Insulin Dependent Diabetes Mellitus

Insulin-Dependent Diabetes Mellitus

Etiology of Diabetes Mellitus
“Diabetes is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of different organs, especially the eyes, kidneys, nerves, heart, and blood vessels.” (Association, National Center for Biotechnology Information , 2009, p. 1)

“The cause of type 1 and type 2 diabetes remains a mystery. Although genetic factors may play a role”. (Association, Diagnosis and Classification of Diabetes Mellitus, 2010, pp. 562-569)
Diabetes mellitus generally results from an insulin deficiency or resistance. Insulin transports sugar into cells for use as energy and storage as glycogen which is a carbohydrate. Insulin also stimulates protein synthesis and free fatty acid storage. Insulin deficiency or resistance compromises the bodies access to essential nutrients for fuel and storage. Several processes called pathogens(capable of causing disease) are involved in the development of diabetes. The reasons of the abnormalities in carbohydrates, fats, and protein metabolism in diabetes is deficient action of insulin on certain tissues in the body. The term Deficient insulin action, results from not enough insulin secretion and/or diminished tissue response to insulin at one or more points in the complex pathways of hormone action (a chemical messenger that transports a signal from one cell to another). If insulin secretion is blocked or impaired, then defects in the insulin action occur in the same patient, and it is often unclear which abnormality, the cause of the hyperglycemia. (Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997, pp. 107-109)
Type 1 Diabetes Mellitus is defined as an autoimmune disorder or simply put an overactive immune response of the body against substances and tissues normally present in the body. In other words, the body actually attacks its own cells (What-is-Autoimmune-Disease).
This form of diabetes is brought on by a viral infection in which certain cells are destroyed which leads to absolute (complete) insulin deficiency and is usually diagnosed in childhood. Many pediatric patients that have diabetes normally have Type 1 diabetes and therefore a lifetime dependency on insulin. “Diabetes mellitus (DM) is a chronic metabolic disorder caused by an absolute or relative deficiency of insulin, an anabolic hormone.” (Diabetes-Mellitus---Definition-Causes-Symptoms-and-Treatment)
In contrast Type 2 Diabetes Mellitus is a more progressive disorder in which the glandular organ in the digestive system and endocrine system known as the pancreas makes less insulin over time. Because the body’s cells have a reduced response to insulin, symptoms arise that include poor control of liver glucose (sugar) output, a decrease in cell function, and eventually cell failure. The true cause of Type 2 diabetes is unknown; however, it usually occurs in adulthood, from heredity, excessive obesity and sedentary lifestyle. These lifestyle choices may play a major role in its development. For both types of diabetes the main feature is chronic high blood glucose (sugar) levels (Ignatavicius, 2006).
Risk factors for Diabetes Mellitus include obesity, physiologic or emotional stress, which can lead to an elevation of stress hormone levels. In women sometimes pregnancy, which causes weight gain and increases levels of estrogen and placental hormones, may aggravate insulin output. There is also something called the metabolic syndrome which is a combination of medical disorders that, when occurring together, increase the risk of developing cardiovascular disease and diabetes.
There are also some medications that can provoke the effects of insulin, including thiazide diuretics, adrenal corticosteroids, and hormonal contraceptives (Mackay, 2004).

