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Diabetic Ketoacidosis - Coggle Diagram
Diabetic Ketoacidosis
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Risk Factors
Illness, infection, physical or emotional stress
Increased hormone production stimulates hepatic glucose release and decreases cellular insulin uptake
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Collaborative Treatment
Prevention
Appropriate education about checking blood glucose, administering insulin, and monitoring ketones
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Restore fluid volume with 0.9% Normal Saline, high rate of infusion for several hours
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Increases renal perfusion, alleviates CV stress
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Pathophysiology/Etiology
Beta cells of the pancreas become unable to produce insulin due to autoimmune damage, leading to diabetes mellitus type 1 (DM1)
Insulin carries glucose into cells. Without it, cells are unable to harness glucose to produce ATP and perform cell functions. Starving cells signal liver to release stored glucose. Hyperglycemia develops as blood glucose levels rise abnormally high (>300 mg/dL).
Liver breaks down stored fat to release energy for cells. Fatty acids and acidic ketone bodies are released as by-products, decreasing blood pH and contributing to metabolic acidosis.
Causes nausea/vomiting, acetone breath
Kidneys filter glucose into urine, causing osmotic diuresis and excess loss of water, potassium, and sodium. Causes polyuria and electrolyte imbalance.
Fluid volume deficit and dehydration decreases renal perfusion. Impaired kidney function decreases bicarbonate production and contributes to development of metabolic acidosis. Causes polydipsia and changes to LOC.
Compensation in the form of Kussmaul breathing may occur to increase blood pH by ridding body of CO2.
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Etiology: mismanaged DM1, infection/stress
Symptoms
Hyperglycemia
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Polyuria
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Electrolyte loss (Na, K, Cl)
Irregular HR, arrhythmias
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Metabolic acidosis
Kussmaul respirations
Hyperventilation, deep, labored breathing
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