Endocrine Dysfunction: Adrenal & Pituitary Endocrine System (comprehensive source) Endocrine Review (narrated online review) Medications-Endocrine (narrated PPTs) Endocrine Drugs Overview Pituitary Drugs Adrenal Drugs Endocrine System Pituitary Gland- “master gland” + Hypothalamus Hypothalamus-functions Hypothalamus- integrative center for endocrine and autonomic nervous system *Hypothalamus and pituitary integrate communication between nervous and endocrine system Control of some endocrine glands by neural and hormonal pathways Two major groups of hormones secreted: inhibiting and releasing Hypothalamus Two major groups of hormones secreted: inhibiting and releasing ANTERIOR PITUITARY (Adenohypophysis) SECRETES 6+ HORMONES: ACTH (adrenocorticotropic hormone) controls release of cortisol in adrenal glands *ACTH release; controlled by corticotropin-releasing hormone (CRH) ANTERIOR PITUITARY(adenohypophysis) TSH (thyroid stimulating hormone) Thyroid –releasing hormone; secreted by hypothalamic neuronscontrol release of TSH GH (growth hormone) (Somatotropin) stimulates growth of bone/tissue Prolactin- promotes mammary gland growth and milk secretion FSH (follicle stimulating hormone)- stimulates growth of ovarian follicles & spermatogenesis in males LH (lutenizing hormone)- regulates growth of gonads & reproductive activities Posterior Pituitary (Neurohypophysis) What hormones are released by the posterior pituitary signaled by the hypothalamus? Antidiuretic hormone (ADH) ____________ Oxytocin & ____________. ANTERIOR PITUITARY DISORDERS ANTERIOR PITUITARY HYPERFUNCTION DISORDERS ETIOLOGY Primary: defect in gland itself -releases a particular hormone that is too much or too little. Secondary: defect is somewhere outside of gland i.e. GHRH from hypothalamus TRH from hypothalamus PITUITARY TUMORS 10% OF ALL BRAIN TUMORS What diagnostic tests diagnose a pituitary tumor? *Determined by symptoms presented; evaluate serum/urine hormone levels; stimulation/suppression tests for hormone levels; CT, MRI, etc Tumors usually cause hyper release of hormones ANTERIOR PITUITARY HYPERFUNCTION What happens if: TOO MUCH secretion of prolactin (prolactinoma)? Anovulation; menstrual irregularities; galactorrhea TOO MUCH release of Lutenizing Hormone (LH)? “Polycystic ovary syndrome;, due to effect on corpus lutea Too much growth hormone secretion? GIGANTISM IN CHILDREN; ACROMEGALY IN ADULTS Which goolish character on the Addam’s Family had too much GH secretion Effects of growth hormone. A, Comparison of (from left to right) gigantism, normal, and dwarfism. B and C, The patient’s hands and face show; Clinical signs of acromegaly. D, Acromegaly. Excessive secretion of growth hormone in the adult caused characteristic malocclusion of the teeth resulting from the overgrowth of the mandible. Sing along TOO MUCH GROWTH HORMONE GIGANTISM IN CHILDREN skeletal growth; may grow up to 8 ft. tall; > 300 lbs ACROMEGALY IN ADULTS enlarged feet/hands, thickening of bones, prognathism (jaw projects forward), diabetes, HTN, wt. gain, H/A, Visual disturbances, diabetes mellitus ACROMEGALY IN ADULTS progessive change in facial features Hand in acromegaly; normal hand What assessment findings would the nurse document? What priority health risks associated with acromegaly? Video-You Tube Lecture “Effects of GH Deficiency in Adults” You Tube-Pituitary Giantism/Agromegaly “Egor” the Giant Video You Tube-Pituitary Giantism- Robert Wadlow “Worlds Tallest Man” died age 22 Cont. Hyperfunction of the Anterior PituitaryAn individual has a tumor of anterior pituitary gland which causes excess ACTH secretion •What “disease” is this? •What signs and symptoms are likely to be found? Cushing’s disease- condition in which pituitary gland releases too much adrenocorticotropic hormone (ATCH). Cushing's disease- a form of Cushing syndrome See next slide for VideoRemember this one-see adrenal disorders Cushing’s Disease- MEDICAL INTERVENTIONS PITUITARY TUMOR *Medications (goal…...reduce GH levels) Somatostatin analogs (octreotide) GH receptor antagonists (Pegvisomant) Dopamine agonists (cabergoline) Dostinex *inhibits prolactin (prolactinoma) FYI- If inadequate