Diabetes & Thyroid Disorders PDF

Diabetes Mellitus What is it? Chronic multisystem disease characterized by hyperglycemia related to: abnormal insulin production (type 1) , impaired insulin utilization (type 2), OR BOTH. Very prevalent disease in the US - 8th leading cause of death Leading cause of: end stage...

Diabetes Mellitus What is it? Chronic multisystem disease characterized by hyperglycemia related to: abnormal insulin production (type 1) , impaired insulin utilization (type 2), OR BOTH. Very prevalent disease in the US - 8th leading cause of death Leading cause of: end stage renal disease (people on dialysis), adult blindness, non traumatic lower limb amputations. Risk Factors Family history Gestational diabetes - could lead to diabetes, start living like you have diabetes. Minority groups (American Indians, AA, Hispanics, Asian Americans) Age > 35 Obesity (BMI of > 30) Given birth to an infant > 9lbs Inactivity Etiology and Pathophysiology Combination: genetic, autoimmune, environmental Regardless of its cause, DM is mainly a disorder of glucose metabolism related to absent or insufficient supply and/or ineffective use of available insulin. Normal insulin metabolism ○ Produced by B cells in islets of Langerhans ○ Released continuously into bloodstream in small increments with larger amounts released after food ○ Stabilizes glucose level in range of 70 to 120 mg/dL **Insulin promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell. GLUCOSE SHOULD BE IN THE CELL NOT IN THE BLOOD. INSULIN IS THE KEY TO ALLOW GLUCOSE INTO THE CELL AND OUT OF THE BLOODSTREAM. Other hormones (counterregulatory hormones): glucagon, epinephrine, GH, cortisol ○ Work against the effects of insulin ○ These hormones increase glucose levels by (1) stimulating glucose production and release by the liver and (2) decreasing the movement of glucose into the cells. ○ Counterregulatory hormones and insulin work together to maintain glucose levels within the normal range by regulating the release of glucose for energy during food intake and periods of fasting. ○ Glucagon = opposite of insulin - release from the liver Increase the amount of glucose in the bloodstream by: Glycogenolysis: breakdown of stored glucose Gluconeogenesis: the liver converts fats and proteins into glucose ○ Cortisol = rises with stress; rises in the morning; when cortisol is released, sugar goes up Ketones, the result of the breakdown of fats are excreted in the urine Protein metabolism causes an elevated Blood Urea Nitrogen (BUN) Prediabetic need to PREVENT diabetes, live life like a diabetic before complications occur. At risk for type 2 diabetes Defined as impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or both. Diagnosis of IGT is made if the 2-hour oral glucose tolerance test (OGTT) values are 140 to 199 IFG is diagnosed when fasting glucose levels are 100 to 125. Usually no symptoms Patient Teaching ○ Have glucose A1C checked regularly. ○ Monitor for symptoms of diabetes such as fatigue, frequent infections, or slow-healing wounds. ○ Maintain a healthy weight, exercise regularly and make healthy food choices. Type 1: insulin dependent (abnormal insulin production) The result of the destruction of the beta cells in the pancreas, the only cells in the body that make insulin When beta cells are destroyed, insulin is no longer produced. Signs/Symptoms ○ POLYDIPSIA- excessive thirst ○ POLYURIA - frequent urination ○ POLYPHAGIA- excessive hunger ○ fatigue/weakness due to the body’s inability to get energy from glucose ○ GI : N/V - body’s attempt to get rid of excess glucose Treatment: must be on both a long acting and short acting insulin Type 2: insulin resistant (impaired insulin utilization) Combination of inadequate insulin secretion and insulin resistance. The pancreas usually makes some endogenous insulin, but the body may not produce enough of it or use it effectively. Signs/Symptoms ○ Slow onset