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Endocrine Disorders

Endocrine Disorders. Irma B. Ancheta, PhD, RN University of North Florida. Endocrine. “ductless” Lock and key Excess production = hyperfunction Decreased production = deficiency. Simple Negative F eedback Mechanism. “ supply and demand”

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Endocrine Disorders

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  1. Endocrine Disorders Irma B. Ancheta, PhD, RN University of North Florida

  2. Endocrine • “ductless” • Lock and key • Excess production = hyperfunction • Decreased production = deficiency

  3. Simple Negative Feedback Mechanism • “ supply and demand” • Glucose insulin = maintain glucose levels insulin (met) glucose insulin

  4. Complex Feedback Effect • Look up this info • Glucocorticoids needed when stressed. Tells hypothalamus… release C?H. Tells pit to release ACTH. Tells adrenals to release cortisol… adrenals then release the cortisol… From one gland to another gland.

  5. hypothalamus • Structure • A. hypothalamuic – hypophysial • Portal system = allows hormones to travel from hypothalamus and APG • B.

  6. Pituitary Gland Posterior Anterior (70% of all hormones produced here) TSH (thyroid stimulating hormone) ACTH LH FSH PRL (prolactin) GH MSH (melanocyte stimulating hormone) • Vasopressin (antidiuretic hormone) = Kidney • Oxytocin

  7. Adrenal Glands Adrenal Cortex (outer layer) adrenal steroids or corticosteroids Adrenal Medulla (inner layer) Catecholamines [1] Epinephrine (85%) = Beta [2] NE (515%) =alpha receptors sites Secreted in small amounts at all times to maintain homeostasis • 90% • OUTER layer (Glumerolosa) [1] mineralocorticosteroids • (aldosterone, regulated by RAAS, ACTH) = [SALT] Na and water retention = K+ excretion • MIDDLE Layer (Fasciculata) • INNER layer (reticularis) [1] [SUGAR] Glucocorticosteroids (cortisol) [2] [SEX] Androgens [3] [SEX] Estrogens

  8. Addison’s Disease(Adrenal Gland Hypofunction) Causes: [1] ACTH [2] dysfunction of hypothalic pituitary control mechanism [3]dysfunction of adrenal gland tissue

  9. Addison’s disease Adrenal Cortex Adrenal Medulla catecholamines (E and NE) • Aldosterone • Cortisol

  10. Adrenal Cortex [1] Aldosterone (needed for Na and water retention/ K+ excretion) = K+ excretion is decreased hyperkalemia ? = Na and water NOT retained hyponatremia ? hypovolemia ?BP

  11. Adrenal Cortex [2] Decreased Cortisol levels Can lead to gluconeogenesis hypoglycemia Hypoglycemia glomerular filtration gastric acid production Both of which urea nitrogen excretion causing Anorexia Weight Loss

  12. Adrenal Cortex [3] Androgens = Levels Decreased in body, axillary and pubic hair growth

  13. Diagnostic Labs Addison’s Disease • Cortisol = Decreased • Aldosterone = Decreased [1] NA = ? [2] K+ = ? [3] Glu = ? [4] Ca = ? [5] BUN = ? • Urinary 17hydroxycorticosteroids (androgen metabolites) • Skull x-rays (?), CT, MRI (pituitary) • ACTH Stimulation test Cushing’s Disease • Cortisol = Increased • Aldosterone = Increased [1] NA = ? [2] K+ = ? [3] Glu = ? [4] Ca = ? [5] BUN = ?

  14. Intervention [1] Fluid Balance (a) Weigh (b) I & O (c) monitor lab values (d) monitor for dysrthmmias [2] Cortisol/ Aldosterone Replacement (prednisone)/ (flurinef)

  15. Treatment [1] Primary Cause: (trauma, surgery, infection) • Cortisol and (b) aldosterone replacement [2] Secondary causes: sudden cessation of high dose glucocorticoid therapy

  16. Cushing’s Disease(Hypercortisolism) Causes: [1] excessive stimulation/production of ACTH [2] excessive amounts of glucorticoids

