Pathology (Joint)

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Pathology (Joint)
2013-09-17 14:06:26
Pathology Joint

Pathology (Joint)
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  1. What are the types of joints?
    • Solid (nonsynovial) and cavitated (synovial).
    • The solid joints (synarthroses)-->lack a joint space; fibrous synarthroses ( cranial sutures and the bonds between roots of teeth and the jawbones); cartilaginous synarthroses (synchondroses) are represented by the symphyses (manubriosternalis and pubic).
  2. What are the features of synovial joints?
    • Have a joint space
    • Situated between the ends of bones formed via enchondral ossification
    • Strengthened by a dense fibrous capsule reinforced by ligaments and muscles.
    • The boundary of the joint space consists of the synovial membrane, which is firmly anchored to the underlying capsule and does not cover the articular surface.
  3. What are the features of synovial membrane?
    • Firmly anchored to the underlying capsule and does not cover the articular surface.
    • Its contour is smooth except near the osseous insertion, where it is thrown into numerous villous folds.
    • Lined by synoviocytes,that synthesize hyaluronic acid.
    • The synovial lining lacks a basement membrane, which allows for quick exchange between blood and synovial fluid.
    • Synovial fluid is clear and viscous, and is a filtrate of plasma containing hyaluronic acid that acts as a lubricant and provides nutrition for the articular hyaline cartilage.
  4. What feature of synovial lining allow for quick exchange between blood and synovial fluid?
    Lack of basement membrane
  5. What is the function of hyaline cartilage?
    shock absorber and wear-resistance
  6. What is the composition of hyaline cartilage?
    • Lacks a blood supply lymphatic drainage or innervation.
    • Hyaline cartilage is composed of type 2 collagen, water, proteoglycans, and chondrocytes.
  7. What are the functions of each part of hyaline cartilage?
    • The collagen--> resist tensile stresses and transmit vertical loads.
    • The water and proteoglycans -->  turgor and elasticity  and limiting friction.
    • The chondrocytes synthesize the matrix as well as enzymatically digest it. 
    • Chondrocytes secrete the degradative enzymes in an inactive form and enrich the matrix with enzyme inhibitors.
  8. How can diseases destroy articular cartilage?
    • Activate the catabolic enzymes and decreasing the production of inhibitors.
    • Cytokines such as IL-1 and TNF trigger the degradative process; their sources include chondrocytes, synoviocytes, fibroblasts, and inflammatory cells.
  9. What is mc joint disease?
  10. What is the main pathophysiology of OA?
    Progressive erosion of articular cartilage (due to intrinsic articular disease)
  11. What are the causes of secondary OA?
    Diabetes, ochronosis, hemochromatosis, marked obesity, trauma, congenital deformity, the shoulder or elbow involvements in baseball players and knees in basketball players
  12. What is the effect of gender on distribution of joints in OA?
    The knees and hands are more commonly affected in women and the hips in men.
  13. What are the RF for OA?
    • 1. genetic (particularly hand)
    • 2. Age (strongest)
    • 3. Biomechanical stress
    • 4. Lack of osteoporosis
    • 5. Obesity (strongest modifiable/ hand and knee but not hip)
    • 6. Any degree of exercise in abnormal joint
    • 7. No or high impact exercise in normal joint
    • 8. Female sex
  14. Which joints are frequently involved by OA?
    Cervical and lumbar spine, First CMC, PIP, DIP, Hip, Knee, Subtalar, First MTP
  15. Which joint involvement is uncommon in primary OA?
    Shoulder, wrist, elbow, MCP
  16. What are the radiological findings of OA?
    • Joint space narrowing
    • Subchondral sclerosis
    • Marginal osteophytes
    • Subchondral cysts
  17. What are the symptoms, signs and synovial fluid analysis of OA?
    • Symptoms: Pain, Stiffness, Gelling
    • Physical examination: Crepitus, Bony enlargement, Decreased range of motion, Malalignment, Tenderness
