NR 507 Alterations in Renal and Urinary

NR 507 Alterations in Renal and Urinary

NR 507 Alterations in Renal and Urinary

I am also not a great fun of DNA and genetics. I read the chapter on epigenetics and disease. One process I found interesting is, gene silencing (Imprinting), in which genes are inevitably silenced, regulated on which parent transfers them (McCance, Huether, Brashers, & Rote, 2013). I also learnt that imprinted genes are densely methylated in comparison to the nonimprinted clone of the allele, which is usually not methylated (McCance et al., 2013). Disease of imprinting that is consorted with deletion of approximately four million base sets (Mb) of the protracted arm of chromosome 15 (McCance et al., 2013). When this genetic deletion is from the father, the child exhibits Prader-Willi syndrome, whose clinical representation includes, short height, loss of muscle tone, small upper and lower extremities, obesity, mild to modest mental retardation and hypogonadism (McCance et al., 2013). The same 4-Mb deletion passed down from the mother results in Angelman syndrome, which is distinguished by severe mental retardation, seizure, ataxic posture and spells of unsuppressed laughter (McCance et al., 2013). According to McCance (2013), these illnesses are both seen in one of every 15,000 live births and chromosome deletions are accountable for about 70 percent of cases in both illnesses.

References

McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby

In this week lesson of the renal system it is whort knowing the difference between the nephrotic syndrome and acute glomerulonephritis.

Both diseases attract the kidney and result in renal dysfunction.  As a nurse practitioner, it is good to pay attention to the hallmark signs of both diseases since acute glomerulonephritis and nephrotic syndrome have a similar characteristic. Glomerulonephritis is the inflammation of the glomerulus resulting to leakage of into the urine.red blood cells (RBCs) and protein tea-colored urine (cola colored) from hematuria recent strep infection. The cause of the patient disease is not due to strep infection but is due to the bodily reaction to antigen in strep

Nephrotic syndrome, on the other hand, is due to changes to the glomerulus of the nephron that causes leakage of massive protein greater than 3 grams (Proteinuria) in the urine, hyperlipidemia, hypoalbuminemia, foamy frothy urine dark yellow in color,  generalized edema that start around the eyes and spreads to  other systems of the body.

The filtrating system in the glomerulus is faulty in nephrotic syndrome they are bigger than their regular size and allows proteins to pass through. In acute glomerulonephritis there is presence of protein but not to compare to the protein loss in the Nephrotic syndrome.

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This week’s reading material is focused on the pathophysiology and alterations of the renal and urologic systems.

NR 507 Alterations in Renal and Urinary
NR 507 Alterations in Renal and Urinary

Both organ systems according to our textbook and knowledge ascertained throughout the years working not only psychiatric, but other medical disciplines. That we care for patients during vulnerabilities secondary to acute exacerbations of medical comorbidities.  Our textbook References the importance of both organs and appendages in maintaining homeostasis the body. Through the regulation of fluid volume and the removal of toxins and excess waste. Over the years in the medical discipline, one the principles that remained a constant in my mind that was learned from nursing school, was the need to discontinue the medication Glucophage also known as metformin. At least 48 hours before a patient would be administered radiocontrast media. The generalized understanding was that the pharmacokinetics of the contrast media and Glucophage would lead to a potential toxic level of lactic acid which could progress to lactic acidosis. As a result of the material used in this week’s lesson, the writer learned another fundamental principle. Which consists of factors that contribute to ischemic acute tubular necrosis (ATN). One of the primary causes of intrarenal acute kidney injury secondary to ischemia have been closely associated with significant exposure to “antibiotics and radio contrast media” and medical conditions such as “glomerulonephritis, disseminated intravascular coagulation (DIC), vascular disease and malignant hypertension” (McCance, Huether, Brashers, & Rote, 2014, p. 1360).

References

McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2014). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, Missouri: Mosby

This week our primary focus is on the renal system. I have always been fascinated with the renal system because it plays such a vital role in filtering out the unwanted substances in the blood stream and can affect all other body organs if the process is interrupted. In the healthcare field I feel it is very common to see renal diagnosis and complications of some diseases such as chronic renal disease. My grandmother had chronic renal disease and it was a long process that involved dialysis and many other health conditions as a result of the renal disease. One topic that I always find interesting in the renal system is obstruction such as kidney stones. While reading this week I found it interesting that depending on where the obstruction is located highly impacts the complications that arise. I have seen many individuals who have kidney stones present with severe flank pain, nausea, and vomiting. I have always found it interesting calcium is one of the main culprits of kidney stone formation. I have visualized a passed kidney stone before and was surprised that something so small can cause so much discomfort however, I have also visualized stones that I would have thought impossible to pass without surgical intervention. Healthcare continues to advance with treatment techniques to remove stones from the ureters of patients who will not be able to pass the stones on their own. I feel this is a very interesting topic along with all of the other great information learned this week in regards to the renal system. This week is also our midterm and I must admit I am very nervous to see the questions that will be asked. I have spent the week in an attempt to review all of the learned information and focus in on the study guide outline. I hope everyone succeeds and does great on the midterm and can continue our journeys to becoming advanced practice nurses.

Reference

McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2014). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, Missouri: Mosby. Chapter 38.

This week has been a very interesting week with regards to our readings and trying to study for the midterm exam.  We covered some great topics this week and I leaned towards the renal system and its function.  At the beginning of my nursing career I worked on a Med/Surg unit and of course we had our fair share of UTI’s and Rental stone patients.

  • Kidney stone– kidney stones affects 10% of people between the ages of twenty and sixty years old, and a recurrence rate within 5-10 years (Dawson & Tomson, 2012). Kidney stones are a result of the growth of crystals into stones.   These crystals are formed in urine that is supersaturated with particular salts such as calcium oxalate, sodium urate, magnesium ammonium phosphate, or cysteine (Sakhaee, 2014). There are mainly four types of kidney stones.

Calcium oxalate stones are the most common type of stones, accounting for over 70% of all stones. These stones develop under a high degree of supersaturation, crystallization inhibitors, and urinary stagnation. Supersaturation occurs with high concentration of salt within the urine. These stones typically form by eating too much calcium or vitamin D. Genetics and certain medications can increase formation also (Rajat, Anu, & Sumeet, 2011).

Kidney stones tend to be located either at the area of prior injury or in gravity dependent locations such as lower pole calices. These stones can be small or large in size. Depending on the size of the stone, it can either be voided with urination, or if the stone is too large, lithotripsy or surgery may be required (Malan et al., 2011).  Depending on the size of the stones, individuals may experience considerable pain during their journey through the urinary tract due to the sharp edges of the large stones that may gouge into the walls of the ureters and sometimes the urethra. This severe pain is called renal colic, and comes in waves that may cause the person to double over. Pain may be localized in the flank or pelvic area, and often to one side. Other symptoms include; nausea, vomiting, fever, sweating, difficulty voiding, and possible hematuria.

Reference

Dawson, C. H., & Tomson, C. V. (2012). Kidney stone disease: pathophysiology, investigation and medical treatment. Clinical Medicine12(5), 467-471.

Rajat, M., Anu, W., Sumeet, G. (2011). New Frontiers on Nephrolithiasis: Pathophysiology andManagement of Kidney Stones. International Journal of Research in Avurveda & Pharmacy, 2(3), 775-786.

Sakhaee, K. (2014). Epidemiology and clinical pathophysiology of uric acid kidney stones. Journal Of Nephrology27(3), 241-245. doi:10.1007/s40620-013-0034-z