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 neurons-control 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?

Tumors usually cause hyper release of hormones

*Determined by symptoms presented; evaluate serum/urine hormone levels; stimulation/suppression tests for hormone levels; CT, MRI, etc

ANTERIOR PITUITARY HYPERFUNCTION

What happens if: TOO MUCH secretion of prolactin (prolactinoma)?

TOO MUCH release of Lutenizing Hormone (LH)?

Too much growth hormone secretion?

Which goolish character on the Addam’s Family had too much GH secretion

Anovulation; menstrual irregularities; galactorrhea

“Polycystic ovary syndrome;, due to effect on corpus lutea

GIGANTISM IN CHILDREN; ACROMEGALY IN ADULTS

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 Pituitary-

An 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 Video-

Remember 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

New Method Click to view!•No incisions !•Less recovery time•Fewer complications

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

What is this disorder called?

Decreased ACTH- require cortisone replacement due to decreased glucocorticoid production (adrenal response)

Can you live without glucocorticoids????

DI

NO

Other deficiencies post hypohysectomy: in sex hormones-lead to infertility due

to decrease production of ova & sperm What are these hormones called?

Gonadotropic hormones-FSH & 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

S & S Anterior Pituitary Hypofunctioning

GH FSH/LH Prolactin ACTH TSH

Define:

*Selective hypopituitarism

*Panhypopituitarium

ANTERIOR PITUITARY-Hypofunction

•Etiology: (rare disorder) may be due to disease, tumor, or destruction of gland.•Diagnostic tests

•CT Scan •Serum hormone levels

Medical Management-Anterior Pituitary

Neurosurgery -- removal of tumor Radiation - tumor size Hormone replacement

cortisol, thyroid, sex hormones

Assessment of S & S of hypo or hyper functioning hormone levels Teaching-Compliance with hormone replacement

therapy Counseling and referrals Support medical interventions

Nursing Management-Anterior Pituitary

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?

ADH has vasoconstrictive or vasodilation properties?

With decreases blood volume, increased concentration of Na+ or other substances (drugs as opiooids, thiazide diuretics) also, pain, stress

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 (500-600ml/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 CareMedical Management-DI Identify etiology, H & P Treat underlying problem *Desmopressin acetate (DDAVP)-

Central DI; orally, nasally, IV Vasopressin (Pitressin) Diabenese, carbamazepine (Tegretol)

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

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

HYPER AND HYPOFUNCTION ADRENAL CORTEX HORMONES: Too much: Too little

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 (review video)

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

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 ________ and _______ retention Marked hypokalemia b.p. from ________

NA water

hypervolemia

SIGNS & SYMPTOMSz; CushingsMENTAL CHANGES

Mood swings Euphoria Depression Anxiety Mild to severe

depression Psychosis Poor concentraion and

memory Sleep disorders

s in hematologyWBCsLymphocytesEosinophils

Summary Signs and symptoms: Summary Signs and symptoms: Related to excess corticosteroidsRelated to excess corticosteroids•Weight gain most common featureWeight gain most common feature

•Trunk (centripetal obesity)Trunk (centripetal obesity)•Face (“moon face”)Face (“moon face”)•Cervical areaCervical area•Transient weight gain;from sodium Transient weight gain;from sodium and water retentionand water retention

•Protein wastingProtein wasting•Catabolic effects of cortisolCatabolic effects of cortisol•Leads to weakness especially in Leads to weakness especially in extremitiesextremities•Protein loss in bones leads to Protein loss in bones leads to osteoporosis, bone and back painosteoporosis, bone and back pain

•Hyperglycemia Hyperglycemia Glucose intolerance associated with Glucose intolerance associated with cortisol-induced insulin resistancecortisol-induced insulin resistance•Increased gluconeogenesis by liverIncreased gluconeogenesis by liver

Loss of collagenLoss of collagen•Wound healing delayedWound healing delayed•Purplish red striae on abdomen, Purplish red striae on abdomen, breast, or buttocksbreast, or buttocks•Mood disturbancesMood disturbances•InsomniaInsomniaIrrationalityIrrationality•PsychosisPsychosis Mineralocorticoid excess Mineralocorticoid excess may cause hypertension secondary to may cause hypertension secondary to fluid retentionfluid retentionAdrenal androgen excess may causeAdrenal androgen excess may cause

•Pronounced acnePronounced acne•Virilization in womenVirilization in women•Feminization in menFeminization in men

•Seen more commonly in adrenal Seen more commonly in adrenal carcinomascarcinomas

•Women: Menstrual disorders Women: Menstrual disorders and hirsutism and hirsutism •Men: Gynecomastia and Men: Gynecomastia and impotenceimpotence

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: Collaborative Care: medical/nursingmedical/nursingPPrimary goal_rimary goal_normalize hormone secretionnormalize hormone secretion•Treatment depends on causeTreatment depends on cause•Pituitary adenomaPituitary adenoma

•Surgical removal of tumor and/or radiationSurgical removal of tumor and/or radiation*Transsphenoidal removal of pituitary tumor

•Adrenal tumors or hyperplasiaAdrenal tumors or hyperplasia•Adrenalectomy; 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 pituitary-hypophysectomy 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 destroyed-

advanced 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 CrisisComplications

*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 CrisisComplications 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 10-

12mg 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

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

Acute intervention Protect against infection Assist with daily hygiene Protect from extremes: light, noise,temperature

Acute intervention 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

Usually due to adrenal tumor

Too much aldosterone secretion Sodium retention

(hypernatremia) Potassium excretion

(hypokalemia) Muscle weakness Fatigue Cardiac dysrhythmias Glucose intolerance Metabolic alkalosis May lead to tetany

Hydrogen ion excretion

HYPERALDOSTERONISM (Conn’ Syndrome)

*Hallmark- hyperaldosteronism•Hypertension with hypokalemic alkalosis

•Usually no edema•Headache

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/INTERVENTIONS-Hyperaldosteronism 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 Produces excessive _________ Mostly in young to middle-aged adults Results in severe hypertension If untreated, may lead to

Diabetes mellitus Cardiomyopathy Death

catecholamines

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