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Rheumatology > Exam 3 Review > Flashcards

Exam 3 Review Flashcards

1
Q

Osteoarthritis definition

A

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

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2
Q

Osteoarthritis joint involvement

A

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

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3
Q

Osteoarthritis predisposing factors

A

Age, obesity, occupational risks (miners, weavers), trauma
Secondary OA: inflammatory, metabolic (hemochromatosis, Wilson’s disease, ochronosis)
Sports in general present no increased risk; exercise may be protective

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4
Q

Components of cartilage

A

1) Collagen: predominantly type II
2) Proteoglycans (chondroitin, keratin sulfate) linked to hyaluronic acid
3) Matrix proteins: MMPs (collagenase, gelatinase, stromelysin), TIMPs
4) Chondrocytes
5) Water: 70% by weight

No nerves, blood vessels

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5
Q

Cartilage changes in osteoarthritis

A

1) Increased chondrocytes
2) Decreased proteoglycan
* 3) Increased metalloproteinases
4) Decreased TIMP
5) Increased water content
6) Lacks systemic features

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6
Q

Synovial fluid in osteoarthritis

A

Noninflammatory, type I (200-2000 WBC/mm^3)

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7
Q

Cytokines/inflammatory mediators in osteoarthritis

A

1) IL-1: stimulates MMP production, PGE2, NO, IL-6
2) NO: increases MMP prodution, inhibits proteoglycan synthesis, induces chondrocyte apoptosis
3) Prostaglandins: increase production/activation of MMPs
4) Other cytokines: TNF, IL-6, IL-17, IL-18
5) Complement activated
6) Adipokines

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8
Q

Radiographic findings of osteoarthritis

A

1) Joint space loss
2) Sclerosis (whitening)
3) Subchondral cysts
4) Osteophytes

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9
Q

Rheumatoid arthritis definition

A

Systemic, inflammatory, autoimmune disorder of unknown etiology that results in peripheral, symmetric synovitis which can result in cartilage and bone destruction

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10
Q

Rheumatoid arthritis joint involvement

A

Bilateral, symmetric
Small joints in hands and feet - but sparing the DIPs
Medium and large joints can also be involved

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11
Q

Radiographic findings of rheumatoid arthritis

A

Marginal joint erosions and deformities

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12
Q

Etiology of rheumatoid arthritis

A

Unknown beyond arthritogenic peptides in genetically susceptible host

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13
Q

Genetic susceptibility in rheumatoid arthritis

A 
Shared epitope (QKRAA, in antigen-binding groove)
In subtypes of HLA-DR4, HLA-DR1
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14
Q

Rheumatoid factor

A 
IgM (sometimes IgG or IgA) antibody directed against Fc portion of IgG
Present in 85% of patients with RA
Not specific for RA or CTDs
Produced locally in synovial tissue
*RF-IgG immune complexes are pathogenic
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15
Q

Anti-CCP antibodies

A

AutoAbs reactive with synthetic peptides containing cirulline (modified arginine residue)
Specifically present in sera of RA patients: 88-99% specificity, 98-100% specific when present with RF
Occur more frequently in individuals with shared epitope - citrullination of peptides enhances binding

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16
Q

Lymphocytes in rheumatoid arthritis synovium

A

Majority are CD4+ T cells (modulation/amplification of local immune response through Ag recognition) and Th17 cells
IL-1, TNF-a
T cell cytokines (IL-2, IFN-y) are sparse
B cells and plasma cells also present

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17
Q

Extra-articular manifestations of rheumatoid arthritis

A

RF-IgG immune complex-induced vasculitis

Rheumatoid nodule formation in tissues/organs

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18
Q

Gout definition

A

Result of tissue deposition of MSU crystals due to hyperuricemia (MSU supersaturation of extracellular fluids)

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19
Q

Joint involvement in gout

A 
1st MTP (podagra)
Cool, peripheral joints of lower and upper extremities
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20
Q

2 reasons for hyperuricemia

A

1) Overproduction of uric acid

* 2) Underexcretion of uric acid (90% of cases)

