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Joint Deposition Diseases

Histologic Considerations 150 Normal US Anatomy and Scanning Technique 153 Pathologic Changes 156 Joint Effusion 156 Rheumatoid Arthritis and Other Inflammatory Arthropathies 158 Septic Arthritis 162 Traumatic Injuries 163 Degenerative Joint Disease (Osteoarthritis) 166 Deposition Diseases 169 Postoperative Complications 173... [Pg.137]

Fig. 5.34a-g. Calcium pyrophosphate deposition disease, a-c Transverse 12-5 MHz US images obtained over a the femoral trochlea, b the posterior aspect of the medial condyle and c the lateral meniscus in a patient with bilateral degenerative osteoarthritis of the knee reveal scattered hyperechoic foci (arrowheads) due to crystal deposition within the hyaline cartilage, the medial meniscus and the joint capsule (arrows). F, femur T, tibia. Note that crystals tend to be deposited in the middle layer of the cartilage, parallel to the subchondral bone, d-f Radiographic correlation, g Schematic drawing illustrates the typical deposition pattern of pyrophosphate crystals within the cartilage... [Pg.171]

Among the degenerative arthropathies that typically involve the shoulder, there are a variety of conditions related to crystal deposition diseases, including renal osteodystrophy, milk alkali syndrome, hyper-vitaminosis D and the so-called Milwaukee shoulder syndrome . This last condition, which is also known as apatite-associated destructive arthritis, hemorrhagic shoulder or rapid destructive arthritis of the shoulder, consists of massive rotator cuff tear, osteoarthritic changes, hlood-stained noninflammatory joint effusion containing calcium hydroxyapatite and calcium pyrophosphate dihydrate crystals, synovial hyperplasia and extensive destruction... [Pg.299]

Cooper AM, Hayward C, Williams BD (1993) Calcium pyrophosphate deposition disease involvement of the acromioclavicular joint with pseudocyst formation. Br J Rheumatol 32 248-250... [Pg.326]

Fig. 11.66a,b. Lateral ligament calcification in a patient with crystal pyrophosphate deposition disease, a Coronal 12-5 MHz US image over the proximal interphalangeal joint with b radio-graphic correlation demonstrates a calcified convex structure (arrows) with posterior acoustic shadowing over the joint line, reflecting a ligament calcification. PP, proximal phalanx MP, middle phalanx... [Pg.542]

Gout is a metabolic disease characterized by recurrent episodes of acute arthritis due to deposits of monosodium urate in joints and cartilage. Uric acid renal calculi, tophi, and interstitial nephritis may also occur. Gout is usually associated with hyperuricemia, high serum levels of uric acid, a poorly soluble substance that is the major end product of purine metabolism. In most mammals, uricase converts uric acid to the more soluble allantoin this enzyme is absent in humans. While clinical gouty episodes are associated with hyperuricemia, most individuals with hyperuricemia may never develop a clinical event from urate crystal deposition. [Pg.813]

For example, normal urine is supersaturated with calcium oxalate. To prevent formation of renal calculi (stones)719 an inhibitory glycoprotein is present and slows the formation and growth of crystals.720 Under some disease conditions calcium carbonate stones may form in pancreatic ducts. A17 kDa lectinlike glycoprotein called lithostatine has been proposed to inhibit stone formation by binding to certain planes on CaC03 microcrystals just as antifreeze proteins (Box 4-D) inhibit ice formation.721 However, this proposed function for lithostatine is doubtful.722 723 Pathological deposits of crystalline calcium pyrophosphate and basic calcium phosphates are sometimes present in joints,724 even in Neanderthal skeletons.725... [Pg.443]

Gout is a familial metabolic disease characterized by recurrent episodes of acute arthritis due to deposits of monosodium urate in joints and cartilage. Formation of uric acid calculi in the kidneys... [Pg.837]

Gout is a metabolic disease in which there is a overproduction of purines. It is characterized by intermittent attacks of acute arthritis produced by the deposition of sodium urate crystals in the synovial tissue of joints. Drugs used for treating gout are allopurinol, probenecid, colchicine, and NSAIDs. [Pg.278]

Gout is a metabolic disease characterized by the painful inflammation of joints. Gout is a type of arthritis- Hyperuricemia is a risk factor for gout and for the development of uric add stones in kidneys. Gout often presents as a violent attack of pain in the big toe. Less commonly, it involves the wrists, ankles, or knees. The pain spontaneously disappears after a feu days, but recurs later, with an increasing fre<)uency. Eventually, cry stalline deposits of uric acid accumulate in the joints and appear as bumps on the skin, each with a diameter of a millimeter to a few centimeters. The deposits of urate lead to erosion of the bone and to destruction of the joints. Gout can be crippling. [Pg.478]

AA protein is often deposited in chronic inflammatory diseases such as rheumatoid arthritis (incidence up to 20%) and other inflammatory joint diseases, and in chronic suppurative and granulomatous infections such as tuberculosis and osteomyelitis. Deposits of AA protein are also observed in nonlymphoid tumors such as renal and gastric carcinomas and in Hodgkin s disease. Deposits of AA protein are most often found in the kidneys, liver, and spleen, usually resulting in nephrotic syndrome and hepatosplenomegaly. [Pg.582]


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