  17. Signs and symptoms [1] increased glucorticoids = leads to hypergycemia carbohydrate metabolism increase in body fat (truncal obesity/ “buffalo hump”) =kill lymphocytes, shrink organs containing lymphocytes ( liver, spleen, lymph nodes) causing decreased eosinophils, macrophages =leading to reduced inflammatory/ immune responses

  18. Signs and symptoms [2] excessive androgens (sex hormone) = hirsutism and oligomenorrhea

  19. Cushing’s Disease = excess of cortisol, secreted by adrenal gland (Endogenous) = bilateral adrenal hyperplasia, Adrenal carcinomas Cushing’s Syndrome = excess cortisol (exogenous) = Use of ACTH or glucoticoids (asthma, auto immune diseaases, organ transplantation,Ca chemo, allergic responses, chronic illness)

  20. Cushing’s Disease General Appearance: [1] moon face [2] Buffalo hump [3] truncal obesity [4] Weight gain CV [1] HTN [2] dependent edema MS [1] osteoporosis/pathologic fracture Immune system [1] Increased risk for infection [2] decreased lymphocytes [3] dcreased eosinophils

  21. Diagnostic Assessment (Cushing’s Disease) [1] check plasma cortisol levels [2] Check plasma ACTH • Ectopic = elevated • Primary cushings (from chronic steroid use)=low [3] Glucose = ? [4] Lymphocytes =? [5] Na = ? [6] Ca =? [7] K+ = ? • 24 hour urine (17k , 17 h) • 3 day low dose dexamethasone suppression test • High dose dexamethasone suppression test

  22. Nursing Diagnosis [1] ? [2] ? [3] ?

  23. The good thing is: = Cushing’s disease is RARE = Occurs 10 patients for every one million

  24. Thyroid Disorders Irma B. Ancheta, PhD, RN Linda Connelly, ARNP, MSN

  25. A Thyroid Story

  26. Management of patient with Thyroid disorders Thyroid Gland • Butterfly shape • Hugs trachea • 2 lobes together produce • T3 and T4 • Calcitonin • T3 - triiodothyronine • T4 - thyroxine • Together Thyroid hormone - body’s major metabolic hormone • Calcitonin helps regulate blood calcium level by inhibiting the release of calcium from the bone

  27. Thyroid Hormone Regulation

  28. TSH released from ant. Pituitary in response to TRH from the hypothalamus TSH stimulate the thyroid to produce T3 and T4 - iodine is crucial to this process Circulating T3 and T4 then exert negative effect on ant pit and hypothalamus to decrease production of TRH and TSH All to maintain therapeutic level of T3 and T4 in the serum and stable metabolic processes in the body

  29. Thyroid Hormone Effects on the Body • Metabolism • Increase BMR - increase body heat production • Stimulate mobilize fat and enhance oxidation in many tissues • Stimulates CHO and fat metabolizm • Other effects • Increase HR, vasodilation, CO, contractility

  30. Physiologic Effects of Thyroid HormonesIt is likely that all cells in the body are targets for thyroid hormones. While not strictly necessary for life, thyroid hormones have profound effects on many "big time" physiologic processes, such as development, growth and metabolism. Many of the effects of thyroid hormone have been delineated by study of deficiency and excess states, as discussed briefly below.

  31. Diagnostic tests • Serum Thyroid Antibody (TA) • Serum TSH • Serum T4 • Serum T3 • Radioactive Iodine Uptake • Serum Calcitonin

  32. TA wnl negative to 1:20 ratio TSH> 1 m/l, T4 4.5 to 11.5 m/dl (microgram, mcg) T3 80-200 ng/dl Radioactive iodine 2hre 1-13%; 6 hrs 2-25%; 24 hrs 15-45% Compare TSH with T4

  33. Major thyroid disorders • Hyperthyroidism • Grave’s Disease • Toxic Multinodular Goiter • Thyroiditis • Thyroid Storm • Hypothyroidism • Iodine Deficiency • Hashimoto’s Thyroiditis • Myxedema Coma