Classification of Diabetes Mellitus
There are several different types of diabetes mellitus; they may differ in cause, clinical course, and treatment. The major classifications of diabetes are:
* Type 1 diabetes (insulin dependent diabetes mellitus) is caused by B-cell destruction, usually leading to absolute insulin deficiency
a) Immune mediated
b) Idiopathic
* Type 2 diabetes (previously referred to as non-insulin dependent diabetes mellitus) ranges from those with predominant insulin resistance associated with relative insulin deficiency, to those with a predominantly insulin secretory defect with insulin resistance (Alberti, 2007).
Insulin is secreted by beta cells, which are one of four types of cells in the islets of Langerhans (dendritic cells = antigen-presenting immune cells) in the pancreas. Insulin is an anabolic, or storage hormone. When a person eats a meal, insulin secretion increases and moves sugar from the blood into muscle, liver, and fat cells. In those cells, insulin transports and metabolizes glucose for energy. Later it stimulates storage of sugar in the liver and muscle (in the form of glycogen). Following this it signals the liver to stop the release of glucose, then enhances storage of dietary fat in adipose which is a storage tissue. Finally it accelerates the transport of amino acids (derived from dietary protein) into the body’s cells.
“Insulin also inhibits the breakdown of stored glucose, protein, and fat. During fasting periods (between meals and overnight), the pancreas continuously releases a small amount of insulin (basal insulin); another pancreatic hormone called glucagon (secreted by the alpha cells of the islets of Langerhans) is released when blood glucose levels decrease and stimulate the liver to release stored glucose. The insulin and the glucagon together maintain a constant level of glucose in the blood by stimulating the release of glucose from the liver. Initially, the liver produces glucose through the breakdown of glycogen (glycogenolysis). Glycogen is the storage form for glucose in the liver and muscles. Glycogenolysis is the conversion of glycogen into glucose in the liver. After 8 to 12 hours without food, the liver forms glucose from the breakdown of non-carbohydrate substances, including amino acids (gluconeogenesis)” (Hamouda, 2012).
Type 1 Diabetes Treatment and Study
This form of diabetes is immune-mediated in over 90% of cases and idiopathic in less than 10%. The rate of pancreatic B cell destruction is quite variable, being rapid in some individuals and slow in others. Type 1 diabetes is usually associated with ketosis in its untreated state. It occurs at any age but most commonly arises in children and young adults with a peak incidence before school age and again at around puberty. It is a catabolic disorder in which circulating insulin is virtually absent, plasma glucagon is elevated, and the pancreatic B cells fail to respond to all insulinogenic stimuli. Exogenous insulin is therefore required to reverse the catabolic state, prevent ketosis, reduce the hyperglucagonemia, and reduce blood glucose.
Clinical manifestations of all types of diabetes include the “three Ps”: polyuria, polydipsia, and polyphagia. Polyuria (increased urination) and polydipsia (increased thirst) occur as a result of the excess loss of fluid associated with osmotic diuresis. The patient also experiences polyphagia (increased appetite) resulting from the catabolic state induced by insulin deficiency and the breakdown of proteins and fats. Other symptoms include fatigue and weakness, sudden vision changes, tingling or numbness in hands or feet, dry skin, skin lesions or wounds that are slow to heal, and recurrent infections (Hamouda, 2012, p. para. 8). The onset of type 1 Diabetes may also be associated with sudden weight loss or nausea, vomiting, or abdominal pains. (Association, Diagnosis and Classification of Diabetes Mellitus, 2010)
In recent years, there has been increasing interest in the impact of diabetes mellitus on the central nervous system (Lukovits TG, 1999).Clinically and epidemiologically, it has been shown that diabetes mellitus is an important risk factor for cerebrovascular accidents (Kannel WB, 1979), and may underlie many of the neuropsychological and cognitive deficits observed in diabetic patients (CM, 1988). Few studies have sought to establish the pathophysiological mechanisms that occur before these deficits appear, with a view to detecting early subclinical abnormalities that could serve as markers of the risk for stroke in patients who might benefit from preventive treatment. The study I read was performed in 15 insulin-dependent diabetics (eight men and seven women) with no history of central neurological symptoms. Their ages ranged from 27 to 59 years (mean 46±8 years) and the mean time since diagnosis of diabetes mellitus was 19±6 years. The characteristics of the patients are given in the Table below. The study was been reviewed by the hospital 's ethics clinical committee, and before being enrolled each patient gave written informed consent.
Characteristics of study subjects
No. 15
Gender (M/F) 8/7
Age (years) 46±8
Arterial hypertension (yes/no) 5/12
Total cholesterol (mg/dl) 214±49
Time from diagnosis of IDDM (years) 19±6
Hemoglobin A1C (%) 8.19±0.8
Diabetic nephropathy (no/micro/macro albuminuria) 10/1/4
Diabetic retinopathy (yes/no) 7/8
Diabetic neuropathy (yes/no) 7/8
IDDM, Insulin-dependent diabetes mellitus

