HESI EXAM CARE OF ADULTS WITH COMPLEX ILLNESS ENDOCRINE - DISORDERS

Nursing Interventions ● Assessments: Serum calcium levels, Serum phosphorus levels, Cardiac monitoring, and Acid-base status. ● Actions: Increase fluid intake to 3000 mL/day, Administer furosemide (Lasix) as ordered, Administer oral phosphates as ordered, Administer calcium chelators, Use a lift sheet in patients with chronic hyperparathyroidism to prevent bone injury, and Strain urine with suspected renal calculi. Teaching: ● Signs of hypocalcemia and hypercalcemia ● Low-calcium diet ● Increase fluids and fiber to decrease complications of constipation ● Patients with hyperparathyroidism are also taught to decrease consumption of calcium-containing antacids and vitamin D. ● Thiazide diuretics are also to be avoided in patients with hyperparathyroidism because these medications increase reabsorption of calcium in the kidney. Risk Factors: Although most commonly diagnosed before age 30, type 1 diabetes can occur at any stage of life, even into the eighth and ninth decades. Patho: Triggered by an autoimmune process in which the insulin-producing beta cells of the pancreas are destroyed, resulting in an absolute lack of insulin. Clinical Manifestations: Predominant features include polyuria, polydipsia, polyphagia, fatigue, glucosuria, hyperglycemia, decreased appetite and weight loss. Dx: ● Hemoglobin A1c (glycosylated hemoglobin) value: Greater than or equal to 6.5% ; 5.7%–6.4% ● Fasting blood glucose: Greater than or equal to 126 mg/dL ; 100–125 mg/dL ● Two-hour postprandial (after meals) or the oral glucose tolerance test (OGTT): Greater than or equal to 200 mg/dL ; 140–199 mg/dL ● Random blood glucose: Greater than or equal to 200 mg/dL Treatment: Insulin, Continuous glucose monitoring (CGM) systems, A1C monitoring and glucose monitoring. Complications: HYPOGLYCEMIA( blood glucose level of less than 65 mg/dL) ● Hypoglycemia is an important and dangerous complication of the treatment of diabetes. It can present as an acute or even life-threatening emergency due to the potentially devastating effects on the central nervous system. ● S/S: Anxiety, hunger, palpitations, sweating, shakiness, irritability, and Circumoral paresthesia (numbness around lips). ● Management: Oral glucose (15–20 g) administration is the preferred treatment for the conscious individual with hypoglycemia, although any form of rapidly absorbed carbohydrate may be used. Juice, soda, honey, jelly, bread, or crackers work well. ○ Carbohydrates that contain fat, such as ice cream or chocolate, are not recommended. ○ In the hospital setting: if a patient is unable to swallow or absorb oral carbohydrates but has IV access, IV dextrose, 25 to 50 mL of 50% dextrose solution (D50), should be administered. If there is no IV access and the patient is unable to swallow or absorb oral carbohydrates, 1 mg of Diabetes Mellitus (including pharm and management of hypoglycemia) Type 1 intramuscular glucagon injection should be administered. Glucagonmobilizes glucose release from stores in the liver. Nursing Interventions: ● Assessments: Vital signs, Serum glucose, Potassium levels, Carbohydrate intake at meals, and Intake and output. ● Actions: Bedside glucose monitoring (finger sticks) done before meals and at bedtime, Administer insulin as ordered, and Administration of isotonic IV fluids as ordered Teaching: ● Signs of hypoglycemia and hyperglycemia ● Subcutaneous insulin administration ● Syringe size ● Rotating sites ● Medication education ● Healthy lifestyle that includes diet and exercise Type 2 Risk Factors: ● Modifiable: Body mass index (BMI) greater than 26; increased risk with BMI greater than 30, Physical inactivity, High-density lipoprotein (HDL) cholesterol level less than or equal to 35 mg/dL (0.90 mmol/L) and/or a triglyceride level greater than or equal to 250 mg/dL (2.82 mmol/L) and Metabolic syndrome. ● Nonmodifiable: First-degree relative with diabetes, African American, Latino, Native American, Asian American, Pacific Islander, Women who delivered a baby weighing greater than or equal to 9 lb or who were diagnosed with gestational diabetes, HTN, Women with polycystic ovary syndrome, HgbA1c greater than or equal to 5.7%, and History of cardiovascular disease ● A condition called prediabetes is a warning sign for the development of type 2 DM. This is defined by blood glucose levels higher than normal but not high enough to be considered diabetes. Patho: Type 2 DM involves defects at the