Module 1 (NHI III) PDF

MED SURG.MOD 1 CHAPTER 38:Understanding the Endocrine System Endocrine System contains: o Pineal Gland: “mystery gland”; “third eye” ▪ Secretes melatonin (for sleep, reproduction and cancer prevention) o Pituitary Gland (hypophysis): controlled by hypothalamus...

MED SURG.MOD 1 CHAPTER 38:Understanding the Endocrine System Endocrine System contains: o Pineal Gland: “mystery gland”; “third eye” ▪ Secretes melatonin (for sleep, reproduction and cancer prevention) o Pituitary Gland (hypophysis): controlled by hypothalamus ▪ Anterior Growth hormone (GH): regulated by growth hormone releasing hormone (GHRH) and by growth hormone inhibiting hormone (GHIH or somatostatin); stimulated by hypothalamus Thyroid stimulating hormone (TSH): stimulates growth and secretions of thyroid gland; stimulated by thyrotropin releasing hormone (TRH) Adrenocorticotropic hormone (ACTH): stimulates secretions of cortisol and related hormones from adrenal cortex; stimulated from Corticotropin releasing hormone (CRH) o CRH: produced during exercise, stress, disease or hypoglycemia ▪ Posterior Antidiuretic hormone (ADH): also known as “vasopressin”; increases water reabsorption by kidney tubules and urine output is decreased (maintains blood pressure)  o Major fluid loss: hemorrhages; large amount of ADH secretion will result in arteriole vasoconstriction Oxytocin (prolactin): contractions and breastfeeding; acts as a positive feedback loop o Thyroid Gland ▪ Triiodothyronine (T3) & Thyroxine (T4): stimulated by TSH in anterior pituitary Increase metabolism of glucose and fatty acids to increase energy and heat production Essential for growth, development, and reproduction Requires intake of iodine ▪ Calcitonin: stimulus is hypercalcemia Inhibits resorption of calcium and phosphorous in blood so they stay in the blood (“TONE IT DOWN”) ***resorption: breaks down bone tissue and releases calcium ions into circulation ***reabsorption: process of absorbing a substance into blood again o Parathyroid Gland: 4 glands: 2 on back of each lobe ▪ Parathyroid hormone (PTH): antagonist to calcitonin Target organs: bone, small intestines, and kidneys Overall raises blood calcium level and lowers blood phosphate levels ***homeostasis of blood calcium level is regulated by calcitonin and PTH o Adrenal Glands ▪ Adrenal cortex: located superior to each kidney; secretes 3 types of steroid hormones Mineralcorticoids (aldosterone): think SALT; promotes reabsorption of sodium and excretes potassium by kidney tubules; helps maintain blood volume and blood pressure Glucocorticoids (cortisol): think SUGAR; stimulates gluconeogenesis in liver and increases lipolysis and protein catabolism for energy; energy is required for proper brain functioning; also helps with anti-inflammatory effects BUT can lower immune response and delay healing Gonadocorticoids (male androgens and female estrogens): sex; only source of estrogen after menopause; contribute to libido ▪ Adrenal Medulla: releases epinephrine and norepinephrine (catecholamines); they are sympathomimetic (fight or flight response) o Pancreas: secretes somatostatin to inhibit both insulin and glucagon (antagonists) ▪ Insulin: secreted by beta cells; stimulated by hyperglycemia; increases movement of glucose from blood into cells lowering blood glucose and making it available as energy ▪ Glucagon: secreted by alpha cells: stimulated by hypoglycemia o Duodenum o Ovaries  o Testis: consist of two lobes connected by a piece of tissue called the isthmus Effects of Aging: most of the endocrine glands decrease secretion with age; normal aging usually does not lead to serious hormone deficiencies or illness o Decreased GH, TSH, and TH o Decreased insulin secretion and glucagon tolerance