    • Synovial fluid: Clear fluid, WBC <2000/mm3, Normal viscosity
  18. What is the difference between RA and OA?
    • RA--> MCP, PIP: soft, warm, tender
    • OA--> DIP, CMC, Heberden Nodes: Hard and bony
  19. What is the major cell in the pathophysiology of OA?
  20. What are the stages of OA?
    • (1) chondrocyte injury
    • (2) early OA, in which chondrocytes proliferate (cloning) and secrete mediators--> remodel the cartilaginous matrix and initiate secondary inflammatory changes in the synovium and subchondral bone
    • (3) late OA, in which repetitive injury and chronic inflammation lead to chondrocyte drop out, marked loss of cartilage, and extensive subchondral bone changes
  21. What are the first histological changes in OA?
    Chondrocytes proliferatation, increased water content of the matrix and decreased concentration of proteoglycans
  22. What are the histological changes in OA?
    • 1. Chondrocytes proliferatation, increased water content of the matrix and decreased concentration of proteoglycans
    • 2. superficial layers of the cartilage and type 2 collagen molecules are degraded. Grossly this manifests as a granular soft articular surface.
    • 3. fibrillation
    • 4. chondrocytes die and full-thickness portions of the cartilage are sloughed (loose bodies)
    • 5. The exposed subchondral bone plate becomes the new articular surface, and friction with the opposing degenerated articular surface smooths and burnishes the exposed bone, giving it the appearance of polished ivory (bone eburnation)
    • 6. sclerosis of the underlying cancellous bone
    • 7. Small fractures through the articulating bone are common, and the fracture gaps allow synovial fluid to be forced into the subchondral regions in a one-way, ball valve–like mechanism. The loculated fluid collection increases in size, forming fibrous-walled cysts.
    • 8. osteophytes
    • 9. The synovium is usually only mildly congested and fibrotic, and may have scattered chronic inflammatory cells.

  23. What is the hallmark of RA?
    nonsuppurative proliferative and inflammatory synovitis that often progresses to destruction of the articular cartilage and ankylosis of the joints
  24. What is the first histological change in RA of a joint?
    Initially the synovium becomes grossly edematous, thickened, and hyperplastic, transforming its smooth contour to one covered by delicate and bulbous fronds
  25. What are the characteristic histological features of RA?
    • 1) infiltration of synovial stroma by a dense perivascular inflammatory infiltrate composed of lymphoid aggregates (mostly CD4+ helper T cells), B cells, plasma cells, dendritic cells, and macrophages (but not neutrophils)
    • 2)increased vascularity due to vasodilation and angiogenesis, with superficial hemosiderin deposits
    • 3) aggregation of organizing fibrin covering portions of the synovium and floating in the joint space as rice bodies 
    • 4) accumulation of neutrophils in the synovial fluid and along the surface of synovium but usually not deep in the synovial stroma
    • 5) osteoclastic activity in underlying bone, allowing the synovium to penetrate into the bone and cause juxta-articular erosions, subchondral cysts, and osteoporosis 
    • 6) pannus formation
  26. Which cells are NOT expected to be found in the synovial stroma of rheumatoid joint?
  27. What allows synovium to penetrate into the bone and cause juxta-articular erosions, subchondral cysts, and osteoporosis in RA?
    osteoclastic activity in underlying bone
  28. What is the most abundant inflammatory cell found in synovium of RA?
    CD4+ T cells
  29. What is a panus?
    • Mass of synovium and synovial stroma consisting of inflammatory cells, granulation tissue, and synovial fibroblasts, which grows over the articular cartilage and causes its erosion.
    • After the cartilage has been destroyed, the pannus bridges the apposing bones to form a fibrous ankylosis, which eventually ossifies and results in bony ankylosis
  30. What are the mc cutaneous lesion in RA?
    Rheumatoid nodules
  31. Which patients are more likely to develop rheumatoid nodules?
    Patients with severe disease
  32. Where do we expect to find rheumatoid nodules more commonly?
    Regions of the skin that are subjected to pressure, including the ulnar aspect of the forearm, elbows, occiput, and lumbosacral area
  33. What are the clinical features of rheumatoid nodules?
    Firm nontender subcutanueos
  34. What is the histological feature of RN?
    • a central zone of fibrinoid necrosis surrounded by a prominent rim of epithelioid histiocytes (activated macrophages) and numerous lymphocytes and plasma cells
  35. What is the mc finding of RA in heart?
    fibrinous pericarditis
  36. What are the manifestations of RA in the heart?
    • fibrinous pericarditis (mc)
    • Rheumatoid valvulitis of aorta
    • RN in myocardium
  37. What features of RA are associated with development of vasculitis?
    severe erosive disease, rheumatoid nodules, and high titers of RF
  38. Which arteries are involved in rheumatoid vasculitis?
    • Medium- to small-size arteries is similar to that occurring in polyarteritis nodosa, except that in rheumatoid arthritis the kidneys are not involved
    • Segments of small arteries such as vasa nervorum and digital arteries are obstructed by an obliterating endarteritis resulting in peripheral neuropathy, ulcers, and gangrene.
