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Endocrine Disorders
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Thyroid Disorders
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“A Delicate Feedback Mechanism”
Thyroid Gland- drop in T3 and T4 Pituitary Gland releases TSH The TSH stimulates the thyroid gland to release of T3 and T4
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Thyroid Gland Hormones
Thyroxine (T4) and Triiodothyronine (T3) These are responsible for increase in metabolic rate increase protein and bone turnover increase responsiveness to catecholamines Fetal and infant growth and development Calcitonin Lowering blood calcium and phosphate levels
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Continuum of Thyroid Dysfunction
Normal
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An increase in release of thyroid hormone
Hyperthyroidism An increase in release of thyroid hormone
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Hyperthyroidism Clinical Manifestations
What are the clinical manifestations in each body system that reflect the increase in metabolism caused by the excessive release of thyroid hormones? Cardiovascular Respiratory Gastrointestinal Integumentary Musculoskeletal Nervous Reproductive Other
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Hyperthyroidism Diagnostic Studies
History Physical examination Ophthalmologic examination ECG Radioactive iodine uptake (RAIU) Indicated to differentiate Graves’ disease from other forms of thyroiditis
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Hyperthyroidism Diagnostic Studies
Laboratory tests TSH RAIU – radioactive iodine uptake
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What is the primary test Diagnose Hyperthyroidism?
used to Diagnose Hyperthyroidism?
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Hyperthyroidism Collaborative Care
Goals Block adverse effects of thyroid hormones Stop hormone oversecretion Three primary treatment options Antithyroid medications Radioactive iodine therapy (RAI) Subtotal thyroidectomy
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Hyperthyroidism Treatment – Drug Therapy Antithyroid Drugs
Action: Inhibit synthesis of thyroid hormone First-line examples Propylthiouracil (PTU) Also blocks conversion of T4 to T3 Methimazole (Tapazole)
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Antithyroid Drugs Nursing Implications:
Instruct the patient that it will take several weeks for the drug to be effective Improvement in 1 to 2 weeks Good results in 4 to 8 weeks Therapy for 6 to 15 months Disadvantages include Patient noncompliance Increased rate of recurrence when medication is discontinued
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Do these medications cure the problem?
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Hyperthyroidism Drug Therapy - Iodine
Uses: Used with other antithyroid drugs in preparation for thyroidectomy or treatment of thyrotoxic crisis Given several weeks preoperatively Decrease the vascularity of thyroid gland decreasing bleeding making surgery safer Action: Inhibit synthesis of T3 & T4 and block release into circulation to slow metabolism Examples Saturated solution of potassium iodine (SSKI) Lugol’s solution Main use is for preparation for surgery in order to decrease the vascularity of the thyroid gland and decrease chance of bleeding therefore making surgery safer.
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Hyperthyroidism Drug Therapy β-Adrenergic blockers
Action: Symptomatic relief of thyrotoxicosis resulting from β-adrenergic receptor stimulation Uses: Helps to control nervousness, tachycardia, tremor, anxiety, and heat tolerance. Example Propranolol (Inderal) administered with other antithyroid agents Some of the symptoms of hyperthyroidism (such as tremor and palpitations, which are caused by excess thyroid hormone acting on the cardiac and nervous system) can be improved within a number of hours by medications called beta-blockers (eg, propranolol; Inderal). These drugs block the effect of the thyroid hormone but don't have an effect on the thyroid itself, thus beta blockers do not cure the hyperthyroidism and do not decrease the amount of thyroid hormone being produced; they just prevent some of the symptoms.
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Hyperthyroidism Radioactive Iodine Therapy (RAI)
Uses: Used to destroy thyroid tissue thereby limiting thyroid hormone secretion. Effects not seen for 2-3 months Dose of RAI is low so no radiation safety precautions are needed Complication High incidence of post-treatment hypothyroidism – need to be taught symptoms RAI Not an option during pregnancy 6. How is radioactive Iodine therapy used in treating hyperthyroidism? What are nursing implications? Radioactive iodine is the most widely-recommended permanent treatment of hyperthyroidism. This treatment takes advantage of the fact that thyroid cells are the only cells in the body which have the ability to absorb iodine. By giving a radioactive form of iodine, the thyroid cells which absorb it will be damaged or killed. Because iodine is not absorbed by any other cells in the body, there is very little radiation exposure (or side effects) for the rest of the body. Radioiodine can be taken by mouth without the need to be hospitalized. This form of therapy often takes one to two months before the thyroid has been killed, but the radioactivity medicine is completely gone from the body within a few days. The majority of patients are cured with a single dose of radioactive iodine. The only common side effect of radioactive iodine treatment is underactivity of the thyroid gland. The problem is that the amount of radioactive iodine given kills too many of the thyroid cells so that the remaining thyroid does not produce enough hormone, causing hypothyroidism.