The study dealt with the Cerebrovascular reserve (CVR) which is the capacity of cerebral arteries and arterioles to dilate, thus increasing blood flow in areas of decreased perfusion pressure (WJ, 1991). It is one of the first mechanisms of the brain to be activated in cases of hemodynamic compromise and is an early indicator of its existence (Baron JC, 1981). The chemical Acetazolamide, a carbonic anhydrase inhibitor, induces dilatation of the cerebral microvasculature and has been widely used in assessing CVR in large series of patients with different cerebrovascular disorders. (Julio F. Jiménez-Bonilla, 2001).
The study concluded that Insulin-dependent diabetic patients with no clinical history of neurological disorders present baseline abnormalities in cerebral perfusion and a decrease in CVR in extensive areas of the brain. The decrease in CVR and the behavior of baseline subclinical abnormalities after administration of acetazolamide suggested the existence of chronic cerebrovascular disease, the severity of which varied between patients and was better assessed with this technique than with baseline SPET (PET scan). In addition, the introduction of acetazolamide made it possible to classify baseline irregularities as being of probable metabolic origin or of probable ischemic origin. They concluded that the post-acetazolamide brain SPET is a valid tool which, in comparison with baseline SPET, provided additional information on cerebral perfusion in insulin-dependent diabetes. The technique should prove useful in evaluating future preventive strategies aimed at reducing the incidence of complications in diabetics. (Julio F. Jiménez-Bonilla, 2001)
The main goal of diabetes treatment is to normalize insulin activity and blood glucose levels to reduce the development of vascular and neuropathic complications. Insulin is indicated for type 1 diabetes as well as for type 2 diabetic patients with insulin openia whose hyperglycemia does not respond to diet therapy either alone or combined with other hypoglycemic drugs. The therapeutic goal for diabetes management is to achieve normal blood glucose levels (euglycemia) without hypoglycemia and without seriously disrupting the patient’s usual lifestyle and activity.
There are five components of diabetes management
• Nutritional management – teaching the patient to eat properly and manage their diet accordingly.
• Exercise
• Monitoring – Use of a glucose meter and watching their numbers.
• Pharmacologic therapy – medicines that help level off sugars in their system.
• Education – finding out all the information they can about the disease so they will be informed as to the preventative measures taken to lead a more normal life.

