wk 8 advanced pathophysiology (1).docx

wk 8 advanced pathophysiology (1).docx - Pyelonephritis is...

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Pyelonephritis is an infection of the ureter, renal pelvis, and kidney interstitium. Urinary blockage and reflux of urine from the bladder (vesicoureteral reflux) are the most common causes. Most commonly occur in young adult women. Acute pyelonephritis usually associated with E. coli, Proteus, or Pseudomonas. The Proteus and Pseudomonas are more commonly associated with infections after urethral instrumentation or urinary tract surgery. These bacteria split the urea into ammonia that makes the urine alkaline that helps in stone formation. The infection is usually spread by ascending infection along the ureters but spreading also may occur through the bloodstream (McCance & Huether, 2014). Cornwall has a pyelonephritis due to bacterial infection of her renal pelvis, calyces, and medulla. The bacterial invasion triggers inflammatory mediators with infiltration of white blood cells within renal pelvis that cause purulent urine. In severe pyelonephritis, abscess formation and necrosis may occur in the medulla. Scar tissue may form with healing. The urine coming from the glomeruli mixes with inflammatory exudate in the renal pelvis and calyces or tubules with extensive infection. This leads to purulent urine with bacteria and white blood cell casts (McCance & Huether, 2014). The acute kidney injury is ranging from minimal or subtle changes in renal function to complete renal failure requiring the renal transplant. The acute renal injury divide into three categories (1) prerenal (2) intrarenal (3) postrenal. Most types of injuries are reversible with early diagnoses and treatment. Prerenal acute renal failure occurs in any condition that causes reduce or no blood supply to the kidney such as hypovolemia, hypotension, shock, hemorrhage, myocardial infarction with poor cardiac output, and left ventricular failure. The kidneys receive up to 25% of the cardiac output and thus any failure of the general circulation or isolated failure of the intrarenal circulation can have a profound impact on renal perfusion. Initially, the kidney in prerenal conditions tries to concentrate the urine maximally and avidly reabsorb sodium in an effort to maintain/increase intravascular volume and normalize renal perfusion. But when the blood supply of the afferent arterioles of the kidney is low for a long time, it results in a low glomerular filtration rate and eventual result in renal ischemia. Ultimately the renal function reduced with high blood urea nitrogen (BUN) and plasma creatinine ( Basile, Anderson, & Sutton, 2012). Intrarenal acute renal failure is caused by impaired blood flow within the kidney such as acute tubular necrosis (ATN), glomerulonephritis, malignant hypertension, disseminated intravascular coagulation (DIC), and renal vasculitis. That result in kidney damage due to ischemia or inflammatory damage (McCance & Huether, 2014).
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