 Greetings, my name is Dr. Cray and I am one of the instructors here at MedSmarter. Today I would like to review the pathophysiology of diabetes mellitus, one of the major causes of morbidity and mortality here in the United States as well as throughout the world. It is a very high yield topic on both your step one and step two examinations. What I would like to do is talk about diabetes mellitus pathophysiology in a general way. That is to say the common features of type one and type two diabetes and as we move through the discussion I will point out some of the distinguishing physiologic features when we compare type one to type two diabetes mellitus. Pathophysiology of diabetes mellitus and another way that we can call this presentation is we're talking about an insulin deficiency or severe insulin insensitivity. The major factor that is responsible for triggering the pathophysiologic cascade in type one diabetes mellitus is autoimmune destruction of 80 to 90% of the beta cells in the islets of Langerhans of the pancreas. The major underlying factor responsible for triggering the pathophysiology in type two diabetes mellitus is an insulin insensitivity in peripheral tissue or insulin resistance which is necessary but not sufficient in order for an individual to have frank clinical type two diabetes mellitus in addition to them having insulin resistance they also need inadequate insulin secretion from the beta cells. In any case both of these situations are going to result in a decrease in tissue glucose uptake. The decrease in tissue glucose uptake is going to result in a decrease in the intercellular glucose and that is going to trigger in the liver glycogenalysis and gluconeogenesis. There is also as a result of this decrease glucose uptake by the cells going to be proteolysis and lipolysis. The decrease in the tissue glucose the glycogenalysis and the gluconeogenesis are going to result in hyperglycemia and glycosuria. In normal circumstances the kidneys filter and reabsorb 100% of the glucose but there is a T max or a threshold and once that threshold is exceeded then sugar spills over into the urine so that the hyperglycemia will just add here is a very nutritious substance for microorganisms so that the extracellular fluid environment is very rich in sugar and this puts the diabetic at an increased risk of contracting infections. The hyperglycemia is going to result in an increase in the plasma osmolarity that increase in plasma osmolarity is going to result in an increase in thirst and so that increase in thirst is where your polydipsia comes in and as a result of that polydipsia along with the increase in osmotic effect as a result of the increase in the plasma sugar there will be a polyuria. The hyperglycemia is also going to result in an osmotic diuresis that osmotic diuresis is going to cause an increased loss of water sodium potassium and other electrolytes such as magnesium and phosphorus in the urine. The loss of the sodium and water is going to result in hypovolemia this hypovolemia will result in circulatory failure and decrease in tissue perfusion tissue hypoxia and if not intervened upon this will result in coma and death. Thank you very much for watching the video and if you would like to take advantage of our USMLE courses please use the promo code below.