Chapter 49 Diabetes Mellitus

Hypoglycemia

(Moist) Hunger Sweating Pallor Tremor Palpitations Lightheadedness Tremors Headache Clammy Lethargy

Hyperglycemia

(dry) Polyuria Polydipsia Polyphagia Fruity/acetone breath Dry Restlessness

Dawn Phenomenon

- characterized by hyperglycemia present on awaking. Possible growth hormone and cortisol excreted in increased amounts in the early morning hours. Adolescence and young adulthood. Treatment in an increase in insulin or adjustment in administration time. Check the blood sugar during the night.

Somogyi effect

- hyperglycemia in the am. High dose of insulin makes a decline in blood glucose levels during the night. Counter regulatory hormones (glucagon, epinephrine, growth hormone, and cortisol) are released. This results in rebound hyperglycemia. So the health care professional may increase the dose due to the hyperglycemia unknowingly. Treatment is less insulin.

Chronic Complications of DM

Angiopathy is one of the leading causes of diabetes-related deaths. Macrovascular large and medium size vessels - Younger person was when DM developed the greater the risk. CVD women with DM have 4 - 6 X greater risk. Men 2 to 3 times. Decrease the risk stop smoking, control HTN, obesity, high fat intake, exercise. Microvascular - eyes, kidneys, skin most notable. Type 2 may have these at time of diagnosis; thickening of vessel membranes in capillaries and arterioles. Retinopathy - microvascular complication - need dilated eye exams - laser photocoagulation - drugs injected into the eye vascular block endothelial growth factor. Nephropathy - microvascular complication - leading cause of ESKD, 20 to 40% diabetics have it. Screened annually random spot urine for albuminuria and measure albumin to creatinine ratio. ACE inhibitor (angiotensin-converting enzyme) (prils). Or angiotensin II receptor antagonists (losartan, Cozaar). Neuropathy - Nerve damage due to metabolic derangement. 60 to 70% have some degree. Most common is sensory which is mainly treated by controlling glucose also meds (capsaicin, tricyclic antidepressants, selective serotonin and norepinephrine reuptake inhibitors (duloxetine) anti-seizure medications (gabapentin) Autonomic neuropathy affect all body systems, lead to hypoglycemic unawareness, bowel incontinence and diarrhea, nausea, vomiting, gastroesophageal reflux, gastroparesis can trigger hypoglycemia by delaying food absorption. ED in men, decreased libido in women. Neurogenic bladder

Pre diabetes

Asymptomatic but long-term damage already occurring Patient teaching important Undergo regular screening Manage risk factors Lifestyle changes Monitor for symptoms of diabetes Maintain healthy weight, exercise, healthy diet

DM etiology

Autoimmune Beta cells destroyed Require exogenous insulin May experience a 'honeymoon' period Prone to develop ketoacidosis when blood glucose is elevated Rapid onset Genetic predisposition Idiopathic diabetes Hispanic, African, or Asian ancestry Autoimmune destruction of beta cells. There is inadequate insulin production and requires insulin to survive. The patient with type 1 diabetes is more prone to develop ketoacidosis with elevated blood glucose levels. Genetic predisposition.

Chronic Complications of DM continued

Complications of Feet and Lower Extremities Sensory neuropathy and PAD Teach foot care Integumentary complications Psychologic considerations Disordered eating behaviors - anorexia, bulimia, binge eating, restriction of calories, intense exercise; decrease insulin to cause weight loss. Depression, anxiety

4 genetic factors for DM

Four major metabolic abnormalities have a role in the development of type 2 diabetes (see Fig. 49-2). The first factor is insulin resistance, a condition in which body tissues do not respond to the action of insulin because insulin receptors are unresponsive, are insufficient in number, or both. Most insulin receptors are located on skeletal muscle, fat, and liver cells. When insulin is not properly used, the entry of glucose into the cell is impeded, resulting in hyperglycemia. In the early stages of insulin resistance, the pancreas responds to high blood glucose by producing greater amounts of insulin (if β-cell function is normal). This creates a temporary state of hyperinsulinemia that coexists with hyperglycemia. A second factor in the development of type 2 diabetes is a marked decrease in the pancreas's ability to produce insulin, as the β cells become fatigued from the compensatory overproduction of insulin or when β-cell mass is lost. The underlying basis for the failure of β cells to adapt is unknown. It may be linked to the adverse effects of chronic hyperglycemia or high circulating free fatty acids. A third factor is inappropriate glucose production by the liver. Instead of properly regulating the release of glucose in response to blood levels, the liver does so in a haphazard way that does not correspond to the body's needs at the time. A fourth factor is altered production of hormones and cytokines by adipose tissue (adipokines). Adipokines secreted by adipose tissue appear to play a role in glucose and fat metabolism and are likely to contribute to the pathophysiology of type 2 diabetes. 5 Adipokines are thought to cause chronic inflammation, a factor involved in insulin resistance, type 2 diabetes, and cardiovascular disease (CVD). The two main adipokines believed to affect insulin sensitivity are adiponectin and leptin.

