Rheumatology Flashcards
Common and chronic conditions (plus some potential rogue ones) to know
List common differentials for an acutely swollen joint
- Most important to rule out –> septic arthritis
- trauma & haemarthrosis
- bursitis
- tendinopathy
- reactive arthritis
- gout
- pseudogout
- enteropathic arthritis
Define gout
What is the pathophysiology?
Gout = crystal arthropathy resulting from excess uric acid leading to precipitation in joints and tissues.
Pathophysiology –> disorder of purine metabolism, uric acid is the breakdown product of purines and is predominantly excreted via the kidneys. Imbalance between production and excretion of uric acid leading to deposits in joints and soft tissues.
3 main mechanisms - increased production with increased cell turnover e.g. psoriasis, chemoT
Increased purine intake - seafood red meat alcohol
Decreased uric acid secretion e.g. furosemide, thiazides, AKI, CKD
Risk factors for gout?
Fuck My HOT And Chronic gout
Family history
Male
High purine diet/ hyperlipidaemia
Obesity
Thiazides
CKD/ CVD/ Chemotherapy / DBM
Presentation of gout
Rapid onset of pain - typically over 1 hour
Monoarticular - often 1st MTP joint (may affect wrists/ carpometacarpal joint/ knee/ ankle)
or oligoarticular (< 4 joints)
joint stiffness, swelling, erythema & warmth
effusion
Gout tophi - often on extensor surfaces - elbow, knee, achilles, helix of ear
FHx of gout
Examination features of gout
- warm red swollen
- considerable tenderness
- limited ROM
- Hard subcutaenous Tophi on extensors - elbow/ knees / achilles/ helix of ears
Investigations for Gout
- Gout is a clinical diagnosis but joint aspiration can be used to confirm it
Bedside:
- BM - Diabetes = RF
- Urine dip - for CKD (protein blood etc)
Bloods:
- FBC
- U& E –> check renal function
- LFTs –> premedication baseline
- Blood cultures –> exclude septicaemia
- Serum Uric acid –> taken 4-6 weeks after acute attack, normal serum uric acid does not exclude gout during an acute attack as plasma urate often falls.
- Serum Calcium
Imaging:
- USS –> more sensitive in Xray in detecting erosions, tophi and gout specific double contour sign
- Xray –> typically normal in acute episodes of gout. In Chronic gout:
- lytic lesions
- punched out erosions
- erosion with sclerotic borders
- joint space maintained
Special test:
- Joint arthocentesis –> gold standard investigation, exclude septic arthritis
- MCS of joint aspirate –> crystal microscopy will show needle shaped monosodium urate crystals, negatively birefringent of polarised light. No bacterial growth
Management of gout
Conservative:
- Rest, ice, elevation
- Weight loss
- Low purine diet
- Reduced alcohol consumption
Medical:
For acute episode:
- NSAID 1st line, Colchicine 2nd line, Steroid 3rd line
- NSAID CI in significant HD or renal impairment, then use oral colchicine
- notable SE colchicine is diarrhoea which is dose dependent.
- If NSAID and colchicine is CI then short course oral steroid or intraarticular steroid
For chronic management:
- urate lowering therapy usually started once initial attack has resolved to enable the patient to make the decision to start urate lowering therapy without any pain
- First line Allopurinol = xanthine oxidase inhibitor that prevents conversion of metabolites to uric acid
- colchicine cover considered for the first 6 months
- Caution with allopurinol in renal impairment
- Second line = Febuxostat (also xanthine oxidase inhibitor) considered if allopurinol is CI.