GH prior to puberty- what “condition” will this individual have? what drug might be given to treat? Pituitary Dwafism (panhypopituitarism)- give GH (somatostatin) MEDICAL INTERVENTIONS PITUITARY TUMOR/REPLACEMENT THERAPY Radiation therapy External radiation- bring down GH levels 80% of time Steriotactic radiosurgery Click to view You Tube video Risk post-procedure-increased risk for seizures Neurosurgery: Transsphenoidal hypophysectomy Most commonly used approach Incision thru floor of nose into sella turcica. Newer Method-EndoscopicTranssphenoidal Hypophysectomy Nursing Management-Pituitary Tumors/Hyperfunction Pre op hypophysectomy Anxiety r/t body changes fear of unknown *brain involvement – tumor extent, deficits *chronic - life long care implications- develop hypopituitary conditions following procedure *Need life-long replacement therapy! Sensory-perceptual alteration r/t a. visual field cuts b. diplopia secondary to pressure on optic nerve. Alteration in comfort (headache) r/t a. tumor growth/edema Knowledge deficit r/t Post-op teaching pain control ambulation hormone replacement Activity Avoid straining, coughing, sneezing *Prevent cerebrospinal fluid leakage Post operative care Post-op complications of hormone insufficiency: Trauma lead to transient (or permanent) inadequate ADH DI What is this disorder called? Decreased ACTH- require cortisone replacement due to decreased glucocorticoid production (adrenal response) Can you live without glucocorticoids???? NO Other deficiencies post hypohysectomy: in sex hormones-lead to infertility due to decrease production of ova & sperm What are these hormones called? Gonadotropic hormonesFSH & LH *Potential for Incisional disruption after transsphenoidal hypophysectomy *Avoid bending and straining X 2 months post transsphenoidal hypophysectomy, Use stool softeners Avoid coughing Saline mouth rinses No toothbrushes for 7-10 days Post-op CSF Leak where sella turcica was entered Ck any clear rhinorrhea - test for glucose + glucose = CSF Leak Notify physician HOB 30 degrees Bedrest CSF leak usually resolves within 72 hrs. If not - spinal taps to decrease pressure Post op problems cont. Periocular edema/ecchymosis Headaches Visual field cuts/diplopia Consider important nursing intervention for these problems Safety ANTERIOR PITUITARYHypofunction S & S Anterior Pituitary Hypofunctioning •Etiology: (rare disorder) may be due to disease, tumor, or destruction of gland. •Diagnostic tests •CT Scan •Serum hormone levels Define: GH FSH/LH Prolactin ACTH TSH *Selective hypopituitarism *Panhypopituitarium Medical Management-Anterior Pituitary Neurosurgery -- removal of tumor Radiation - tumor size Hormone replacement cortisol, thyroid, sex hormones Nursing Management-Anterior Pituitary Assessment of S & S of hypo or hyper functioning hormone levels Teaching-Compliance with hormone replacement therapy Counseling and referrals Support medical interventions Posterior Pituitary-(Neurohypophysis) Name the hormones released by posterior pituitary when signaled by hypothalamus! ADH (vasopressin) and oxytocin ADH (Vasopressin) secreted by cells in hypothalmus-stored in posterior pituitary acts on distal & collecting tubules of kidneys making more permeable to H20 volume excreted ADH is released when? With decreases blood volume, increased concentration of Na+ or other substances (drugs as opiooids, thiazide diuretics) also, pain, stress ADH has vasoconstrictive or vasodilation properties? vasocontrictive Oxytocin Controls lactation & stimulates uterine contractions ‘Cuddle hormone’ Research links oxytocin and socio-sexual behaviors Posterior Pituitary Disorders SIADH (TOO MUCH ADH!!) Numerous causes: *Small cell lung cancer , other types cancer CNS disorders *Medications as, thiazide diuretics, opioids, general anesthetics, tricyclic antidepressants, others Miscellaneous SIADH (Syndrome of Inappropriate Antidiuretic Hormone Secretion) If too much ADH, what clinical signs and symptoms are “typical”? Weight gain urine output serum Na levels (less than120mEq/L) weakness muscle cramps H/A SIADH-if hyponatremia worsens-high risk neuro manifestations lethargy decrease tendon reflexes *seizures-life threatening! (if serum Na less than 120mEq/L) Diagnostic Tests-SIADH Serum Na+ <134meq/l Serum osmolality <280 OSM/kg H2O urine specific gravity >1.005 (elevated) or normal BUN Collaborative Care Medical/Nursing Management ***FLUID RESTRICTION (LIMIT TO 1000ML/24HRS (500600ml/24hrs if severe) May require IV 3% NaCl to replace Na (very slow infusion) IF CHF -- Lasix (temporary fix) Treat underlying problem --Chemo, radiation Declomycin 600 po-1200mg/day (block effect ADH on renal tubules) Daily weights-1 lb. weight = 500ml fluid retention Accurate I & O; monitor F & E imbalances High risk for injury r/t complications of fluid overload (seizures) Posterior Hypopituitary-ADH disorders Diabetes Insipidus-(DI) (too little ADH) Etiology: (50% idiopathic) •*Central- neurogenic- i.e. brain tumors •Nephrogenic - inability of tubules to respond to ADH •Psychogenic- What Clinical Manifestations-DI? Polydipsia Polyuria (10L in 24 hours) Severe fluid volume deficit wt loss tachycardia constipation shock Diagnostic Tests-DI urine specific gravity serum Na serum osmolality *Water deprivation test: Determine if central DI Risk of dehydration *Vasopressin (ADH) given; show rise in urine osmolality if central DI Collaborative Care Medical Management-DI Identify etiology, H & P Treat underlying problem *Desmopressin acetate (DDAVP) Vasopressin (Pitressin) Diabenese, carbamazepine (Tegretol) Central DI; orally, nasally, IV Partial central DI Dietary, low Na etc if neprhogenic cause Nursing Management-DI Assess for F & E imbalances High risk for sleep disturbances Increase po/IV fluids RF Injury (hypovolemic shock) Knowledge deficit High risk for ineffective coping FOCUS-DISORDERS OF ADRENAL GLANDS Adrenal Cortex Adrenal Medulla How Stuff Works ADRENAL CORTEX Think Salt Sugar Sex SUGAR SALT Mineralocorticoids (F & E balance) Aldosterone (renin from kidneys controls adrenal cortex production of aldosterone) Na retention Water retention K excretion Question: If Na level is low, does aldosterone promote renal reabsorption of sodium and excretion (loss) of potassium? YES or NO?? YES SUGAR (Cortisol) GLUCOCORTICOIDS (regulate metabolism; critical in stress response) CORTISOL responsible for control & metabolism of CHO (carbohydrates) amt. glucose formed amt. glucose released FATS-control of fat metabolism Stimulates fatty acid mobilization from adipose tissue PROTEINS-control of protein metabolism stimulates protein synthesis in liver protein breakdown in tissues INFLAMMATORY and allergic response immune system-more prone to infection SEX ANDROGENS hormones which male characteristics release of testosterone Seen more in women than men What is the RELEASE OF GLUCOCORTICOIDS CONTROLLED BY ______ ACTH (adrenocorticotropic hormone) Produced in anterior pituitary gland ACTH Circulating levels of cortisol levels cause stimulation of ACTH levels cause dec. release of ACTH What type of feedback mechanism is this?? Negative AFFECTED BY: Individual biorhythms ACTH LEVELS -HIGHEST 2 HOURS BEFORE AND JUST AFTER AWAKENING. usually 5AM - 7AM Gradually decrease rest of day Stress- cortisol production and secretion ADRENAL MEDULLA Fight or flight What is released by the adrenal medulla? CATECHOLAMINE RELEASE •Epinephrine •Norepinephrine HYPER AND HYPOFUNCTION ADRENAL CORTEX HORMONES: Too much: Too little CUSHING’S Syndrome (TOO MUCH CORTISOL!) secretion of cortisol from adrenal cortex 4X more frequent in females Usually occurs at 35-50 years of age *Cushing’s disease if due to inc ACTH secreting tumor from pituitary ETIOLOGY: Cushing’s Syndrome Due to Excess of corticosteroids, particularly glucocorticoids: most common cause: Iatrogenic administration of exogenous corticosteroids Prolonged adm. of coricosteroids 85% of endogenous cases due to ACTH-secreting pituitary tumor (Cushing’s disease) Other causes include Adrenal tumors (Cortisol secreting neoplasm within adrenal cortex) Ectopic ACTH production in tumors outside hypothalamic–pituitary– adrenal axis :usually lung and pancreas tumors SIGNS & SYMPTOMS: Cushing’s protein catabolism muscle wasting loss of collagen support thin, fragile skin, bruises easily poor wound healing