of manifestations, the person may go for many years with undetected hyperglycemia and few, if any, symptoms. ○ May have polyuria and polydipsia ** To differentiate between type 1 and type 2, we can look at the beta cells and insulin. Gestational Develops during pregnancy Increase risk for c-section and perinatal complications Screen high risk patients at first visit; others at 24 - 28 weeks Usually glucose levels normal 6 weeks postpartum Diagnostics (Can be used for all types but mostly secondary onset) Fasting plasma glucose (FPG) ○ Impaired fasting glucose: >100 and < 126 ○ If glucose is greater than 126, DM is present ○ Goal = keep FPG of 99 or lower Hemoglobin A1C ○ Gives an average of glucose levels for the past 3 months  ○ Glucose “sticks” to red blood cells. RBCs last about 3 months ○ Goal: 6.5% - 7% ○ 6.5% or > = DIABETIC Estimated Average Glucose (eAG) ○ A calculated conversion of HbA1c ○ It’s reported in mg/dL, the same units as their home blood glucose tests ○ Makes results more meaningful to patients Urine glucose, ketone, and protein levels ○ The presence of glucose in the urine indicates hyperglycemia ○ Ketonuria occurs with the breakdown of fats ○ Albuminuria may indicate early onset of nephropathy Serum cholesterol ○ Diabetics are at risk for atherosclerosis ○ Treatment goal is LDL < 100 Insulin - KNOW! Mixing Insulin (NR -> RN) Wipe off tops of vials with alcohol wipe Draw air for NPH dose, inject air into NPH Draw air for regular insulin, inject air into regular insulin Draw back regular insulin Draw back NPH **draw clear then cloudy Storage of Insulin Do no heat/freeze In-use vials may be left at room temperature for up to 4 weeks Extra insulin should be refrigerated Avoid exposure to direct sunlight, extreme heat or cold Stored prefilled syringes upright for 1 week if two insulin types; 30 days for one Administration of Insulin Typically given 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. Absorption is the fastest from the abdomen,followed by the arm, thigh, and buttock. Teach patients to rotate the injection within and between sites to prevent excess bruising. Usually available as U100 insulin (1mL contains 100 U of insulin) Inject at 45 to 90 degree angle NO alcohol swab for self injection; wash with soap and water - can dry out skin Insulin Pump Delivers a continuous subcutaneous insulin infusion through a small device worn on the belt, in the pocket, or under clothing. Deliver short-acting insulin Preprogrammed to deliver varying hourly basal rates. Ideal candidate ○ A person who has failed to control diabetes on other regimens ○ Pregnant ○ Desires increased daily flexibility Very expensive ($7,000) Risk of infection at site progressing to sepsis Change the infusion site every 24-48 hours. Problems with Insulin Therapy Hypoglycemia ○ Treatment includes administering glucagon 0.5-2 mg IM. After 20 minutes of no progression, administer again ○ When aroused, give 15 g of carbs and wait 15 minutes Allergic reaction ○ Local inflammatory reactions to insulin may occur, such as itching, and burning around the injection site. ○ Local reactions may be self-limiting within 1 to 3 months or may improve with a low dose of antihistamine. Lipodystrophy ○ Changes in subcutaneous tissue ○ May occur if the same injection sites are used frequently.  Somogyi Effect ○ Hyperglycemia in the morning may be due to the Somogyi effect. ○ Pt takes insulin at night time, then in morning the sugar is very low ○ Rebound hyperglycemia occurs because a high dose of insulin causes a decline in glucose levels overnight, and counterregulatory hormones are released. Dawn Phenomenon ○ Also characterized by hyperglycemia that is present on awakening ○ Due to the release of counterregulatory hormones ○ Unrelated to amount of insulin given at night. ○ The treatment for the dawn phenomenon is an increase in insulin or an adjustment in administration time. Acute Complications