Nur204 Care of clients w/ problems on endocrine function Endocrine system- the nervous system of the interconnected network of glands

controls body system with far reaching effects Nervous system: hypothalamus Pituitary gland (ACTH) - master gland, located at the sphenoid sinus at the base of the brain. Renal system: Adrenal medulla- inner part; epinephrine, norepinephrine, erythropoietin. Adrenal cortex- outside part; o Sex = androgen o Sugar = glucocorticoid o Salt = mineralocorticoid Immune system: Regulation Interleukins, interferons when there are foreign agents Cytokines Gastrointestinal system: Gastrin Secretin Cholycystokinin Nervous system (automatic)

-binding with the specific receptors located on the membrane on the target cell or by penetrating the cellmembrane and forming a complex that influences cellular metabolism. - target cell response reflected through production

Hormone Action Regulate overall metabolic rate and storage, conversion and release of energy. Regulate fluid and electrolyte balance. Initiate coping responses to stressors. Regulate growth and development. Regulate reproduction processes. Regulation of hormones 1. Negative feedback system a. Fall in blood concentration of hormone leads to activation of the required endocrine gland and to release its STIMULATOR HORMONES b. Elevations in blood concentrations of target cell hormone or of changes in blood composition resulting from target cell activity can cause INHIBITION OF HORMONES. 2. Endocrine disorders are manifested as states of hormone deficiency or excess. a. Primary- secreting glands releases inappropriate hormone because of the disease of the gland itself. b. Secondary- secreting gland release abnormal amount of hormone because of a disease in a regulator gland(pituitary) c. Tertiary- secreting gland release inappropriately because of hypothalamic dysfunction, resulting in abnormal stimulation of pituitary. 3. Abnormal concentrations may also be caused by hormone-producing tumors (adenomas) located at remote site. The glands and function: Assessment b.1. history ask about: 1. Changes in usual energy leves (t3, t4, testosterone, gh)

Hypothalamus (link)

Endocrine system Glands of the endocrine system: -secretes products directly into the bloodstream. P ituitary T hyroid P arathyroid A drenals P ancreatic islets (insulin, somatostatin) O varies T estes Hormones- stimulatory or inhibitory effect on target tissues or glands.

2. How the changes affect the patients ability to carry out activities of daily life. 3. Changes in heat and cold tolerances, recent weight changes(adrenal, thyroid) , changes in fat distribution, fluid loss / retention. 4. Changes in sexual function and secondary sex characteristics. a. Females(data on menarche, menses, patterns, pregnancies) b. Male (onset of puberty, erectile function, testicular size and volume) c. Assess partner issues d. Frequency and type of sexual contact e. Arousal capabilities f. Ability to achieve orgasm g. STDs h. Fertility ( mild hypothyroid, polycystic ovarian syndrome(PCOS)) 5. Changes in mood, memory, ability to concentrate, altered sleep pattern (hyperthyroid) 6. Changes in appetite, food and fluid intake (hyperthyroid-voracious) a. Dietary treatment DM CHO consistency SIADH fluid restrictions b. Hyerparathyroid- I-205-DIOH vit D supplementation 7. Changes in urine frequency, volume, characteristics (turbidity, color, odor, SG) a. Excessive: DI & DM b. Subnormal: SIADH 8. Volume and type of oral fluid intake (DI crave for colds) 9. Perceptions of body characteristics (review photograph if available and relevant) a. Hirsutism- PCOS Cushings syndrome b. Hair loss Thyroid dx c. Hoarse voice hypothyroidism d. Proptosis and ophthalmopathy- graves disease e. Darkening skin pigmentation- Addisons (primary adrenal insufficiency) f. Excessive sweating- hyperthyroidism, acromegaly

