When a person with diabetes and heart failure takes a sulfonylurea, her body may release antidiuretic hormone-and the resulting water retention and hyponatremia can spell danger.If you’re caring for such a patient, watch for signs and symptoms of the syndrome of in -

• Appropriate antidiuretic hormone
• Weight gain despite anorexia
• Nausea and vomiting
• Muscle weakness
• restlessness
• Possibly seizures and coma.

If you note these signs and symptoms, begin emergency treatment as prescribed to increase sodium levels and prevent central nervous system injury and death. If the patient experiences hyponatremia associated with increased blood volume, a physician will prescribe normal or hypertonic saline solution and furosemide to induce the excretion of more dilute urine.

This test places exercise demands on the heart and can uncover CAD not detected with an ECG. Many patients with diabetes have additional risk factors for CAD, such as obesity, hypertension, and abnormal blood lipid levels. Thus, a physician may have a patient undergo an exercise stress test even if her ECG is normal.

A stress test can also be used to monitor the progression of CAD. A patient may require periodic stress tests, especially if new symptoms of CAD appear or new risk factors are identified.

Nursing Considerations

Review your patient’s drug history and find out from her physician which drugs should be with­held and which she should take on the day of the stress test. A physician may withhold oral antidiabetic drugs because exercise lowers blood glucose levels. If your patient uses insulin, her physician may prescribe a lower dose to avoid hypoglycemia during the test.

Instruct your patient to rest the day before the test so that she has the energy to perform it. She should also fast for at least 3 hours and avoid smoking for at least 1 hour before the test. Explain to your patient what she can expect during the test and what she should wear. This information may ease her anxiety.

Determine if your patient has autonomic neuropathy, which affects involuntary functions, such as heart rate and blood pressure. During stress testing, patients with such neuropathy may not experience chest pain even though ischemia develops. Also, the blood pressure may go very high or very low when exercising. If your patient has autonomic neuropathy, closely monitor her throughout the test. The physician may even decide that an exercise stress test is inappropriate for such a patient and substitute a dipyridamole­thallium test. With this test, dipyridamole, instead of exercise, is used to put stress on the heart. The thallium acts as a contrast agent.

All patients with Type 1 diabetes must use insulin. Because the insulin dose is determined by blood glucose levels, you and your patient must monitor those levels with particular care.People with Type 2 diabetes produce some insulin, but generally not enough to lower their blood glucose levels. If other treatments can’t control their blood glucose levels, they may also require insulin. Some patients with Type 2 diabetes may require insulin only temporarily during times of stress.

All insulins are administered subcutaneously. Regular insulin may be administered I.V. Because of its protein nature, insulin must be administered by injection. Given orally, it would be digested and destroyed in the GI tract.

Insulin restores the cells’ ability to use glucose as a source of energy, but researchers don’t know exactly how. Insulin is involved in cell membrane transport, so it increases cell growth and the metabolism of carbohydrates, proteins, and fats.

Insulin maintains blood glucose levels through several mechanisms. In the liver, insulin decreases the breakdown of glycogen, prevents the formation of new sources of glucose from amino acids, and prevents the formation of ketone bodies. At the same time, insulin increases the synthesis and storage of glycogen and fatty acids and decreases the breakdown of fat in adipose tissue. Insulin also enhances the use of amino acids and decreases the breakdown of protein in muscle tissue.

Types of Insulin

Insulin is classified as rapid-acting, intermediate­acting, or long-acting, depending on its onset, peak, and duration of activity .

Most rapid-acting insulins begin working in 30 minutes and reach their peak in 2 to 5 hours. Their duration of action is 6 to 8 hours. One form of rapid-acting insulin, lispro, begins working in 5 to 15 minutes and reaches its peak in 30 to 90 minutes. Its duration of action is 2 to 4 hours. Rapid-acting insulins compensate for the meals eaten after injection. For some patients, using lispro before a meal improves postprandial glycemic control and reduces the risk of hypoglycemia because of its short duration of action. Other rapid-acting insulins include regular and Semilente insulin.

Intermediate-acting insulin starts working in 1 to 3 hours and reaches its peak in 4 to 15 hours. Its duration of action is 18 to 24 hours. It may be given in split doses, before meals, but the patient must eat at the time of peak action to prevent hypoglycemia. Intermediate-acting insulins include neutral protamine Hagedorn (NPH) and Lente insulins. NPH insulin contains protamine sulfate, a protein derived from fish that can cause an allergic reaction. Lente insulin is a good choice for people sensitive to protamine.

