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Diabetic Ketoacidosis
is caused by an absence or markedly inadequate amount of insulin. the most serious metabolic disturbance deficit in insulin results in disorder in the metabolism of carbohydrate, protein and fat. 3 main clinical features/events of DKA:
Hyperglycemia Dehydration Acidosis- an abnormal increase in hydrogen ion conc. In the body, resulting from an accumulation of an acid or the loss of a base.
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Pathophysiology
Without insulin, the amount of glucose entering the cells is reduced and the liver increases glucose production. Both factors lead to hyperglycemia. To rid the body of the excess glucose, the kidneys excrete the glucose along with water and electrolytes. This osmotic diuresis, which is characterized by excessive urination (polyuria), leads to dehydration and marked electrolyte loss.
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Another effect of insulin deficit is the breakdown of fat (lipolysis) into free fatty acids and glycerol. The free fatty acids are converted into ketone bodies by the liver. In DKA, there is excessive production of ketone bodies because of the lack of insulin that would normally prevent this from occuring. Ketone bodies are acids, their accumulation in the circulation leads to metabolic acidosis.
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This condition occurs most often in older people (50-70 with no known history of diabetes of with mild type II diabetes. HHNS can be traced to a precipitating event such as an acute illness (pneumonia, stroke), medications that exacerbate hyperglycemia (Thiazides), or treatments, such as dialysis. The history, includes days to weeks of polyuria with adequate fluid intake. What distinguishes HHNS from DKA is that ketosis and acidosis do not occur in HHNS partly because of differences in insulin levels. In DKA no insulin is present, and this promotes the breakdown of stored glucose, protein, and fats, which needs to the production of ketoacidosis.
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The insulin level is too low to prevent hyperglycemia (and subsequent osmotic diuresis), but it is high enough to prevent fat breakdown. Patients with HHNS do not have the ketosis-related GI symptoms that lead them to seek medical attention. Instead, they may tolerate polyuria and polydipsia until neurologic changes or an underlying illness prompts them to seek treatment. Because of possible delays in therapy, hyperglycemia, dehydration, and hyperosmolarity maybe more severe in HHNS.
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Clinical Manifestations
Hypotension Profound dehydrating (dry mucous membranes, poor skin turgor) Tachycardia Variable neurologic signs (alteration of sensorium, seizures, hemiparesis).
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