Diabetes Mellitus (DM) is a metabolic disorder caused by pancreatic dysfunction resulting in absence or insufficient insulin secretion. Different categories of DM are as follows; type 1 DM, type 2 DM, other specific type and gestational DM (GDM) (Huether & McCance 2012). Type 1 DM is caused by autoimmune where there is no insulin production, type 2 DM happens later in life due to insulin resistance from obesity, low level of HDL(good cholesterol), or polycystic ovary disease (Blair, 2016). Other specific types could be idiopathic, and lastly GDM which is seen only during pregnancy due to increased pregnancy hormone. Diabetes Insipidus (DI) is caused by vasopressin (antidiuretic hormone (ADH) deficiency resulting in disorder of water metabolism. Hypotonic polyuria, increased thirst and excessive fluid intake is common with DI. In addition, DI has four classification; namely neurogenic, nephrogenic, gestagenic, and dipsogenic types (Walsh & March, 2016). Pathophysiology of Diabetes Mellitus
Type 1 DM is caused by autoimmune disorder where the T cell mediated disease damage the pancreatic beta cell (Huether & McCance, 2012). At the onset of the disease process, lymphocytic infiltrates of macrophage activating CD4+ cells with cytokine secreting, cytotoxic CD8+cells surround the necrotic B cells (McPhee & Hammer, 2010) (p.507). This is a gradual process that happens over several years. However, the production of glucagon increases due to the damage to the beta cells of islet
Type 1 diabetes is also called insulin-dependent because the pancreas produce little to no insulin due to the destruction of beta cell in pancreas(Bardsley et al, 2004). Therefore, the insulin have to be injected manually for body to function normally. (Seewaldt et.al, 2000) states that in type 1 diabetes, the beta cell located in the islets of Langerhans have antigen that cause the immune system to produce antibodies and kill the insulin producing cells. The autoimmune response is thought to be caused by the autoreactive CD4 and CD8 effector cells that recognise islet self-antigens, as an outcome there is greater than 90% destruction on insulin producing cell BACH (1994). Similarly, (Nakayama et al,2005) and (Kent et al, 2005) supports that insulin in itself is a
Diabetes mellitus is a group of metabolic disorders characterized by inadequate insulin secretion by the pancreas or cellular destruction leading to an insulin deficiency. Depending on the cause of the insulin shortage, diabetes can be subcategorized into type I and type II. Type I diabetes (T1DM) is usually mediated by the destruction of b-cells in the pancreas resulting in decreased insulin production and secretion. Type II diabetes (T2DM) is the failure of these b-cells to secrete adequate amounts of insulin to compensate for insulin resistance and increased gluconeogenesis combined with an overall resistance to the insulin action (8., 1997). T2DM accounts
Diabetes Mellitus (DM) or Type 2 Diabetes is seen as a metabolic disease that is categorized by abnormally high blood glucose or hyperglycemia. Diabetes Mellitus is also formerly known as noninsulin-dependent diabetes mellitus and is the most common form of diabetes that is seen. Insulin is a hormone that is supplied to the body that allows us to efficiently use glucose as fuel. When carbohydrates are broken down into sugars in the stomach glucose enters the blood circulation simulating the pancreas to release insulin in an appropriate amount to become used for energy. With diabetes mellitus the body does not properly make use of the insulin supplied for the body. This causes the pancreas to produced an extra amount if insulin which the body cannot keep up with, causing an imbalance to the blood glucose levels (American Diabetes Association, 2015). In the united states diabetes affects almost 29.1 million people, while the another 86 million people have pre-diabetes but do not know. It is also known as the 7th leading cause of death in the country in the recent years (MedicineNet.com, 2016). For a patient suffering from a chronic form of diabetes mellitus understanding how these mechanisms lead to the condition can be used as preventative measures. Potential consequences as well as the causes and clinical manifestations will ensure a better knowledge on the issue to monitor the condition.
For unknown reasons, the body of a T1D attacks the insulin producing cells, called islets, that are formed in the pancreas and destroys them. This type of attack is known as an autoimmune disorder (Diabetes Research Institute Foundation [DRIF], n.d.). Insulin is the hormone that allows sugar to enter cells, and produce energy. The body now sees islet cells as foreign and eventually the pancreas yields little to no islet cells. Once there are no more islet cells to produce the insulin hormone the sugar levels in the blood become high, called hyperglycemia. This disturbance in homeostasis is not like type 2 diabetes (T2D), where the body becomes insulin resistant. In a T2D, the pancreas still produces islet cells and they are still
Type 1 diabetes is a chronic autoimmune disorder, in which beta cells in the Islets of Langerhans are destroyed resulting in insulin deficiency and hyperglycemia. “The exact cause of why these normal cells are attacked by the immune system is a combination of genetic predisposition and certain viral infections such as the mumps and coxosackievirus which appear to trigger the destruction of pancreatic beta cells.” (Ignatavicius & Workman, 2013, p 1416) When these cells do not work properly, the body can no longer produce insulin. Insulin is a hormone that allows the body to use glucose that is found in foods for
In recent studies, Diabetes type 1 has been scientifically linked to a chronic autoimmune disorder. The immune system attacks the beta cells, in the Islets of Langerham, located in the pancreas. This leads to the insulin producing cells to be destroyed and damaged, which ultimately ends up with very limited blood glucose or no insulin production at all.