Long-acting insulin starts to work in 4 to 6 hours and reaches its peak in 8 to 20 hours. Its duration of action is 24 to 28 hours. Ultralente, the only long-acting insulin, gives patients a consistent insulin effect.

Some patients need a mixture of insulins. One that’s rapid-acting, such as regular insulin, for a fast onset and one that’s intermediate-acting, such as NPH, for a longer duration of action. These insulin mixtures are available in premixed bottles. For example, NPH and regular insulin are available in 70/30 and 50/50 mixtures. The premixed bottles are especially useful for elderly patients or patients with vision loss.

Sources of Insulin

Extracts of beef and pork pancreas were once the only sources of insulin. Beef insulin is no longer used, except in some beef and pork mixtures, and pork insulin is rarely used. Today, human insulin, which is derived from recombinant deoxyribonucleic acid technology, and the human analog lispro are the two forms most commonly used. Insulin from all sources appears to be equally effective at controlling blood glucose levels. However, human insulin causes less lipoatrophy, less antibody production, and fewer allergic reactions. And it’s absorbed faster than pork insulins.

Changing between pork and human sources of insulin can disrupt blood glucose levels and require dosage adjustments. People who need insulin only temporarily-a patient with Type 2 diabetes undergoing surgery, for example-should use human insulin.

Indications and Contraindications

Insulin is essential for everyone with Type 1 diabetes. Type 2 patients may need it if diet, exercise, weight control, and oral antidiabetic drugs haven’t been effective. They may also need it during periods of stress involving fever, severe trauma, infection, major surgery, DKA, and HHNK syndrome. Insulin therapy is recommended for women with gestational diabetes if diet alone doesn’t control blood glucose levels.

Adverse Effects and Interactions

Hypoglycemia is the most common adverse effect of insulin therapy. Other adverse effects include lipodystrophy, insulin resistance, and, in rare cases,insulin allergy.

The two types of lipodystrophy are lipoatrophy and lipohypertrophy. Lipoatrophy, which is caused by animal insulins, results from the breakdown of adipose tissue at the injection site or in areas away from the injection site and causes a loss of fatty tissue. Dimpling may result from an injection with an impure insulin preparation or may be an immune response. Treatment includes injecting human insulin or steroids around the area of breakdown.

Lipohypertrophy occurs after repeated injections into the same site. The skin in the hypertrophied area eventually loses sensation. Because the hypertrophied area is an accumulation of fatty tissue, tell your patient not to use it for additional injections because the insulin will be absorbed erratically.

Insulin resistance results from the formation of antibodies that bind to insulin, making it inactive. Patients with cirrhosis of the liver or a disease of the endocrine glands may also develop insulin resistance. The patient becomes unresponsive to usual doses and may need as much as several hundred units of insulin a day. Changing from animal to human insulin or purified pork insulin may correct the problem. Or a corticosteroid may treat it. For obese patients who have nonimmunologic insulin resistance, the treatment is weight loss.

A patient with an insulin allergy may develop redness, swelling, aching, and pruritus at the injection site 4 to 8 hours after the injection. Or she may develop systemic allergic reactions.

Insulin products derived from animal sources cause allergies in some patients. The physician will probably substitute human insulin.

Some people are allergic to the insulin preparations or to the preservatives in the solution. Other people may be hypersensitive to the skin­cleansing agent used before injectionShould . Some patients are allergic to the latex in the stopper of the vial or in the plunger of the syringe. If any allergic reactions occur, your patient should contact her physician immediately.

Systemic allergic reactions to insulin are uncommon, especially with purified insulin preparations. If an anaphylactic reaction occurs, however, it may be life threatening. The signs and symptoms include rash, shortness of breath, tachycar­dia, hypotension, diaphoresis, angioedema, and anaphylaxis. Patients with severe systemic reactions should have a skin test before they begin using a new insulin preparation.

Several drugs can increase or decrease the action of insulin . No foods interact with insulin. However, to achieve optimal glycemic control, patients should follow their prescribed meal plan in conjunction with their insulin prescription.