    • Leukocytoclastic venulitis produces purpura, cutaneous ulcers, and nail bed infarction
  39. Vasculitis of which organ is not seen in RA?
  40. What is the pathogenesis of neuropathy in RA?
    obliterative endarteritis of vasa nervorum
  41. What are the features of leukocytoclastic venulitis in RA?
    Purpura, cutaneous ulcers, and nail bed infarction
  42. What is the general pathogenesis of RA?
    rheumatoid arthritis is triggered by exposure of a genetically susceptible host to an arthritogenic antigenresulting in a breakdown of immunological self-tolerance and a chronic inflammatory reaction. In this manner, an acute arthritis is initiated, but it is the continuingautoimmune reaction, the activation of CD4+ helper T cells, and the local release of inflammatory mediators and cytokines that ultimately destroys the joint
  43. What are the genetic RF for RA?
    • HLA-DRB1 (DR4)
    • PTPN22 (inhibitor of T cells)
  44. Which autoantigen may be important in RA?
    citrullinated proteins
  45. What are the citrullinated proteins?
    proteins modified by the enzymatic conversion of arginine to citrulline, many of which are fibrins) formed in the body (especially in the lungs of smokers)
  46. Which inflammatory cells appear early in joints of RA?
    activated CD4+ effector and memory T cells
  47. What is the most important cell in pathophysiology of RA?
    T helper
  48. What are the two major cells that initiate inflammation in RA?
    TH1 and TH17
  49. What is the most abundant inflammatory cells in joints of RA?
    CD4+ with a memory phenotype
  50. What is responsible for destruction of articular cartilage in RA?
    Activated synovium (Pannus)
  51. The destruction of cartilage, bone, and tendons in RA is initiated largely by ......
  52. What is rheumatoid factor?
    IgM autoantibodies to the Fc portion of autologous IgG
  53. What is the specific serologic test for RA?
    Antibodies to citrulline-modified peptides (high titers more chronicity)
  54. What is the pathophysiology of RA?
  55. What is the key cytokine in pathogenesis of RA?
  56. How is the initial course of RA?
    • Begins slowly in more than half of affected individuals.
    • Initially there is malaise, fatigue, and generalized musculoskeletal pain, and only after several weeks to months do the joints become involved. 
    • Symmetrical and the small joints are affected before the larger ones (metacarpophalangeal and proximal interphalangeal joints) and feet.
    • Lumbosacral region and hips are usually spared.
  57. Which joints are not involved in RA?
    Lumbosacral region and hips
  58. What are the radiographic hallmarks of RA?
    • Joint effusions
    • Juxta-articular osteopenia
    • Erosions
    • Narrowing of the joint space with loss of articular cartilage
  59. How are characteristic deformities of RA produced?
    Destruction of tendons, ligaments, and joint capsules
  60. What is the pathophysiology of Baker cyst?
    increased intra-articular pressure causes outpunching of the synovium
  61. What are the criteria for diagnosing RA?
    (1) morning stiffness, (2) arthritis in three or more joint areas, (3) arthritis of hand joints, (4) symmetric arthritis, (5) rheumatoid nodules, (6) serum rheumatoid factor, and (7) typical radiographic changes.
  62. Which drug can inhibit articular damage in RA?
  63. What is the risk of Anti-TNF?
  64. How is the nomenclature for cytokine inhibitors?
    • “-cept” refers to fusion of a receptor to the Fc part of human IgG1
    • “-mab” indicates a monoclonal antibody (mAb)
    • “-ximab” indicates a chimeric mAb
    • “-zumab” indicates a humanized mAb
  65. What are the three types of cytokine inhibitors?
    • Soluble receptor (etanercept) bind their target cytokine while it is in serum, thereby inhibiting the cytokine’s ability to interact with its cell surface receptors
    • Monoclonal antibodies binds to cytokine in both serum and on cell surface
    • Cell surface receptor antagonists (Anakinra): compete with a cytokine for binding to the cytokine’s membrane receptor.
