Endocrine Dysfunction:

Adrenal & Pituitary

Endocrine System

Endocrine System (comprehensive source)

Endocrine Review (narrated online review)
Medications-Endocrine (narrated PPTs)

Endocrine Drugs Overview

Pituitary Drugs
Adrenal Drugs

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 Addams 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 patients 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?
Cushings 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

Cushings 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 MethodEndoscopicTranssphenoidal
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
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
*Avoid bending and straining X 2 months
hypophysectomy

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

Weight gain
signs and symptoms are

urine output
typical?
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 ManifestationsDI?

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

Questio
n:
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
CUSHINGS Syndrome
(TOO MUCH CORTISOL!)

secretion of cortisol from adrenal cortex

4X more frequent in females
Usually occurs at 35-50
years of age
*Cushings disease if due to inc ACTH
secreting tumor from pituitary

ETIOLOGY: Cushings 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 (Cushings 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: Cushings

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: Cushings Syndrome!

Androgen secretion
excessive hair growth
acne
change in voice
receding hairline
Mineralocorticoid activity
water retention

NA
________
and _______
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 Cushings

*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 Cushings

High or normal ACTH levels indicate ACTH-dependent Cushings

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,
SCDs 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-(postadrenalectomy)

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
Cushings

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- ADDISONS

DISEASE

Remember-Adrenocortical insufficiency may be

Addisons disease (hypofunction of adrenal
cortex)*primary cause
From lack of pituitary ACTH *secondary cause

What hormones will BE LACKING/decreased in Addisons

disease
Glucocorticoids (corticosteroids as cortisol,
hydrocortisone)
Mineralocorticoids (aldosterone)
Androgens (testosterone, androsterone) and estrogen
____________

Trivia Question: Which President had

Addisons Disease?

Addisons Disease

Addisons Disease:
Etiology/Pathophysiology
Common
cause-autoimmune response to adrenal tissue (esp. white
females)
Susceptibility genes; other endocrine conditions often found
Other causes of Addisons disease
Tuberculosis (rare in North America)
Infarction
Fungal infections
AIDS
Metastatic cancer
*Iatrogenic Addisons 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

Addisons 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

Addisons Disease: Clinical

Orthostatic hypotension
Manifestations

*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 Addisons disease

Patients characteristically lack hyperpigmentation

Addisons 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

Addisons DiseaseAddisonian
Crisis
Manifestations (contd)
Hyperkalemia
Complications
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 Addisons who doesnt respond to

tx or has stress without
dose
Pt. with Addisons but undiagnosed who
is exposed to stress
Pt. on steroids that are dcd without
tapering
Pt. with Addisons not controlled

Addisons 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

Addisons 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: Addisons

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: Addisons

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: Addisons

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
Usually no edema
(hypokalemia)
Headache
Muscle weakness
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/INTERVENTION
S
Hyperaldosteronism
Primary aldosteronism
Preferred treatment of

Plasma aldosterone
levels
Sodium levels
Potassium levels
Renin activity

Adenomas are
localized by CT
or MRI

primary
hyperaldosteronism is
surgical removal of the
adenoma
(ADRENALECTOMY)

INTERVENTIONSHyperaldosteronism (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