Administration

The dosage and number of daily insulin injections depend on each patient’s circumstances. Many patients are on an insulin regimen that requires different kinds or mixes of insulin. The physician considers the time of insulin administration, diet, and exercise when determining dosages. After initial insulin dosages have been determined, monitor the effects of the insulin.

Your patient will inject insulin subcutaneously with a short (1/2 inch), small-bore (27, 28, or 29 gauge) needle .

The rate of absorption of insulins other than lispro varies with the injection site. Insulin is absorbed from the abdomen faster than from any other site. The upper arm provides the next most rapid absorption, followed by the thigh and but­tock. Instruct your patient not to administer insulin within a 2-inch radius of the umbilicus to prevent injection into a blood vessel. Because the rate of absorption of insulin changes with the injection site, patients should rotate injection sites within one area, such as the abdomen, before moving to another, such as the upper arm.

Body temperature also affects absorption. Increased blood flow from sitting in a sauna, having a fever, or exercising a muscle causes insulin to be absorbed more quickly than usual.

Storage: Tell your patient that she can keep unopened bottles of insulin in the refrigerator for up to 3 months. She shouldn’t freeze the insulin because freezing can cause clumping. A bottle in current use can be stored at room temperature, out of direct sunlight and extreme heat, for up to 1 month. Prefilled syringes may be stored in the refrigerator vertically (needle up) for 1 to 2 weeks. Instruct her to check the expiration date on the insulin bottle periodically and to discard the insulin when it expires.

Injection: When teaching your patient how to inject insulin, first instruct her to roll the bottle of insulin suspension gently between her hands so that the contents don’t form bubbles or foam. If a bottle of insulin contains granules or clumps after mixing, instruct her to discard the bottle. Because regular insulin is clear, the bottle doesn’t have to be rolled before use. Instruct your patient to discard the bottle of regular insulin if it’s discolored or cloudy or contains granular material.

Next, instruct your patient to stretch the skin at the injection site and insert the needle at a 90­degree angle .

Several new alternatives to syringes simplify insulin injection. Spring-operated insulin pens,which metal container with a are preloaded with bottles of insulin, are convenient and accurate. The cartridges, which don’t have to be refrigerated, supply enough insulin for 3 to 5 days. Using the pen, however, requires skill and dexterity. Patients with impaired vision can buy devices that facilitate drawing up and administering insulin with a syringe, including syringe magnifiers, needle guides, bottle stabilizers, and nonvisual insulin measurement systems.

Disposal: Advise your patient to dispose of needles and lancets in a hard plastic container, such as an empty detergent bottle, or a tightly secured lid. If the patient uses coffee cans to dispose of needles, caution her to reinforce the plastic lid with several layers of duct tape. Some drugstores sell commercial containers like the ones used in hospitals.

Tell your patient to put needle containers in the regular trashnever with recyclables. If she lives in an area with a depot system for dropping off used syringes, encourage her to do that.

Insulin Pumps: Instead of using subcutaneous injections, some patients can use insulin-pump therapy, a method of insulin administration that more closely mimics the normal function of the pancreas. To be a candidate for the insulin pump, a patient must have Type 1 diabetes, be able to monitor her own blood glucose levels, and be able to operate the pump. Patients using pump therapy also must be highly motivated; they’ll have to monitor their blood glucose levels at least four times a day and keep careful records to help evaluate their therapy.

The battery-powered pump contains a syringe and a computer chip that stores information for insulin administration. To administer insulin, the patient attaches an infusion set with a small catheter to the pump. She then inserts the catheter into her abdomen, arm, or thigh. She can wear the pump 24 hours a day but should change the injection site every 72 hours. She should also change the site when it becomes inflamed or painful, or whenever the system leaks or becomes clogged.

Using the pump provides several benefits. Because blood glucose levels can be more tightly controlled, glycosylated hemoglobin levels and the number of hyperglycemic episodes can be reduced. The pump may also help lower the number of congenital birth defects in children who are born to mothers with diabetes. Insulin-pump therapy also may help delay the progression of microvascular and macrovascular complications and neuropathy.

Providing nursing care to a patient with DKA presents a multisystem challenge. To prevent serious complications, think critically and act quickly.During fluid replacement, assess your patient’s fluid balance to ensure adequate hydration without the complications of fluid overload. Evaluate her vital signs, level of consciousness, body weight, intake and output, urine specific gravity, and blood osmolality. And assess her skin turgor and mucous membranes for signs of improved hydration.

