The Disorder of Type II Diabetes - Case Study Example

? Running Head: CASE PRESENTATION FOR TYPE II DIABETES Case Presentation for Type II Diabetes Sasha---- -- Brief Definition of the Disorder Type II diabetes is defined as the inability of the body to tolerate carbohydrate as exemplified by insulin resistance, relative deficiency of insulin, excessive production of glucose in the liver, and hyperglycemia. (Brashers 2006, cited in National Diabetes Data Group and the World Health Organization, undated). Epidemiology of the Disorder In the United States, around 25.8 million people are identified to have diabetes, and out of these, about 7.0 million belong to the criteria of undiagnosed population for diabetes. The Centers for Disease Control and Prevention (2011) reported that approximately 1.9 million new cases of diabetes among people ages 20 years old and above were reported in 2010. Other than accidents or injury, diabetes became the leading cause of blindness, kidney failure, and amputation of feet and legs, making diabetes as the 7th leading cause of death listed in the year 2007. Lastly, CDC (2011) noted that a diabetic person has twice the risk of dying compared to individuals not diagnosed with diabetes, establishing a fact that a diabetic person has a shorter life expectancy. Pathophysiology of the Disorder Type 2 diabetes mellitus is a multifactorial disorder caused by genetics and environmental elements affecting the functioning of the beta – cell of the pancreas, and insulin sensitivity to muscle, liver, adipose, and pancreatic tissue (Scheen, 2003 and Kardori, 2011). It is characterized by a combination of inadequate secretion of insulin by beta – cells of the pancreas and resistance to peripheral insulin resulting to elevated free fatty acids in the plasma and decreased transport of glucose into muscle cells, elevated production of glucose in the liver, increased breakdown of fat, and deteriorating functioning of beta cell that eventually leads to failure of the beta cells (Mahler and Adler, 1999 and Khardori, 2011). Scheen (2003) added that although the mechanisms remain unclear, these factors including dysfunction of the beta – cell and reduced sensitivity to insulin were agreed to play an important role in the pathogenesis of diabetes. Adipose tissue is also recognized to play an essential role in the pathogenesis of type II diabetes mellitus since most of the individuals with type 2 diabetes are obese with truncal obesity (Scheen, 2003). The following is a case presentation study that illustrates the use of medical research knowledge in managing a patient diagnosed with type 2 diabetes mellitus. Hypothetical Patient Presentation with the Disorder History P.G. is a 59 year old man with a 10 year history of type II diabetes. The initial symptoms of easy fatigability, polyuria, polydipsia, slight blurring of vision and erectile dysfunction brought P.G. to seek consult in 2001. Fasting blood sugar, obtained twice, revealed he had diabetes (145 mg/dL and 140 mg/dL). The hemoglobin A1c test result of 7% also suggests positive findings for diabetes. He has a positive family history of type II diabetes in the maternal side. P.G. was referred to an endocrinologist, and was advised to take Metformin 500 three times daily and to exercise at least 45 minutes daily; however, he was not compliant with his medication and exercise regimen. Recently, P.G. complained of slight numbness in the right lower extremity, polyuria, fatigue, and erectile dysfunction. Symptoms P.G. presented with initial symptoms of easy fatigability, polyuria, polydipsia, slight blurring of vision, and erectile dysfunction, which are consistent with the symptoms of diabetes, namely, weight gain, frequent infection of the urinary bladder, kidney, and skin, yeast infection especially in the skin and vagina, fatigue, hunger, increased thirst and urination, nocturia, loss of visual acuity, erectile dysfunction, numbness and tingling of both hands and feet, and neuropathy (PubMed Health, 2011 and Brashers, 2006). Physical Exam Findings Physical examination findings revealed the following: Weight: 220 lb and height 5’5”, BP of 140/90 mmHg (taken left arm, sitting position), Pulse rate of 70 bpm; respirations of 17 cycles per minute. HEENT: (+) pupillary light reflex, clear fundi, (-) retinopathy, (-) palpable nodes Lungs: clear breath sounds; Heart: regular rate and rhythm Neurological findings: no significant findings although patient complained of previous episodes of numbness in the big toe of the right foot. Significant Laboratory Results were: Fasting blood sugar: 156 mg/dl (normal range: 65 – 109 mg/dl) hemoglobin A1c: 8%, Creatinine: 0.9 mg/dl (normal range: 0.5 – 1.4 mg/dl) Lipid profile: Total cholesterol: 170mg /dl (normal: less than 200 mg/dl), HDL: 40 mg/dl (normal: more than 40 mg/dl), LDL: 110mg/dL (normal: less than 100 mg/dL), Triglycerides: 170 mg/dl (normal: less than 150mg/dl), and Cholesterol to HDL ratio: 4.5 (normal: less than 5.0) Differential Diagnosis The following are the differential diagnosis for type 2 diabetes: (1) Diabetes mellitus type 1, (2) Diabetic ketoacidosis, (3) Gestational diabetes, (4) Drug – induced glucose intolerance, (5) Pancreatitis, (6) Cystic fibrosis, (7) In