NUR 229 Diabetes, Endocrine, Stress, Hemodynamics PDF

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Diabetes 

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Diabetes Mellitus (DM) o DM is a disorder of ______ _______  Carbohydrate metabolism o What is diabetes characterized by?  High levels of blood glucose, resulting from the body’s inability to produce or utilize insulin o What are the four major categories of Diabetes Mellitus?  Type 1  Type 2  Gestational Diabetes  Other specific types of diabetes Insulin o What is insulin?  A hormone produced by the beta cells of the islets of Langerhans  What are the islets of Langerhans? o Specialized tissue within the pancreas o What does the rise in blood glucose stimulate?  The pancreas to release insulin Insulin + glucose = diffuses into cell o After absorption into cells, what can glucose be used for?  Energy production  Be stored in the form of glycogen  Be converted into fat. o All cells can store some glucose in the form of glycogen, but the ___ and ___ cells can store the largest amounts.  Liver  Muscle Basics of Carbohydrate Metabolism o What is a major source of glucose in the bloodstream?  Monosaccharides o Before glucose can be utilized for energy, it must be transported through the ____ ____ into _____ of cells  Plasma membrane into cytoplasm o What is the name of the process it requires?  Facilitated diffusion  What is this? o An insulin-supported process that occurs at the cell’s plasma membrane Glycogenesis, Glycogenolysis, Gluconeogenesis o What is glycogenesis?  The process of glycogen formation o What is glycogenolysis?  The process of glycogen breakdown o What is gluconeogenesis?  The conversion of amino acids and fats into glucose during times when fasting is prolonged or starvation occurs Fat Breakdown  Fatty Acids  Ketoacids o As fatty acids accumulate, they are converted into…  Acetoacetic acid  Beta-hydroxybutyric acid

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Acetone What are these three substances referred to as?  Ketoacids or ketones o What is ketone accumulation in the bloodstream known as?  Ketosis or ketoacidosis Diabetic Ketoacidosis (DKA) o What is Diabetic Ketoacidosis (DKA)?  A condition that develops in those with no insulin reserves, such as those with uncontrolled type 1 diabetes  Does DKA require immediate treatment?  Yes, it is a critical condition that requires immediate treatment o Why?  When there is no glucose entering cells because of either a lack of insulin or resistance to insulin, the cells go into starvation mode Starvation  Liver Glycogen, Fat, and Muscle Breakdown o During periods of starvation, the liver is called to release its glucose storage  What is this called?  Glycogenolysis o What is adipose tissue breakdown utilized for?  To yield fatty acids to manufacture glucose o What may muscle mass be called upon to release?  Proteins  amino acids used to manufacture glucose in the liver o What does prolonged starvation cause?  Depletion of fat stores and muscle mass Hypoglycemia o What characterizes hypoglycemia?  Very low glucose levels in the blood  What is a side effect of this? o Cannot support efficient brain function o What happens when blood glucose levels fall to hypoglycemic levels (lower than 70 mg/dL)?  The hypothalamic region of brain and portal vein of liver sense the drop in glucose  Then what happens? o These glycemic sensors initiate a compensatory response mainly involving the adrenal gland, pancreas, and liver o Epinephrine and glucagon are released, causing…  Activation of sympathetic nervous system and rise in blood glucose o Signs and symptoms of Hypoglycemia (activation of the sympathetic nervous system)  What are the signs and symptoms of hypoglycemia?  Sweating  Hunger  Dizziness  Nervousness, Tremulousness  Irritability  Headache  Heart palpitations  Confusion, Disorientation, Inability to concentrate  Seizures  Loss of consciousness Hyperglycemia o What is hyperglycemia?

