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Musculoskeletal and Rheumatology > Introduction to Rheumatology > Flashcards

Introduction to Rheumatology Flashcards

1
Q

What are fibrous joints

A

No space between the bones Sutures in skull Syndesmosis (sheet of connective tissue) in tibia and fibula joint Synarthroses, amphiathroses

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2
Q

What are cartilaginous joints

A

Bones connected by cartilage e.g. joints between spinal vertebrae

Synarthroses, amphiathroses

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3
Q

What are synovial joints

A

Space between joining bones Filled with synovial fluid Diarthroses

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4
Q

What is the synovium

A

1-3 cell deep lining containing macrophage-like phagocytic cells (type A synviocyte) and fibroblast-like cells that produce hyaluronic acid - lubricate joint

Type 1 collagen

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5
Q

What is synovial fluid

A

Hyaluronic acid rich lubricating fluid

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6
Q

What is articular cartilage

A

Smooth lining to end of bone

Type 2 collagen

Proteoglycan (aggrecan)

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7
Q

What is the composition of cartilage

A

Chondrocytes

Extracellular matrix: water, collagen and proteoglycans

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8
Q

Why is cartilage being avascular important

A

No blood supply so poorly heals

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9
Q

What is aggrecan

A

Proteoglycan which possesses many chondroitin sulfate and keratin sulfate chain

characterised by its ability to interact with hyaluronan to form large aggregates

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10
Q

Diagram of cartilage structure

A
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11
Q

What is arthritis

A

Disease of the joints

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12
Q

What is the epidemiology of esteoarthritis

A

Joint trauma (footballer’s knees)

prevalent as age increase

heavy manual labour (spinal arthritis)

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13
Q

what is the onset of osteoarthritis

A

gradual. slowly progressive

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14
Q

which joints are affected in osteoarthritis

A

Distal interphalangeal joints

Proximal interphalangeal joints

First carpometacarpal joints

Spine

Weight bearing joints of lower limbs = knees and hips

First metatarsophalangeal joint - toe

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15
Q

What are the symptoms and signs of OA

A

Joint paint - worse with activity, bettery with rest

Joint instability

Join crepitus - creaking, cracking grinding sound

Joint stiffness

Limited range of motions

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16
Q

What are heberdens nodes

A

swelling at DIP

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17
Q

What are bouchard nodes

A

Swelling at the PIP

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18
Q

Radiographic features of OA

A

Joint space narrowing

Subchondral bony sclerosis - white spaces

Osteophytes - bone spurs

Subchondral cysts

19
Q

Picture of bony spurs

A
20
Q

What is inflammation

A

Physiological repsonse to deal with injury and infection

21
Q

How does inflammation manifest

A

Red (rubor)

Pain (dolor)

Hot (calor)

Swelling (tumour)

Loss of function

22
Q

Inflammation of joint physiological changes

A

Increased blood flow

Migration of white blood cells

Activation/differentiation of leucocytes

Cytokine production e.g. TNF-alpha IL1, 6 17

23
Q

Causes of joint inflammation

A

Infection - septic arthritis (acute), TB (chronic)

Crystal arthritis - gout, pseudgout

Autoimmune - rheumatoid, psoriatic, reactive arthritis, systemic lupus erythematosus

24
Q

Septic arthritis fact sheet

A

CAUSE: bacterial infection from spread of blood

RISK FACTORS: immunosuppressed, pre-existing joint damage, intravenous drug use - spread bacteria

MEDICAL EMERGENCY

usually only one joint affected- monoarthritis

SYMPTOMS: acute painful, red, hot, swelling, fever

DIAGNOSIS: joint aspiration and sent to lab

COMMON ORGANISMS: staphylococcus aureus, streptococci, gonococcus (polyarthritis, less likely to cause joint destruction)

TREATMENT: surgical wash-out (lavage) and IV antibiotics

25
Q

Crystal arthritis gout fact sheet

A

CAUSE: deposition of urate (uric acid) crystals which leads to inflammation, genetic tendency, increase intake of purine rich foods: beer, reduced excretion (kidney failure)

RISK FACTOR: high uric acid levels

SYMPTOMS: first metatarsopphalangeal joint most commonly affected, red, hot, swollen, joints in foot ankle knee wrist figner and elbow, crystal deposits (tophi) may develop around hands, feet elbows and ears

XRAY IMAGING: rate bite erosions juxta-articular

26
Q

Crystal arthritic pseudogout

A

CAUSE: deposition of calcium pyrophosphate dihydrate - inflammation

RISK FACTOR: background osteoarthritis, elderly patients, intercurrent infection

27
Q
A
28
Q

xray of crystal arthritis gout

A
29
Q

How to diagnosis crystal arthritis

A

Use polarised light

Gout - needle shaped crystals with negative birefrignence

Pseudogout - rhomboid shaped crystal with postivie birefringence

30
Q

RA fact sheet

A

CAUSE: inflammation of synovium

RISK FACTORS: immunosuppressed, pre-existing joint damage, intravenous drug use - spread bacteria

