Diabetes mellitus type 1 BUILD MINDMAP + HEAD TO TOE – Flashcards

Multisystem chronic disease of carbohydrate, fat, and protein metabolism, resulting in hyperglycemia Caused by pancreatic insufficiency (deficiency) of insulin production because of autoimmune destruction of the beta cells Long-term medical attention required to limit end-organ complications (such as accelerated atherosclerosis, neuropathy, nephropathy, and retinopathy) Lifelong insulin therapy required

Autoimmunity is considered a major factor in type 1 diabetes mellitus (DM), placing the beta cell at special risk for inflammatory damage; human leukocyte antigen (HLA)DR3 or HLA-DR4, specific markers of type 1 DM susceptibility, have been found in about 95% of patients. Amino acid metabolism and low vitamin D levels may also play a role in the pathogenesis of diabetes. Type 1 DM may result from damage to pancreatic beta cells from infectious or environmental agents, an autoimmune response against altered pancreatic beta-cell antigens, the presence of anti-insulin antibodies, or a combination of these factors. Most islet cell antibodies are directed against glutamic acid decarboxylase (GAD) within pancreatic beta cells. Lymphocytic infiltration and destruction of insulin-secreting cells of the islets of Langerhans result, causing low levels or absence of circulating insulin, elevated levels of plasma glucagon, and failure of pancreatic beta cells to respond to stimuli.

Genetic inheritance, with an increased risk associated with the presence of both HLA-DR3 and HLA-DR4 Immunologically mediated destruction of the beta cells by enterovirus infection, viruses, (coxsackievirus B4, mumps, rubella), cytotoxins, toxic chemicals, exposure to cow's milk in infancy, or a combination of these factors Infant weight velocity (small effect on adult insulin resistance) Diet high in nitrosamines Environmental toxins

Certain HLA types Presence of a specific 64,000 molecular weight protein, which may be responsible for antibody formation Family history of insulin-dependent or noninsulin-dependent diabetes in any 1st-degree relatives; slightly greater risk for a child if the father has type 1 diabetes Exposure to Epstein-Barr virus, coxsackievirus B4, mumps, rubella, or cytomegalovirus Exposure to cow's milk at an early age (with possible protection against the disease if breastfed) Lower maternal age at birth (younger than age 25) Preeclampsia during gestation

In the United States, about 1 million people have type 1 DM, and roughly 10,000 new cases are diagnosed every year; there is a yearly incidence of about 15 cases per 100,000 in patients younger than age 18. Type 1 DM was commonly called juvenile-onset diabetes, as it commonly occurs early in life; however, 50% of patients with new-onset type 1 DM are older than 20 years of age. About one in every 400 to 600 children and adolescents has type 1 DM; the mean age of onset is age 8 to 12, with a peak incidence of age 11 to 13, coinciding with adolescence and puberty. A slower-onset and less aggressive adult form of type 1A (early hyperglycemia without ketoacidosis and gradual onset of ketosis) has shown a high incidence in those in their late 30s and early 40s; it is referred to as latent autoimmune diabetes of the adult (LADA). Type 1 DM is more common among non-Hispanic whites, African Americans, and Hispanic Americans. It's uncommon among Asians, and whites are more commonly affected than blacks. It's more common in men than women, but incidence in postmenopausal women is similar to that of men. Incidence is increased in people living farther from the equator; people in Finland have the highest incidence of type I DM. Those affected generally are not obese, and they may present with diabetic ketoacidosis (DKA). Young children are more likely to present withDKA.

Chronic foot ulcers Lower-extremity amputation Hypoglycemia Hyperlipidemia Increased risk for preeclampsia and preterm delivery Macrovascular disease (coronary and cerebral artery disease) Microvascular disease (retinopathy, nephropathy, neuropathy) Diabetic ketoacidosis Excessive weight gain Excessive weight loss Skin and mouth conditions, particularly gum infections Osteoporosis For women, pregnancy complications Hearing impairment Psychological problems of chronic disease, such as depression and anxiety

