Glycaemic Control for Type 2 Diabetes
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Case study 1: Glycaemic Status
A newly diagnosed type 2 diabetic patient attended his outpatient appointment and reported that he had been tightly monitoring his glycaemic control. The biochemical analysis produced the following results:
[Plasma Glucose] fasting sample 12 mmol/l 4-6 mmol/l
Urea 10.1 mmol/l 3.3-6.8 mmol/l
HbA1c 10% <6.5%
Osmolality (mosm/kg) 277 mosm/kg 285-295 mosm/kg
1] Consider each of these findings and give an assessment of the patient’s glycaemic control.
The above type 2 diabetic patient with abnormal biochemical values [high fasting plasma glucose, HbA1C, urea and borderline Osmolality] showing hyperglycaemic condition though the patient reported, that he had been tightly monitoring his glycaemic control. This describes either 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  about the disease monitoring  and management [5-7], medication [medication regimen] alterations.
The high fasting plasma glucose value 12 mmol/l shows patient is having high blood sugar levels at the time of testing and high HbA1C value [10%] gives a retrospective assessment of the mean plasma glucose concentration during the preceding 6-8 weeks. As the percentage is twice the normal value [<6.5%] it shows poor glycaemic control [9-11].
High urea value 10.1 mmol/l shows that renal impairment caused by diabetes mellitus. Plasma creatinine and urea levels are established 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 system [12-14, 16].
Borderline osmolality 277 mosm/kg suggests possibility of disrupted water balance from either excessive water intake [polydipsia caused 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].
Thus above all classical symptoms are suggestive of uncontrolled diabetes mellitus.
2] Discuss the importance of glycaemic control and the effects that poor control can cause in these patients.
It is very essential to control the hyper glycaemia in diabetic patients as uncontrolled diabetes can 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 present as coronary artery, cerebrovascular or peripheral vascular insufficiency. A number of risk factors have been associated with the metabolic syndrome, including hypertension, poor glycaemic control, central obesity, smoking, dyslipidaemia and glycated end products .
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 erectile dysfunction is also most 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, Charcot’s joints .
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 commonly caused by accidental over administration of insulin or oral anti diabetic drugs [9, 19].
3] Describe how this particular patient could achieve a better 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 combination with other agents to promote daily glycaemic control without increasing the risk of hypoglycaemia or weight gain .
In this patient insulin secretion can be stimulated by sulphonyl urea drugs. Metformin decreases intestinal glucose absorption and hepatic gluconeogenesis as well as increasing tissue insulin sensitivity and which is particularly used in obese patients .
Acarbose delays postprandial absorption of glucose by inhibiting alpha-glucosidase. Glitazones activate γ-peroxisome proliferator activated receptors and which can reduce insulin resistance. Repaglinide increases insulin release from pancreatic β-cells .
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 lifetime strategy for diabetes management might involve aggressive efforts to control glycaemia daily and early in type 2 diabetes, with less stringent glucose targets and avoidance of hypoglycaemia as possibility of comorbidities, such as advanced cardiovascular disease and renal impairment [8, 14, 16, and 20].
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