Introduction to rheumatology actual Flashcards
(32 cards)
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.