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21
Q

Uric acid involvement in gout

A

Product of purine metabolism

Humans lack uricase - oxidizes uric acid into allantoin

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22
Q

Two X-linked defects causing overproduction of uric acid

A

1) PRPP synthetase overactivity

2) HGPRT deficiency (complete: Lesch-Nyhan)

23
Q

Crystal arthritis diagnosis

A

Arthrocentesis

Crystal identification by polarized microscopy: MSU crystals are needle-shaped and negatively birefringent

24
Q

Mechanism of MSU crystal-induced inflammation

A

Initial recognition by TLR2/TLR4

Engage caspase-1, activating NLRP3 inflammasome leading to IL-1b production

25
Q

Self-limiting nature of acute gouty arthritis

A

1) IgG (not specific anti-crystal antibodies)-coating promotes phagocytosis by PMNs
2) Apolipoprotein B coating inhibits phagocytosis and further inflammatory response

Phagocytosis of crystals decreases concentration
Local heat of inflammation increases MSU solubility
ACTH secretion suppresses inflammation
IL-1 and TNF are modulated by inhibitors

26
Q

CPDDD definition

A

Abnormal PPi metabolism (metabolism of NTPs from chondrocytes)
NTPPPH hydrolyzes phosphodiester bond, generating NMP and PPi
Leads to PPi precipitates with calcium forming CPPD crystals in mid-zonal cartilage layers
Crystal release into joint space: shedding phenomenon, enzymatic strip mining

27
Q

CPDDD genetic mutation

A

Mutations in ANKH gene
Results in transmembrane PPi transporter protein in chondrocytes
Allows excess intracellular PPi egress from chondrocytes

28
Q

CPPD crystal identification

A

Rhomboid, positively birefringent

29
Q

Ankylosing spondylitis genetic association

A

HLA-B27
2% chance of developing AS if HLA-B27+
20% chance if HLA-B27+ and have a first-degree relative with AS
Concordance rate in identical twins: 60%
HLA-B27 represents 40% of genetic risk - at least 9 other genes involved (also environment)

30
Q

Reactive arthritis

A

Asymmetric, oligoarticular (<5 joints), lower extremity arthritis
Dactylitis (sausage fingers) in 20-50%

31
Q

Reactive arthritis causes (generally + 4 specific hypotheses)

A

Bacterial environmental triggers transported to joints inside monocytes (ex. latent Chlamydia)
Hypotheses:
1) Molecular mimicry
2) Arthritogenic peptide hypothesis: unique presentation of processed peptide by HLA-B27
3) HLA-B27 heavy chain theory: NK cell activation
Unfolded protein hypothesis: ER stress response causing inflammation
4) Th2 (IL-4, IL-10) response: ? bacterial persistence

32
Q

Reiter’s syndrome

A

Clinical triad of conjunctivitis, urethritis, arthritis

33
Q

SLE definition

A

Chronic, systemic autoimmune disease that affects multiple organ systems (skin, joints, serosal surfaces, lungs, kidneys, CNS, hematologic system)

34
Q

Fundamental defect in SLE

A

Misdirected recognition of self as foreign, resulting in autoimmune process. T and B cell process
T cell: antibody responses toward autoantigens are antigen-driven, require CD4+ T cells
B cell: loss of T cell tolerance allows autoreactive B cell stimulation

35
Q

Genetic susceptibility to SLE

A

Association with HLA-DR3 and C4A null allele (greatest risk)
Concordance among monozygotic twins: 35%
Increased incidence among relatives (RR 2-3)
More common in African Americans, Asians, Hispanic Americans

36
Q

Environmental triggers of SLE

A

Sex hormones: female to male ratio 9:1
Increased incidence in women of childbearing age
Sun exposure: exacerbates systemic disease

37
Q

ANAs

A

Hallmark of abnormal antibody production in SLE
>95% of patients with SLE have + ANAs
Not specific for SLE, can occur in other CTDs

38
Q

3 types of ANAs (and common diseases they cause)