  66. What are the biological drugs for RA?
    • TNF INHIBITION: Etanercept, Infliximab, Adalimumab, Certolizumab (only Fab), Golimumab
    • IL-1 INHIBITION (not used widely): Anakinra, Canakinumab
    • IL-6 INHIBITION: Tocilizumab
    • COSTIMULATION BLOCKADE: Abatacept--> CTLA4-Ig:  It prevents CD28 from binding to its counter-receptor, CD80/CD86, due to its higher affinity for CD80/CD86--> T cell blockade
    • B-CELL DEPLETION: Rituximab (monoclonal )anti-CD20 antibody
  67. What is the mcc of secondary Sjogren syndrome?
    Rheumatoid Arthritis
  68. What is the cause of sicca in Sjogren syndrome?
    lymphocytic infiltration and fibrosis of the lacrimal and salivary glands.
  69. What are the predominant cell type in glands of Sjogren disease?
    Activated CD4+ T
  70. What is the most sensitive antibody test in Sjogren?
    SS-A (Ro) and SS-B (La) (RNP)
  71. What are the antibodies found in Sjogren?
    • RF
    • ANA
    • SS-A
    • SS-B
  72. What is the clinical significance of anti SS-A ?
    more likely to have early disease onset, longer disease duration, and extraglandular manifestations, such as cutaneous vasculitis and nephritis
  73. What is the mc haplotype for Sjogren?
    DR3, B8, DQ2
  74. What is the earliest histologic manifestation of Sjogren syndrome?
    periductal and perivascular lymphocytic infiltration
  75. What are the histological characteristics of Sjogren syndrome?
    • periductal and perivascular lymphocytic infiltration
    • ductal epithelial hyperplasia
    • lymphoid follicles with germinal centers
    • Atrophy, fibrosis and fat (late)
  76. What are the symptoms of Sjogren syndrome?
    • Sicca
    • Parotid gland enlargement (half the patients) 
    • Dryness of the nasal mucosa, epistaxis, recurrent bronchitis, and pneumonitis are other symptoms.
    • Synovitis, diffuse pulmonary fibrosis, and peripheral neuropathy.
    • In contrast to SLE, glomerular lesions are extremely rare in Sjögren syndrome.
    • RTA, uricosuria, and phosphaturia, are often seen and are associated histologically with tubulointerstitial nephritis.
    • About 60% of patients have another accompanying autoimmune disorder.
  77. What is essential for the diagnosis of Sjögren syndrome?
    Biopsy of the lip (to examine minor salivary glands)
  78. What is the mc lymphoma in Sjogren and Hashimoto?
    B cell marginal zone lymphoma
  79. Which lymphoma often arise in the setting of chronic lymphocytic inflammation?
    Marginal B cell
  80. What are the types of JIA?
    (1) systemic arthritis, (2) oligoarthritis, (3) rheumatoid factor–positive polyarthritis, (4) rheumatoid factor–negative polyarthritis, (5) enthesitis (inflammation of a point of attachment of skeletal muscle to bone)-associated arthritis, (6) psoriatic arthritis, and (7) undifferentiated arthritis.
  81. What is the difference between JIA and RA?
    • (1) oligoarthritis is more common in JIA, (2) systemic disease is more frequent, (3) large joints are affected more often than small joints, (4) rheumatoid nodules and rheumatoid factor are usually absent, and (5) antinuclear antibody (ANA) seropositivity is common.
    • Similar histology (CD4 memory cells)
  82. What are the features of systemic arthritis?
    • Abrupt onset
    • Remitting, high spiking fevers
    • Migratory and transient skin rash,
    • HSM
    • Serositis
  83. How is JIA diagnosed?
    Developing arthritis before 16 years of age and that persist for a minimum of 6 weeks
  84. What is oligoarticular JIA?
    Arthritis affecting four or fewer joints during the first 6 months of disease in the absence of psoriasis and an HLA-B27 genotype defines the oligoarthritis variant. The arthritis is asymmetric, develops at an early age (younger than 6 years), and is commonly associated with iridocylitis and a positive ANA.
  85. What are the features of Enthesitis-related arthritis of JIA?
    mainly affects male children younger than 6 years, and most affected individuals are HLA-B27 positive. The enthesitis and arthritis affects tendoligamentous insertion sites and joints of the lower extremities.
