Ch. 48 Textbook Notes

Diabetes Diagnotics (powerpoint : part 1)

Fasting plasma glucose (FPG) Normal: 100 or less Prediabetes: 100-126 Diabetes: > 126 - two separate tests under similar circumstances Two-hour plasma glucose level > 200 Oral Glucose Tolerance Test (OGTT) Normal 2 Hr Post Prandial:- < 140/mg/dL Impaired Glucose Tolerance Test (IGT) : 141 mg - 199 mg/dL Diabetes diagnosis > 200 mg/dL Glycosolated Hemoglobin A1c Normal A1c 4-6 % Greater than 6.5% diagnostic for diabetes 5.7 - 6.4% Pre-diabetes

hypoglycemia Tx

Follow the "Rule of 15" to treat hypoglycemia. A blood glucose less than 70 mg/dL is treated by ingesting 15 g of a simple (fast-acting) carbohydrate, such as 4 to 6 oz of fruit juice or a regular soft drink. Commercial products such as gels or tablets containing specific amounts of glucose are convenient for carrying in a purse or pocket to be used in such situations. Recheck the blood glucose 15 minutes later. If the value is still 1147less than 70 mg/dL, ingest 15 g more of carbohydrate and recheck the blood glucose in 15 minutes. If no significant improvement occurs after two or three doses of 15 g of simple carbohydrate, contact the HCP. After an acute episode of hypoglycemia, have the patient ingest a complex carbohydrate after recovery to prevent repeat hypoglycemia.

Factors that can falsely elevate values of diabetes diagnostic tests

For example, factors that can falsely elevate values include recent severe restrictions of dietary carbohydrate, acute illness, medications (e.g., contraceptives, corticosteroids), and restricted activity such as bed rest. A patient with impaired gastrointestinal absorption or one who has recently taken acetaminophen may have false-negative results

Type 2 Diabetes ( formerly known as adult-onset diabetes (AODM) or non-insulin-dependent diabetes (NIDDM).)

Type 2 diabetes is, by far, the most prevalent type of diabetes, accounting for approximately 90% to 95% of patients with diabetes. Many risk factors contribute to the development of type 2 diabetes, including 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. Type 2 diabetes is characterized by a combination of inadequate insulin secretion and insulin resistance. The pancreas usually produces some endogenous (self-made) insulin. However, the body either does not produce enough insulin or does not use it effectively, 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.)

intermediate acting NPH (Humulin N, Novolin N)

onset: 1.5 to 4 hour peak:4-12 hr duration:12-18 hour

inhaled insulin (Afrezza)

onset: 12-15 min peak:60 min duration:2.5-3 hour

Self-monitoring of blood glucose

recommendation for patients who use multiple insulin injections or insulin pumps is to monitor their blood glucose four or more times each day. Patients using less frequent insulin injections, noninsulin therapy, or nutrition management will monitor as often as needed to achieve their glycemic goals

Lipodystrophy

(atrophy or hypertrophy of subcutaneous tissue) may occur if the same injection sites are used frequently. The use of human insulin has significantly reduced the risk for lipodystrophy. Atrophy is the wasting of subcutaneous tissue and presents as indentations in injection sites. Hypertrophy, a thickening of the subcutaneous tissue, eventually regresses if the patient does not use the site for at least 6 months. The use of hypertrophied sites may result in erratic insulin absorption.

DKA Tx

. Because fluid imbalance is potentially life threatening, the initial goal of therapy is to establish IV access and begin fluid and electrolyte replacement. Typically, an infusion of 0.45% or 0.9% NaCl at a rate to restore urine output to 30 to 60 mL/hr and to raise BP constitutes the initial fluid therapy regimen. When blood glucose levels approach 250 mg/dL (13.9 mmol/L), add 5% to 10% dextrose to the fluid regimen to prevent hypoglycemia and a sudden drop in glucose that can be associated with cerebral edema. Overzealous rehydration, especially with hypotonic IV solutions, can result in cerebral edema. Obtain a serum potassium level before starting insulin. If the patient is hypokalemic, insulin administration will further decrease the potassium levels, making early potassium replacement essential. Although initial serum potassium may be normal or high, levels can rapidly decrease once therapy starts as insulin drives potassium into the cells, leading to life-threatening hypokalemia. IV insulin administration therapy is directed toward correcting hyperglycemia and hyperketonemia. Insulin is immediately started at 0.1 U/kg/hr by a continuous infusion. It is important to prevent rapid drops in serum glucose to avoid cerebral edema. A blood glucose reduction of 36 to 54 mg/dL/hr (2 to 3 mmol/L/hr) will avoid complications. Insulin allows water and potassium to enter the cell along with glucose and can lead 1145to a depletion of vascular volume and hypokalemia, so monitor the patient's fluid balance and potassium levels.

4 DIagnostic studies to diagnose diabetes

1. A1C of 6.5% or higher. 2. Fasting plasma glucose (FPG) level greater than or equal to 126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 hours. 3. Two-hour plasma glucose level greater than or equal to 200 mg/dL (11.1 mmol/L) during an OGTT, using a glucose load of 75 g. 4. In a patient with classic symptoms of hyperglycemia (polyuria, polydipsia, unexplained weight loss) or hyperglycemic crisis, a random plasma glucose greater than or equal to 200 mg/dL (11.1 mmol/L). If a patient is seen with a hyperglycemic crisis or clear symptoms of hyperglycemia (polyuria, polydipsia, polyphagia) with a random plasma glucose greater than or equal to 200 mg/dL, repeat testing is not warranted. Otherwise, criteria 1 through 3 should be confirmed by repeat testing to rule out laboratory error. It is preferable for the repeat test to be the same test used initially. For example, if a random blood glucose test showed an elevated blood glucose, that same test should be used again when the person is retested