Frequently check the I.V. site for signs of infiltration or infection. If your patient has a central line, check all connections. During rapid fluid replacement, monitor your patient for signs and symptoms of fluid overload especially if she’s elderly, a child, or at risk for heart failure. Signs and symptoms of heart failure include pulmonary crackles, labored respirations, hypotension, tachycardia, and heart sounds.

Monitor your patient’s blood sodium, potassium, bicarbonate, magnesium, and phosphate levels closely. And evaluate her electrocardiogram (ECG) tracings to detect arrhythmias or characteristic changes from abnormally high or low potassium levels.

Before starting the insulin infusion, flush the tubing with 50 ml of insulin solution to saturate the tubing with insulin. Remember, insulin adheres to I.V. tubing, so if you don’t saturate it with insulin, your patient won’t receive the full insulin dose. Use an infusion pump to ensure insulin delivery at the prescribed rate.

Monitor the blood glucose level hourly. As the level falls, monitor your patient closely for signs and symptoms of hypoglycemia.

Your patient also requires basic nursing interventions for comfort and hygiene. Although she’s dehydrated and thirsty, she may not be able to eat or drink anything until she’s no longer feeling nauseated, vomiting, or complaining of abdominal pain. Providing frequent oral care helps moisten dry lips and mucous membranes, increasing her comfort and giving you an opportunity to assess her hydration.

Skin care is especially important because dehydration and poor tissue perfusion from DKA increase the risk of skin breakdown. Turn and reposition your patient every 2 hours. Use an emollient to keep her skin from becoming scaly, flaky, and vulnerable to breakdown. As you provide skin care, check your patient’s skin turgor, color, temperature, and perfusion.

Assessment

You can use a health history and physical examination in two distinct ways to investigate diabetes. When you suspect that a patient has the disorder, you can perform a health history and physical examination to discover the characteristic signs and symptoms and confirm your suspicion. When you already know that a patient has diabetes, you can use a health history and physical examination to help monitor the disease and uncover any complications.

Diabetes looks different in different patients. The signs and symptoms, the severity, and even the type of diabetes can vary. But one thing is always the same, hyperglycemia.

Any patient with diabetes has one or both of these problems. She either produces little or no insulin, or her body can’t use insulin effectively. As a result, she has difficulty metabolizing carbohydrates, fats, and proteins, so hyperglycemia develops.

To diagnose diabetes, a physician needs to determine if a patient has hyperglycemia. Depending on the patient’s history and her signs and symptoms, one of three tests may be performed. For a patient with the typical signs and symptoms of diabetes, such as polydipsia, polyuria, polyphagia, blurry vision, and unexplained weight loss, a physician can base the diagnosis on a single random blood glucose level of 200 mg/dl or more. If a patient doesn’t have the typical signs and symptoms of diabetes, the physician needs a fasting blood glucose level of 126 mg/dl or more to make the diagnosis. For a patient who is at risk for developing diabetes (for example, someone who has a family history of diabetes or who is obese) and who has a normal fasting blood glucose level, a physician will use the 2-hour oral glucose tolerance test. He’ll make a diagnosis of diabetes if an initial test and one follow-up test reveal blood glucose levels of 200 mg/dl or more.

Treating diabetes consists of keeping blood glucose levels as close to normal as possible, using a combination of medication, diet, exercise, and stress control. By closely monitoring blood glucose levels and keeping them as close to normal as possible, a patient can reduce the risks of acute and long-term complications. The acute life-threatening complications of diabetes include hypoglycemia, diabetic ketoacidosis (DKA), and hyperglycemic hyperosmolar nonketotic (HHNK) syndrome. Long-term complications, which develop because chronic hyperglycemia causes damage to organs and tissues, include nephropathy, cardiovascular disease, peripheral vascular disease, cerebral vascular disease, neuropathy, and retinopathy.

An acute complication of diabetes can quickly deteriorate into a metabolic crisis. Hypoglycemia, for instance, can make your patient’s mental status decrease quickly. Left untreated, she can become comatose and suffer permanent brain damage. Acute hyperglycemia can also trigger dangerous consequences.As a nurse, you’re in an excellent position to detect the early signs and symptoms of hypoglycemia, hyperglycemia, and other acute complications such as diabetic ketoacidosis (DKA), and hyperglycemic hyperosmolar nonketotic (HHNK) syndrome . You can also identify findings that suggest the Somogyi phenomenon, an acute complication of treatment, and the dawn phenomenon, another problem related to diabetes. And your quick detection can lead to swift interventions that save your patient from life-threatening consequences.