  86. What is the mcc of the gout?
    Reduced excretion of uric acid with normal production
  87. Why in the mammals only human is prone to gout?
    Because they lack uricase that turn uric acid into allantoin (a water-soluble non-toxic substance)
  88. What is the hallmark of chronic gout?
  89. What is the major risk for those who develop chronic gouty arthritis?
    Gout nephropathy
  90. What is the relationship of hyperuricemia to gout?
    Hyperuricemia (plasma urate level above 6.8 mg/dL) is necessary but not sufficient for the development of gout
  91. What are the causes of gout?
    • PRIMARY GOUT (90% OF CASES)  1): Overproduction of uric acid: Diet, Unknown enzyme defects (80% to 90%), Known enzyme defects (e.g., partial HGPRT deficiency, rare)  2) Reduced excretion of uric acid with normal production (mc)
    • SECONDARY GOUT (10% OF CASES)  1): Overproduction of uric acid with increased urinary excretion:  Increased nucleic acid turnover (e.g., leukemias and other aggressive neoplasms),  Inborn errors of metabolism (e.g., complete HGPRT deficiency)  2) Reduced excretion of uric acid with normal production: CRF
  92. How much of urate is reabsorbed?
    Approximately 90% of the filtered urate is reabsorbed, and the urate transporter 1 gene (URAT1) has an important role in the reabsorption process
  93. What happens in HGPRT deficiency?
    • It leads to increased synthesis of purine nucleotides through the de novo pathway and hence increased production of uric acid.
    • A complete lack of HGPRT occurs in the uncommon X-linked Lesch-Nyhan syndrome, seen only in males and characterized by hyperuricemia, severe neurologic deficits with mental retardation, self-mutilation, and in some cases gouty arthritis.
  94. Which enzyme is responsible for synthesis of PRPP from 5-ribose phosphate?
    PRPP synthetase
  95. How is conversion of PRPP to purine nucleotides catalyzed in de novo and salvage pathways?
    • by amido-PRT in the de novo pathway and by APRT and HGPRT in the salvage pathway
  96. What can predispose to gout?
    • Age
    • Obesity (asymptomatic hyperuricemia)
    • Heavy alcohol (acute attack)
    • Genetic
    • Thiazide (reduce excretion), low dose ASA, cyclosporine
    • Lead toxicity
  97. What is central to pathogenesis of gouty attack?
    precipitation of monosodium urate (MSU) crystals into the joints
  98. How is the solubility of MSU in a joint modulated ?
    by temperature (the lower the less soluble) and by the intra-articular concentration of urate and cations. Crystallization is dependent on the presence of nucleating agents
  99. What happens in an acute gout attack?
    • MSU crystals are phagocytosed by macrophages 
    • activate the NALP3 inflammasome, a multiprotein complex that includes the protease caspase 1.
    • The inflammasome-activated caspase 1, in turn, cleaves and activates several cytokines, most notably IL-1β and IL-18. IL-1β induces the expression of adhesion molecules and the synthesis of the neurophil chemokine CXCL8, which is essential for the localization of neutrophils at the site of acute inflammation.
    • The neutrophils pour fuel on the fire by releasing toxic free radicals, leukotrienes (leukotriene B4), and lysosomal enzymes
  100. What is the major cell in acute gout?
  101. What is the histology of acute gout?
    • Dense neutrophilic infiltrate that permeates the synovium and synovial fluid.
    • The MSU crystals are frequently found in the cytoplasm of the neutrophils and are arranged in small clusters in the synovium. They are long, slender, and needle shaped, and are negatively birefringent. 
  102. What are the features of chronic gouty arthritis?
    • Due to repetitive precipitation of urate crystals during acute attacks.
    • The urates form visible deposits in the synovium.
    • The synovium forms a pannus that destroys the underlying cartilage leading to juxta-articular bone erosions.
    • In severe cases, fibrous or bony ankylosis
  103. What are the histology of tophi?
    large aggregations of urate crystals surrounded by an intense inflammatory reaction of macrophages, lymphocytes, and large foreign body giant cells, which may have completely or partially engulfed masses of crystals
  104. What are the features of gouty nephropathy?
    • Deposition of MSU crystals in the renal medullary interstitium,
    • Intratubular precipitations,
    • or free uric acid crystals
    • production of uric acid renal stones.
    • Secondary complications, such pyelonephritis
  105. What is the mc joint involved in gout?
    first metatarsophalangeal
  106. What are the four stages of gout?
    (1) asymptomatic hyperuricemia, (2) acute gouty arthritis, (3) intercritical gout, and (4) chronic tophaceous gout
  107. When does asymptomatic hyperuricemia appear?
    around puberty in males and after menopause in females
  108. What are the symptoms of acute gout?
    • Sudden onset of excruciating joint pain associated with localized hyperemia, warmth, and exquisite tenderness.
