Introduction to rheumatology actual Flashcards
What is Rheumatology?
The medical specialty dealing with diseases of the musculoskeletal system including:
- Joints = where 2 bone meets
- Tendons = cords of strong fibrous collagen tissue attaching muscle to bone
- Ligaments = flexible fibrous connective tissue which connect two bones
- Muscles
- Bones
Session overview and learning objectives
Components of a synovial joint
Have 2 bones forming joint and between that have joint cavity
Synovial fluid is in middle-hyluronic acid rich viscous fluid
Joint diseases - overview
-Main condition we deal with is arthritis
What is inflammation?
•= a physiological response to deal with injury or infection
Clinically manifests as: Calor-hot, dolor-painful, tumour-swollen and rubor-red. Because of these can get loss of function.
Often specific cytokines which is how we target medications
Causes of joint inflammation
1) Crystal arthritis
Gout
Pseudogout
2) Immune-mediated (“autoimmune”)
E.g.
Rheumatoid arthritis
Seronegative spondyloarthropathies
Connective tissue diseases
3) Infection
Septic arthritis
Tuberculosis
- Crystal arthritis-2 main types:
=Gout-urate crystal deposition
purine rich food-eg alcohol is a risk factor, and also some other medications
High-Purine Foods Include:
- Alcoholic beverages (all types)
- Some fish, seafood and shellfish, including anchovies, sardines, herring, mussels, codfish, scallops, trout and haddock.
- Some meats, such as bacon, turkey, veal, venison and organ meats like liver.
Pseudogout-calcium pyrophosphate dihydrate crystal deposition
Crystal Arthritis – Gout
Urate crystals deposited in joints and also generally jus in body
Ears and joints of hands can see Tophi-white looking deposit
Extremely painful and comes on suddenly, has all features of inflammation. Can be so painful that patients may not even be able to touch the joint.
Purine rich food-meaty foods and rich foods eg fish
•Acute gout is a good example of arthritis
•A disease in which tissue deposition of monosodium urate (MSU) crystals occurs as a result of hyperuricaemia and leads to one or more of the following:
- Gouty arthritis
- Tophi (aggregated deposits of MSU in tissue)
•Gouty arthritis commonly affects the metatarsophalangeal joint of the big toe (‘1st MTP joint’) podagra
- Abrupt onset
- Extremely painful
- Joint red, warm, swollen and tender
- Resolves spontaneously over 3-10 days
Crystal Arthritis – Gout
X-ray finding:
erosions on either side
Crystal Arthritis – Gout
Investigations and management
Investigations
•Joint aspiration – synovial fluid analysis (to see what crystals look like)
Management-tend to split into 2 groups
- Acute attack – colcihine (has antiinflammatory properties), NSAIDs, Steroids
- Chronic – allopurinol (reduces uric acid production in body)
SYNOVIAL FLUID examination
- Would send fluid for crystal microscopy but also microscopy and culture to check for pathogens
- Slightly different appearance of crystals
Pseudogout starts with P and it is Positive for birefringence!
- Immune-mediated inflammatory joint disease
What is the most common one?
Rheumatoid arthritis: pathogenesis revision
RA-abnormal synovial membrane
due to neovascularisation-formation of new blood vessels and other inflammatory processes going on at the joint
Excess of pro-inflammatory cytokines such as Il-1, TNF-alpha and IL-6 compared to anti-inflammatory cytokines
Rheumatoid arthritis: pathogenesis
TNF-alpha inhibition via biologics eg inflixumab. Show how implicative TNF-alpha is in inflammatory process of RA
Ultimately TNF-alpha results in boney erosion, reduction in joint space etc. as it causes other pro-inflammatory cytokines to be released which leads to bone resorption etc.