-measurement of hormone or substances using radioisotope-labeled antigen Thyroid function (RIA) a. T3 and T4 (levels meaningful after 6-8 wks of hormone replacement therapy; hyperthyroidism hypothyroidism b. TSH hyperpituitarism hypopituitarism Electro-chemoluminescence immunoassay Parathyroid function (RIA method) o PTH hyperparathyroidism hypoparathyroidism o Serum Ca hyperpara hypopara o Serum Ph hypopara hyperpara Ca Ph Adrenal function Plasma cortisol = varies w/ circadian rhythm (8 am: typically2x that of 8pm) Dexamethasone suppresion test= supress cortocotropin. ACTH w/ch stimulates cortisol 11pm test, 8am result: low=normal, inc=abnormal Clonidine suppresion test= suppress production of catecholamines; pheochromocytoma (tumor secreting) Pituitary function S. GH = stimulation test for deficiency states and suppression test for hormone excess condition. Glucose suppression test= post prandial elevations of glucose Radiology/ Imaging a) Radioactive 131 I uptake Thyroid uptake patterns of iodine Hyper= 90% removal of Iodine from bloodstream(graves) Hypo=low uptake *IV test for sensitivity for I. betadine for home b) Thyroid scan =123 or technecium for best images as contrast imaging agents

test Diagnostic studies Radioimmunoassay

Risk factors of endocrine disorders 1. Heredity 2. Congenital 3. Trauma 4. Environmental 5. Consrquence of other disorders DISORDERS OF THE THYROID GLAND Levothyroxine(T4) contains 4 iodine atoms, maintains body metabolism in a steady state Triiodothyronine(T3) contains 3 iodine atoms, has more rapid metabolic action and utilization than T4 does Most conversion of T4 to T3 occurs at the cellular level in the periphery.

Predisposing factors: Age(30-60) 5x more to female Congenital Hashimotos Iodine deficiency Atrophy of thyroid gland w/ aging Drug therapy Etc Declined function of TG Low level of T3, T4 conc in blood Stimulation of hypothalamus TRH Stimulation of PG

Hypothyroidism Inadequate amount of thyroid hormone in the bloodstream Primary- autoimmune dx (hashimotos thyroiditis) -use or radioactive iodine -destruction, suppression or removal of all of the thyroid tissue by thyroidectomy. - Iodine deficiency - sub acute thyroiditis - Lithium therapy, overtreatment w/ antithyroid Secondary- inadequate secretion of TSH by disease of pituitary gland -inadequate TH= gen. slowing of all physical and mental processes - gen depression of most cellular enzyme system and oxidative processes occurs *depression=less oxygen Metabolic activity of all cells of the body decreases, reducing O2 consumption, decrease oxidation of nutrients for energy and producing less body heat (cold intolerant) s/sx- range from vague, nonspecific complaints that make dx difficult to sever sx that may be life threatening if unrecognized or untreated.

Release of TSH Failure of negative mechanism T3 & T4 remains at low level HYPOTHYROIDISM CLINCAL MANIFESTATIONS fatigue and lethargy wt gain complaint of cold hands and feet temp. and pulse become subnormanl; pt cant tolerate cold and desires increased room temp. reduced attention span; impaired short term memory severe constipation, dec peristalsis. Generalized appearance of thick, puffy skin Subcutaneous swelling of hands, feet and eyelids Hair thins Menorrhagia/ amenorrhea- may have difficulty conceiving/ spontaneous abortion, decreased libido Neurologic signs: plynueropathy, cerebellar ataxia, muscle aches or weakness, clumsiness, prolonged DTR(ankle jerk) Hyperlipoproteinemia and hypercholesterolemia Enlarged heart and chest x-ray Inc. susceptibility to all hypnotic and sedative drugs and anesthetic agents DIAGNOSTIC EVALUATION Low T3 and T4 levels

Elevated TSH levels in primary hypothyroidism serum cholesterol ECG- sinus bradycardia, low voltage of QRS complexes and flat or inverted T waves

