![ Clinical Manifestations:
• Severe tachycardia,
• Heart failure,
• Shock,
• Hyperthermia (up to 105.3° F [40.7° C]),
• Restlessness,
• Agitation : A state of anxiety or nervous excitement
• Seizures,
• Abdominal pain,
• Nausea, vomiting,
• Diarrhea,
• Delirium, and coma.](https://image.slidesharecdn.com/hyperthyrodism-190618111349/75/Hyperthyrodism-15-2048.jpg)
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Hyperthyrodism
- 1. Mrs Dipali Dumbre MScNursing Medical Surgical Nursing SCON
- 3. “Hyperthyroidism is hyperactivityof the thyroid gland with sustained increase in synthesis and release of thyroid hormones.” Hyperthyroidism is sometimes called thyrotoxicosis, the technical term for too much thyroid hormone in the blood.
- 4. Graves’ disease.(In Graves’ disease, immune system creates antibodies known as thyroid-stimulating immunoglobulins. These antibodies attach to healthy thyroid cells can cause thyroid to create too much thyroid hormone.) Toxic nodular goiter, Thyroiditis, Exogenous iodine excess, Pituitary tumors Thyroid cancer
- 5. Graves’ diseaseis an autoimmune disease of unknown etiology marked by diffuse thyroid enlargement and excessive thyroid hormone secretion. Precipitating factors such as infection, and stressful life events may interact with genetic factors to cause Graves’ disease. Graves’ disease accounts for 75% of the cases of hyperthyroidism. The patient develops antibodies to the TSH receptor.
- 6. These antibodiesattach to the receptors and stimulate the thyroid gland to release T3, T4, or both. The excessive release of thyroid hormones leads to the clinical manifestations associated with thyrotoxicosis. The disease is characterized by remissions and exacerbations, with or without treatment. It may progress to destruction of the thyroid tissue, causing hypothyroidism.
- 7. Nodular goitersare thyroid hormone–secreting nodules that function independent of TSH stimulation. If these nodules are associated with hyperthyroidism, they are termed toxic. The nodules are usually benign follicular adenomas.
- 8. Increases metabolism. It also increases tissue sensitivity to stimulation by the sympathetic nervous system. Palpation of the thyroid gland may reveal a goiter. Auscultation of the thyroid gland may reveal bruits, a reflection of increased blood supply. Ophthalmopathy, a term used to describe abnormal eye appearance or function. A classic finding in Graves’ disease is exophthalmos, a protrusion of the eyeballs from the orbits.
- 9. Exophthalmos isa type of infiltrative ophthalmopathy that is due to impaired venous drainage from the orbit, which causes increased fat deposits and fluid (edema) in the retroorbital tissues.
- 10. Acropachy: Acropachyrefers to a dermopathy associated with Graves' disease. It is characterized by soft-tissue swelling of the hands and clubbing of the fingers.
- 11. Cardiovascular Manifestation: •Systolic hypertension • Increased rate and force of cardiac contractions • Bounding, rapid pulse • Increased cardiac output • Cardiac hypertrophy • Systolic murmurs • Dysrhythmias • Palpitations • Atrial fibrillation (more common in the older adult)
- 12. Respiratory System: •Increased respiratory rate • Dyspnea on mild exertion Gastrointestinal: • Increased appetite, thirst • Weight loss • Increased peristalsis • Diarrhea, frequent defecation • Increased bowel sounds
- 13. Nervous System •Difficulty in focusing eyes • Nervousness • Fine tremor (of fingers and tongue) • Insomnia • Lability of mood, delirium • Restlessness • Personality changes of irritability, agitation • Exhaustion • Hyperreflexia of tendon reflexes • Depression, fatigue, apathy (in the older adult) • Lack of ability to concentrate • Stupor, coma
- 14. Thyrotoxic crisis(also called thyroid storm) is an acute, rare condition in which all hyperthyroid manifestations are heightened. Although it is considered a life-threatening emergency, death is rare when treatment is vigorous and initiated early. Causes: It is thought to be stressors (e.g., infection, trauma, surgery) in a patient with preexisting hyperthyroidism, either diagnosed or undiagnosed.
- 15. Clinical Manifestations: •Severe tachycardia, • Heart failure, • Shock, • Hyperthermia (up to 105.3° F [40.7° C]), • Restlessness, • Agitation : A state of anxiety or nervous excitement • Seizures, • Abdominal pain, • Nausea, vomiting, • Diarrhea, • Delirium, and coma.
- 16. Treatment: • It isaimed at reducing circulating thyroid hormone levels by appropriate drug therapy. • Supportive therapy is directed at managing respiratory distress, fever reduction, fluid replacement, and elimination or management of the initiating stressor(s).
