Pyonephrosis pathophysiology: Difference between revisions
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==Overview== | |||
[[File:Pathophysiology of Pyonephrosis.jpg|thumb|Pathophysiology of Pyonephrosis]] | [[File:Pathophysiology of Pyonephrosis.jpg|thumb|Pathophysiology of Pyonephrosis]] | ||
[[Pyonephrosis]] can be seen as a complication of [[Acute Pyelonephritis]], usually seen with complete or incomplete obstruction of tubules<ref>{{cite book | last = Kumar | first = Vinay | title = Robbins and Cotran pathologic basis of disease | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2015 | isbn = 978-1-4557-2613-4 }}</ref>. Obstruction of [[ureter]] and [[renal pelvis]] leads to dilatation of tubular system and leads to [[Hydronephrosis]]. This dilatation becomes a nidus for infection. The pathogen multiply easily in obstructed and dilated tubules leading to suppurative inflammation. The exudates fill the tubules, renal pelvis, calyces and ureter with pus that is difficult to drain. | [[Pyonephrosis]] can be seen as a complication of [[Acute Pyelonephritis]], usually seen with complete or incomplete obstruction of tubules<ref>{{cite book | last = Kumar | first = Vinay | title = Robbins and Cotran pathologic basis of disease | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2015 | isbn = 978-1-4557-2613-4 }}</ref>. Obstruction of [[ureter]] and [[renal pelvis]] leads to dilatation of tubular system and leads to [[Hydronephrosis]]. This dilatation becomes a nidus for infection. The pathogen multiply easily in obstructed and dilated tubules leading to suppurative inflammation. The exudates fill the tubules, renal pelvis, calyces and ureter with pus that is difficult to drain. | ||
Revision as of 14:08, 15 October 2021
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Harsh Vardhan Chawla, M.B.B.S.[2]
Overview
Pyonephrosis can be seen as a complication of Acute Pyelonephritis, usually seen with complete or incomplete obstruction of tubules[1]. Obstruction of ureter and renal pelvis leads to dilatation of tubular system and leads to Hydronephrosis. This dilatation becomes a nidus for infection. The pathogen multiply easily in obstructed and dilated tubules leading to suppurative inflammation. The exudates fill the tubules, renal pelvis, calyces and ureter with pus that is difficult to drain.
The accumulation of pus in the tubules eventually lead to structural and functional loss of the renal parenchyma. There may be a complete or incomplete loss of function initially. The combination of obstruction with the infections rapidly progresses to sepsis. Therefore to prevent renal loss of function and blood stream infection leading to sepsis it is important to diagnose and treat the condition.[2]
References
- ↑ Kumar, Vinay (2015). Robbins and Cotran pathologic basis of disease. Philadelphia, PA: Elsevier/Saunders. ISBN 978-1-4557-2613-4.
- ↑ Tanagho, Emil (2008). Smith's general urology. New York: McGraw-Hill Medical. ISBN 978-0-07-163260-7.