s in CHO metabolism hyperglycemia Can get diabetes insufficient insulin production Polyuria s in fat metabolism truncal obesity buffalo hump “moon face” weight but strength (review video) Cushigns-SIGNS & SYMPTOMS immune response More prone to infection resistance to stress Death usually from infection Before Cushings After Cushings What assessment findings indicate Cushings’ syndrome? SIGNS & SYMPTOMS: Cushing’s Syndrome! Androgen secretion excessive hair growth acne change in voice receding hairline Mineralocorticoid activity water retention ________ and _______ NA Marked hypokalemia hypervolemia b.p. from ________ SIGNS & SYMPTOMSz; Cushings MENTAL CHANGES Mood swings Euphoria Depression Anxiety Mild to severe depression Psychosis Poor concentraion and memory Sleep disorders s in hematology WBCs Lymphocytes Eosinophils Summary Signs and symptoms: Related to excess corticosteroids •Weight gain most common feature •Trunk (centripetal obesity) •Face (“moon face”) •Cervical area •Transient weight gain;from sodium and water retention •Protein wasting •Catabolic effects of cortisol •Leads to weakness especially in extremities •Protein loss in bones leads to osteoporosis, bone and back pain •Hyperglycemia Glucose intolerance associated with cortisol-induced insulin resistance •Increased gluconeogenesis by liver Loss of collagen •Wound healing delayed •Purplish red striae on abdomen, breast, or buttocks •Mood disturbances •Insomnia Irrationality •Psychosis Mineralocorticoid excess may cause hypertension secondary to fluid retention Adrenal androgen excess may cause •Pronounced acne •Virilization in women •Feminization in men •Seen more commonly in adrenal carcinomas •Women: Menstrual disorders and hirsutism •Men: Gynecomastia and impotence DIAGNOSIS of Cushing’s *24-Hour urine for free cortisol Levels of 50 to 100 mcg/day in adults indicates Cushing syndrome High-dose dexamethasone suppression test used for borderline results of 24-hour urine cortisol False positives with depression, stress, or alcoholism Plasma cortisol (main glucocorticoid) levels may be elevated with loss of diurnal variation Plasma ACTH levels High level-Cushings disease –pituitary cause Low level-adrenal or exogenous origin CT and MRI of pituitary and adrenal glands Hypokalemia and alkalosis-seen in ectopic ACTH syndrome and adrenal carcinoma Plasma ACTH may be low, normal, or elevated depending on problem ACTH and cortisol DIAGNOSIS of Cushing’s High or normal ACTH levels indicate ACTH-dependent Cushing’s disease Low or undetectable ACTH levels indicate an adrenal or exogenous etiology Collaborative Care: medical/nursing Primary goal_normalize hormone secretion •Treatment depends on cause •Pituitary adenoma •Surgical removal of tumor and/or radiation *Transsphenoidal removal of pituitary tumor •Adrenal tumors or hyperplasia •Adrenalectomy; can be unilateral or bilateral; if bilateral, need hormone replacement for life; if ectopic-try to remove source of ACTH secretion Adrenalectomy-Cushings Preoperative care Achieve optimal physical condition Control hypertension/ hyperglycemia Correct hypokalemia with diet/potassium supplements *Teaching depends on surgical approach (laproscopic/open): NG tube, urinary cath, IV, CVP, SCD’s etc *if etiology is pituitaryhypophysectomy may be indicated. Postoperative care Risk of hemorrhage- increased due to high vascularity of adrenal glands Wide hormonal fluctuation due to manipulation of glandular tissue cause unstable BP, fluid balance, and electrolyte levels Need high doses of corticosteroids IV during and several days after surgery Important-report any significant changes in VS Bed rest until BP is stabilized post-op Meticulous care (avoid infection) as normal inflammatory responses are suppressed Cushing Syndrome-(post-adrenalectomy) Ambulatory and home care Discharge instructions based on lack of endogenous corticosteroids Wear MedicAlert bracelet at all times Avoid exposure to stress, extremes of temperature, and infections Lifetime replacement therapy is required for many patients Non-Surgical Management Cushing’s Radiation to tumors Medications-goal-inhibit adrenal function MITOTANE (Lysodern) Suppresses cortisol production Alters peripheral metabolism of cortisol ↓ Plasma and urine corticosteroid levels Metyrapone, ketoconazole (Nizoril) and aminolglutethimide (Cytadren) inhibit cortisol synthesis Common side effects of drug therapy Anorexia Nausea and vomiting GI bleeding Depression Vertigo Skin rashes Diplopia (double vision) Cushing Syndrome If Cushing syndrome develops during use of corticosteroids Gradually discontinue therapy Decrease dose Convert to an alternate-day regimen Gradual tapering avoids potentially life-threatening adrenal insufficiency Nursing Diagnosis Risk for infection Imbalanced nutrition related to decreased appetite Disturbed self-esteem related to altered body image Impaired skin integrity Hypofunction Adrenal Cortex- ADDISON’S DISEASE Remember-Adrenocortical insufficiency may be Addison’s disease (hypofunction of adrenal cortex)*primary cause From lack of pituitary ACTH *secondary cause What hormones will BE LACKING/decreased in Addison’s disease Glucocorticoids (corticosteroids as cortisol, hydrocortisone) Mineralocorticoids (aldosterone) Androgens (testosterone, androsterone) and estrogen ____________ Trivia Question: Which President had Addison’s Disease? Addison’s Disease Addison’s Disease: Etiology/Pathophysiology Common cause-autoimmune response to adrenal tissue (esp. white females) Susceptibility genes; other endocrine conditions often found Other causes of Addison’s disease Tuberculosis (rare in North America) Infarction Fungal infections AIDS Metastatic cancer *Iatrogenic Addison’s disease-due to adrenal hemorrhage Most often occurs in adults <60 years old Affects both genders equally Disease not evident until 90% of adrenal cortex destroyedadvanced before diagnosis Addison’s Disease: Clinical Manifestations Primary features Progressive weakness Fatigue Weight loss Anorexia Skin hyperpigmentation primarily in Areas exposed to sun Pressure points Over joints In skin creases, especially palmar creases Addison’s Disease: Clinical Manifestations Orthostatic hypotension *Hyponatremia (why??- think aldosterone) *Hyperkalemia (why??- think aldosterone) *Hypoglycemia (why??- think cortisol) Nausea and vomiting Diarrhea *Secondary adrenocortical hypofunction (pituitary cause) Signs and symptoms common with Addison’s disease Patients characteristically lack hyperpigmentation Addison’s Disease-Addisonian Crisis Complications *Risk for life-threatening Addisonian Crisis caused by Insufficient adrenocortical hormones Sudden, sharp decrease in these hormones Triggered by stress from infection, surgery, trauma, hemorrhage, psychologic Sudden withdrawal of corticosteroid replacement therapy Severe manifestations of glucocorticosteroid and mineralocorticoid deficiencies Hypotension Tachycardia Dehydration Hyponatremia Addison’s Disease-Addisonian Crisis Complications Manifestations (cont’d) Hyperkalemia Hypoglycemia Fever Weakness Confusion Hypotension can lead to shock Circulatory collapse is often unresponsive to usual treatment GI manifestations- severe vomiting, diarrhea, and abdomen pain Pain in lower back or legs *Renal shutdown, death! CAUSES Pt. with Addison’s who doesn’t respond to tx or has stress without dose Pt. with Addison’s but undiagnosed who is exposed to stress Pt. on steroids that are dc’d without tapering Pt. with Addison’s not controlled Addison’s Disease: Diagnostic Studies Subnormal levels of serum cortisol Levels fail to rise over basal levels with ACTH stimulation test Latter indicates primary adrenal disease Positive response to ACTH stimulation indicates functioning adrenal gland Abnormal laboratory findings Hyperkalemia Hypochloremia Hyponatremia Hypoglycemia Addison’s Disease-Diagnostic Studies Abnormal laboratory findings Anemia ↑ BUN Low urine cortisol levels urinary 17-OHCS and 17 KS Other abnormal findings ECG Low voltage, vertical QRS axis, peaked T waves from hyperkalemia CT and MRI used to Localize tumors Identify adrenal calcifications or enlargement Collaborative Care: Addison’s Disease Life long hormone replacement primary-need oral cortisone 20-25mgs in AM and 1012mg in PM also need mineralocorticoid-(FLORINEF) Hydrocortisone