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Y1 BRS > Rheumatology COPY > Flashcards

Rheumatology COPY 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
Cellular changes with inflammation?
* Migration of white blood cells (leucocytes) into the tissues * Activation/differentiation of leucocytes * Cytokine production E.g. TNF-alpha, IL1, IL6, IL17
26
The 3 main causes of joint inflammation?
* Infection e.g septic arthritis * Crystal arthritis e.g gout * Autoimmune(includes RA,PA,SLE)
27
What causes septic arthritis?
Bacterial infection of a joint (usually caused by spread from the blood)
28
Risk factor for septic arthritis?
immunosuppressed, pre-existing joint damage, intravenous drug use (IVDU)
29
How to diagnose septic arthritis?
Aspiration of joint fluid e.g pus. Sent for gram stain and culture (often S.aureus or streptococci)
30
How to treat septic arthritis?
Surgical washout and IV antibiotics.
31
2 main types of crystal arthritis?
Gout and pseudogout
32
What is gout?
Gout is a syndrome caused by deposition of urate (uric acid) crystals -\> inflammation
33
What is pseudogout?
Pseudogout is a syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystal deposition crystals -\> inflammation
34
How to diagnose crystal arthritis?
aspirating fluid from the affected joint and examining it under a microscope using polarized light Gout: needle shaped crystals with **negative** birefringence **P**seudogout: rhomboid shaped crystals with **positive** birefringence
35
What is rheumatoid arthritis?
Chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis
36
How does RhA affect joints?
Symetrically and polyarthritis. Esp hands and feet e.g MCP, PIP, wrists,knees and ankles.
37
Where is the primary site of pathology in RhA?
Synovium including synovial joints,tenosynovium and bursa.
38
What are the extra-articular features of RhA?
* Fever * weight loss * Subcutaneous nodules * Vasculitis/episcleritis(uncommon)
39
What are subcutaneous nodules?
Central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue. Associated with severe disease.
40
Describe the pathogenesis of rhA?
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
What is the dominant cytokine in the rheumatoid synvium?
TNF-alpha
42
What is TNF-alpha
Pro-inflammatory cytokine mainly produced by activated macrophages.Causes angiogenesis,osteoclast activation and chondroycte activation.
43
What do osteoclasts cause?
Bone resorption leading to bone erosion
44
What do synoviocytes cause?
Pain and joint swelling
45
What do chondrocytes cause?
Cartilage degradation and joint space narrowing
46
What are the autoantibodies involved in RhA?
Rheumatoid factor IgM anti-IgG antibody ACPA
47
What does ACPA mean?
Antibodies to citrullinated peptides including anti-cyclic citrullinated peptide antibody(anti-CCP antibody)
48
Which enzymes citrullinate peptides?
Peptidyl arginine deiminases (PADs)
49
How to manage RhA?
* Early recognition of symptoms, referral and diagnosis * Prompt initiation of treatment: joint destruction = inflammation x time * Aggressive treatment to suppress inflammation
50
Drug treatments for RhA?
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
Why is prednisolone not used long-term?
Glucocorticoid therapy important but has side effects.
52
What are the biological therapies against RhA?
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
Compare OA with rheumatoid arthritits?
54
What is psioriatic arthritis?
* Present in 10% of psoriasis patients * Seronegative * Classically asymmetrical arthritis affecting IPJs
55
What is reactive arthritis?
* 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
* What is Systemic Lupus Erythematous?
* Multi-site inflammation * Presence of autoantibodies e.g antinuclear or anti-dsDNA

Y1 BRS (39 decks)

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