Thursday, November 15, 2012

PATHOPHYSIOLOGY OF DIABETES MELLITUS

In both type 1 and 2, individual will by hyperglycemic. Glucosuria occur after the renal tubular transport system for glucose becomes saturated. This happens when glucose concentration of plasma exceeds 180 mg/dL i.e. increase more than renal threshold. As hepatic glucose over production continues the plasma glucose concentration reaches a plateau of 300-500 mg/dL.


(Source: medscape.org)
The individual with type 1 diabetes has higher tendency to produce ketones. Patient with type 2 diabetes seldom generates ketones but instead have greater tendency to develop hyperosmolar nonketotic states. The difference in glucagon and insulin concentrations in these two groups appears to be responsible for the generation of ketone through increased β-oxidation. In type 1 there is an absence of insulin with an excess of glucagon. This permits gluconeogenesis and lipolysis to occur. In type 2 insulin is present therefore glucagon is attenuated. Fatty acid oxidation is inhibited in type 2. This causes fatty acids to be incorporated into Tg for release as VLDL.

The laboratory findings of patients with diabetes with ketoacidosis tend to reflect dehydration, electrolyte disturbances, and acidosis. Acetate, beta hydroxybutyrate and acetone are produced from the oxidation of fatty acids which leads to acidosis along with lactate, fatty acids and other organic acids. Bicarbonate and total carbon dioxide are usually decreased due to Kussmaul-Kien respiration. This is a compensatory mechanism to blow off carbon dioxide and remove hydrogen ions. The anion gap in this acidosis can exceed 16 mmol/L. Serum osmolality is high as a result of hyperglycemia; sodium concentrations tend to be low due in part to losses (polyuria) and in part to shift of water from cells because of the hyperglycemia. Grossly elevated Tg will displace plasma volume and give the appearance of decreased electrolytes with flame photometry or if sample is diluted. Hyperkalemia is almost always present as a result of displacement of potassium from cells in acidosis.

More typical of the untreated patient with type 2 diabetes is a nonketotic hyperosmolar state. The individual presenting with this syndrome has an overproduction of glucose; however, there appears to be an imbalance between production and elimination in urine. Glucose concentration exceeds 300-500 mg/dL and severe dehydration is present. The severe dehydration contributes to the inability to excrete glucose in urine. Mortality is high with this condition. Ketones are not observed because of severe hyperosmolar state inhibits the ability of glucagon to stimulate lipolysis. The laboratory findings of non ketotic hyperosmolar coma include plasma glucose value more than 1000 mg/dL, normal or elevated sodium and potassium, slightly elevated bicarbonate, elevated BUN and creatinine, and elevated osmolality. 

(Source: thenursingcorner.blogspot.com)

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