A Revitalized Battle Against Diabetes Mellitus for the New Millennium

MedSurg Nursing, Dec, 1998 by Theresa Capriotti, Susan McLaughlin

Despite great advances in control and treatment, diabetes mellitus (DM) remains a formidable opponent for the health care team. A major cause of morbidity and mortality throughout the world, DM continues to increase in prevalence. Nurses are in a strategic position to employ new research findings and aggressive strategies to fight this killer disease.

Diabetes is one of the nation's most prevalent and serious health problems. In fact, many public health experts consider the chronic and potentially disabling disease to be epidemic in proportion. More than 16 million Americans live with the disease, and many more are affected but undiagnosed (Amos, McCarty, & Zimmet, 1997). Further, a significant percentage of the population have one or more risk factors for developing diabetes. A complex disorder caused by pathologic mechanisms in the secretion and metabolism of the hormone insulin causes alterations in the metabolism of carbohydrates, proteins, and fats. This results in elevated blood sugar levels. These in turn damage organ systems. While there are several types of diabetes, type 1 and type 2 are primarily of interest to adult health nurses. Recently, the diagnosis, epidemiology, and clinical management of type 1 and type 2 diabetes have undergone substantive changes. The purpose of this review is to discuss these changes and their implications for adult health nurses and their patients.

Pathophysiology and Epidemiology

Type 1 and type 2 diabetes differ with respect to pathophysiology, diagnosis, epidemiology, and clinical management (see Table 1). In type 1 diabetes, pathogenesis involves a genetic susceptibility and a triggering environmental insult. Specific triggering factors are not clearly delineated. However, it has been shown that an autoimmune attack on insulin secreting cells occurs. Islet cells of the pancreas become infiltrated with cytotoxic T cells and macrophages resulting in an "insulitis" (Bullock, 1996; Cotran, Kumar, & Robbins, 1994). While this immune attack is occurring the client endures a silent autoimmune disease with diminishing levels of insulin reserve. With diminishing ability to produce insulin, glucose is less facilitated into cells, and glucose levels rise in the bloodstream (Foster, 1998; Guyton & Hall, 1996).

Table 1. Diabetes Subtypes

Type 1 Diabetes

* Autoimmune pancreatic islet
cell destruction and resultant
insulin deficiency

Type 2 Diabetes

* Dysfunctional secretion of insulin

* Insulin resistance in the peripheral tissues

The pathogenesis of type 2 diabetes is less well understood. Research has increasingly pointed to an etiology related to insulin resistance of peripheral tissues. The disease is caused by a combination of genetic predisposition, pancreatic cell defects, and peripheral resistance to insulin. Individuals with type 2 diabetes endure a state of abnormal insulin secretion and target tissue resistance to insulin. It is believed that peripheral tissues become increasingly insensitive to insulin over time. Glucose needs insulin for facilitated entrance into cells. Therefore, higher and higher amounts of insulin are needed to keep up with the worsening peripheral cell resistance. Greater amounts of insulin must be secreted by the pancreatic cells, and pancreatic cells eventually become "exhausted." Obesity can cause insulin resistance; however, nonobese individuals with type 2 diabetes also have insulin resistance (Foster, 1998; Guyton & Hall, 1996). Ninety to 95% of affected individuals suffer from type 2 diabetes.

The two types of diabetes have different etiologic mechanisms, but basically cause impaired glucose tolerance and hyperglycemia. The hyperglycemic state causes multiple problems on the cellular and systemic levels. In the body, glucose is reduced to sorbitol which can function as a tissue toxin. Sorbitol accumulation causes abnormal cell metabolism, particularly of the retinal cells, neurons, and kidney cells. Glucose also causes glycosylation of major proteins in the body such as hemoglobin, albumin, collagen, and lipoproteins. These altered proteins undergo biochemical changes which result in accumulation of glycosylation end products (Clark & Lee, 1995). These end products bind to endothelial cells which then release a substance called endothelin-1. Endothelin-1 causes potent vasoconstriction, stimulates mitosis of vascular smooth muscle, and enhances platelet adhesion (Foster, 1998). Simultaneously, the glycosylation of lipoproteins causes alterations which prime LDL for formation of plaque. Cardiovascular research has shown that the atherosclerotic lesion is initiated by this alteration or oxidation of low-density lipoproteins, hypertrophy or mitosis of vascular smooth muscle, and enhanced platelet adhesiveness (Foster, 1998; Guyton & Hall, 1996). Diabetes then provides all the conditions necessary for the development of atherosclerotic damage of the vasculature.

Additionally from a cellular perspective, high amounts of circulating glucose exert a large amount of osmotic pressure in the extracellular fluid. When glucose rises to excessive values, fluid shifts occur, resulting in considerable cellular dehydration, Intracellular water exits in attempting to balance out the high osmolarity of the extracellular fluid. As a result, the patient experiences thirst and excessive urination. Concurrently, white blood cells function with less efficiency in a hyperglycemic environment. This results in diminished immune function, increasing the patient's susceptibility to infection. Neurons are also affected by high levels of glucose, causing nerve dysfunction, particularly evident in the sensory nerves of the lower extremities (Guyton & Hall, 1996).