Somogyi effect

A high dose of insulin produces a decline in blood glucose levels during the night. As a result, counterregulatory hormones (e.g., glucagon, epinephrine, growth hormone, cortisol) are released, stimulating lipolysis, gluconeogenesis, and glycogenolysis, which in turn produce rebound hyperglycemia. The danger of this effect is that when blood glucose levels are measured in the morning, hyperglycemia is apparent and the patient (or the HCP) may increase the insulin dose. If a patient is experiencing morning hyperglycemia, checking blood glucose levels between 2:00 and 4:00 AM for hypoglycemia will help determine if the cause is the Somogyi effect. The patient may report headaches on awakening and recall having night sweats or nightmares. A bedtime snack, a reduction in the dose of insulin, or both can help to prevent the Somogyi effect.

infection and diabetes

A person with diabetes is more susceptible to infections because of a defect in the mobilization of white blood cells and an impaired phagocytosis by neutrophils and monocytes. Recurring or persistent infections such as Candida albicans, as well as boils and furuncles, in the undiagnosed patient often lead the HCP to suspect diabetes. Loss of sensation (neuropathy) may delay the detection of an infection. Persistent glycosuria may predispose patients to bladder infections, especially patients with a neurogenic bladder. Decreased circulation resulting from angiopathy can prevent or delay the immune response. Antibiotic therapy has prevented infection from being a major cause of death in patients with diabetes. The 1152treatment of infections must be prompt and vigorous. Teach patients to prevent infection by practicing good hand hygiene, avoiding exposure to individuals who have a communicable illness, and getting an annual influenza vaccine and pneumococcal vaccine

A1C measures

A1c measures the amount of hemoglobin that has glucose attached to it compared to the total hemoglobin A1c of 7 means that 7% of the total hemoglobin has glucose attached to it.

Acanthosis nigricans

Acanthosis nigricans is a manifestation of insulin resistance. It can appear as a velvety light brown to black skin thickening, predominantly seen on flexures, axillae, and the neck

Sodium-Glucose Co-Transporter 2 (SGLT2) Inhibitors:canagliflozin (Invokana) dapagliflozin (Farxiga) empagliflozin (Jardiance)

Action: Decreases renal glucose reabsorption and increases urinary glucose excretion Side effect:Increased risk of genital and urinary tract infections. Hypoglycemia. *work by blocking the reabsorption of glucose by the kidney, increasing glucose excretion, and lowering blood glucose levels. Drugs in this class include canagliflozin (Invokana), dapagliflozin (Farxiga), and empagliflozin (Jardiance).

Dopamine Receptor Agonists:bromocriptine (Cycloset)

Action:Activates dopamine receptors in central nervous system. Unknown how it improves glycemic levels. Side effects:Orthostatic hypotension. *Bromocriptine (Cycloset) is a dopamine receptor agonist that improves glycemic levels. The mechanism of action is unknown. Patients with type 2 diabetes are thought to have low levels of dopamine activity in the morning. These low levels of dopamine may interfere with the body's ability to control blood glucose. Bromocriptine increases dopamine receptor activity. It can be used alone or as an add-on to another type 2 diabetes treatment.

Dipeptidyl Peptidase-4 (DPP-4) Inhibitors:linagliptin (Tradjenta) saxagliptin (Onglyza) sitagliptin (Januvia) alogliptin (Nesina)

Action:Enhance activity of incretins. Stimulate release of insulin from pancreatic β-cells. Decrease hepatic glucose production. Side effects:pancreatitis, allergic reactions *DPP-4 inhibitors block the action of the DPP-4 enzyme, which is responsible for inactivating incretin hormones (gastric inhibitory peptide [GIP] and glucagon-like peptide-1 [GLP-1]). The result is an increase in insulin release, decrease in glucagon secretion, 1132and decrease in hepatic glucose production. Since the DPP-4 inhibitors are glucose dependent, they lower the potential for hypoglycemia. The main benefit of these drugs over other medications for diabetes with similar effects is the absence of weight gain as a side effect.

Thiazolidinediones:pioglitazone (Actos) rosiglitazone (Avandia)

Action:Increase glucose uptake in muscle. Decrease endogenous glucose production Side effects:Weight gain, edema. pioglitazone: may increase risk for bladder cancer and exacerbate heart failure. rosiglitazone: may increase risk for cardiovascular events (e.g., myocardial infarction, stroke). -insulin sensitizers * They are most effective for people who have insulin resistance. These agents improve insulin sensitivity, transport, and utilization at target tissues. Because they do not increase insulin production, thiazolidinediones do not cause hypoglycemia when used alone. However, these drugs are rarely used today because of their adverse effects. Rosiglitazone is associated with adverse cardiovascular events (e.g., myocardial infarction) and can be obtained only through restricted access programs. Pioglitazone can worsen heart failure and is associated with an increased risk of bladder cancer.

Meglitinides:nateglinide (Starlix) repaglinide (Prandin)

Actions: Stimulate a rapid and short-lived release of insulin from the pancreas. Side effects: weight gain, hypo glycemia * increase insulin production by the pancreas. However, because they are more rapidly absorbed and eliminated than sulfonylureas, they are less likely to cause hypoglycemia. When they are taken just before meals, pancreatic insulin production increases during and after the meal, mimicking the normal response to eating. Instruct patients to take meglitinides any time from 30 minutes before each meal right up to the time of the meal. These drugs should not be taken if a meal is skipped.