o Reduced sex hormones o Increased ADH o Reduced liver & kidney functions, use hormone replacements cautiously Nursing Assessment: o INSPECTION ▪ Mood and affect (emotional tone) ▪ Inspect the neck for thyroid enlargement ▪ Building eyes (exophthalmos) ▪ Weight change ▪ Tremors ▪ Posture ▪ Fat pads o PHYSICAL ASSESSMENT ▪ Palpation (thyroid gland is the only palpable endocrine gland) ▪ Peripheral pulses (posterior tibial and dorsalis pedis may be diminished in circulation issues) ▪ Skin turgor (sternum is common): dehydration = ADH insufficiency ▪ ***Remember the thyroid gland should NEVER be palpated in a patient with uncontrolled hyperthyroidism because this can stimulate secretion of additional thyroid hormone o DIAGNOSTIC TESTS ▪ Hormone test: (serum hormone levels, stimulation tests, suppression tests) ▪ Urine Tests ▪ Nuclear Scans (thyroid, radioactive iodine Uptake, PET Scans) ▪ Radiographic Tests (CT, MRI) ▪ Ultrasound ▪ Biopsy CHAPTER 39: Adrenal Disorders Pheochromocytoma: tumor of chromaffin cells of adrenal medulla; secretes catecholamines; usually benign o Etiology ▪ Usually unknown; mostly just hereditary o S/S (fight or flight) ▪ ***HTN (main one; diastolic can be 115 or higher; increased risk of CVA) ▪ Tachycardia ▪ Palpations ▪ Anxiety ▪ Headache  ▪ Vison changes ▪ ***Risk for stroke, heart attacks, heart failure, vison changes, seizures, psychosis, and organ damage o Diagnostic tests ▪ 24hr urine (no caffeine or meds before) ▪ CT or MRI to find the tumor o Treatment ▪ Medications: beta blockers, alpha blockers, and calcium channel blockers ▪ Surgery: adrenalectomy o Nursing Care ▪ Monitor vitals ▪ Quiet and calm environment; reduce stressors ▪ No stressors ▪ Replace corticosteroids postoperatively Addison’s Disease: involves adrenal cortex; not enough cortisol; and/or not enough aldosterone or androgens; lack of mineralocorticoids and glucocorticoids o Etiology ▪ Autoimmune ▪ AIDS ▪ Cancer ▪ Pituitary or hypothalamus problems ▪ Abrupt discontinuance of steroids o S/S ▪ Hypotension (specifically postural hypotension) ▪ Hyponatremia (sodium loss) ▪ Hyperkalemia (potassium retention) ▪ Hypoglycemia ▪ Weakness and fatigue ▪ Weight loss ▪ GI disturbances ▪ Bronzed skin ▪ Changes in distribution of body hair ▪ Nausea and vomiting o Complications ▪ Occurs with exposure to stress, infection, trauma, psychological pressure ▪ ***Adrenal crisis: profound fatigue, dehydration, vascular collapse (decreased bp), renal shut down, hyponatremia and hyperkalemia which can lead to cardiac arrythmias o Treatment ▪ Glucocorticoids (hydrocortisone) and mineralcorticoids (fludrocortisone (Florinef)) are taken daily for remainder of life 2/3 of dose in AM and 1/3 in PM; double or triple dose during stress ▪ Patients should wear a medic-alert bracelet  ▪ Replace electrolytes o Nursing care ▪ Risk for deficient fluid volume: monitor vitals and fluid volume; daily weights ▪ Ineffective health management: lifelong treatment; identify causes of stress; educate about IM emergency kit (if pt is unable to take oral meds); may need to increase sodium intake during hot weather ▪ ***remember to NEVER ABRUPTLY DISCONTINUE STEROIDS; taper down to avoid adrenal crisis Cushing’s Syndrome: excess adrenal cortex hormones o Etiology ▪ ***most common cause: increased glucocorticoids (prednisone- taken for chronic inflammatory disorders- rheumatoid arthritis, COPD, Chron’s) ▪ Hypersecretion of ACTH by pituitary gland (result of benign pituitary tumor/adenoma which results in Cushing’s disease) o S/S ▪ Weight gain ▪ Truncal obesity (central obesity) ▪ Thin arms and legs ▪ Buffalo hump (fatty pad) ▪ Moon face (round face due to excess adipose tissue) ▪ Muscle wasting ▪ Striae ▪ Risk for osteoporosis, fractures (due to muscle