cell membrane that prevent the normal action of insulin, insulin resistance develops that requires increased levels of insulin in order to drive glucose into the cell. Clinical Manifestations: polyuria, polydipsia, polyphagia, Fatigue, Poor wound healing, Cardiovascular disease, Visual disturbances, Renal insufficiency, and Recurring infection. Dx: The diagnosis of type 2 DM is done through evaluation of the same laboratory analyses as type 1 DM: HgbA1c levels, fasting blood glucose levels, 2-hr postprandial blood levels, and random blood glucose level. Treatment: Education, Monitoring glycemic control, Nutrition, Exercise, and Monitoring for complications. ● Pharm: metformin (Glucophage), glucagon-like peptide-1 (GLP-1) receptor agonist, Sulfonylureas, Meglitinides, Thiazolidinedione, Alpha-glucosidase inhibitors, DPP-4 inhibitors, and SGLT-2 inhibitors Nursing Interventions: ● Assessments: Vital signs, Serum glucose, Capillary refill in lower extremities, Skin assessment, especially lower extremities and feet, looking for breaks in the skin, erythema, trauma ; Intake and output, WBC count, Serum blood urea nitrogen (BUN) and creatinine levels, Carbohydrate intake at meals and Spot urine for microalbuminuria. ● Actions: Blood glucose monitoring (finger sticks) completed before meals and at bedtime, Administer oral diabetes medications as ordered, Administer insulin as ordered, Administer isotonic IV fluids as ordered, and Administer antibiotics as ordered. Teaching: ● Medication education ● Regular blood glucose checks via finger sticks, alternate site testing, and CGM ● Healthy lifestyle that includes meal planning and exercise ● Signs of hypoglycemia and hyperglycemia ● Foot care ● Monitoring for complications Diabetic Ketoacidosis Risk Factors: 1. Intentional or unintentional missed or reduced doses of insulin 2. Inadequate insulin due to increased insulin needs secondary to stress or infection 3. New onset of type 1 diabetes Patho: There is inadequate insulin for cells to obtain adequate glucose for normal metabolism. The body attempts to obtain energy by the rapid breakdown of fat stores, releasing fatty acids from adipose tissues. The liver converts the fatty acids into ketone bodies, which can serve as an energy source in the absence of glucose. The ketone bodies, however, have a low pH, resulting in metabolic acidosis. The absence of insulin also results in an increased release of hormones, such as glucagon and cortisol, in response to inadequate glucose transport into the cells. This leads to gluconeogenesis and glycogenolysis, resulting in severe hyperglycemia leading to hyperosmolality and osmotic diuresis, as discussed previously. Clinical Manifestations: polyuria, polydipsia, polyphagia, hyperkalemia or hypokalemia, Kussmaul respirations, glycosuria, nausea, vomiting, abdominal pain, blurred vision, breath smells of acetone, and lethargy. ● Can lead to a coma Dx: ● Blood glucose level greater than 250 mg/dL ● Ketonuria (ketones in the urine) ● Arterial pH of less than or equal to 7.3 ● Serum bicarbonate level of less than or equal to 18 mEq/L Hyperosmolar Hyperglycemic Syndrome (HHS) ● Positive anion gap Treatment: ● Fluid replacement with isotonic normal saline ● Correction of electrolyte imbalances, focusing on monitoring and correction of decreased potassium level if necessary, prior to insulin administration ● Insulin administration, usually by intravenous delivery Risk Factors: Hyperosmolar hyperglycemic state (HHS) is a serious metabolic derangement that occurs in patients with DM. Patho: The condition is characterized by hyperglycemia, hyperosmolality, and dehydration without significant ketoacidosis. It occurs when there is sufficient insulin to prevent rapid fat breakdown and ketone release. However, there is not enough insulin to prevent severe hyperglycemia. Clinical Manifestations: Electrolyte imbalances, dehydration, most patients present with global neurological defects. Dx: ● Blood glucose level of 600 mg/dL or greater ● Serum osmolality of 320 mOsm/kg or greater ● Profound dehydration ● Serum pH greater than 7.4 ● Bicarbonate concentration greater than 15 mEq/L ● Low ketonuria and absent to low ketonemia ● alteration in level of consciousness Treatment: Treatment prioritiesinclude standard care for dehydration with IV fluid andtreatment for altered mental status, including airway management as appropriate. Patients may respond to fluids alone, but IV insulin may be necessary to correcthyperglycemia.