Endocrine Disorders

CHAPTER 6 Endocrine Disorders


Section One Disorders of the Thyroid Gland



imageHyperthyroidism



Overview/Pathophysiology


Hyperthyroidism is a clinical syndrome caused by excessive circulating thyroid hormone. Because thyroid activity affects all body systems, excessive thyroid hormone exaggerates normal body functions and produces a hypermetabolic state.


Lymphocytic (“painless”) thyroiditis and postpartum thyroiditis are autoimmune disorders that result in thyroid inflammation with release of stored thyroid hormone into systemic circulation. Postpartum thyroiditis may ensue several months after delivery and remain active for several months, sometimes followed by hypothyroidism lasting several months.


Subacute (granulomatous) thyroiditis is a viral syndrome resulting in a painful, enlarged, overactive thyroid until the infection is controlled. Hyperthyroid symptoms also result from ingestion of too much thyroid replacement medication.


Graves’ disease (diffuse toxic goiter) accounts for approximately 85% of reported cases of hyperthyroidism. It is characterized by spontaneous exacerbations and remissions that appear to be unaffected by therapy. The cause of Graves’ disease is unknown, but an immunoglobulin known as long-acting thyroid stimulator has been isolated in a majority of patients with this disorder, a finding suggesting that Graves’ disease is an autoimmune response.


Thyrotoxic crisis, or thyroid storm, is the most severe form of hyperthyroidism. It results from a sudden surge of large amounts of thyroid hormones into the bloodstream that cause an even greater increase in body metabolism. This is a medical emergency. Precipitating factors include infection, trauma, and emotional stress, all of which increase demands on body metabolism. Thyrotoxic crisis also can occur following thyroidectomy because of manipulation of the gland during surgery.





Collaborative Management



Pharmacotherapy









Nursing Diagnoses and Interventions



Imbalanced nutrition: less than body requirements


related to hypermetabolic state and/or inadequate nutrient absorption










Nursing Interventions








Implement emergency treatment if signs of thyroid storm are present:






























imageHypothyroidism








Nursing Diagnoses and Interventions



Ineffective breathing pattern


(or risk for same) related to upper airway obstruction occurring with enlarged thyroid gland and/or decreased ventilatory drive caused by greatly decreased metabolism



















Nursing Interventions











Section Two Disorders of the Parathyroid Glands


The parathyroid glands regulate serum calcium (Ca++) and phosphorus levels via release of parathyroid hormone (PTH). This is accomplished by a negative-feedback mechanism: when serum Ca++ levels rise, PTH secretion is suppressed. PTH acts on bone to decrease Ca++ binding, and it stimulates the kidneys to increase resorption of Ca++. Parathyroid glands affect serum phosphorus levels in two ways: (1) directly, in that PTH causes increased renal excretion of phosphorus; and (2) indirectly, in that phosphorus and Ca++ combine readily to form an insoluble salt, and increased serum phosphorus facilitates this reaction, thus effectively lowering circulating Ca++ levels. PTH is also involved in the synthesis of a renal enzyme that catalyzes formation of vitamin D, which, in conjunction with PTH, increases absorption of Ca++ from the gastrointestinal (GI) tract.



imageHyperparathyroidism



Overview/Pathophysiology


Hyperparathyroidism is a clinical syndrome occurring from excessive secretion of parathyroid hormone (PTH). Primary hyperparathyroidism is caused by pathology of one or more of the parathyroid glands. Approximately 80% of these cases are caused by a benign adenoma of one gland, another 10% by multigland involvement, and in rare cases by carcinoma. In this disorder, excessive PTH acts on the skeletal, renal, and gastrointestinal (GI) systems, and the overall effects are increased serum calcium (Ca++) levels and decreased phosphate levels.


Hyperparathyroidism is the second most common cause of hypercalcemia. Incidence of this diagnosis increases dramatically after age 50 yr and is much more prevalent in female patients than in male patients. Secondary hyperparathyroidism is usually caused by renal insufficiency with decreased glomerular filtration. Although Ca++ and phosphorus are retained because of the lack of renal filtration, the high serum phosphate level depresses Ca++ concentration because phosphorus combines with Ca++ to form insoluble salts, with resulting hypocalcemia. This hypocalcemia, in turn, stimulates the parathyroid glands to release PTH in an effort to increase serum Ca++ levels. Bone resorption occurs because of increased PTH, but absorption of calcium from the GI tract is depressed because of Ca++ binding with high-phosphate GI secretions. The overall effects are decreased Ca++ levels and increased phosphate levels. Tertiary hyperparathyroidism occurs when secondary hyperparathyroidism progresses to a state in which excessive PTH is released independent of serum Ca++ levels.




Diagnostic Tests













Medical Treatment for Hyperparathyroidism







Pharmacotherapy












Nursing Diagnoses and Interventions



Impaired physical mobility


related to neuromuscular weakness and joint pain secondary to increased serum Ca++ and altered phosphate levels

























imageHypoparathyroidism







Nursing Diagnoses and Interventions



Activity intolerance


related to weakness and fatigue secondary to decreased cardiac contractility






Sep 1, 2016 | Posted by in NURSING | Comments Off on Endocrine Disorders

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