Diabetes mellitus, type 2

Resulting from a combination of resistance to insulin action and impairment in insulin secretion, producing hyperglycemia and related complications to many systems of the body, including microvascular (retinal andrenal), macrovascular (coronary and peripheral vascular), and neuropathic manifestations
One of the leading causes of morbidity and mortality in the United States, and a contributing factor leading to blindness, renal failure, and lower limb amputations
Long-term medical treatment required to manage as well as limit the development of complications
Remaining ability to secrete some endogenous insulin so that the patient isn’t dependent upon insulin administration, although it may still be needed in treatment
Previously called adult-onset diabetes, but diagnosed in children as young as age 2

Characterized by a combination of peripheral insulin resistance and inadequate insulin secretion by pancreatic beta cells, the results are a progressive loss of beta cell function and mass.
Insulin resistance elevates levels of free fatty acids in plasma, leading to decreased glucose transport into muscle cells, elevated hepatic glucose production, and increased breakdown of fat.
Abnormal glucose tolerance occurs and postprandial blood glucose levels increase; hepatic gluconeogenesis suppression fails and fasting hyperglycemia develops.
Cellular damage occurs in the capillary endothelial cells of the retina, mesangial cells in the renal glomerulus, and the neurons and Schwann cells in peripheral nerves due to the inability of cells to regulate the uptake of glucose.
Insulin resistance, combined with the presence of lipid and thrombotic abnormalities and atherosclerotic risk factors, determines cardiovascular risk; increased cardiovascular risk begins prior to hyperglycemia, possibly because of insulin resistance.
Other types of diabetes (secondary diabetes) are caused by other illnesses or medications, or may be gestational.

Environmental pollutants (long-term exposure to traffic-related pollution)
In utero environment, resulting in low birth weight
Genetics (involvement of multiple genes in pancreatic beta-cell failure and insulin resistance)
Genetic defects (maturity onset diabetes of youth [MODY],which has been reclassified as a variety of defects in beta-cell function); autosomal dominant trait with 6 mutations identified (HNF-4-alpha, glucokinase gene, HNF-1-alpha, IPF-1, HNF-1-beta, NEUROD1)
Genotype susceptibility (increased risk for diabetes with excess weight that varies with different races)
Lifestyle (excessive caloric intake, inadequate caloric expenditure, obesity)
Medical conditions that antagonize the actions of insulin (Cushing syndrome, acromegaly, pheochromocytoma)
Medications (glucocorticoids)

Age greater than 45 years
Dyslipidemia (high-density lipoprotein [HDL] cholesterol level less than 40 mg/dL or triglyceride level greater than 150 mg/dL)
Race and ethnicity (African American, Latino, Native American, Asian American, and Pacific Islander)
Family history of type 2 diabetes in a first-degree relative
History of previous impaired glucose tolerance (IGT) or impaired fasting glucose (IFG)
Hypertension (greater than 140/90 mm Hg)
History of gestational diabetes mellitus or delivering a baby with a birth weight greater than 9 lb
Impaired fasting glucose (IFG) or impaired glucose tolerance (IGT)
Obesity, which induces resistance to insulin-mediated peripheral glucose uptake (especially abdominal obesity)
Polycystic ovarian syndrome, which results in insulin resistance
Sedentary lifestyle
History of prediabetes or gestational diabetes

A 2011 Centers for Disease Control and Prevention (CDC) report estimated that 26 million Americans have diabetes,and an estimated 79 million have prediabetes. Type 2 diabetes affects 8.3% of Americans of all ages and 11.3% of adults ages 20 and older. About 27% of those with diabetes (7 million Americans) don’t know they have the disease.
Worldwide, about 171 million people currently have diabetes, with the largest numbers found in India, China, the United States, Indonesia, Japan, Pakistan, Russia, Brazil, Italy, and Bangladesh. It’s less common in non-Western countries where the diet contains fewer calories and daily caloric expenditure is higher.
Its prevalence varies widely among racial and ethnic groups. It’s more prevalent among Hispanics, Native Americans, African Americans, Asians, and Pacific Islanders than in non-Hispanic whites.
Type 2 diabetes mellitus occurs most commonly in adults at age 40, with prevalence increasing with advancing age.