Biguanides: metformin (Glucophage, Glucophage XR, Riomet, Fortamet, Glumetza)

Actions:Decreases rate of hepatic glucose production. Augments glucose uptake by tissues, especially muscles. Side effects:Diarrhea, lactic acidosis. Must be held 1-2 days before IV contrast media given and for 48 hr after. *The most widely used oral diabetes agent is metformin, the only medication in the biguanide class available in the United States. Metformin is the most effective first-line treatment for type 2 diabetes *The primary action of metformin is to reduce glucose production by the liver. It also enhances insulin sensitivity at the tissue level and improves glucose transport into the cells. Additionally, it has beneficial effects on plasma lipids. it may cause moderate weight loss, metformin may be useful for people with type 2 diabetes and prediabetes who are overweight or obese. It is also used in the prevention of type 2 diabetes in those with prediabetes who are less than age 60 and have risk factors such as hypertension or a history of gestational diabetes. Patients who are undergoing surgery or any radiologic procedures that involve the use of a contrast medium are instructed to temporarily discontinue metformin before surgery or the procedure. They should not resume the metformin until 48 hours afterward, once their serum creatinine has been checked and is normal. imageDrug Alert

α-Glucosidase Inhibitors: acarbose (Precose) miglitol (Glyset)

Actions:Delay absorption of complex carbohydrates (starches) from GI tract. Side effects:Gas, abdominal pain, diarrhea. * slowing down the absorption of carbohydrate in the small intestine. Acarbose (Precose) and miglitol (Glyset) are the available drugs in this class. Taken with the first bite of each main meal, they are most effective in lowering postprandial blood glucose. Their effectiveness is measured by checking 2-hour postprandial glucose levels. *known as "starch blockers"

Sulfonylureas: glipizide (Glucotrol, Glucotrol XL) glyburide (DiaBeta, Glynase) glimepiride (Amaryl)

Actions:Stimulate release of insulin from pancreatic islets. Decrease glycogenolysis and gluconeogenesis. Enhance cellular sensitivity to insulin. Side effects: weight gain, hypoglycemia *The primary action of the sulfonylureas is to increase insulin production by the pancreas. Therefore hypoglycemia is the major side effect with sulfonylureas.

Type 1 Diabetes clinical manifestations

Because the onset of type 1 diabetes is rapid, the initial manifestations are usually acute. The classic symptoms are polyuria, polydipsia, and polyphagia. The osmotic effect of glucose produces the manifestations of polydipsia and polyuria. Polyphagia is a consequence of cellular malnourishment when insulin deficiency prevents utilization of glucose for energy. Weight loss may occur because the body cannot get glucose and turns to other energy sources, such as fat and protein. Weakness and fatigue may result because body cells lack needed energy from glucose. Ketoacidosis, a complication most common in those with untreated type 1 diabetes

autonomic neuropathy

Autonomic neuropathy can affect nearly all body systems and lead to hypoglycemia unawareness, bowel incontinence and diarrhea, and urinary retention. Gastroparesis (delayed gastric emptying) is a complication of autonomic neuropathy that can produce anorexia, nausea, vomiting, gastroesophageal reflux, and persistent feelings of fullness. Gastroparesis can trigger hypoglycemia by delaying food absorption. Cardiovascular abnormalities associated with autonomic neuropathy are postural hypotension, resting tachycardia, and painless myocardial infarction. Assess patients with diabetes for postural hypotension to determine if they are at risk for falls. Instruct the patient with postural hypotension to change from a lying or sitting position slowly

Acute illness/ surgery and diabetes

Both emotional and physical stress can increase the blood glucose level and result in hyperglycemia. Because stress is unavoidable, certain situations may require more intense treatment, such as extra insulin and more frequent blood glucose monitoring, to maintain glycemic goals and avoid hyperglycemia. Acute illness, injury, and surgery are situations that may evoke a counterregulatory hormone response, resulting in hyperglycemia. Even common illnesses such as a viral upper respiratory tract infection or the flu can cause this response. Encourage patients with diabetes to check blood glucose at least every 4 hours during times of illness. Acutely ill patients with type 1 diabetes with a blood glucose greater than 240 mg/dL (13.3 mmol/L) should also check urine for ketones every 3 to 4 hours. Teach patients to report to the HCP when glucose levels are over 300 mg/dL twice in a row or urine ketone levels are moderate to high. A patient with type 1 diabetes may need an increase in insulin to prevent DKA. Elevated blood glucose levels can lead to poor healing and infection. Insulin therapy may be required for a patient with type 2 diabetes to prevent or treat hyperglycemia symptoms and avoid an acute hyperglycemia emergency. In critically ill patients, insulin therapy may be started if the blood glucose is persistently greater than 180 mg/dL. These patients have a higher targeted blood glucose goal, which is usually 140 to 180 mg/dL. Food intake is important during times of stress and illness, when the body requires extra energy. If patients are able to eat normally, they can continue with their regular meal plan while increasing the intake of noncaloric fluids, such as water, sugar-free gelatin, and other decaffeinated beverages, and continue taking OAs, noninsulin injectable agents, and insulin as prescribed. When illness causes patients to eat less than normal, they can continue to take OAs, noninsulin injectable agents, and/or insulin as prescribed while supplementing food intake with carbohydrate-containing fluids. Examples include low-sodium soups, juices, and regular, sugar-sweetened decaffeinated soft drinks. It is important to tell the patient to contact an HCP if he or she is unable to keep down food or fluid. During the intraoperative period, adjustments in the diabetes regimen can be planned to ensure safe and healthy blood glucose levels. The patient is given IV fluids and insulin (if needed) immediately before, during, and after surgery when there is no oral intake. Explain to the patient with type 2 diabetes who has been on OAs that this is a temporary measure, not a sign of worsening diabetes. When caring for an unconscious surgical patient receiving insulin, be alert for signs of hypoglycemia such as sweating, tachycardia, and tremors. Frequent monitoring of blood glucose can prevent episodes of severe hypoglycemia.

causes of hypoglycemia

Causes of hypoglycemia are often related to a mismatch in the timing of food intake and the peak action of insulin or oral hypoglycemic agents that increase endogenous insulin secretion. The balance between blood glucose and insulin can be disrupted by administering too much insulin or medication, ingesting too little food, delaying the time of eating, and performing unusual amounts of exercise. Hypoglycemia can occur at any time, but most episodes occur when the OA or insulin is at its peak of action or when the patient's daily routine is disrupted without adequate adjustments in diet, medications, and activity. Although hypoglycemia is more common with insulin therapy, it can occur with noninsulin injectable agents and OAs, and it may be severe and persist for an extended time because of the longer duration of action of these drugs. Symptoms of hypoglycemia may occur when a very high blood glucose level falls too rapidly (e.g., a blood glucose level of 300 mg/dL [16.7 mmol/L] falling quickly to 180 mg/dL [10 mmol/L]). Although the blood glucose level is above normal by definition and measurement, the sudden metabolic shift can evoke hypoglycemia symptoms. Too vigorous management of hyperglycemia with insulin can cause this type of situation.