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Hyperthyroidism Surgery Therapy Thyroidectomy
Indications Unresponsive to drug therapy Large goiters with tracheal compression Possible malignancy
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Thyroidectomy Oxygen, suction equipment, tracheostomy tray available in room Postoperative care Every 2 hours for 24 hours Assess for signs of hemorrhage Assess for tracheal compression Irregular breathing, neck swelling, frequent swallowing, choking Semi-Fowler’s position Support head with pillows Avoid flexion of neck Tension on suture lines
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Thyroidectomy Postoperative care Monitor vitals Control pain
Check for tetany Muscle cramps or laryngeal stridor – treat with calcium gluconate Trousseau’s and Chvostek sign should be monitored Monitor for 72 hours Evaluate difficulty in speaking/hoarseness Some hoarseness for 3 to 4 days is expected
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Thyroidectomy Ambulatory and home care Discharge teaching
Monitor hormone balance periodically Decrease caloric intake to prevent weight gain Adequate iodine Regular exercise Avoid ↑environmental temperature
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Hyperthyroidism Nutritional Therapy
Why is the patient placed on a High-calorie diet ( kcal/day)? What foods are encouraged? What foods should be avoided?
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Hyperthyroidism Nursing Implementation
Change linens frequently if diaphoretic Eye Care for exophthalmos Apply artificial tears to prevent corneal ulceration Elevate HOB and salt restriction for edema Tape eyelids shut for sleep if they cannot close Dark glasses to reduce glare and prevent environmental irritants
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Hyperthyroidism Complications
Thyrotoxic crisis (Thyroid Storm) Acute, rare condition where all manifestations of hyperthyroidism are heightened Life-threatening emergency/death rare when treatment initiated early and is vigorous.
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Hyperthyroidism Thyrotoxic crisis/ Thyroid Storm
Manifestations include: Respiratory distress – dyspnea Hyperthermia – up to Tachycardia – pulse > 130 BPM Heart failure, chest pain Shock Restlessness, Agitation Seizures Abdominal pain, Nausea Delirium Coma
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Thyrotoxic crisis/ Thyroid Storm
Goal of Treatment ↓ Thyroid hormone levels and clinical manifestations with drug therapy Interventions Manage respiratory distress – oxygen Fever reduction – with antipyretics or cooling blankets, cool room fluid replacement – IV fluids and electrolytes, and management of stressors Administer medications – PTU, methimazole, Iodine, β-blockers Treatment of Heart failure
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Review on Hyperthyroidism
Case Study: Beth Minton, 43 y/o, Admitted to hospital with high fever. Following an endocrine workup she was diagnosed with Graves Disease. Objective Data: Has fever of 1040 F, B/P of 150/78, P - 11, Flushed, with hot, moist skin Has fine hand tremors and appears nervous Has 4+ deep tendon reflexes R – 24
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Critical Thinking Questions
What is the etiology of Beth’s symptoms? What diagnostic studies were probably ordered? What would the results have been to establish the diagnosis of Grave’s Disease? She has a subtotal Thyroidectomy planned for 2 months later – why is surgery being delayed? Beth is started on propylthiouracil (PTU) and propranolol (Inderal). What is the purpose of drug therapy for Beth? Beth has Graves’ disease (diffuse toxic goiter), which is an autoimmune disease of unknown etiology marked by diffuse thyroid enlargement and increased production of thyroid hormone. The hyperthyroidism and diffuse thyroid hyperplasia are caused by antibodies that attack thyroid tissue and thus stimulate hyperplasia. Precipitating factors such as insufficient iodine supply, infection, and stressful life events may interact with genetic factors to cause Graves’ disease. The two primary laboratory findings used to confirm the diagnosis of hyperthyroidism are decreased TSH levels and elevated free thyroxine (free T4) levels. Total T3 and T4 may also be assessed, but these are not as useful. Measurements of total T3 and T4 measure both free and bound (to protein) hormone levels. The free hormone is the only form of the hormone that is biologically active. In the nonpregnant, nonlactating patient, a 6- or 24-hour radioactive iodine uptake (RAIU) may be done. The RAIU test is used to differentiate Graves’ disease from other forms of thyroiditis. The patient with Graves’ disease will show a diffuse, homogeneous uptake of 35% to 95%, whereas the patient with thyroiditis will show an uptake of less than 2%. The person with a nodular goiter will have an uptake in the high normal range. This test can differentiate Graves’ disease from other forms of thyroiditis. The patient is usually given antithyroid drugs to produce a