Define pseudogout
Pseudo gout = Microcrystal synovitis caused by the deposition of calcium pyrophosphate crystals in the synovium
What is the pathophysiology of pseudogout
What are the risk factors
- Pathophysiology:
- excess CPP production leads to supersaturation and crystal formation / deposition in the synovium. There is an inflammatory response to calcium in the synovium
- Risk factors: usually pseudogout is associated with increasing age therefore patients developing it at a younger age have a secondary condition:
- haemochromatosis
- hyperparathyroidism
- hypomagnesaemia
- familial CPPD disease (calcium pyrophosphate disease)
- acromegaly
- wilsons
- gout
Presentation of pseudogout
Asymmetrical arthropathy of larger peripheral joints
key risk factors of increasing age, family history, previous inury or surgery to the joint, metabolic disorders
often affects knee 50%, can affect the shoulders, elbows, wrists, hips, ankles and feet
sudden worsening of osteoarthritis and involvement of joints not commonly involved in OA e.g wrists and shoulders may suggest CPP arthritis
joint swelling
erythema
restricted ROM
with or without fever
Investigations for pseudogout
- Bedside: BM ( diabetes), Urine dipstick (kidney function)
- Bloods:
- FBC
- U&Es (kidney function)
- LFTs baseline premedication
- Blood cultures –> rule out septicaemia
- Serum calcium / bone profile (check for hyperparathyroidism)
- Serum urate
- Imaging:
- Xray –> chondrocalcinosis is the classical XR finding (pathognomonic of gout)
- Other XR changes similar to OA (LOSS) (Loss of joint space, osteophytes, subchondral sclerosis, subchondral cysts)
- Special tests:
- Synovial fluid analysis –> rhomboid shaped crystals positively birefringent in polarised light with no bacterial growth
Management of pseudogout
- Flares usually self resolve within a few weeks
- Conservative:
- ice packs, immobilisation, rest for first 48 hours
- Medical management:
- NSAID - naproxen first line
- colchicine - if NSAID CI
- Steroids PO or joint injection if no response to above
- Recurrent episodes may need prolonged colchicine
- Surgical:
- Joint washout in severe cases
Define reactive arthritis
Reactive arthritis - one of the group of seronegative spondyloarthropathies, arthritis occurring after an infection with “Sterile inflammation”.
Occurs several weeks following an infection with organisms that infect the urogenital or GI tract
Common organisms causing reactive arthritis?
- Urogenital infections –> chlaymidia, gonorrhoea, Ureaplasma urealyticum
- GI –> campylobacter jejuni, shigella, salmonella, yersinia, C diff
- Rare – >TB
Presentation of Reactive arthritis
Key: cant see, pee, or climb a tree
- Conjunctivitis
- urethritis
- acute monoarthritis
- Patients with clear history of preceding infection either diarrhoea or urethritis
- often 1- 4 weeks before onset of joint pain
- Peripheral asymmetrical oligoarthritis most common
- can cause monoarticular or polyarticular arthritis
- acutely hot swollen red painful joint
- worse in the morning
- axial arthritis –> inflammatory back pain, buttock pain, stiffness at rest, relieved by exercise
- enthesitis - often achilles
- dactylitis
Extraarticular manifestations:
- fever
- fatigue
- ocular –> bilateral conjunctivitis
- oral ulcers
- Skin –> circinate balanitis (inflammation of head of penis) and keratoderma blenorrhagica, erythema nodosum
- GI –> diarrhoea
- Urogenital –> urethritis & dysuria
Investigations : reactive arthritis
- Bedside:
- urine dipstick & urinalysis for source of infection
- Stool culture (often negative at onset of arthritis)
- urethral / cervical swab for STI screen
- Bloods:
- FBC
- U&E
- LFT
- CRP/ESR
- blood cultures - rule out septic arthritis
- STI screen - HIV/ hep/ syphilis
- ANA (should be -ve)
- RF (should be -ve)
- Imaging/ special test:
- Xray of pelvis –> asymmetric sacroilities or enthesitis of achilles tendon
- Joint aspiration to exclude septic arthritis, gout and pseudogout
Management : reactive arthritis
- Conservative: RICE
- Medical –> 1) indentify and eradicate underying infection, 2) NSAID& paracetamol, 3) Steroid PO or joint injection
- Medical if chronic ReA –> use DMARDs methotrexate or sulfasalazine
Often self limiting but up to 20% develop chronic arthritis
Key risk factors reactive arthritis
DDX reactive arthritis
Key risk factors: Male, HLA B27 +VE, preceding chlaymidia or GI infection
DDX:
Septic arthritis (key)
disseminated gonococcal infection
Gout
pseudogout
RA
SLE
Traumatic arthritis / haemarthrosis
Differential diagnosis for chronic joint pain
- Monoarthritis:
- OA
- Chronic tophaceous gout
- Polyarthritis:
- RA
- Ankylosing spondylitis
- psoriatic arthritis
- Systemic sclerosis
- SLE
- Sjogrens
- PMR
- Fibromyalgia
Define osteoarthritis
- Osteoarthritis is a chronic degenerative joint disorder caused by degeneration of the cartilage within a joint, leading to exposure of the underlying bone and bone - bone interaction. Leads to pain, stiffness and reduced function of the joint involved.
