- Pancreatic disorder resulting in insufficient or lack of insulin production leading to elevated blood sugar
- Insulin is the key to allow glucose to be used by the cells for energy
Diabetes: Type 1 occurs when there is an autoimmune (the body attacks the pancreas) response. The beta cells are attacked and can no longer produce and secrete insulin. Insulin is necessary to take sugar from the blood to the cells for energy. Without insulin delivery sugar to the cells, hyperglycemia (high blood sugar) occurs.
Type II DM usually occurs because of genetics and or environmental factors. In type II the pancreas either does not secrete enough insulin or has difficulty with insulin action and insulin resistance occurs in the cells. Hyperglycemia occurs because the cells are resistant to insulin or because there is not adequate insulin production/secretion. When the body can not sufficiently move sugar from the blood to the cells, blood sugars rise and hyperglycemia occurs.
- Type I
- Immune disorder
- Body attacks beta cells in pancreas (responsible for insulin production)
- Pancreas makes NO insulin
- Patient is insulin-dependent
- Ketosis due to gluconeogenesis (body making glucose from fat cells)
- Type II
- Beta cells do not produce enough insulin for body’s needs
- OR – Body becomes resistant to insulin
- May or may not require insulin, depending on severity
- Coronary Artery Disease → increases morbidity & mortality
- Vascular and Nerve Damage
- Related to inflammation and hyperosmolarity in vessels
- Poor circulation
- Poor wound healing
- Retinopathy → blurry vision
- Neuropathy → decreased sensation, especially in feet/toes
- Nephropathy → may result in Chronic Kidney Disease
- Loss of SubQ fat at insulin injection site (rotate sites)
- Fatty mass at insulin injection site (rotate sites)
- Dawn Phenomenon
- Reduced insulin sensitivity between 5-8am
- Evening insulin administration may help
- Somogyi Phenomenon
- Night time hypoglycemia results in rebound hyperglycemia in the morning hours
- Bedtime snack may help
- Diabetic Ketoacidosis (DKA)
- Acute exacerbation of Type I Diabetes Mellitus
- See DKA Lesson
- Hyperglycemic Hyperosmolar Nonketotic State (HHNS)
- Acute exacerbation of Type II Diabetes Mellitus
- See HHNS Lesson
- See Diabetes Management Lesson
- See Diabetes Management Lesson
- See Diabetes Management Lesson
Okay guys, we’re going to talk about Diabetes Mellitus. Now, even if you’re brand new into nursing school, you’ve probably heard of this or know someone who has it, or have at least heard about it on the news. Diabetes is one of the leading comorbidities in the US and it’s a serious problem for our patients. In this lesson we’re going to review what happens in the patient’s body with Diabetes Mellitus, and in the next lesson we’re going to talk about what we do about it medically and in our nursing care.
So first, let’s look at the basic patho – Diabetes is an immune disorder where the body attacks the beta cells of the pancreas. Those are the cells responsible for secretion of insulin. So if the beta cells are attacked, we have either a lack of insulin or an insufficient supply of insulin for our body’s needs. So let’s remind ourselves what insulin does. Insulin is like the key that helps to unlock the cell to allow glucose to get into the cell. So you can see here, that glucose channel is closed until insulin comes in and unlocks it. Now glucose can get into the cells so they can use it for energy or ATP. If we don’t have insulin, all of this glucose will have to stay outside of the cells – so the amount of sugar left in our bloodstream will be elevated – hence our increased blood sugar levels. There are two types – Type 1 and Type 2, so let’s look at each of those a little closer.
In Type 1 Diabetes Mellitus, patients have absolutely NO insulin production. All of the beta cells in their pancreas have been destroyed and they’ve completely lost their ability to produce insulin. So, what does that mean for them? Well remember normally the insulin helps unlock the cells so that glucose can move into them. If there’s no insulin, all of this sugar just hangs out in the bloodstream and the cells get NOTHING. But cells REQUIRE glucose for energy, so they’re going to have to find it another way. That can create a lot of problems for the patient, as we’ll see in the DKA lesson. So – as you can imagine, these patients are considered insulin-dependent. This used to be called juvenile diabetes or juvenile onset diabetes, but they’ve found that it can actually develop later in life as well, so we stick to Type 1 or insulin-dependent.
