1. Endocrine<br />Chapter 18<br />Review the anatomy and physiology of the endocrine system.<br />Pituitary gland – “master” gland; hormones regulates many body fxns<br />Anterior Pituitary – Somatotropin (GH – growth hormone = cells increase protein production and growth of epiphyseal plates of long bones)<br /> PRL – breast milk<br />TSH – synthesis/release of TH from thyroid <br />ACTH – stimulates release of hormones (esp. glucocorticoids) from adrenal cortex<br />Gonadotropin – FSH – generation of estrogen and sperm, LH – when combines with FSH = ovulation<br />Posterior Pituitary – nervous tissue, release and store ADH/Oxytocin<br />ADH – vasopressin – inhibits urine production, renal tubules reabsorb water from urine<br />Oxytocin – contraction of smooth muscles in reproductive organs, uterus during labor, milk from breasts<br />Thyroid gland – secretes TH (T3, T4) which increase metabolism (growth and development in <br />children) and secretes calcitonin (decreases levels of Ca in blood by slowing Ca-release <br />from bone cells)<br />Parathyroid glands – secrete PTH (Ca levels in blood fall, PTH released) which controls <br />phosphate metabolism – increase renal excretion of phosphorus, decrease Ca <br />excretion, increase bone reabsorption of Ca. Normal levels of Vit D needed to reg PTH<br />Adrenal Medula – produces acetylcholamines (epinephrine/adrenaline and norepinephrine/noradrenaline) – not essential to life<br />Epi – increases BGL and stimulates ACTH (release glucocorticoids), increase rate and <br />force of heart contractions, constricts vessels in skin, mucous membranes, kidneys, <br />dilates BVs in skeletal muscles/coronary arteries/pulm arteries<br />Norepi – increase HR and force of cardiac contractions, constricts BVs throughout body<br />Adrenal Cortex – secretes corticosteroids, essential to life – mineral and gluco corticoids<br />Mineral corticoids – renin controlled – in response to decrease in drop in BP or <br />hyponatremic conditions in kidneys<br />Glucocorticoids – released during stressful pds, depresses body’s inflammatory <br />response and inhibits efficacy of immune system<br />Pancreas – produces hormones and digestive enzymes – regulate carb metabolism in islets of <br />langerhans (four types of cells)<br />Alpha – produce glucagon<br />Beta – produce insulin<br />Delta – produce/secrete somostatin, inhibits secretion of glucagon and insulin<br />F cells – secretes pancreatic polypeptide (inhibits the exocrine activity/digestive <br />enzymes)<br />Gonads – testes/ovaries – produce androgens which maintain reproductive functioning and secondary sexual characteristics<br />What are hormones?<br />Chemical messengers secreted by endocrine organs and transported through the body where they exert specific actions on target cells. Do not cause reactions, but regulate tissue responses producing generalized or local effects.<br />How are they transported?<br />Four ways:<br />Endocrine glands release into blood stream, with or without protein carriers.<br />Adrenal glands release to blood stream, neuroendocrine route.<br />Hypothalamus releases directly to target cells by nerve cell extension.<br />Messengers diffuse through interstitial fluid, via peptides released through vital organs and cells and act locally.<br />What is a negative feedback system?<br />Most feedback systems are negative. I.e. Controlled much as the thermostat in a house <br />regulates temperature. Sensors detect hormone level changes and adjust hormone secretion <br />to maintain body at normal levels.<br />What diagnostic tests are used to assess pituitary and adrenal function?<br />Pituitary: blood test for hormone levels sometimes at multiple times, stimulation tests - insulin tolerance test (ITT), synacthen and glucagon tests, etc.<br />Adrenal: serum or saliva cortisol tests (often taken 4 x day), 24 hr cumulative urine test, ACTH baseline, dexamethasone tests, etc.<br />Chapter 19<br />What is Cushing’s syndrome?