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 Elevated blood glucose level commonly caused by…  The body’s lack of insulin or cellular resistance to insulin o Why is hypoglycemia harmful?  It causes cellular damage and harms the endothelium Diagnostic Criteria for DM o Fasting blood glucose  What is the normal range?  Normal: 70 to 99 mg/dL  What is the prediabetic range?  Prediabetic: 100 to 125 mg/dL  What is the diabetic range?  Diabetes: 126 mg/dL or higher o Two-hour plasma glucose during oral glucose tolerance test  What is the prediabetic range?  Prediabetes: 140 to 199 mg/dL  What is the diabetic range?  Diabetes: 200 mg/dL or higher o Random plasma glucose  What is the diabetic range?  Diabetes: 200 mg/dL or higher o Hgb A1c glycated hemoglobin (used for diagnosis or tracking glucose control)  What is the prediabetic range?  Prediabetes: 5.7% to 6.4%  What is the diabetic range?  Diabetes: 6.5% or higher Hyperinsulinism o What is Hyperinsulinism?  A condition that can occur when body cells are resistant to insulin o What does the pancreas attempt to compensate for in this condition?  The body’s cellular resistance to insulin by overworking and increasing secretion, which increases the level of insulin in blood to high levels o With time, what normally happens in this condition?  Cellular insulin resistance usually worsens  Pancreatic secretion ability declines  Blood glucose levels begin to rise Glucagon o What is glucagon secreted by?  The alpha cells of the pancreas that regulate blood glucose levels o What does pancreatic glucagon do in hypoglycemia?  Pancreatic glucagon breaks down glycogen stores & raises blood glucose o What does a rise in blood glucose concentration inhibit?  Glucagon secretion and a fall in blood glucose stimulates its excretion o When may glucagon be administered as an injectable medication? Why?  In severe hypoglycemia to raise blood glucose levels Other Hormones That Increase Insulin o What are other hormones that increase insulin secretion?  Growth hormone, cortisol, epinephrine, progesterone, and estrogen Immune-Mediated T1DM o What is immune-mediated T1DM caused by?  Immunological destruction of the insulin–secreting beta cells within the islets of Langerhans of pancreas.

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o What percent of individuals with T1DM have the immune-mediated form?  Approximately 90% Cellular Insulin Resistance T2DM o What is T2DM mainly characterized by?  Cellular resistance to insulin  What does this eventually cause? Why? o Pancreatic beta cell exhaustion o For unknown reasons, body cells are insensitive to effects of insulin and, therefore, do not allow entry of glucose o What is a major contributing factor to development of T2DM?  Obesity  Why? o Fat cells are particularly resistant to insulin o What risks are associated with developing T2DM?  Age, obesity, and lack of physical activity T1DM o What are the initial symptoms of T1DM?  Polydipsia (constant thirst)  Polyuria (excessive urination)  Polyphagia (increased appetite) o What is the first sign of T1DM?  Diabetic ketoacidosis T2DM o What are the initial symptoms of T2DM?  Polydipsia (excessive thirst)  Polyuria (excessive urination)  Polyphagia (increased appetite) o Do they experience diabetic ketoacidosis?  No o What may occur in T2DM?  Hyperosmolar hyperglycemia Pathological Mechanism of T2DM o What is a major pathophysiological process that causes T2DM?  Insulin resistance o What does insensitivity of body cells to insulin cause?  The pancreas attempts to compensate by secreting increasing amounts of insulin  Why may this cause the pancreas to overwork? o Greater-than-normal amounts of pancreatic insulin are required to produce a normal biological response, causing the pancreas to overwork Metabolic Syndrome o What do persons with metabolic syndrome present with?  Insulin resistance, hypertension, dyslipidemia, hyperinsulinism, centralized or “appleshaped” obesity, glucose intolerance, and a predisposition to T2DM o What does metabolic syndrome increase the risk of?  Coronary artery disease and other diseases related to arteriosclerosis, such as stroke and peripheral vascular disease Gestational DM (GDM) o What is gestational diabetes?  Any degree of glucose intolerance that occurs during pregnancy o Why does GDM require treatment?

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 To normalize maternal blood glucose levels in order to avoid complications in the infant o What can happen in the absence of treatment of GDM?  Fetal defects, premature delivery, hypoglycemia in the newborn, and large-forgestational-age infants o When are pregnant women screened for GDM?  During the second trimester o What does gestational DM increase the risk for?  T2DM  GDM in future pregnancies o Studies show that about __% of women who get gestational diabetes will develop type 2 diabetes within the first 5 years after delivery  50% HgbA1c (A1c) o What is the glycated hemoglobin (HbA1c) test (also called A1c) used to diagnose?  Diabetes and assess blood glucose control over preceding 3 months o When is screening for diabetes recommended?  Every 3 years beginning at age 45 Glucosuria o What is glucosuria?  Glucose in the urine Ketonuria o What is ketonuria?  Urine that contains ketones Treatment of Hypoglycemia o What will remedy an acute episode of hypoglycemia?  Ingestion of fast-acting carbohydrates such as glucose tablets or gels, juices, soft drinks, or candy o What is the suggested amount of carbohydrate consumption in hypoglycemia?  15 grams  If, after 15 minutes, blood glucose is still lower than 70 mg/dL and symptoms have not diminished, what is recommended? o An additional dose of 15 grams is recommended  Intravenous injection of 50 mL of 50% dextrose is often used  What is an alternative to this? o A 1 mg dose of glucagon by subcutaneous injection Somogyi Effect o What is the Somogyi Effect?  Nocturnal hypoglycemia while asleep o What is the Somogyi effect usually a consequence of?  Excessive insulin dosage or peaking of insulin action during sleep o What happens by morning?  Epinephrine, growth hormone, cortisol, and glucagon are all released in response to hypoglycemia and raises blood glucose further; in the morning, the patient will be hyperglycemic Dawn Phenomenon o Explain what occurs during Dawn Phenomenon  During the night, peaks of growth hormone slow cellular utilization of glucose allowing glucose levels to rise in the bloodstream resulting in a morning fasting hyperglycemic blood glucose measurement. o What is the difference between the Somogyi Effect and Dawn Phenomenon?