Management: Replacement therapy in mild cases Life saving support and treatment in severe cases, monitor closely Restoration of normal metabolic rate o T4- levothyroid o T3- liothyronine Monitor to anticipate: Diuresis Decrease puffiness Improved reflexes/ muscle tone Accelerated pulse rate Slightly higher level of serum T4 Signs disappear in 3-12 wks Decrease TSH level Complication: myxedema coma(dec functions) Nsg assessment: Obtain history of sx- med prog., past hx of thyroid disease, surgery or treatment Perform multisystem assessmentcardiac, respiratory, neurologic, GI system Nursing diagnosis: Decrease cardiac output r/t decreased metabolic rate, decreased cardiac conduction per minute(<5-7 liters) Increase cardiac output: - Monitor VS - Monitor ECG tracings, arrhythmias and deterioration of cardiovascular status - Prevent chilling- avoid inc, metabolic rate that places strain on the heart - Avoid rapid rewarming techniques because results in o2 requirement increase= vasodilation=hypotension - Administer fluids cautiously - Administer all prescribed drugs with caution before and after thyroid replacement begins Effects Thyroid replacement may inc effects of digoxin(monitor

pulse) and anticoagulants(signs of bleeding) Report angina(chest pain/discomfort, crushing feeling) Monitor for cardiac failure Monitor ABG

Nsg diagnosis: Constipation r/t dec bowel motility caused by hypotonic of the thyroid gland Activity intolerance r/t reduced metabolic rate Deficient knowledge r/t self-care need for Th replacement therapy HYPERTHYROIDISM Excessive amounts of thyroid hormone in the blood stream Women> men Graves disease (most prevalent)- diffuse hyperfunction of the thyroid gland with autoimmune etiology and associated with ophthalmopathy Toxic nodular goiter ( singular/multiple) Hypertrophy and hyperplasia of the thyroid gland which is accompanied by inc. vascularity and blood flow and enlargement of the gland

Clinical manifestation results in increased metabolic rate, excessive heat production, increased neuromascular and cardiovascular activity, hyperactivity of the sympathetic nervous system. Thyrotoxicosis- (mild increase in metabolic rate to severe hyperactivity) thyroid storm, thyroid crisis Result of ingestion of excessive amount of thyroid hormone medication(factitious hyperthyroidism)

Clinical manifestations: Nervousness, emotional lability, irritability, apprehension Difficulty in sitting quietly Rapid pulse at rest and on exertion (90160) Palpitations Heat intolerance; profuse perspirations; flushed skin (hands may be warm, soft, moist)

Fine tremor of hands; changes in bowel habits- constipation and diarrhea Increase appetite and progressive weight loss; frequent stools Muscle fatigability and weakness; amenorrhea Atrial fibrillation(possible cardiac decompensation common in older patients) Exophthalmos- seen only in graves disease Thyroid gland may be palpable and a bruit may be auscultated over gland Course may be mild, characterized by remissions and exacerbations May progress to maciation, extreme nervousness, delirium, disorientation, thyroid storm or crisis and death.

If euthyroidism not maintained radiation or surgery 2) Drugs to control peripheral manifestations Propanolol (inderal) - Act as beta-adrenergic blocker - Inhibits peripheral conversion of T4 T3 - Abolishes tachycardia, tremor, excess sweating, and nervousness. - Control hyperthyroid until antithyroid drugs or radioiodine can take effect. Glucocorticoid - Decrease conversion of T4-T3 aside from being a steroid - More steroid=thyroid disease Radioactive iodine - Limits secretion hormone by destroying thyroid tissue - Dosage is contolled so that hypothyroidism does not occur - Advantage: lasting remission can be achieved - Disadvantage: permanent hypothyroidism can be produced. Surgery - Used for those with large goiters - For those whom the use of radioiodine ir thioamides is contraindicated - Subtotal thyroidectomy- removal of most of the thyroid gland Emergency management of thyroid storm: - PTU (inhibitionof new hormone synthesis with thioamides - Lugols solution (inhibition of thyroid hormone release using iodine) - Propanolol(inderal) corticostreroids, and thioamides(PTU) inhibition of oeripheral effects of thyroid hormones *hyperthermia- cooling effects *dehydration- IVF Complications: Thioamides toxicity- agranulocytosis Hypothyroidism- overtreated/ radiation treatment Radiation thyroiditis- transcient axacerbation of hyperthyroidism