Atherosclerotic cardiovascular and peripheral vascular disease
Blindness
Cataracts
Charcot joints
Damage of macro- and microvascular arterial cell walls
Gangrene of the extremities
Glaucoma
Hyperosmolar coma
Nephropathy and chronic renal failure
Osteoporosis
Peripheral neuropathy
Proliferative retinopathy
Skin and mouth conditions
Increased risk of Alzheimer’s disease and vascular dementia
Hearing impairment

Polyuria, polydipsia, polyphagia, weight loss, weakness, fatigue, and frequent infections.
Other symptoms suggesting hyperglycemia include blurred vision, lower extremity paresthesias, and yeast and skin infections.
At the time of diagnosis, the typical patient has had diabetes for at least 4 years.
At the time of diagnosis, about 25% have retinopathy, 9% have neuropathy, and 8% have nephropathy.

Complications of hyperglycemia may be revealed on assessment (retinopathy, neuropathy, and poor wound healing).
Vital signs may be useful in assessing volume status and detecting the presence of autonomic neuropathy as well as other complications; for example, Kussmaul respirations may be present in DKA.
Fundoscopic examination may reveal the presence of hemorrhages or exudates.
Monitoring of the dorsalis pedis and posterior tibialis pulses may detect poor lower-extremity blood flow, which can delay healing and increase the risk of amputation.
Lower-extremity sensory neuropathy assessment may reveal decreased sensation with foot ulceration.

Fasting plasma glucose (FPG) level of 126 mg/dL (7.0 mmol/L) or higher on 2 occasions is diagnostic; 100 to 125mg/dL is considered prediabetes.
Random glucose level of 200 mg/dL (11.1 mmol/L) or higher and classic symptoms of diabetes mellitus (such as polyuria, polydipsia, polyphagia, and weight loss) indicates diabetes; 140 to 199 mg/dL 2 hours after ingestion of 75g of glucose is considered prediabetes.
HbA1C level of 6.5% or greater confirms the diagnosis; HbA1c between 5.7% and 6.4% is prediabetes.
A 2-hour oral glucose tolerance test (OGTT) value of 200 mg/dL or higher confirms the diagnosis, but is reserved for gestational diabetes mellitus or impaired glucose tolerance (IGT); a glucose tolerance test (GTT) may be used to diagnose gestational diabetes.
Normal urine albumin excretion is less than 30 mg/dL; microalbuminuria is 30 to 300 mg/dL(20 to 200 mcg/min) and is a common finding as well as a risk factor for macrovascular (especially coronary) disease and a weaker predictor for future kidney disease in type 2 diabetes.
A fasting C-peptide level more than 1 ng/dL in those with diabetes for more than 1 to 2 years suggests type 2 diabetes (residual beta-cell function); absence of a C-peptide response to carbohydrate ingestion may indicate total beta-cell failure.
Antibodies to insulin, islet cells, or glutamic acid decarboxylase (GAD) are absent in type 2 diabetes mellitus.

Ideally, blood glucose maintained at near-normal levels (preprandial levels of 90 to 130 mg/dL)or goal fasting plasma glucose (FPG)less than 110 mg/dL (5.5 mmol/L)and hemoglobin A1C [HbA1c] levels less than 7%, if possible, as recommended by the American College of Physicians (ACP) (ADA endorses less than 7.5%; American Association of Clinical Endocrinologists and the International Diabetes Federation recommend a glycemic target of HbA1c less than 6.5%.)
Blood sugar control using medications from different classes; possible addition of insulin if uncontrolled by oral agents
Goal of eliminating symptoms and preventing or slowing the development of complications
Metabolic and neurologic risk reduction through control of glycemia
Microvascular (eye and kidney disease) risk reduction through control of glycemia and blood pressure (BP); possibly strict control of hypertension (goal BP less than 130/80 mm Hg), if necessary
Macrovascular (coronary, cerebrovascular, peripheral vascular) risk reduction through control of lipids and hypertension, smoking cessation, and aspirin therapy
Low-density lipoprotein cholesterol goal of less than 70 mg/dL recommended in patients with cardiovascular disease or risk factors for cardiovascular disease
Dietary and exercise modifications
Appropriate self-monitoring of blood glucose
Regular monitoring for complications and laboratory assessment
Foot examination at every visit for neuropathy (monofilament), arterial insufficiency, and ulcers
Urine analysis to check microalbumin yearly and detect nephropathy
Yearly eye examinations to determine the extent of retinopathy
Low-dose aspirin recommended for all adults with diabetes, unless there is a contraindication

