THE ADRENAL

GLANDS
DISORDERS

Adrenal Glands

THE
ADRENAL
GLANDS
Each gland composed of two parts:
1. Adrenal Cortex: outer part
2. Adrenal Medulla: inner part
1.Cortex: 90% of adrenal gland. Its a life-sustaining
physiologic activities
Three layers:
1. glomerulosa
2. fasciculata
3. reticularis
Cortex secretes three types of STEROIDS
hormones:
1.Mineralocorticoids
2.Glucocorticoids
3.Gonadocorticoids (Sex Hormones)
Androgens or Estrogens

THE ADRENAL GLANDS

2. Medulla: 10% of the glands and secretes two
hormones Catecholamines:

1. Norepinephrine (noradrenaline)
2. Epinephrine (adrenaline)
Cathecolamines are sympathomimetic
Function:
Adaptation to stress, by the fight-or-flight
response,
For Example: Fear - heart rate = Epinephrine
Heavy Load - Adrenaline

ADRENAL CORTEX
1. Mineralocorticoids: produced by zona
HORMONES
glomerulosa in the Adrenal Cortex maintain

extracellular fluid volume through RAA System:

When there is decrease perfusion the

juxtaglomerular (JG) cells of the kidneys
stimulate Renin
Renin converts angiotensinogen from the liver
into Angiotensin I which is converted to
Angiotensin II by angiotensin-converting
enzyme (ACE) found in lung capillaries.
Angiotensin II is a potent vasoconstrictor
causing blood pressure to increase.
Angiotensin II stimulates release of aldosterone
from the adrenal cortex.

ADRENAL CORTEX
HORMONES
The RAA system can be activated when
there are:
1. Loss of blood volume
2. Drop in blood pressure
example: hemorrhage or dehydration
3. Decrease in plasma SODIUM
concentration

RAA SYSTEM: ANGIOTENSIN II

Aldosterone acts on kidney tubules:
Function of the Aldosterone:
1.increases reabsorption of sodium and
excretion of potassium and hydrogen by kidney
tubules
2.increases water retention increase blood
volume and, therefore, increases blood pressure
3.secretion of hydrogen ions kidney tubules and
excreted in the urine to prevent acidosis
ADH is reabsorption of water causing water
retention.
ALDOSTERNE is reabsorption of sodium and
water causing water retention (fluid overload).

RAA SYSTEM: ANGIOTENSIN II

Angiotensin II stimulates release of anti-diuretic

hormone (ADH) also called vasopressin to stimulate
reabsorption of water .

ADH and Aldosterone are long-term regulator of blood

pressure, the (RAA system) has a constant baseline level
of activity to keep blood pressure steady over the long term.

RAA System watches blood pressure. If blood pressure

declines ADH and Aldosterone conserve water and cause
vasoconstriction.

Sudden blood pressure fluctuation can speed up its activity.

ADRENAL GLANDS: CORTEX

2. Glucocorticoids: produced by the zona reticularis
and zona fasciculata of the adrenal cortex
Cortisol (hydrocortisone): Essential for survival
Levels increased in AM
Levels increased during
stress
Function of Cortisol:
Anti-inflammatory & Stimulate Hyperglycemia
ANTI-INFLAMMATORY RESPOSE
Immunological: anti-inflammatory by inhibiting
WBC leukocyte inflammatory events decrease
immune responses and can delay healing of
damaged tissues

ADRENAL GLANDS: CORTEX

Function of Cortisol:
Anti-inflammatory & Stimulate
Hyperglycemia
METABOLIC/STIMULATE HYPERGLYCEMIA
Metabolic: stimulates gluconeogenesis,
increases lipolysis and protein catabolism.
The Metabolic function of cortisol is
hyperglycemia.
Stimulates hyperglycemia by producing
glucose for energy production. By
providing energy sources to body tissues,
cortisol ensures that glucose will be
available for the brain (Metabolic)
If you give Steriods blood GLUCOSE Immune
System WBC