Thyroid storm crisis- extreme form of hyperthyroidism characterized by: hyperpyrexia, diarrhea, dehydration, tachycardia, arrhythmias, extreme irritation, delirium, coma, shock and death if not adequately treated. Precipitated by stress (surgery, infection) or inadequate preparation for surgery. Diagnostic evaluation: elevated T3, T4 Management: Remissions of hyperthyroidism occurs spontaneously within 1-2 yrs however relapses can be expected in half of the patients. Treatment: Anthyroid drugs, radiation, surgery Nodular toxic goiter- surgery or use of radioiodine is preferred Thyroid carcinoma- surgery or radiation is used Goal of therapy: To bring the metabolic rate to normal as soon as possible and to maintain it as this level Pharmacotherapy: 1) Drugs that inhibit hormone formation Thioamides- propylthiouracil (PTU), methimazole (Tapazole) - Depressing the synthesis of thyroid hormone by inhibiting perioxidase - Given in divided but daily doses (PTU) or in a single daily dose Duration of treatment is determined until patient becomes clinically euthyroid; 3 mos. 2 yrs

-Leakage of TH in circulation from damaged follicles Infiltrative ophthalmopathy- occurs in 50% of patients Nursing assessment: Obtain history PA Temperature Nursing diagnosis: Imbalanced nutrition: less that body requirements r/t hyper metabolic state and fluid loss through diaphoresis Risk for impaired skin integrity r/t diaphoresis, hyperpyrexia, restlessness and rapid weight loss Disturbed thyroid process 1. Providing adequate nutrition - High calories food, fluids - Quiet, calm environment - Restrict stimulants - Encourage and permit the patient to eat alone food preferences - Monitor IV infusion - Monitor fluid and nutritional status by weighing and MIO - Monitor skin turgor, mucous membranes 2. Maintain skin integrity - Assess skin frequently to detect diaphoresis - Bath with cool water, change linen - No soap, use lotions - Relieve pressure from bony prominences 3. Promote normal thought process - Explain calm - Avoid stimulation, limit visitors - Reduce stressors - Sleep and relaxations - Minimize disruption - Safety measures reduce risk of trauma or falls 4. Relieve anxiety - Encourage verbalization of concerns or fears about illness or treatment - Support patient undergoing various diagnostic test - Clear misconceptions about treatment options

Patient education and health maintenance 1. Instruct patient as follows: a. When to take medicines b. Signs and symptoms of insufficient/ excessive medication c. Necessity of having blood evaluation. d. Signs of agranulocytosis- fever, sore throat, URTI or rash, urticaria e. s/sx of thyroid storm- tachycardia, hyperrexia, extreme irritation 2. predisposing factors to thyroid storminfection, surgery, stress, abrupt withdrawal of medications 3. Reinforce teaching by written instructions 4. Assist identifying resources of information

DISORDERS OF PARATHYROID GLANDS Parathyroid gland- small bean-sized atructure embedded in the posterior section of the thyroid gland. -production, storage and release of PTH HYPERPARATHYROIDISM Women <50 Primary hyperparathyroidism single parathyroid adenoma Parathyroid hyperplasia parathyroid carcinoma Secondary hyperparathyroidism primarily result of the renal failure Clinical manifestations Decalcification of bones - Skeletal pain - Backache - Pain on weight bearing - Pathologic fractures (innate pathology that soften bones) - Formation of bone tumors - Formation of calcium-containing kidney stones Depression of neuromascular function - Show general fatigue - Lose memory for recent events - Emotional instability - Changes in level of consciousness - Stupor and coma Diagnostic evaluation

Elevated serum Ca, test 2 occassions for consistency. PTH levels are increased Alkaline phosphatase levels are elevated Serum phosphorus will be decreased Skeletal changes are revealed by x-ray

