endocrine dysfunction: adrenal & pituitary endocrine systemendocrine system (comprehensive...
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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