Pathophysiology of Type 1 Diabetes, Essay Example

Introduction

The goal of the research paper was to review the available information on diabetes type I and II. The emphasis of the research will be placed on the case study. The case study is directed towards Brenda. The patient is seventeen years of age. She has been recently hospitalized for elevated blood glucose and dehydration. In addition, Brenda was discovered to be six weeks into the fetal development of her child. She has sustained weight loss and mood changes prior to her hospitalization.

Overview

The research directed attention to the participation of the immune system in the eradication of the beta cells and the production of diabetes type 1. In addition, the eradication of the beta cells will be explored with regards to the administration of glucose within the blood stream. The second question that was reviewed had been the severe influences of blood glucose administration. The correlation of diabetes with regards to mood alterations, hyperglycemia and unsubstantiated weight loss was explored. In addition, the patient´s enhanced appetite, increased urges to urinate and severe thirst were detailed. Furthermore, the potential outcomes on the six-week fetus within the first trimester of Brenda´s pregnancy had been detailed. Finally, the correlations between obesity, genetic vulnerability and the production of diabetes type II were detailed.

Explanation of the Pathophysiology of Type 1 Diabetes

Diabetes type 1 is the outcome of the reaction of the autoimmune system which is produced as a result of the destruction of the beta cells from the pancreas. The evidence that has been linked to diabetes type 1 has been indirectly associated on the results of the islet cell antibodies, T cell reaction to the antigens that have the beta cell quality and a limited category of the alleles associated with the class II primary histocompatibility. In addition, the examination for the presence of type 1 diabetes is reliant on evidence of insulitis. Notwithstanding, the mechanism which start the malfunction of the immunological system tolerance continue to be undiscovered in the conventional diabetes type 1. Diabetes type 1 has been detailed as a multifactorial dysfunction which are catalyzed by the immunization against the patient’s proprietary tissues. It has been theorized for a number of years that the reactions of the autoimmune system against foreign antigens was a causal attribute of diabetes type 1. Diabetes type 1 is a multifaceted dysfunction in which the environmental aspects are aligned with an elevated level of multi-genetic vulnerability which facilitates the intolerance of the autoimmune system with regards to the beta cells (Faideau, Larger, Lepault, Carel & Boitard 2005).

As a result of the experimentation that has taken place since the 1950s it had been hypothesized that the immunization of the autoimmune antigens attacked the patient’s proprietary cells. It has also been postulated that there is an environmental cause which imitates the foreign antigens. This environmental causal attribute catalyzes and motivates the immune system in the initiation and activation of autoreactive lymphocytes. The introduction of the autoantigens occurs at locations which are remote in correlation to the targeted tissues. In the Brenda´s system, there may be extraordinary situations which precede the occurrences of the production of autoantigens. This type of production of autoantigens has been observed in cases involving paraneoplastic illnesses during pregnancy (Faideau et al.2005).

Insulin is produced in the pancreas which is positioned to the posterior of Brenda´s stomach. Brenda´s pancreas possesses cellular clusters which are designated islets. The function of the islets in Brenda’s pancreas is to produce insulin and liberate the insulin into the bloodstream.  In the event that the beta cells do not develop sufficient insulin or if Brenda’s body is unable to respond to the insulin that is in her bloodstream, the glucose accumulates in the blood instead of being subjected to absorption by the cells in Brenda´s body. This can lead to the manifestation of prediabetes. Prediabetes is a situation which causes the indexes of the blood glucose to be more elevated than normal. The blood glucose in prediabetes is not sufficient to warrant a diagnosis of diabetes. In diabetes type one and two, the cells are deprived of glucose notwithstanding the high glucose levels that Brenda may be demonstrating (National Institute of Diabetes and Digestive and Kidney Diseases 2014).

Explain the Pathophysiology of the Signs and Symptoms

Some of the primary complications of diabetes which may cause   Carol´s excessive thirst elevated appetite, unsubstantiated weight loss, frequent urges to urinate and mood changes may be attributed to elevated blood glucose. Hyperglycemia is designated as high blood glucose. This is one of the defining qualities of all of the categories of diabetes. The excessive thirst, frequent urination, increased appetite, undetailed weight loss and mood changes are attributed to the patient´s inability to maintain normal blood levels of glucose. This takes place due to the deficiency of the production of insulin in the pancreas. It can also be attributed to the cells increased resistance to insulin that the pancreas becomes unable to maintain the pace of insulin production. As a result of the pancreas´ inability to maintain the production of insulin, the glucose accrues in the bloodstream and is not transported to the cells (Mazze, Strock, Bergenstal, Criego, Cuddihy, Langer, Simonson & Powers 2011).