SYMPTOMS: early morning stiffness, polyarthritis, symmetrical, particularly hands and feets (MCP, PIP, wrists, knees, ankles, MTP), fever, weight loss, subcutaneous nodules, rheumatoid nodules, vasculitis, episcleritis, ocular inflammation, neuropathies, amyloidosis, lung disease, felty syndrome

DIAGNOSIS: autoantibody against IgG - antibody against antibody “rheumatoid factor”

COMMON ORGANISMS: staphylococcus aureus, streptococci, gonococcus (polyarthritis, less likely to cause joint destruction)

TREATMENT: surgical wash-out (lavage) and IV antibiotics

31
Q

RA subcutaneous nodules

A

Clasically found distal to elbow, also on fingers

central area of fibronoid necrosis surrounded by histocytes and peripheral layer of connective tissue

30% of patients

Severe disease, extra-articular manifestations, rheumatoid factor

32
Q

What is the pathogenesis of RA

A

Synovium becomes proliferated mass of tissue (pannus)

Neovascularisation - ingrowth of new blood vessels

Lymphangiogenesis - ingrowth of lymphatic

inflammatory cells - activated B and T cell, plasma cells, mast cells, activated macrophages

Excess of proinflammatory vs anti-inflammatory

TNFalpha - pleotropic - important cytokine

Therapy - targeting TNFa inhibition

33
Q

What are the autoantibodies in RA

A
  1. Rheumatoid factor - recognise Fc portion of IgG as their target antigen - IgM antibodies targeting IgG antibodies - immune complexes triggers inflammation
  2. Antibodies to citrullinated protein antigens (ACPA) - highly specific to rheumatoid arthritis - citrullination of peptides is mediated by enzymes: peptidyl arginine deiminases (convert arginine to citrulline)
34
Q

What is the treatment of RA

A

Prevent joint damage

Early recognition of symptoms, referral and diagnosis

AGGRESSIVE treatment

DRUGS: Disease modifying anti-rheumatic drugs

1ST LINE TREATMENT: methotrexate in combination with hydroxycholoroquine or sulfasalazine

2ND LINE TREATMETN: Biological therapies, tafcitinib and baricitinib

Glucocorticoid - injected into joints, however side effects

35
Q

What are the biological therapies of RA

A

Usually proteins that specifically target a protein such as an inflammatory cytokine

  1. Inhibition of TNF alpha - infliximab antibodies, fusion proteins (etanercept)
  2. B cell depletion - ritucimab - antibody against the B cell antigen CD20 - depletion of B cells from peripheral blood
  3. Modulation of T cell co-stimulation - abatacept - fusion protein - combines extracellular domain of human cytotoxic T lymphocyte associated antigen 4 (CTLA-4) linked to modified Fc (hinge, CH2 and CH3) of human immunoglobulin G1, stops t cells getting stimulated
  4. Inhibition of IL6 - tocilizumab and sarilumab
36
Q

What is the problem with part mouse part human antibodies

A

Patient will develop antibodies to mouse component

37
Q

What is anakinra

A

Il1 receptor antagonist

38
Q

X ray of RA and OA

A
39
Q

Psoriatic arthritis fact sheet

A

Autoimmune disease of the skin

10% of psoriasis patients have joint inflammation

Rheumatoid factors are not present

PRESENTATION: asymmetrical arthritis affecting IPJs, index and little finger

Can present with RA symptoms

Spinal inflammation and sacro-iliac inflammation

Can present with oligoarthritis and arthritis mutilans

40
Q

What is oligoarthritis

A

Inflammation of just a few joints - 2 to 4

Affects large joints of knee and ankle

41
Q

Arthritis mutilans

A

Bones around joint get dissolved

Shorten fingers and excess skin - telescoping

42
Q

Reactive arthritis

A

Sterile inflammation in joints following infection especially urogenital and gastrointestinal (chlamydia, salmonella, shigella, campylobacter)

OTHER MANIFESTATIONS: tendon inflammation (enthesitis), skin and eye inflammation

May be first manifestation of HIV or hepatitis C

Genetic predisposition (HLA-B27) and environmental trigger such as salmonella

Symptoms may be mild

Immune reaction to a previous infection

43
Q

Systemic Lupus Eythematous

A

Multisystem autoimmune disease

Almost any organ

MANIFISTATIONS: joint pain, skin rash, kidney involvement, blood abnormalities, lung and CNS involvement, mallat butterfly rash

Autoantibodies directed to cell nucleus (nucleic acid and proteins)

Clinical tests: Antinuclear antiboides, high sensitivity for SLE but not specific, neg test rules out but pos test does not mean SLE

Clinical tests: Anti-double stranded DNA antibodies: high specifity for SLE

Epidemiology: F:M 9:1, 15-40 yrs, increase prevalence in african and asian

Musculoskeletal and Rheumatology (3 decks)

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