Essay dealers patho dqr wk 8 nanoxia deep silence 4 matx

The symptoms presented by Ms. Cornwall are classic symptomology of pyelonephritis. anxiety disorder meaning in bengali The upper urinary tract is usually a sterile system, it consists of the ureter, renal pelvis and kidney interstitium. Bacteria can enter the system via the lower urinary tract or through the bloodstream (Macon, Yu, & Nall, 2018). The most common etiology cause is infection with Escherichia coli (E-coli). When E-coli is introduced to the area, it causes an inflammatory process that brings white blood cells to the area. When Ms. Cornwall urinates the inflammatory process brings infectious waste (exudate) and white blood cells are excreted in the urine (Macon, Yu, & Nall, 2018). The bacteria cause inflammation and pain resulting in a rise in white blood cells.


The bacterial infectious process from E-coli arises from either by ascending through the ureters or blood stream (Doig & Heuther, 2014).

In pyelonephritis, abscess and necrosis may occur in the medulla. The presence of white blood cells casts usually neutrophils, indicate an inflammatory response to the presence of bacteria. During the diagnosing stage, a urinalysis will reveal bacteria and white blood cell casts as the out flow of urine attempts to flush the kidneys of the infection (Doig & Heuther, 2014). Urine cultures are positive in 90 percent of patients with pyelonephritis.

Prerenal acute renal injury is caused by decreased perfusion leading to a decrease in renal function (Macedo, & Mehta, 2009). The loss of blood flow causes a loss of kidney function, however there’s no damage to the kidney itself at this stage. Certain medication, dehydration, hypotension, sepsis, blood loss due to injury can cause this lack of blood flow. Kidneys receive 25% of cardiac output, thus any failure in systematic circulating blood volume causes a profound impact on renal perfusion (Makris & Spanou, 2016). An example would be septic shock, causing wide vasodilation and hypoperfusion due to low blood pressure.

Intrarenal (intrinsic) kidney injury is a sudden loss in renal function due to a direct damage to the kidney. Acute tubular necrosis (ATN) related to the prerenal AKI can cause it. Acute glomerulonephritis, vascular disease, infection can cause intrarenal kidney injury. ATN caused by ischemic occurs most often after surgery, it accounts for 40 to 50 percent of cases (Macedo & Mehta, 2009).

Postrenal acute kidney injury is usually caused by an obstruction of the urinary tract that affects the kidneys bilateral (Kazama & Nakajima, 2017). Post renal injury increases intratubular, thus decrease GFR, leading to impaired renal blood flow and inflammation process (Makris & Spanou, 2016). An example would be an obstruction cause by kidney stones, neurogenic bladder, and tumors (Kazama & Nakajima, 2017).

Acute pyelonephritis is a severe form of urinary tract infection (UTI) involving the renal parenchyma, calices, and pelvis, usually caused by Escherichia Coli (E. Coli) or other gram-negative bacilli (Johnson, & Russo, 2018). E. unspecified anxiety disorder dsm 5 code Coli is an enteric bacterium capable of attaching to uroepithelial cells (Hanson, Kaijser, & Svanborg Eden, 1981), thus called a uropathogen and is known to be the most common cause of severe UTI. E. Coli ascends from the lower urinary tract along the ureters to the kidneys. However, according to Doig and Huether (2014), the spread of infection can also be via the bloodstream. E. Coli accounts for 70-90% of UTI (Shields, & Maxwell, 2010). Pyelonephritis can be acute, chronic, or recurrent, and would present with fever, chills, accompanied by severe back pain or flank pain, nausea, vomiting, and costovertebral angle tenderness (“Acute Pyelonephritis,” 2018). Other symptoms include urinary frequency, urgency, and dysuria. Pyelonephritis may lead to sepsis and septic shock (Johnson, & Russo, 2018). The incidence of acute pyelonephritis is higher in younger women. Risk factors for uncomplicated acute pyelonephritis include recent sexual intercourse, acute cystitis, stress incontinence, and diabetes. For complicated acute pyelonephritis, predisposing factors include pregnancy, diabetes, anatomical abnormalities of the urinary tract, and renal calculi (Shields, & Maxwell, 2010). Diagnosis is primarily made through urinalysis and urine culture. Urinalysis may reveal white blood cell casts indicating a renal-origin pyuria, confirming the diagnosis of acute pyelonephritis (Colgan, Williams, Johnson, 2011). anoxic brain injury mayo clinic All casts originates from the renal tubules, and white casts are linked to an inflammatory process occurring in the tubules, such as in the case of pyelonephritis. Complicated pyelonephritis may need to have blood culture and imaging of the urinary tract (Doig, & Huether, 2014). Intravenous pyelography and voiding cystourethrography are imaging used to assist in determining the possible cause of the urinary tract obstruction that had led to infection. Intravenous pyelography is a series of x-rays performed on the kidneys, the ureters, and the bladder to locate the suspected obstruction in the urine flow, the most common cause of which are kidney stones (Cheong, 2017). Cystourethrography is also a radiologic test of the bladder using a contrast medium to evaluate for anatomical and functional abnormalities (Cheung, 2017). Treatment for pyelonephritis is microorganism-specific antibiotic therapy for 2-3 weeks (Doig, & Huether, 2014). Complications include acute kidney injury, papillary necrosis, renal or perinephric abscess, and/or the development of emphysematous pyelonephritis. plexus anxiety testimonials A rising incidence in the community had been seen with UTI caused by bacteria that produce extended spectrum beta-lactamase (ESBL) enzymes, resistant to antibiotics such as penicillin, cephalosporin, and quinolone (Shields, & Maxwell, 2010).

