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rheumatology Flashcards

1
Q

What do joints do? What do ligaments do? What do tendons do?

A

Joints are where bones meet. Ligaments connect 2 bones. Tendons connect muscle to bone.

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2
Q

What is diarthroses, amphiarthroses, synarthroses? What types of joint are they?

A
  • Diarthroses is free joint movement (synovial joint).
  • Amphiarthroses is limited joint movement.
  • Synarthroses is no movement (both of these can be cartilaginous or fibrous joints)
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3
Q

What is the structure of a synovial joint?

A

Each bone lined with articular cartilage, synovium lines synovial cavity (filled with synovial fluid)

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4
Q

What is structure of synovium?

A

1-2 cell thick lining with macrophage like phagocytic cells (type A synoviocytes) & fibroblast like cells that produce hylauronic acid for joint lubrication (type B synoviocytes) & have type I collagen in ECM

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5
Q

What is structure of synovial fluid?

A

Rich in hyaluronic acid for lubrication

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6
Q

What is structure of articular cartilage?

A

Made of some cells & ECM made of type II collagen & proteoglycan (aggrecan)

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7
Q

What is structure of cartilage?

A

Made of specialized cells (chondrocytes) & ECM (water, collagen & proteolgycan - aggrecan).
-Avascular so heals poorly

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8
Q

What is aggrecan?

A

Proteoglycan with many chondroitin sulfate & keratin sulfate chains.
Ability to interact with hylauronic acid to form large proteocyglycan aggregates

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9
Q

What happens in osteoarthritis?

A

Articular cartilage is worn out & attempt at bony repair leads to bone spurs

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10
Q

What is epidemiology of osteoarthritis? Onset?

A

Increasing age, previous joint trauma, heavy manual labour.

Onset is gradual & slowly progressive

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11
Q

Which joints are usually affected in osteoarthritis?

A

Distal interphalangeal joint DIP, proximal interphalangeal joint PIP, 1st carpometacarpal joint of thumb (CMC), spine, knees, hips, 1st metatarsophalangeal joint of big toe

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12
Q

What are features of joints in osteoarthritis?

A
  • Joint pain worse with movement/better with rest, joint crepitus, joint instability, joint enlargement (swelling)
  • heberden’s nodes (DIP), bouchard’s nodes (PIP), joint stiffness/immobility, but not as prolonged as RA, limited ROM
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13
Q

What are osteoarthritic nodes on DIP?

A

Heberden’s nodes

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14
Q

What are osteoarthritic nodes on PIP?

A

Bouchard’s nodes

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15
Q

What does radiography show in osteoarthritis?

A
  • Joint space narrowing
  • osteophytes (bone spurs - lumps next to joints)
  • subchondral bony sclerosis (increased white)
  • subchondral cysts
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16
Q

How does inflammation manifest in inflammatory arthritis?

A
  • Rubor (redness), dolor (pain), calor (warm), tumor (swlling) & loss of function.
  • Increased blood flow, migration of WBC & activation, cytokine production TNF-a, IL-1, IL-6, IL-17
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17
Q

What is septic arthritis? What needs to be done and why? How does it usually present?

A
  • Bacterial infection of the joint that usually spread from blood.
  • Need emergency treatment because can rapidly destroy joint permanently.
  • Usually monoarthritic (but can be polyarthritic with gonococcal infection)
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18
Q

What are risk factors for septic arthritis?

A

Immunosuppresion, joint damage, IV drug use

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19
Q

How is diagnosis of septic arthritis made?

A

joint aspiration - aspirate fluid with needle & syringe & send for gram stain/culture

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20
Q

What are common organisms of septic arthritis?

A

S.aureus, streptococci, gonoccocus

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21
Q

Which organism causes polyarthritic septic arthritis?

A

gonococcus

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22
Q

What is treatment of septic arthritis?

A

Surgical lavage of joint & IV antibiotics

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23
Q

What are the 2 types of crystal arthritis?

A

Gout & pseudogout

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24
Q

What is gout due to?

A

Deposition of urate (uric acid) crystals

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25
Q

What are risk factors for gout?

