Good Research Paper About Pharmacology - Diabetes Type 2
Health ailments that are of common occurrence in the society are the problematic public concerns. They interfere with the normal psychosocial wellbeing of the individuals and disturb their quality of life. They also tend to induce financial burden on the patient, their family members and the overall healthcare system. In certain cases, they even become worsen and appears as a life threatening condition. So, a thorough management appears mandatory to minimise the consequences of such health abnormalities. In such context, the present description deals with highlighting a topic entitled Type 2 diabetes.
Briefly, diabetes is a metabolic disorder where the levels of blood sugar or glucose exceed beyond the normal. The food that a person consumes induces the synthesis of glucose in the body. Here, a hormone insulin assists in making the glucose enter the body cells to provide them energy. A type 1 diabetes could occur if the body fails to synthesize insulin. On the other hand, Type 2 Diabetes is defined as the condition where the body fails to absorb or utilise the insulin. Due to this, glucose begins to accumulate in the circulation. The person could thus develop prediabetes which serves as the risk contributing agent for type 2 diabetes.
Type 2 diabetes is considered as the most common form of diabetes. Type 2 diabetes symptoms were reported to manifest at at a slow rate. Few individuals even fail to recognise or discover the symptoms. The symptoms could be frequent urination, increased thirstiness, increased hunger, fatigue, weight loss with no attempts, sores that slowly recover and presence of blurred eyesight.
Research evidence states that Type 2 diabetes mellitus is a heterogeneous condition accompanied by the difficulties in fat and carbohydrate (Scheen, 2003). It was believed to be induced by the genetic and environmental factors that alter the function of beta-cell and tissues such as pancreas, adipose tissue, liver and muscle cell. The pathophysiology of type 2 diabetes was believed to rely beta-cell dysfunction and minimised sensitivity to insulin. But the pathways regulating the interaction of such factors are not fully known. Several factors were thought to mediate the link between beta-cell dysfunction and insulin resistance (Scheen, 2003).
Many people facing the type 2 diabetes appear to be obese and especially have central visceral adiposity. So, the adipose tissue could be much involved in the pathophysiology of type 2 diabetes. Some authors recently hypothesized that ectopic fat storage syndrome could play key role. This could involve accumulation of triglycerides in pancreatic cells, liver, and muscle. The other hypothesis is that adipose tissue could serve as anendocrine organ where it intends to secrete adiponectin, resistin, TNF-alpha, and leptin in the processes of beta-cell dysfunction and insulin resistance (Scheen, 2003).
Researchers have employed certain mathematic models and mentioned that the association between insulin secretion and sensitivity reflects the hyperbolic function, that indicates the role of a feedback loop that regulates the communication between peripheral tissue and β-cells (Adamo & Caprio, 2011). So, as the reduction in the insulin sensitivity occurs, there would be an increase in the insulin secretion for glucose tolerance to stay normal. This activity refers to “disposition index” (DI)’ which is the outcome of β-cell function and insulin sensitivity. DI is thus regarded as the indicator of β-cell function determined by the sensitivity to insulin. Investigations on adult individuals gave revealed that DI is not the only parameter for recognising subjects with abnormal β-cell function but also a potent agent in predicting type 2 diabetes (Adamo & Caprio, 2011).
Likewise, some researchers mentioned that type 2 diabetes could become responsible for the increased mortality if the metabolic syndrome and hepatic insulin resistance are associated with
cardiovascular disease and atherosclerosis(Yki-Järvinen, 2011). This could involve increased synthesis of very-low-density lipoprotein that in turn causes the production of minute, weighty and atherogenic substances. This mode of typ2 diabetic condition where hepatic insulin resistance occurs was referred to as non-alcoholic fatty liver disease (NAFLD) (Yki-Järvinen, 2011).