- 17. History andphysical examination Ophthalmologic examination ECG Laboratory tests : • Decreased TSH levels • Elevated free thyroxine (free T4) levels Radioactive iodine uptake (RAIU): 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%.
- 18. Antithyroid Drugs. Thefirst-line antithyroid drugs are Propylthiouracil (PTU) and methimazole (Tapazole). These drugs inhibit the synthesis of thyroid hormones. PTU also blocks peripheral conversion of T4 to T3.
- 19. Iodine. Iodine isused with other antithyroid drugs to prepare the patient for thyroidectomy or for treatment of thyrotoxic crisis. The administration of iodine in large doses rapidly inhibits synthesis of T3 and T4 and blocks the release of these hormones into circulation. It also decreases the vascularity of the thyroid gland, making surgery safer and easier.
- 20. β-Adrenergic Blockers. β-Adrenergic blockers are used for symptomatic relief of thyrotoxicosis that results from increased β-adrenergic receptor stimulation caused by excess thyroid hormones. Propranolol (Inderal) is usually administered with other antithyroid agents and rapidly provides symptomatic relief. Atenolol (Tenormin) is the preferred β-adrenergic blocker for use in the hyperthyroid patient with asthma or heart disease
- 21. Radioactive Iodine Therapy Radioactive iodine (RAI) therapy is the treatment of choice for most nonpregnant adults. RAI damages or destroys thyroid tissue, thus limiting thyroid hormone secretion. RAI has a delayed response, and the maximum effect may not be seen for 2 to 3 months. For this reason, the patient is usually treated with antithyroid drugs and propranolol before and during the first 3 months after the initiation of RAI until the effects of radiation become apparent.
- 22. Surgical Therapy Thyroidectomyis indicated for individuals who have been unresponsive to antithyroid therapy, for individuals with very large goiters causing tracheal compression, and for individuals with a possible malignancy. Additionally, this surgery may be done when an individual is not a good candidate for RAI. One advantage thyroidectomy has over RAI is a more rapid reduction in T3 and T4 levels. A Subtotal thyroidectomy is the preferred surgical procedure and involves the removal of a significant portion of the thyroid gland.
- 23. Endoscopic thyroidectomyis a minimally invasive procedure. It is an appropriate procedure for patients with small nodules (less than 3 cm) where there is no evidence of malignancy. Advantages of endoscopic thyroidectomy over open thyroidectomy include less scarring, less pain, and a faster return to normal activity.
- 24. When subtotalthyroidectomy is the treatment of choice, the patient must be adequately prepared to avoid postoperative complications. Preoperative Preoperative teaching should include comfort and safety measures in which the patient can participate. Coughing, deep breathing, and leg exercises should be practiced and their importance explained. The patient should be taught how to support the head manually while turning in bed, because this maneuver minimizes stress on the suture line after surgery. Range-of-motion exercises of the neck should be practiced.
- 25. Post Operative Oxygen,suction equipment, and a tracheostomy tray should be readily available. A tracheostomy tray is required in case airway obstruction occurs. Recurrent laryngeal nerve damage leads to vocal cord paralysis. If there is paralysis of both cords, airway obstruction will occur, requiring an immediate tracheostomy. Respiration may also become difficult because of excess swelling of the neck tissues, hemorrhage, hematoma formation, and laryngeal stridor. Laryngeal stridor (harsh, vibratory sound) may occur during inspiration and expiration as a result of edema of the laryngeal nerve. Laryngeal stridor may also be related to tetany, which occurs if the parathyroid glands are removed or damaged during surgery leading to hypocalcemia. To treat tetany, IV calcium salts such as calcium gluconate should be available.
- 26. After a thyroidectomythe nurse should do the following: Assess the patient every 2 hours for 24 hours for signs of hemorrhage or tracheal compression such as irregular breathing, neck swelling, frequent swallowing, sensations of fullness at the incision site, choking, and blood on the anterior or posterior dressings. Place the patient in a semi-Fowler position and support the patient's head with pillows, and avoid flexion of the neck and any tension on the suture lines. Monitor vital signs. Complete the initial assessment by checking for signs of tetany secondary to hypoparathyroidism (e.g., tingling in toes, fingers, or around the mouth; muscular twitching) and by evaluating difficulty in speaking and hoarseness.
- 27. Trousseau's signand Chvostek's sign should be monitored for 72 hours. Trousseau's sign: Inflating the BP cuff for several mintues causes muscular contraction,including flexion of the wrist and metacapophalangeal joints
- 28. Chvostek's sign:Tapping on the facial nerve causes twitching of facial muscles. Some hoarseness is to be expected for 3 to 4 days after surgery because of edema. Control postoperative pain by giving medication.