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MHD2 > Block 9 - L16, 17 > Flashcards

Block 9 - L16, 17 Flashcards

1
Q

What percent of US adults are diagnosed with arthritis?

A

20%

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2
Q

What is the most common form of arthritis?

A

Osteoarthritis

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3
Q

Compare the frequency of arthritis in men and women.

A

More common in women

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4
Q

What happens in osteoarthritis (aka degenerative arthritis)?

A

Degeneration of articular cartilage (chondrocytes respond to stress in a way that results in breakdown of the matrix)

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5
Q

List some causes of secondary osteoarthritis.

A
  1. Trauma
  2. Inflammatory arthritis (RA, infectious, seronegative spondyloarthropathies)
  3. Dysplastic and hereditary conditions
  4. Kashin-Beck disease (joint hypermobility)
  5. Bone disorders
  6. Metabolic and endocrine disorders
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6
Q

What age group is osteoarthritis most commonly seen in?

A

> 65 y/o

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7
Q

In OA, ___ changes can be seen beginning at 45 years of age, but these are fairly unsymptomatic.

A

Radiographic (37% - knee, 27% - hip, >90% - hands)

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8
Q

What are the risk factors for OA? What is the strongest risk factor?

A
  1. Age (strongest)
  2. Obesity (leptin may influence chondrocytes)
  3. Chronic repetitive impact loading (long term weight bearing sports)
  4. Genetics (family history)
  5. Joint dysplasia (increases risk for hip OA)
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9
Q

List the components of normal morphology in this connective tissue.

A
  1. Collagen
  2. Proteoglycans
  3. Water
  4. Chondrocytes
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10
Q

What type of collagen is most prominent in this connective tissue and what is its role?

A

Type II collagen; distributes compressive forces, tethers cartilage to subchondral bone, dissipates weight bearing force

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11
Q

What type of proteoglycans are seen in this connective tissue and what is its role?

A

Aggrecans - high fixed negative charge allows for retention of water

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12
Q

What is the role of chondrocytes here?

A

Mediate turnover of matrix components

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13
Q

Discuss the morphologic changes seen in OA.

A

The articular cartilage loses homogeneity, becomes disrupted, and the surface fragments.

Deeper layers of cartilage are invaded by capillaries from calcified cartilage.

Chondrocytes (normally isolated) proliferate and cluster.

Osteophytes form.

Water content increases.

Increase in both anabolic and catabolic activity. Eventually, catabolic > anabolic.

Chondrocytes release degradative enzymes.

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14
Q

List the clinical characteristics of OA.

A
  1. Localized joint pain
  2. Stiffness (but very little morning stiffness)
  3. Worse with weight bearing
  4. Better with rest
  5. Involved areas: DIP, PIP joints, knees, hips, cervical/lumbar spine
  6. Joint crepitus
  7. Swelling NOT common
  8. Bony enlargement
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15
Q

What is seen on X-ray in OA?

A

Decreased joint space
Subchondral sclerosis and cysts
Osteophytes (spurs)

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16
Q

What lab tests are useful in OA?

A

None

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17
Q

How is OA managed?

A
  1. No cure
  2. Manage risk factors (PT, exercise, weight loss, dietary measures)
  3. Pharmacologic (acetaminophen, NSAIDs, intra-articular steroid injections in selected cases)
  4. Joint replacement surgery
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18
Q

What is rheumatoid arthritis?

A

Systemic, chronic, inflammatory, autoimmune disease primarily involving joints

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19
Q

What extra-articular organs may be involved in RA?

A
  1. Lungs (interstitial lung disease, pleural effusion)
  2. Anemia of chronic disease
  3. Eyes (episcleritis, scleritis)
  4. Skin (vasculitis), soft tissue (rheumatoid nodules)
  5. Heart (pericarditis)
  6. CNS rarely, peripheral neuropathy
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20
Q

Discuss the prevalence of RA, particularly in F vs. M.

A

Overall - 1%

F>M (5:1)

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21
Q

What is the peak incidence age range of RA?

A

20-50 y/o

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22
Q

What are environmental risk factors for RA?

A
  1. Infectious triggers (P. gingivalis)

2. Smoking (anti-CCP Ab)

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23
Q

Compare RA and OA.