euthyroid state and possibly iodine and -adrenergic blockers to relieve symptoms preoperatively. Iodine decreases the size and vascularity of the thyroid, making resection safer and easier. Administration of propylthiouracil (PTU) and iodine for 10 days before surgery is a common method for surgical preparation. . The most commonly used antithyroid drugs are classified as thioamides; an example of one is propylthiouracil (PTU). These drugs inhibit the synthesis of thyroid hormones. PTU also blocks peripheral conversion of T4 to T3. Propranolol (Inderal) is the most frequently used -adrenergic blocker. It relieves the symptoms of thyrotoxicosis that result from increased -adrenergic receptors caused by excess thyroid hormones. These symptoms include heat intolerance, palpitations, nervousness, tremor, and muscle weakness. Propranolol is used with other antithyroid treatment and rapidly relieves the symptoms that cause such discomfort to the patient with hyperthyroidism.
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Critical Thinking Questions
What are Beth’s immediate learning needs; pre-op needs, and post-op needs? What are the nursing interventions for successful long-term management of Beth after the subtotal thyroidectomy? Based on assessment data presented, write appropriate nursing diagnosis pertinent to Beth while hospitalized. Preoperatively, Beth needs to be taught comfort and safety measures that she can perform. Coughing, deep breathing, and leg exercises should be practiced and their importance explained. Beth is taught how to support her head manually while turning in bed, since this maneuver minimizes stress on the suture line after surgery. Range-of-motion exercises of the neck should be practiced. The nurse should explain routine postoperative care such as IV infusions. The patient should be told that talking is likely to be difficult for a short time after surgery. If Beth could not read, the nurse could use videos and demonstration for education purposes. Postoperatively, Beth will need to cough and deep breathe. She will also be assessed for respiratory symptoms, speech difficulties (e.g., hoarseness), and hypocalcemia. She will be instructed to report symptoms related to these problems. Beth needs to know that her thyroid balance should be monitored periodically to ensure that normal function has returned. Caloric intake must be reduced substantially below the amount that was required before surgery to prevent weight gain. Regular exercise helps stimulate the thyroid and should be encouraged. Exposure to alternating extremes of temperature, such as hot and cold showers, also promotes thyroid hyperplasia but is not acceptable to many individuals because of cold intolerance 6. . Regular follow-up care is necessary. Beth should be seen biweekly for a month and then at least semiannually to assess for the development of hypothyroidism. She should be taught the signs and symptoms of progressive thyroid failure and instructed to seek medical care if these develop. 7. Nursing diagnoses: anxiety, hyperthermia, insomnia, fatigue, activity intolerance, imbalanced nutrition: less than body requirements, ineffective coping, risk for injury Collaborative problems: corneal abrasions, malnutrition, cardiac dysrhythmias, electrolyte imbalances
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A condition in which the body lacks thyroid hormones
Hypothyroidism A condition in which the body lacks thyroid hormones
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Hypothyroidism Clinical Manifestations
What are the clinical manifestations in each body system that reflect the decrease in metabolism caused by the lack of thyroid hormones? Cardiovascular Respiratory Gastrointestinal Integumentary Musculoskeletal Nervous Reproductive Other
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Hypothyroidism Diagnostic Studies
History and physical examination Laboratory tests Serum TSH Determines cause of hypothyroidism Other abnormal findings are ↑ cholesterol and triglycerides, anemia, and ↑ creatine kinase
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Hypothyroidism Treatment - Drug Therapy
Levothyroxine (Synthroid) Must take regularly Monitor for angina and cardiac dysrhythmias Monitor thyroid hormone levels and adjust (as needed) Patient/family teaching Because of the impaired memory - Be sure to provide patient with written instructions and teach family as well as patient Lifelong therapy
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Nursing Management Ambulatory and Home Care
Teach measures to prevent skin breakdown Emphasize need for warm environment Caution patient to avoid sedatives or use lowest dose possible Discuss measures to minimize constipation Avoid enemas because of vagal stimulation in cardiac patient Teach patient to notify physician immediately if signs of overdose appear Orthopnea, dyspnea, rapid pulse, palpitations, nervousness, insomnia
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Hypothyroidism Complication