common causes of HHS

Common causes of HHS are urinary tract infections, pneumonia, sepsis, any acute illness, and newly diagnosed type 2 diabetes. HHS is often related to impaired thirst sensation and/or a functional inability to replace fluids. There is usually a history of inadequate fluid intake, increasing mental depression, and polyuria. The main difference between HHS and DKA is that the patient with HHS usually has enough circulating insulin so that ketoacidosis does not occur. Because HHS produces fewer symptoms in the earlier stages, blood glucose levels can climb quite high before the problem is recognized. The higher blood glucose levels increase serum osmolality and produce more severe neurologic manifestations, such as somnolence, coma, seizures, hemiparesis, and aphasia. Since these manifestations resemble a stroke, immediate determination of the glucose level is critical for correct diagnosis and treatment. Laboratory values in HHS include a blood glucose level greater than 600 mg/dL (33.33 mmol/L) and a marked increase in serum osmolality. Ketone bodies are absent or minimal in both blood and urine.

Other diseases/ conditions that can cause diabetes

Cushing syndrome, hyperthyroidism, recurrent pancreatitis, cystic fibrosis, hemochromatosis, and parenteral nutrition. Commonly used medications that can induce diabetes in some people include corticosteroids (prednisone), thiazides, phenytoin (Dilantin), and atypical antipsychotics (e.g., clozapine [Clozaril]). Diabetes caused by medical conditions or medications can resolve when the underlying condition is treated or the medication discontinued.

diabetic ketoacidosis clinical manifestations

Dehydration occurs in DKA with manifestations of poor skin turgor, dry mucous membranes, tachycardia, and orthostatic hypotension. Early symptoms may include lethargy and 1144weakness. As the patient becomes severely dehydrated, the skin becomes dry and loose, and the eyes become soft and sunken. Abdominal pain may be present and accompanied by anorexia, nausea, and vomiting. Kussmaul respirations (rapid, deep breathing associated with dyspnea) are the body's attempt to reverse metabolic acidosis through the exhalation of excess CO2. Acetone is noted on the breath as a sweet, fruity odor. Laboratory findings include a blood glucose level greater than or equal to 250 mg/dL (13.9 mmol/L), arterial blood pH less than 7.30, serum bicarbonate level less than 16 mEq/L (16 mmol/L), and moderate to large ketones in the urine or serum.

Diabetes-related dermopathy

Diabetes-related dermopathy, the most common diabetic skin lesion, is characterized by reddish brown, round or oval patches. They initially are scaly, then they flatten out and become indented. The lesions appear most frequently on the shins but can also be found on the front of the thighs, forearm, side of the foot, scalp, and trunk.

diabetic nephropathy

Diabetic nephropathy is a microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney. It is the leading cause of end-stage renal disease in the United States and is seen in 20% to 40% of people with diabetes. Risk factors for diabetes-related nephropathy include hypertension, genetic predisposition, smoking, and chronic hyperglycemia. Results of the DCCT and UKPDS research have demonstrated that kidney disease can be significantly reduced when near-normal blood glucose levels are maintained. Patients with diabetes are screened for nephropathy annually with a random spot urine collection to assess for albuminuria and measure the albumin-to-creatinine ratio. Serum creatinine is also measured to provide an estimation of the glomerular filtration rate and thus the degree of kidney function. Patients with diabetes who have albuminuria receive either angiotensin-converting enzyme (ACE) inhibitor drugs (e.g., lisinopril [Prinivil, Zestril]) or angiotensin II receptor antagonists (e.g., losartan [Cozaar]). Both classifications of these drugs are used to treat hypertension and have been found to delay the progression of nephropathy in patients with diabetes. Hypertension significantly accelerates the progression of nephropathy. Therefore aggressive BP management is indicated for all patients with diabetes. Keeping blood glucose levels in a healthy range is also critical in the prevention and delay of diabetes-related nephropathy

diabetic neuropathy

Diabetic neuropathy is nerve damage that occurs because of the metabolic derangements associated with diabetes mellitus. About 60% to 70% of patients with diabetes have some degree of neuropathy. The most common type of neuropathy affecting persons with diabetes is sensory neuropathy. This can lead to the loss of protective sensation in the lower extremities, and, coupled with other factors, significantly increases the risk for complications that result in a lower limb amputation. More than 60% of nontraumatic amputations in the United States occur in people with diabetes.2 Screening for neuropathy begins at the time of diagnosis in patients with type 2 diabetes and 5 years after diagnosis in patients with type 1 diabetes

HHS Tx

HHS is a medical emergency and has a high mortality rate. The management of DKA and HHS is similar and includes immediate IV administration of insulin and either 0.9% or 0.45% NaCl. HHS usually requires large volumes of fluid replacement. This should be accomplished slowly and carefully. Patients with HHS are commonly older and may have cardiac or renal compromise, requiring hemodynamic monitoring to avoid fluid overload during fluid replacement. When blood glucose levels fall to approximately 250 mg/dL (13.9 mmol/L), IV fluids containing dextrose are administered to prevent hypoglycemia. Electrolytes are monitored and replaced as needed. Hypokalemia is not as significant in HHS as it is in DKA, although fluid losses may result in milder potassium deficits that require replacement. Assess vital signs, intake and output, tissue turgor, laboratory values, and cardiac monitoring to check the efficacy of fluid and electrolyte replacement. This includes monitoring serum osmolality and frequently assessing cardiac, renal, and mental status. Once the patient is stabilized, initiate attempts to detect and correct the underlying cause

hypoglycemia

Hypoglycemia, or low blood glucose, occurs when there is too much insulin in proportion to available glucose in the blood. This causes the blood glucose level to drop to less than 70 mg/dL (3.9 mmol/L). When plasma glucose drops below 70 mg/dL, counterregulatory hormones are released and the autonomic nervous system is activated. Suppression of insulin secretion and production of glucagon and epinephrine provide a defense against hypoglycemia. Epinephrine release causes manifestations that include shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, and pallor. Because the brain requires a constant supply of glucose in sufficient quantities to function properly, hypoglycemia can affect mental functioning. These manifestations are difficulty speaking, visual disturbances, stupor, confusion, and coma. Manifestations of hypoglycemia can mimic alcohol intoxication. Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death.