A

High uric acid (hyperuricaemia) due to genetics, consumption of purine rich foods, kidney failure (reduced removal of uric acid)

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26
Q

How does gout present? What is usually affected? How does it resolve?

A

Acutely, monoarthritic, affects toe (podagra) (1st metatarsophalangeal joint) and other joints in foot, wrist, ankle, knee etc.

  • really painful, joint red, warm, tender, swollen.
  • Resolves spontaneously after 3-10 days
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27
Q

What can be seen in gout under skin?

A

Crystal deposits (tophi) under skin (yellow appearance)

28
Q

What is seen on x-ray of gout?

A

If chronic can lead to damage of joint (erosion) like rat -bites at MTPJ of toe

29
Q

How Is diagnosis of gout made? What is seen?

A

Aspirate fluid & under polarized light with microscope see needle shaped crystals with negative birefringence

30
Q

How is gout managed acutely & chronically?

A

Acutely: colchicine, NSAIDS, steroids.
Chronically: allopurinol (lowers uric acid levels)

31
Q

What is pseudogout caused by?

A

Deposition of calcium pyrophosphate dihydrate crystals

32
Q

What are risk factors for pseudogout?

A

Osteoarthritis, elderly, intercurrent infection

33
Q

How is diagnosis of pseudogout made?

A

Aspirate fluid and under polarized light with microscope see rhomboid shaped crystals with positive birefringence

34
Q

What is rheumatoid arthritis? How does it present?

A

Chronic autoimmune disease with pain, stiffness, symmetrical synovitis, can have tenosynovium surrounding tendons and bursa swelling.

35
Q

What is seen on radiograph in RA?

A

Joint space narrowing, osteopenia & bony erosions

36
Q

What are extra-articular diseases of rheumatoid arthritis?

A

Systemic inflammation eg. Rheumatoid nodules, vasculitis, episcleritis, neuropathies, amyloidosis, lung disease with nodules, pleuritis, fibrosis, felty’s syndrome (triad of splenomegaly, leukopenia & RA), commonly fever, weight loss, subcutaneous nodules

37
Q

Which joints are commonly affected in rheumatoid arhtitis? Which joint usually spared?

A

MCP, PIP, MPT but usually spares DIP

38
Q

What are subcutaneous nodules seen in RA?

A
  • Central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue.
  • Found just distal to elbow or extensor surfaces of fingers.
  • Associated with severe disease, extra-articular manifestations & rheumatoid factor.
  • Rheumatoid nodule in hands and elbow (ulnar border of forearm)
39
Q

What is pathogenesis of rheumatoid arthritis?

A
  • Synovium inflammation & proliferation so it becomes big pannus because of neovasculairsation and lympangiogenesis & infiltrate of inflammatory cells.
  • Excess pro-infalmmatory cytokines in RA
40
Q

What is the key cytokine in rheumatoid arthritis? What does it do?

A

TNF-a.
pro-inflammatory cytokine in synovium that affects osteoclasts activating them (erosion), affects synoviocytes (iinflammation) affects chrondrocytes (cartilage degradation, joint narrowing)

41
Q

What 2 antibodies are found in RA?

A
  1. rheumatoid factors (RF)

2. antibodies to citrullinated protein antigens (ACPA)

42
Q

What is rheumatoid factor?

A

IgM antibodies against IgG (Fc region) forming complexes leading to inflammation

43
Q

What are antibodies to citrullinated protein antigens (ACPA)?

A

Highly specific to RA - citrullination of peptides mediated by enzymes named peptidyl arginine deiminases (PADs) that convert arginine to citrilline

44
Q

What is treatment of RA?

A

Disease modifying anti-rheumatic drugs DMARDs.

  • 1st line - methotrexate (folate antagonist) in combination with hydroxychloroquinine or sulfasalzine.
  • 2nd line - biological therapies eg. Janus kinase inhibitors (tofacitinib & baricitinib).
  • Glucocorticoids (anti-inflammatory eg prednisolone) but avoid long term because side effects.
  • MDT team - physio, OCT, hydrotherapy, surgery
45
Q

What are biological therapies offered for RA?

