Lupus, Gout, Reactive Arthritis & CPPD Flashcards
What is Systemtic Lupus Erthematosus?
An auto-immune disease that is usually characterized by clinical manifestations that are multi-system.
What is the pathogenesis of SLE?
- Results from recurrent activation of the immune system
- Production of antibodies and protein products that then contribute to high levels of inflammation and tissue destruction
- Activation of B & T cells (adaptive immune response)
What are the risk factors for SLE?
- Genetic: Siblings of someone with SLE are 30% more likely to have the disease.
- Environmental (UV over, Epstein-Barr Virus, Drug induced Lupus)
- Hormonal (High Oestrogen, OCP use, Pregnancy)
How does SLE present?
CAN AFFECT ANY ORGAN SYSTEM Most common key clinical features: o Cutaneous manifestations o Malar and/or Discoid rash o Usually photosensitive
How is SLE Diagnosed?
Blood testing
- Serological hallmark (98% sensitive)
- Antinuclear antibodies (ANA)
- Double Stranded DNA (dsDNA)
- ENA antibodies
- Raised ESR/CRP
How is ‘mild’ Lupus managed?
- Reduce environmental triggers
- UV, hormone therapy, CV risk
- NSAIDs Antimalarials
How is ‘severe’ Lupus managed?
- Corticosteroids
- Be aware of osteoporosis risk.
- Immunosuppressive drugs
What is reactive arthritis?
“Reactive arthritis (or Reiter’s syndrome) is a form of inflammatory arthritis that develops in response to an infection in another part of the body (cross-reactivity). Coming into contact with bacteria and developing an infection can trigger the disease.
What condition does reactive arthritis present similarly to?
Septic Arthritis
Reactive arthritis is associated with an acute monoarthitis, what does this mean?
Affecting one joint, usually in the lower limb (knee or talocrural)
What two bodily systems usually respond to reactive arthritis?
Seronegative spondyloarthropathy secondary to a bacterial infection in the GI or GU tract
Postulated pathogenesis of Reactive Arthritis?
Unclear but the common theories postulate that:
- Immune response to the bacteria in systemic circulation
- T-cell activation, leading to synovitis, monoarticular arthritis
- Cross-reactivity with HLA-B27
Common pathogens to trigger reactive arthritis?
Most common: chlamydia, salmonella and shingella
Less common: Ecoli
What are some clinical manifestations of reactive arthritis?
- Asymmetrical Oliglioarthritis
- Ocular involvement
- Penile Lesions
- Skin Lesions
- Cardiac Involvement
What does “The patient cant see, cant pee, cant climb a tree” refer to for reactive arthritis?
It refers to the clinical manifestations - Ocular: Uveitis, Conjunctivitis - Penile lesions: Urethritis, Balanitis circinate - Oliglioarthritis: Larger joints of lower extremity, Dactylitis, Enthesitis (achillies or PF), Bursitis, Sacroiliitis
How is reactive arthritis diagnosed?
No specific testing or imaging!
- Hx taking and clinical features ensuring to rule out other causes of arthritis and the presence of predisposing infection
- Blood testing: ESR and CRP to rule out an inflammatory arthritis
- Testing for specific infection
What is the suggested treatment and management for reactive arthritis?
- Management of underlying infection with antibiotics
- NSAIDs and paracetamol: NSAID use may be contraindicated in patients with gastric issues
- DMARDs: For late-stage diseases
- General mobility and treatment of arthritis compensations
What is GOUT?
A form of arthritis characterised by severe pain, redness and tenderness in joints.
What is a Monosodium urate crystal disorder?
An abnormality of uric acid metabolism that results in hyperuricemia and urate crystal deposition
(Inflammatory crystal monoarthropathy)
Where do the crystals usually deposit in the body?
- Joints- acute gout arthritis
- Soft tissue- tophi and tenosynovitis
- Urinary tract- urate stones
What age group/ sex is most likely to suffer from gout?
Mainly a disorder of men between 40-50
In women onset is usually 60+
What nationalities are at an increased risk for gout?
More common in Maori, Pacific Islander and Indigenous Australians
What is the enzyme that transforms xanthine into uric acid?
Xanthine oxidase
Pathogenesis of gout?
- Lack the ability to degrade uric acid therefore deposited out of the urine
- Hyperuricemia: Urate increases in the kidneys to a point where there is too much in the urine. It then congregates in the blood/ synovial fluid/ soft tissues then crystal precipitate and development of tophi.
