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Pathophysiology
Process
Individuals with Type 1 do not produce insulin. Without insulin, muscle and adipose cells cannot access glucose to meet energy requirements. Glucose production goes unopposed in the liver. Glucagon is produced in response to the glucose deprivation of muscle and adipose tissues, prompting glycogenolysis and gluconeogenesis. Glucose levels rise in the blood.
The kidneys cannot absorb the ever-increasing glucose, so the excess is excreted in the urine (polyuria). The brain, prompted by this loss of fluid, signals thirst (polydypsia) and hunger (polyphagia). If this process continues, stored fats are metabolized and transformed by the liver into keto acids, which leads to lower pH levels and acidosis. The drop in pH level and loss of ketones in urine signals the onset of ketoacidosis.
Intracellular potassium ions are exchanged for hydrogen ions. These potassium ions are lost in urine along with sodium, magnesium and phosphorus. Blood volume drops, increasing hematocrit, hemoglobin and white blood cell counts. Respiratory compensation results in labored, deep respiration (Kussmaul respiration) in an attempt to lower the PCO2 values.
This process is acute but may extend over several days. Ketoacidosis is a likely presenting symptom in an initial Type 1 diagnosis. (3,6,7)
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