3APPLIED PATHOPHYSIOLOGYIntracellular starvation of the tissues (insulin dependent)Hyperventilationvenous rightHYPERGLYCEMIA KETOACIDOSISHepatic ketogenesisDehydrationRelease of catecholamines, Cortisol, growth hormone and glucagon Base lossVomitingInsulin deficiencyStimulates lipolysisIncreased glucose utilisation oProteolysis & hepatic gluconeogensisTissue hyper fusionOsmotic diuresisLactic acidosissecurityrityus getvenous rightDiabetic Ketoacidosis in CarlyNausea, vomiting, dehydration, polydipsia, and polyuria, deep breathing, abdominal pain, acetone smelling breathing Presents to the emergency departmentDehydration causes tachycardia, poor skin turgor, dry mucous membranes, and orthostatic hypotension.Osmotic diuresis- loss of magnesium ions, potassium ions, sodium phosphate, and phosphate ionsTreatment with IV fluids and an IV insulin infusionNeurological deterioration, tonic-clonic seizuresecurityrityus getvenous rightTreatment with Mannitol Discharge of CarlyPathophysiologyDiabetic Ketoacidosis is a condition characterized by the serum bicarbonateconcentration<15 mmol/L, high serum glucose concentration (> 200 mg/dL) along withketonuria, ketonemia, and glucosuria. In this condition, the venous pH is found to be <7.3(Srinivas, 2016). Pathophysiology is the study of disordered physiological events occurringinside the body due to illness or injury. It is the convergence of physiology and pathology thathelps explains the conditions observed during disease. This section deals with thePathophysiology of Diabetic Ketoacidosis, experienced by Carly.According to Boling & Pravikoff, (2016) the main cause of Diabetic Ketoacidosis is thecritical deficit of insulin. This leads to intracellular starvation of the insulin-dependent tissues. Inthis situation the growth hormone and other like Cortisol, catecholamines, and glucagon arereleased stimulating the production of the glucose, lipolysis, proteolysis and oxidation if the fattyacids to release ketone bodies. However, these bodies are not processed unlike in the physiologicfasting. The reason for this outcome is the fact that the blood glucose regulation is mainlyperformed by insulin. In the absence of the insulin the hepatic and renal glucose productionincreases resulting in the decreased uptake of the peripheral glucose. It prevents the peripheralfat disposition. In the presence of insulin, the glycogen synthesis is stimulated, while switchingof the hepatic gluconeogenesis (Srinivas, 2016). This may occur to some extent in the case ofnormal fasting. However, in a case of the insulin deficiency, the normal response to fasting isexaggerated. It stimulates the liver production of the glucose. This process is called as thegluconeogenesis from protein and fat. Simultaneously the breakdown of the liver glycogen

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