<br />Chronic disorder in which hyperfunction of adrenal cortex produces and circulates excessive amts of ACTH. More common in female 30-50. <br />S/S: weakness, muscle wasting, osteoporosis, thin bruisable skin, infections, poor wound healing, stretch marks, hirsutism, echymosis, peptic ulcers, emotional liability, psychsoes, renal calculi, polyuria, glycosuria, htn, hypona/kalemia, impotence, decreased libido, amenorrhea, etc.<br />Discuss the common causes and complications.<br />Result from pharmacologic therapy (steroids for long pds of time - tx of arthritis, s/p organ transplant, or as adjunct to chemotherapy), etc. Pituitary form (caused by tumor), ectopic form (ACTH-secreting tumors – small cell lung cancer), adrenal form (adrenal tumor), Iatrogenic Cushings syndrome (from long term pharmacologic therapy).<br />Complications (if untreateated): electrolyte imbalance (hyperglycemia, hypernatremia, hypokalemia), htn, emotional disturbances, increased susceptibility to infections, compression fxs from osteoporosis, aseptic necrosis (of femoral head), acute deficit of cortisol (if pt undergoes bilateral adrenalectomy).<br />How is it diagnosed?<br />Plasma cortisol – (+) Cushing’s = loss of normal diuretic variations of higher levels in AM and lower levels in PM<br />Plasma ACTH levels – determine etiology of syndrome. Levels normally highest from 0700-1000, lowest from 1900-2200, (+) 2ndary cushings ACTH elevated, primary cushings ACTH decreased<br />24 hr Urine Tests – measure free cortisol and androgens (+) cushings = elevated levels<br />Serum K, Ca, BGL – measured to ID electrolyte imbalance<br />ACTH suppression test – used to ID cause of d/o, dexamethasone given to suppress levels /production of ACTH – plasma cortisol levels are measured, if extremely high dose is required (primary d/o is adrenal cortex hyperplasia), if levels not suppressed adrenal tumor is suspected<br />How is it treated?<br />Meds: Mitotaine – suppresses activity of adrenal cortex, decreases peripheral <br />metabolism of cortico’s – used to tx metastatic adrenal ca<br />Metyrapone/Ketoconazole/both – inhibit cortisol synthesis by adrenal cortex, used for ectopic ACTH secreting tumors<br />Somatostatis analog (octreotide) – suppresses ACTH secretion<br />Surgery: (unilateral) adrenalectomy, bilateral adrenalectomy (both require lifelong hormone <br />replacement), surgical removal of pituitary (hypohphysectomy) via transphenoidal or craniotomy<br />Discuss the nursing care and common diagnoses.<br />Fluid Volume Excess: excess cortisol = sodium and water reabsorption, wt gain, edema, htn<br />Weigh at same time QD (1L = 2lbs)<br />Monitor BP, pulse, RR, breath sounds, etc.<br />Teach reasons for restricting fluid<br />Risk for injury: elevated cortisol levels increase Ca retention and demineralization of bones, pathologic fxs<br />Teach client and family to maintain safe environment<br />Risk for infection: elevated cortisol impairs the immune response, affects protein synthesis, causing delayed wound healing, inhibits collagen formation, results in epidermal atrophy, altered cellular nutrition, etc.<br />Private room, limit visitors<br />Monitor VS q 4<br />What is Addisons disease?<br />Results from destruction/dysfunction of adrenal cortex. Chronic deficiency of cortisol, aldosterone, and adrenal androgens, accompanied by skin pigmentation. Women under 60. <br />Discuss the common causes and pathophysiology.<br />Causes: autoimmune dysfunction of adrenals, clients who are taking anticoaguluants, have major trauma injuries, etc. Adrenoleukodystrophy (accumulation of fatty acid chains in adrenal cortex), ACTH deficit (from pituitary tumors), clients abruptly withdrawn from steroid therapy.<br />What are its manifestations?<br />Delayed wound healing, hyperpigmentation, postural hypotension, tachycardia, arrhythmias, emotional lability, confusion, lethargy, tremors, join/muscle pain, weakness, muscle wasting, diarrhea, anorexia, N/V, hyperkalemia/hypoglycemia/hyponatremia.<br />What is Addisonian Crisis?<br />Life threatening response to an acute adrenal insufficiency. Occurs in pt w/Addisons disease (poorly controlled), or pt abruptly w/drawn from glucocorticoid therapy. <br />S/S?<br />Primary sx = high fever, weakness, abd pain, severe hypotension, circulatory collapse, shock, coma.<br />Tx?