Diabetic ketoacidosis (DKA): associated excessive levels of ketones in the body ○ Serious condition that proceeds rapidly and must be promptly treated, and is caused by a profound deficiency of insulin. ○ It is characterized by hyperglycemia, ketosis, acidosis, and dehydration. Hyperglycemia: cells don't have insulin to allow glucose in. This forces the body to use fat cells to break down glucose for energy. Ketoacidosis: the after-effect of fat cells being broken down for glucose stores Dehydration: cells are hungry. They have no food, so the body goes into severe dehydration. Overload of sugar in the ECF leads to vomiting in an attempt to excrete excess sugar. ○ Clinical manifestations Dehydration, lethargy SWEET FRUITY BREATH! KUSSMAUL RESPIRATIONS (rapid, deep breathing w/dyspnea) Labs - Blood Glucose > 250, pH < 7.3 ○ Interprofessional Care First goal = establish IV for fluid and electrolyte replacement Assess renal status, cardiopulmonary status, LOC Hyperosmolar Hyperglycemic Syndrome (HHS): due to insulin deficiency ○ Blood sugar like 600, will be in ICU, very life-threatening ○ Life-threatening syndrome that can occur in a patient with diabetes who is able to make enough insulin to prevent DKA, but not enough to prevent severe hyperglycemia. ○ HHS is less common than DKA. It often occurs in patients over 60 years of age with 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 entail, increasing mental depression or cognitive impairment. ○ Lab values in HHS include a blood glucose level > 600 mg/dL and a marked increase in serum osmolality. Ketone bodies are absent or minimal in both blood and urine. ○ Nursing Management HHS is a medical emergency and has a high mortality rate Immediate IV administration of insulin and either 0.9% or 0.45% NaCl Monitor administration of (1) IV fluids to correct dehydration (2) insulin therapy to reduce blood glucose and serum ketone levels, and (3) electrolytes given. Hypoglycemia: low blood glucose due to too much insulin ○ IV access available - obtain blood glucose level, administer glucagon 0.5 - 2 mg IM  ○ When aroused - give 45 g carbohydrates to replace glycogen stores Drug Therapy (Oral Agents) Only for type 2 diabetes (insulin resistance, decreased insulin production, increased hepatic glucose production) For oral medications we want glucose to be 70 - 99 mg/dL **a patient can be on both oral and insulin injection at the same time. Drug: MOA: Nursing Considerations: Biguanides: Metformin Decreases the overproduction of causes moderate weight loss; glucose by the liver; decreases can be used for people with type insulin resistance. 2 diabetes and prediabetes who are overweight or obese. a-Glucosidase Inhibitors: Works in the small intestine to Taken with the first bite of Glyset, Precose slow carb metabolism and each main meal, they are most delays glucose absorption effective in lowering postprandial blood glucose. Their effectiveness is measured by checking 2-hour postprandial glucose levels. Sulfonylureas: Glucotrol, Stimulates the pancreatic cells Most common side effect is Glynase to secrete more insulin and hypoglycemia peripheral cells’ sensitivity to insulin Meglitinides: Prandin Stimulates the of insulin from Hypoglycemia is a common the pancreatic islet cells; rapid side effect acting Long term Diabetes Complications Nephropathy ○ Damage to the kidneys ○ Early glomerular hypertrophy ○ Increased glomerular filtration ○ Microalbuminuria Cardiovascular ○ Coronary artery disease ○ Stroke ○ Hypertension American diabetes association recommends < 140/90 130/80 if high risk  Retinopathy ○ Can lead to blindness ○ Encourage eye exam once a year Neuropathy ○ Decreased feeling in feet or hands ○ Hot, burning sensation Gastroparesis - low GI motility ○ Constipation, vomiting, anorexia, heartburn Infections Sexual Dysfunction Nursing Assessment Health history: visual changes, numbness in hands or feet, pain when