Summary
Diabetes mellitus is a disease that affects many systems in the body; it has both anatomical and biochemical consequences which are manifested in various ways. In simple terms, diabetes mellitus is a chronic disease mainly resulting from insulin deficiency or reduction in the body to an extent that metabolism of carbohydrate, fat and protein is severely interrupted and disabled.
Diabetes mellitus manifests itself in two forms – type 1 diabetes mellitus and type 2 diabetes mellitus. Type 2 diabetes mellitus is the most common form of the disease, and differs from the type 1 diabetes mellitus in that, type 2 diabetes mellitus is caused by abnormalities in both the insulin secretion and action whereas type 1 diabetes mellitus is mainly caused by the abnormalities in the insulin secretion. Diabetes mellitus type 1 is mostly found among the juveniles, with the peak age for its occurrence being usually between the age of 10 and 16. However, it can also occur among the adults mostly to those who are in the late 30s or early 40s.
Definition
Type 1 Diabetes mellitus (TID) is an autoimmunity disease caused by the destruction of the beta cells of the islets of Langerhans by islet-reactive T cells (Von Herrath p 1). According to Tortora and Derrickson (2008, p. 698) pancreatic islets are important in the body as they play the role of releasing insulin and glucose in the body, failure to which the disease manifests in the body. The beta cells produce insulin, a hormone that helps in the regulation of blood sugar (glucose) level. Hence, their destruction leads to a decrease in the levels of insulin in the body, which in turn leads to a decrease in the amount of glucose in the body. The onset of the disease is usually during the youth age; hence, it was formerly referred to as juvenile onset diabetes. The patients who suffer from the disease usually required taking insulin daily for survival (Lavin p. 589). Insulin may be administered via intravenous injections; the physician may prefer “insulin pumps and inhaled insulin” as alternative methods (Werner, 2008).
Signs and symptoms of the disease
Type 1 Diabetes mellitus is mainly manifested via the following symptoms
Polyuria and thirst: polyuria refers to frequent urination of the patients. Polyuria is mainly brought about by osmotic diuresis secondary to hyperglycemia. The thirst is mainly due to the dehydration of the body (Hussain and Vincent 2010).
Polyphagia and weight loss: polyphagia refers to an increase in the appetite of the patients. However, the increase in the increase in the appetite is coupled with weight loss, as the patient is not able to eat enough food to compensate for the calories, which are usually lost via the urine (Hussain and Vincent 2010).
Fatigue and weakness: this is mainly as a result of wasting away of the muscles through catabolism resulting from the deficiency of insulin (Hussain and Vincent, 2010).
Nocturnal enuresis: this refers to the tendency of patients urinating in their beds while sleeping. Nocturnal enuresis “can be an indication of onset of diabetes in young children” (Hussain and Vincent 2010).
Pathophysiology of the disease
Type 1 diabetes mellitus is caused by both the genetic and environmental influences. Studies have indicated that the susceptibility of an identical twin suffering from the disease is far much higher if the other twin suffers from the disease (Braun and Anderson p 461). Most of the medical professionals believe that the disease arises when people who are susceptible to the disease are exposed to environmental factors that trigger the autoimmune response of the body. However, the nature of the environmental trigger to the disease is not well understood.
Medical professionals believe that the trigger may be a viral infection, environmental toxin, or dietary component taken by the individual concerned (Niewoehner p 169). After the triggering of the disease, the destruction of the beta cells commences leading to their progressive decrease. The rate in which the beta cells are destroyed is usually varied from person to person; however, it is widely believed to be faster for people who are diagnosed with the disease when they are young and in their childhood. The presence of type 1 diabetes mellitus can be detected when about 90 percent of the beta cells have been destroyed (Niewoehner 2004 p 169). This makes it very difficult to detect the disease at an early stage and hence effectively treat it or determine the factors that lead to the development of the disease (McPhee, Lingappa and Ganong, 2006).