A
  1. inhibition of TNF-a (infliximab, etanercept)
  2. modulation of T cell stimulation (abatecept)
  3. B cell depletion (rituximab)
  4. inhibition of IL-6 signalling (toclizumab, sarilumab)
46
Q

What is the goal of management in RA?

A

Early recognition, fast initiation of treatment, aggressive treatment against inflammation

47
Q

What are differences between OA & RA?

A

RA onset more rapid, RA symmetrical OA asymmetrical, RA pain better with movement OA worse, morning stiffness prolonged RA, OA usually DIP, RA spared DIP, RA affects wrist, elbow ankle,( uncommon in OA). RA systemic symptoms high inflammation ESR CRP but not in OA. Radiograph: both have joint space narrowing. Osteophytes & subchondral sclerosis only OA. Osteopenia & bony erosions only RA

48
Q

What is psoriatic arthritis and what does it cause?

A

-Autoimmune condition of skin (scaly red plaques on extensor surfaces), usually symmetric affecting interphalangeal joints, can have symmetrical involvement of small joints (rheumatoid pattern), spinal/sacroiliac inflammation, oligoarthritis of large joints, arthritis mutilans (severe)

49
Q

What are investigations for psoriatic arthritis and what do you see?

A

-X-ray of joint (pencil in cup abnormality), MRI showing sacroilitis & enthesitis. Blood seronegative

50
Q

What Is management for psoriatic arthtitis?

A

DMARDS (methotrexate), avoid oral steroids (risk of pustular psoriasis due to skin lesions)

51
Q

What is reactive arthritis? Cause?

A
  • Sterile inflammation in joint following infection eg urogenital, GI (chlamydia, salmonella).
  • Genetic predisposition + environmental trigger
52
Q

hat are extra-articular manifestations of reactive arthritis?

A

Enthesitis (tendon inflammation), skin inflammation, eye inflammation

53
Q

Epidemiology of reactive arthritis?

A

young people with genetic predisposition (eg HLA-B27) & environmental trigger (infection)

54
Q

What can reactive arthritis be the first manifestation of?

A

HIV or hepatitis C

55
Q

How does reactive arthritis present?

A

1-4 weeks after infection which may be mild

56
Q

How is reactive arthritis managed?

A

Usually self limiting - managed with NSAIDs or DMARDs if needed

57
Q

What is SLE and what does it affect?

A

Autoimmune condition affecting many organs. Autoantibodies against cell nucleus components

58
Q

What are diagnostic antibodies used in SLE?

A

1 anti-nuclear antibodies ANA (high sensitivity but not specific) - negative rules it out but positive doesn’t mean SLE.
2. anti-double stranded DNA antibodies (anti-dsNDA) - high specificity for SLE in context of clinical signs

59
Q

What is epidemiology of SLE?

A

Mostly females, child-bearing age, more african/asian

60
Q

What is a common sign of SLE?

A

Malar butterfly rash on face to nose triggered by sun

61
Q

What is ankylosing spondylitis?

A

Seronegative spondyloarthropathy (no positive antibodies), chronic sacroilitis, results in spinal fusion (ankylosis)

62
Q

What are demographics of ankylosing spondylitis?

A

20-30yrs, male, associated with HLA-B27

63
Q

How does ankylosing spondylitis present?

A

-Lower back pain + stiffness (early morning improves with exercise), reduced spinal movements, peripheral arthritis, planar fasciitis, achilles tendonitis, fatigue, hyperextended neck, loss of lumbar lordosis, flexed hips + knees

64
Q

What are investigations for ankylosing spondylitis and what can you see?

A
  • Blood - normocytic anaemia, high CRP, ESR, HLA-B27.
  • X-ray/MRI: squaring vertebral bodies, romanus lesion, erosions, sclerosis, narrowing of SIJ, bamboo spine, bone marrow oedema
65
Q

What is management of ankylosing spondylitis?

A

Physiotherapy, exercise regimen, NSAIDS, DMARDS for peripheral joint disease

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