sturge_weber
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a girl comes to the clinic with diarrhea and oliguria. examination of blood reveals numerous schistocytes. reticulocyte count 2.4%. what would a kidney biopsy reveal???
a.acute tubular necrosis
b. effecement of foot processes
c.intimal thickening of small arteries and glomerular thrombosis
d mesangial and subendothelial deposits
e. PMN s in the glomerular capillaries
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| msyamp
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a. hypovolemia> atn> uremia > schystozoites
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| sturge_weber
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try again
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| msyamp
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it is hus. answer is c sorry for the first
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| sturge_weber
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well can u explain hus, i alwya get it wrong....
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| msyamp
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Heamolytic uremic syndrome
The disease process begins with systemic absorption from the gastrointestinal tract of a toxin that causes endothelial damage. The major toxins that cause HUS, Shiga toxin 1 (Stx1) and Shiga toxin 2 (Stx2), are similar in structure to the classic Shiga toxin (Stx). Organ injury occurs after binding of Stx1 and/or Stx2 to globotriaosylceramide (Gb3), a glycolipid receptor molecule on the surface of endothelial cells. Damage primarily occurs in the kidney but may occur in other organs as well. The predominance of renal injury may be caused by differential expression of Gb3 on glomerular capillaries versus other endothelial cells. Damaged endothelial cells of the glomerular capillaries release vasoactive and platelet-aggregating substances. The endothelial cells swell, and fibrin is deposited on the injured vessel walls.
Swelling and microthrombi formation within the glomerular capillaries produce a localized intravascular coagulopathy. The glomerular filtration rate is reduced, and renal insufficiency ensues. Erythrocytes are damaged and fragmented as they traverse the narrowed glomerular capillaries. This leads to the characteristic microangiopathic hemolytic anemia. Hemolysis also may be a result of lipid peroxidation.
Thrombocytopenia is believed to result from a combination of platelet destruction, increased consumption, sequestration in the liver and spleen, and intrarenal aggregation. Platelets are damaged as they pass through the affected glomerular capillaries. Remaining platelets circulate in a degranulated form and show impaired aggregation
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| sturge_weber
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great explanation msyamp
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| ssrpk
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How would the PT and aPTT present in HUS?
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| sturge_weber
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normal as only platelets consumed. hence prolonged bleeding, n pt and ptt
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| ssrpk
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yeah right 
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| druas
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thanks god i got it right...yes its HUS. Diarrhea and oligouria in a patient with shistocyte(GI+Kidney)...strongly suggest it..2 more thngs to add...shiga toxin of 0157:H7 of e. coli and hamburger eating(undercooked beef)
Edited by druas on 01/05/06 - 08:05 AM
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