Metformin, classified as a biguanide, doesn’t enhance insulin secretion, so it won’t predispose the patient to hypoglycemia or cause the weight gain associated with other glucose-lowering drugs. Metformin lowers blood glucose levels and improves glucose tolerance by decreasing glucose production in the liver and increasing the muscles’ use of insulin. It also decreases intestinal absorption of glucose.Metformin increases the binding of insulin to its cellular receptor sites and decreases the potential for insulin resistance. The drug enhances the uptake of glucose by the muscles and adipose tissue. During the day, especially after lunch, the drug lowers postprandial blood glucose levels. This phenomenon may be attributed to delayed glucose absorption or to the time required for metformin to be absorbed and accumulate in the tissues.

Taking the drug also reduces levels of serum triglycerides, total cholesterol, LDL cholesterol and increases levels of HDL cholesterol.

The initial dose of metformin is 500 mg twice a day, with morning and evening meals. A physiciangradually increases the dose by 500 mg per week until the patient’s fasting blood glucose and glycosylated hemoglobin levels are as close to normal as possible. The total recommended dosage is 2,500 mg per day in three doses. Metformin can be used alone or with sulfonylurea therapy.

Indications and Contraindications

Patients with Type 2 diabetes whose disease can’t be managed satisfactorily by diet and exercise alone take metformin to reduce hyperglycemia. If metformin and diet therapy are ineffective, a physician may add a sulfonylurea.

Before your patient begins metformin therapy, assess her kidney function and verify that her serum creatinine levels are below 1.5 mg/dl to prevent lactic acidosis. If they’re above 1.5 mg/dl, her physician will substitute another drug. Instruct your patient to contact her physician immediately if she experiences difficulty breathing, muscle aches, fatigue, unusual sleepiness, or nonspecific symptoms, which may indicate lactic acidosis.

Metformin is contraindicated for patients with kidney dysfunction, cardiopulmonary disease, infection, hypersensitivity to the drug, or ketosis. Patients undergoing radiologic tests such as excretory urography, angiography, and scans that use parenteral iodinated contrast media shouldn’t receive metformin within 48 hours of the test. The contrast media can predispose a patient to acute kidney failure and an accumulation of metformin in the kidneys, which can lead to lactic acidosis.

A physician should stop metformin therapy before surgery if food and fluid intake is restricted. The patient shouldn’t resume therapy until kidney function has returned to her base­line and she’s eating meals.

Usually, insulin and metformin aren’t used simultaneously. If a patient needs insulin, metform in should be discontinued.

Adverse Effects and Interactions

The most common adverse effects of metformin are GI signs and symptoms such as diarrhea, anorexia, nausea, bloating, and a metallic taste in the mouth. Tell your patient that she can prevent GI irritation by taking metformin with food, which also helps to delay rapid drug absorption. Patients who have difficulty swallowing may crush metformin and mix it with food or liquids. If diarrhea or vomiting is severe, your patient’s physician may stop metformin therapy temporarily.

Patients who don’t get enough vitamin B 12 or calcium may develop asymptomatic vitamin B 12 deficiency when taking metformin because the drug interferes with the absorption of the vitamin. Taking vitamin B 12 supplements or discontinuing metformin therapy rapidly reverses the deficiency.

If your patient is taking a drug for a bacterial infection, angina, thyroid disease, coughing, asthma, a skin condition, or anxiety, it may alter the effects of her metformin therapy. For example, many calcium channel blockers and corticosteroids can decrease the effects of metformin and may seriously undermine blood glucose control.

A chronic disorder, Type 1 diabetes results from a complete or partial lack of insulin. Without insulin, glucose can’t enter the cells. Thus, the cells starve while high levels of glucose remain in the bloodstream. The body, sensing a lack of glucose in the cells, tries to increase its availability by breaking down fat and protein sources and glycogen stores to produce glucose. In another attempt to compensate, the body secretes counterregulatory hormones (glucagon, epinephrine, growth hormone, and cortisol) to increase blood glucose levels. But without insulin, these increases in glucose only contribute further to hyperglycemia.When the amount of glucose filtered by the kidneys surpasses the amount the kidneys can reabsorb, glucose appears in the urine. The glucose acts as an osmotic diuretic, causing the patient to produce increased amounts of urine. Elevated blood glucose levels also increase the osmotic pull of the blood, which causes water to move from the cells in the tissues into the bloodstream. This intracellular dehydration, along with the dehydration caused by increased urination, produces excessive thirst. Because the cells lack the glucose they need for energy, the person is continually hungry.