Sudden onset, with the presentation of an infection, such as a prolonged or recurrent candidal infection in young children, usually in the diaper area Possibly present with diabetic ketoacidosis (DKA) Polydipsia due to the hyperosmolar state and dehydration Polyphagia with weight loss (normal or increased appetite due to depletion of water and a catabolic state with reduced glycogen, proteins, and triglycerides and normal weight or wasting, depending on the interval between the onset of the disease and initiation of treatment) Polyuria that presents as nocturia, bedwetting, or incontinence in a previously continent childdue to osmotic diuresis secondary to hyperglycemia Increased fatigue and lethargydue to muscle wasting from the catabolic state of insulin deficiency, hypovolemia, and hypokalemia Muscle crampsdue to electrolyte imbalance Vision changes (blurriness), due to a hyperosmolar effect on the lens and vitreous humor, and dilation of the lens, altering focal length Abdominal discomfort, nausea, and a change in bowel habits in acute DKA Recurrent skin infections and rashes Anxiety attacks, irritability, emotional lability, headaches, and altered school or work performance Peripheral neuropathy; numbness and tingling in hands and feet in a glove and stocking pattern; and bilateral, symmetric, and ascending neuropathy that results from many factors due to sustained hyperglycemia

Orthostatic vital signs, which can indicate volume status and suggest the presence of autonomic neuropathy Kussmaul's respirations if DKA is present Possible retinopathy on ophthalmological examination that may be viewed as hemorrhages or exudates Possible foot infections with the presence or absence of the dorsalis pedis and posterior tibialis pulses due to poor lower-extremity blood flow, which can delay healing and increase the risk of amputation Peripheral neuropathy possibly present in the lower extremities in patients who present with foot ulcers Skin infections, such as staphylococcal follicular skin infections, superficial fungal infections, cellulitis, erysipelas, and oral or genital candidal infections (common) Lower urinary tract infections (common), increasing the risk of acute pyelonephritis Malignant otitis externa, rhinocerebral mucormycosis, and emphysematous pyelonephritis, which occur almost exclusively in patients with diabetes Staphylococcal sepsis, which occurs more commonly in those with diabetes and has an increased mortality rate, and pneumococcal pneumonia

Fasting glucose is greater than 126 mg/dL (7.0 mmol/L) and may be elevated on two separate occasions for diagnosis. Random glucose of greater than 200 mg/dL (11.1 mmol/L)suggests diabetes. Glycosylated hemoglobin (HbA1c) level is greater than 6.5%,which may be confirmed on repeat testing. An insulin or C-peptide level below 5 µU/mL, or 0.6 ng/mL, suggests type 1 DM; C-peptide is formed during conversion of proinsulin to insulin; a fasting C-peptide level greater than 1 ng/dL in a patient who has had diabetes suggests type 2 DM (residual beta-cell function). A high positive titer of glutamic acid decarboxylase antibodies suggests type 1 DM, except in a patient with type 2DM who hashyperglycemia (greater than 300 mg/dL) and temporarily has a low insulin or C-peptide level but recovers insulin production once normoglycemic. Serum electrolytes may be elevated, especially in those with ketoacidosis. Urinalysis reveals glucosuria, ketonuria, and microalbuminuria. Pancreatic autoantibodies help diagnose type 1A diabetes (islet cells, insulin, GAD, and tyrosine phosphatase antibodies). Complete blood count may reveal an elevated white blood cell count and hemoglobin level.

Pancreatic biopsy reveals inflammatory changes, lymphocytic infiltration around the islets of Langerhans, or islet cell loss.

Maintaining normal blood glucose levels through diet, exercise, and medication to greatly reduce the development and progression of retinopathy, microalbuminuria, proteinuria, and neuropathy; in children, a goal of normal growth and development and overall good health Control of carbohydrate metabolism through diet, exercise, and medication to achieve normoglycemia (adjusted to age), with the goal of blood glucose levels ranging from 80 to 150 mg/dL (4.4 to 8.3 mmol/L), or 80 to 120 mg/dL (4.4 to 6.6 mmol/L) in older patients, at all times Avoidance of hypoglycemic episodes, especially in children, who are more prone to hypoglycemia and in whom tight glucose control might be dangerous Hemoglobin A1c target levels: Children under age 6, 7.5% to 8.5%; children ages 6 to 12, less than 8.0%; adolescents ages 13 to 19, 7.5% (less than 7.0% if achieved without excessive hypoglycemia); and adults, less than 6.0% Prevention of acute complications, including ketoacidosis, and delay or prevention of chronic complications

Carbohydrate counting using insulin-to-carbohydrate ratio with all meals and snacks to allow flexibility in eating Dietary treatment based on nutritional assessment, treatment goals, and the patient's eating habits and lifestyle, according to ADA policy Diet management, including timing, size, frequency, and composition of meals to avoid hypoglycemia or postprandial hyperglycemia Comprehensive diet plan that includes daily caloric intake prescription and allowable amounts of dietary carbohydrate, fat, and protein, with calories divided between meals and snacks Individual diet plan created by a professional dietitian, with individualized or group teaching provided