Type 1 Diabetes Onset

In type 1 diabetes, the islet cell autoantibodies responsible for β-cell destruction are present for months to years before the onset of symptoms. Manifestations of type 1 diabetes develop when the person's pancreas can no longer produce sufficient amounts of insulin to maintain normal glucose. Once this occurs, the onset of symptoms is usually rapid, and patients often are initially seen with impending or actual ketoacidosis. The patient usually has a history of recent and sudden weight loss and the classic symptoms of polydipsia (excessive thirst), polyuria (frequent urination), and polyphagia (excessive hunger). The individual with type 1 diabetes requires insulin from an outside source (exogenous insulin) to sustain life. Without insulin, the patient will develop diabetic ketoacidosis (DKA), a life-threatening condition resulting in metabolic acidosis. Newly diagnosed patients with type 1 diabetes may experience a remission, or "honeymoon period," for 3 to 12 months after treatment is initiated. During this time, the patient requires little injected insulin because β-cell insulin production remains sufficient for healthy blood glucose levels. Eventually, as more β-cells are destroyed and blood glucose levels increase, the honeymoon period ends and the patient will require insulin on a permanent basis.

how is insulin synthesized

Insulin is synthesized from a precursor, proinsulin. Enzymes split proinsulin to form insulin and C-peptide, and then the two substances are released in equal amounts. Therefore measuring C-peptide in serum and urine is a useful clinical indicator of pancreatic β-cell function.

Counterregulatory hormones and their mechanism of action

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 (1) stimulating glucose production and release by the liver and (2) 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.

pancreas transplantation

Pancreas transplantation can be used as a treatment option for patients with type 1 diabetes. Usually it is done for patients who have end-stage renal disease and have had or plan to have a kidney transplant. Kidney and pancreas transplants are often performed together, or a pancreas may be transplanted after a kidney transplant. If renal failure is not present, the ADA recommends that pancreas transplantation be considered only for patients who exhibit the following three criteria: (1) a history of frequent, acute, and severe metabolic complications (e.g., hypoglycemia, hyperglycemia, ketoacidosis) requiring medical attention; (2) clinical and emotional problems with the use of exogenous insulin therapy that are so severe as to be incapacitating; and (3) consistent failure of insulin-based management to prevent acute complications.

Type 2 Diabetes clinical manifestations

The clinical manifestations of type 2 diabetes are often nonspecific, although it is possible that an individual with type 2 diabetes will experience some of the classic symptoms associated with type 1 diabetes, including polyuria, polydipsia, and polyphagia. * Some of the more common manifestations associated with type 2 diabetes are fatigue, recurrent infections, recurrent vaginal yeast or candidal infections, prolonged wound healing, and visual changes.

diabetes and psychological considerations

Patients with diabetes have high rates of depression, anxiety, and eating disorders. Depression contributes to diminished diabetes self-care, feelings of helplessness related to chronic illness, and poor outcomes.12 Assess patients for manifestations of depression and/or diabetes distress. Disordered eating behaviors (DEB) can occur in people with both type 1 and type 2 diabetes. DEBs include anorexia, bulimia, binge eating, excessive restriction of calories, and intense exercise. The greatest incidence of eating disorders is seen in females. Adolescent girls with diabetes are more than twice as likely to develop DEB than those who do not have diabetes.28 Patients may intentionally decrease their dose of insulin or omit the dose. This is called "diabulimia" and leads to weight loss, hyperglycemia, and glycosuria because the food ingested cannot be used for energy without adequate insulin. Insulin omission and DEBs can have serious consequences, including retinopathy, neuropathy, lipid abnormalities, DKA, and death Open communication is critical to identify these behaviors early. Patients with eating disorders need to be seen by a mental health professional with expertise in eating disorders and an understanding of diabetes management.

Amylin Analogs

Pramlintide (Symlin) is the only available amylin analog. Amylin, a hormone secreted by the β-cells of the pancreas in response to food intake, slows gastric emptying, reduces glucagon secretion, and increases satiety.12 Pramlintide is used in addition to mealtime insulin in patients with type 1 or type 2 diabetes who have elevated blood glucose levels on insulin therapy. It is only used concurrently with insulin and is not a replacement for insulin. Pramlintide is administered before major meals subcutaneously into the thigh or abdomen. It cannot be injected into the arm because absorption from this site is too variable. The drug cannot be mixed in the same syringe with insulin. The concurrent use of pramlintide and insulin increases the risk of severe hypoglycemia during the 3 hours after injection, especially in patients with type 1 diabetes. Instruct patients to eat a meal with at least 250 calories and keep a form of fast-acting glucose on hand in the event that hypoglycemia develops. When pramlintide is used, the bolus dose of insulin should be reduced.

Short acting insulin

Regular (Humulin R, Novolin R) onset- 30 min to 1 hr peak - 2 to 5 hour duration- 5 to 8 hour

exercise

Regular, consistent exercise is an essential part of diabetes and prediabetes management. The ADA recommends that people with diabetes engage in at least 150 min/wk (30 minutes, 5 days/week) of a moderate-intensity aerobic physical activity. The ADA also encourages people with type 2 diabetes to perform resistance training three times a week in the absence of contraindications. Exercise decreases insulin resistance and can have a direct effect on lowering blood glucose levels. It also contributes to weight loss, which further decreases insulin resistance. The therapeutic benefits of regular physical activity may result in a decreased need for diabetes medications to reach target blood glucose goals in people with type 2 diabetes. Regular exercise may also help reduce triglyceride and low-density lipoprotein (LDL) cholesterol levels, increase high-density lipoprotein (HDL), reduce BP, and improve circulation

