CUA Presentation_0

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Calcific Uremic Arteriolopathy ‘Calciphylaxis’ QuickTimeª and a decompressor are needed to see this picture QuickTimeª and a decompressor are needed to see this p David Shure
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Calciphylaxis Syndrome ‘Coined by Hans Selye ‘62 Nephrectomized rat model 1) Systemic Sensitization induced by agents i.e. PTH, vitamin D, or high Ca, P diet 2) After ‘critical period’, exposure to appropriate challengers via SC injections of iron salt, egg albumin, polymyxin, glucocorticoids, causing local trauma, led to macroscopic visible deposits of calcium salts systemically and at site of injection
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Calciphylaxis CUA Calciphylaxis Metastatic systemic calcifications after invasive manipulation of animal model No vascular calcifications found QuickTimeª and a decompressor are needed to see this p CUA Occurs in presence of uremia Abnormalities in divalent ion ie PTH, Ca, PO4 (not required) Vascular calcifications at site of lesions
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CUA First Described Early 1970’s Cutaneous eruptions usu in pt’s on HD or after Renal Tx Painful skin lesions with superficial violaceous nodules on tips of digits, ankles, thighs or buttocks Progressed to hemorrhagic eruptions with ischemic necrosis Bilaterally symmetrical, superficial, maintained persistent distal pulses Progressed to necrosis, ischemic severe pain, gangrene
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Pathogenesis Unclear Pathogenic Factors Uremic milieu + high Ca x P Ca content of skin noted to be high in HD pts and higher when dialysate Ca concentrations of 4.0 meq/L. Lowering dialysate Ca improved CUA in some pts. Also avoiding ca based po4 binders Presence of high PTH levels: PTX effective in some pts
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CUA associated with: Most primary renal diseases including DM Occurs rarely in non-renal failure diseases, ie primary hyperparathyroidism and alcohol- related cirrhosis
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Necrotic Skin Lesions QuickTimeª and a decompressor are needed to see this picture QuickTimeª and a decompressor are needed to see this picture.
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Lesion Evolution Primary: calcium salts accumulate in media of small arteries intima is thickened by loose CT lumen narrows Secondary Lesion Infarcts of the subcut tissue and skin comprise the secondary lesions, responsible for initial clinical manifestations of the syndrome. Before skin ulcerations, tissue ischemia leads to hard lumpy and/or plaque-like charac to the SC tissue.
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Secondary Lesion Primary lesion alone not sufficient to initiate infarction ie, thrombosis or reduced perfusion contribute Thrombi often found in primary lesios Preexisting disturbances of coagulation are relevant to the pathogenesis: protein c/s and cryofibrinogen Also iron dextran suggested to aggravate or initiate the secondary lesions
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Pt HE Stain Intimal Constriction
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This note was uploaded on 12/24/2011 for the course STEP 1 taught by Professor Dr.aslam during the Fall '11 term at Montgomery College.

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CUA Presentation_0 - QuickTime and a decompressor are...

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