A

RA: inflammatory (swelling), prolonged morning stiffness, systemic manifestations, joints involved = PIPs, MCPs, wrists, NO lumbar spine

OA: degenerative (no swelling), limited morning stiffness, localized symptoms, joints involved = DIPs, PIPs, CMC, lumbar spine

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24
Q

Compare the morphology of RA vs. OA.

A

RA - more inflammation, forms a panus that erodes into bone

OA - general wear and tear, more symmetrical

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25
Q

Discuss the pathogenesis of RA.

A
  1. Activation of CD4+ helper T cells
  2. T and B cells respond to self-antigens, leading to an inflamed synovium and increased inflammatory cytokines
  3. Fibroblasts, chondrocytes, synovial cells respond to the pro-inflammatory milieu, release destructive enzymes
  4. Osteoclasts are activated, leading to bone erosions
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26
Q

What cytokines are common in RA?

A

IL-1, IL-6, TNF-alpha

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27
Q

Describe the morphology of RA.

A
  1. Chronic papillary synovitis
  2. Synovial cell hyperplasia and proliferation (thickening) - pannus formation
  3. Perivascular inflammatory cell infiltrates (dense)
  4. Angiogenesis
  5. Neutrophils and organizing fibrin on synovial surface (layered)
  6. Increased osteoclast activity (erosion)
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28
Q

What is a pannus?

A

Thickening of the synovium

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29
Q

How is RA diagnosed clinically?

A
  1. Chronic, symemtrical, inflammatory polyarthritis

2. +/- extra-articular manifestations (rheumatoid nodules, ILD)

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30
Q

How is RA diagnosed with blood tests?

A
  1. Rheumatoid factors (auto-Ab against Fc portion of normal polyclonal IgG)
  2. Anti-CCP Ab
  3. Elevated inflammatory markers
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31
Q

What is seen on x-ray in RA?

A

Erosions and peri-articular osteoporosis

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32
Q

What is seen in the synovial fluid in RA?

A

WBCs, low glucose (non-specific)

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33
Q

What is a rheumatoid nodules?

A

Area of fibrinoid necrosis surrounded by palisading histiocytes

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34
Q

How is RA treated?

A
  1. NSAIDs
  2. Corticosteroids (prednisone) - bridge, not monotherapy
  3. DMARDs (disease modifying anti-rheumatic drugs - mainstay of long-term treatment)
  4. Non-biologic DMARDs (methotrexate, leflunomide)
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35
Q

What is the first line biologic treatment for RA and what does it do?

A

Etanercept, Adalimumab, Infliximab - anti-TNF-alpha

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36
Q

What are seronegative spondyloarthropathies?

A

Group of inflammatory arthritides which primarily involve ankylosing of the spine

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37
Q

Describe the symptoms of seronegative spondyloarthropathies.

A

Inflammatory back pain that improves with exercise, not relieved by rest

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38
Q

Describe the pattern of joint involvement of seronegative spondyloarthropathy.

A

Oligoarticular, asymmetric, more large joints involved, axial involvement (sacroiliitis), bamboo spine (fusion of the vertebrae), enthesitis

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39
Q

What is enthesitis?

A

Inflammation of tendon insertions

40
Q

What are the extra-articular manifestations of seronegative spondyloarthropathy?

A

Uveitis (not seen in RA), genitourinary tract (in reactive), skin (in psoriatic), GI tract (in IBD-associated)

41
Q

List the types of spondyloarthropathies.

A
  1. Psoriatic arthritis
  2. Ankylosing sponylitis
  3. IBD-related
  4. Reactive arthritis
  5. Undifferentiated spondyloarthropathy
42
Q

What is the typical age of onset for spondyloarthropathy?

A

16-30 y/o

43
Q

Discuss the arithrogenic theory of spondyloarthropathy pathogenesis.

A

Molecular mimicry via infection with bacteria such as Yersinia, Shigella, Salmonella, Campylobacter, Chlamydia, body forms Ab against self because they look like the bacterial Ag

44
Q

Discuss the theory of spondyloarthropathy pathogenesis related to dimerization.