Most commonly used as replacement therapy Glucocorticoid dosage must be **↑ during times of stress to prevent addisonian crisis INTERVENTIONS Salt food liberally Do not fast or omit meals Eat between meals and snack Eat diet high in carbs and proteins Wear medic-alert bracelet Kit of 100mg hydrocortisone IM Keep parenteral glucocorticoids at home for injection during illness Avoid infections/stress Collaborative Care: Addison’s Disease (Crisis)-Keys Treatment directed at Shock management High-dose hydrocortisone replacement Rapid infusion of IV fluids Check VS /urine output frequently Monitor EKG Give Solu-cortef IV hours until S & S disappear Try to decrease anxiety May require vasopressors Dopamine or Epinepherine Avoid additional stress Collaborative Care: Addison’s Disease (Crisis) Large volumes 0.9% saline/5% dextrose to reverse hypotension and electrolyte imbalances until BP returns to normal Acute intervention Acute intervention Protect against infection Assist with daily hygiene Protect from extremes: light, noise,temperature Acute intervention Frequent assessment Assess vital signs/signs of fluid and electrolyte imbalances every 30 minutes to 4 hours for first 24 hours Take daily weights Administer corticosteroid therapy diligently Discharge usually occurs before maintenance dose reached Instruct on importance of follow-up appointments Ambulatory and home care Vomiting and diarrhea may indicate Adisonian crisis Notify health care provider since electrolyte replacement may be necessary HYPERALDOSTERONISM (Conn’ Syndrome) Usually due to adrenal tumor Too much aldosterone secretion *Hallmark- hyperaldosteronism Sodium retention •Hypertension with (hypernatremia) hypokalemic alkalosis Potassium excretion (hypokalemia) •Usually no edema Muscle weakness •Headache Fatigue Cardiac dysrhythmias Glucose intolerance Metabolic alkalosis May lead to tetany Hydrogen ion excretion Review renin/aldosterone effect! Hyperaldosteronism Etiology and Pathophysiology Primary hyperaldosteronism Usually caused by adrenocortical adenoma Secondary hyperaldosteronism Due to renal artery stenosis, renin-secreting tumors, and chronic kidney disease DIAGNOSIS/INTERVENTIONSHyperaldosteronism Primary aldosteronism ↑ Plasma aldosterone levels ↑ Sodium levels ↓ Potassium levels ↓ Renin activity Adenomas are localized by CT or MRI Preferred treatment of primary hyperaldosteronism is surgical removal of the adenoma (ADRENALECTOMY) INTERVENTIONS-Hyperaldosteronism (before surgery) BP -aldactone=Aldosterone antagonist: what effect on Na, H2O, and K? (potassium sparing) Correct hypokalemia/hypernatremia K+ supplements; low Na diet Assess vital signs/BP PHEOCHROMOCYTOMA Rare, benign tumor of the adrenal medulla catecholamines Produces excessive _________ Mostly in young to middle-aged adults Results in severe hypertension If untreated, may lead to Diabetes mellitus Cardiomyopathy Death Clinical Manifestations Hallmark-hypertension-200/150 or greater “Spells”-paroxymal attacks bladder distension,emotional distress, exposure to cold. Norepinephrine and Epinepherine released sporadically Clinical features include Severe, episodic hypertension Severe, pounding headache Tachycardia with palpitations Profuse sweating Abdominal or chest pain Diagnosis is often missed DIAGNOSIS Best test- Urinary fractionated metanephrines (catecholamines metabolites) Plasma catecholamines (elevated during an attack) 24 hour urine-VMA (metabolite of Epinepherine) CT/MRI to locate tumor Pheochromocytoma Treatment Surgical removal of tumor Medications Calcium channel blockers control BP nicardipine (Cardene) Sympathetic blocking agents may ↓ BP ; ↓ Symptoms of catecholamine excess Prazosin (Minipress) Beta blockers to ↓ dysrhythmias, BP Inderal Diet high in vitamin, mineral, calorie, no caffeine Sedatives INTERVENTIONS-cont Monitor b.p. Eliminate attacks/keep comfortable If attack- complete bedrest and HOB 45 degrees Monitor glucose DURING/POST SURGERY May require REGITINE AND NIPRIDE TO PREVENT HYPERTENSIVE CRISIS b.p. may be initially, BUT CAN DROP RAPIDLY Need plasma expanders/Vasopressors Hourly I and O Observe for hemorrhage*vascular adrenal gland The End