Pathophysiology of Diabetes Mellitus

Modifiable: Lifestyle Diet Stress Exercise Insulin deficiency Insulin resistance Non-Modifiable: Heriditary Age

Intracellular: failure of glucose to enter into intracellular space or inside the cell Decrease in the tissue uptake

Decrease source of glucose for ATP production

Extracellular Hyperglycemia

Cellular starvation. s/s polyphagia, polydipsia

body compensates: by converting proteins (amino acid), fats and other noncarbohydrate through the liver Gluconeogenesis

Newly formed glucose in the blood fail to enter the cell tissues due to insulin resistance (lack of insulin receptor in the membrane of cell for glucose transport). Therefore it adds more glucose in the blood.

breakdown of fats resulting to high ketone levels. Ketones bodies are low in pH causing diabetic acidosis (ketoacidosis) s/s fast, deep breathing a smell of acetone on your breath nausea and vomiting stomach pains.

decreased anabolism and increased catabolism of protein s/s cachexia lethargy polyphagia decrease production of gamma globulins (decrease WBC) increase susceptibility to infection impaired wound healing

Systemic blood Viscosity Impaired tissue perfussion

osmotic diuresis. High glucose levels spill over into the urine, taking water and solutes (such as sodium and potassium)

Poor oxygen delivery to peripheral area Poor wound healing

Dehydration s/s Hypokalemia Hyponatremia Polyuria polydipsia