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Endocrine Dysfunction:
Adrenal & Pituitary
Endocrine System (comprehensive source)
Endocrine Review (narrated online review)
Medications-Endocrine (narrated PPTs)
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
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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
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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
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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)
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
Large volumes 0.9% saline/5% dextrose to reverse hypotension and
electrolyte imbalances until BP returns to normal
Acute intervention
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Acute intervention
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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
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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

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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

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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
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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