atrophy) ▪ Risk for infection (due to anti- inflammatory and immunosuppressive action of cortisol) ▪ Mental status changes ▪ Androgen effects (acne, facial hair, amenorrhea) ▪ Sodium and water retention ▪ Hypokalemia ▪ Hyperglycemia ▪ Thin skin o Complications ▪ ***Secondary diabetes mellitus (insulin resistance and stimulates gluconeogenesis, resulting in glucose intolerance) o Diagnostic Tests ▪ Cushingoid appearance ▪ History of taking steroids ▪ Plasma and urine cortisol ▪ Plasma ACTH ▪ 24hur urine test for cortisol  o Treatment ▪ Surgery (if tumor is present) ▪ Diet (high potassium, low sodium, high protein) ▪ Diabetes treatment if necessary ▪ Potassium supplements ▪ ***Alternate day therapy for steroids (before 9am): used when the cause is due to medications; the goal is to trick to pituitary to release ACTH so that the patient can taper off meds; doesn’t apply to those who have had adrenalectomies as they would need lifelong treatment o Nursing problems ▪ Excess fluid volume: stick with HCP’s ordered diet ▪ Risk for impaired skin integrity: Q2 turns, avoid harsh soaps and hot water, refrain from use of tape, pressure reducing mattress ▪ Risk for infection: hand hygiene, vaccinations for flu and pneumonia ▪ Risk for unstable blood glucose levels: insulin (remember that oral hypoglycemics usually aren’t effective) ▪ Disturbed body image: develop trust, allow patient to verbalize feelings Adrenalectomy: removal of the adrenal gland o Pre-op: monitor electrolytes and blood sugar o Post-op: assess for fluid and electrolyte balance, assess for adrenal crisis, educate about lifelong hormone replacement therapy (HCT), educate pt to contact HCP if unable to take HRT orally CHAPTER 39: Pituitary disorders Diabetes Insipidus (DI): insufficient ADH (water loss- think “DRY INSIDE”); extreme diuresis o Etiology ▪ Tumors ▪ Trauma of pituitary gland ▪ Glucocorticoids ▪ Alcohol o Pathophysiology ▪ Decreased ADH causing water to not be reabsorbed in the kidneys o S/S ▪ Polyuria (3-15 L/day) ▪ Dehydration ▪ Polydipsia (extreme thirst) ▪ Increased blood osmolality; concentrated blood (>295 mOsm/kg) ▪ Nocturia (peeing throughout the night) ▪ Electrolyte imbalance ▪ Hypovolemic shock can lead to death if left untreated o Diagnosis ▪ Low specific gravity; diluted urine (will be 100bpm (teach pt to take pulse at home) o Nursing Process ▪ Activity intolerance ▪ Risk for impaired skin integrity ▪ Imbalanced nutrition (more than body requirements Hyperthyroidism: too much TH o Etiology ▪ Multinodular goiter ▪ Grave’s disease (autoimmune disease where TSH makes too much TH) ▪ Pituitary tumor ▪ Levothyroxine overdosage o S/S ▪ Hypermetabolic state ▪ Heat intolerance ▪ Increased appetite ▪ Weight loss ▪ Frequent stools ▪ Nervousness ▪ Tachycardia and palpitations ▪ Tremors ▪ Heart failure ▪ Warm, smooth skin ▪ Exophthalmos (eye buldging) o Gerontological s/s: heart failure, a-fib, palpitations, fatigue, depression o Complications ▪ Thyrotoxic crisis (can occur after thyroidectomy) S/S: Tachycardia, HTN, ARDs, fever of up to 106, dehydration ***Coma (death within 2 hours if not treated; MEDICAL EMERGENCY) Treatment: IV fluids, cooling blanket, iodine, beta blockers (propranolol), Tylenol for fever, oxygen administration ▪ Hypothyroidism (overmedicating) o Treatment ▪ Methimazole (monitor for agranulocytosis) ▪ Beta blockers (propanalol) ▪ Oral or radioactive iodine Radioactive: limit time in pt’s room, avoid contact with pregnant women, dispose of bodily fluids properly, and encourage pt to drink fluids ▪ Thyroidectomy  o Nursing care ▪ Report elevated BP or pulse ▪ Monitor crackles and lung sounds ▪ Assess anxiety and coping mechanisms ▪ Assess eyes ▪ ***NEVER PALPATE THYROID o Nursing Process ▪ Hyperthermia ▪ Diarrhea ▪ Imbalanced nutrition: less than body requirements ▪ Disturbed sleep pattern ▪ Anxiety ▪ Risk for injury (tape eyes at night for Graves’ disease) Goiter: enlarged thyroid; low TH and high TSH o Etiology ▪ Iodine deficiency ▪ Virus ▪ Genetics ▪ Goitrogens (medications that interfere with body’s use of iodine) o Pathophysiology ▪ Enlarged thyroid gland; may he high, low, or euthyroid state o S/S ▪ Dysphagia ▪ Difficulty breathing o Treatment (treat cause) ▪ Avoid goitrogens ▪ Thyroidectomy ▪ Treat iodine deficiency ***iodine foods: seaweed, cod, Greek yogurt, oysters, milk, iodized salt o Nursing care ▪ Monitor breathing and watch for stridor ▪ Monitor swallowing ▪ Dietary consult for soft foods ▪ Speech therapy Cancer of thyroid: most common endocrine cancer and occurs more in women; most tumors are benign; TH is usually in normal range o Etiology ▪ Radiation ▪ Iodine deficiency ▪ Goitrogens ▪ Hyperplasia o S/S ▪ Hard and painless nodules ▪ Dysphagia ▪ Dyspnea if there is an obstruction o Diagnosis  ▪ Thyroid scan shows “cold spots” ▪ Biopsy o Treatment ▪ Radioactive iodine ▪ Thyroidectomy: can be partial or total Thyroidectomy o Pre-op care ▪ Monitor airway (breathing and swallowing) ▪ Assess nutrition ▪ Monitor VS ▪ Administer iodine or antithyroid drugs to achieve a euthyroid state ▪ Educate: gentle ROM, never hyperextend, support neck, incentive spirometry o Post-op care ▪ Monitor airway and swelling, vitals, bleeding, and voice changes ▪ Have trach at beside ▪ Keep in semi-fowlers position; support head and neck (be gentle when doing ROM) ▪ Keep pain controlled ▪ No coughing!!! ▪ Dietician consult ▪ Monitor serum calcium levels (have calcium gluconate in case of tetany- twitching and muscle cramps) o Complications ▪ Airway obstruction ▪ Hemorrhage ▪ Tetany (will occur 24-73 hours after surgery) ▪ Thyrotoxic crisis (thyroid storm) ▪ Laryngeal nerve damage o Nursing problems ▪ Ineffective airway clearance ▪ Risk for injury ▪ Acute pain ▪ Ineffective health management Parathyroid hormone: PTH; regulates blood level of calcium Hypoparathyroidism: decreased PTH o Etiology ▪ Hereditary ▪ Accidental removal of parathyroids during thyroidectomy ▪ Hypomagnesemia: occurs with chronic alcoholism or nutrition issues o Pathophysiology ▪ Calcium stays in the bones and leads to hypocalcemia o S/S ▪ ***Tetany: neuromuscular irritability, numbness and tingling of fingers and perioral areas, muscle spasms and twitching o Diagnosis ▪ Low PTH and serum calcium ▪ High phosphorous  ▪ Positive Chvostek’s sign (tapping cheek causes facial nerve to twitch) ▪ Positive Trousseau’s sign (and contracts when bp cuff is inflated) ▪ Exaggerated reflexes o Treatment ▪ IV calcium gluconate (acute instances) ▪ Long term: oral calcium with Vitamin D and a high calcium diet o Nursing problems ▪ Risk for injury Hyperparathyroidism: increased PTH o Etiology ▪ Hyperplasia ▪ Benign tumor ▪ Hereditary ▪ Kidney disease due to failure to activate vitamin D (which is necessary for absorption in small intestine) o Pathophysiology ▪ Overactive parathyroid that leads to hypercalcemia o S/S ▪ Fatigue ▪ Muscle weakness ▪ Polyuria ▪ Nausea and vomiting; anorexia ▪ ***Kidney stones (1st sign) ▪ ***Pathologic fractures (1st sign) ▪ Cardiac arrythmias ▪ Abdominal pain ▪ Peptic ulcers o Complications ▪ Coma ▪ Cardiac arrest o Diagnosis ▪ High PTH and serum calcium ▪ X-rays for decreased bone density ▪ 24 hour urine test o Treatment ▪ Mild cases: extra IV fluids to dilute calcium, monitor bone changes and renal function, educate about weight bearing exercises ▪ Patients will take oral calcium and vitamin D (but levels are monitored very closely) ▪ Acute cases: IV NS to dilute, furosemide, calcitonin or alendronate, parathyroidectomy o Nursing problems ▪ Risk for injury: smoking cessation, keep bones strong, encourage safe ambulation Chapter 40: Diabetes Insulin: produced by beta cells and is necessary for glucose to enter cells o Allows for glucose to be used as energy  o Lowers BG levels o Helps body store excess glucose in the liver (stored as glycogen) Glucagon: produced by alpha cells o Raises BG levels by releasing glycogen from the liver and muscle stores Diabetes: OVERALL o S/S ▪ 3 Ps: polyuria, polydipsia, and polyphagia ▪ Glycosuria and nocturia ▪ Fatigue, blurry vision, abdominal pain, headaches ▪ Ketones in T1DM and advances T2DM o Diagnosis ▪ FBG (fasting blood glucose) Normal: 70-99 Prediabetes: 100-125 Diabetes: 126 or higher ▪ Random blood glucose: over 200 (indicates diabetes) ▪ OGTT (oral glucose tolerance test) Prediabetes: 140-199 Diabetes: 200 or more ▪ Glycohemoglobin (HbA1c): “glycosylated hemoglobin”; measures glucose saturated RBCs within the last 3 months Normal: less than 5.7% Prediabetes: 5.7%-6.4% Diabetes: 6.5% or higher ▪ Ketones, blood, and urine ▪ Additional: lipids, serum creatinine, urine microalbumin, urinalysis, EKG Type 1: juvenile diabetes/early onset before 15 years old; IDDM (insulin dependent); about 5% of diabetics o Pathophysiology ▪ Destruction of beta cells in pancreas which means the body is unable to produce any insulin; fast/rapid onset o S/S ▪ Polyuria (increased urination) ▪ Polydipsia (increased thirst ▪ Polyphagia (increased hunger) ▪ Weight loss ▪ Fatigues ▪ Increased infections ▪ Ketoacidosis (pt is usually young and thin) o Treatment ▪ Insulin must be injected o Prone to develop ketoacidosis (patient is usually young and thin) Type 2: adult onset; NIDDM (non-insulin dependent) o Etiology ▪ Hereditary ▪ Obesity ▪ Sedentary lifestyle  ▪ Over 50 years old ▪ History of HTN o Pathophysiology ▪ Tissues may become resistant to insulin due to lifestyle (nutrition, obesity, HTN, etc.); slow onset ▪ Insulin is still made but disease progression causes insulin production to diminish o S/S ▪ Fatigue ▪ Decreased energy ▪ Polyuria ▪ Polydipsia ▪ Recurrent infections ▪ FBS >126 mg/dl o Treatment ▪ Insulin or oral hypoglycemics ▪ weightloss Gestational diabetes o Pathophysiology ▪ Can result form stressors ▪ Occurs in 2%-10% of pregnancies Prediabetes: higher than normal BG levels but not enough to be diagnosed as a diabetic o Etiology: occurs before onset of type 2 o Diagnosis: 100-125 after fasting Metabolic Syndrome: must have 3 or more of the following o Risk Factors ▪ Physical inactivity (sedentary life) ▪ Aging ▪ Hormone imbalance ▪ Genetics or Hispanic ethnicity ▪ Obesity o Treatment ▪ Monitor for T2DM and heart disease ▪ Educate about low salty foods, low fatty foods, weight loss, maintenance of BP and cholesterol levels o Diagnosis ▪ Increased waist circumference Women: 35 inches Men: 40 inches ▪ Increased triglycerides (150 or higher) ▪ Decreased HDLs Women: 50 Men: 40 ▪ Increased BP (130/85 or higher) ▪ Increased FBG (100 or higher) Hyperglycemia o Etiology ▪ Calories eaten are more than the insulin readily available in the body (overeating)  ▪ Epinephrine, cortisol, GH, and glucagon count regulate against stress ▪ Inadequate amount of insulin o S/S ▪ 3 Ps ▪ Blurry vision ▪ Headache ▪ Lethargy ▪ Abdominal pain ▪ Ketonuria ▪ Possible coma Hypoglycemia: not enough glucose available in body: 30 min away, follow up with a complex carb and protein ▪ Elderly on beta blockers may not recognize s/s (check BG more often) ▪ Educate diabetic patients about always carrying a “fast sugar” on them Reactive hypoglycemia: BG drops to 50 without diabetes; possible impending diabetes diagnosis o Pathophysiology ▪ Pancreas overproduces insulin ▪ Low BG level causes epinephrine release (fight or flight response) o