walking, appetite, N/V, frequent vomiting, infections Physical assessment: height/weight, VS, peripheral pulses, skin, feet, injection sites Patient Education ○ Medications ○ How to administer insulin ○ Finger sticks or CGM ○ Foot care ○ Diet Tests and/or Areas to check annually ○ Glycohemoglobin (2-4 times a year) ○ Kidney function ○ Cholesterol & triglycerides, foot exam, eye exam, BP **If a patient is sick, you SHOULD still take your oral antidiabetic because because of the stress from sickness, cortisol is released and increases the blood sugar. Disorders of the Parathyroid Glands Parathyroid gland: four small glands that are located on the posterior surface of the thyroid and releases parathyroid hormone; about the size of a grain of rice PRIMARY FUNCTION: regulate calcium levels; to a lesser degree regulates phosphate levels Calcium is stored in the bones; it is readily available to the rest of the body at the request of the parathyroid glands. Osteoclasts = deconstructs bone Osteoblasts = build bone Parathyroid Hormone ○ Regulates how much calcium is: Absorbed from diet Excreted by kidneys Stored in bones ○ Increases formation of active vitamin D  ○ Active vitamin D increases intestinal calcium and phosphorus absorption HYPERPARATHYROIDISM Most common disease of the parathyroid glands Characterized by excess PTH - so you get excess calcium in the blood Parathyroid glands continue to make large amounts of PTH even when the calcium level is normal. Most common cause: benign tumor called an adenoma on one of parathyroid glands that secretes too much PTH Symptoms: ○ Kidney stones - due to kidneys’ inability to keep up with the excretion of calcium ○ Abdominal pain ○ Bone and joint pain - too much calcium in the blood and not in the bone ○ Fragile bones (osteoporosis) ○ irritability/Depression/Anxiety ○ Heart palpitations/arrhythmias Diagnostic Studies: Serum PTH: Serum Calcium: Serum Urine Calcium: Bone Density Phosphate: ⬆ ⬆(8.5-10) ⬇(2.5-4.5) ⬆ ⬇ Management: It depends on the severity of disease Surgical: partial or complete removal of the parathyroid glands Nonsurgical: ○ Ongoing measures of lab values ○ Exercise ○ Increase fluids ○ Moderate calcium intake ○ Calcimimetic agents, bisphosphonates, and phosphate Severe: ○ IV sodium chloride ○ Loop Diuretics ○ IV bisphosphonates: rapidly lower serum calcium in patients with dangerous levels Nursing Management: Patient education If postoperative: ○ Pain control ○ Monitor for bleeding ○ Monitor for tetany (due to sudden decrease in calcium level) HYPOPARATHYROIDISM Very rare; characterized by inadequate circulating PTH Most common cause: iatrogenic (this may include accidental removal of parathyroid glands or damage to the vascular supply of the glands during neck surgery) Symptoms Due to hypocalcemia: ○ Tetany ○ Tingling of lips and stiffness of limbs ○ Painful spasms of muscles ○ Trousseau’s sign Inflate BP cuff above SBP for several minutes Positive response: muscle contractions in hand Indicates hypocalcemia ○ Chstvoek’s Sign Elicited by tapping the patient’s face slightly over the facial nerve anterior to the ear lobe Positive finding: facial muscle twitching Indicates hypocalcemia Diagnostic Studies: Serum PTH: Serum Calcium: Serum Phosphate: ⬇(10-65) ⬇ ⬆(2.5-4.5) Management: Calcium supplements Vitamin D Magnesium High calcium diet Teach patient that it is a lifelong disorder Treatment goals are to treat acute complications, such as tetany, maintain normal calcium levels, and prevent long-term complications Give IV calcium slowly. USE ECG monitoring when giving calcium (can cause arrhythmias/cardiac arrest) Need to be in ICU Anatomy and Physiology: Thyroid Gland: The thyroid gland is located in the front of the neck with the primary function being to produce thyroid hormone. the thyroid hormone controls:  ○ metabolic rate ○ Metabolism ○ growth/development Thyroid Hormones ○ Calcitonin: controls body use of