Regular exercise and education about the effects of exercise on blood glucose level and possible resultant hypoglycemia as well as ways to prevent hypoglycemia, such as reducing insulin by 10% to 20% or consuming an extra snack Maintaining hydration during exercise

Lifelong treatment with insulin to promote glucose utilization Rapid-acting insulins (regular insulin, lispro, glulisine, and aspart), preparations of zinc insulin crystals in solution with an onset of action ½ hour to 1 hour, a peak of 2½ to 5 hours, and a duration of action of 6 to 8 hours (with lispro and aspart absorbed more quickly,with a rapid onset [5 to 10 minutes], peak [1 hour], and duration of action [4 hours], allowing administration shortly before eating) Intermediate-acting insulins,including neutral protamine Hagedorn(NPH), which contains a mixture of regular and protamine zinc insulin, and Lente, which contains 30% Semilente insulin and 70% Ultralente insulin in an acetate buffer Long-acting insulins, including Ultralente, containing large zinc insulin crystals in an acetate buffer, and insulin glargine, having no peak and providing a stable level lasting more than 24 hours, with both supplying basal 24-hour insulin with a single daily injection Mixtures of insulin preparations with different onsets and durations of action administered by drawing doses of the two preparations into the same syringe immediately before use (also available in premixed syringes) Insulin replacement, given as a basal insulin (long-acting glargine or detemir or intermediate-acting NPH) and preprandial (premeal) insulin (rapid-acting lispro, aspart, or glulisine or short-acting regular insulin) Preprandial dose for patients requiring multiple daily doses by injection or insulin infusion pump based on the carbohydrate content of the meal, plus a correction dose if the blood glucose level is elevated (with careful monitoring of blood glucose level) I.V. administration of only regular, lispro, and aspart insulins Amylin analogs (pramlintide acetate or Symlin), which delay gastric emptying, decrease postprandial glucagon release, and modulate appetite by improving control of glucose levels, reducing fluctuation of levels during the day and lowering blood glucose levels after meals as well as improving HbA1c levels Glucagon (GlucaGen), an antidote to insulin that elevates blood glucose levels by inhibiting glycogen synthesis, increasing the formation of glucose from proteins and fats (gluconeogenesis), increasing hydrolysis of glycogen to glucose in the liver, and increasing hepatic glycogenolysis and lipolysis in adipose tissue

Pancreatic transplantation, which is a possibility and is performed most commonly with simultaneous kidney transplantation for end-stage renal disease

Activity intolerance Deficient fluid volume Deficient knowledge: Disease process Deficient knowledge: Treatment Disabled family coping Imbalanced nutrition: Less than body requirements Impaired urinary elimination Ineffective peripheral tissue perfusion Risk for decreased cardiac perfusion Risk for electrolyte imbalance Risk for impaired skin integrity Risk for ineffective renal perfusion Risk for infection 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 and appropriate body weight achieve and maintain balanced fluid intake and output demonstrate adequate peripheral tissue perfusion maintain an adequate cardiac output and hemodynamic stability verbalize an understanding of the causative factors of electrolyte imbalance and demonstrate behaviors to correct the deficit, as appropriate demonstrate intact skin integrity achieve and maintain adequate renal perfusion and function state actions that will decrease the risk of infection maintain appropriate glucose levels.

Assess vital signs and level of consciousness frequently; monitor for signs of dehydration. 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

12-lead electrocardiogram (ECG) 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 secondary line drug infusion 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 (such as foot and neurologic examinations), and referrals to specialists (such as the ophthalmologist and podiatrist) specific diet control education to the patient and family how to administer self—insulin injection and perform finger sticks for blood glucose level monitoring as well asproper storage and use of insulin how to perform daily foot examinations 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 prescribed treatment causes and signs of hypoglycemia, how to avoid hypoglycemia, and the treatment required if it occurs as well as advising the patient to carry candy or sugar cubes how to administer subcutaneous injections of glucagon in an emergency signs and symptoms of infections and the need for close glucose monitoring and insulin adjustment during periods of medical illness and surgery procedures, including the rationale for a procedure and its possible outcome drug dosages, adverse reactions, and signs of toxicity to watch for medications that may affect glucose level prevention of infection (including appropriate immunizations and 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.