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Disease and Defense: Unit 4 > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What are the characteristics of spondyloarthropathies?

A 
Axial arthritis 
Peripheral arthritis 
Enthesitis 
Mucocutaneous lesions
HLA-B27
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2
Q

What patient population does ankylosing spondylitis effect most often?

A

Caucausian men between the ages of 16 and 40 years of age.

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3
Q

What is the common history of someone with AS?

A

Pain > 3 moths
Prolonged morning stiffness
Improvement of pain with exercise

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4
Q

What is cytokine is increased in the synovium of a patient with AS?

A

TNF-alpha

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5
Q

What is enthesitis?

A

Inflammation of ligamentous-, fibrous-, and thendinous- osseous junciton

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6
Q

What percent of Caucasians are HLA-B27 positive?

A

6-9%

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7
Q

What is the percent chance that someone who is HLA-B27 has of developing AS?

A

2%

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8
Q

What is the percent chance that someone who is HLA-B27 has of developing AS if they have a first degree relative with AS?

A

20%

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9
Q

What is the incidence of AS?

A

0.1-0.2%

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10
Q

Do mice with HLA-B27 develop AS?

A

Yes, unless they are raised in a sterile environment

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11
Q

What patient population most often develops reactive arthritis?

A

Caucasian males between the age of 40-50.

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12
Q

What would the history look like of a patient with reactive arthritis?

A

Diarrhea caused by shingella, salmonella, yersinia, campylobacter or urethritis caused by chlamydia 2-4 weeks prior to the onset of arthritis.

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13
Q

What is Reiter’s syndrome?

A

Conjunctivitis- Can’t see
Urethritis- Can’t pee
Arthritis- Can’t climb a tree

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14
Q

Reiter’s syndrome is commonly linked to what?

A

Reactive arthritis

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15
Q

What is the common site of arthritis in reactive arthritis?

A

Lower extremities-

  • —Enthesopathy- Achilles and plantar
  • —Dactylitis- Sausage toes
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16
Q

In what way can bacterial antigens get to the sites of arthritis?

A

Bacterial environmental triggers are transported to the joints in monocytes (Chlamydia can be latent)

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17
Q

What are the four possible theories of how HLA-B27 can predispose a person to develop AS?

A
  1. Arthritogenic peptide hypothesis
  2. Molecular mimicry
  3. Free heavy chain hypothesis
  4. Unfolded protein hypothesis
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18
Q

Define vasculitis.

A

Inflammation within or through the vessel wall resulting in damage to vessel intergrity flow

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19
Q

Name some of the cells that infiltrate vessels in vasculitis.

A 
Lymphocytes
Monocytes
Histiocytes
Eosinophils 
PMNs
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20
Q

Fibrinoid necrosis of vessel wall occurs secondary to what?

A

Immune complex deposition

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21
Q

What is the nature of lesions in all types of vasculitis?

A

Focal and segmental

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22
Q

What two vasculitis’ affect large ARTERIES?

A

Giant cell arteritis

Takayasu’s arteritis

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23
Q

What two vasculitis’ affect medium ARTERIES?

A

Polyarteritis nodosa

Kawasaki’s disease

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24
Q

What three vasculitis’ affect small ARTERIOLES/VENULES and are ANCA positive?

A
  1. Granulomatous with polyangiitis (Wegner’s) GPA
  2. Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
  3. Microscopic polyangiitis (MPA)
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25
Q

What threevasculitis’ affect small ARTERIOLES/VENULES and are ANCA negative?

A
  1. Henoch-Schonlein Purpura
  2. Essential cytoglobulinemic vasculitis
  3. Cutaneous leukoclastic angiitis
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26
Q

What are the five mechanisms suspected of vascular damage?

A
  1. Immune complexes (IC)
  2. Antineutrophil cytoplasmic antibodies (ANCA)
  3. Antiendothelial antibodies
  4. T cell dependent mediated endothelial cell injury
  5. Infection of endothelial cells
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27
Q

Name four sources of antigen for immune complexes.

A
  1. Drugs
  2. Bugs: infectious agents
  3. Connective tissue disease: autoimmune process
  4. Malignancy
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28
Q

What are the primary granules of PMNs associated with generalized GPA?

Which antibody binds these primary granules?

A

Proteinase-3 (PR3)

Cytoplasmic ANCA (c-ANCA)

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29
Q

What are the primary granules of PMNs associated with microscopic polyangiitis (MPA)?

What antibody binds to these primary granules?