Normal Insulin Metabolism

Insulin is a hormone produced by the β cells in the islets of Langerhans of the pancreas. Under normal conditions, insulin is continuously released into the bloodstream in small pulsatile increments, with increased release when food is ingested (Fig. 49-1). Insulin lowers blood glucose and facilitates a stable, normal glucose range of approximately 70 to 120 mg/dL (3.9 to 6.66 mmol/L). The average amount of insulin secreted daily by an adult is approximately 40 to 50 U, or 0.6 U/kg of body weight. Insulin promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell. The rise in plasma insulin after a meal stimulates storage of glucose as glycogen in liver and muscle, inhibits gluconeogenesis, enhances fat deposition of adipose tissue, and increases protein synthesis. For this reason insulin is an anabolic, or storage, hormone. The fall in insulin level during normal overnight fasting facilitates the release of stored glucose from the liver, protein from muscle, and fat from adipose tissue. Skeletal muscle and adipose tissue have specific receptors for insulin and are considered insulin-dependent tissues. Insulin is required to "unlock" these receptor sites, allowing the transport of glucose into the cells to be used for energy. Other tissues (e.g., brain, liver, blood cells) do not directly depend on insulin for glucose transport but require an adequate glucose supply for normal function. Although liver cells are not considered insulindependent tissue, insulin receptor sites on the liver facilitate hepatic uptake of glucose and its conversion to glycogen. Other hormones (glucagon, epinephrine, growth hormone, and cortisol) work to oppose the effects of insulin and are referred to as counterregulatory hormones. These hormones increase blood glucose levels by stimulating glucose production and output by the liver and by decreasing the movement of glucose into the cells. The counterregulatory hormones and insulin usually maintain blood glucose levels within the normal range by regulating the release of glucose for energy during food intake and periods of fasting.

DM type 1 continued

Low incidence Must have insulin to survive Usually < 40 Occurring more frequently in younger children Normal or low body weight Classic symptoms Polyuria Polydipsia Polyphagia Once known as juvenile-onset diabetes, or IDDM. 5% of those with DM are type 1. The patient with type 1 diabetes is usually young, under 40 and 40% develop under 20, thin. There is inadequate insulin production and requires insulin to survive.

DM type 2 continued

Most prevalent Risk factors Overweight or Obese Age of and client is usually >40 Family history Ethnic populations Type 2 also know as adult onset or NIDDM. Accounts for 90 to 95% of patients with diabetes Body type - obese or overweight - this is the most important factor especially abdominal and visceral adiposity. (produce cytokines) Age of onset is usually >40, incidence is increasing in children. Risk factors include family history of T2DM African Americans, Native Americans, Asian Americans, Hispanics, Native Hawaiians or other Pacific Islanders have higher incidence than white

Type 1 DM

Type 1 diabetes mellitus, formerly known as juvenile-onset diabetes or insulin-dependent diabetes, accounts for approximately 5% of all people with diabetes. Type 1 diabetes generally affects people under 40 years of age, and 40% develop it before 20 years of age. The incidence of type 1 diabetes has increased 3% to 5% over recent decades, and for unknown reasons it is occurring more frequently in younger children. 3 Etiology and Pathophysiology. Type 1 diabetes is an immunemediated disease, caused by autoimmune destruction of the pancreatic β cells, the site of insulin production. This eventually results in a total absence of insulin production. Autoantibodies to the islet cells cause a reduction of 80% to 90% of normal function before hyperglycemia and other manifestations occur (Fig. 49-2). A genetic predisposition and exposure to a virus are factors that may contribute to the pathogenesis of immunerelated type 1 diabetes..

Type 2 DM

Type 2 diabetes mellitus was formerly known as adult-onset diabetes (AODM) or non-insulindependent diabetes (NIDDM). Type 2 diabetes mellitus is, by far, the most prevalent type of diabetes, accounting for approximately 90% to 95% of patients with diabetes. 2 Risk factors for developing type 2 diabetes include being overweight or obese, being older, and having a family history of type 2 diabetes. Although the disease is seen less frequently in children, the incidence is increasing due to the increasing prevalence of childhood obesity. Type 2 diabetes is more prevalent in some ethnic populations. African Americans, Asian Americans, Hispanics, Native Hawaiians or other Pacific Islanders, and Native Americans have a higher rate of type 2 diabetes than whites. 4 Etiology and Pathophysiology. In type 2 diabetes the pancreas usually continues to produce some endogenous (self-made) insulin. However, the insulin that is produced is either insufficient for the needs of the body or is poorly used by the tissues, or both. The presence of endogenous insulin is a major distinction between type 1 and type 2 diabetes. (In type 1 diabetes, there is an absence of endogenous insulin.) Many factors contribute to the development of type 2 diabetes. The most powerful risk factor is obesity, especially abdominal and visceral adiposity.

DM

is a chronic multisystem disease related to abnormal insulin production, impaired insulin utilization, or both. Diabetes mellitus is a serious health problem throughout the world, and its prevalence is rapidly increasing. Currently in the United States an estimated 25.8 million people, or 8.3% of the population, have diabetes mellitus, and 79 million more people have prediabetes.