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Y1 BRS > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What effect arises from IL-1 and TNF-alpha?

A

Stimulates cell to secrete proteases (serine proteases, and matrix metalloproteinases), hydrolyses the joint.

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2
Q

What are the 3 main mechanisms of action of rheumatoid disorders?

A

1) Erosion of hyaline cartilage
2) Inflammation of synovial membrane
3) Reduced joint space

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3
Q

What are the main 3 symptoms of rheumatoid arthritis?

A
  • Joint pain
  • Stiffness
  • Swelling
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4
Q

What is vasculitis?

A

Collection of disorders that destroy blood vessels by inflammation

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5
Q

What are DMARDs?

A

Disease modifying drugs

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6
Q

What are joints?

A

Where 2 bones meet

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7
Q

What are tendons?

A

Cords of strong fibrous collagen tissue attaching muscle to bone

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8
Q

What are ligaments?

A

Flexible fibrous connective tissue which connects two bones

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9
Q

Describe fibrous joints

A

No space between bones e.g sutures in skull. Allow no/very limited movement.

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10
Q

Describe cartilaginous joints and examples

A

Bones connected by cartilage e.g joints between spinal vertebrae. Allow no/very limited movement.

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11
Q

Describe synovial joints

A

Have a space between adjoining bones (e.g glenohumeral).Allow for free movement of the joint.

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12
Q

What is the synovium?

A

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

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13
Q

What is synovial fluid?

A

Hyaluronic acid-rich viscous fluid.

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14
Q

What is articular cartilage made of?

A

Type II collagen and proteoglycan (aggrecan)

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15
Q

What is cartilage composed of?

A

1) specialized cells (chondrocytes)
2) extracellular matrix: water, collagen and proteoglycans (mainly aggrecan)

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16
Q

What is aggrecan?

A

-a proteoglycan that possesses many chondroitin sulfate and keratin sulfate chains -characterized by its ability to interact with hyaluronan (HA) to form large proteoglycan aggregates

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17
Q

What does arthritis mean?

A

Disease of the joints

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18
Q

What are the 2 major divisions of arthritis?

A

Osteoarthritis and inflammatory

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19
Q

Pathology of osteoarthritis?

A

Cartilage worn out(wear and tear) and bony remodelling occurs. Gradual onset.

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20
Q

Epidemiology of OA?

A

More prevalent with increasing age,previous joint trauma and heavy manual labour.

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21
Q

Examples of joints affected by OA?

A
  • DIP -distal interphalangeal
  • PIP-proximal interphalangeal
  • First CMC
  • Spine
  • First MTP-metatarsophlangeal
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22
Q

Symptoms and signs of OA?

A
  • Joint pain worse with activity, better with rest
  • Joint crepitus (creaking cracking grinding sound on moving affected joint)
  • Joint instability (‘giving way’)
  • Joint enlargement e.g. Heberden’s nodes
  • Joint stiffness after immobility (‘gelling’)
  • Limitation of range of motion
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23
Q

Radiographic features of OA?

A
  • Joint space narrowing
  • Subchondral bony sclerosis
  • Osteophytes(Bone spurs)
  • Subchondral cysts
24
Q

Physiological change with inflammation?

A

Increased blood flow

25
Q

Cellular changes with inflammation?

A
  • Migration of white blood cells (leucocytes) into the tissues
  • Activation/differentiation of leucocytes
  • Cytokine production E.g. TNF-alpha, IL1, IL6, IL17
26
Q

The 3 main causes of joint inflammation?

A
  • Infection e.g septic arthritis
  • Crystal arthritis e.g gout
  • Autoimmune(includes RA,PA,SLE)
27
Q

What causes septic arthritis?

A

Bacterial infection of a joint (usually caused by spread from the blood)

28
Q

Risk factor for septic arthritis?

A

immunosuppressed, pre-existing joint damage, intravenous drug use (IVDU)

29
Q

How to diagnose septic arthritis?

A

Aspiration of joint fluid e.g pus. Sent for gram stain and culture (often S.aureus or streptococci)

30
Q

How to treat septic arthritis?

A

Surgical washout and IV antibiotics.