So if stop TNF-alpha, can stop other processes
Rheumatoid arthritis: overview
key features
Key features:
•Chronic arthritis
- Polyarthritis - swelling of the small joints of the hand and wrists is common, but can happen in any synovial joints
- Symmetrical (eg similar in both hands)
- Early morning stiffness in and around joints
- May lead to joint damage and destruction - ‘joint erosions’ on radiographs
•Extra-articular disease can occur (due to inflammatory processes going on in the body)
- Rheumatoid nodules (nodules that appear on the skin)
- Others rare e.g. lung fibrosis, vasculitis, episcleritis (eye involevement)
•Rheumatoid ‘factor’ may be detected in blood
•Autoantibody against IgG - should really call this rheumatoid ‘antibody’ not ‘factor’
Rheumatoid arthritis: pattern of joint involvement
Polyarthritis eg affects over 5 joints
Rheumatoid arthritis: synovial inflammation
Can see swelling in PIP joints
Can also get inflammation, not only in joints but also in other areas in hand eg tenosynovitis, synovium around tendons
Can also get inflammation of bursae
Rheumatoid arthritis: extra-articular features
Vasculitis-inflammation of blood vessels, can lead to side effects such as digital ischaemia
Neuropathies-damage to nerve endings
Rheumatoid arthritis: subcutaneous nodules
Tend to be found in those who have a strongly positive rheumatoid factor
Elbow-typical place to see nodules and can help confirm diagnosis of arthritis
Rheumatoid arthritis: autoantibodies
RF-antibodies that recognise Fc portion of IgG as target antigen
Also check for anti-CCP antibodies
Rheumatoid arthritis: management
-referral from GP services to amke sure patients are treated as soon as possible to reduce joint destruction
DRUGS-eg DMARDS eg methotrexate which is often used with another DMARD eg hydroxychloroquine, can also use steroids for acute episodes, but not long term, also use biologics such as anti-TNF
Rheumatoid arthritis: biological therapies (2nd line treatment often reserved for severe cases)
RA vs OA
RA-inflammatory arthritis
- tends to affect MCP joints, so knuckles, can see loss of joint space, but also deformity
- Osteoporosis around joint
- Boney erosions (dark areas)
OA
-DIP lots of loss of joint space
Name any other conditions that can cause inflammatory arthritis
Ankylosing spondylitis
Seronegative as no specific positive autoantibodies
Inflammation of sacroiliac joints ie at bottom of spine
Associated with: HLA-b27 so genetic predisposition
HLA B27 is a contributory factor in the development of AS. However arounf 5-10% of population have AS and most don’t get AS. So by itself it’s not sufficient. HLA molecules are encoded by the MHC region on chr 6. T cells recognise peptide presented in association with HLA. CD4 T cells recognise HLA class 2, CD8 T cells recognise HLA class 1. HLA A,B and C are class 1.
AS: Clinical Presentation
Back pain >3 months, <45 years is suggestive of possible Ank Spond
Reduced spinal movements-so often ask them to touch toes
Patient may have flexed hips and knees to reduce pain or due to fusion of sacroiliac joints.
Anaemia common across most inflammatory diseases. Its the effect of cytokines on bone marrow (which produces the blood cells)
AS: Investigations and Management
- Look for HLA-B27 association
- Inflammatory markers important to check for
- MRI is very good investigation
- Bamboo spine is shown in X-ray
- Tends to improve with exercise, NSAIDs help reduce inflammation
Psoriatic arthritis
- Again look for HLA-B27 association
- Tends to affect IPJ rather than proximal joints
- Can cause Arthritis mutilans which is a very destructive form and joints get worn down very quickly in the hands
Psoriatic arthritis-investigations and management
Check for Rheumatoid factor to rule out RA, check for anti-CCP, ANA etc to rule out other factors and then together with skin involvement and joint involvement we would diagnose with psoriatic arthritis.
- Primarily DMARDs are used eg methotrexate
- Avoid oral steroids as can make skin involvement worse
Reactive arthritis
- Tends to occur after an infection, specifically urogenital or gastrointestinal
- Reiter’s syndrome, also known as reactive arthritis, is the classic triad of conjunctivitis, urethritis, and arthritis occurring after an infection, particularly those in the urogenital or gastrointestinal tract.
Sterile-means no bacteria
Self-limiting ie within a maximum of 6 weeks conditon will ressolve itself without active treatment.
Reative arthritis tends to affect only one joint. This is the same in septic arthritis but there is a pathogen within joint, but in reactive arthritis there is just a sterile inflammation within joint caused by previous infection, but won’t get systemic factors such as fever in reactive arthritis like you would in septic arthritis
Connective tissue disease eg
Systemic Lupus Erythematous (SLE)
- Positive test of ANA doesn’t mean specifically SLE and it could just be a small amount so not enough for SLE
- Affects females more than males 9:1
Other connective tissue disease:
- Systemic Sclerosis
- Myositis
- Sjogrens syndrome
- Mixed connective tissue disease
Overlap between these and lupus and especially in the antibodies that we use to try and diagnose them. ANA is positive in lots of the connective tissue disorders, which is why if it is negative, lupus is unlikely, but if it is positive it is not definitely lupus.
DMARDs:
Disease-modifying antirheumatic drugs (DMARDs) are a class of drugs indicated for the treatment of inflammatory arthritides including rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS).