The management of type 2 diabetes requires suitable treatment strategies at the earliest. Drug manufacturers have been striving hard to come up with the drugs that could produce significant outcome. In fact, the three common therapeutic modalities are lifestyle adjustments intended for enhancing the effect of insulin or endogenous insulin sensitivity (Chehade & Mooradian,2000). This could be accomplished by enhanced physical activit, working on reducing the bodyweight with food, modification of the behaviour, and the application of pharmacological substances or surgical invasion. Type 2 diabetic individuals could get and enhancing availability of insulin by providing insulin,analogues, exogenous insulin, sulphonylureas and repaglinide, a novel insulin secretagogue (Chehade & Mooradian,2000). The other options are biguanides and thiazolidinediones that improve sensitivity to insulin or the agents that minimise the insulin needs such as the alpha-glucosidase inhibitors. Likewise, Krentz, Patel & Bailey (2008) highlighted that the safe application of Oral therapy could help type 2 diabetic patients to attain the necessary glycaemic values in the short period. The outcome would be more significant if the care professionals use two or more oral medications for extended duration.
Recent, health care researchers have started some novel interventions such as community based life style programs. This approach was able to enhance glucose control and also minimise associated complications like cardiovascular disease in type 2 diabetics (West-Pollack et al ., 2014).
The drug treatment addresses the pathophysiology of type 2 diabetes by normalizing the glucose levels and correcting the insulin sensitivity aberrations.
Say, metamorfin is a drug of the class biguanides (Mitchell, 2014). It assists in decreasing the quantity of gluocose levels in the circulation by minimizing its synthesis in the live. This event finally retards the glucose absorption from the gastrointestinal tract into the circulation following the diet consumption and enhances the insulin’s muscle sensitivity. Examples include Riomet, Glucophage, Fortamet etc. Similarly, sulfonylureas enable the cells of body use insulin and enable the pancreas synthesize insulin in increased quantity (Mitchell, 2014) Examples include Tolbutamide, Glipizide, Chlopropamide etc (Mitchell, 2014).
On the other hand, some drugs like Pramlintide could decrease the insulin dose and body mass whereas others facilitate weight loss and exert positive effect on hyperglycaemia or metabolic syndrome in type 2 diabetics (Krentz, Patel, & Bailey,2008).
So, it could seem that the drugs exert their effects on the pathophysiology by interfering with the diet, glucose metabolism and insulin production by mainly acting on liver and pancreas.
However, apart from the benefits, many drugs do carry negative outcomes which range from common side effects to risks.
The side effects include nausea, diarrhea, swollen leg, and liver inflammation (Type 2 Diabetes Mellitus, 2015).
Rosiglitazone was described to be detrimental for type 2 diabetics who are susceptible to heart failure (Krentz, Patel, & Bailey,2008).
Holstein and Egberts (2003) described that antidiabetic drugs could induce a hypoglycaemia. Some of these include oral drugs, acarbose, thiazolidinediones and Metformin.
In fact, the individuals considered at high risk for hypoglycaemia are geriatric patients. So, these patients need to be monitored for the risk as they have other complications such as malnutrition, cardiovascular multimorbidity, hepatic or renal dysfunction, and polypharmacy. In addition, it is also a worth noting point that in type 2 diabetic patients, the magnitude of glucose regulation is under the influence of age, presence of concomitant disorders and life expectancy.
Finally, patients with type 2 diabetes need to incur high treatment costs over their life time if a suitable drug relevant to their medical history was not identified at the earliest.
According to the American Journal of Preventive Medicine, the treatment cost for a given individual with type 2 diabetes and its consequences could be approximately $85,500 (High Lifetime Costs for Type 2 Diabetes, 2015). Investigators working on simulation model at the Research Triangle International and CDC revealed that men with a confirmed diagnosis for type 2 diabetes and in the age between 25 and 44 could spend $124,700. On the other hand, women could spend $130,800. Especially, the consequences associated with diabetes treatment are 53% of their lifetime expenses. A 57% was attributable to large blood vessel damage that could result in stroke or coronary heart disease (High Lifetime Costs for Type 2 Diabetes, 2015).
Likewise, the American Diabetes Association (ADA) had reported that the total expenditure of diagnosed diabetes had increased from $174 billion in 2007 to $245 billion in 2012. Out of 245 billion, a $ 176 was attributable to direct medical expenditure. Here, the cost incurred for prescription drugs for treating diabetic complications accounted for 18%. This is next to the inpatient care received in hospitals that accounts for 43%. Overall, this could more likely reflect a treatment cost burden on the diabetic patient (The cost of diabetes, 2015).
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