Summary

This document contains information on different endocrine disorders such as hypoadrenalism, Cushing's Syndrome, and hyper and hypothyroidism. It covers topics like causes, clinical features, and management of the various disorders. It's intended for medical students or professionals.

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Endocrine Disorders The endocrine system The feedback system of the hypothalamus, pituitary, and target glands (From Ignatavicius DD, Workman ML, Mishler MA. Medical-surgical nursing across the health care continuum , 3rd ed. Philadelphia: Saunders;1999.) ...

Endocrine Disorders The endocrine system The feedback system of the hypothalamus, pituitary, and target glands (From Ignatavicius DD, Workman ML, Mishler MA. Medical-surgical nursing across the health care continuum , 3rd ed. Philadelphia: Saunders;1999.) Alterations of pituitary function Pituitary hormones. From Patton & Thibodeau, 2016 Disorders of Pituitary Secretion  Posterior Pituitary Syndrome of inappropriate antidiuretic hormone secretion (SIADH) High levels of antidiuretic hormone without the normal physiological stimuli for its release Symptoms of water intoxication Hyponatraemia resulting from enhanced renal (low serum sodium) water retention or increases in total body water Disorders of Pituitary Secretion  Posterior Pituitary Diabetes insipidus is related to an insufficiency of antidiuretic hormone, leading to polyuria and polydipsia Two Forms: 1) Neurogenic form Caused by the absence of antidiuretic hormone 2) Nephrogenic form Caused by inadequate response of the renal tubules to antidiuretic hormone Partial or total inability to concentrate urine Insufficient antidiuretic hormone secretion causes polyuria (excretion of large volumes of dilute urine) The thirst mechanism is stimulated and induces polydipsia Alterations of adrenal function Image Source: Endocrine Society of Australia Hypoadrenalism Primary (Addison’s) Adrenal insufficiency Secondary 1) Impaired secretion of cortisol decreased gluconeogenesis and decreased liver and muscle glycogen decreases supplies of available glucose Hypoglycemia 2) Decreased levels of aldosterone Potassium excretion is decreased Hyperkalemia Acute Adrenal Crisis (Addisonian Crisis) A sudden marked decrease in available adrenal hormones  hypotension, tachycardia, dehydration, confusion, hyponatremia, hyperkalemia, hypercalcemia, and hypoglycemia Adrenal Hypersecretion (Cushing Syndrome) Hypersecretion of the adrenal cortex Hypercortisolism means excessive levels of serum cortisol When chronic, it leads to Cushing's syndrome Causes: 1) Endogenous  e.g., pituitary tumors 2) Exogenous  e.g., prolonged administration of high doses of corticosteroids List, Sarah Published January 2, 2019. Pages 255-278. Cushing Syndrome The hallmark findings that lead to a diagnosis of Cushing syndrome: Truncal obesity (excess adipose in body trunk) Protein wasting (slender extremities and very thin and friable skin) Facial fullness, often called a moon face Purple striae on the abdomen, breasts, buttocks, or thighs Osteoporosis (a significant finding in premenopausal women) Hypokalemia of uncertain cause List, Sarah Published January 2, 2019. Pages 255-278. Management of Cushing Syndrome Abnormal laboratory findings include polycythemia, hypokalemia, hypernatremia, hyperglycemia, leukocytosis, glycosuria, hypocalcemia, and elevated plasma cortisol. Drug therapy, radiation, and surgery: Surgery – e.g., benign adrenal tumor Surgery and Radiation e.g., metastatic tumor Drug Therapy- e.g., mitotane (cytotoxic), ketoconazole, metyrapone The drugs must be promptly discontinued if trauma or shock occurs because the patient's ability to adapt is diminished Nursing Considerations: Potential for infection related to high serum cortisol levels Anxiety related to depression, mood swings, anxiety, irrational behavior Potential for disrupted skin integrity related to changes in skin and connective tissue and edema Potential for injury (fracture) related to osteoporosis Altered body image related to changes in physical appearance and function Ineffective management related to lack of understanding of disease, drug therapy, diet, and self-care Alterations of thyroid function Linton ,Matteson. Endocrine System Introduction, eds. Medical-Surgical Nursing; 2020:911-28. M. Clark, J. Choi, and M. Douglas, Biology, 2018. Hyperthyroidism or Thyrotoxicosis Abnormally increased synthesis and secretion of thyroid hormones. When these high levels result in a hypermetabolic state, this is known as thyrotoxicosis. Graves' disease Graves' disease is the most common cause of hyperthyroidism. It is an autoimmune condition. Clinical Features of Grave’s Disease Management: Antithyroid medication e.g., Carbimazole and propylthiouracil Complication: Thyrotoxic crisis ( thyroid storm ) is a rare but dangerous worsening of the thyrotoxic state, in which death occurs within 48 hours without treatment. Hypothyroidism Deficient production of thyroid hormone by the thyroid gland results in hypothyroidism. Clinical Features of Hypothyroidism Management: Supplemental thyroxine References Hooter, L. (2020). Diabetes and Hypoglycemia. In Linton, F. & Matteson, F. (Eds.), Medical-Surgical Nursing (pp. 967- 995). https://doi.org/http://dx.doi.org/10.1016/B978-0-323-55459-6.00050-5 Lapiz-Bluhm, M. D. S., & Linton, A. D. (2020). Pituitary and Adrenal Disorders. In Linton, F. & Matteson, F. (Eds.), Medical-Surgical Nursing (pp. 929-949). https://doi.org/http://dx.doi.org/10.1016/B978-0-323-55459-6.00048-7 Linton, F.& Matteson, F. (Eds.), Medical-Surgical Nursing (pp. 911-928). https://doi.org/http://dx.doi.org/10.1016/B978-0-323-55459-6.00047-5 List, S. (2019). Alterations of endocrine function across the life span. In J. A. Craft, C. J. Gordon, S. E. Huether, K. L. McCance, V. L. Brashers, & N. S. Rote (Eds.), Understanding Pathophysiology, ANZ Edition (pp. 255-278). https://doi.org/http://dx.doi.org/10.1016/B978-0-7295-4264-7.00011-X Patton, K. T. P., & Thibodeau, G. A. P. (2016). Endocrine glands. In K. T. P. Patton & G. A. P. Thibodeau (Eds.), Anatomy & Physiology (pp. 579-608). https://doi.org/http://dx.doi.org/10.1016/B978-0-323-29883-4.00038-X

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