<br />Rapid IV replacement of fluids and glucocorticoids, fluid balance restored within 4-6 hrs.<br />How is it diagnosed?<br />Serum cortisol levels, BGLs, Serum Na/K levels, BUN levels, Urinary 17 hydrocorticoids/ketosteroids, Plasma ACTH, ACTH stimulation test, CT scans of head, etc.<br />Discuss the nursing mgmt.<br />Primary tx of Addisons disease includes replacement of corticosteroids and mineralcorticoids accompanied by increased sodium in the diet. Hydrocortisone is given PO to replace cortisol, fludrocortisones given PO to replace mineralcorticoids.<br />Cortisol replacements: <br />Establish baseline data (VS, MS, wt)<br />ID meds that might interact negatively: Antidiabetic agents, cardiac glycosides, PO contraceptives, anticoagulants.<br />Document /report increased BP, edema, wt gain, bleeding or bruising, weakness, or manifestations of Cushings disease.<br />Monitor for increased Na or decreased K.<br />Take meds w/food or milk and report any dark, tarry stools.<br />Diet must be high in K, low in Na, high in protein. <br />Weight QD at same time. <br />Abruptly d/cing med is dangerous.<br />Use safety measures in home to prevent falls. <br />Report dizziness on standing/standing, N/V, feelings of thirst, malaise, infections, etc. to MD.<br />What are the d/o of the anterior pituitary gland?<br />Hyperfunction of pituitary, excess production/secretion of one or more trophic hormones result of Pit. Tumor or hyperplasia, benign adenoma, etc. Manifestations result from excess in GH or PRL or ACTH.<br />Define gigantism and acromegaly.<br />Gigantism – when GH hypersecretion begins before puberty and closure of epiphyseal plates. Abnormally tall, exceeding 7ft; body proportions are normal. <br />Acromegaly – excess of GH during adulthood, “enlarged extremities” usually because of pituitary tumors. Bone and connective tissue continue to grow, forehead, tongue, jaw enlarges, voice deepens. Other s/s = entrapment of nerves: headache, htn, CHF, visual disturbances, sensitivity to sugars, etc.<br />What is a transphenoidal surgical procedure?<br />Go in through the nose, dissect the phenoidal frontal bone and take out the pituitary tumor. (Ch 42)<br />What drug is used to suppress the anterior pituitary gland and decrease GH levels?l<br />Octreotide – man made mimic drug that acts like somatostatin and inhibits HGH, LH, glucagon, insulin<br />What common complication is associated with its use?<br />Bradycardia, palpitations<br />What are the common disorders of the posterior pituitary gland?<br />R/T to excessive or deficient amounts of ADH. When ADH secreted, renal water reabsorbed. When ADH suppressed, renal water excreted. SIADH/Diabetes Insipidus.<br />What is SIADH?<br />Serum of Inappropriate Anti-Diuretic Hormone.<br />High levels of ADH in absence of serum hypo-osmolality. Caused by ectopic production ofADH by malignant tumors. <br />What are its manifestations?<br />Result of H2O retention, hyponatremia, serum hupo-osmolality. S/S BV expands, plasma diluted. Aldosterone suppressed, renal exretion fo sodium increases. Water moves from hypotonic plasma and interstitial spaces into cells causing edema.<br />Brain cells swell = neurologic deficits. No peripheral/abd edema present.<br />How is it treated?<br />Treated by correcting underlying causes. Treating hyponatremia w/hypertonic saline, restricting PO fluids to <800 cc day.<br />What is Diabetes Insipidus?<br />Result of ADH insufficiency. Two types:<br />Neurogenic DI: result from disruption of hypothalamus and pituitary gland (from trauma, irradiation, or cranial surgery) or can idiopathic.<br />Nephrogenic DI: renal tubules are not sensitive to ADH, may be familial in origin or result of renal failure<br />What causes it?<br />Brain tumors, infxns, pituitary surgery, CVAs, and renal/organ failure. Complication of closed head trauma, increased ICP.<br />What are the symptoms?<br />Polyuria, polydipsia, dehydration, hypernatremia, hyperosmolality. Urine still clear and dilute.<br />What is the treatment?<br />Correcting underlying causes. IV hyptonic fluids, increase PO fluids, replacing ADH hormone. Desmopressin acetate is drug of choice.<br />