post- Monica

Respond  on two different days who selected different factors than you, in one or more of the following ways:
Share insights on how the factor you selected impacts the pathophysiology of diabetes mellitus and diabetes insipidus.
Offer alternative diagnoses and prescription of treatment options for diabetes mellitus and diabetes insipidus.
Validate an idea with your own experience and additional research.

                                               Main Post
Pathophysiology of Diabetes Insipidus     
Diabetes insipidus is either the loss of antidiuretic hormone (ADH) action or secretion.  ADH is secreted by the posterior pituitary and causes water reabsorption from the collecting ducts.  Increases of ADH increases water reabsorption; this results in concentrated urine and more dilute serum.  Decreases of ADH decreases water reabsorption, this results in an increase and dilute urine output, and the by-product is a more concentrated serum because ADH is lost with DI, urine output increases and leaves behind a more concentrated hypernatremic serum.  There are two categories of DI, central and nephrogenic.  Central DI involves a decrease of ADH in the posterior pituitary; this is usually secondary to head trauma, encephalitis, meningitis, and the like.   Nephrogenic DI consists of a kidney sensitivity to the decrease of ADH; this form is typically hereditary or congenital and originates from the kidneys (Berkowitz, 2007).   Signs and symptoms of DI are much like those of DM and can be, polyuria, polydipsia, and nocturia.  Treatment is based on the type of DI and may involve ADH replacement (Huether & McCance, 2017).
Pathophysiology of Diabetes Mellitus    
 DM is broken down into type I and type II.  Type I was previously known as insulin-dependent, and type II was formerly known as non-insulin dependent, that is no longer how these two disorders are classified.  Type I is more common in adolescents and associated with the human leukocyte antigen (HLA).  Ketone development commonly occurs in type I, and islet cell antibodies are in 90% of patients within the first year.  Type I is thought to be caused by infectious or toxic environment that insults the B cells of the pancreas in a genetically predisposed person.  Type II DM makes up greater than 90% of the DM cases in the United States.  Type II is an inadequate production of insulin; this can be caused by tissue insensitivity and results in impaired insulin production or resistance.  There is no link to the islet cell antibodies or HLA.  With Type II, there is an association with abnormal lipid profile, obesity, and hypertension.  Signs and symptoms of type I and II resemble DI in regards to polyuria, polydipsia.  Type I involves weight loss, fatigue, and weakness.  Type II includes weight gain, peripheral neuropathy, blurred vision, and chronic skin infections.  Treatment might be insulin, oral antidiabetic choices, diet, and exercise (Barkley, 2018).
Patient Behavior and Ethnic Factors     
First degree relatives and infection, infection and illness, are contributing factors to DM type I.  Family history, sedentary lifestyle, obesity, women with polycystic ovary syndrome, gestational diabetes, insulin resistance, and impaired glucose tolerance are all patient and behavior factors that contribute to DMII.  DM is more prevalent with African-Americans, Hispanic/Latino Americans, Asian-Americans, Native-Americans, Alaska Natives, and Pacific Islanders (WedMD, 2019).  For DI there are no apparent contributing patient behaviors or ethnic links.

                                               References
Barkley, T.  (2018).  Adult-gerontology primary care nurse practitioner.  West Hollywood, CA:  Barkley & Associates.Berkowitz, A. (2007).  Clinical pathophysiology made ridiculously simple. Miami, FL:  Medmaster.Huether, S. E., & McCance, K. L. (2012). Understanding pathophysiology (Laureate custom ed.). St. Louis, MO: Mosby.WebMD.  (2019).  What increases my risk of diabetes?  Retrieved from             https://www.webmd.com/diabetes/guide/risk-factors-for-diabetes#1