31
Q

2 main types of crystal arthritis?

A

Gout and pseudogout

32
Q

What is gout?

A

Gout is a syndrome caused by deposition of urate (uric acid) crystals -> inflammation

33
Q

What is pseudogout?

A

Pseudogout is a syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystal deposition crystals -> inflammation

34
Q

How to diagnose crystal arthritis?

A

aspirating fluid from the affected joint and examining it under a microscope using polarized light

Gout: needle shaped crystals with negative birefringence

Pseudogout: rhomboid shaped crystals with positive birefringence

35
Q

What is rheumatoid arthritis?

A

Chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis

36
Q

How does RhA affect joints?

A

Symetrically and polyarthritis. Esp hands and feet e.g MCP, PIP, wrists,knees and ankles.

37
Q

Where is the primary site of pathology in RhA?

A

Synovium including synovial joints,tenosynovium and bursa.

38
Q

What are the extra-articular features of RhA?

A
  • Fever
  • weight loss
  • Subcutaneous nodules
  • Vasculitis/episcleritis(uncommon)
39
Q

What are subcutaneous nodules?

A

Central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue. Associated with severe disease.

40
Q

Describe the pathogenesis of rhA?

A

Synovial membrane is abnormal in rheumatoid arthritis:

The synovium becomes a proliferated mass of tissue (pannus) due to:

  • Neovascularisation
  • Lymphangiogenesis
  • inflammatory cells: activated B and T cells plasma cells mast cells activated macrophages
41
Q

What is the dominant cytokine in the rheumatoid synvium?

A

TNF-alpha

42
Q

What is TNF-alpha

A

Pro-inflammatory cytokine mainly produced by activated macrophages.Causes angiogenesis,osteoclast activation and chondroycte activation.

43
Q

What do osteoclasts cause?

A

Bone resorption leading to bone erosion

44
Q

What do synoviocytes cause?

A

Pain and joint swelling

45
Q

What do chondrocytes cause?

A

Cartilage degradation and joint space narrowing

46
Q

What are the autoantibodies involved in RhA?

A

Rheumatoid factor IgM anti-IgG antibody ACPA

47
Q

What does ACPA mean?

A

Antibodies to citrullinated peptides including anti-cyclic citrullinated peptide antibody(anti-CCP antibody)

48
Q

Which enzymes citrullinate peptides?

A

Peptidyl arginine deiminases (PADs)

49
Q

How to manage RhA?

A
  • Early recognition of symptoms, referral and diagnosis
  • Prompt initiation of treatment: joint destruction = inflammation x time
  • Aggressive treatment to suppress inflammation
50
Q

Drug treatments for RhA?

A

DMARDS.

1st line treatment: methotrexate in combination with hydroxychloroquine or sulfasalazine

2nd line: Biological therapies offer potent and targeted treatment strategies.New therapies include Janus Kinase inhibitors : Tofacitinib & Baricitinib

51
Q

Why is prednisolone not used long-term?

A

Glucocorticoid therapy important but has side effects.

52
Q

What are the biological therapies against RhA?

A
  1. Inhibition of tumour necrosis factor-alpha (‘anti-TNF’) antibodies (infliximab, and others) fusion proteins (etanercept)
  2. B cell depletion Rituximab – antibody against the B cell antigen, CD20
  3. Modulation of T cell co-stimulation Abatacept - fusion protein linked to modified Fc of human immunoglobulin G1
  4. Inhibition of interleukin-6 signalling- Tocilizumab and Sarilumab
53
Q

Compare OA with rheumatoid arthritits?

A
54
Q

What is psioriatic arthritis?

A
  • Present in 10% of psoriasis patients
  • Seronegative
  • Classically asymmetrical arthritis affecting IPJs
55
Q

What is reactive arthritis?

A
  • Sterile inflammation in joints AFTER infection
  • Can include skin and eye inflammation
  • Symptoms occur 1-4 weeks after infection
  • Could be first signs of HIV/Hep C
56
Q
  • What is Systemic Lupus Erythematous?
A
  • Multi-site inflammation
  • Presence of autoantibodies e.g antinuclear or anti-dsDNA

Y1 BRS (39 decks)

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