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During Dawn Phenomenon, the patient will not experience hypoglycemia during the night Remedy for Somogyi Effect or Dawn Phenomenon o How do you remedy the Somogyi effect or dawn phenomenon?  The clinician needs to re-evaluate the patient’s insulin or antidiabetic medication regimen, mealtimes, and exercise patterns Diabetic Ketoacidosis (DKA) o When can DKA occur?  When there is no insulin secreted by the pancreas o Does DKA occur in the presence of insulin?  No, DKA does not occur Electrolyte Disturbances in DKA o What does hyperglycemia raise?  The osmotic pressure of the bloodstream which sucks in intracellular fluid into the bloodstream and leads to cellular dehydration and excess water in blood o What are other electrolyte imbalances that may occur in DKA?  Dilutional hyponatremia  False hyperkalemia  Excess water in the bloodstream causing polyuria  Excess glucose in the blood causing glucosuria  Hyperglycemia  What does this cause? o Cell dehydration DKA Clinical Presentation o What is the clinical presentation of DKA?  Polyuria  Polydipsia  Polyphagia  Weakness  Abdominal pain  Kussmaul’s respirations; compensatory  Nausea  Vomiting  Dehydration  Dry mucous membranes, tachycardia, hypotension  Ketonuria  Ketone body odor – fruity odor Treatment of DKA o How is DKA treated?  Fluid replacement  Intravenous insulin (administered until blood glucose diminishes to fewer than 250 mg/dL)  Subcutaneous insulin to maintain blood glucose in range of 150 to 200 mg/dL o What is a potential side effect of fluid and insulin treatment?  They normalize blood pH and cause movement of K+ into intracellular compartment, which may leave patient hypokalemic Fatal Consequences of DKA o What is a severe complication that can develop in DKA?  Cerebral edema  What are early signs of cerebral edema? o Headache, confusion, and lethargy

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o Papilledema, which is swelling of the optic disc o Hypertension o Hyperpyrexia Hyperosmolar Hyperglycemia Syndrome (HHS) o What is Hyperosmolar Hyperglycemia Syndrome (HHS)?  Major short-term complication of T2DM  What is it characterized by? o Severe hyperglycemia, hyperosmolarity, and dehydration o How does Hyperosmolar Hyperglycemia Syndrome manifest?  The presence of insulin prevents fat breakdown, which prevents fatty acid and ketone formation  Cells sense starvation leading to hepatic glycogen breakdown and activation of gluconeogenesis  These mechanisms attempt to compensate for cellular starvation. As a result, with cells continually resisting glucose, blood glucose levels rise higher and higher. o Does HHS develop gradually or quickly?  Gradually o What are common complaints associated with HHS?  Anorexia, weight loss, weakness, visual disturbances, poor tissue turgor, tachycardia, and confusion  Seizures and neurological disturbances can occur o What may occur due to the effect of blood hyperosmolarity in the brain?  Approximately 25% of patients present in coma Treatment of HHS o How do we treat HHS?  IV rehydration  Electrolyte replacement  IV insulin  Adequate fluids should be administered first.  Why? o If insulin is administered before fluids, extracellular water will move intracellularly, worsening hypotension and possible hypovolemic shock Long-Term Complications of DM o Arteriosclerosis can lead to myocardial infarction o Peripheral angiopathy (lack of circulation) can lead to limb ischemia o Diabetic retinopathy can lead to blindness o Diabetic neuropathy can lead to lack of sensation in lower limbs, burning, tingling o Autonomic neuropathy can lead to a lack of sympathetic nervous system stimulation in hypoglycemia o Diabetic nephropathy can lead to kidney failure o Poor wound healing can cause gangrene o Immunosuppression can cause infection Amputation in DM o Why does amputation occur in DM?  Peripheral neuropathy causes a lack of sensation in lower extremities  Peripheral angiopathy causes poor circulation in lower extremities which can result in ischemia of lower extremities  A wound in the lower extremity can occur without patient sensing the skin breakdown  Immunosuppression results in increased infection susceptibility  Infection and ischemia of limb can cause gangrene which may lead to amputation