As the person burns fat and proteins for energy, fatigue and weight loss result. As body fats continue to break down, toxic levels of ketones are produced. Ketones can’t be used efficiently as energy, and as they accumulate in the blood, the pH drops, and metabolic acidosis develops. As the kidneys filter ketones, ketonuria develops. Insulin replacement is necessary to prevent DKA. The signs and symptoms of DKA include nausea, vomiting, electrolyte imbalances, a fruity breath odor, weight loss, and muscle wasting. Without treatment, DKA can progress to coma and death.

After being diagnosed with Type 1 diabetes, many patients experience a remission during which little or no insulin therapy is needed to control blood glucose levels. This honeymoon period can last up to a year, but once it ends, blood glucose levels rise, and insulin requirements increase.

Even when the disease is treated with exogenous insulin, it progresses, producing long-term complications. These complications can be classified as microvascular, macrovascular, and neuropathic. Microvascular complications include retinopathy, which can lead to blindness, and nephropathy, which can lead to renal failure. Macrovascular complications include coronary artery disease, cerebrovascular disease, and peripheral vascular disease. Neuropathies can lead to conditions including impotence and a loss of sensation in the arms and legs. Among patients with Type 1 diabetes, renal disease is the most common cause of death, followed by cardiovascular disease.

After a patient has been diagnosed with diabetes mellitus, a physician determines the type so that treatment can begin. In some cases, a physician can determine the type only after evaluating the patient’s initial response to treatment.

The four types are -

a) Type 1, or insulin-dependent diabetes mellitus.

b) Type 2, or non-insulin-dependent diabetes mellitus.

c) Gestational diabetes mellitus.

d) Diabetes secondary to other medical conditions.

Borderline and chemical diabetes are now called impaired glucose tolerance and aren’t classified as diabetes at all.

For the first 5 to 10 minutes of exercise, the main fuel used by a person without diabetes is stored muscle glycogen. But it can be used only to meet the energy needs of the muscle in which it’s contained. With prolonged exercise, the body uses glycogen from the liver, fat in the form of triglycerides and nonesterified fatty acids (NEFA).

As a person continues to exercise, muscle glycogen stores are depleted. Muscle glycogen depletion stimulates liver gluconeogenesis, which begins the replacement of glycogen stores. This happens in two stages. First, immediately after exercise, cell permeability to glucose increases, and muscle glycogen stores are restored rapidly with no need for insulin. In the second stage, muscle glycogen returns to near-normal levels, glucose uptake decreases, and insulin action increases.

In a person who has diabetes, the body’s use of muscle glycogen, triglycerides, liver glycogen, and NEFA differs. During short-term exercise, the rate of gluconeogenesis rises to two to three times above her baseline. Her liver’s response to brief exercise resembles the response to prolonged exercise in people without diabetes.

In people without diabetes and in those with diabetes who have mildly elevated blood glucose levels, an initial drop in NEFA concentration is followed by a gradual increase as exercise continues. In patients with diabetes who have severe hyperglycemia and ketosis, levels of NEFA are elevated, even at rest. For them, the increase in NEFA during exercise is even greater.

Normally, ketones aren’t a major source of fuel for the muscles. The body of a patient with diabetes who has mild ketosis, however, uses ketones for fuel during exercise.

A minimum amount of insulin is needed for glucose uptake by muscles and for the regulation of gluconeogenesis by the liver. An insulin deficiency triggers the abnormal secretion of counterregulatory hormones, which raise blood glucose levels. If exercise fails to lower high blood glucose levels, hyperglycemia results .

In patients with Type 1 diabetes, hypoglycemia rarely occurs during exercise but can occur up to a day later. Possible causes for late-onset hypoglycemia include glycogen depletion in the liver or muscles from intense or prolonged exercise, increases in insulin sensitivity, the use of glucose to replenish glycogen stores, counterregulatory response defect, and inappropriate adjustments of food intake or insulin therapy.