Reply separately to two of your classmates posts (See attached classmates posts, post#1 and post#2). INSTRUCTIONS: In your reply posts, use scholarly references and offer constructive feedback within

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of your classmates posts (See attached classmates posts, post#1 and post#2).


In your reply posts, use scholarly references and offer constructive feedback within your post. Provide at least one online web resource that provides additional knowledge for APRNs and or patient education on the presented topic.

“In your reply to each of your peers, discuss content that you learned while exploring the website and a resource they might find helpful as well.

The expectation is not that you “agree” or “disagree” with your peers but that you develop a reply post with information that is validated via citations to encourage learning and to bring your own perspective to the conversation.

– Utilize at least two scholarly references per peer post.

Please, send me the two documents separately, for example one is the reply to my peers Post #1, and the second one is the reply to my other peer Post #2.

– Minimum of 300 words per peer reply.


Background: I am currently enrolled in the Psych Mental Health Practitioner Program, I am a Registered Nurse, I work at a Psychiatric Hospital.

Reply separately to two of your classmates posts (See attached classmates posts, post#1 and post#2). INSTRUCTIONS: In your reply posts, use scholarly references and offer constructive feedback within
POST # 1 KEARA For your reply, consider elaborating on the statement — There are a couple different types of diabetes insipidus that exist – what are they? Diabetes InsipidusDiabetes Insipidus is a condition that occurs because of an impairment in the endocrine system of the body. The endocrine system is composed of various glands and organs that play a role in the hormonal function of the body. The hypothalamus, pituitary, pineal, adrenal, thyroid, parathyroid, endocrine gland of pancreas, gonads, and thymus gland all play a role in the hormonal messengers that travel throughout the body and maintain homeostasis (VanMeter & Hubert, 2018). When considering the condition of diabetes insipidus, the focus is primarily on the posterior lobe of the pituitary gland and specifically, antidiuretic hormone (ADH, vasopressin). The purpose of this discussion post is to discuss the pathophysiology and symptoms of diabetes insipidus, explain the typical routine diagnosed of the condition, provide a standardized treatment plan for a patient, and provide any supplementary links for readers to enhance their knowledge on the condition related to the treatment guidelines that exist.The body utilizes hormones to maintain homeostasis. Specific changes occur in the body that contribute to diabetes insipidus. The overall water balance is maintained by ADH, kidney function, and thirst mechanism. Hui (2019) describes the pathophysiology of diabetes insipidus as ADH being released form the posterior pituitary and enters blood supply. This hormone targets the kidneys and specifically bind to receptors in the collecting tubules. When this occurs, water flow is promoted to retain water to keep electrolyte balances stable and ensure dehydration does not occurs. However, diabetes insipidus occurs when there is either a deficiency of ADH or the kidneys are not responding to the release of the hormone (Hui & Radbel, 2019). VanMeter and Hubert (2018) support this statement and explain that this can occur due to a head injury, may be temporary, and can be genetic, or linked to an electrolyte imbalance or drugs (VanMeter & Hubert, 2018). There are a couple different types of diabetes insipidus that exist, but primarily this discussion post will focus on central diabetes insipidus.Symptoms that are commonly presented in this condition are polyuria and polydipsia. Additionally, dizziness, weakness, nocturia, fatigues, and generalized symptoms related to dehydration are common. More clinical symptoms are hypotension and tachycardia (Hui & Radbel, 2019). Large amounts of dilute urine are excreted by the body due to the deficit of ADH and thirst is initiated by the hypothalamus to assist in making up for the dumping of water out of the body in order to avoid possible dehydration (VanMeter & Hubert, 2018). Kalra (2016) and colleagues explains that polyuria is defined as more than 3 liters of output in a 24-hour period. Using the symptoms that are present, this assists health care professionals in diagnosing this condition. Patients often present with most of these symptoms due to the fast progression of this condition. Hui and Radbel (2019) explains a diagnostic algorithm that is used to diagnosed diabetes insipidus. First and foremost, clinical symptoms must be present to initiate the algorithm. If symptoms are present, a 24-hour urine collection is performed to confirm the presence of polydipsia and polyuria. If the volume is > 40-50 ml/kg, then a blood and urine examination should be completed. This blood test evaluates sodium levels, plasma osmolality, and urine osmolality. Depending on the results, determines whether or not a desmopressin challenge is performed or if a patient must undergo a water deprivation test to determine if diabetes insipidus is present (Hui & Radbel, 2019). If desmopressin is not administered, a water deprivation trial is the most accurate to increase urine osmolality and determine if diabetes insipidus is the primary cause of the “dumping” of water (Kalra et al., 2016). Standard treatment and management vary. Kalra (2016) and colleagues explains that DDAVP (desmopressin) is often administered orally, intranasally, subcutaneously, or through an IV. Secondly, replacing the fluid losses is an important intervention to implement because often times thirst impairment can be reduced, specifically with those that are older, and may not respond to an increase in water intake (Kalra et al., 2016). Because there are a couple different forms of diabetes insipidus that exist, there are different treatment plans. The medications that are often used to treat diabetes insipidus are carbamazepine, chlorpropamide, clofibrate, thiazide diuretics, indapamide, indomethacin, amiloride, and pharmacokinetic desmopressin (Kalra et al., 2016). Every individual responds differently to treatments, so it is important to keep continual follow up until the condition has improved. The standardized treatment algorithm is the plan that providers should follow to confirm the presence of the condition and determine the most effective treatment due to the type of diabetes insipidus diagnosis made. Baldeweg (2018) and colleagues provides clinical guidance for impatient treatment and provides a step-by-step protocol on how to treat each underlying condition or outcome of diabetes insipidus. To summarize, diabetes insipidus is a condition that is a result of a deficit of antidiuretic hormone. There are many causes of diabetes insipidus and occasionally treatment of the underlying cause is necessary to reduce the symptoms. In some situations, it is not possible to treat the underlying cause, and this results in some patients being on replacement therapy for ADH. Maintaining homeostasis of these hormones in the body is important to ensure that negative outcomes do not occur. Additionally, it is important for individuals to understand that diabetes insipidus does not mean that they have diabetes, in fact, the pathophysiological process does not have many similarities. Diagnosis and treatment can be made based on an algorithm provided by Endocrine Connection and the authors provide step-by-step instructions to effectively treat and manage this condition.ReferencesBaldeweg, S. E., Ball, S., Brooke, A., Gleeson, H. K., Levy, M. J., Prentice, M., Wass, J., & Society for Endocrinology Clinical Committee (2018). Society of endocrinology clinical guideance: Inpatient management of cranial diabetes insipidus. Endocrine connections, 7(7), G8–G11., C. & Radbel, J. (2019) Diabetes Insipidus. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Retrieved from:, S., Zargar, A. H., Jain, S. M., Sethi, B., Chowdhury, S., Singh, A. K., Thomas, N., Unnikrishnan, A. G., Thakkar, P. B., & Malve, H. (2016). Diabetes insipidus: the other diabetes. Indian journal of endocrinology and metabolism, 20(1), 9–21.
Reply separately to two of your classmates posts (See attached classmates posts, post#1 and post#2). INSTRUCTIONS: In your reply posts, use scholarly references and offer constructive feedback within
POST # 2 SYDNEY Gestational Diabetes The purpose of this post is to discuss the diagnosis and treatment of gestational diabetes, along with the pathophysiology and presenting symptoms. Gestational diabetes is a glucose intolerance in pregnancy when the woman was not previously diagnosed with diabetes (Plows et al., 2018). The authors state that gestational diabetes is caused by B-cell disfunction and insulin resistance in the tissue that progressively worsens in pregnancy. B-cells store insulin and secrete the insulin in response to the glucose level in the body. Pregnancy can cause changes that can create a decrease in insulin sensitivity. The insulin sensitivity can be decreased because of higher levels of estrogen and cortisol made in the placenta. Gestational diabetes occurs when the woman cannot create a sufficient response to the normal resistance of insulin in pregnancy (Kampmann et al., 2015). The mother then transfers the glucose to the placenta. The fetus creates hyperinsulinemia to counter the excess of glucose in the placenta. The high levels of insulin in the fetus allow for the fetus to grow larger than a normal fetus (2015). According to the CDC, gestational diabetes does not typically have any symptoms. The patient could have certain risk factors that make them more susceptible to get gestational diabetes. These risk factors include being overweight, having gestational diabetes in a previous pregnancy, older than 25 years old, and have a family history of type two diabetes (CDC, 2020). Women who have a family history of diabetes should have their glucose monitored closely throughout their pregnancy (Hubert & Vanmenter, 2018). Gestational diabetes can be detected between the 24th and 28th week of pregnancy. The patient drinks a liquid that contains glucose, and the blood sugar is checked one hour later (CDC, 2020). The patient passes the glucose test if the blood sugar is 140 or lower. If the patient does not pass the one-hour glucose test, the patient will have a glucose tolerance test. The glucose tolerance test measures a fasting blood sugar on the patient before the test. Once the patient drinks the glucose, the blood sugar is tested every hour for three hours (CDC, 2020). The patient can be determined to have gestational diabetes if they do not pass the three-hour glucose test.  Gestational diabetes cannot be cured until the patient delivers the infant, but it can be managed. The standard treatment for gestational diabetes is diet, glucose monitoring and insulin. The patient can typically control their blood sugar with diet and some exercise (Kampmann et al., 2015). It is important for the healthcare provider to provide guidance on the proper diet to control the patient’s blood sugar. Physical activity is important to manage gestational diabetes because it lowers the blood sugar and makes the body more sensitive to insulin, so it will not require as much (CDC, 2020). The patient can continue to monitor glucose closely to make sure that the diet and exercise are controlling the blood glucose levels. If the patient is having trouble maintaining their blood glucose levels, the patient can be started on insulin for better control. The baby will also be monitored closely by the healthcare provider to watch for macrosomia and ensure that the baby is healthy throughout the pregnancy. This link provides a detailed treatment guide: link provides a detailed treatment guide: Centers for Disease Control and Prevention. (2020). Diabetes tests. Retrieved from, R. J. & VanMeter, K. C. (2018). Gould’s pathophysiology for the health professions. St. Louis, MO: Elsevier Saunders.Kampmann, U., Madsen, L. R., Skajaa, G., Iversen, D. S., Moeller, N., & Ovesen, P. (2017). Gestational diabetes: a clinical update. Retrieved from 10.4239/wjd.v6.i8.1065Plows, J. F., Stanley, J. L., Baker, P. N., Reynolds, C. M., & Vickers, M. H. (2018). The pathophysiology of gestational diabetes mellitus. Retrieved from 663 words

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