Bibliography

Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. (1997). Diabetes Care, 20:1183-97.
CITATIONS AND CLINICIANS ' NOTES: ETIOLOGY, PREDICTION, AND INCIDENCE OF DIABETES. (2005). Current Medical Literature: Diabetes, 22(2), 32-33.
Alberti, K. M. (2007). International Diabetes Federation: a consensus on Type 2 diabetes prevention. Diabetic Medicine, 24(5), 451-463. doi:10.1111/j.1464-5491.2007.02157.x.
Association, A. D. (2009, January). National Center for Biotechnology Information . Retrieved from PMC US National Library of Medicine : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2613584/
Association, A. D. (2010, January). Diagnosis and Classification of Diabetes Mellitus. Diabetes Care, pp. 562-569.
Baron JC, B. M. (1981). Reversal of focal “misery-perfusion syndrome” by extra-intracranial arterial bypass in hemodynamic cerebral ischemia. A case study. Stroke, 12: 454-459.
CM, R. (1988). Neurobehavioral complications of type I diabetes. Examination of possible risk factors. Diabetes Care, 11: 499-505.
Diabetes-Mellitus---Definition-Causes-Symptoms-and-Treatment. (n.d.). Retrieved 12 15, 2012, from www.healthguidance.org: http://www.healthguidance.org/entry/7366/1/Diabetes-Mellitus---Definition-Causes-Symptoms-and-Treatment.html
Hamouda, M. (2012, May 24). Diabetes/articles/B28Nm6tfL09/nursing+process+for+diabetes. Retrieved from http://www.zimbio.com: http://www.zimbio.com/Diabetes/articles/B28Nm6tfL09/nursing+process+for+diabetes
Ignatavicius, D. &. (2006). Medical surgical nursing: Critical thinking for collaborative care (5th ed.). St. Louis, MO: Elsiever Saunders.
J R Porter, T. G. (2004, April 17). Archives of Disease in Childhood. Retrieved from BMJ.com: http://adc.bmj.com/content/89/12/1138.full#xref-ref-1-1
Julio F. Jiménez-Bonilla, R. Q. (2001). Assessment of cerebral perfusion and cerebrovascular reserve in insulin-dependent diabetic patients. European Journal of Nuclear Medicine, 11:1647-1654.
Kannel WB, M. D. (1979). Diabetes and cardiovascular disease: The Framingham study. JAMA, 241: 2035-2038.
Lukovits TG, M. T. (1999). Diabetes mellitus and cerebrovascular disease. Neuroepidemiology, 18; 1-14.
Mackay, J. &. (2004). Chapter 10: Risk factor: diabetes. In Atlas of Heart Disease & Stroke. (pp. (pp. 38-39)). World Health Organization.
What-is-Autoimmune-Disease. (n.d.). Retrieved from www.news-medical.net: http://www.news-medical.net/health/What-is-Autoimmune-Disease.aspx
WJ, P. (1991). Cerebral hemodynamics in ischemic cerebrovascular disease. Ann Neurol, 29: 231-240.

Citations: AND CLINICIANS ' NOTES: ETIOLOGY, PREDICTION, AND INCIDENCE OF DIABETES. (2005). Current Medical Literature: Diabetes, 22(2), 32-33. Alberti, K. M. (2007). International Diabetes Federation: a consensus on Type 2 diabetes prevention. Diabetic Medicine, 24(5), 451-463. doi:10.1111/j.1464-5491.2007.02157.x. Association, A. D. (2009, January). National Center for Biotechnology Information . Retrieved from PMC US National Library of Medicine : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2613584/ Association, A Baron JC, B. M. (1981). Reversal of focal “misery-perfusion syndrome” by extra-intracranial arterial bypass in hemodynamic cerebral ischemia. A case study. Stroke, 12: 454-459. CM, R. (1988). Neurobehavioral complications of type I diabetes. Examination of possible risk factors. Diabetes Care, 11: 499-505. Diabetes-Mellitus---Definition-Causes-Symptoms-and-Treatment. (n.d.). Retrieved 12 15, 2012, from www.healthguidance.org: http://www.healthguidance.org/entry/7366/1/Diabetes-Mellitus---Definition-Causes-Symptoms-and-Treatment.html Hamouda, M Ignatavicius, D. &. (2006). Medical surgical nursing: Critical thinking for collaborative care (5th ed.). St. Louis, MO: Elsiever Saunders. J R Porter, T. G. (2004, April 17). Archives of Disease in Childhood. Retrieved from BMJ.com: http://adc.bmj.com/content/89/12/1138.full#xref-ref-1-1 Julio F Kannel WB, M. D. (1979). Diabetes and cardiovascular disease: The Framingham study. JAMA, 241: 2035-2038. Lukovits TG, M. T. (1999). Diabetes mellitus and cerebrovascular disease. Neuroepidemiology, 18; 1-14. Mackay, J. &. (2004). Chapter 10: Risk factor: diabetes. In Atlas of Heart Disease & Stroke. (pp. (pp. 38-39)). World Health Organization.