear formation Histology: focal lymphocytic infiltration Hypergammaglobulinaemia Low C4
Management of Sjögren’s syndrome
Artificial saliva and tears
Pilocarpine may stimulate saliva production
Paget’s disease of the bone pathophysiology
Increased but uncontrolled bone turnover
Thought to be primarily a disorder of osteoclasts, with excessive osteoclast resorption followed by increased osteoblast activity
Features of Pagets disease of the bone
Stereotypical presentation: older male with bone pain and an isolated raised ALP
Bone pain (Pelvis, lumbar spine, femur)
Classical, untreated features: bowing of tibia, bossing of skull
Raised ALP (calcium and phosphate normal)
Skull X-ray: thickened vault, osteoporosis circumscripta
Ill defined sclerotic and lucent areas throughout X-ray
Treatment and complications of pagets disease of the bone
Treatment with bisphosphonates or calcitonin indicated if bone pain, skull/long bone deformity, fracture or periarticular pagets
Complications: deafness (cranial nerve entrapment), bone sarcoma, fracture, skull thickening, high output cardiac failure
Osteoporosis risk factors
Age, female, caucasian/asian
Important risk factors: History of glucocorticoid use RA Alcohol excess Hx of parental hip fracture Low BMI Current smoking
Other risk factors: Sedentary lifestyle Premature menopause Hyperthyroidism Hypogonadism/GH deficiency Hyperparathyroidism DM Multiple myeloma/ Lymphoma IBD Liver disease CKD Osteogenesis imperfecta
Drugs which may worsen osteoporosis
Glucocorticoids SSRIs Antiepileptics PPIs Glitazones Long term heparin therapy Aromatase inhibitors
What is a FRAX tool
Used in osteoporosis to assess the 10 year risk of patient developing a fragility fracture
treatment of osteoporosis and indication for treatment
Indication for treatment is a DEXA scan T score of < -2.5
First line treatment is an oral bisphosphonate
DEXA scan scores
T score: based on bone mass of young reference population
T score > -1.0 = normal
-1 to -2.5 = osteopenia
>-2.5 = osteoporosis
Management of patients at risk of corticosteroid-induced ostoporosis
Risk of osteoporosis rises significantly one a patient is taking the equivalent of prednisolone 7.5mg OD for 3+ months. Start bone protection if this is likely.
Management of patients at risk of corticosteroid induced osteoporosis:
- Patients >65 or those who’ve previously had a fragility fracture should be offered bone protection
- Patients <65 should be offered a bone density scan, if T score < -1.5 then bone protection should be offered
First line treatment is bisphosphonate (alendronate) and calcium and vitamin D.
Marfans syndrome features
Tall stature High arched palate Arachnodactyly Pectus excavatum Pes planus Scoliosis Heart: aortic aneurysm, aortic dissection, aortic regurgitation, mitral valve prolapse Lungs: repeated pneumothoraces Eyes: upwards lens dislocation
Cause of Marfans syndrome
Autosomal dominant connective tissue disorder
FBN1 gene on chromosome 15 -> defect in protein fibrillin-1
Causes of hip pain in adults
Osteoarthritis Inflammatory arthritis Referred lumbar spine pain Trochanteric bursitis Meralgia paraesthetica Avascular necrosis Pubic symphysis dysfunction Transient idiopathic osteoporosis
Ehlers-Danlos syndrome cause
Autosomal dominant connective tissue disorder affecting type 3 collagen -> tissue more elastic than normal -> hypermobility and increased skin elasticity
Features and complications of ehlers danlos
Elastic, fragile skin Joint hypermobility (recurrent joint dislocation) Easy bruising Aortic regurgitation Mitral valve prolapse Aortic dissection SAH Angioid retinal streaks
Features of Behcet’s syndrome
Classic triad of oral ulcers, genital ulcers and anterior uveitis
Thrombophlebitis, DVT Arthritis Neuro involvement Abdo pain, diarrhoea, colitis Erythema nodosum
Epidemiology of Behcet’s syndrome
Eastern mediterranean (eg. Turkey) More common in men Typically 20-40 Associated with HLA B51 30% have positive FHx