    • Constitutional symptoms are uncommon except possibly mild fever.
    • Most first attacks are monoarticular; 50% occur in the first metatarsophalangeal joint.
    • Eventually, about 90% of affected individuals experience acute attacks in the following locations (in descending order of frequency): insteps, ankles, heels, knees, wrists, fingers, and elbows.
  109. What are the radiological manifestations of chronic gout?
    • Juxta-articular bone erosion caused by osteoclastic bone resorption
    • loss of the joint space
  110. What other diseases are common in patients with gout?
    • Cardiovascular and HTN
    • Renal disease (20% die of CRF)
  111. What is mechanism of hereditary CPPD?
    mutation in pyrophosphate transport channel
  112. What are the causes of secondary CPPD?
    • previous joint damage
    • hyperparathyroidism
    • hemochromatosis
    • hypomagnesemia
    • hypothyroidism
    • ochronosis
    • diabetes
  113. Where do crystals first form in CPPD?
    articular matrix, menisci, and intervertebral discs
  114. What is the mc joint involved in CPPD?
  115. Which joints are involved in CPPD?
    knee>wrist> elbow>shoulder>ankle
  116. What are the features of crystals in CPPD?
    • The crystals form chalky white friable deposits, which are seen histologically in stained preparations as oval blue-purple aggregates.
    • Weakly birefringent, and have geometric shapes
  117. What is the main cell involved in AS?
    T cell
  118. What is the hallmark of SNSA?
    chronic synovitis that causes destruction of articular cartilage and resultant bony ankylosis, especially of the sacroiliac and apophyseal joints
  119. What are the other manifestation of AS?
    • low back pain, which frequently follows a chronic progressive course. Involvement of peripheral joints, such as the hips, knees, and shoulders, occurs in at least one third of affected individuals. Fracture of the spine, uveitis, aortitis, and amyloidosis are other recognized complications
    • Extremely good response to NSAIDs within 24-48 h

  120. What is the hallmark x ray of AS?
    Bamboo spine and fused SI joints
  121. Which drug prevent disease progression in AS?
    TNF inhibitor
  122. Which other gene may be involved in AS?
    IL23R (activate TH17)
  123. Which cytokine has a central role in AS?
  124. What are the features of ReA?
    reactive arthritis that is defined by a triad of arthritis, nongonococcal urethritis or cervicitis, and conjunctivitis
  125. Which patients are particularly susceptible to ReA?
  126. What are the other symptoms of ReA?
    • 1. Arthritic symptoms usually develop within several weeks of the inciting bout of urethritis or diarrhea.
    • 2. The ankles, knees, and feet are affected most often, frequently in an asymmetric pattern.
    • 3. Synovitis of a digital tendon sheath produces the sausage finger or toe, and ossification of tendoligamentous insertion sites leads to calcaneal spurs and bony outgrowths.
    • 4. Balanitis, Keratoderma blenorrhagica (crusted hyperkeratotic lesion in palm and sole), conjunctivitis, cardiac conduction abnormalities, and aortic regurgitation.
  127. What are the pathophysiology of sausage digit and bony spur in ReA?
    Synovitis of a digital tendon sheath produces the sausage finger or toe, and ossification of tendoligamentous insertion sites leads to calcaneal spurs and bony outgrowths.
  128. What is the hallmark of enteritis associated arthritis?
    • Association with Yersinia, Salmonella, Shigella, and Campylobacter
    • Abrupt onset and involvement of knee and ankle
  129. What are the hallmarks of PsA?
    • HLA-B27 and HLA-Cw6 association
    • Assymetric DIP of hand and feet (sausage digit)
    • SI and spondylitis<40%
    • Aside from conjunctivitis and iritis, extra-articular manifestations are uncommon
  130. What is the least associated of SNSA with HLA-B27?
    • IBD
    • Associated with NOD2/CARD15 (CD)