Mild caloric restriction suggested by the ADA to achieve mild to moderate weight loss, with carbohydrates consisting of less than 45% to 65% of caloric consumption per day, fat at less than 30%, protein at less than 15%, and fiber at 50 g/day, taking into account dietary preferences
Emphasis on intake of fruits, vegetables, and fiber
Increase in risk factor reduction with losses of 10% to 15% of body weight

Increased activity of the patient’s choice, with aerobic exercise to improve insulin sensitivity and possibly glycemia, markedly in some patients
Greater HbA1c reduction from structured exercise training (more than 150 minutes per week) when combined with dietary modifications
Slow start to activities in sedentary patients
Cardiovascular evaluation for older patients and those with longstanding disease, multiple risk factors, or previous atherosclerotic disease prior to beginning a significant exercise regimen

Sulfonylureas, such as glyburide (Micronase, DiaBeta, Glynase), glipizide (Glucotrol, Glucotrol XL), and glimepiride (Amaryl), which are insulin secretagogues that stimulate insulin release from pancreatic beta cells
Meglitinides, such as repaglinide (Prandin) and nateglinide (Starlix)], which are short-acting insulin secretagogues that work by stimulating insulin release from pancreatic beta cells, with nateglinide mimicking endogenous insulin patterns
Biguanides, such as metformin (Glucophage),to reduce hepatic glucose production and utilization and increase peripheral insulin sensitivity
Alpha-glucosidase inhibitors, such as acarbose (Precose) and miglitol (Glyset),to delay absorption of carbohydrates and help prevent postprandial glucose surges
Pioglitazone (Actos) to reduce insulin resistance (acting as an insulin sensitizer) in the periphery (sensitizing muscle and fat to the actions of insulin) and, to a small degree, in the liver; decrease triglycerides; and help with inflammation and the vasculature
Incretin-mimetic agents (administered by injection), such asexenatide (Byetta, Bydureon) and liraglutide (Victoza), which mimic incretin, a glucagonlike peptide-1 (GLP-1), to stimulate glucose-dependent insulin release, reduce glucagon, and slow gastric emptying
Dipeptidyl peptidase IV (DPP-4) inhibitors, such assitagliptin (Januvia), saxagliptin (Onglyza), and linagliptin (Tradjenta), to prolong action of incretin hormones, degrade numerous biologically active peptides (endogenous incretins GLP-1 and GIP), and significantly increase beta cell secretory capacity (vildagliptin)
Insulins, including rapid (Aspart, Lispro, Glulisine), short (regular insulin), intermediate (NPH), long/peakless (Glargine), and long/peak (Detemir), with individualized therapy and possibly in combination with oral agents due to the variability of insulin resistance from patient to patient
Amylin analogs, such as pramlintide acetate (Symlin), which mimic endogenous amylin effects by delaying gastric emptying, decreasing postprandial glucagon release, and affecting appetite through centrally mediated appetite modulation
Leptin (metreleptin), which marginally reduces HbA1c levels in obese patients
Bile acid sequestrant, such as colesevelam (WelChol), which is an adjunct to diet and exercise to improve glycemic control, to reduce LDL cholesterol in patients with prediabetes (but to be avoided in patients with hypertriglyceridemia)

