Project #89667 - Responses

Responses #1 and 2


Response # 1 Response to Chelsea



Chelsea Van Rooy

Main Discussion Post

            Diseases of hormonal regulation can occur within the endocrine system when hormones are not secreted or received normally (Huether & McCance, 2012). The purpose of this discussion is to cover the pathophysiology and hormone regulation of diabetes mellitus (DM) and diabetes insipidus (DI). There will also be a discussion of how behaviors and genetics affect the diagnosis and treatment of these diseases.

Pathophysiology of Diabetes Mellitus and Diabetes Insipidus

             DM progresses slowly as beta cells of the pancreas are destroyed due to genetic susceptibility and multiple environmental factors (Heuther & McCance, 2012). Beta cells serve as the body’s insulin producer (Heuther & McCance, 2012). When these cells are destroyed the human body does not have enough insulin to counteract glucagon (Heuther & McCance, 2012). Glucagon then stimulates increased blood glucose production in the liver (Heuther & McCance, 2012). Amylin production, which is meant to suppress glucagon release, is also suppressed (Heuther & McCance, 2012). Hyperglycemia then develops.

            DI is a disorder in which antidiuretic hormone (ADH) is not effective enough to concentrate urine properly (Heuther & McCance, 2012). In neurogenic DI, there is inefficient secretion of ADH (Heuther & McCance, 2012). In nephrogenic DI, there is an inadequate response by the renal tubules to ADH (Heuther & McCance, 2012). “Insufficient ADH causes excretion of large volumes of dilute urine, leading to increased plasma molality” (Heuther & McCance, 2012, p. 449). DI can be caused by diseases of the central nervous system, diseases of the kidneys, head injury, or pregnancy (McPhee & Hammer, 2012).

Hormonal Regulation

             DM occurs when the body does not produce an adequate amount of the hormone insulin. Another hormone, glucagon, acts to increase blood sugar through glycogenolysis and gluconeogenesis (Heuther & McCance, 2012). In DM, glucagon is increased. Amylin, a glucagon suppressing hormone, is decreased (Heuther & McCance, 2012). These changes in hormonal regulation may result in clinical manifestations such as polyuria, polydipsia, fatigue, pruritus, infections, visual changes, delayed healing, and neuropathy (Heuther & McCance, 2012).

             DI is caused by insufficient ADH. This hormone increases the kidneys ability to collect water (Heuther & McCance, 2012). A lack of AHD results in the body’s inability to conserve as much water as it excretes in the urine (Heuther & McCance, 2012). This hormonal regulation can result in clinical manifestations such as thirst, dehydration, and hypernatremia (Heuther & McCance, 2012).

Behavior and Genetics Effects on Diagnosis and Treatment

            Valencia, Oropesa-Gonzales, Hogue, & Florez (2014) stated that certain behaviors and attitudes are based on ethnic backgrounds. Valencia et al. (2014) give an example of a Hispanic that moves to the United States, continues to eat food from his home country but also enjoys our fast food. This individual also had a notable decrease in activity (Valencia et al., 2014). This patient slowly puts on weight putting him at higher risk for diseases such as diabetes. Heuther & McCance (2014) stated that 10-13% of those with Type 1 DM have a first degree relative with the same diagnosis. The Center for Genetics Education (2013) stated that DM has an inherited predisposition. Genetics plays a role in the alteration of hormone regulation in DM (Heuther & McCance, 2012). Diagnosis of diabetes should include a thorough history to assess for behavioral habits and genetic disposition. Diagnosis of DM also includes multiple lab tests to check blood glucose levels at differing times (Heuther & McCance, 2012). Treatment for DM can include diet modification, exercise, weight loss, and diabetic medications (Heuther & McCance, 2012).

            Knoers (2012) stated that poor eating habits and dehydration can worsen the symptoms of DI. Inadequate intake to compensate for increased urine output can have detrimental effects on the body (Heuther & McCance, 2012). The Mayo Clinic (2013) stated that DI usually has a genetic link that alters the kidney’s ability to concentrate urine. The history portion of making a diagnosis of DI should include behavioral considerations as well as any past family history. Diagnosing DI should also include blood and urine testing. Treatment for some requires ADH replacement, medication, and correction of any electrolyte imbalances (Heuther & McCance, 2012).   


             DM and DI are disorders of hormonal regulation. DM occurs with an inadequate amount of insulin and DI happens with an insufficient supply of ADH (Heuther & McCance, 2012). Many factors can influence the incidence and progression rate of DM and DI. These factors can include behaviors such as poor eating habits and genetics. Diagnosis and treatment of these disorders varies and depends on the patient's age and the severity of the disease process (Huether & McCance, 2012).


Centers for Genetics Education. (2013). Diabetes types 1 and 2 and inherited predisposition. Retrieved from

Huether, S. E., & McCance, K. L. (2012). Understanding pathophysiology (Laureate custom ed.). St. Louis, MO: Mosby.