In Type 2 Diabetes Mellitus, the patient is making SOME insulin…However, one of two things is happening. Either they just aren’t making enough to deal with the excess blood glucose, or, their body has become resistant to the effect of insulin. If the body is insulin resistant, then it requires much more insulin to have the same effect on the blood glucose. But, their body just isn’t providing it. So we have some cells able to get glucose, but the rest of that sugar stays out here in the bloodstream. The difference here is that the body is getting Just Enough glucose into the cells to not have to find that same workaround like Type 1 does. We’ll talk about this more in the HHNS lesson. They used to call this Adult Onset, but more and more we’re seeing children diagnosed because of poor lifestyle and eating habits. Just remember Type 1 is NO insulin, Type 2 is not enough insulin or insulin resistance. Either way, sugars can become dangerously elevated.
So there are quite a few complications of having elevated blood sugars, which we’ll continue to look at throughout this module. But, one of the big ones we want you to see is the amount of damage it can cause in the vascular system. Elevated blood sugars can cause inflammatory processes inside the vessels. They also cause a hyperosmolar state or a super concentrated state in the blood. Both that inflammation and that hyperosmolarity can do damage to the vessels as well as nerves surrounding them. So patients tend to have poor circulation, especially in the smaller vessels in the body – like in their hands and feet. That poor circulation and pro-inflammatory process can also lead to poor wound healing, so you’ll see in nursing care we’ll talk about inspecting every inch of their skin, especially on their feet and between their toes. Even the smallest wound can become massive and infected and they could lose their toe, foot, or even their leg because of it. Now, because of the damage to the small vessels and nerves, we’re also going to see neuropathy – they’ll get numbness and tingling in their hands and feet – that just makes the poor wound healing worse because they may not even be able to feel that something is wrong. We could also see retinopathy, which affects the tiny vessels in the eyes and can lead to vision loss. And finally, high blood sugars are very hard on the kidneys, so all patients with diabetes are at risk for nephropathy and ultimately chronic kidney disease if their sugars aren’t well controlled.
There are a couple of other complications that we can see, especially in patients who receive SubQ insulin therapy. Lipoatrophy is a loss of SubQ fat, remember atrophy means shrinking. Lipohypertrophy is a SubQ fat mass, remember hypertrophy means excess growth. Both of these can occur at the site of SubQ insulin injection. That’s why it’s SO important that we rotate sites when we’re administering insulin. We draw quadrants on the abdomen and rotate around, we can even further divide and rotate within the quadrants as well. We can also use the upper arms or the outer thighs. If we give insulin in the same spot multiple times in a row, it can start causing a lot of problems in that Subcutaneous tissue.
Other things we see in diabetic patients are the dawn phenomenon and the somogyi phenomenon. In the Dawn phenomenon, we see that patients tend to be less sensitive to insulin in the morning – so their sugars will be higher. We can sometimes combat this with an evening dose of insulin. In the Somogyi Phenomenon, patients who are a bit hypoglycemic at bedtime tend to have a rebound hyperglycemia and have super high sugars in the morning. For these patients we encourage a small bedtime snack. Either way, you’ll notice patients may tend to have higher sugars in the mornings than they do in the afternoon. I know, for me, as a night shift nurse it was always frustrating because they wanted the 6AM blood sugar to be under 200 or super controlled after surgery – but it was always the highest one of the day. My 9pm and 3am blood glucose levels would be fine, then I’d take the 6am and it would be 250. So this is something we need to be aware of.
Then, patients can also experience Diabetic Ketoacidosis or Hyperglycemic Hyperosmolar Nonketotic Syndrome – which will each have their own lesson, so make sure you review those.
So let’s recap. Diabetes mellitus is a condition of insufficient insulin production or action – either because all of their beta cells have been destroyed and they have NO insulin, like in Type 1, or because they just aren’t producing enough or they’re resistant to it, like in Type 2. Because the glucose can’t enter the cells to be used for energy without insulin, we see significant hyperglycemia. This hyperglycemia can lead to inflammation and hyperosmolarity in the vessels which can cause damage to the small vessels and nerves, leading to things like neuropathy, retinopathy, and poor wound healing. We want to monitor and manage their sugars closely and prevent complications by rotating injection sites, evaluating whether they need a bedtime snack or bedtime insulin, and monitoring for signs and symptoms of DKA or HHNS, which we’ll learn about later in this module.
Those are the basics of the pathophysiology and complications of Diabetes. Make sure you check out the rest of this module to learn about nursing care, as well as DKA, and HHNS. Now, go out and be your best selves today. And, as always, happy nursing!