Administration of insulin

Routine doses of insulin are administered by subcutaneous injection. Regular insulin can be given IV when immediate onset of action is desired. Insulin is not taken orally because it is inactivated by gastric fluids. Teach patients to avoid injecting insulin IM because rapid and unpredictable absorption could result in hypoglycemia

Short Acting insulin Bolus

Short-acting regular insulin has an onset of action of 30 to 60 minutes and is injected 30 to 45 minutes before a meal to ensure that the onset of action coincides with meal absorption. Because timing an injection 30 to 45 minutes before a meal is difficult for people to incorporate into their lifestyles, the flexibility that rapid-acting insulins offer is preferred by those taking insulin with their meals. Short-acting insulin is also more likely to cause hypoglycemia because of a longer duration of action.

dawn phenomenon

The dawn phenomenon is also characterized by hyperglycemia that is present on awakening. Two counterregulatory hormones (growth hormone and cortisol), which are excreted in increased amounts in the early morning hours, may be the cause of this phenomenon. The dawn phenomenon affects a majority of people with diabetes and tends to be most severe when growth hormone is at its peak in adolescence and young adulthood

Type 2 Diabetes onset

The disease onset in type 2 diabetes is usually gradual. The person may go for many years with undetected hyperglycemia that may produce few, if any, symptoms. Many people are diagnosed on routine laboratory testing or when they undergo treatment for other conditions, and elevated glucose or glycosylated hemoglobin (A1C) levels are found. The signs and symptoms of hyperglycemia develop when about 50% to 80% of β-cells are no longer secreting insulin. At the time of diagnosis, the average person has had type 2 diabetes for 6 1/2 years.

Type 2 Diabetes Factors in Development

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 ability of the pancreas 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. In addition, the α-cells of the pancreas increase production of glucagon. This leads to a third factor, which 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.

exercise: special considerations

The glucose-lowering effects of exercise can last up to 48 hours after the activity, so it is possible for hypoglycemia to occur long after the activity. It is recommended that patients who use medications that can cause hypoglycemia schedule exercise about 1 hour after a meal or that they have a 10- to 15-g carbohydrate snack and check their blood glucose before exercising. They can eat small carbohydrate snacks every 30 minutes during exercise to prevent hypoglycemia. Patients using medications that place them at risk for hypoglycemia should always carry a fast-acting source of carbohydrate, such as glucose tablets or hard candies, when exercising *Although exercise is generally beneficial to blood glucose levels, strenuous activity can be perceived by the body as a stress, causing a release of counterregulatory hormones and a temporary elevation of blood glucose. In a person with type 1 diabetes 1135who has hyperglycemia and ketones, exercise can worsen these conditions. Teach these patients to delay activity if the blood glucose level is over 250 mg/dL and ketones are present in the urine. If hyperglycemia is present without ketosis, it is not necessary to postpone exercise.

long and intermediate acting background insulin

The long-acting insulins include glargine (Lantus, Toujeo), detemir (Levemir), and degludec (Tresiba). This type of insulin is released steadily and continuously, and for many people does not have a peak of action. The action time for long-acting insulin varies. Although they can be used for once-daily subcutaneous administration, detemir is often given twice daily. Because they lack peak action time, the risk for hypoglycemia from this type of insulin is greatly reduced. Glargine and detemir must not be diluted or mixed with any other insulin or solution in the same syringe. Ryzodeg 70/30 is a mixture of degludec and aspart (rapid-acting) insulin. If oral agents and long-acting insulin are not adequate to achieve glycemic goals, mealtime insulin may also be added. Intermediate-acting insulin (NPH) is also used as a basal insulin. It has a duration of 12 to 18 hours. The disadvantage of NPH is that it has a peak ranging from 4 to 12 hours, which can result in hypoglycemia. NPH can be mixed with short- and rapid-acting insulins. NPH insulin should never be given IV.

sensory neuropathy

The most common form of sensory neuropathy is distal symmetric polyneuropathy, which affects the hands and/or feet bilaterally. This is sometimes referred to as stocking-glove neuropathy. Characteristics of distal symmetric polyneuropathy include loss of sensation, abnormal sensations, pain, and paresthesias. The pain, which is often described as burning, cramping, crushing, or tearing, is usually worse at night and may occur only at that time. The paresthesias may be associated with tingling, burning, and itching sensations. The patient may report a feeling of walking on pillows or numb feet. At times the skin becomes so sensitive (hyperesthesia) that even light pressure from bed sheets cannot be tolerated. Complete or partial loss of sensitivity to touch and temperature is common. Foot injury and ulcerations can occur without the patient ever having pain . Neuropathy can also cause atrophy of the small muscles of the hands and feet, causing deformity and limiting fine movement.

Treatment for the dawn phenomenon and somogyi effect

The treatment for Somogyi effect is less insulin in the evening. The treatment for dawn phenomenon is an increase in insulin or an adjustment in administration time. Your assessment must include insulin dose, injection sites, and variability in the time of meals or insulin administration. Ask the patient to measure and document bedtime, nighttime (between 2:00 and 4:00 AM), and morning fasting blood glucose levels on several occasions. If the predawn levels are less than 60 mg/dL (3.3 mmol/L) and signs and symptoms of hypoglycemia are present, the insulin dosage should be reduced. If the 2:00 to 4:00 AM blood glucose is high, the insulin dosage should be increased. In addition, counsel the patient on appropriate bedtime snacks. Inhaled Insulin. * low= less *high=more

Rapid Acting insulin Bolus

To manage postprandial blood glucose levels, the timing of rapid- and short-acting insulin in relation to meals is crucial. Rapid-acting synthetic insulin analogs, which include lispro (Humalog), aspart (NovoLog), and glulisine (Apidra), have an onset of action of approximately 15 minutes and should be injected within 15 minutes of mealtime. The rapid-acting analogs most closely mimic natural insulin secretion in response to a meal.

