5.7: Introduction to rheumatology (part 1 of 2) Flashcards
Arthritis is a
Disease of the joints
2 major divisions of arthritis
Degenerative joint disease (osteoarthritis)
Inflammatory joint disease
Pathological changes during osteoarthritis
Cartilage loss, bony remodelling
Epidemiology of osteoarthritis
More prevalent with increasing age
Previous joint trauma
Jobs involving heavy manual labour
What kind of onset and progression does osteoarthritis present with
Gradual onset
Slow progressive disorder
4 symptoms and signs of osteoarthritis
Joint pain - worse with activity better with rest
Joint crepitus - creaking, cracking, grinding sound on moving joint
Joint enlargement
Limitation of range of motion
3 types of joints affected by degenerative joint disease
Joints of the hand (: Distal interphalangeal joints, proximal interphalangeal joints, first carpometacarpal joint )
Spine
Weight bearing joints of lower limbs (: knees, hips, first metatarsophalangeal joint)
4 radio graphic features of osteoarthritis
Joint space narrowing
Subchondral bony sclerosis
Osteophytes
Subchondral cysts
Define inflammation
A physiological response to deal with injury or infection
What can excess or inappropriate inflammatory reactions lead to
Damage to host tissues
What 5 things does inflammation manifest clinically as
Red (rubor)
Pain (dolor)
Hot (calor)
Swelling (tumor)
Loss of function
4 Physiological, cellular and molecular changes during inflammation
Increased blood flow
Migration of white blood cells (leucocytes)
Activation p/differentiation of leucocytes
Cytokine production
3 main causes of joint inflammation
Infection (secondary inflammation)
Crystal arthritis (secondary inflammation)
Immune- mediated (autoimmune) primary inflammation
Secondary inflammation occurs in response to
A noxious insult
Example of Non-sterile inflammation
Infection
2 examples of sterile inflammation
Crystal arthritis
Immune-mediated inflammation
Cause of septic arthritis
Bacterial infection of a joint (spread of blood)
3 risk factors of septic arthritis
Immunosuppressed (e.g. diabetes)
Pre-existing joint damage
Intravenous drug use (IVDU)
Why is septic arthritis a medical emergency
If untreated can rapidly destroy a joint
Clinical presentations of septic arthritis
Acute, red, hot, painful swollen joint
Usually only one joint affected
Typically fever - systemically unwell
Diagnosis of septic arthritis
Joint aspiration
Sample sent for urgent gram stain and culture
Common organisms causing septic arthritis
Staphylococcus aureus, strepococci
Gonococcus (affects multiple joints - polyarthritis, less likely to cause joint destruction)
Treatment of septic arthritis
Surgical wash out and intravenous antibiotics
2 types of Crystal arthritis
Gout
Pseudogout
Gout is caused by deposition of
Momosodium urate (MSU) crystals around/in joints leading to inflammation
A risk factor if gout is
High Uric acid levels
3 causes of hyperuricaemia
Genetic tendency
Increased intake of purine rich foods
Reduced excretion (kidney failure)
What is pseudogout caused by deposition of
Calcium pyrophosohate dihydrate (CPPD) crystals
Risk factors of pseudogout
Background osteoarthritis
Elderly patients
Intercurrent infection
In Crystal arthritis, tissue deposition of monosodium urate (MSU) crystals leads to:
Gouty arthritis
Top hi (depositions of MSU in tissue, often around hands, feet, elbows and ears)
4 Clinical features of Crystal arthritis
Abrupt onset
Usually monoarthritis
Big toe 1st MTPJ most commonly affected
Can also affect other joints- feet,ankle,knee,wrist,finger,elbow
What would a blood test in a patient with gout show
Increased C-reactive protein - inflammatory marker
Increased serum urate
What would an X-ray of a patient presenting with gout show
Normal X-ray
If recurrent attacks - juxta-articular erosions develop
Gout Crystal shape and birefringence
Urate crystals have a needle shape
Negative for light microscopy
What is the key investigation for any acute monoarthritis
Joint aspiration
Synovial fluid analysis
Send to lab for : microbiology
Polarising light microscopy to detect crystals
Pseudogout Crystal shape and birefringence
CPPD crystals are rhomboid shaped
Positive for birefringence
Gout treatment for an acute attack
Main aim to reduce inflammation
- non-steroidal anti-inflammatory drugs NSAIDs
Glucocorticoids
Chronic Gifu treatment
Aim - reduce uric acid levels
Lifestyle : avoids purine rich food e.g. beer
Pharmacological - allopurinol, febuxostat (xanthine oxidase inhibitors)
3main categories of immune-mediated inflammatory joint diseases
Rheumatoid arthritis
Seronegative inflammatory arthritis
Systemic lupus erythematosus
What kind of condition is rheumatoid arthritis
Chronic autoimmune disease