ADRENAL GLANDS: CORTEX

3. Sex hormones:

Adrenal androgens: class of steroids produced

in the zona fasciculata and zona reticularis
Testosterone: primary function is
masculinization, and contribute to libido
In women, androgens are converted to
estrogen and progesterone:
In men, these contribute little to reproductive
maturation
In women, estrogens are mostly supplied by
the ovaries and adrenal glands
In postmenopausal women, the adrenal
cortex is the only primary source of
endogenous estrogen

ADRENAL
GLANDS:
History Present illness: Decreased energy,
depression, nervousness and sexual dysfunction
ASSESSMENT
Past medical history: Radiation to the head or
abdomen, intracranial surgery, recent and current
medications , Tuberculosis is the most common cause
of primary adrenal insufficiency
Review of systems
Patients perception of his/her general state of health
Changes in skin color, especially bronzed or smoky
pigmentation, and increased facial hair in women.
Note changes in weight and appetite
Headache, lightheadedness with position
changes, muscle weakness, nausea, vomiting,
abdominal pain, anorexia, menstrual dysfunction,
erectile dysfunction

ADRENAL GLANDS:
Functional assessment: Usual diet and activity
ASSESSMENT
patterns; disruptions in lifestyle

Physical

Examination:
Height, weight, and vital signs
Skin: bronzed/smoky pigmentation, bruising,
petechiae, vitiligo (skin losing pigment), pallor,
excess facial hair of female
Examine oral mucous membranes for color
changes
Inspect anterior thorax for fat pads under the
clavicles, and posterior thorax for the buffalo
hump
Obesity of the trunk
Examine breasts for striae and darkening of the
areola
Inspect abdomen for striae; extremities for muscle
wasting and edema, atrophy, hair loss,
appropriateness for age of genitalia

AGE-RELATED CHANGES

Under normal circumstances, adrenal

function remains adequate in older
person
Some decline in cortisol secretion,
but this is balanced by decrease in
cortisol metabolism such that blood
levels remain normal
Secretion of aldosterone and plasma
renin activity decline, thus abilities to
conserve sodium and adapt to position
changes less efficient

ADRENAL
MEDULLA
Pheochromocytoma: tumors of chromaffin tissues
in the adrenal medulla
DISORDERS
secretes excessive cathecholamines (epinephrine
and norepinephrine) in excessive amounts
Cause is unknown, some hereditary
90% of pheochromcytoma is benign, 10% malignant
Precipitating causes of a catecholamine surge:
anesthesia, opiates and opiate antagonists
(naloxone), dopamine antagonists
(phenothiazines), drugs that inhibit
catecholamines (tricyclic antidepressants)
childbirth
foods high in tyramine (aged cheese, red wine)
radiographic contrast media
increased abdominal pressure (abdominal
palpation) can cause hypertensive episode

PHEOCHROMOCYTOMA
fight or flight signs and symptoms:

Exaggerated

Prominent characteristic is intermittent,

unstable HYPERTENSION. Triggered by emotional
distress, exercise, manipulation of tumor, postural
changes, major trauma, surgery
tachycardia, palpitations, diaphoresis, nausea,
vomiting, apprehension, hyperglycemia, pounding
headache, heat intolerance, pallor, weight loss,
anxiety, vision changes, constipation
Can be fatal if it causes malignant
hypertension (diastolic >115), risk for stroke,
risk for organ damage
Diagnostics: 24-hour urine for vanillymandelic acid
(VMA), cathecolamine levels (caffeine, vanilla, licorice,
ASA and anti-hypertensives restricted for 2-3 days
before VMA test), metanephrine levels, CT scan, MRI

PHEOCHROMOCYTOMA

Management:
surgical removal of the tumor or gland

(adrenalectomy), control of Hypertension

Lifelong glucocorticoid supplementation
and mineralocoticoid replacement after
bilateral adrenalectomy
If catecholamine surge is recognized promptly,
it is potentially curable, if missed patient can
suffer cardiac and neurologic damage
Monitors cardiovascular status: VS: check BP,
PR
Preop and post op care. After surgery, at
risk for hypotension and hypoglycemia
Avoid caffeine
Emotional support to avoid panic attacks
Complications: Hypertensive crisis!! Closely
monitor BP. Administer calcium-channel
blockers, alpha blockers, beta-blockers

