logo

Diabetes Pathophysiology | Assessment

   

Added on  2020-01-16

15 Pages4955 Words181 Views
Disease and DisordersNutrition and WellnessHealthcare and Research
 | 
 | 
 | 
Running head: ASSESSMENT TASK 2 - DIABETES PATHOPHYSIOLOGY1Assessment Task 2 - Diabetes Pathophysiology Student's Name: Student's Number:Word Count:
Diabetes Pathophysiology | Assessment_1

Running head: ASSESSMENT TASK 2 - DIABETES PATHOPHYSIOLOGY2Assessment Task 2 - Diabetes Pathophysiology Introduction:Diabetes mellitus of type 2 is characterized as a complex condition or disease of metabolism or ametabolic disorder (De Fronzo, 2010). Additionally, it is one of the most common disorders across the world (De Fronzo, 2010). Diabetes mellitus is known to affect almost 100 million individuals across the world (Creager et al., 2003). Type 1 diabetes is present in approximately five to ten percent of the total number of individuals affected by Diabetes (Creager et al., 2003). Type 2 diabetes is primarily affected by lifestyle and can eventually lead to obesity (Creager et al., 2003). The disease is further complicated by the incidence of macrovascular and microvascular diseases (Creager et al., 2003). Hyperglycaemia has been regarded as one of the primary risk factors in the incidence of microvascular anomalies in diabetes (De Fronzo, 2010). The incidence of insulin resistance is a major hallmark event in the indication of diabetes of type 2 (De Fronzo, 2010). It has been known to have a predominant link with a combination or group of several abnormalities of the cardiovascular system and metabolism (De Fronzo, 2010). A few of the primary metabolic disorders that occur along with type 2 diabetes include hypertension, visceral obesity, dyslipidaemia, impaired glucose tolerance or intolerance for glucose, and dysfunction of the endothelial system (De Fronzo, 2010). Each of these is regarded as an etiological and stand-alone causative risk for the onset of disease of the cardiovascular system (De Fronzo, 2010). Several studies in research present documented evidence that suggests a possible association between the catalyzed development of cardiovascular complications and resistance to insulin in persons with type 2 diabetes (De Fronzo, 2010). Alternately, there could be a similar association between resistance to insulin and the development of complications of the cardiovascular system amongst the persons without the condition as well (De Fronzo, 2010).
Diabetes Pathophysiology | Assessment_2

Running head: ASSESSMENT TASK 2 - DIABETES PATHOPHYSIOLOGY3Aim/Purpose: The following article discusses the onset of diabetes type 2 along with its link to insulin resistance. It further critiques the mechanism of development of macrovascular complications due to insulin resistance, the various risk factors of metabolic disorder and their impact on individuals with impaired glucose tolerance, and renal diseases along with increase death incidence in individuals having diabetes type 2.Part 1:Insulin resistance is regarded as a critical hallmark event in the disease condition of diabetes (Taylor, 2012). The link between the insulin resistance and diabetes mellitus is established as a crucial marker for several years in research (Taylor, 2012). Innate resistance to insulin is regarded as an important aspect for the progression of diabetes mellitus (Taylor, 2012). It is considered as a crucial hallmark predicting factor for the development of diabetes mellitus of type 2 (Taylor, 2012). It is an important target of therapy of therapeutic site once the presence of hyperglycaemia is confirmed in a patient (Taylor, 2012). Studies have indicated the presence of alikely genetic mechanism that links the expression of the enzyme lipoprotein lipase (LPL) to the peroxisome proliferator-activated receptor- and the function of mitochondria in cells (Taylor, 2012). This genetic event is likely to have a significant contribution to the insulin resistance in the muscle which is a predisposing factor in type 2 diabetes mellitus (Taylor, 2012). The initial in vitro evidence of abnormal mitochondrial function in cases of type 2 diabetes mellitus was subsequently observed again in vivo in persons with insulin resistance through genetic first degree relationships with persons with diabetes type 2 (Taylor, 2012). It is demonstrated in research that mitochondrial function, although at a risk of being defective, can be modified with the availability of fatty acids and total concentration of blood glucose (Taylor, 2012). The determination of insulin resistance in the muscle is carried out by a euglycemic-hyperinsulinemic
Diabetes Pathophysiology | Assessment_3

Running head: ASSESSMENT TASK 2 - DIABETES PATHOPHYSIOLOGY4clamp which acts as an important characteristic causative occurrence in the progression of diabetes type 2 (Taylor, 2012). The pathophysiology of hyperglycaemia indicates that its incidence in diabetes has an association with hepatic resistance of insulin as compared to muscle insulin resistance (Taylor, 2012). The levels of fasting and postprandial blood glucose are found to be in a normoglycaemic state (Taylor, 2012). Normoglycaemia can thus be restored in type 2 diabetes mellitus without any resultant changes in the resistance of muscle insulin (Taylor, 2012). Individuals having an inactive level of muscle glycogen synthase are not found all to be hyperglycaemic (Taylor, 2012). The link between resistance insulin and the onset of diabetes type 2 is complex and more indefinite than that of hepatic insulin resistance (Taylor, 2012). Hyperinsulinemia consistently leads to the accumulation of hepatic fat along with causing hepatic resistance of insulin (Taylor, 2012). The onset of hyperglycaemia can be determined definitely only when there is an observed failure in the secretion of nutrient-stimulated insulin (Taylor, 2012). Hyperglycaemia in diabetes and macrovascular disease development: Hyperglycaemia in diabetes is reported to be developed from insulin resistance in the muscle (Taylor, 2012). A possible mechanism for this is the mRNA expression of LPL was determined to be crucial by theknockdown method of LPL gene (Taylor, 2012). In cases where hyperglycaemia occurs in diabetes, there is a damage caused in certain cells such as mesangial and endothelial cells, due to hyperglycaemia, thus impairing the transport of glucose (Brownlee, 2005). Hyperglycaemia has been found to cause the elevation of the overall flux that exists through polyol biochemical cycle and cause the protein kinase C to get activated (Brownlee, 2005). Intracellular hyperglycaemia leads to the activation of protein kinase – C (Brownlee, 2005). A unified mechanism indicates that hyperglycaemia leads to the activation of hexosamine which is a necessary predisposing
Diabetes Pathophysiology | Assessment_4

End of preview

Want to access all the pages? Upload your documents or become a member.

Related Documents
Macrovascular Complication of Diabetes
|11
|2908
|363

Type 2 Diabetes Assignment
|12
|2696
|149

Macrovascular Complications of Diabetes: Pathophysiology, Assessment, and Management
|10
|2619
|460

Youth Diabetes Type 2
|7
|1680
|44

Diabetes Mellitus: Progression to Microvascular and Macrovascular Complications
|16
|4593
|186

Pathophysiology and Treatment of Diabetes Type 2
|21
|4308
|491