Glycaemic Control for Type 2 Diabetes

Glycaemic Control for token 2 DiabetesCase issue 1 Glycaemic StatusA newly diagnosed caseful 2 diabetic affected role of att subverted his out patient of appointment and reported that he had been tightly supervise his glycaemic mince. The biochemical analysis produced the following resultsValue RangePlasma Glucose abstinence sampling 12 mmol/l 4-6 mmol/lUrea 10.1 mmol/l 3.3-6.8 mmol/lHbA1c 10% Osmolality (mosm/kg) 277 mosm/kg 285-295 mosm/kg1 Consider each of these findings and give an assessment of the patients glycaemic sway.The supra type 2 diabetic patient with super everyday biochemical values high fasting relationship plasma glucose, HbA1C, urea and borderline Osmolality cover hyperglycaemic condition though the patient reported, that he had been tightly monitoring his glycaemic suppress. This describes any his nonadherance to medication 1-4 or fluctuations in plasma glucose levels as he is a newly diagnosed diabetic patient. So he requires more counselling 14 some the sickness monitoring 8 and management 5-7, medication medication regimen alterations.The high fasting plasma glucose value 12 mmol/l shows patient is having high demarcation scratch levels at the time of testing and high HbA1C value 10% gives a retro assessment of the mean plasma glucose concentration during the preceding 6-8 weeks. As the dower is twice the normal value High urea value 10.1 mmol/l shows that nephritic impairment designerd by diabetes mellitus. Plasma creatinine and urea levels are effected markers of Glomerular filtration rate GFR. High urea value in above patient suggests that impaired function of the nephrons. It could be attributed to a fall in the filtering capacity of the kidney thus leading to accumulation of waste products within the administration 12-14, 16.Borderline osmolality 277 mosm/kg suggests possibility of disrupted body of water balance from either excessive water intake polydipsia energised by hyperglycaemia or inadequate water excretion impaired kidney function. In this case further investigations like measurement of urine osmolality, urine volume and urine, plasma electrolytes sodium to confirm the reason for hypo osmolality 9, 22. thereof above all classical symptoms are suggestive of uncontrolled diabetes mellitus.2 deal the sizeableness of glycaemic control and the effects that poor control plenty cause in these patients.It is very essential to control the hyper glycaemia in diabetic patients as uncontrolled diabetes sess cause life threatening consequences 14, 20.Vascular disease is a common complication of persistent poor glycaemic control in diabetes 9, 13, 14-16.Macro vascular disease due to abnormalities of large vessels may drive home as coronary artery, cerebrovascular or peripheral vascular insufficiency. A number of venture factors have been associated with the metabolic syndrome, including hypertension, poor glycaemic control, central obesity, smoking, dyslipidaemia and glycated end products 16.Microvascular disease due to abnormalities of small blood vessels particularly affects the retina diabetic retinopathy and the kidney nephropathy both may be related to inadequate glucose control.Microvascular disease of the kidney is associated with proteinuria and progressive renal failure. Diffuse nodular glomerulosclerosis Kimmelstiel Wilson lesions may cause the nephrotic syndrome. The renal complications may be partly due to the increased glycation of structural proteins in the arterial walls supplying the glomerular basement membrane glycation of protein in the lens may cause cataracts.Skin disorders, Infections like urinary tract or chest infections, cellulitis, candida and vertical dysfunction is also some common and partly neurologically mediated. diabetic neuropathy, which can be peripheral symmetric sensory, peripheral painful, acute mononueropathies or autonomic. diabetic ulcers, which can be ischemic, infective. The joints can also be affected, Charcots joints 9.Type 2 diabetic patients are more likely to suffer from a hyperosmolar hyperglycaemic non-ketotic state HONK when their diabetic control is deranged 17, 18.Hypoglycaemia is most ordinarily caused by accidental over administration of insulin or oral anti diabetic drugs 9, 19.3 Describe how this particular patient could action a crack glycaemic control.The above diabetic patient with abnormal biochemical values could achieve a better glycaemic control, by diet control, weight reduction if patient is overweight, and increased physical activity, medication adherence, medication regimen alteration and most importantly high dose of insulin may be required to control the hyperglycaemic status 7, 9,17. Additionally care providers must educate and motivate the patient to monitor glucose levels, control carbohydrate consumption and aggressively participate in self-care to control disorder.In type 2 diabetic patients incretin hormones glucagon-like peptide-1 and glucose-dependant insulinotropic polypeptide maintain normal glucose homeostasis. Thus dipeptidyl peptidase-4 inhibitors, which enhance endogenous incretin function, are well suited for junto with other agents to promote periodical glycaemic control without increasing the risk