7 Nov 2022

110

Diabetes Mellitus: An Overview

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Academic level: College

Paper type: Case Study

Words: 1181

Pages: 4

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1. Explain the cause for her low calcium and sodium levels. 

The calcium and sodium levels are low due to increased levels of antidiuretic hormone (ADH). The hormone, which is involved in water retention in the body is produced in the hypothalamus in the brain and stored in the posterior pituitary gland until a signal is received on need for water retention control. ADH is also called arginine vasopressin and regulates and balances water in the body through kidney tubules. Sarah’s condition is due to hyponatremia, which means the sodium is diluted. Hyponatremia occurs when there is too little sodium in the body for the amount of fluid in circulation. The condition is mainly caused by kidney disease and cirrhosis, and makes the body to retain more fluid than sodium. 

Her low calcium level is called hypocalcemia. Hypocalcemia occurs when not enough calcium is moved from bones into the blood or too much of it is lost in urine. The causes of hypocalcemia include Vitamin D deficiency due to kidney dysfunction ( Calvo, 2014) . Where the kidney lacks proper balance ability, more calcium is excreted in urine and the kidney becomes less capable of activating vitamin D. 

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2. Explain the cause of her anemia. What laboratory test should indicate she is suffering from anemia? 

The cause for her anemia is renal disease, as it affects the kidneys and impairs their functioning. In this case, her anemia is because the kidneys do not produce sufficient amounts of erythropoietin. Erythropoietin is a hormone synthesized by the kidneys then released into the bloodstream in response to low blood oxygen levels. It is then carried to the bone marrow, where it triggers release of red blood cells. However the hormone is active for a short period then destroyed and excreted through urine. Sarah's kidneys are damaged and cannot produce sufficient erythropoietin, thus not enough red blood cells are released into the blood, resulting into anemia. 

The red blood cell count laboratory test indicates it is low because the standard level is from 4.2 to 5.4 million cells per ul for females who are not pregnant, but Sarah’s is 3.9 cells per ul ( Daru, Sobhy & Pavord, 2019) . In addition to the tests that Sarah received to assess whether she was anemic, other tests such as a bone marrow biopsy, iron level, Vitamin B12, and foliate levels tests can also be done. 

3. Explain the cause of her hypotension. How will her body attempt to establish homeostasis? 

The normal blood pressure is approximately 120/80; therefore, Sarah's is in the range of hypotension (low blood pressure) since its 92/64. Hypotension is either caused by the blood volume being reduced involving loss of salt and water from urinate, or the increasing of ADH and the decrease of renin. Increased water retention slows down the release of hormone renin from the kidneys. As the hormone renin is inhibited, the blood pressure reduces as more water is lost through the kidney. The body restores homeostasis by the decreasing secretion of ADH from the hypothalamus, which in turn increases release of renin to stimulate the hormone angiotensinogen then the lungs convert angiotensin I to angiotensin II which is a vasoconstrictor, alleviating hypotension. 

4. What type of acid-base disorder has she developed, and how will her body compensate? 

According to the blood test results, her HCO3 is low at 12 mmol/L and so is pH at 7.2, which implies she has metabolic acidosis. Metabolic acidosis occurs when the body produces excess acid. The patient has end-stage renal disease, which means her kidneys are not able to excrete acid sufficiently from the body. Acidosis also becomes more dangerous in patients with diabetes since lack of insulin causes ketones to be excessively produced, which turns blood acidic. 

However Sarah's body is compensating by increased absorption of hydrogen ions (H+) and bicarbonate ions (HCO3-) in the kidneys. The respiratory compensation also helps reduce metabolic acidosis by the lungs increasing the respiratory rate to remove CO2 and readjust the bicarbonate to carbonic acid ratio to the usual 20:1 ratio. 

5. Explain the cause of her elevated ADH and glucose levels. 

Sarah's has insulin deficiency due to the increased level of glucose in the blood. When the glucose level is elevated, the hormone is not produced because the nervous system does not receive signals to release insulin (American Diabetes Association, 2017). She also has smoking 30-pack a day history; thus may be at risk of lung cancer. Lung cancer causes syndrome of inappropriate ADH, as it causes an increased release of the hormone. 

6. What is the correlation between her illnesses and the low vitamins (D, K, E, and A), renin, and aldosterone levels? 

Low vitamin D causes hypocalcemia because not enough calcium is moved from bones into the blood. 

