Sample Answer for NUR-631 Topic 12 DQ 1 Included After Question
Select two of the following questions for your discussion response. Indicate which questions you have chosen using the format displayed in the “Discussion Forum Sample.”
Explain the concept of azotemia (including prerenal, renal, and postrenal), causes, and diagnostic measures used to identify each.
Identify and discuss the pathophysiology underlying one pediatric urological disorder.
Spinal cord injuries carry a high risk of neurogenic bladder and reflex incontinence. Explain the mechanisms responsible for these disorders.
A Sample Answer For the Assignment: NUR-631 Topic 12 DQ 1
Title: NUR-631 Topic 12 DQ 1
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MH
Explain the concept of azotemia (including prerenal, renal, and postrenal), causes, and diagnostic measures used to identify each.
In acute kidney injury (AKI), clinical classification is placed to identify the severity, stage, progression, and location of damage to kidneys. Furthermore, the clinical term azotemia is part of one of the determinants of renal function by characterized in serum laboratory findings of increased urea and creatinine level; creatinine level normal value is 0.7-1.4 mg/dL; the renal insufficiency or renal failure causes azotemia and in general the term is used to describe the accumulation of waste products that the circulatory system contains. Moreover, for acute kidney injury the literature describes a sudden onset of decline in kidney function by the decrease of glomerular filtration and urine output with accumulation of nitrogenous waste products in blood circulation and developed by Kidney Disease: Improving Global Outcomes (KDIGO) Working Group aid in determining diagnosis of acute renal injury (McCance et al., 2018).
Staging of acute kidney injury is set in stages; Stage 1 is a serum create of 1.5-1.9 times baseline or greater or equal to 0.3mg.dL increase, Stage 2 is 2.0-2.9 times baseline, Stage 3 is 3.0 times baseline or increase in serum create to >/= 4.0 mg/dL or start on renal replacement therapy or in clients < 18 yrs, decrease in eGFR to < 35mL/min per 1.73m2. . In addition, AKI results from extracellular volume depletion and decrease perfusion to renal system, tosxic/inflammatory injury to cells in kidney changing the morphology and secondary changes occur in filtration and are classified accordingly. 1) Hypoperfusion is a prerenal AKI in which not enough blood reaches the kidney for perfusion for example hypovolemia 2’ hemorrhage 2’ large vessel or vessels are broken by trauma ex motor vehicle accident. The loss of blood is decreased and cell in afferent artery sense by baroreceptors causing a cascade of events by activation of the RAAS system (McCance et al., 2018).
2) Intrarenal is usually by nephrotoxic agents, medications, herbal, home remedies culture, and drug allergies in which cause an acute tubular necrosis ATN. In consequence, the ATN causes ischemia necrosis affecting the tubules most often seen in the medullary area of the kidney that is the highest oxygen ectracton rate of all the body tissues approximately 80% (McCance et al., 2018). Finally, postrenal acute kidney injury is 2’ to urinary tract obstruction, for example, bladder outlet obstruction (BOO), causes and increase in intravesicle pressure, ureter vesicle junction UVJ sphincter dilates and urine is retrograde into ureter back into kidneys creating hydronephrosis, hydroureter reflux, all contribute to AKI and GFR decreases (McCance et al., 2018).
Spinal cord injuries carry a high risk of neurogenic bladder and reflex incontinence. Explain the mechanisms responsible for these disorders.
Neurogenic bladder in general term can be 2’ to spinal cord injury and detrusor hyperreflexia or dyssynergia depending on injury of spinal cord lesion will create the disorder. Furthermore, micturition center between C2 and S1 are upper motor neurons and result in detrusor hyperreflexia with DSD. Therefore, the initial response of the bladder and miscommunication of the adrenergic innervation will develop OAB syndrome and detrusor sphincter dyssynergia in simplicity terms the bladder contracts by detrusor muscle and the outlet internal sphincter contracts resulting in sporadic spontaneous incontinence. Moreover, the treatment is based on mechanics by intermittent catheterization and emptying the bladder on time management and if antimuscarinics or anticholinergic medication are given the problem will worsen the outcomes. In addition, one of the gold standards of physiological functions is performing a urodynamics test to determine in what stage is the patient in NGB w/ Hyperreflexia or NGB w/Hypotonic bladder or Atonic Bladder (McCance et al., 2018).
McCance, K. L., & Huether, S. E. (2018). Pathophysiology – e-book (8th ed.). Elsevier Health Sciences.
REPLY
JG
What are the pathophysiological differences between prerenal, intrarenal, and postrenal failure? Can anyone give examples of each scenario.
How can you help to determine the cause of acute renal failure in your patient?
REPLY
RM
Hello Marco. I enjoyed reading your post. To add to spinal cord injuries and high risk of neurogenic bladder and reflex incontinence. According to the national association for continence. Bladder function, bladder and bowel external sphincters, sexual functions, and some leg muscles are the domain of the sacral spinal cord. A very important part of voiding involves the sacral spinal cord. The micturition, center receives and sends signals directly to and from the bladder. When the bladder becomes filled with urine, it sends signals to the sacral spinal cord. If this communication is disrupted, through disease or injury, the message is delayed or not received. The result is incontinence (NAFC, 2022).