  34. Thyroid Disease States Disease is associated with both inadequate production and overproduction of thyroid hormones. Both types of disease are relatively common afflictions of man and animals.Hypothyroidism is the result from any condition that results in thyroid hormone deficiency. Two well-known examples include:･Iodine deficiency: Iodide is absolutely necessary for production of thyroid hormones; without adequate iodine intake, thyroid hormones cannot be synthesized. Historically, this problem was seen particularly in areas with iodine-deficient soils, and frank iodine deficiency has been virtually eliminated by iodine supplementation of salt. ･Primary thyroid disease: Inflammatory diseases of the thyroid that destroy parts of the gland are clearly an important cause of hypothyroidism.Common symptoms of hypothyroidism arising after early childhood include lethargy, fatigue, cold-intolerance, weakness, hair loss and reproductive failure. If these signs are severe, the clinical condition is called myxedema. In the case of iodide deficiency, the thyroid becomes inordinantly large and is called a goiter.

  35. Hyperthyroidism • Hypermetabolic condition with elevated T3 and T4 • Arises from many different factors • Autoimmune reactions (Graves) • Excess TSH from Anterior Pituitary • Thryoiditis • Neoplasms (multinodular goiter) • Excessive intake of thyroid medications

  36. Grave’s Disease • Most common cause of hyperthyroidism (75% of cases) • 5 times more prevalent in women than men • Occurs most frequently between 20 and 40 years of age • Seen worldwide, incidence correlated with amount of iodine in diet • Precipitated by stress, infections, genetic factors

  37. Clinical Manifestations EXOPHTHALMOS GOITER

  38. Exophthalmos • Impaired drainage from orbit, increasing fat and edema in retroorbital tissues • Eyeballs forced outward and protrude • Corneal surfaces become dry and irritated

  39. Toxic Multinodular Goiter • Slower to develop than Grave’s disease • Multiple nodules in the thyroid secrete excessive amounts of TH • Usually women 60-70 years of age • Characteristic massive enlargement of neck (goiter)

  40. Thyroid Storm • Life threatening condition • Precipitated by severe illness or injury, or surgical manipulation of thyroid • Rapid increase in metabolic rate • Hyperthermia up to 106 deg. F, respiratory distress, tachycardia, hypertension, severe GI symptoms, confusion, delirium, coma • High mortality rate

  41. Diagnostic Studies Primary hyperthyroidism • T3 and T4 elevated • TSH suppressed • Radioactive iodine uptake is increased in Graves' disease

  42. Hyperthyroidism: goals and treatment • Goals • Reduce production of TH • Establish euthyroid state • Prevent and/or treat complications • Collaborative treatment • Medications • Radioactive iodine therapy • Surgery

  43. Pharmacologic therapy antithyroid medications • Potassium iodide (SSKI, Thyro-Block) • CHECK ALLERGIES to shellfish • Bleeding precautions • Bitter taste - give with OJ • Maximum effect in 2 weeks • Tapazole, Propylthiouracil • Monitor for s/s hypothyroidism especially if taking lithium • Bleeding precautions • Effects may take up to 12 weeks

  44. SSKI - Inhibits TH synthesis and release Hyperplastic thyroid less vascular before surgery Hastens ability of other antithyroid drugs to reduce natural hormone output PTU inhibits TH production only

  45. Radioactive iodine therapy • Measured dose given orally • Results in 6-8 weeks • 131I concentrates in thyroid cells and damages them so they produce less TH • TAKEN AT HOME, NO RADIATION PRECAUTIONS NEEDED • Contraindicated in pregnant women

  46. Surgery: thyroidectomy • Subtotal thyroidectomy indicated when thyroid pressing on trachea • leaves enough gland to produce TH • Total thyroidectomy primarily for cancer of the thyroid • Requires lifelong hormone replacement • Endoscopic thyroidectomy appropriate with small nodules with no malignancy • Less scarring, pain, and recovery time

  47. Breathing or swallowing problems • Subtotal thyroidectomy involves removal of significant portion of thyroid • 90% removed to be effective • If too much is removed, regeneration will not occur, results in hypothyroidism • Surgical Therapy • Indicated for those • unresponsive to drug therapy • with large goiters causing tracheal compression • with possible malignancy

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