Nursing Care ▪ Small frequent meals, avoid fasting and simple sugars, increase fiber and complex carbs , protein is recomended Diabetic ketoacidosis (DKA): o Etiology  ▪ Deficient insulin levels ▪ T1DM (most often) and T2DM (late stage) ▪ Stress or illness o Pathophysiology ▪ Insufficient insulin leads to starvation of cells ▪ Body breaks down fat for energy and it releases ketones ▪ Ketones build up in the blood and make the BG extremely high o S/S ▪ Kussmaul breathing (body tries to correct acidosis by deepening breathing to blow off excess CO2) ▪ Fruity breath/ acetone breath ▪ Dehydration ▪ Polyuria ▪ Tachycardia, hypotension, and shock ▪ Initial hyperkalemia (K builds up in the blood then is excreted through urine causing hypokalemia) ▪ Abdominal pain ▪ Vomiting ▪ Dry skin and mucous membranes ▪ Thirst ▪ Possible loss of consciousness and death if untreated o Treatment ▪ Iv fluids or subcutaneous insulin (may add glucose to IVF when BG drops to 180 to decrease risk of hypoglycemia) ▪ Monitor BG levels and potassium levels ▪ Monitor ABGs o Prevention ▪ Educate about monitoring levels at home, checking urine for ketones, drink plenty water, and to never stop insulin without HCP consult Hyperosmolar Hyperglycemic state (HHS): no ketones o Etiology ▪ More common with T2DM ▪ Stress and illness ▪ More often seen in older adults o Pathophysiology ▪ Some insulins present so there is no starvation of cells o S/S (develops slowly) ▪ Extreme thirst ▪ Lethargy ▪ Mental confusion ▪ Polyuria ▪ Extreme dehydration ▪ BG levels may rise to 1500mg/dL ▪ May lack clinical manifestations (pt may delay seeking treatment) ▪ Shock, coma and death if untreated (mortality rate is 20%)  o Treatment ▪ IV fluids and insulin ▪ Glucose and electrolyte monitoring o Prevention ▪ Educate about monitoring BG levels at home ▪ Increase fluids if BG are getting high Long term complications of diabetes o Macrovascular: circulatory system ▪ Atherosclerosis and arteriosclerosis ▪ HTN, high LDL and triglycerides ▪ Increased clotting ▪ Higher risk of strokes, heart attacks, poor circulation in lower extremities ▪ Educate: control BG, BP and cholesterol; avoid smoking, maintain healthy weight, exercise regularly ▪ Meds: ASA therapy, ACE inhibitors, statins and ARBs for BP o Microvascular system ▪ Eyes: retinopathy, small hemorrhages that could lead to blindness, high incidence of cataracts Educate: control BG, frequent eye exams and diluted eye exams yearly ▪ Kidneys: nephropathy (kidneys cannot rid waste products and excess fluid); end stage renal disease (ESRD) Treatment: hemodialysis or peritoneal dialysis; kidney transplant; routine urine tests to check for albumin; renal dietician Meds: ACE inhibitors, ARBs Educate: control BG to prevent delayed kidney disease ▪ Nerve complications: neuropathy Numbness and pain in extremities, sexual or erectile dysfunction, gastroparesis (delayed stomach emptying) Treatment: antidepressants, anticonvulsants (gabapentin) ▪ Infection: slower healing WBCs become sluggish and ineffective Poor blood supply makes antibiotics harder to reach (may use topical) Periodontal/gum disease increases Educate: good oral hygiene and regular dental visits, routine vaccines (flu, pneumonia, hepatitis) ▪ Foot complications: risk for gangrene and nasty infections Soft tissue damage (ulcers) Charcot arthropathy: “Charcot foot”; due to neuropathy and development of unrecognized injuries; with inadequate blood supply and abnormal regulation problems occur (dislocations and deformities) Educate: monitor pressure points, foot care, referral to podiatrist Diabetics and surgery o What will happen: decreased immunity and healing, increased infection risk o Nursing care: monitor frequently o Extremely ill patients: keep BG between 