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o Why should individuals with DM seek care by a podiatrist?  There is sensory loss in the feet Candida Infection Common in DM o What may be a presenting feature of diabetes even before other signs?  Chronic Candida vaginitis o Why is a candida infection common in diabetes?  Because with hyperglycemia, the vaginal cells become glycogen rich  High glucose changes the pH of the vaginal canal, making it more conducive to proliferation of Candida organisms Peripheral Neuropathy Blunts Pain Sensation o The pain of inflammatory conditions and myocardial ischemia (MI) or myocardial infarction may not be perceived. o Silent MI is particularly common in those with diabetes. Psychological Resistance o ___ is common among many individuals with diabetes  Denial o Many affected individuals refuse to comply with insulin administration, who is this particularly common in?  Persons with T2DM who initially obtain good glycemic control with oral medications and later in the course of the disease require insulin Eating Disorders in Adolescents o What does insulin prevent?  Lipolysis o What can decreasing insulin dosage lead to?  Fat breakdown and weight loss, which can be a desirable effect, particularly in adolescent females o What should be suspected in patients with recurrent DKA or chronically poor glycemic control?  Eating disorders Treating DM o What should be maintained within a narrow range?  Blood glucose (70 to 140 mg/dL) regardless of food intake or physical activity. o What indices does the clinician use to guide and evaluate treatment efficacy?  HbA1c level  Fasting blood glucose level  Postprandial blood glucose level o What type of diet should be implemented in a patient who has DM?  200 gram carbohydrates per day  Low-fat/low-salt diet to prevent CV disease  Daily exercise  The diabetic diet should consist of __% carbohydrates, __% fats, and __% protein  50% carbs  30% fats  20% protein Low Glycemic Index Diet o What does the glycemic index measure?  How a carbohydrate-containing food raises blood glucose o What are carbohydrate-containing foods with a low glycemic index?  Dried beans and legumes, most vegetables, most fruit, and whole grain breads and cereals o As a general rule, the more ___ a food, the ___ the glycemic index  Processed  Higher

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Exercise Increases Skeletal Muscle Glucose Uptake o What must individuals with diabetes remember in regard to strenuous muscle activity?  It will reduce blood glucose levels, which can lead to hypoglycemia o When should exercise be scheduled?  1 to 2 hours after a meal or when insulin is not at peak levels o What other precautions should the individual take during sustained exercise?  Ingest carbohydrate snacks and vigilantly monitor blood glucose Patient Self-Monitoring of Glucose o What is preprandial blood glucose?  Measurement of blood glucose before eating o What is postprandial glucose?  Measurement of blood glucose 2 hours after eating o When do clinicians recommend measurement of blood glucose?  Before eating  2 hours after eating  At bedtime Insulin Therapy o What is the goal of insulin therapy?  To mimic physiological control of blood glucose levels, as well as basal and postprandial levels of insulin o When do basal insulin levels occur?  During fasting o What are the two types of insulin?  Conventional insulins and insulin analogues  When can the combined use of these types of insulin be used?  To simulate fasting and postprandial pancreatic insulin Insulin Analogues o What are insulin analogues?  Synthetic preparations with a slightly different structure than human insulin  They have pharmacokinetic profiles that closely approximate physiological endogenous insulin secretion.  **I didn’t include the names of the medications** Basal-Bolus Regimen o What is the basal-prandial insulin regimen (basal-bolus)?  A common type of treatment for optimal glycemic control o What does this regimen use?  A once-daily injection of a long-acting insulin to control fasting plasma glucose level (basal insulin) and boluses of a rapid-acting insulin for post meal glucose elevations (prandial insulin). Oral Antidiabetic Medication o When are oral antidiabetic agents initiated?  When lifestyle modifications prove insufficient to maintain glycemic control

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Endocrine Disorders o Hypothalamic-Pituitary-Hormonal Axis  What does the hypothalamic portion of the brain secrete? What does it stimulate?  A releasing factor that stimulates the pituitary gland o What does the pituitary gland do after it is stimulated?  It releases a substance referred to as a tropic hormone  What does this target? o An endocrine organ – what does this secrete?  A hormone that acts on the body and causes a physiological effect Hormone Feedback System o How are hormones kept in check?  By a unique endocrine feedback system  What happens after the...