adults, latent autoimmune diabetes, which is very rare, (8) Secondary diabetes mellitus due to pancreatic and hormonal disorder and drug – induced diabetes, and (9) Chromium deficiency, a rare clinical and genetic syndrome which is associated with diabetes (Brashers, 2006 and Robbins, et al., 1995) Keys to Assessment 1. It is encouraged that all patients especially the obese with more than 120% ideal body weight or have significant weight gain as well as patients with positive family history for type II diabetes, members of the ethnic population at risk for diabetes, positive history for gestational diabetes, hypertensive, abnormal lipid profile, exhibit symptoms of diabetes, and recurrent infections especially in the skin, urinary tract, and vagina must be screened for type II diabetes (Brashers, 2006). 2. Diagnosis for type 2 diabetes must be established by five criteria, namely; fasting plasma glucose level, any casual plasma glucose concentration, 2-hour plasma glucose level, HgA1C level, and identification of diabetic retinopathy characteristic (Brashers, 2006). 3. Signs for any complications associated with type II diabetes such as proteinuria, albuminuria, glycosuria, diabetic renal disease, and abnormalities in the retina must be examined. It is also necessary to evaluate creatinine clearance, total protein and albumin, BUN, and lipid profile to assess the renal function, and to investigate for any possibility of diabetic nephropathy (Brashers, 2006). Keys to Management include Patient Education Managing patients with type 2 diabetes mellitus is a lifetime exercise of active and concerting effort to educate patients that require his physician, nutritionist, diabetes educator, and other health professionals to get involved in the management (Khardori, 2011). Nathan, et al (2009) noted that the principle in selecting interventions in elevated blood sugar is by choosing specific antihyperglycemic agents that is effective to lower glucose level and has the capacity to reduce unforeseen complications as well as safe, tolerable, easy to use and less expensive. The first approach to P.G. was non pharmacological. He was referred to a dietitian to address his concern in losing weight. Weight loss does not only reduce elevated glucose levels but it is also an important step to reduce his blood pressure. P.G. and his family were informed on the significance and role of exercise in reducing blood pressure and blood sugar. After discussion, the family agreed to take turns to walk with P.G. for at least 45 minutes per day, 5 days a week, between 7 a.m. to 8 a.m. For pharmacologic approach to treatment, P.G. was given ACE inhibitor because of elevated BP of 140/90 mmHg. Statin therapy is recommended to correct LDL to normal. A low dose of aspirin was also given because P.G. was at risk of cardiovascular disease, as evidenced by increase BP and abnormal lipid panel. After discussing the treatment option with P.G. and his family, Metformin 500 mg was prescribed twice daily. Metformin is ideal for overweight patients and is used to decrease glucose output of the liver. Hence, lowers the hemoglobin A1c level (Nathan, et al., 2009). References Brashers, V. (Ed). (2006). Clinical Applications of Pathophysiology: An Evidence-Based Approach (3rd ed). St. Louis, Missouri: Mosby. Centers for Disease Control and Prevention. (2011). Diabetes Successes and Opportunities for Population – Based Prevention and Control at a Glance 2011. Retrieved November 28, 2011, from http://www.cdc.gov/chronicdisease/resources/publications/AAG/ddt.htm Khardori, R. (2011). Type 2 Diabetes Mellitus. Retrieved November 26, 2011, from http://emedicine.medscape.com/article/117853-overview#a0156 Kishore, P. (2008). The Merck Manual Home Health Handbook: Diabetes Mellitus. Whitehouse Station, NJ: Merck Sharpe & Dohme Corp. Retrieved from http://www.merckmanuals.com/home/hormonal_and_metabolic_disorders/diabetes_mellitus_dm/diabetes_mellitus.html Lee, J. (2008). Why Young Adults Hold the Key to Assessing the Obesity Epidemic in Children. Archives of Pediatrics and Adolescent Medicine, 162(7):682-287. Retrieved from http://archpedi.ama-assn.org/cgi/reprint/162/7/682.pdf Mahler, R. and Adler, M. (1999). Type 2 Diabetes Mellitus: Update on Diagnosis, Pathophysiology, and Treatment. The Journal of Clinical Endocrinology and Metabolism, 84(4): 1165-1171. Retrieved from http://jcem.endojournals.org/content/84/4/1165.full Nathan, D., Buse, J., Davidson, M., Ferrannini, M., Holman, R., Sherwin, R., and Zinman, B. (2009). Medical Management of Hyperglycemia in Type 2 Diabetes: A Consensus Algorithm for the Initiation and Adjustment of Therapy. Diabetes Care, 32(1): 193-203. Retrieved from PubMed Central Journal List, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2606813/ PubMed Health. (2011). Type 2 Diabetes. Retrieved November 26, 2011, from http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001356/ Robbins, S., Cotran, R., and Kumar, V. (1995). Robbins Pathologic Basis of Disease (2nd Edition). Philadelphia: W.B. Saunders Company. Scheen, J. (2003). Pathophysiology of Type 2 Diabetes. Acta Clinica Belgica, 28(6): 335-41. Retrieved November 26, 2011, from http://www.ncbi.nlm.nih.gov/pubmed/15068125 Read More