Why is there hypercalemiaemia in diabetic ketoacidosis
In the diabetic ketoacidosis, short DKA, it is a serious metabolic imbalance (ketoacidosis) due to insulin deficiency, which requires immediate intensive medical treatment. Ketoacidosis is a form of metabolic acidosis.
Ketoacidosis is metabolic acidosis (acidosis) caused by the increased formation of ketone bodies. It is primarily a complication of type 1 diabetes and a consequence of severe insulin deficiency. The body then covers its energy needs by breaking down fats, which leads to an increased build-up of ketone bodies. The consequences are ketonemia, hyperlipoproteinemia, and hypercholesterolemia.
The hyperglycaemia excretes more water and thus electrolytes, since the kidney threshold of maximum reabsorption of glucose is exceeded from a glucose level of approx. 180 mg / dl. These changes result in desiccation and pronounced electrolyte imbalances.
The insulin deficiency has several biochemical consequences.
3.1 Breakdown of free fatty acids
Although there is hyperglycaemia, the transport of glucose into the cell is disturbed. Ultimately, there is a lack of glucose as an energy supplier intracellularly and free fatty acids are broken down via beta oxidation to acetyl-CoA and NADH / H +.
Since NADH / H + inhibits the citric acid cycle, acetyl-CoA is used as an alternative to ketogenesis and cholesterol synthesis. This creates the ketone bodies acetoacetate and ß-hydroxybutyrate. By submitting H+-Ions the body's alkali reserves, which leads to metabolic acidosis with negative base excess.
Acetoacetate is released from the liver under physiological circumstances, in order to be split again into two acetyl-CoA in target cells and broken down in the citric acid cycle. However, acetoacetate can spontaneously decarboxylate, producing acetone with the release of carbon dioxide. The volatile acetone is exhaled and causes the characteristic odor of the air we breathe.
The insulin deficiency also leads to a disinhibition of the hormone-sensitive lipase (HSL) and thus to increased lipolysis in the fat cells. HSL splits off the fatty acid in position 3 on triacylglycerols (TAG). The released fatty acids are transported to the liver, where they are also broken down into acetyl-CoA and NADH / H + in the beta oxidation.
3.3 Disturbed fatty acid synthesis
The reduced glucose turnover in the pentose phosphate cycle leads to a deficiency in NADPH / H +, which in turn slows down fatty acid synthesis. The increased concentration of free acetyl compounds also blocks another enzyme involved in fatty acid synthesis, acetyl-CoA carboxylase.
Possible symptoms of diabetic ketoacidosis include:
With increasing severity of the clinical picture, disturbances of consciousness up to coma diabeticum can occur.
Evidence of diabetic ketoacidosis is marked hyperglycaemia combined with acidosis with a pH of 7.3 or below. There is marked hyponatremia while the serum potassium is normal to slightly elevated. There is an anion gap.
5.1 Sample findings
- pH value: 6.8 - 7.3 (metabolic acidosis)
- pCO2: 20-30 mmHg (hyperventilation as a compensation attempt)
- HCO3-: <15 mmol / l (metabolic acidosis)
- Lactate:> 6 mmol / l
- Blood glucose:> 400 mg / dl
Due to the severity of the clinical picture, intensive medical treatment is required.
The cornerstones of diabetic ketoacidosis treatment are the intravenous infusion of large amounts of fluids and insulin. It is particularly important to ensure that sufficiently high amounts of potassium are supplied in good time, as this is shifted from the extracellular space into the cells by the action of insulin - an original hyperkalaemia results in hypokalaemia. The acidosis can be balanced with sodium bicarbonate.
When blood sugar is lowered, the "cellular memory" enables excessive translocation of GLUT-4 transporters into the cell membrane, which can trigger dangerous hypoglycaemia. The blood sugar should therefore be lowered slowly and carefully, possibly even IV glucose. to administer.
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