140-180 mg/dL Nursing Process  o Assessment: table 40.8 (page 783) o Care plan: page 784-785 o Evaluation: best indicator of success is controlled BG levels and HbA1c Goals of treatment o Pre-prandial: 80-130 o Peak prandial: lower than 180 o HgA1c: lower than 7% o Blood pressure: lower than 140/90 Nutrition therapy o Carbohydrates contribute the most to BG levels; consistent carbs are important o Patients with DM should eat every 4-5 hours while awake o Sucrose should be incorporated into meal plan o Build a plate: ½ with nonstarchy veggies, ¼ with starches, ¼ with meats/protein, add a serving of fruit or 8 oz of non-fat milk o Fiber: 25-30 grams per day; reduces the amount of insulin needed by lowering BG levels; also lowers cholesterol; helps pt feel fuller; increases the need for water o Exercise: lowers BG for up to 48 hours; improves lipids and circulation; 150 min/week over 3 or more days; resistance exercise; avoid if ketones are present ▪ ***ketones: indicate insufficient insulin and glycogen may be released during workouts and BG will increase significatly ▪ Important to check BG before working out and if it’s less than 100, have a carbohydrate snack before Insulins o Route ▪ All given Ssubcutaneous ▪ IV: clear insulins (Novolog, Apidra, and regular insulin) ▪ DO NOT ASPIRATE or rub site after injection ▪ Roate sites (prevents lipodystrophy) ▪ Insulin pens: NOT SHARED, change needle each time, hold for 10 seconds o Insulin pump ▪ Delivers insulin continuously ▪ Needle is in thigh and is administer 2-3 days at a time ▪ Can be bloused before meals or snacks ▪ Allows for a more flexible lifestyle ▪ Use of carb counting o Timing ▪ Onset: time that elapses before insulin starts to lower BG ▪ Peak: when max effect occurs and BG is at its lowest point ▪ Duration: length of time insulin works before it’s used up o Regimens ▪ More frequent injections=better control (decreased risk of complications; increased risk for hypoglycemia) ▪ Basal insulin: long acting (glargine); given once a day ▪ Bolus insulin: short acting (lispro); given before meals o Sliding scale (ACHS): dose is based on BG level o Mixing insulins: CLEAR THEN CLOUDY ▪ ***air into cloudy, air into clear, draw up clear, draw up cloudy  o Oral hypoglycemic agents: helps with T2DM; NEVER T1DM ▪ NOT insulin ▪ Administer before meals and make sure to eat within 30 minutes after receiving ▪ Insulin may be added if oral meds aren’t helping (doesn’t mean they’re diagnosed with T1DM) o Injectables ▪ Incretin mimetics: secreted by GI tract and stimulate insulin release and reduce glucagon release ▪ Amylin mimetics: hormone that naturally releases and is used with insulin; may cause hypoglycemia and promotes weight loss o Natural remedies ▪ Cinnamon is common ▪ ALWAYS ask HCP first o Self monitoring of glucose (ACHS) ▪ Most of the cost involved is the test strips ▪ Keep a diary ▪ HCP will explain a normal BG range for each individual o Urine Glucose: usually 180 mg/dL ▪ No longer recommended (difficult to base treatment off of urine glucose levels) o Urine Ketones ▪ Tested during stress, illness, pregnancy, if BG is consistently over 300 ▪ T1DM are most at risk for DKA ▪ Indicates insulin deficiency Insulin Type Example Onset Peak Duration When to give Very short Lispro (Humalog) 15 min 1-2 hr 2-4 hr No more than 15 acting Aspart (Novolog) min before meal Glulisine (Apidra) Inhaled insulin (Afrezza) 12-15 min 30 min 3 hr Short acting Regular (Humulin R, Novolin R) 30 min 2-3 hr 3-6 hr No more than 30 min before meal Intermediate Neutral protamine Hagedorn (NPH) 2-4 hr 4-12 hr 12-18 hr No more than 30 acting (Humulin N, Novolin N) min before meal Long acting Glargine (Lantus AE), Detemir 1-2 hr None Up to 24 hours The same time (Levemir) each day