ADRENAL
CORTEX
DISORDERS
Disease
(AD): insufficiency
of the

Addisons

hormones of adrenal cortex leading to reduced levels of

cortisol, aldosterone, androgens, estrogens.
Two

Types:

1. Primary AD: dysfunction of the entire (90%)

adrenal cortex causing deficiencies of cortisol and
aldosterone. ACTH levels from the pituitary can be
elevated to stimulate adrenal cortex to synthesize
more hormones.
Common causes of primary AD:
Auto-immune dysfunction associated with TB, fungal
infection, AIDS, metastatic Ca, thyroiditis, gramnegative sepsis
Adrenalectomy, idiopathic atrophy (common
cause), adrenal hemorrhage due to anticoagulants
abrupt discontinue long-term use of exogenous
corticosteroids that suppresses adrenals intrinsic
activity

ADDISONS DISEASE

2. Secondary AD: dysfunction of hypothalamus

or pituitary leading to decreased androgen and

cortisol production. Unlike primary AD, aldosterone
may not be affected. ACTH fails to stimulate the
adrenal cortex to synthesize more hormones.
Common causes of secondary AD:
ACTH deficit due to pituitary tumors,
radiation, Sheehans syndrome (postpartum
necrosis), hypophysectomy
Prolonged use of corticosteroid drugs can
depress ACTH and corticotropin-releasing
hormone production which in turn reduces
cortisol production. It may take a year before
ACTH is produced normally again

ADDISONS and
DISEASE
signs and symptoms

Pathophysiology

1.Impaired secretion of cortisol: decreased

gluconeogenesis, decreased liver and muscle
glycogen causing hypoglycemia: fatigue, muscle
weakness, weight loss, confusion, psychosis
2.Decreased levels of aldosterone alter the
clearance of potassium, water, sodium by the kidney
leading to:
loss of sodium (hyponatremia) and water
(hypovolemia): the most significant sign of AD
is HYPOTENSION, tachycardia, craving for salty
foods, fluid and electrolyte imbalance
potassium retention (hyperkalemia) due to
decreased excretion of potassium: cardiac
dysrrythmia, tachycardia, confusion, metabolic
acidosis

ADDISONS DISEASE:
PATHOPHYSIOLOGY
2. Decreased levels of aldosterone:

Decreased Glomerular filtration rate leads

to decreased urea nitrogen excretion (BUN):
irritability, metabolic acidosis
Decreased gastric acid production of the
stomach: anorexia, nausea and vomiting,
diarrhea, weight loss
3. Increased secretion of melanocytestimulating hormone (MSH). ACTH can be
broken down to produce melanocyte-stimulating
hormone leading to hyperpigmentation of the skin
in sun-exposed areas, pressure points, joints and
creases of the body
4. Decreased androgen levels lead to decreased
or loss of body, facial, axillary and pubic hair, lack
of secondary sex characteristics

ADDISONS
DISEASE:
ACTH stimulation test: low serum and urinary cortisol
level
after ACTH injection,TESTS
measures cortisol response in
DIAGNOSTIC
30 and 60 minutes
Serum electrolytes: decreased FBS
(hypoglycemia), hyponatremia, hyperkalemia,
hypercalcemia, BUN and creatinine
Urinary 17-hydroxycorticosteroids: measures
glucocorticoids and androgen metabolites which are low
Plasma ACTH levels: in primary AD (adrenals do not
respond) and in secondary AD (pituitary do not
produce)
Radiographic studies: skull films, arteriograms, MRI
and CT scans of brain for pituitary tumors and size of
adrenal glands
ECG: cardiac dysrythmias in hyperkalemia (peaked T
waves, wide QRS and increase PR interval)

