Pathophysiology of Diabetes Mellitus (DM) – Advanced patho week 9 response 2
Type of document Essay
1 Page Double Spaced
Subject area Nursing
Academic Level Master
Style APA
References 3
Order description:
Please respond to Necki post in one 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. and use the readings and resources for at least 2 references or it will not count
Resources
Learning Resources
Required Readings
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Chapter 18, “Mechanisms of Hormonal Regulation”
This chapter explores mechanisms of hormonal regulation and the structure and function of the endocrine glands. It provides a foundation for examining alterations of the endocrine system, as well as the effects of aging on the endocrine glands.
Chapter 19, “Alterations of Hormonal Regulation”
This chapter begins with an explanation of the mechanisms of hormonal alterations. It then discusses alterations of the hypothalamic-pituitary system, thyroid function, parathyroid function, endocrine pancreas, and adrenal function. It also covers the pathophysiology, clinical manifestations, and evaluation and treatment of type 1 and type 2 diabetes.
Hammer, G. G. , & McPhee, S. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.) New York, NY: McGraw-Hill Education.
Chapter 17, “Disorders of the Parathyroids & Calcium & Phosphorus Metabolism”
This chapter explores the anatomy, histology, and associated mechanisms of the parathyroid glands, bone, vitamin D, and C cells. It then examines various disorders involving altered regulation of parathyroids, calcium, and phosphorous metabolism.
Chapter 18, “Disorders of the Endocrine Pancreas”
This chapter explores the anatomy, histology, and physiology of the endocrine pancreas. It then covers the clinical presentation, etiology, pathophysiology, and clinical manifestations of endocrine pancreas disorders such as diabetes mellitus.
Chapter 19, “Disorders of the Hypothalamus & Pituitary Gland”
This chapter covers the structure and function of the hypothalamus and pituitary glands. It then explores disorders relating to alterations of the hypothalamus and pituitary glands.
Chapter 20, “Thyroid Disease”
This chapter explains thyroid hormones, including how they are formed and secreted. It then examines thyroid diseases such as hyperthyroidism, hypothyroidism, and goiters.
Optional Resources
American Diabetes Association. (2012). Retrieved from http://www.diabetes.org/
The Endocrine Society. (2012). Retrieved from http://www.endo-society.org/
The Hormone Foundation. (2012). Retrieved from http://www.hormone.org/
Neckhi post
Nkechi Jiabana
Week 9 Discussion Initial Post
COLLAPSE
Nkechi Jiabana
Introduction
Diabetes mellitus (DM) is a common disease where there is too much sugar (glucose) floating around in the blood. This occurs because either the pancreas can’t produce enough insulin or the cells in the body have become resistant to insulin. Diabetes is a chronic health problem affecting more than 17million people in the united states. According to Huether & McCance (2017), diabetes involves group of metabolic diseases characterized by hyperglycemia due to defects in insulin secretion, insulin action or both. In the United States, the cost of healthcare for diabetic patients is skyrocketing daily. According to CDC (2017), it is approximately 30.3 million people of all ages or about 9.4% that had diabetes in 2015. American Diabetes Association (2012), classified diabetes mellitus (DM) into four different groups; type 1, type 2; other specific types and gestational diabetes. Other types of diabetes recognized by Huether and McCance (2017) are diabetes insipidus (DI) which is neurogenic or central and nephrogenic.
Pathophysiology of Diabetes Mellitus (DM)
When one eats, the food is converted into glucose which in turn enters our blood stream to be transported to the cells where it can be used for energy. There are special cells in one’s pancreas that sense the increase of glucose and thus release insulin in the blood stream. The main job of this insulin is to help decrease blood glucose levels and it does this by activating a system which transports glucose from one’s blood into the cells and it also decreases blood glucose by stimulating an enzyme called glycogen synthase in the liver. American Diabetes Association (2012) further classified Diabetes Mellitus into: Typ1, Type 2, other specific types and gestational diabetes.
According to Gutherie & Gutheria (2004), Type 1 diabetes is an insulin dependent form of diabetes that is also called juvenile diabetes. It is a form of DM that resulted from autoimmune that destroys the insulin producing beta cells of the pancreas. With this, lack of insulin creates increase blood and urine glucose. Huether and McCance (2017) added that autoimmune type1 diabetes mellitus is a slowly progressive autoimmune T-Cell mediated disease that destroys beta cells of pancreas and destruction of beta cells is related to genetic susceptibility (involving histocompatibility leucocyte antigen-HLA) and environmental factors (involving exposure to certain drugs, foods, and viruses). Type 1 diabetics therefore suffer from lack of insulin due to destruction of beta cells resulting from lymphocyte and macrophage infiltration of the islets which leads to release of inflammatory cytokines leading to death of islets beta cells. Although the exact cause has not been identified, however, it is understood that cells which make insulin are destroyed by the body’s own immune system due to autoimmune process resulting to manifestation of diabetes (Huether and McCance 2017).
