Introduction to rheumatology actual Flashcards

1
Q

What is Rheumatology?

A

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
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2
Q

Session overview and learning objectives

A
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3
Q

Components of a synovial joint

A

Have 2 bones forming joint and between that have joint cavity

Synovial fluid is in middle-hyluronic acid rich viscous fluid

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4
Q

Joint diseases - overview

A

-Main condition we deal with is arthritis

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5
Q

What is inflammation?

A

•= 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

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6
Q

Causes of joint inflammation

A

1) Crystal arthritis

Gout

Pseudogout

2) Immune-mediated (“autoimmune”)

E.g.

Rheumatoid arthritis

Seronegative spondyloarthropathies

Connective tissue diseases

3) Infection

Septic arthritis

Tuberculosis

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7
Q
  1. Crystal arthritis-2 main types:
A

=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

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8
Q

Crystal Arthritis – Gout

A

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
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9
Q

Crystal Arthritis – Gout

X-ray finding:

A

erosions on either side

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10
Q

Crystal Arthritis – Gout

Investigations and management

A

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)
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11
Q

SYNOVIAL FLUID examination

A
  • 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!

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12
Q
  1. Immune-mediated inflammatory joint disease

What is the most common one?

A
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13
Q

Rheumatoid arthritis: pathogenesis revision

A

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

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14
Q

Rheumatoid arthritis: pathogenesis

TNF-alpha inhibition via biologics eg inflixumab. Show how implicative TNF-alpha is in inflammatory process of RA

A

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

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15
Q

Rheumatoid arthritis: overview

key features

A

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’

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16
Q

Rheumatoid arthritis: pattern of joint involvement

A

Polyarthritis eg affects over 5 joints

17
Q

Rheumatoid arthritis: synovial inflammation

A

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

18
Q

Rheumatoid arthritis: extra-articular features

A

Vasculitis-inflammation of blood vessels, can lead to side effects such as digital ischaemia

Neuropathies-damage to nerve endings

19
Q

Rheumatoid arthritis: subcutaneous nodules

A

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

20
Q

Rheumatoid arthritis: autoantibodies

RF-antibodies that recognise Fc portion of IgG as target antigen

A

Also check for anti-CCP antibodies

21
Q

Rheumatoid arthritis: management

A

-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

22
Q

Rheumatoid arthritis: biological therapies (2nd line treatment often reserved for severe cases)

A
23
Q

RA vs OA

A

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

24
Q

Name any other conditions that can cause inflammatory arthritis

A

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.

25
Q

AS: Clinical Presentation

A

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)

26
Q

AS: Investigations and Management

A
  • 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
27
Q

Psoriatic arthritis

A
  • 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
28
Q

Psoriatic arthritis-investigations and management

A

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
29
Q

Reactive arthritis

A
  • 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

30
Q

Connective tissue disease eg

Systemic Lupus Erythematous (SLE)

A
  • 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
31
Q

Other connective tissue disease:

A
  • 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.

32
Q

DMARDs:

A

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).