Treatment of hypercalcemia Hydration and diuresis furosemide Pral phosphate dutihypercalcemic agent Pamidronate (aredia) calcitonin (Cibacalcin) Dietary calcium is restricted Dialysis renal failure Digoxin is reduced because they are more sensitive to toxic effects of this drug Monitor serum calcium, BUN, pottasium, magnesium levels Treatment of primary hyperparathyroidism Surgery for abnormal parathyroid hormone Complications Renal stones Calcification of kidney parenchyma Renal shutdown Ulceration of upper GI tract Demineralization of bones Hypoparathyroidism Nursing assessment Multisystem exam Monitor I&O and serum electrolytes Nursing diagnosis Deficient fluid volume related to effects of elevated serum calcium levels. Impaired urinary elimination related to renal calculi and calcium deposits in kidneys. Impaired physical mobility Anxiety related to surgery Risk for injury related to hypocalcemia Nursing intervention Achieving fluid and electrolyte balance - MIO - Adequate hydration - Prevent or promptly treat dehydration - Avoid dietary sources of calcium dairy products like milk, broccoli, calciumcontaining antacids Promote urinary elimination - Strain all urine for stones - Increase fluid intake to 3000 ml/day

Observe signs of UTI, hematuria, renal colic - Assess renal function (BUN, Serum creatinine) Increase physical mobility - Assist patient in hygiene and activities if bone pain is severe - Protect from falls or injury - Turn the patient cautiously and handle extremities gently - Administer analgesia as prescribed - Correct body mechanics to reduce strain, backache and injury. Relieving anxiety - Encourage patient to verbalize fears and feelings - Explain test and procedures - Reassure the patient Monitor post operative hypocalcemia - Monitor ECG - Monitor serum calcium level - Evaluate signs and symptoms of hypocalcemia - Tetany Health education 1. Instruct about Ca-reducing medications a. Calcitonin (cibacalcin) given subcutaneously b. Etidonate disodium (didronel) avoid Carich food with 24hrs of dose; response may take 1-3 months c. Pamidronate (arcdia) monitor hypercalcemia and vitamin d to prevent hypocalcemia d. Biphosphanates - used with caution with upper GI problems Teach signs and symptoms of teteny : numbness on the mouth Evaluation Output = intake Normal skin turgor Moist mucous membrane No s/sx of kidney stone or UTI Normal serum creatinine, BUN Less bone and joint pain Appears less anxious ECG have no changes ( QT, T wave) No numbness or tingling reported HYPOPARATHYROIDISM

Deficiency of PTH characterized by hypocalcemia and neuromascular hyperexcitability. Pathophysiology and etiology - Accidental removal or destruction of parathyroid tissue during thyroidectomy - Autoimmune or familial origin - Malignant metastasis from cancer - Resistance to PTH action Inadequate PTH secretion and decrease serum calcium - Causing symptoms of muscular hyperirritability, uncontrolled spasm, hypocalcemic tetany - Serum phosphate level rises - Phosphate excretion by the kidney decreases Clinical manifestations Tetany general muscular hypertonia - Tremors and spasm - Uncoordinated movement Chvosteks sign spasm of facial muscles - Occurs when facial muscle are tapped Troseaus sign carpopedal spasm - Within 3 mins after Bp cuff is inflated 2ommHg above patients systolic pressure Severe anxiety and apprehension Renal colic Diagnostic evaluation Increased Ph level Decreased Ca level: 7.5 mg/100ml or less (normal: 9-11mg/dl) Decreased PTH Management IV Ca administration - Administer slowly - Cause rapid relief of anxiety - Slow IV drip of IV saline containing Ca gluconate is given until control of tetany is ensured - Later, vitamin D is added to Ca intake to increase absorption of Ca - Thiazide diuretics Ca retaining effect on the kidney - Doses of Ca and Vitamin D may be lowered Other measures Treat kidney stones Monitor for hypercalciuria Periodic 24 hr urinary Ca determinations

Monitor blood Ca level

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