The elevated blood glucose occurs when the blood glucose is more elevated than 130 mg/ dl prior to a meal. In addition, high blood glucose takes place when the glucose indexes in the bloodstream are more elevated than 180 mg/dl two hours subsequent to the initial bite of a meal. The majority of the symptoms which include frequent urination, excessive thirst, unexplained weight loss, increased appetite and mood changes do not become manifest until the blood glucose levels reach 250 mg/ dl. There are several symptoms which have a quick onset (i.e., excessive thirst, frequent urges to urinate and increased appetite that require a short period of elevated glucose levels in order to become manifest). These symptoms are acknowledged as polyphagia (increased appetite), polydipsia (excessive thirst) and polyuria (excessive urges to urinate). Once these symptoms become manifest, the blood glucose level should be reviewed (Mazze, Strock, Bergenstal, Criego, Cuddihy, Langer, Simonson & Powers 2011).

Polyuria takes place due to the patient´s elevated levels of blood glucose pulling the intracellular fluid into the patient’s blood stream by means of osmosis. Consequently, in the kidneys, there is a correlated dysfunction that is initiating. As the glucose indexes in the kidneys attain a level of 250 mg/ dl, the capacity of the kidneys to reabsorb cleansed fluid is deterred. The result is osmotic diuresis where the patient releases substantial quantities of urine. The cells are releasing fluids into the bloodstream and the kidneys are releasing water from the body. This is the cause of polyuria (Mazze, Strock, Bergenstal, Criego, Cuddihy, Langer, Simonson & Powers 2011).

The increased appetite is caused by lowered insulin indexes. Insulin is required to move the glucose from the blood to the cells.  The unexplained weight loss is caused by the excessive urination that causes the body to reach a low level of bodily fluids. In addition, if the levels of insulin are deficient for the maintenance of glucose metabolism, the body will convert to consuming fat in order to sustain the cellular metabolism. Furthermore, the weight loss takes place due to the elevated levels of glucose which may reach levels as elevated as 1000mg/dl. This level of glucose in the urine infers that the body is urinating the calories instead of consuming the glucose (Mazze, Strock, Bergenstal, Criego, Cuddihy, Langer, Simonson & Powers 2011).

Moodiness takes place due to the elevated levels of blood glucose influencing the decision making abilities and rapid thinking. In addition to polyuria, polydipsia and polyphagia, these combinations of symptoms are sufficient to cause moodiness. The patient experiences excessive thirst (polydipsia) due to the need for the body to engage in rehydration subsequent to polyuria. Polydipsia or excessive thirst is initiated by the osmoreceptors in the hypothalamus which define that the level of plasma osmolality is extremely low (Mazze, Strock, Bergenstal, Criego, Cuddihy, Langer, Simonson & Powers 2011).

Patients who are affected with diabetes type 1 have the requisite of receiving daily dosages of insulin in order to administrate their blood glucose levels. The additional parts of the treatment may incorporate:

1. A suitable diet in order to administrate the levels of blood glucose in Carol´s body.
2. Adequate amounts of exercise.
3. Precautionary self-administration and supervision of the ketone indexes in the urine various times within the day.
4. Constant supervision of the hemoglobin A_1c The A_1c examination demonstrates the mean levels of sugar present in Carol´s blood during the past three months. The outcome of the examination will show if Carol´s blood sugar is well administrated. The regularity of the A_1c examination is prescribed by the attending physician. It is suggested that Carol undergo the A1c examination semi_annually in the event that her blood sugar is within the acceptable range. The A_1c should be conducted more frequently ion the case that Carol’s blood sugar is not within acceptable levels (National Institute of Diabetes and Digestive and Kidney Diseases 2014).

Progress in diabetes research has been the reason for enhanced methods of administrating diabetes and providing interventions for its complications. Notwithstanding, clinicians continue exploring the causal attributes of diabetes while finding manners of preventing and mediating the disorder. There are additional methods for the ingestion of insulin that are being reviewed. These interventions include inhalers that supply insulin and pill that can be taken orally. Researchers are studying the genetic participation in Diabetes type 1 and type 2. There have been some of the genetic markers that have been found for Diabetes type 1. There is also research being conducted in the area of the transplantation of the islet cells and the pancreas (National Institute of Diabetes and Digestive and Kidney Diseases 2014).