The type 1 Diabetes that Ava lives with differentiates from type 2 Diabetes in that it is characterized by the complete autoimmune destruction of the pancreatic Beta (B) cells that produce and secrete Insulin in the Islet’s of Langerhans (Craft & Gordon, 2015, pg253). By contrast, type 2 Diabetes is a combination of B cell destruction, B cell dysfunction, and insulin resistance (Turner & Wass, 2009, pg803). The Beta cells of a non-Diabetic person would rapidly respond to glucose, however in type 1 Diabetes antibodies are produced against the body’s own B cells and consequently all the Islets are destroyed (Montague, 1983, pg50 and Craft & Gordon, 2015, pg253). This results in the failure of negative feedback loops in maintaining the body’s
We learned that Type 1 is an autoimmune condition where the body attacks its own beta cells in the pancreas via antibodies. Specifically, the person’s body produces antibodies that come down and destroy the beta cells in their pancreas. By having no beta cells, the person will not be able to secrete insulin; therefore, leaving the body in a hyperglycemic state. Some of the first symptoms of hyperglycemia are polyuria or polydipsia. Normal levels of blood glucose are between 70-110mg/100ml. Symptoms such as polyuria and polydipsia are diagnosed when diuresis via osmolarity of glucose becomes more than the Transport maximum (200mg/100ml). The protein responsible for this reabsorption of glucose is located in the proximal convoluted tubule, called the Sodium Glucose Transporter. In essence, 100mg/100ml of glucose can be easily reabsorbed, but 500mg of glucose will exceed the Tranport maximum. As a result, the person will have diuresis because 200mg will be reabsorbed, but 300mg will be left which ends up in the urine. This condition is also called diabetes mellitus or honey
Type 1 diabetes (T1D) is the autoimmune destruction of insulin-producing-β-cells located in the pancreas, specifically in the islets of Langerhans, responsible for regulating blood glucose levels in the blood. Insulin is a hormone which when released, signals the live, muscle and fat cells to take in glucose to be used as energy. If the body has sufficient energy, then the liver can store the glucose through the passage of insulin into glycogen. Glucagon, the antagonistic hormone to insulin produced by Alpha cells in the pancreas, is released when the blood sugar levels are too low and causes the liver to convert the stored glycogen into glucose. The difference between type1 and type 2 diabetes is that T2D is when the body does not effectively respond to
Diabetes is considered a metabolic disorder. Glucose is obtained from the food we ingest and normally insulin is released as the glucose levels rise. Insulin is produced in the pancreas by cells called Beta cells. Diabetes results from an imbalance of the hormone insulin. When Beta Cells fail to produce insulin the levels of glucose in the blood rise as the kidney is not able to filtrate the high amounts of glucose in the blood. Another cause of diabetes can be insulin resistance. Insulin resistance occurs when the body is not able to utilize the available insulin. Insulin is in charge of maintaining the proper levels of glucose in the plasma. Insulin levels are raised when the levels of glucose in the blood are high. Insulin activates the absorption of glucose by the cells that need it. The excess glucose is filtered out of the body as urine. This is the cause for constant urination in diabetics. As the body tries to get rid of the excess glucose polyuria occurs. Glucose is of great importance as it provides energy to cells such as those in the muscles and brain to properly function. In diabetics even though there is high levels of glucose the organs are not able to utilize it because insulin is not sufficient and the absorption of glucose by the cells does not occur. Symptoms may not be evident but the may increase as the disease progresses. There are three major types of diabetes, type 1, type 2, and gestational diabetes which will be fully explained
The pathophysiology of type I diabetes, insulin-dependent diabetes mellitus (IDDM), is the autoimmune destruction of pancreatic β-cells, leads to a deficiency of insulin secretion which results
T1D is an autoimmune disorder, that develops when the immune system attacks and destroys the pancreatic beta cells that produce insulin by mistakenly identifying them as foreign (autoimmune disorders: MedlinePlus) (Dugdale, 2013). The Pancreas gland is positioned at the posterior of the stomach in our bodies, and plays an important role in digestion and in regulating blood sugar. It makes enzymes to digest proteins, fats, and carbohydrates in the intestines and produces the hormones insulin and glucagon. A well-known effect of insulin is to decrease the concentration of glucose in blood. This lowers blood sugar levels and allows the body’s cells to use glucose for energy (Ediger et al. 2014).
Diabetes mellitus (DM) is a group of metabolic diseases characterized by high blood sugar levels over an extended period of time. With symptoms including increased urination, thirst, and hunger, diabetes is mainly due to loss of insulin production in the pancreas or lack of response to insulin produced. As of 2015, nearly 415 million people worldwide have diabetes with the three main types being Type 1, Type 2, and gestational. 90% of all diabetes cases are Type 2 (T2D) which is characterized by insulin resistance, high blood sugar, and lack of insulin. Also known as noninsulin-dependent diabetes mellitus (NIDDM), this disease is primary caused by obesity and lack of exercise in genetically predisposed people and affects in nearly 29 million people in the US alone, making it the 7th leading cause of death in the country (American Diabetes Association 2016).
Patients with type 1 DM have problem with insulin secretion from their pancreatic β-cells and patients with
Diabetes Mellitus (DM) is a serious disease that affects much of the U.S. population. DM occurs when the body had trouble regulating the amount of glucose in the blood stream. Although they share a similar name, Diabetes Insipidus (DI) is a different process, which involves kidney-related fluid retention problems. As advanced practice nurses (APNs) one must be able to differentiate, diagnose, and treat all three disorders appropriately. The purpose of this paper is to discuss the hormonal regulation alterations in both DM and DI respectively.