Afrezza

a rapid-acting inhaled insulin, is administered at the beginning of each meal or within 20 minutes after starting a meal. It is not a substitute for long-acting insulin. Afrezza must be used in combination with long-acting insulin in patients with type 1 diabetes. It is not recommended for the treatment of diabetic ketoacidosis or in patients who smoke. The most common adverse reactions are hypoglycemia, cough, and throat pain or irritation. Afrezza should not be used in patients with chronic lung disease, such as asthma or COPD, because bronchospasm can occur.

macrovascular complications

are diseases of the large and medium-size blood vessels that occur with greater frequency and with an earlier onset in people with diabetes. Macrovascular diseases include cerebrovascular, cardiovascular, and peripheral vascular diseas

Type 1 Diabetes (formerly known as juvenile-onset diabetes or insulin-dependent diabetes)

accounts for about 5% to 10% of all people with diabetes. Type 1 diabetes generally affects people under 40 years of age, although it can occur at any age. An autoimmune disorder, in which the body develops antibodies against insulin and/or the pancreatic β-cells that produce insulin. This eventually results in not enough insulin for a person to survive. Autoantibodies to the islet cells cause a reduction of 80% to 90% of normal function before hyperglycemia and other manifestations occur. A genetic predisposition and exposure to a virus are factors that may contribute to the pathogenesis of immune-related type 1 diabetes. • Increased susceptibility (40%-50%) when one has specific human leukocyte antigens (HLA-DR3, HLA-DR4). • Polygenic (>40 genes influence susceptibility).

diabetic ketoacidosis

caused by a profound deficiency of insulin and is characterized by hyperglycemia, ketosis, acidosis, and dehydration. It is most likely to occur in people with type 1 diabetes but may be seen in people with type 2 diabetes in conditions of severe illness or stress when the pancreas cannot meet the extra demand for insulin. Precipitating factors include illness and infection, inadequate insulin dosage, undiagnosed type 1 diabetes, poor self-management, and neglect. When the circulating supply of insulin is insufficient, glucose cannot be properly used for energy. The body compensates by breaking down fat stores as a secondary source of fuel. Ketones are acidic by-products of fat metabolism that can cause serious problems when they become excessive in the blood. Ketosis alters the pH balance, causing metabolic acidosis to develop. Ketonuria is a process that occurs when ketone bodies are excreted in the urine. During this process, electrolytes become depleted as cations are eliminated along with the anionic ketones in an attempt to maintain electrical neutrality. Insulin deficiency impairs protein synthesis and causes excessive protein degradation. This results in nitrogen losses from the tissues. Insulin deficiency also stimulates the production of glucose from amino acids (from proteins) in the liver and leads to further hyperglycemia. Because of the deficiency of insulin, the additional glucose cannot be used and the blood glucose level rises further, adding to the osmotic diuresis. If not treated, the patient will develop severe depletion of sodium, potassium, chloride, magnesium, and phosphate. Vomiting caused by the acidosis results in more fluid and electrolyte losses. Eventually, hypovolemia followed by shock will ensue. Renal failure, which may eventually occur from hypovolemic shock, causes the retention of ketones and glucose, and the acidosis progresses. Untreated, the patient becomes comatose as a result of dehydration, electrolyte imbalance, and acidosis. If the condition is not treated, death is inevitable.

insulin pump

delivers a continuous subcutaneous insulin infusion through a small device worn on the belt, in a pocket, or under clothing. Insulin pumps use rapid-acting insulin, which is loaded into a reservoir or cartridge and connected via plastic tubing to a catheter inserted into the subcutaneous tissue. All insulin pumps are programmed to deliver a continuous infusion of rapid-acting insulin 24 hours a day, known as the basal rate. Basal insulin can be temporarily increased or decreased based on carbohy1129drate intake, activity changes, or illness. Many individuals require different basal rates at different times of the day.

Gestational Diabetes

develops during pregnancy and occurs in about 4.6% to 9.2% of pregnancies in the United States.8 Women with gestational diabetes have a higher risk for cesarean delivery, and their babies have increased risk for perinatal death, birth injury, and neonatal complications. Women who are at high risk for gestational diabetes are screened at the first prenatal visit.9 Those at high risk include women who are obese, are of advanced maternal age, or have a family history of diabetes. Women with an average 1124risk for gestational diabetes are screened using an OGTT at 24 to 28 weeks of gestation. Most women with gestational diabetes have normal glucose levels within 6 weeks postpartum. Be aware that women with a history of gestational diabetes have up to a 63% chance of developing type 2 diabetes within 16 years

Metabolic Syndrome

has five components: elevated glucose levels, abdominal obesity, elevated BP, high levels of triglycerides, and decreased levels of high-density lipoproteins (HDLs). An individual with three of the five components is considered to have metabolic syndrome. Overweight individuals with metabolic syndrome can reduce their risk for diabetes through a program of weight loss and regular physical activity

hypoglycemia unawareness

is a condition in which a person does not experience the warning signs and symptoms of hypoglycemia until the glucose levels reach a critical point. Then the person may become incoherent and combative or lose consciousness. This is often related to autonomic neuropathy of diabetes that interferes with the secretion of counterregulatory hormones that produce these symptoms. Patients at risk for hypoglycemia unawareness include those who have had repeated episodes of hypoglycemia, older patients, and patients who use β-adrenergic blockers. Using intensive treatment to get tight blood glucose levels in patients who are at risk for hypoglycemia unawareness may not be an appropriate goal because a major drawback is hypoglycemia. These patients are usually managed with blood glucose goals that are somewhat higher than those of patients who are able to detect and manage the onset of hypoglycemia.