Acute kidney injury (AKI) is defined as the abrupt reduction in the function of the kidneys usually within 48 hours, manifested by a build-up of nitrogenous wastes in the blood, and a decrease in glomerular filtration. AKI is caused by volume depletion, diminished blood flow to the kidneys, and/or toxic injury to the kidney cells. AKI can either be prerenal, intrarenal, or post-renal. Pre-renal injury is caused by poor perfusion resulting from renal artery thrombosis, hypotension secondary to volume depletion, hemorrhage, and renal vasoconstriction. Intrarenal or intrinsic renal injury is an injury that causes direct damage to the kidneys. The most common cause of intrinsic renal injury is called acute tubular necrosis (ATN) which can either be ischemic or nephrotoxic. Ischemic injury results from persistent hypotension, hypoperfusion, and hypoxemia in cases such as glomerulonephritis, systemic lupus erythematous, allograft rejection, malignant hypertension, disseminated intravascular coagulation, severe sepsis, severe trauma, severe burns, and obstetric complications. Nephrotoxic ATN may result from exposure to nephrotoxic drugs such as aminoglycosides, radiocontrast agents, and cisplatin (Doig, & Huether, 2014). Other nephrotoxic drugs are methotrexate, ethylene glycol, amphotericin B, angiotensin-converting enzymes (ACE) inhibitors, angiotensin receptor blockers, and non-steroidal anti-inflammatory drugs. Other substances that are toxic to the kidney tubules are excessive myoglobin and hemoglobin in rhabdomyolysis and hemolysis (Rahman, Shad, & Smith, 2012). Postrenal AKI is usually caused by obstruction in the urinary tract found in ureteral and urethral obstruction, prostatic hypertrophy, tumors, and neurogenic bladder (Doig, & Huether, 2014).

Risk factors for acute kidney injury includes pre-existing chronic kidney disease, cardiac failure, liver failure, older age, hypovolemic shock, exposure to contrast media. Management of AKI is geared primarily on fluid resuscitation, avoidance of nephrotoxic agents, and correction of electrolyte imbalances. Renal replacement therapy (dialysis) will be required for intractable metabolic acidosis, and refractory hyperkalemia, volume overload, uremic encephalopathy, pericarditis, pleuritis, and removal of toxins (Rahman, Shad, & Smith, 2012).

Doig, A. K., & Huether, S. E. (2014). Alterations of renal and urinary tract function. In K. L. McCance, S. E. Huether, V. L. nanoxia deep silence 5 Brashers, & N. S. Rote (Eds.). Pathophysiology: The Biologic Basis for Disease in Adults and Children (7thed.). St Louis, Missouri: Elsevier

Hanson, L. A., Fasth, A., Jodal, U., Kaijser, B., & Svanborg Eden, C. (1981). Biology and pathology of urinary tract infections. Journal of Clinical Pathology, 34 (7). Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC493796/?page=3