- Accumulation of crystals in the soft-tissues then leads to macrophages engulfing them
What are the risk factors for gout?
- Genetic factors: 35% increase in males if another male relative has had gout
- Natonality: Maori, Pacific Islander and indigenous
- Long term renal disease
- Long term medication use: Diuretics, Salcylates
- Diet: High purine diet (Shellfish, somefish, crab, lobster), Meats (especially bacon, turkey, veal and organ meats),
- High alcohol consumption (Beer higher than spirits or wine)
- High soft-drink consumption (Especially high fructose corn syrup)
What are the four stages of gout?
Stage 1: Asymptomatic hyperuricaemia
Stage 2: Acute Gouty Arthritis
Stage 3: Intercrtial gout
Stage 4: Chronic tophacious gout and chronic gouty arthritis.
How does Stage 1 (asymptomatic hyeruricaemia) present?
Usually no clinical manifestations and no treatment necessary other than lifestyle modifications.
Elevated serum uric acid:
o >0.42 mmol/L in men
o >0.36mmol/L in women
How does Stage 2 (Acute gouty arthritis) present?
- Acute attack of severe pain
- Usually in great toe but can be elsewhere – knees, other toes, ankle
- Often in the early hours of the morning and wakes the patient
- Skin over the joint is red, shiny, hot and swollen
- VERY tender to touch
- Sheet overlying is too much- Can’t bear socks
- May be precipitated by:
o Alcohol or dietary excess
o Starvation
o Surgical operation - Can subside in 3-10 days
How does Stage 3 (Intercritical gout) present?
- Time between attacks.
- Low to no pain.
- Low-level inflammation causing joint destruction
- Time for aggressive management strategies.
How does Stage 4 (Chronic tophacious gout and chronic gouty arthritis) present?
- Unlikely to be the first indication of Gout
- Stone like deposits of monosodium urate in soft tissue, synovial tissue or in bone near joints (Ears, elbows, big toe, fingers)
- Pathognomonic
- Uric acid levels remain high over a number of years.
- Attacks more frequent and more painful
- Permanent joint destruction
How is gout Diagnosed?
Synovial fluid aspirate: - Uric acid crystals present - Only real diaganostic feature Elevated Serum Uric acid: - Around 30% of all gout sufferers will be in normal limits. Xray: - Punched out joint erosions - Visible tophi and joint effusion
What are some pharmaceutical management for gout?
NSAIDs
- In acute attacks
- Contraindicated in kidney disease
Corticosteroids
- For chronic inflammation
Allopurinol- Serious potential adverse reaction (hypersensitivity)
- Xanthine oxidase inhibitor
- Indicated when frequent attacks
- Presence of tophi, kidney stones or uric acid nephropathy
- Usually not indicated in kidney disease or elderly
- Used as both a prophylaxis and a maintenance
What is Calcium Pyrophosphate Deposition Disease (CPPD)?
A disease of crystal deposition in the joint and soft tissue, almost exclusive to articular cartilage.
What are some risk factors for CPPD?
- Disease of the elderly – most common in 65+ years
- OA
- Previous joint trauma
- Metabolic disease – diabetes
- Family Hx
What is the pathophysiology of CPPD?
-Largely unknown how it is exactly caused but what occurs in the joint is an excess of pyrophosphate production in the cartilage
What are the clinical features of CPPD?
- Acute attacks that mimic gout
- Pain, synovitis or tenderness in one OR multiple joints (Knee, MCP, wrist and hand most common)
- Systemic features
- Can also mimic RA, OA and tendonitis
How is CPPD diagnosed?
- Synovial fluid analysis (differs to gout via rhomboid shaped crystals)
- X-ray (shows chondrocalcinosis which reduces joint space and forms new bone around the cartilage making it appear hyper-white)
How is CPPD managed?
- Treating acute flare ups and symptoms of an attack
- After being diagnosed cortisone is usually injected into the joint
- Managed with paracetamol/oral corticosteroids depending on age and co-morbidities
How can you distinguish CPPD from GOUT?
- Present with similar symptoms and often indistinguishable in early stages
- Joint aspiration for fluid analysis necessary
- Treatment is also similar in early stages
- In chronic stage gout must be treated with hypouricemic agent to prevent severe deformity.