Hyperosmolar hyperglycemic syndrome (HHS)

is a life-threatening syndrome that can occur in the patient with diabetes who is able to produce enough insulin to prevent DKA, but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion often occurs in those over 60 years of age with diabetes type 2

prediabetes

is defined as impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or both. It is an intermediate stage between normal glucose homeostasis and diabetes, in which the blood glucose levels are elevated but not high enough to meet the diagnostic criteria for diabetes. A diagnosis of IGT is made if the 2-hour oral glucose tolerance test (OGTT) values are 140 to 199 mg/dL (7.8 to 11.0 mmol/L).3 IFG is diagnosed when fasting blood glucose levels are 100 to 125 mg/dL (5.56 to 6.9 mmol/L). Persons with prediabetes usually do not have symptoms. However, long-term damage to the body, especially the heart and blood vessels, may already be occurring. It is important for patients to undergo screening and to understand risk factors for diabetes. Patients with prediabetes can take action to prevent or delay the development of type 2 diabetes. Encourage those with prediabetes to have their blood glucose and A1C checked regularly and monitor for symptoms of diabetes, such as fatigue, frequent infections, or slow healing wounds. Maintaining a healthy weight, exercising regularly, and making healthy food choices have all been found to reduce the risk of developing overt type 2 diabetes in people with prediabetes.

Rapid Acting Insulin

lispro (humalog) lispart (novlog) glulisine (Apidra) onset- 10- 30 min peak- 30min-3 hour duration- 3-5 hour

Long Acting glargine (lantus), detemir (levemir), degludec (tresiba)

onset: 0.8- 4 hour peak: less defined or no pronounced peak duration: 16-24 hour

diabetic retinopathy

refers to the process of microvascular damage to the retina as a result of chronic hyperglycemia, nephropathy, and hypertension in patients with diabetes. Diabetic retinopathy is estimated to be the most common cause of new cases of adult blindness. Retinopathy can be classified as nonproliferative or proliferative. In nonproliferative retinopathy, the most common form, partial occlusion of the small blood vessels in the retina causes microaneurysms to develop in the capillary walls. The walls of these microaneurysms are so weak that capillary fluid leaks out, causing retinal edema and eventually hard exudates or intraretinal hemorrhages. This may cause mild to severe vision loss, depending on which parts of the retina are affected. If the center of the retina (macula) is affected, vision loss can be severe. Proliferative retinopathy, the most severe form, involves the retina and vitreous. When retinal capillaries become occluded, the body compensates by forming new blood vessels to supply the retina with blood, a pathologic process known as neovascularization. These new vessels are extremely fragile and hemorrhage easily, producing vitreous contraction. Eventually light is prevented from reaching the retina as the vessels become torn and bleed into the vitreous cavity. The patient sees black or red spots or lines. If these new blood vessels pull the retina while the vitreous contracts, causing a tear, partial or complete retinal detachment will occur. If the macula is involved, vision is lost. Without treatment, more than half of patients with proliferative diabetic retinopathy will be blind. Persons with diabetes are also prone to other visual problems. Glaucoma occurs as a result of the occlusion of the outflow channels secondary to neovascularization. This type of glaucoma is difficult to treat and often results in blindness. Cataracts develop at an earlier age and progress more rapidly in people with diabetes. *The earliest and most treatable stages of diabetic retinopathy often produce no changes in the vision. Therefore patients with type 2 diabetes should have a dilated eye examination by an ophthalmologist or a specially trained optometrist at the time of diagnosis and annually thereafter for early detection and treatment. A person with type 1 diabetes should have a dilated eye examination within 5 years after the onset of diabetes and then repeated annually.

microvascular complications

result from thickening of the vessel membranes in the capillaries and arterioles in response to conditions of chronic hyperglycemia. They differ from the macrovascular complications in that they are specific to diabetes. Although microangiopathy can be found throughout the body, the areas most noticeably affected are the eyes (retinopathy), kidneys (nephropathy), and nerves (neuropathy). Microvascular changes are present in some patients with type 2 diabetes at the time of diagnosis

insulin-dependent tissues

skeletal muscle adipose tissue

The fastest site for insulin absorption?

stomach -followed by: arm, thigh, and buttock * Caution the patient about injecting into a site that is to be exercised. For example, injecting into the thigh and then going jogging could increase body heat and circulation, which could increase the rate of insulin absorption and speed the onset of action, thus resulting in hypoglycemia.

Necrobiosis lipoidica diabeticorum

usually appears as red-yellow lesions, with atrophic skin that becomes shiny and transparent revealing tiny blood vessels under the surface. This condition is uncommon and occurs more frequently in young women. It may appear before other clinical signs or symptoms of diabetes. Because the thin skin is prone to injury, special care must be taken to protect affected areas from injury and ulceration

hypoglycemia causes

• Alcohol intake without food • Too little food—delayed, omitted, inadequate intake • Too much diabetes medication • Too much exercise without adequate food intake • Diabetes medication or food taken at wrong time • Loss of weight without change in medication • Use of β-adrenergic blockers interfering with recognition of symptoms

hypoglycemia manifestations

• Blood glucose <70 mg/dL (3.9 mmol/L) • Cold, clammy skin • Numbness of fingers, toes, mouth • Rapid heartbeat • Emotional changes • Headache • Nervousness, tremors • Faintness, dizziness • Unsteady gait, slurred speech • Hunger • Changes in vision • Seizures, coma

hyperglycemia manifestations

• Elevated blood glucose† • Increase in urination • Increase in appetite followed by lack of appetite • Weakness, fatigue • Blurred vision • Headache • Glycosuria • Nausea and vomiting • Abdominal cramps • Progression to DKA or HHS

hyperglycemia tx

• Get medical care • Continue diabetes medication as prescribed • Check blood glucose frequently and check urine for ketones; record results • Drink fluids at least on an hourly basis • Contact HCP regarding ketonuria

hyperglycemia causes

• Illness, infection • Corticosteroids • Too much food • Too little or no diabetes medication • Inactivity • Emotional, physical stress • Poor absorption of insulin

Nutritional therapy

• Minimize trans fat. • Dietary cholesterol <200 mg/day. • ≥2 servings of fish per week to provide polyunsaturated fatty acids. • Fiber intake at 25-30 g/day. Alcohol: Limit to moderate amount (maximum 1 drink per day for women and 2 drinks per day for men). • Consume alcohol with food to reduce risk of nocturnal hypoglycemia in those using insulin or insulin secretagogues. • Moderate alcohol consumption has no acute effect on glucose and insulin concentrations, but carbohydrate taken with the alcohol (mixed drink) may raise blood glucos