Diabetes mellitus: Nursing pathophysiology

Diabetes mellitus is a group of endocrine disorders characterized by hyperglycemia, or elevated blood glucose. The two main types are type 1 diabetes, which is caused by an absolute insulin deficiency; and type 2 diabetes which is caused by insulin resistance.

Okay, so, the pancreas is an organ located in the abdomen that plays a role in glucose regulation and digestion. Scattered throughout the pancreas are small clusters of cells, called islets of Langerhans. Among these cells are α-cells and β-cells. The α-cells secrete glucagon in response to decreasing blood glucose. Glucagon increases blood glucose by stimulating the liver to breakdown glycogen, or stored glucose, by a process called glycogenolysis.

Conversely, β-cells secrete insulin in response to increasing blood glucose. Insulin lowers blood glucose, which also suppresses α-cell secretion of glucagon. Along with insulin, β-cells co-secrete amylin, which prevents postprandial, or post-meal, spikes in blood glucose by inhibiting gastric emptying, increasing satiety, and suppressing glucagon release.

Now, for cells to function, they need glucose as a source of energy. However, cell membranes are impermeable to glucose; so, for glucose to get inside the cell, insulin must first bind to insulin receptors on the cell membrane. This binding activates the cell’s glucose transporters that will then facilitate the movement of glucose into the cell.

Type 1 diabetes is most commonly caused by an autoimmune destruction of β-cells, resulting in an inability to produce insulin. In other cases, the cause is idiopathic, meaning there’s no known cause. Risk factors include exposure to certain viruses and a family history of type 1 diabetes.

As for type 2 diabetes, the main cause is insulin resistance in the tissues, which is when cells don’t respond as easily to insulin. Risk factors include obesity, physical inactivity, and a diet high in simple carbohydrates, saturated fats, and red meat. Additionally, those older than 65 years and those with a history of hypertension are at increased risk.

Alright, now with type 1 diabetes, a lack of insulin means glucose can’t enter the cells, and without glucose the cells begin to starve. Additionally, α-cells will continue to secrete glucagon because they become less responsive to high levels of glucose; so, the liver continues to break down glycogen into glucose, which contributes to a further increase in blood glucose, resulting in hyperglycemia.

On the other hand, with type 2 diabetes, cells in the tissues become insulin resistant, and additional insulin is required to get glucose to enter the cells. The β-cells respond by releasing more insulin. Over time, however, it becomes more difficult for the β-cells to keep up with the demand. They become exhausted, dysfunctional, and progressively lose their ability to produce enough insulin to overcome resistance. Eventually, β-cells begin to undergo apoptosis, or cell death, leaving less β-cells available to produce insulin. Losing β-cells means less insulin, and less insulin means glucose will build up in the blood, resulting in hyperglycemia.

Now, sustained hyperglycemia has detrimental effects on the rest of the body. The kidneys reach the maximum amount of glucose they can reabsorb, so extra glucose spills into the urine, causing glycosuria. Additionally, since glucose is osmotically active, glycosuria is accompanied by a large amount of water in the urine. Glucose also pulls water out of cells and into the bloodstream, expanding the blood volume and leaving the cells dehydrated.