Risk factors for OA
- Age
- Female
- Fhx
- Physically demanding occupation or sport
- anything leading to altered joint loading –> hypermobility, osteoporosis, trauma within the joint e.g. fracture, meniscal or ligament tears
Presentation of OA (symptoms)
- Pain and stiffness within joints
- worsened by activity and weight bearing
- background ache at rest
- lasts less than 30 mins in the morning
- pain better with rest
- pain not present at night unless advanced
- often affects larger weight bearing joints : Hips, knees, SI joints, cervical spine
- Hands –> DIPs and 1st CMC joint (base of the thumb) & wrist
- often > 50 years
- slow onset over months - years
- functional difficulty
Signs of OA on examination?
- Check weight, height, calculate BMI
- Watch for gait abnormality and malalignment of the joints
- Look:
- joint swelling
- erythema
- bony swellings –> osteophytes
- effusion
- fixed flexion deformity at the knee or hip (+ve thomas test)
- Feel:
- crepitus
- limited ROM
- Effusion
- Joint line tenderness
- Move:
- assess ROM, both active and passive (will be reduced)
- crepitus felt
- assess for ligament laxity (may be a cause)
- Hand signs:
- Heberdens DIP
- Bouchards PIP
- Squaring of 1st CMC joint
- Weakened grip
- reduced ROM
Diagnosis of OA?
Diagnosis of OA is often a clinical diagnosis based of age, symptoms and examination findings. Clinical diagnosis is considered in a patient with a typical OA presentation:
Activity related joint pain
morning stiffness no longer than 30 mins
> 45 yrs
Investigations for OA
Bedside: BMI
Bloods:
- To exclude RA:
- CRP
- ESR
- RF
- AntiCCP
- XR of affected joint:
- Loss of joint space
- Osteophytes
- Subchondral sclerosis
- Subchondral cysts
- MRI if soft tissue injury is suggested in the history e.g with locking or instability of the joint
- MRI of the spine if there is any neurological deficit and spinal OA
Management of OA
Conservative:
- Weight loss to reduce any load on the joint
- physiotherapy and occupational therapy
- orthotics to support function
- low impact exercise such as swimming or cycling
Medical:
Stepwise analgesia:
- paracetamol + topical NSAID/ topical capsaicin
- oral NSAID + PPI omeprazole
- Consider stronger opiates e.g. codeine/ morphine –> caution with dependence tolerance and withdrawal
- Intraarticular steroid injections
Surgical:
Joint replacement of hip or knee in severe OA that is not responding to conservative measures & is severely impacting the patients QOL
Define rheumatoid arthritis
Quick pathophysiology
RA = chronic symmetrical polyarthritis with systemic inflammation
Pathophysiology: autoimmune disease with development of autoantibodies - RF and Anti CCP. Leads to inflammation in the synvoium of joints, activation of osteoclasts leading to bone and cartilage breakdown, formation of a pannus of proliferating synoviocytes & immune cells. Antigen immune complexes in the joint leads to chronic inflammation and joint destruction. Chronic inflammation leads to increased vascular permeability and joint effusion.
Key risk factors for RA
- 20-50 yrs
- white
- female
- HLA DR4 HLA DR1
- family history
- other AI condition
- Environmental trigger e.g. smoking or infections
Presentation of RA - symptoms
- Swollen painful stiff joints in hands and feet
- DIPS rarely affected
- PIP, MCP and wrist common, MTP common
- joints are hot, red, swollen, with stiffness worse in the morning, lasting > 1hr
- (due to drop in cortisol overnight allowing more inflammation)
- gradually worsens with larger joints involved - knee hip elbow, shoulders, ankle, TMJ, atlantoaxial joint, cervical spine
- presentation over a few months
- Systemic symptoms:
- fatigue
- low grade fever
- weight loss
- myalgia
- low mood
Signs of RA on examination
- Look: Hands
- Z shaped deformity of thumb
- swan neck deformity
- boutonniere deformity
- ulnar deviation of fingers at knuckles
- muscle atrophy –> guttering between the extensor tendons in the hands due to wasting of interossei muscles
- Feel:
- boggy joint swelling
- pain on palpation
- +ve squeeze test of metacarpal and metatarsal joints
- Move:
- reduced ROM
- Difficulty with fine motor tasks
Extraarticular manifestations of RA?