The symptoms which have been demonstrated are also commonly encountered in prediabetes. In the manifestation of prediabetes. The levels of blood glucose are at a more elevated index than normal. There are many who have prediabetes who are at risk for developing prediabetes within a decade. In the cases which involve prediabetes, there is an increased hazard for stroke and heart disease. In the event that Carol is suffering from prediabetes, the onset of diabetes type 2 can be deterred or delayed with moderate exercise and a suitable diet. There are more than 79 million Americans who are affected with prediabetes (National Institute of Diabetes and Digestive and Kidney Diseases 2014).

Carol may also be suffering from diabetes type two. Diabetes type two is the most commonly occurring form of diabetes. Approximately 93% of the cases involving diabetes are with diabetes type two. Diabetes type two is an illness which is the outcome of the physiognomy´s deficiency to produce sufficient insulin. Previously, type two diabetes was known as diabetes mellitus which is non-insulin dependent. Diabetes type 2 is usually the outcome of prediabetes. It is a chronic disease which has no known remedy. It is quite easy to confuse the manifestations of diabetes type two with the process of normal aging. Studies have demonstrated that 50% of all Americans who have diabetes are unaware that they have it (National Institute of Diabetes and Digestive and Kidney Diseases 2014).

Carol may also be suffering from gestational diabetes. Gestational diabetes manifests elevated levels of glucose during pregnancy. These symptoms may take place in women who have not previously manifested symptoms of diabetes. In gestational diabetes, all of the symptoms which are connected with diabetes dissipate during the childbirth delivery process. Gestational diabetes is not an outcome of an insulin deficiency. It is an outcome of the hormones which are present in the anatomy blocking the absorption of insulin. This is also known as insulin resistance. Studies have demonstrated that approximately 6% of the women who are pregnant in the United States manifest symptoms of gestational diabetes. There are some theories with regards to the causal attributes of gestational diabetes. It is not fully understood why the gestational diabetes manifests symptoms and disappears during the childbirth delivery process (National Institute of Diabetes and Digestive and Kidney Diseases 2014; University of Chicago Medical Center 2015).

Potential Effects of Diabetes in the Developing Embryo during Brenda’s First Trimester

The potential risks to the mother and the child is the macrosomia and hypoglycemia. Macrosomia is when the baby becomes larger than what would be normally anticipated. Hypoglycemia is when there is a drop in the fetal blood sugar prior to the delivery process. In the event that the insulin level demonstrated by the baby is less than normal, there may be the need to provide the baby with glucose intravenously (Diabetes Control and Complications Trial 2005).

Explain the Correlation between Genetic Susceptibility, Obesity and the Development of Type 2 Diabetes

The condition of obesity occurs when an individual has accrued bodily fat to the point where it has a detrimental influence on their well-being. In the event that an individual’s bodily fat is 20% more elevated than normal, the person would be considered as being obese. In the event that the bodily mass index, (BMI) is found in the range of 25 to 29.9, the person would be considered as overweight. In the circumstance that the bodily mass index is more than 30, the person would be considered as obese. People become obese due to the intake of too many calories. In the year 2000, it had been assessed that over 30% of the United States’ population was considered as obese. In addition, individuals who have a sedentary lifestyle are at risk of obesity. The less movement that an individual engages, the less potential of burning calories. In addition, insufficient sleep has increased the risk of obesity. Furthermore, there are some hormone disruptors which cause the metabolizing of fructose in the liver. Finally, there are many who are obese due to their genetic predisposition. There is a defective gene that is delineated ass FTO. This gene is the cause of 16.6% of people having the quality of being obese (Medical News Today 2015).