A

Myeloperoxidase (MPO)

Perinuclear ANCA (p-ANCA)

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30
Q

Do antineutrophil cytoplasmic antibodies begin or amplify inclammatory vascular response?

A

AMPLIFY response

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31
Q

Where is the location of the muscle weakness in PM/DM?

A

Proximal muscle weakness

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32
Q

Identify the typical skin rashes associated with DM.

A 
Gottron's papules
Heliotrope rash
V-sign and shawl-sign
Mechanic's hands
Periungual changes/erythema
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33
Q

What is the worst presentation associated with PM or DM?

A

Intersitial lung disease (ILD)

34
Q

Name two of the anti-synthetase antibodies found in PM/DM.

A

Anti-aminoacyl-tRNA synthetases (cytoplasm)

Anti-Jo-1= anti-histadyl-tRNA synthetase

35
Q

Are the anti-synthetase antibodies pathologic or myotoxic?

A

No

36
Q

Polymyositis is characterized by what inflammatory cells?

Where are they located?

A

CD8+ T cells

Endomysial distribution surrounding and invading muscle fibers resulting in DIRECT muscle injury

37
Q

Dermatomyositis is characterized by what inflammatory cells?

Where are they located?

A

CD4+ T cells

Perivascular and perifascicular inflammatory infiltrate and is complement-mediated

38
Q

What is the potential etiology of PM/DM?

A

Evidence suggests a viral etiology:

  • Influenza and HIV
  • No live virus has been cultured but viral RNA has been detected
  • Juvenile DM: coxsackie B antibodies
  • Seasonal pattern: anti-Jo-1 antibodies and spring
  • DM: Interferon responsive pathways
39
Q

What is SLE?

A

A chronic, systemic autoimmune disease which affects multiple organ systems including the skin, joints, serosal surfaces, lungs, kidneys, CNS

40
Q

What is the fundamental defect in systemic lupus erythematosus (SLE)?

A

Misdirected recognition of self as foreign, resulting in an autoimmune process; T cell AND B cell process

41
Q

Antibody responses toward autoantigens are antigen-driven, but what do they require?

A

CD4+ T cells

42
Q

What are some of the theories to explain autoimmunity in SLE?

A
  1. Polyclonal B cell activation
  2. Molecular mimicry
  3. “Illicit help”
  4. Sequestered antigen
  5. Immunodeficiency
  6. Loss of T cell tolerance
43
Q

Is the defect that causes self-reactive lymphocytes a central or peripheral abnormality?

A

PERIPHERAL

44
Q

Name some genetic predispositions of SLE.

A
  1. HLA-DR3 and C4A null allele (C4A is the greatest risk)
  2. Increase incidence of SLE among relatives
  3. Concordance rate in monzygotic twins
  4. More common in some ethnic groups: African Americans, Hispanic Americans, and Asians
45
Q

What are some environmental factors that are associated with systemic lupus erythematosus?

A

Sex Hormones: Female more than male Increased incidence in women of childbearing age

Sun exposure: exacerbates systemic disease

46
Q

What percent of patients with SLE are ANA+?

A

> 95%

47
Q

Is a positive ANA specific for SLE?

A

NO. they can be found in other diseases

48
Q

Name some antibodies that are directed to multiple nuclear antigens

A

Anti-dsDNA antibodies: Renal disease

Anti-histone antibodies: SLE and drug-induced lupus

Antibodies to non-DNA, non-histone nuclear antigens:

  • SSA
  • SSB
  • Smith
  • Ribonuclear protein (RNP)
49
Q

Name the specific antibody-mediated disease (Type II).

A

Anti-RBC antibodies&raquo_space; hemolytic anemia

Anti-WBC antibodies, anti-Plt antibodies

Anti-phospholipid antibodies»block prothrombin activation > prolonged PTT > Clotting in a way we don’t know yet

50
Q

Define osteoarthritis.

A

Degeneration of articular cartilage with hypertrophy of contiguous bone: joint space loss, subchondral cysts, sclerosis, osteophytes

51
Q

Name some of the joints involved in osteoarthritis

A

DIP (Heberden’s), PIP (Bouchard’s), 1st CMC
Hips and knees
Spine: cervical and lumbar
First MTP

52
Q

What are some predisposing factors of OA?

A 
Age
Obesity
Occupational risk 
Trauma
Secondary OA: Inflammatory, metabolic 
SPORTS DO NOT HAVE ASSOCIATED INCREASE EXERCISE IS PROTECTIVE
53
Q

What are the five components of cartilage?

A 
Collagen
Proteoglycans 
Matrix proteins 
Chondrocytes 
Water
54
Q

What type of collagen is damaged in osteoarthritis?