A

Tendency to misfold and form dimers leads to inappropriate stimuli and inflammation. TNF-alpha is induced, NK, dendritic, and CD4 T cells are activated, IL-17 is produced.

45
Q

Discuss the cytokines involved in sponyloarthropathy.

A

TNF-alpha (similar to RA), IL-17, IL-23 (Th17 cells)

46
Q

What is the role of IL-17?

A

Important role in defense against extracellular bacteria; dysregulated expression leads to joint destruction

47
Q

What is the role of IL-23 in spondyloarthropathy?

A

Strongly overexpressed int he gust of AS patients, promotes highly specific entheseal inflammation

48
Q

What happens in sacroiliitis?

A

Granulation tissue erodes through the bone and cartilage into the joint cavity. Inflammation occurs. Bone may erode, cartilage may fuse, sclerosis may occur. Osteoblast activation eventually leads to replacement of cartilage by new bone, which causes anklyosis.

49
Q

What happens in spinal ankylosis?

A

Inflammation at vertebral corners leads to development of syndesmophytes

50
Q

What are syndesmophytes?

A

Sclerosis and squaring of vertebral corners; leads to complete bridging ossification

51
Q

What are the features of spondyloarthropathy?

A
  1. Inflammatory back and/or buttock pain
  2. Chest wall pain
  3. Enthesitis
  4. Dactylitis (sausage shaped swelling of digit)
  5. Uveitis
  6. Sacroiliitis on imaging
52
Q

What is the triad of symptoms in reactive arthritis?

A
  1. Non-gonococcal urethritis
  2. Conjunctivitis
  3. Arthritis

*Can have only arthritis
Follows certain enteric infections and sexually acquired infections

53
Q

What is a mucocutaneous features sometimes seen in reactive arthritis?

A

Keratoderma blennorhagica

54
Q

How is spondyloarthropathy treated?

A
  1. Education and PT
  2. NSAIDs
  3. Oral DMARDS
  4. Biologics (anti-TNF-alpha, anti-IL-23)
55
Q

List the types of crystal-induced arthropathy.

A
  1. Gout

2. Pseudogout

56
Q

What crystal causes gout?

A

Monosodium urate monohydrate

57
Q

What crystal causes pseudogout?

A

Calcium pyrophosphate dihydrate

58
Q

What happens in crystal-induced arthropathy?

A

Inflammatory arthritis (episodic and acute, but can be chronic)

59
Q

What is the pathogenesis of crystal-induced arthropathy?

A
  1. Supersaturation of uric acid
  2. Cyrstal formation
  3. Crystals activate the immune system - complement cascade recruits neutrophils, monocyte phagocytosis activates the intracellular inflammasome.
  4. Inflammasome activation leads to increased IL-1b
60
Q

Discuss the epidemiology of gout.

A

M»F

Age 65 and older (can happen younger)

61
Q

What is the crystallization point for uric acid?

A

6.3 mg/dL

62
Q

Why are women at a lower risk of gout until menopause?

A

Estrogen has uricosuric effects (excreted in urine)

63
Q

What are additional risk factors for gout?

A

Obesity, metabolic syndrome, high purine diet, fructose, medications

64
Q

What medications put you at higher risk for gout?

A

Thiazide diuretics and low dose aspirin

65
Q

What foods have the highest levels of purines?

A

Red meat, beer (hops), shellfish, beans

66
Q

Gout may be caused by overproduction or underexcretion of urea - which is more common?

A

Underexcretion (90%)

67
Q

What enzyme leads to the formation of uric acid?

A

Xanthine oxidase

68
Q

What are the clinical features of gout?

A
  1. Acute inflammatory arthritis
  2. Usually monoarticular (can be oligo or poly)
  3. Podagra
  4. Resolves in days to weeks
  5. Repeated attacks (show characteristic erosions on x-ray)
  6. Tophi
69
Q

What is podagra?

A

Acute involvement of the first MTP seen in gout

70
Q

How is gout diagnosed definitively?

A

Demonstration of crystals on polarized microscopy

71
Q

How do urate crystals appear?

A

Parallel, negative biorefringence - eyellow

Perpendicular, negative biofrefringence - blue

72
Q

How is gout treated?