Research has demonstrated that inflammation is caused by obesity. Inflammation is the one of the cause of type II diabetes. It has not been directly established the manner by which inflammation is a causal attribute of diabetes. Studies have demonstrated that there is an inflammatory molecule that is designated LTB4 which is a promoter of insulin resistance. The resistance to insulin is one of the primary stages in the production of diabetes type II. It had been reviewed that extracting the LTB4 genetic element in rodents enhances the sensitivity to insulin. Obesity has been determined to be a root cause in diabetes. The excess fat which accumulates in the liver, catalyzes macrophages. The macrophages are the immunological cells which are found in the liver. The macrophages perform their function when they are catalyzed. The macrophages liberate LBT4 molecules and start a chain reaction between other macrophages. As a result, there is a greater amount of LBt4 liberated in the liver tissues (Buschman 2015).

The reaction that is associated with the inflammatory reaction would be positive if it were applied in order to ward off infection. The muscle cells and the fat cells also are composed of the LBT4 receptors. Consequently, these cells become catalyzed when the LBt4 receptors connect. In the case of obesity, these cells also become engorged. The engorgement of the cells as a result of the activation of the LBT4 cells is the causal attribute of the insulin resistance encountered in obese patients (Buschman 2015).

Diabetes is a multifactorial illness. As a result, there has been a development of an approach which has been delineated as the genome wide perspective (GWAS). These categories of approaches evolved as an outcome of the information that had been acquired from the international Hap Mop Program. This program supplied a blueprint for the genetic variances that occur in the comprehensive genome. In the program, it become possible to ascertain that specific solitary nucleotide polymorphisms (SNPs) migrated in conjunction with genetic blocks. Consequently, the haplotypes had the potential of being reviewed by the determination of the order of a minute collection of SNPs. This comprehension was the causal attribute for the production of cost avoidant elevated level prototyping matrices that had the capacity of precisely ascertaining the genome wide variances in any sample that was provided (Basile, Johnson, Xia & Grant 2014).

The application of this category of innovation caused the inception of a genome wide associated study. These perspectives are most appropriately adapted to the classification of the mutual variations within a sample that provide a moderate risk for a particular dysfunction. The genome wide associated study has been integral in discovering the main genetic elements that are linked to type II diabetes. Before the application of GWAS, there had only been several genetic occurrences which were demonstrated to be linked with diabetes type II. These elements were classified by means of the analysis of the candidate gene though linkages which were based on heredity. These studies included proliferator activation reception gamma (PPARG), potassium inward rectification channels, subcategory J, and member number 11 (KCNJ11). Notwithstanding the inception of the GWAS in the middle of the last decade that there had been innovation with regards to the discovery of the genetic components accountable for diabetes type II (Basile et al. 2014).

These genetic elements have been categorized and verified by means of a variety of GWAS evaluations. The primary research found the diabetes type II linked variations in the genetic elements which included the CDK5 regulating subunit assorted protein 1, like 1 otherwise known as CDKAL1. These genetic elements are encountered in the solute carrier category 30 (zinc transporting) and member number 8 (SLC30A8) hematopoietically homeobox expressed HHEX. This genetic information regulates an insulin type growth factor linking protein in addition to a cyclin reliant inhibitor (Basile et al. 2014).

The insulin that is encountered in the skeletal muscular tissue is the main feature of type II diabetes. The skeletal muscular tissues’ insulin has a substantial participation in the pathogenesis of diabetes type II. It had been perceived that it was only the malfunction of the beta cells that were the causal attribute for the production of diabetes type II. Notwithstanding, the skeletal muscular tissue has been demonstrated to the main defect that catalyzes type II diabetes. The resistance to insulin is delineated as a diminished reaction of the targeted tissues in comparison with the tissues that have a conventional glucose tolerance (DeFronzo & Tripathy 2009).

In the manifestations of gestational diabetes, the maternal placenta provides the   developing fetus with water and nutrients. In addition, there are diverse hormones which are produced during the pregnancy. There are some of the hormones which are developed that include cortisol, estrogen and the placental lactogenic hormone which have an inhibiting outcome on the distribution and absorption of insulin. This is normally known as the contra insulin influence and is normally initiates within the twentieth to twenty fourth week of pregnancy. As the placenta develops, there are greater quantities of the hormones which are manufactures. Consequently, the insulin resistance increases. Under normal circumstances, the pancreas has the ability of creating additional insulin in order to counteract the insulin resistance. There are circumstances where the pancreas cannot compensate for the inability of inulin absorption. As a result, gestational diabetes develops. Women who have developed gestational diabetes have a higher probability of producing type II diabetes (Li, Zhao, Luan, Langenberg, Luben, Khaw, Wareham & Loos 2011).

Reference List

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