Rheumatology Flashcards
How many joints does oligoarthritis affect?
2-4 joints
How many joints does polyarthritis affect?
5+
What are the two types of arthritis?
Degenerative joint disease and inflammatory joint disease.
Signs on inflammation?
Red, Pain, Hot, Swelling and loss of function.
Two types of secondary joint inflammation?
Infection and crystal arthritis.
Type of primary joint inflammation?
Immune mediated.
Example of non sterile inflammation of joint?
Infection of joint.
Example of sterile inflammation of joint?
Crystal arthritis and immune mediated arthritis.
What causes septic arthritis?
Bacterial infection of joint.
Symptoms of septic arthritis?
Acute onset. Inflammation symptoms of joint. Monoarthritis. Fever.
How do you diagnose septic arthritis?
Joint aspiration to get bacteria sample. Gram stain and culture done.
Treatment of septic arthritis?
Surgical washout and iv antibiotics.
Risk factors of septic arthritis?
Immunosupressed and IV drug use.
What is an exception for septic arthritis that displays different symptoms?
Gonococcal septic arthritis causes polyarthritis.
2 types of crystal arthritis?
Gout and pseudogout.
What causes gout?
Deposition of monosodium urate crystals around joints. This results in inflammation.
What is a key risk factor for gout?
High uric acid levels.
What causes hyperuricemia?
Genetic tendency, increase intake of high purine foods and reduced excretion due to kidney failure.
What causes pseudogout?
Deposition of calcium pyrophosphate dihydrate crystals around joints which results in inflammation.
What are the symptoms of gout?
Acute onset, monoarthritis and formation of tophi.
What are tophi?
Stone deposits on skin.
Gout biomarkers?
High CRP and high serum urate.
What is a definitive test for crystal arthritis?
Synovial fluid analysis.,
How is synovial fluid analysed?
Use of microscopy and polarising light microscopy.
Shape of gout crystal?
Needle shaped.
Shape of pseudogout crystal?
Brick shaped.
Birefringerence test result for gout?
Negative.
Birefringerence test result for pseudogout?
Positive.
What may you administer to treat gout?
Non steroidal anti inflammatory drugs. Use of glucocorticoids.
What may you prescribe to treat chronic gout?
Xanthine oxidase inhibitor.
Lifestyle changes for chronic gout?
Avoid purine rich foods.
How does a xanthine oxidase inhibitor help treat chronic gout?
Reduces serum urate levels by inhibiting purine metabolism.
How are osteoarthritis different to rheumatoid arthritis?
Osteoarthritis is a gradual onset. OA worsens with movement. There is joint enlargement in OA but no swelling. RA has morning stiffness.
How is OA different on an Xray to rheumatoid arthritis?
OA has osteophytes and has subchondral sclerosis (increased whiteness at joint). RA can have osteopenia and bony erosions.
What is subchondral sclerosis?
Thickening of bone below cartilage surface.
What are the 3 types of joints?
Fibrous joints, cartilaginous joints and synovial joints.
What is a fibrous joint and give an example
No space between bones such as sutures in skull.
What is a cartilaginous joint and give an example
Joints in which the bones are connected by cartilage such as joints between spinal vertebrae.
What is a synovial joint and give an example
Have synovial cavity between adjoining bones that is filled with synovial fluid. Knee joint.
What is the proteoglycan in articular cartilage?
Aggrecan.
What is a main compound present in synovial fluid?
Hyaluronic acid.
What is the synovium made up of?
Type 1 collagen. Synoviocytes.
What is the main reason to why cartilage doesn’t heal well?
Cartilage is avascular (lacks blood supply).
What is cartilage composed of?
Chondrocytes and ECM.
What is ECM made up of?
Water, collagen and proteoglycans.
What is the main proteoglycan in the ECM of cartilage?
Aggrecan.
What can happens to the two bones in a joint if there is a loss of articular cartilage in OA?
Bone in contact with bone.
What structure in the joint does rheumatoid arthritis affect?
Synovium.
Describe the pattern of joint involvement in rheumatoid arthritis
Polyarthritis and symmetrical.
What joints does rheumatoid arthritis commonly affect?
Joints in hands, wrists and feet.
Metacarpophalangeal joints (MCP)
Proximal interphalangeal joints (PIP)
NOT distal interphalangeal joints
Metatarsophalangeal joints (MTP)
What are common extra articular features present in a rheumatoid arthritis patient?
Fever, weight loss. Subcutaneous nodules.
What are some uncommon extra articular features present in a rheumatoid arthritis patient?
Vasculitis and episcleritis.
What causes proliferation of the synovium into a mass of tissue in rheumatoid arthritis?
Neovascularisation, lymphangiogenesis and recruitment of inflammatory cells. Excess of pro inflammatory cytokines.
What is the dominant pro inflammatory cytokine in rheumatoid arthritis? How does it cause symptoms of rheumatoid arthritis?