A

Acutely - NSAIDs, other pain control (IL-1 inibitor)
Anti-inflammatory prophylaxis
Reduction of urate burden (allopurinal)

73
Q

What is calcium pyrophosphate deposition disease (CPPD, aka pseudogout)?

A

Caused by calcium pyrophosphate dihydrate crystals, acute presentation similar to gout - podagra not characteristic, knees and wrists most involved (also elbows, shoulders, ankles)

May see chondrocalcinosis on XR, but not sensitive or specific

74
Q

What are the 4 presentations of CPPD?

A
  1. Asymptomatic (chondrocalcinosis on XR, no symptoms)
  2. Acute (pseudogout)
  3. OA + CPPD (pseudoOA)
  4. Chronic CCP cyrstal inflammatory arthritis (pseudoRA)
75
Q

Discuss the epidemiology of CPPD.

A

More common in older individuals

76
Q

What are some secondary causes of CPPD?

A

Hemochromatosis, hyperparathyroidism, hypophosphatasia, hypomagnesemia

77
Q

What is chondrocalcinosis?

A

Calcium deposition

78
Q

How do crystals of pseudogout appear?

A

Positive + parallel = blue

Positive + perpendicular = yellow

79
Q

How is acute CPPD treated?

A

Similar to acute gout - NSAIDs, oral steroids, steroid injection, colcichicine, rarely anti-IL-1

80
Q

Basic calcium phosphate crystals such as ___ may deposit in joints and soft tissues. One example is the Milwaukee shoulder - explain.

A

Hydroxyapatite

Destructive arthritis associated with hyroxyapatite; seen in elderly females, destruction of rotator cuff and glenohumeral joint, monoarticular (can be bilateral)

81
Q

What is polymyalgia rheumatica?

A

AI disorder with pain and stiffness in the proximal joints and muscles - shoulders, hips, neck + constitutional symtpoms

82
Q

Polymyalgia rheumatic may be seen in the setting of ___.

A

Giant cell arteritis

83
Q

Discuss the epidemiology of polymyalgia rheumatica.

A

50+ y/o
2/3 F
Highest incidence rates in northern Europe, Scandinavian countries

84
Q

The etiology of polymyalgia rheumatic is still unclear, but it may involve what cytokines?

A

IL-6

85
Q

What lab findings are seen in polymyalgia rheumatica?

A

Increased ESR, CRP, IL-6, no serologies or Ab

86
Q

How is polymyalgia rheumatica treated?

A

Corticosteroids

87
Q

What is fibromyalgia?

A

Chronic widespread pain at 11+ tender points; must rule out organic and mechanical causes of pain; NOT AI or inflammatory

88
Q

What are risk factors for fibromyalgia?

A

Female, worry or expectation of chronicity, lack of control of the stressor, intensity of the initial symptoms, inactivity following stressor

89
Q

How is fibromyalgia managed?

A

Minimize chronic stressors, restorative sleep

90
Q

What is the most common benign neoplasm of the synovium?

A

Tenosynovial giant cell tumor

91
Q

What causes tenosynovial giant cell tumor?

A

Translocation fusing the promoter of the collagen 6A3 gene to the coding sequence of M-CSF

92
Q

What are the two types of TSGCT?

A
  1. Diffuse

2. Localized

93
Q

What happens in diffuse TSGCT?

A

Involves joint synovium, leads to monoarticular arthritis with recurrent swelling, erosions develop, knee, hip, ankle

Contorted mass of red brown folds, fingerlike projections, nodules

94
Q

What happens in localized TSGCT?

A

Giant cell tumor of the tendon sheath, painless mass involving wrist and finger tendon sheaths; most common soft tissue tumor of the hand

95
Q

Describe the histologic findings of TSGCT (both types).

A

Multiple hemosiderin-laden macrophages, osteoclast-like giant cells

96
Q

What is synovial chondromatosis?

A

Multiple nodules of hyaline cartilage within subsynovial connective tissue that can undergo enchondral ossification; benign, does not metastasize; joint point, swelling, stiffness, crepitance, limited motion with locking, grating sensation

Knee most common

MHD2 (34 decks)

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