A Case Study Diabetes Mellitus Type II

.PATHOPHYSIOLOGY Diabetes Mellitus Type 2 is referred to as non-insulin dependent diabetes mellitus(NIDDM), or adult onset diabetes mellitus (AODM).In case our patient we classified the risk factor into two categories the modifiable and non-modifiable. Under modifiable is the diet because diet high in cholesterol increases number of adipose tissue and this tissue are resistant toinsulin therefore glucose uptake by cell is poor and the stress because stress stimulates secretion22

of epinephrine, norepinephrine and glucocorticoids and this neurotransmitters increases glucose level. In the non-modifiable factor hereditary because it can be transfer from parents to offspring. In the case of our father has diabetes also. And the age with strong heritability patterns which present as type 2 diabetes early in life, usually before 30 years in the case of our patient he was diagnosed at the age of 37 years old. In type 2 diabetes,can still produce insulin, but do so relatively inadequately for their body's needs, beta cells are primary affected and there is a poor production of insulin. Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from the beta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. If the insulin is deficient the intracellur and the intravascular space are affected. In the intracellular space there is a failure of glucose to enter in the intracellular space because there is a lack of insulin and insulin acts as the key to be able the glucose to enter in the cell. And when this happened the glucose supposed to be absorbed by the cells are staying in the blood and this term is hyperglycemia. If cell was not able to absorb the sugar their will be intracellular and extracellular dehydration and body will compensate and the person will have the urge to drink more water it is term polydipsia. Also if cell has no glucose intake their will be cellular starvation and the person will have the urge to eat and eat and it is termed polyphagia.in the intravascular area if the insulin is insufficient and glucose are not absorb by the cell the glucose is staying in the blood stream and the glucose level in the blood will increase as the sugar in blood increase the blood circulation will become viscose. Prolonged high blood glucose level leads to sluggish circulation and when the glucose concentration in the blood is raised beyond its renal reabsorption of glucose in the proximal renal tubulis incomplete, and part of the glucose remains in the urine(glycosuria). This increases the pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production ( polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst. In a sluggish circulation due to high blood content in blood the oxygen supply in the peripheral site is insufficient and when this happened there is a proliferation of microorganism in the case of our patient his wound doesnt easily heal due to poor oxygen delivery and microorganism take place and multiply