What is the primary site of pathology of RA
Synovium
Synovitis is
Inflammation of the synovial membrane
What 3 locations is synovium found at
Synovial joints
Tenosynovium surrounding tendons
Bursa
5 key features of chronic arthritis
Polyarthritis
Early morning stiffness around joints
MY lead to joint damage and destruction
Auto-antibodies usually detected in blood
Extra-articular disease can occur
Pattern of joint involvement in RA
Symmetrical
Polyarthritis
Affects both small and large joints- most commonly hands, wrists and feet
Describe a healthy synovial membrane
1-3 cell layer that lines synovial joints - maintains synovial fluid
Synovial membrane in RA
Synovium becomes proliferated mass of tissue due to :
Neovascularisation
Lymphangiogenesis
Inflammatory cells : activated B and T cells, plasma cells, mast cells, activated macrophages
Why does inflammation of Synovium occur in RA
Cytokine network controls recruitment, activation and effector functions
Cytokine imbalance - excess of pro-inflammatory and anti-inflammatory cytokines
Pathogenesis of RA
Cytokine tumour necrosis factor-alpha (TNFa) is the dominant pro-inflammatory cytokine in the rheumatoid Synovium
Compare blood test Haemoglobin levels in RA, Osteoarthritis and septic arthritis
RA - low (anaemia)
OA- normal
SA- usually normal
Compare white cell count in RA, Osteoarthritis and septic arthritis
RA - normal
OA-normal
SA- increased (leucocytosis)
Compare levels of C-reactive protein in RA, Osteoarthritis and septic arthritis
RA- high
OA- normal
SA- high
Two types of antibodies found in blood of RA patients
Rheumatoid factor
Antibodies to citrullinated protein antigens (ACPA)
Rheumatoid factor is an antibody that
Recognises the Fc portion of IgG as their target antigen
Typically IgM antibodies
Positive in 80% of RA patients
Clinical test to detect ACPA
Anti-cyclic citrullinated peptide antibody ‘anti-CCP antibody’
Which antibodies are more specific for RA, Anti-CCP or RF
Anti-CCP antibodies
Ab positivity is associated with more aggressive/erosive disease
What 3 identifiable features would be present on an X-ray of a patient with RA
Soft tissue swelling
Peri-articular osteopenia
Bony erosions - only in established disease
What 3 identifiable features would be present in an Ultrasound of a patient with RA
Better test for detecting synovitis
-synovial hypertrophy
-increased blood flow
May detect early erosions (not visible on X-ray)
What 3 imaging investigations can be carried out to diagnose RA and which one is the best at diagnosing
X-ray
MRI - can be expensive and time-consuming
Ultrasound - nest as can be used in assessment in early arthritis
Principles or management of RA
Early recognition of symptoms, referral and diagnosis
Prompt initiation of treatment : joint destruction = inflammation x time
Aggressive pharmacological treatment to surprises inflammation
Two pharmacological treatments of RA and their function
Glucocorticoid therapy (steroids) : useful acutely but avoid long term use due to side effects
DMARDs - disease modifying anti-rheumatic drugs , immunomodulatory drugs that half or slow disease process
Seronegative inflammatory arthritis includes (4)
Psoriatic arthritis
Reactive arthritis
Ankylosing spondylitis
IBD-associated arthritis
What is Seronegative inflammatory arthritis
Family of conditions with overlapping clinical features and oathogenesis
RF and CCP antibodies not present in blood but immune mediated conditions
Main clinical presentation of psoriatic arthritis
Classically asymmetrical arthritis affecting IPJs
What 3 things can psoriatic arthritis also manifest as
Symmetrical involvement of small joints
Oligoarthritis of large joints
Spinal and sacroiliac joint inflammation
What is Reactive arthritis and what does it present following
Sterile inflammation following Infection elsewhere in the body
Two common infections of reactive arthritis
Urogenital (chlamydia trachomatis)
Gastrointestinal (samonella, shingella)
3 Important extra-articular manifestations of Reactive arthritis
Enthesitis
Skin inflammation
Eye inflammation
What can reactive arthritis be a first manifestation of
HIV
Hep C
What age group is most at risk of developing reactive arthritis
Young adults with genetic predisposition and environmental trigger
When do symptoms of reactive arthritis onset
1-4weeks after infection (may be mild)
How is synovial fluid culture different in septic arthritis compared to reactive arthritis
SA - positive
RA- sterile
Use of antibiotic therapy for septic arthritis compared to reactive arthritis
SA- yes
RA- no (not for joint disease but in cases of STIs treatment may be required)
Joint lavage in septic arthritis compared to reactive arthritis
SA- yes for large joints
RA - no