calcium; lowers excess calcium in the blood (calciTONin TONES down calcium in the blood) ○ T3: composed of iodine, regulates metabolism - iodine comes from salt! You can get goiter from lack of iodine. ○ T4 : composed of iodine and regulates metabolism ○ With iodine deficiency, the thyroid is unable to secrete sufficient thyroid hormone. ○ TSH: released from the pituitary gland that stimulates the thyroid to release T3/T4 Disorders of the Thyroid Gland TSH and T4 levels are measured to determine whether a goiter is associated with normal thyroid function, hyperthyroidism, or hypothyroidism. HYPOTHYROIDISM Condition in which the thyroid gland produces inadequate amounts of thyroid hormone Primary hypothyroidism: thyroid gland malfunction; the thyroid gland fails to produce sufficient thyroid hormone to sustain normal metabolic function. ○ Causes: Insufficient iodine diet Hashimoto’s disease: autoimmune disease in which the body attacks its own thyroid gland Surgical removal of the thyroid Therapeutic radiation as a result of hyperthyroidism Atrophy of the thyroid gland Tumors of the thyroid gland Secondary hypothyroidism: cause is related to pituitary tumors and other pituitary disorders; results from alterations in the hypothalamic-pituitary axis. Clinical manifestations - Fatigue Weight gain Cold intolerance Constipation Dry skin Thinning hair Periorbital edema Myxedema Coma Severe hypothyroidism A loss of brain function as a result of severe, long standing low level of thyroid hormone Life-threatening! Causes: acute illness, surgery, chemo, or DC of medications Lab Tests TSH = high T4 Low Thyroid Scan Fine-needle biopsy Ultrasonography Management **restore a euthyroid state as safely and rapidly as possible with hormone therapy Administration of synthetic thyroid hormone ○ Levothyroxine (Synthroid) : drug of choice for hypothyroidism Taken in the morning on an empty stomach Follow-up: TSH and T4 levels will be drawn in 4-8 weeks to assess levels Nursing Management Guided by the severity of the disease Directed at symptom management Note signs and symptoms Monitor patient progress ○ Weight loss ○ Resolution of fatigue ○ Skin and hair returning to normal Nursing Diagnosis Activity intolerance RT fatigue & depressed cognitive process Altered body temperature Constipation RT depressed GI function Altered thought process RT depressed metabolism & altered CV & respiratory status. HYPERTHYROIDISM - Excessive production of thyroid hormone. Patient is in a continuous hypermetabolic state Etiology: Graves Disease: Most common cause of hyperthyroidism ○ Autoimmune disorder ○ TSH is activated ○ Thyroid produces too much thyroid hormone Thyroiditis Nodules on thyroid gland Over treatment of hypothyroidism Signs/Symptoms - CAN LEAD TO THYROID STORM Weight loss tachycardia/palpitations Warm, moist skin Heat intolerance Fine tremors of the hand and tongue Hyperactivity, weakness, insomnia, exophthalmos , goiter Diagnostic Tests TSH: extremely low T4: high Management Synthroid dose will be decreased dose if applicable Antithyroid drugs: Tapapzole, PTU (Propylthiouracil) ○ Inhibit production or conversion of active thyroid hormone (T4 to T3) Beta-Blockers Radioactive Iodine ○ Destroys all or part of the thyroid gland ○ Post treatment: hypothyroid ○ Potassium iodine (SSK) and Lugol’s solution  Give with a straw Metallic taste Surgical Therapy ○ Subtotal thyroidectomy ○ Indications: failure of antithyroid drugs, not good candidate for radioactive iodine, large goiter (tracheal compression), malignancy ○ Makes thyroid gland unable to produce excessive thyroid hormone ○ Complication: accidental removal of parathyroid gland (hypocalcemia) ○ Post-op Assess for hemorrhage and tracheal compression Vital signs Voice Symptoms of hypocalcemia Paresthesia Facial spasm Muscular twitching Spasm of larynx Check for positive Chvostek’s sign ○ Nursing Management VS:BP, Pulse, respirations Exopht