Diagnosis
The disease can be detected in children by measuring their circulating islet-cell antibodies in their serum. The children also have insulin antibodies in their serum, which are not usually secreted to counter the antigen that triggers the autoimmune process. The antibodies are secreted in response to the destruction of the beta cells of the islets of Langerhans. However, adults do not have the antibodies in their serum when they are diagnosed to have the type 1 diabetes mellitus (Werner, 2008). This is mainly because, in adults, the beginning of the autoimmune process occurred many years prior to their diagnosis. The rate of destruction of the beta cells is also lower in adults hence the production of the antibodies may have disappeared (Niewoehner, 2004, p 170).
However, in most of the situations, the manifestation of the clinical conditions mentioned above is enough evidence of the patient suffering from the disease. Tests are also carried out to determine the level of blood glucose. If the level is above 126mg/dL for a fasting individual or 200mg/dL for the random check of the individual, then the person is deemed to have type 1 diabetes mellitus. Urine tests can also be used to determine whether a person suffers from diabetes mellitus or not. The tests usually involve checking the urine for ketones to determine the presence of hyperketonemia. By assessing urine to establish whether it contains ketones, one can determine whether there is a high or low concentration of the same in the blood (Braun and Anderson 2006 p. 462).
Prevention
There are currently no methods to prevent the disease. This is due to the fact that the causes of the disease are not well understood in the medical world. However, many programs are underway to determine methods that may be used to prevent the disease. The approach of the prevention methods is mainly centered on how to prevent the infants from contracting the disease and how to prevent the adults from contracting the disease.
Various researchers believe that vitamin D deficiency may be the trigger for the disease. They are therefore devising methods through which infants will have to be given the vitamin to help protect them from suffering from the disease (Bollyky et al, 2008, p 387). Research is also being done to determine the omega 3 fatty acids protect against the autoimmunity as it has been shown a change in the diet, which lacks the fatty acids leads to development of the disease (Bollyky et al, 2008 p 387). Other measures are taken to prevent the disease in the secondary stage. There are also other methods, which are mainly aimed protecting the beta cells from being destroyed by the antigens. These methods mainly involve the immunotherapy of the individuals concerned.
Management
There is currently no cure for the disease; the methods used by the medical practitioners are mainly to help the person live a comfortable life. The management methods are usually to maintain the levels of blood sugar in the body, and such methods involve nutrition planning, exercising, and taking regular doses of insulin (Rolfes, Pinna and Whitney 2008 p 818).
The most common form of treatment of the type 1 diabetes mellitus is “insulin therapy to control initial hyperglycemia and maintain serum electrolytes and hydration” (Rolfes, Pinna and Whitney 2008 p 818). The initial treatment of the disease is usually followed by a period when the patient does not manifest any of the symptoms of the disease. The length of the period is usually varied. It may take a few weeks, months, or 1 to 2 years. However, the disease will ultimately manifest itself again.
The treatment and management methods the type 1 diabetes mellitus places so much of the responsibility of the treatment of the disease on the individual suffering from the disease. The individuals are therefore educated on how to effectively treat themselves (Rolfes, Pinna and Whitney, 2008 p 818).
References
Bollyky, J. B. et al. (2008). Type 1 diabetes mellitus: primary, secondary and tertiary prevention. Mount Sinai journal of medicine. Web.
Braun, C. A. and Anderson, C. M. (2006). Pathophysiology: functional alterations in human health. PA: Lippincott Williams & Wilkins.
Hussain, A. N. and Vincent, M. T. (2010). Diabetes Mellitus, Type 1. medscape. Web.
Lavin, N. (2009). Manual of Endocrinology and Metabolism. PA: Lippincott Williams & Wilkins.
McPhee, S., Lingappa, V. and Ganong, W. (2006). Pathophysiology of disease: an introduction to clinical medicine. CT: Appleton & Lange.
Niewoehner, C. B. (2004). Endocrine Pathophysiology. North Carolina: Hayes Barton Press. Web.
Rolfes, S. R., Pinna, K. and Whitney, E. (2008). Understanding Normal and Clinical Nutrition. OH: Cengage Learning.
Tortora, G. and Derrickson, B. (2008). Principles of anatomy and physiology. NJ: John Wiley and Sons.
Von Herrath, M. G. (2001). Molecular pathology of type 1 diabetes mellitus. Basel: Karger Publishers.
Werner, R. (2008). A Massage Therapist’s Guide to Pathology. PA: Lippincott Williams & Wilkins.