Pathophysiology of Diabetic Ketoacidosis

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Pathophysiology of Diabetic Ketoacidosis

Diabetic Ketoacidosis(DKA) is a complication of diabetes mellitus that is life-


threatening, if not treated. It is due to the breakdown of fats which turn into ketones
because there is no insulin present in the body to take glucose into the cell.
Therefore, you will see hyperglycemia, ketosis, and acidosis.
DKA primarily occurs in Type I diabetes(DM) due to the absence of insulin.
However, it will manifest on Type II DM due to conditions such as septicemia. Insulin
plays a vital role in the regulation of blood glucose and fatty acid metabolism. In
normal conditions, insulin facilitates the transport of glucose into the cell.
Conversely, it will also inhibit fatty acid metabolism inside the cell. In DKA, the body
is experiencing starvation metabolism. Where the cells are starving from glucose to
form energy due to the absence of insulin. Glucose is present in excessive amount
in the blood, however the body is not able to utilize it and reacts as if it is starving.
The body sends signals into the brain to activate emergency pathways to produce
glucose. Processes such as Proteolysis, Glycogenolysis, Ketogenesis,
Gluconeogenesis, and Lipolysis are commenced. The end product of this pathways
will increase both the ketone and glucose in the bloodstream.
Ketone bodies are considered acids thus predisposing the body to Metabolic
acidosis. The body tends to compensate on this condition so the kidneys increase in
ketone excretion and the lungs compensate by getting rid of the excess Carbon
dioxide. Anion gap acidosis will cause the potassium ions to leave inside the cells
due the proton-potassium exchange mechanism. Despite the hyperkalemia, the
body has total depletion of potassium intracellularly.
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