A

Type II

55
Q

What two proteoglycans are linked to hyaluronic acid?

A

Chondroitin and keratin sulfate

56
Q

Name tow matrix proteins found in cartilage.

A

Metalloproteinases (MMPs) and Tissue inhibitors of metalloproteinases (TIMPS)

57
Q

What percentage of cartilage is made up of water?

A

70%

58
Q

Does cartilage have a blood supply or nerve supply?

A

Neither

59
Q

What are the following changes you see in cartilage in early osteoarthritis?

  • Chrondroccytes
  • Proteoglycans
  • Metalloproteinases
  • TIMP
  • Water content
A 
Increase of chondrocytes 
Decrease of proteoglycan
Increase metalloproteinases
Decrease in TIMP 
Increase in water content

Lack so systemic features
Synovial fluid is noninflammatory in type I (200-2000 WBC)

60
Q

What two structures produce cytokines and inflammatory mediators implicated in articular cartilage destruction?

A

Chrondrocytes and synovium

61
Q

Name three cytokines and inflammatory mediators implicated in articular cartilage destruction.

A
  1. Interleukin-1
  2. Nitric oxide
  3. Prostaglandins
    - Other cytokines: TNF, IL-6, IL-17 and IL-18

> > > > > Complement activation and adipokines

62
Q

Define: Rheumatoid arthritis

A

A systemic, inflammatory, autoimmune disorder of unknown etiology that results predominantly in a peripheral, SYMMETRIC SYNOVITIS which can result in cartilage and bone destruction

63
Q

What are the joints most commonly involved in rheumatoid arthritis?

A

Bilateral, symmetric-small joints of the hands and feel sparing the DIPs

Medium and large joints can be involved

X-rays: marginal joint erosions and deformities

64
Q

What is the etiology of rheumatoid arthritis?

A

Arthritogenic peptide/s in the genetically susceptible host

Disease susceptibility and severity associated with shared epitope (QKRAA; in antigen binding groove) in subtypes of HLA-DR4 and HLA-DR1

65
Q

What is the rheumatoid factor?

A

Antibody directed against the Fc portion of IgG; RF usually IgM, can be IgG or IgA

In 85% of patients with RA

Produced locally in the synovial tissue

RF-IgG immune compleses are PATHOGENIC

66
Q

What two autoantibodies when found in the same patient have a 98-100% specificity for RA?

A

Anti-CCP and RF

67
Q

What are the major lymphocytes found in the synovium of RA patients?

A

CD4+ T cells and Th17
Plasma cells
NO PMNs

68
Q

What is the role of CD4+ memory T cells in rheumatoid arthritis?

A

Modulation and amplificaiton of local immune response through antigen recognition

69
Q

What causes vasculitis in RA?

What causes rheumatoid nodule formation in the tissue of patients with RA?

A

RF-IgG immune complex

70
Q

What is the cause of gout?

A

The result of tissue deposition of monosodium urate (MSU) crystals due to hyperuricemia supersaturation

71
Q

What joints are commonly involved in gout?

A

1st MTP

Cool, peripheral joints of lower and upper extremities

72
Q

What is more common over-production or underextretors?

A

Underexcretors

73
Q

Uric acid is a product of ________ metabolism.

A

Purine

74
Q

Humans lack ________ which oxidizes uric acid into allantoin

A

Uricase

75
Q

Overproduction of uric acid is associated with what two X-linked disorders?

A 
PRPP synthetase overactivity 
HGPRT deficiency (complete: Lesch-Nyhan)
76
Q

How are crystal arthropathies diagnosed?

A

Arthrocentesis to look for needle-shaped, negatively birefringent

77
Q

What two drugs inhibit xanthine oxidase?

A

Allopurinol and Febuxostat

78
Q

How does MSU crystals induce inflammation?

A
  1. Naked MSU crystals bind TLR2/ TLR4

2. MSU crytals engage the caspase-1 activating NLRP3 inflammasome resulting in IL-1Beta production

79
Q

What does IgG-coating of crystals promote?

A

Phagocytosis by PMNs but IgG is NOT specific anti-crystal antibodies

80
Q

What does the coating of crystals by apolipoprotein B do?

A

Inhibits phagocytosis

81
Q

PPi perceipitates with calcium forming CPPD crystals in mid-zonal cartilage layers. These crystals are released into the joint space called
-“shedding phenomenon
-“enzymatic strip mining”
Describe CPPD crystals

A

Rhomboid, positively birefringent

Disease and Defense: Unit 4 (5 decks)

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