Type 2 DM: Per Baynes (2015), people with type 2 diabetes can still make insulin, but their cells have some degree of insulin resistance and this can lead to loss of insulin secretion. When cells initially become resistant to insulin, the body increases the amount of insulin made to counteract this effect and keep glucose levels in a normal range. Eventually, the body cannot compensate enough, and blood glucose levels begin to rise. The pancreatic cells begin to work overtime to produce more and more insulin and eventually burn out. Most individuals with Type 2 diabetes exhibit intra-abdominal (visceral) obesity, which is closely related to the presence of insulin resistance. In addition, hypertension and dyslipidemia (high triglyceride and low HDL-cholesterol levels; postprandial hyperlipidemia) often are present in these individuals. This is the most common form of diabetes mellitus and is highly associated with a family history of diabetes, older age, obesity and lack of exercise. It is more common in women, especially women with a history of gestational diabetes, and in Blacks, Hispanics and Native Americans (Gutherie & Gutheria, 2004).
Other Specific Types of DM
Baynes (2015), indicated that types of diabetes mellitus of various known etiologies are grouped together to form the classification called “Other Specific Types”. This group includes persons with genetic defects of beta-cell function (this type of diabetes was formerly called MODY or maturity-onset diabetes in youth) or with defects of insulin action; persons with diseases of the exocrine pancreas, such as pancreatitis or cystic fibrosis; persons with dysfunction associated with other endocrinopathies (e.g. acromegaly); and persons with pancreatic dysfunction caused by drugs, chemicals or infections and they comprise less than 10% of DM cases.
Gestational Diabetes occurs as a result of surplus counter-insulin hormones during pregnancy and that lead to insulin resistance. Huether and McCance (2017) article noted that fetal pancreatic hypertrophy with neonatal impediments was as a result of maternal hyperglycemia that is transferred to fetus during pregnancy.
Pathophysiology of Diabetes Insipidus (DI)
Diabetes Insipidus is caused by a deficiency of or a decreased response to antidiuretic hormone (ADH). DI is characterized by excessive urination (polyuria-usually greater than 2l/day). Two types of DI include: Central or Neurogenic diabetes insipidus which occurs due to defect in the synthesis or release of ADH and Nephrogenic diabetes insipidus which occurs because kidneys do not respond to ADH (Huether and McCance 2017). Nephrogenic DI is usually acquired or genetic and acquired type is related to disorders or drugs that damage renal tubules. Central DI is related to traumatic brain injury and can also be caused by hereditary disorders that affect the ADH genes (Huether and McCance 2017). People with DI are unable to concentrate urine and tend to excrete large volumes of urine and this is accompanied with excessive thirst. complications are dehydration, low blood pressure, and high sodium levels in the blood.
Differences and Similarities
Huether & McCance, (2017) expressed that some of the resultant symptoms are similar, but the disease processes and pathophysiology are different. Diabetes mellitus is more common than diabetes insipidus. Both involve frequent urination and excessive thirst, but in diabetes mellitus, urination is less frequent. DM is characterized by hyperglycemia resulting from defects from insulin secretion, insulin action, or both, while DI is a disorder of insufficient activity of ADH (Huether and McCance 2017). Diabetes insipidus is a kidney disorder whilst diabetes mellitus is a pancreatic disorder. Furthermore, DM is associated with high blood sugar, excessive urination, extensive thirst, and increased hunger. The risk factors that relate to this are: genetics, lifestyle, and infection. The suggestive treatments are insulin administration, lifestyle changes and management. The following are the symptoms associated with DI: are extreme thirsts and severely diluted urine. Obviously, there are main causes of DI such as brain tumor, head injury, medications such as lithium, and genetics. As for the treatment, patients have been advised to concentrate on low-salt diet, and water intake modification.
Genetics and Pregnancy
Nearly all forms of diabetes have a genetic component. Type 1 diabetes and type 2 diabetes are caused by a complex interaction of genetic and environmental/lifestyle factors. Guthrie, & Guthrie, (2004) indicated that the position of the gene or combination of genes can be dominant, recessive, or in between, while the hereditary form of nephrogenic DI can be caused by mutations in at least two genes. At least, about 90 percent of hereditary nephrogenic DI cases result from mutations in the AVPR2 gene. Pregnancy is responsible with a number of changes found in salt and water regulation. A transient central DI may develop as a result of decreased osmotic level for thirst and AVP release, and a decrease in plasma osmolality. Nearly all forms of diabetes can be diagnosed before pregnancy and affect some women and their pregnancies as pre-gestational diabetes, whereas other women are only diagnosed with gestational diabetes mellitus (GDM) during pregnancy. As such, pregnancy may aggravate the seriousness of any existing nephrogenic or central DI. As for gestational diabetes, such occur due to excess hormones during pregnancy resulting to insulin resistance.
References
American Diabetes Association. (2012). Retrieved from http://www.diabetes.org/
Baynes, H. W., (2015) Classification, Pathophysiology, Diagnosis and Management of Diabetes
Mellitus. J Diabetes Metab 6:541. doi:10.4172/2155-6156.1000541
Center for Disease Control (2017). National Diabetes Statistics Report, 2017: Estimates of
Diabetes and Its Burden in the United States. Retrieved from: https://www.cdc.gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report.pdf
Guthrie, R. A., & Guthrie, D. W. (2004) Pathophysiology of Diabetes Mellitus. Critical Care Nursing Quarterly, 27(2); 113-125
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis,
MO: Mosby.