Activity intolerance
Deficient fluid volume
Deficient knowledge: Disease process
Deficient knowledge: Treatment
Disabled family coping
Imbalanced nutrition: Less than body requirements
Imbalanced nutrition: More than body requirements
Impaired skin integrity
Impaired urinary elimination
Ineffective health maintenance
Ineffective peripheral tissue perfusion
Risk for decreased cardiac perfusion
Risk for electrolyte imbalance
Risk for ineffective renal perfusion
Risk for infection
Risk for peripheral neurovascular dysfunction
Risk for unstable glucose level

perform activities of daily living without excessive fatigue or exhaustion
demonstrate stable vital signs and normal laboratory values
verbalize an understanding of the disease process
comply with the treatment regimen
exhibit adequate coping skills
maintain adequate nutritional intake
achieve an appropriate body weight
demonstrate intact skin integrity
achieve and maintain balanced fluid intake and output
identify and alter actions that are detrimental to his health
demonstrate adequate peripheral tissue perfusion
maintain an adequate cardiac output and hemodynamic stability
verbalize an understanding of causative factors of electrolyte imbalance and demonstrate behaviors to correct the deficit, as appropriate
achieve and maintain adequate renal perfusion and functioning
state actions that will decrease the risk of infection
alter behavior that increases the risk of neurovascular dysfunction
maintain appropriate glucose levels.

Assess vital signs and level of consciousness frequently; monitor for signs of dehydration and complications of hyperglycemia.
Assess oxygenation status and anticipate the need for intervention.
Assess for signs of fluid and electrolyte imbalances.
Monitor for arrhythmias and assess for an underlying cardiac condition.
Administer prescribed medications; assess the I.V. insertion site and ensure I.V. patency.
Organize patient care and activities to provide uninterrupted rest.
Provide a prescribed diet to meet nutritional needs and maintain blood glucose levels.
Provide skin care, as indicated.
Provide emotional support, and help reduce stress and anxiety.

Vital signs, cardiac monitoring
Peripheral pulses
Neurologic status
Bedside glucose levels and laboratory test results
Culture and sensitivity reports
Intake and output
Energy level; activity tolerance
Daily weight

Assessment techniques
Blood culture sample collection
Blood glucose monitoring
Blood pressure assessment
Calculating and setting an IV drip rate
Cardiac monitoring
Indwelling urinary catheter (Foley) care and management
IV bag preparation
IV bottle preparation, nonvented
IV bolus injection
IV catheter insertion
IV catheter removal
IV dressing change
IV pump use
IV solution change
IV time tape use
IV tubing change
IV volume-control set preparation
Oxygen administration
Pulse assessment
Pulse oximetry
Respiration assessment
Subcutaneous injection
Temperature assessment
Urine glucose and ketone tests
Urine pH

disease process, management, goals, lifestyle modification, and long-term complications
signs and symptoms of hypoglycemia and ways to manage it
treatment plan, including laboratory tests, examinations (foot, neurologic, ophthalmological, cardiac), and referrals to specialists, as indicated
specific diet control education to the patient and family
need for regular exercise and weight reduction or maintenance, as indicated
how to administer self—insulin injection, perform fingersticks for blood glucose level monitoring, and store and use insulin properly
how and when to test plasma glucose (daily before meals, in some cases 1 to 2 hours after meals, and at bedtime)
signs and causes of hyperglycemia and the prescribed treatment
need to examine feet regularly
causes and signs of hypoglycemia, how to avoid hypoglycemia, and the treatment required if it occurs as well as the need to carry candy or sugar cubes
signs and symptoms of infections and the need for close glucose monitoring and insulin adjustment during periods of medical illness and surgery
drug dosages, adverse reactions, and signs of toxicity to watch for
medications that may affect glucose level
prevention of infection (appropriate immunizations, avoiding crowds in flu season)
need for exercise and weight control.

Refer the patient to a diabetic education program and consultation with a dietitian for nutritional counseling.
Refer the patient to a smoking-cessation program, if needed.
Refer the patient to a weight-reduction program, if needed.