- Neurological - atlanto axial subluxation with impingement of cervical spine, CTS
- Eyes - dry eyes, (sicca syndrome), episcleritis, scleritis
- Oral - dry mouth, oral ulcers
- Pulmonary - interstital lung disease, inflammation of the pleura, costochondritis
- cardiac - pericarditis, myocarditis, endocarditis
- Increased risk IHD - due to inflammation of arteries
- Renal - glomerulonephritis
- Haem - anaemia, neutropenia and splenomegaly (feltys syndrome), thrombocytopenia or cytosis
- Derm - rheumatoid nodules on extensor surfaces
- MSK - increased risk osteopenia, muscle weakness, tenosynovitis and trigger finger
Investigations for RA
Bedside
Bloods:
- FBC - anaemia
- ESR (raised)
- CRP (Raised)
- U&E - glomerulonephritis
- Ca2+ and bone profile
- LFTs - feltys syndrome
- Rheumatoid factor 70% positive but non specific
- Anti CCP - very specific but low sensitivity, if positive it predicts worse disease and can be detected up to 10 yrs before symptoms. If negative for RF test Anti ccp.
Imaging:
- LESS
- Loss of joint - destruction and deformity
- erosions of bone
- soft tissue swelling
- soft bones - periarticular osteopenia
- Other –> USS for effusion, tendonitis or MRI for cervical spine
Special tests –> joint aspiration if effusion is present
Investigations in ankylosing spondylitis
- Bedside:
- ECG - for AV node involvement
- Urine - if worried about kidney involvement
- Bloods:
- FBC -anaemia
- ESR and CRP - often raised, markers of disease activity
- RF and Anti CCP- negative to rule out RA
- LFTs - raised ALP
- U&E - kidney involvement and baseline pre tx
- HLA B27 genetic testing but of limited use as 90% +Ve with AS, 10% positive with no AS.
- Imaging: X ray of the spine & pelvis
- Sacroilitis with subchondral erosions and sclerosis
- Squaring of the vertebral bodies
- vertebral syndesmophytes - ossification of the annulus fibrosis
- ossification of ligaments, discs and joints - dagger sign ossification of interspinous ligament
- fusion of syndesmophytes with vertebral body above (ankylosis) + calcification leading to bamboo spine
- CXR: apical fibrosis
- If xray is negative for AS but high index of suspicion use MRI to detect active inflammation
Special test - spirometry for restrictive lung disease in apical fibrosis or due to kyphosis
Investigations for psoriatic arthritis
- Bloods: FBC for anaemia, CRP and ESR often raised can be normal, RF negative, genetic testing HLA B27 +ve
- Imaging: XR:
- periositis - inflammation of the periosteum
- ankylosis (fusion of bones)
- osteolysis (Destruction of bone)
- dactylitis (soft tissue swelling entire digit)
- pencil in cup appearance
- arthritis mutilans (Severe psoriatic arthritis with destruction of the ends of digits that shrink and shorten, skin folds in on itself with telescopic finger)
What are the main presenting symptoms of SLE?
SLE affects multiple systems:
Systemic symptoms –> Fatigue, fever, weight loss, lymphadenopathy, splenomegaly.
Skin & eyes –> malar rash, discoid rash, photosensitivity, raynauds, alopecia, livedo reticularis, dry eyes, mouth ulcers
MSK–> arthralgia, myalgia, non erositve arthritis - symmetrical small joint polyarticular
CV/ Haem –> anaemia of chronic disease (SOB), Vasculitis (antiphospholipid), reduced WBC/ platelets, pericarditis, myocarditis, heart block
Resp –> SOB, pleuritic chest pain and pulmonary fibrosis
Renal –> glomerulonephritis, proteinuria and haematuria
Neuro & psychiatric –> anxiety and depression, fluctating cognition, ataxia, psychosis, seizures
Presentation of systemic sclerosis?
- Fatigue
- weight loss
- Hands:
- Hand stiffness & swelling - worse in the morning improves in the day
- Raynauds
- Skin thickening and tightness
- loss of tight grasp, reduced ROM
- loss of fat pads and ulceration
- Calcinosis
- telangiectasia
- GI
- heartburn and reflux
- dysphagia
- distention & constipation - small bowel disease
- MSK:
- arthralgia
- myalgia
- muscle weakness
- resp:
- sob
- dry cough
- CV:
- severe HTN
- renal failure
Core features PMR?
Systemic features PMR?
- Should be present for at least 2 weeks:
- bilateral shoulder pain
- bilateral pelvic girdle pain
- worse with movement and worse in the morning
- interferes with sleep
- stiffness about 45 mins in the morning
- affects shoulders, hips, neck and torso
- systemic features:
- WL
- Fatigue
- fever
- low mood
- upper arm tenderness
- arthritis in knees and wrists
- CTS