A

1) Anti-dsDNA antibodies: renal disease
2) Anti-histone antibodies: SLE and drug-induced lupus
3) Antibodies to non-DNA, non-histone nuclear antigens - ex. SSA, SSB, Smith, Ribonuclear protein (RNP)

39
Q

Specific antibody-mediated disease in SLE

A

Type II immunopathology
Anti-RBC antibodies (hemolytic anemia)
Anti-WBC antibodies, anti-platelet antibodies
Anti-phospholipid antibodies: block prothrombin activation in clotting cascade, associated with increased clotting, but do not cause a vasculitis

40
Q

Immune complex-mediated disease in SLE

A

Type III immunopathology
Anti-dsDNA-DNA immune complexes
Glomerulonephritis (lumpy-bumpy immunofluorescence)

41
Q

Vasculitis definition

A

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

42
Q

Pathology of vasculitis

A

Varying degree of infiltrating lymphs, monocytes, histiocytes, eosinophils, and PMNs
Granulomas and/or giant cells in vessel wall in some types of vasculitis (large vessel)
Fibrinoid necrosis of vessel wall secondary to immune complex deposition
Focal and segmental nature of vascular lesions common to all types of vasculitis

43
Q

Pathophysiology of vasculitis

A

Immune complexes: inflammation –> PAFs –> increased vascular permeability –> immune complex deposition, palpable purpura
Antineutrophil cytoplasmic antibodies (ANCAs)
Anti-endothelial antibodies
T-cell dependent-mediated endothelial cell injury: HLA-DR4 and giant cell arteritis; suggests antigen-driven vascular inflammation
Infection of vascular endothelial cells

44
Q

4 sources of antigen for immune complexes

A

Drugs
Bugs: infectious agents
Connective tissue disease: autoimmune process
Malignancy (leukemias, lymphomas)

45
Q

Cytoplasmic ANCA (c-ANCA)

A

Proteinase-3 (PR3) in primary granules of PMNs
Associated with generalized GPA (Wegener’s)
Likely play a role in amplifying the inflammatory vascular response

46
Q

Perinuclear ANCA (p-ANCA)

A

Myeloperoxidase (MPO) in primary granules of PMNs
Associated with microscopic polyangiitis (MPA)
Likely play a role in amplifying the inflammatory vascular response

47
Q

Polymyositis/Dermatomyositis (PM/DM) definition

A

Inflammatory myopathies, characterized by proximal muscle weakness, low endurance
Usually idiopathic, may occur in association with neoplastic diseases or in overlap with CTD

48
Q

Typical skin rashes in dermatomyositis

A

Gottron’s papules: over MCP or IP joints, also elbows and knees
Heliotrope rash: eyelids
V-sign and shawl-sign: on trunk, in photodistributed regions
Mechanic’s hands: fingertips
Periungual changes/erythema: right below nail bed

49
Q

Anti-synthetase syndrome presentation

A

PM or DM presenting with:

  • 1) Interstitial lung disease (ILD): 60%
    2) Fever: 20%
    3) Arthritis: 50%
    4) Mechanic’s hands: 30%
    5) Raynaud’s phenomenon: 40%
50
Q

Anti-synthetase antibodies

A

Anti-aminoacyl-tRNA synthetases (cytoplasm)
Anti-Jo-1 = anti-histadyl-tRNA synthetase
Not pathologic or myotoxic antibodies

51
Q

Polymyositis histological findings

A

Endomysial distribution of inflammatory cells (CD8+ T cells) surrounding/invading muscle fibers

52
Q

Dermatomyositis histological findings

A

Perivascular (CD4+ T cells) and perifascicular inflammatory infiltrate

53
Q

Etiology of polymyositis/dermatomyositis

A

Evidence suggests viral etiology:
HIV/influenza can cause myositis
Viral particles by EM and viral RNA detected in muscle from PM/DM patients - no live virus has been cultured from muscle
Juvenile DM: increased antibodies to coxsackie B
Seasonal pattern: anti-Jo-1 antibodies and spring
DM: microarray mRNA profiling with predominance of interferon-responsive pathways suggesting anti-viral response

Rheumatology (1 decks)

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