Knoers, N. (2012). Nephrogenic diabetes insipidus. Medical Genetics. Retrieved from

Mayo Clinic. (2013). Diseases and conditions: Diabetes insipidus. Retrieved from

McPhee, S. J., & Hammer, G. D. (2012). Pathophysiology of disease: An introduction to clinical medicine (Laureate Education, Inc., custom ed.). New York, NY: McGraw-Hill Medical.

Valencia, W.M., Oropesa-Gonzales, L., Hogue, C.M., & Florez, H.J. (2014). Diabetes in older Hispanic/Latino Americans: Understanding who is a greatest risk. Journal of the American Society on Aging, 38(4), 33-40. Retrieved from



Response # 2 To Whitney


Whitney Lindsey

Week 9 Initial Post

Walden University

Pathophysiology: DM and DI


Diabetes Mellitus

Diabetes mellitus is a term used to discuss a group of diseases that are from either faulty insulin secretion, insulin action, or both (Huether & McCance, 2012).  This disease group is categorized by hyperglycemia (Huether & McCance, 2012).  Nearly 26 million people in the United States suffer from DM(Huether & McCance, 2012).  The way that glucose attaches to hemoglobin molecules and its behavior over approximately 120 days is how the Hemoglobin A1C is determined and further defined by classification of either as impaired glucose tolerance or impaired fasting glucose (Huether & McCance, 2012.  Diabetes mellitus is subcategorized in to Type 1 or Type 2. 

Type 1 is defined by beta cell destruction leading to insulin deficiency.  Furthermore the text defines Type 1 as having autoimmune destruction of pancreatic cells that causes little or no insulin production(Huether & McCance, 2012). Autoantigens are formed and eventually destroy beta-cells through autoimmunity, furthering decreased insulin synthesis (Huether & McCance, 2012).  The final result being hyperglycemia that develops over time additionally accounting for 80-90% of the islet of Langerhans beta cells being destroyed (Huether & McCance, 2012).   This classification of diabetes requires insulin and approximately 75% of all cases develop before a patient reaches the age of 30.  There is a small percentage of approximately 10% of patients that develop DM type 1 with no defined etiology (Huether & McCance, 2012).  Type 1 DM affects the digestive metabolism of fats, proteins and carbohydrates with variant glucose accumulations in organs such as the kidneys and liver (Huether & McCance, 2012).  This systemic affect over time can cause organ failure and has a wide variety of associated complications (Huether & McCance, 2012).

Type 2 diabetes accounts for most of the Diabetes cases in the United States.  Type DM is on the rise and has been directly related to the rise in obesity (Huether & McCance, 2012).  This type of DM results from genetic beta cell function, insulin receptors, and other cell communication with insulin production (Huether & McCance, 2012).  When cell abnormalities and mutations combine with external factors such as obesity there is insulin resistance and decreased secretion by beta cells causing DM Type 2(Huether & McCance, 2012).  With prolonged beta cell dysfunction DM Type 2 develops overtime (Huether & McCance, 2012).  Insulin resistance is felt to be multifactorial and even affected by hormones produced in the GI tract that contribute to insulin resistance (Huether & McCance, 2012).  Most individuals are over 30 years of age onset although the number of children with onset is growing in recent years (Huether & McCance, 2012).

Diabetes Insipidus

            This form of diabetes is directly related to the hormone ADH and insufficient response with causes excessive urination and severe thirst and need for fluid intake (Huether & McCance, 2012).  Two forms can occur Neurogenic and Nephrogenic.  Neurogenic occurs from some type of lesion that inadvertently interferes with the absorption and production of ADH (Huether & McCance, 2012).  This can be brain injuries and most often closed head injuries.  Not totally limited to injury this disorder can be hereditary.  Nephrogenic DI is directly resulted from some type of alteration in the renal tubules either from injury or malformation(Huether & McCance, 2012).  This deficit in ADH causes excessive urine production with inadequate concentration appropriate for osmolality and results in chronic dehydration and electrolyte imbalance of sodium (Huether & McCance, 2012)

Age as a Factor

In both type of Diabetes Mellitus age is a defining factor for onset and type.  DM type 1 is generally felt to be a pediatric disorder with very early age onset (Huether & McCance, 2012).  Type 2 is generally later in life due to the mechanism of chronic damage to beta-cells although Type 2 can have pediatric onset(Huether & McCance, 2012).  Both type and type 2 affect males and females equal in the respective age onset categories (Huether & McCance, 2012).  Diabetes insipidus does not have a defining age category as it is caused by injury or hereditary mutation.   The peak age for DM I is around the age of 11-13, whereas DMII has a more prevalent onset after age 40(Huether & McCance, 2012)


Huether, S. E., & McCance, K. L. (2012). Understanding pathophysiology (5th ed.). St. Louis, MO: Mosby/


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