Tumour necrosis factor alpha. Osteoclast activation, chondrocyte activation which results in production of MMP and pro inflammatory cytokine release.
Example of TNF-alpha inhibitor?
Adalimumab.
Rheumatoid arthritis biomarkers?
Normocytic anaemia (low Hb but normal MCV). Raised platelets, raised ESR and CRP.
What biomarker can differentiate septic arthritis from rheumatoid arthritis?
Raise white blood cell count in septic arthritis but normal in rheumatoid arthritis.
What are the two main biomarkers for septic arthritis?
Raise white cell count and CRP.
What class of antibody is rheumatoid factor?
IgM.
What are the two self antigens targeted in rheumatoid arthritis?
Fc portion of IgG antibodies. Citrullinated proteins.
What are the two types of autoantibodies in rheumatoid arthritis?
Rheumatoid factor and anti-CCP antibody (anti-cyclic citrullinated protein antibody).
What is the most specific test for rheumatoid arthritis?
Anti-CCP antibody test.
When do bony erosions present in RA?
Later on in disease once its fully established.
Why is ultrasound better that xrays for RA?
Synovium can be visualised better.
What would you seen in the ultrasound of a joint in a rheumatoid arthritis patient?
Thickening of the synovium. Increased blood flow due to neovascularisation of synovium (doppler ultrasound) and erosions (IF RA IS ESTABLISHED).
1st line treatment for rheumatoid arthritis?
Glucocorticoids and DMARDs (disease modifiying anti rheumatic drugs).
Example of a disease modifying anti rheumatic drug?
Methotrexate.
2nd line treatment for rheumatoid arthritis?
Biologics such as JAK inhibitors (Janus kinase inhibitors).
Mechanism for how methotrexate works?
Acts as a folate antagonist by inhibiting dihydrofolate reductase.
Side effects of methotrexate?
Abnormal liver function and fall in white cell count.
Examples of biological therapies for rheumatoid arthritis?
Anti TNF alpha, antibody against B cell antigen or CD20, antibody against IL-6 receptor, blocking of T cell co stimulation proteins.
What is seronegative arthritis?
When you have inflammatory joint disease symptoms but don’t have rheumatoid factor or anti ccp.
Types of seronegative arthritis?
Psoriatic arthritis, reactive arthritis, ankylosing spondylitis and IBD associated arthritis.
Presentation of psoriatic arthritis
Scaly red plaques on extensor surfaces (elbows and knees). Asymmetrical pattern of joint involvement. Usually affects interphalangeal joints.
Doesn’t affect MCPJ’s unlike RA.
What is reactive arthritis?
Sterile inflammation of joint following infection elsewhere in the body.
What type of infections usually cause reactive arthritis?
Urogenital (chlamydia) and gastrointestinal (salmonella).
What extra articular features might be present in reactive arthritis?
Enthesistis (inflammation where tendon or ligament attached to bone), skin inflammation and eye inflammation.
What serious infections can trigger reactive arthritis?
HIV or Hepatitis C infection.
What test can you do to see if someone is more likely to develop reactive arthritis?
HLA-B27
What is HLA-B27?
MHC I class molecule.
How does ankylosing spondylitis present?
Inflammation of spine. Inflammation of sacro iliac joints. Enthesistis
Extra articular features in ankylosing spondylitis?
4 A’S. Anterior uveitus (iris), Apical lung fibrosis, aortitis (inflammation of aorta), amyloidosis.
What is Enthesitis
Inflammation where tendon or ligament joins bone.
What is a big risk factor for ankylosing spondylitis?
HLA-B27 positive.
Main cytokines involved in ankylosing spondylitis?
TNF alpha, IL-17 and IL-23.
Untreated ankylosing spondylitis can lead to what?
Bone growth between adjacent vertebrae leading to spinal fusion.
What diagnostic imaging technique is used for ankylosing spondylitits?
MRI.
Lifestyle changes to improve ankylosing spondylitis?
Physiotherapy and exercise.
First line treatment for ankylosing spondylitis?
NSAID’s
How do NSAID’s work?
Reduce inflammation by blocking COX1 and COX2 resulting in inhibition of prostaglandin production.
Risks of NSAID’s
Can make asthma worse. Peptic ulcer.
Second line treatments for ankylosing spondylitis?
Biologics such as anti TNF alpha and anti IL17.
Why do NSAID’s cause asthma to get worse?
Increased production of leukotrienes which cause bronchoconstriction.
Autoantibodies in SLE (systemic lupus erythematous) target what?
Nucleic acids and other cell nucleus proteins.
Key symptom present in SLE (systemic lupus erythematous)?
Butterfly rash.
Two types of autoantibodies produced in SLE that can be measured in the blood?
Antinuclear antibodies and anti-double stranded DNA antibodies.
What is a big risk factor for SLE (systemic lupus erythematous)?
Sex (Women are a lot more likely to get it).
Which of the two autoantibodies is more specific for SLE?
Anti-double stranded DNA antibodies.
Where does gout usually occur?
Big toe.