  131. What is the mcc of infectious arthritis?
    Staph aureus
  132. What is the mc path for infectious arthritis?
  133. What other path is involved in septic arthritis of neonate?
    contiguous spread from underlying epiphyseal osteomyelitis
  134. What is the mcc of arthritis in the young?
  135. What agents are associated with arthritis in the neonate?
    GBS, Gr negatives, Staph aureus
  136. In what condition is the arthritis with CONS prevalent?
    Prosthetic joints
  137. What are the mc joints involved in septic or lyme arthritis?
  138. What is the mc joint involved in TB arthritis?
    Hip>knee> ankle
  139. What are the features of TB arthritis?
    • Hip mc
    • Pannus formation
    • Ankylosis
  140. What is the mcc of arthritis by human and animal bites?
    Polymicrobial (mc Eikenella, Pasteurella respectively)
  141. What location is more likely to be involved in arthritis associated with IDU?
    Axial skeleton
  142. What are the features of DGI?
    • Female
    • Purulent arthritis alone (knee)--> B/C negative no systemic symptom
    • Triad of tenosynovitis, dermatitis (small painless vesiculopustular), and polyarthralgias without frank arthritis--> B/C positive, systemic symptom 
  143. What is the cause of HIV-associated arthritis?
  144. What are the features of joint involvement in Lyme?
    remitting and migratory, and primarily involves large joints, especially the knees, shoulders, elbows, and ankles in descending order of frequency
  145. What is the morphology of Lyme arthritis?
    • Infected synovium exhibits a chronic papillary synovitis with synoviocyte hyperplasia, fibrin deposition, mononuclear cell infiltrates (especially CD4+ T cells), and onion-skin thickening of arterial walls.
    • Silver stains may reveal small numbers of organisms in the vicinity of blood vessels in approximately 25% of cases
  146. What is the pathophysiology of Chronic arthritis that is antibiotic refractory in Lyme disease?
    • Develops in approximately 10% of affected individuals and results from infection-induced autoimmunity.
    • It is hypothesized that specific HLA-DR molecules bind an epitope of B. burgdorferi outer surface protein A, which initiates a T-cell reaction to this epitope. The T-cells may cross-react with an unknown self-antigen (molecular mimicry).
    • The joints in these patients have synovial pannus
  147. What are the features of a ganglion?
    • Small (1–1.5 cm) cyst that is almost always located near a joint capsule or tendon sheath (joints of the wrist)
    • Firm, fluctuant, pea-sized translucent nodule.
    • It arises as a result of cystic or myxoid degeneration of connective tissue; hence the cyst wall lacks a true cell lining.
    • The fluid that fills the cyst is similar to synovial fluid; however, there is no communication with the joint space.
  148. What are the features of a synovial cyst?
    • Herniation of synovium through a joint capsule or massive enlargement of a bursa may produce a synovial cyst (Baker cyst).
    • The synovial lining may be hyperplastic and contain inflammatory cells and fibrin but is otherwise unremarkable.
  149. What is tenosynovial GCT?
    • Benign neoplasms that develop in the synovial lining of joints, tendon sheaths, and bursae.
    • They harbor a consistent chromosomal translocation, t(1;2)(p13;q37), which fuses colony-stimulating factor 1 (CSF1) coding sequences to the promoter of the collagen type VI alpha-3 gene.
    • As a result, the tumor cells overexpress CSF1, a chemoattractant for macrophages, which infiltrate the tumor in large numbers
  150. What are the characteristic features of tenosynovial GCT?
    • 1. High number of infiltrating MQ or MNGC
    • 2. t(1;2)
  151. What are the variants of tenosynovial GCT?
    Diffuse type (previously known as pigmented villonodular synovitis)--> involve Joints (knee)

    Localized type (also known as giant-cell tumor of tendon sheath)--> involve tendon sheath (hand)
  152. What is the morphology of tenosynovial GCT?
    • In diffuse tumors the normally smooth joint synovium is converted into a tangled mat by red-brown folds, finger-like projections, and nodules.
    • Localized tumors are well circumscribed and resemble a small walnut.
    • The neoplastic cells, which account for only 2% to 16% of the cells in the mass, resemble synoviocytes.
    • Diffuse variant may infiltrate the subsynovial issue.
    • Both variants are heavily infiltrated by macrophages  and multinucleated giant cells.
  153. What are the clinical course of tenosynovial GCT?
    • Diffuse tenosynovial giant-cell tumor usually presents in the knee in 80% of cases, by pain, locking, and recurrent swelling.
    • Localized variant manifests as a solitary, slow-growing, painless mass that frequently involves the tendon sheaths along the wrists and fingers
  154. What is the mc mesenchymal neoplasm of the hand?
    Localized tenosynovial GCT