Those with severe longstanding hypothyroidism may display myxedema Accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues Causes puffiness, periorbital edema, masklike effect
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Hypothyroidism Complications Myxedema Coma
Medical emergency Hypoventilation- respiratory drive is decreased resulting in alveolar hypoventilation Mental sluggishness Drowsiness Lethargy progressing gradually or suddenly to impairment of consciousness or coma Subnormal temperature Hypotension Decrease pulse – does not perfuse tissues
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Myxedema Coma Treatment
Vital functions must be supported Mechanical respiratory support Cardiac monitoring Administer IV thyroid hormone replacement If hyponatremic – give Hypertonic saline solution Close assessment VS monitoring Monitor core temperature
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Think of this when comparing Hyper vs Hypo thyroidism
Hyperthyroidism
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Hyperparathyroidism
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Hyperparathyroidism There is overproduction of parathormone which is characterized by bone decalcification. The patient will have an increase in blood calcium. What is a complication of increase in calcium in the blood?
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Hyperparathyroidism Clinical Manifestations
What are the clinical manifestations of hyperparathyroidism? Hint: They Mimic those of Hypercalcemia
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Hyperparathyroidism Diagnosis
Serology Parathyroid hormone levels - Serum calcium - >10 mg/dl Serum phosphorus - < 3 mg/dl Urine calcium, serum chloride, creatinine, amylase, alkaline phosphatase – all elevated Bone x-rays and bone scans Ultrasound and MRI
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Most common way to diagnose Hyperparathyroidism is by persistent elevated _____ ______levels and PTH
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Hyperparathyroidism Treatment and Nursing Care
Hydration Therapy – force fluids. WHY? Avoid Immobility / Active Lifestyle Bones subjected to normal stress give up less calcium so encourage walking Dietary measures- avoid diet with excess calcium
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Hyperparathyroidism: Surgery
Post – op Nursing Care Assess for hemorrhage Assess Fluid and Electrolytes Assess for Tetany – occurs with sudden decrease in calcium levels What medication should be available at the bedside?
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Hyperparathyroidism Drug Therapy
Explain the use of the following medications in treatment: Bisphosphates Fosamax Calcimimetic Agent Cinacalcet
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Results from abnormally low levels of PTH low Ca level
Hypoparathyroidism Results from abnormally low levels of PTH low Ca level
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Hypoparathyroidism Clinical Manifestations
What are the clinical manifestations of hypoparathyroidism: Hint: They mimic those of hypocalcemia
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Sign that Calcium Level is Low
Chvostek’s sign: tap on the facial nerve just below the temple. Positive - when nose, eye, lip & facial muscles twitch
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Signs of Low Calcium Trousseau’s sign: temporarily occlude arterial blood flow (with BP cuff inflated) above the normal systolic pressure. Positive Trousseau’s sign occurs when the hand and fingers contract from ischemia
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Increase Serum Calcium
Goal of Care Increase Serum Calcium
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Hypoparathyroidism Treatment and Nursing Care
IV calcium such as calcium gluconate – infuse slowly Prevent hypotension, cardiac dysrhythmia, cardiac arrest ECG monitoring Rebreathing using paper bag – increases carbonic acid in blood lowering blood pH. Other Drugs Calcium Vitamin D – promotes intestinal calcium absorption and bone resorption
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Hypoparathyroidism Treatment and Nursing Care
Diet Therapy Encourage high-calcium What are examples of foods high in calcium?
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Key Points Use a gait belt when assisting a patient with muscle weakness Collaborate with dietitian to teach patients about diets that are restricted in calcium Use a lift sheet to move or reposition a patient with hypocalcemia Keep environment of a patient with risk for thyroid storm cool, dark, quiet. Keep emergency suctioning and trach tray in room of patient who has had thyroid or parathyroid surgery.
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Key Points Monitor the hydration status of patients who have hypercalcemia Teach patients that hormone replacement therapy for hypothyroidism is lifelong Teach patients to use clinical manifestations such as number of bowel movements, ability to sleep as indicators of therapy effectiveness
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