Type 1 diabetes (T1DM) is a chronic metabolic disorder wherein an immune response targets the insulin-producing beta-cells of the pancreas leading to cellular damage sufficient enough to significantly reduce, and later on eliminate, the synthesis of insulin (Van Belle et al., 2011). It typically manifests in people below 30 years of age. The American Diabetes Association (ADA) (2016) estimates that 29.1 million or 9.3% of Americans are diabetics but of this number, only 1.25 million or around 5% have type 1 diabetes. The purpose of this paper is to describe the pathophysiology, clinical presentation, diagnosis, treatment and management, and complications of type 1 diabetes.
Pathophysiology
Genetic defects either in one gene or multiple genes predispose individuals to T1DM. One example of such defects is the mutation that causes dysfunction in the regulation of T lymphocytes leading to an autoimmune attack on body organs including the pancreas (Van Belle et al., 2011). Another is a defect in chromosome 6p21 which instigates an autoimmune response following an environmental trigger (Van Belle et al., 2011). Such triggers are commonly viral and bacterial infections but can also be certain foods such as wheat proteins and cow’s milk (Van Belle et al., 2011). It often takes sustained autoimmune responses through multiple triggers before complete beta cell destruction and T1DM symptoms occur.
Clinical Presentation
Classical T1DM can occur during childhood or adolescence and manifests as a lean body build and acute onset of glycosuria and diuresis due to hyperglycemia resulting in frequent thirst (ADA, 2016; Thrower & Bingley, 2014). Patients are also prone to ketosis when the body metabolizes fat for energy given the lack of insulin to facilitate the cellular absorption of glucose from the blood (Thrower & Bingley, 2014). Ketoacidosis manifests as shortness of breath, a fruity odor in the breath, dryness in the mouth, nausea, and vomiting (ADA, 2016). In T1DM in adulthood, weight loss is a common occurrence with shorter symptom durations, and patients typically also have other autoimmune diseases including autoimmune thyroiditis, pernicious anemia or celiac disease (Thrower & Bingley, 2014).
Diagnosis
Diagnosing diabetes mellitus involves performing tests to detect hyperglycemia, investigate glucose control, and classify the type of diabetes. The fasting glucose test, 2-hour oral glucose tolerance test (OGTT), and the random glucose test are used to detect hyperglycemia; the latter is most appropriate in symptomatic patients (Patel & Maurollo, 2010). Meanwhile, the glycated hemoglobin (HbA1c) test is employed to check the level of glucose control within the past few months. To distinguish between T1DM and T2DM, tests such as for C peptide aim to evaluate the functioning of beta cells (Patel & Maurollo, 2010). There are also tests to detect autoantibodies, such as islet cell cytoplasmic autoantibodies (ICA), which serve as markers of autoimmune beta cell damage (Patel & Maurollo, 2010).
Treatment and Management
The lack of endogenous insulin production in T1DM warrants exogenous insulin therapy administered either through 3-4 subcutaneous injections per day or through continuous subcutaneous infusion (ADA, 2015). The dose of rapid-acting insulin will need to match the patient’s intake of carbohydrates, blood glucose level before a meal, and physical activities. As insulin causes a reduction of blood sugar levels, hypoglycemia is an unintended effect of therapy so that insulin analogs are preferred to decrease the risk of hypoglycemia (ADA, 2015). Pramlinitide may also be prescribed in adults to slow the rate of gastric emptying, enhance satiety, facilitate weight loss, and decrease the insulin dose (ADA, 2015). It is important to note that there is disparity in insulin therapy methods and outcomes based on race or ethnicity and negatively affects Black and Hispanic children (AAP, 2015). Addressing the causes of disparity should be part of care planning.
Because of the chronic nature of T1DM, effective self-management is needed to ensure good glucose control, prevent complications, reduce emergency department or hospital admissions, and guarantee quality of life despite a life-long disease. The American Association of Diabetes Educators (AADE) (2010) recommend 7 key self-care behaviors that would help achieve optimal outcomes. These are healthy eating, physical activity, glucose monitoring, medication adherence, problem solving, risk reduction, and positive coping (AADE, 2010). These behaviors address lifestyle, behavioral, and psychological factors that influence the achievement of treatment goals thereby warranting a multifaceted management of disease. Referral to a diabetes educator for self-management education, counseling, and follow-up fosters a holistic and person-centered care (AADE, 2010).
Complications
Poor blood glucose control owing to lack of treatment or non-adherence leads to diabetes complications. Hyperglycemia damages nerves leading to peripheral neuropathy and limb amputation (IDF, 2015). It also causes vasoconstriction and atherosclerosis resulting in heart disease, stroke, renal disease, and retinopathy leading to vision loss (AOA, 2015; IDF, 2015). Furthermore, poorly controlled blood glucose blunts immune responses to infections and injury leading to susceptibility and delayed healing. For this reason, it is important to follow up the patient and conduct periodic physical examination, HbA1c testing, and retinopathy screening to evaluate treatment effectiveness and self-management (AADE, 2010; Patel & Maurollo, 2010).
Conclusion
T1DM is a chronic autoimmune-mediated metabolic disorder affecting persons younger than 30 years. Genetic mutations are known to increase the likelihood of T1DM in the presence of certain foods and diseases that trigger the autoimmune response. The clinical manifestation varies slightly in T1DM that occurs in children and adolescents and that which occurs in adults. Diagnosis focuses on establishing hyperglycemia and suboptimal glucose control and differentiating between different types of diabetes. Treatment is a combination of pharmacotherapy and patient self-management of a chronic illness. There are multiple complications that occur with poor management necessitating regular patient follow up.
References
American Academy of Pediatrics (AAP) (2015). Study finds racial disparities in treating type 1 diabetes in children. Retrieved from https://www.aap.org/en-us/about-the-aap/aap- press-room/pages/Study-Finds-Racial-Disparities-in-Treating-Type-1-Diabetes-in- Children.aspx
American Association of Diabetes Educators (AADE) (2010). AADE 7 self-care behaviors. Retrieved from https://www.diabeteseducator.org/patient-resources/aade7-self-care- behaviors
American Diabetes Association (2015). Standards of medical care in diabetes – 2015. Diabetes Care, 38(1), S1-S94. Retrieved from http://care.diabetesjournals.org/content/suppl/2014/12/23/38.Supplement_1.DC1/Janu ary_Supplement_Combined_Final.6-99.pdf
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Van Belle, T.L., Coppieters, K.T., & Von Herrath, M.G. (2011). Type 1 diabetes: Etiology, immunology, and therapeutic strategies. Physiology Reviews, 91, 79-118. doi:10.1152/physrev.00003.2010.