Spinal Cord Injury and incontinence. National Association For Continence. (2022). https://nafc.org/spinal-cord/
REPLY
KM
Explain the concept of azotemia (including prerenal, renal, and postrenal), causes, and diagnostic measures used to identify each.
Azotemia is a biochemical abnormality that is defined as the elevation of nitrogenous products, creatinine in the blood, or other secondary waste products in the body. The raising of nitrogenous waste is due to the renal system’s inability to filter them out adequately. This is seen in both acute and chronic kidney injury. Prerenal azotemia results from an insult or injury source before the kidney. This is most commonly caused by hypoperfusion or decreased blood flow to the kidneys due to such things as volume depletion seen in shock, dehydration, hemorrhage, over-diuresis, burns, and intravascular depletion in low oncotic pressure states. Renal azotemia occurs from damage to the structure of the kidney. The glomeruli, renal tubules, and interstitium, and renal vasculature are all structures that can be affected. Common causes include inflammatory conditions such as vasculitis, toxins, drugs, infection, and damage from hypoperfusion. Post renal azotemia is seen when there are problems with the ureters and bladder. Typically, there is some type of obstruction. This is seen in those patients with risk factors such as recurrent urinary tract infections, nephrolithiasis, hydronephrosis, and benign prostatic hyperplasia. Diagnosis of azotemia can be made by a BUN >21mg/dL.
Significant findings for prerenal azotemia include BUN: Cr ratio > 20:1; Urine osmolality of 500mOsm/kg; UA can show hyaline casts. Significant findings for renal azotemia: BUN: Cr ratio < 20:1; Urine Osmolality less than 300mOsm/kg; UA shows cellular debris, muddy brown casts, red cell casts, eosinophils, + proteinuria. Significant findings of post renal azotemia include BUN:Cr ratio < 20:1; urine osmo < 300mOsm/kg; UA WBC casts; imagining findings: pyelonephritis, nephrolithiasis, bladder mass (Tyagi & Aeddula, 2023).
Spinal cord injuries carry a high risk of neurogenic bladder and reflex incontinence. Explain the mechanisms responsible for these disorders.
Neurogenic bladder is a broad term used to describe bladder dysfunction caused by neurologic disorders and involves problems with storage or voiding. The type of dysfunction is determined by the related sites in the nervous system that control sensory and motor bladder function. In lesions that develop in the upper motor neurons of the brain and spinal cord, dyssynergia and overactive or hyper reflexive bladder function develop. Lesions in the sacral area of the spinal cord or peripheral nerves result in underactive, hypotonic, or atonic bladder function usually with loss of bladder sensation. In neurologic disorders that develop above the pontine micturition center, the result is detrusor hyperreflexia, also known as reflex bladder. In this upper motor neuron disorder, the bladder empties automatically when it becomes full and the external sphincter functions normally. Because the pontine micturition center remains intact, coordination between detrusor muscle contraction and the relaxation of the urethral sphincter remains. Neurologic lesions that occur below the pontine micturition center but above the sacral micturition center leads to detrusor hyperreflexia with detrusor sphincter dyssynergia. This leads to functional obstruction of the bladder. (McCance & Huether, 2019).
Tyagi, A., Aeddula, N. (2023). Azotemia. StatPearls Internet. Retrieved on July 22,2023 from https://www.ncbi.nlm.nih.gov/books/NBK538145/
McCance, K., Huether, S. (2019). Pathophysiology: The Biological Basis of Disease in Adults and Children. (8th ed). Elsevier.
REPLY
JG
Good. What age related changes occur in the genitourinary system as a person ages?
Why is urine specific gravity not always a good indicator of fluid status in the older adult?
REPLY
KM
In the kidneys, the glomeruli increase in diameter and the tubules enlarge effectively to maintain the regulatory functions of the kidney. This hypertrophy occurs most quickly and to a larger degree in younger individuals and in those with a high protein intake. Hypertrophy is a compensatory mechanism due to an increased workload and occurs throughout life. With aging, the number and size of nephrons decrease. This is due to multiple factors including oxidative stress, inflammation, hypertension, and diabetes. The mechanism of this change is primarily due to a change in the renal vasculature and perfusion patterns due to atherosclerosis, leading to a reduction in the number of nephrons. The nephron population is reduced by 30 to 50% by 75 years of age with the loss of renal mass occurring primarily in the cortex. Other degenerative changes also occur. The glomerular capillaries become sclerotic, the glomeruli may disappear completely, the arcuate and interlobular arteries become tortuous, contributing to ischemia. Tubular transport changes with aging. The tubules may function normally under normal conditions but they do not adapt to stressful situations as easily. Glucose, bicarbonate, and sodium are not reabsorbed as efficiently and hyperkalemia is seen more often due to decreased secretion. In drugs eliminated by renal processes, does modifications and more frequent observations may be required. Contrast agents and nonsteroidal anti-inflammatory drugs should be used with caution (McCance & Huether, 2019). Due to this change in renal status, older adults have a more difficult time concentrating urine, making specific gravity less accurate of an indicator of fluid status.
McCance, K., Huether, S. (2019). Pathophysiology: The Biologic Basis for Disease in Adults and Children. (8th ed). Elsevier.