of hypoglycaemia or weight gain 21.In this patient insulin secretion can be stimulated by sulphonyl urea drugs. Metformin decreases intestinal glucose submerging and hepatic gluconeogenesis as well as increasing tissue insulin esthesia and which is particularly used in obese patients 9.Acarbose delays postprandial absorption of glucose by inhibiting alpha-glucosidase. Glitazones activate -peroxisome proliferator activated receptors and which can reduce insulin resistance. Repaglinide increases insulin release from pancreatic -cells 9.Glycaemic control efforts should involve quarterly glycated haemoglobin assessments, routine monitoring of daily blood glucose values and combination therapy that targets both fasting and post prandial hyperglycaemia. The life sentence strategy for diabetes management might involve aggressive efforts to control glycaemia daily and early in type 2 diabetes, with less stringent glucose targets and dodging of hypoglycaemia as possibility of comorbidities, such as advanced cardiovascular disease and renal impairment 8, 14, 16, and 20.References1 Khattab, M. et Al. 2010 Factors associated with poor glycemic control among patients with type 2 diabetes. daybook of Diabetes and its Complications, 24, 84-89. Accessed 12th February 2015.2 Almutairi, A.M. et Al. 2013 Predictors of poor glycemic control among type 2 diabetic patients. American journal of Medical Sciences, 3 (2), 17-21. Accesses 12th February 2015.3 Blackburn, F D., Swidrovich, J., Lemstra, M. 2013 Nonadherence in type 2 diabetes, practical consideration for interpreting the literature. Patient gustatory perception and Adherence, 7, 183-189. Accessed 12th February 2015.4 Di Bonaventura, M. et Al. 2014 The associa tion between nonadherence and glycated haemoglobin among type 2 diabetes patients victimisation basal insulin analogs. Patient Preference and Adherence, 8, 873-882. Accessed 11th February 2015.5 Moreira, Jr. D E. et Al. 2013 Glycemic control and diabetes management in hospitalized patients in Brazil. Diabetology and Metabolic Syndrome, 5, 62. on hand(predicate) from http//www.dmsjournal.com/content/5/1/62 Accessed 11th February 2015.6 Schmeltz, R.L. et Al. 2011 Management of inpatient hyperglycemia. Lab Med, 42 (2), 427-434. Available from http//www.medscape.com/viewarticle/744866_4 Accessed thirteenth February.7 Fowler, J. M. et Al. 2011 Pitfalls in outpatient diabetes management and inpatient glycemic control. clinical. Diabetes daybook.Org, 29 (2), 79-85. Available from http//clinical.diabetesjournals.org/content/29/2/79.full Accessed 13th February 2015.8 Clarke, S. F. and Foster, J.R. 2012 A history of blood glucose meters and their role in self-monitoring of diabetes mellitu s. British Journal of Biomedical Science, 69 (2), 83-93. Accessed 13th February 2015.9 Crook, M.A. (2006) Clinical biochemistry. 7th ed. Hodder Arnold10 Walker, S., Beckett, G., Rae, P. and Ashby, P. (2010) Lecture notes on clinical biochemistry. 8th ed. Wiley Blackwell.11 Marshall, WJ. and Bangert, SK. (2004) Clinical chemistry. 5th ed. Mosby12 Idonije, O. B. et Al 2011 Plasma glucose, creatinine and urea levels in type 2 diabetic patients attending a Nigerian teaching hospital. Research Journal of Medical Sciences, 5 (1), 1-3. Available from http//www.medwelljournals.com/fulltext/?doi=rjmsci.2011.1.3 Accessed 13th February 2015.13 Alao, O. et Al. 2009 Cardiovascular risk factors among diabetic patients attending a Nigerian teaching hospital. The Internet Journal of Endocrinology, 6 (1), 1-8. Available from https//ispub.com/IJEN/6/1/11009 Accessed 13th February 2015.14 The management of type 2 diabetes 2014 NICE clinical guidelines 87. Available from http//www.nice.org.uk/guidance /cg87 Accessed 13th February 2015.15 Wallace, T. M and Matthews, D. R. 2000 Poor glycaemic control in type 2 diabetes a combination of disease, suboptimal therapy and attitude. The Quarterly Journal of Medicine, 93, 369-374. Accessed 13th February 2015.16 Goud B. K, M. et Al. 2011 Serum urea, creatinine in relation to fasting plasma glucose levels in type 2 diabetic patients. International Journal of Pharmacy and Biological Sciences, 1 (3), 279-283. Accessed 13th February 2015.17 Pesce, J. A. and Kaplan, A. L. 1987 Methods in Clinical Chemistry. Mosby.18 Diabetic ketoacidosis. Information about DKA. Patient.co.uk. Available from http//www.patient.co.uk/doctor/diabeticketoacidosis Accessed 14th February 2015.19 Tight diabetic control. American Diabetes Association. Available from http//www.diabetes.org/livingwithdiabetes/treatmentandcare/bloodglucosecontrol/tightdiabetescontrol.html Accessed 14th February 2015.20 Ousman, MD. Y. and Sharma, MD. M. 2001 The irrefutable importance of g lycemic control. Clinical Diabetes Journal.Org, 19 (2), 71-72. Available from http//clinical.diabetesjournals.org/content/19/2/71.full Accessed 14th February 2015.21 Bode, BW. 2009 Defining the importance of daily glycemic control and implications for type 2 diabetes management. Postgrad Med., 121 (5), 82-93. Available from http//www.ncbi.nlm.nih.gov/pubmed/19820277 Accessed 14th February 2015.22 Weiner, D. pee regulation and osmolality. Available from http//ocw.tufts.edu/data/33/497472.pdf Accessed 17th February 2015