Deficiency in vitamin K is also responsible for the multiple bruises on Sarah’s body as the vitamin is responsible for skin health. 

Low vitamin E also causes general body weakness since vitamin E is an antioxidant. When in low levels, the body experiences oxidative stress, thus weakness. 

Low vitamins A cause Sarah’s skin discoloration, and sclera. 

Renin hormone is needed for the activation of angiotensinogen to angiotensin II, which increase blood pressure. She has hypotension because the low levels of renin. 

Low levels of aldosterone results in reduced level of sodium because it is necessary for the reabsorption of sodium ions in the kidneys. 

7. Which hormone would the body elevate in response to her low calcium levels? Why? 

Parathyroid hormone is released when calcium levels are below optimum. The parathyroid glands release parathyroid hormone (PTH) when low levels of calcium are detected in the body. PTH increases decalcification of bones to release calcium into blood and also increases reabsorption of calcium in the kidneys, altogether raising calcium levels in blood. 

8. Explain the physiological reason behind her physical findings (yellowish hint of the skin, sclera, multiple bruises, weakness, and edema). 

Sarah’s physical findings are due to deficiencies and malfunctioning systems. Yellowish and discolored skin and sclera were caused by cirrhosis; a chronic liver damage or liver failure disease ( Verald et al., 2020) . Skin bruises are due to Vitamin K deficiency, as the vitamin serves to keep the skin healthy. Sarah had body weakness because of the decreased Vitamin E levels, as it translates into low antioxidants activity. Due to increased ADH levels, edema occurred from excessive retention of salt and water in the body. 

9. Explain the cause of her abnormal stool and urine sample. 

The abnormal stool is due to a malfunctioning liver due to cirrhosis, resulting in insufficient excretion of bilirubin. The spleen destroys old RBCs and converts hemoglobin to bilirubin, then metabolized into bile or passed in urine. If there are not enough old RBCs, it means there will not be enough bilirubin to accumulate and excrete, and therefore this gives abnormal color to the stool and urine. 

10. What cell does Glisten work on? Explain how this medication is able to stimulate insulin secretion. 

Glisten causes ATP-sensitive potassium channels to close ( O’Neill et al., 2015) . It works on the beta cells of the pancreas to reduce glucose levels in the body, thus induce insulin release. Potassium ions cause depolarization and the opening of voltage-gated calcium ions. Depolarization causes closing of potassium channels, thus Glisten causes their depolarization. Physiologically, the potassium channels become depolarized after a series of reactions that are triggered by eating. Therefore after a meal, insulin levels spike to remove the excess sugar in blood. When ATP binds to the K+ channel, the gate to the channel closes to prevent the K+ from leaking in the membrane ( Wu, Song, Graaf, & Stevens, 2017) . Glisten therefore acts in a similar way, causing the nervous system to act like the individual has just had a meal. 

References 

American Diabetes Association (2017, May 03). Diabetes Mellitus: An Overview. 

O’Neill, E. D., Wilding, J. P., Kahn, C. R., Van Remmen, H., McArdle, A., Jackson, M. J., & Close, G. L. (2015). Absence of insulin signaling in skeletal muscle is associated with reduced muscle mass and function: evidence for decreased protein synthesis and not increased degradation.  Age 32 (2), 209-222. 

Calvo, M. S. (2014). Dietary phosphorus, calcium metabolism and bone.  The Journal of nutrition 123 (9), 1627-1633. 

Daru, J., Sobhy, S., & Pavord, S. (2019). Revisiting the basis for hemoglobin screening in pregnancy.  Current Opinion in Obstetrics and Gynecology 31 (6), 388-392. 

Wu, F., Song, G., de Graaf, C., & Stevens, R. C. (2017). Structure and function of peptide-binding G protein-coupled receptors.  Journal of molecular biology 429 (17), 2726-2745. 

Veraldi, S., Pietrobattista, A., Liccardo, D., Basso, M. S., Mosca, A., Alterio, T., & Candusso, M. (2020). Fat soluble vitamins deficiency in pediatric chronic liver disease: The impact of liver transplantation.  Digestive and Liver Disease 52 (3), 308-313. 

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StudyBounty. (2023, September 16). Diabetes Mellitus: An Overview.
https://studybounty.com/diabetes-mellitus-an-overview-case-study

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