ADDISONS DISEASE:
Replacement therapy with glucocorticoids and
MANAGEMENT
mineralocorticoids
with medications. IV or po
glucocorticoids: dexamethasone (Decadron),
cortisone (Cortone), prednisolone (Prednisone,
Prelone), hydrocortisone (Cortef) to replace cortisol.
Dosage schedule based on human variations: 2/3 dose in
am and 1/3 dose in pm to mimic bodys normal
secretion daily
Mineralocorticoids: Fludrocortisone (Florinef) given
once daily to prevent loss of K and Na and fluid volume.
Know side effects, monitor VS, I&O, weight, monitor
electrolytes (hypokalemia and hypocalcemia), prevent
infection. This is lifelong therapy
Dont discontinue suddenly!!
Fluid replacement: Normal saline, Dextrose in
0.5%NS

ADDISONS DISEASE:
Collection of data: VS for orthostatic hypotension,
NURSING
CARE
poor
skin turgor, weight
loss, muscle weakness, salt

craving, nausea and vomiting, hyponatremia,

hyperkalemia, hypoglycemia. Report to PMD
immediately. Abdominal cramps, diarrhea, decreased
libido, amenorrhea, pale skin with bronzed areas,
emaciation, sparse body hair,
Compliance for lifelong treatment care: keep
medication with them at all times, teach how to inject IM if
cannot take by po.
Increase cortisol dose as prescribed during stress
times
Increase Florinef dose as prescribed at summertime
and intense exercise due to sweating. Increase salt
intake in hot weather. Wear medical alert bracelet
Daily weights, I & O, VS, fluid replacements, identify S/S of
stress: illness, infection

ADDISONS DISEASE

Sudden marked decrease of adrenal hormones can

lead to acute adrenal crisis (Addisonian crisis)
Complication:
Addisonian crisis!! A life-threatening
emergency from sudden marked decrease
in available adrenal hormones
Precipitating factors are adrenal surgery,
pituitary destruction, abrupt withdrawal of
steroid therapy, and major stressors such
as trauma, infections, illness. and
emotional or psychiatric disturbances
The body may be unable to respond
normally with secretions of cortisol
(natural stress hormone)
It is a Medical emergency!!

Addisonian crisis:
IfManifestations
untreated, fluid and electrolyte imbalances
can lead to circulatory collapse, cardiac
arrhythmias, cardiac arrest, coma, and
death
include symptoms of mineralocorticoid
and glucocorticoid deficiencies but are
more severe: HYPOTENSION, tachycardia,
dehydration, confusion, hyponatremia,
hyperkalemia, hypercalcemia, and
hypoglycemia
fever, weakness, sudden pain in the legs,
lower back or abdomen pain, vomiting,
diarrhea (dehydration), severe
hypotension, loss of consciousness,
convulsions shock, coma.

Addisonian crisis:
Management
Establish baseline, collect data to guide

treatment: blood sample to determine

plasma cortisol levels
Establish intravenous access for administration
of normal saline with 5% dextrose, access for
IV drugs
Provide loading steroid dose and
maintenance of IV infusion: Intravenous
hydrocortisone (Solu-cortef) followed by IV
saline infusion and dextrose for 8 hours
Ensure continuous source of glucocorticoids:
additional doses of hydrocortisone

ADDISONS DISEASE: NURSING

Ineffective Tissue Perfusion related to fluid
DIAGNOSIS
and electrolyte imbalance, hypotension,
hypovolemia, cardiac dysrythmia. Outcome:
warm dry skin, strong peripheral pulses,
normal VS, pulse oximetry and cap refill, LOC
Risk for deficient Fluid volume related to
deficient adrenal hormones. Outcome: stable
VS (BP and HR), body weight, normal skin
turgor, equal I and O
Deficient knowledge related to diagnosis,
long-term medications replacement, lab tests,
prevention of stressors, plan of care
Risk for Injury related to complications: crisis,
shock, postural hypotension, falls

ADRENAL HYPERSECRETION: CUSHINGS

excess amounts of corticosteroids (cortisol) is a
SYNDROME

condition called Cushing's Syndrome, secretion not

related to stress. Excess cortisol may results from :
1.Endogenous (internal) causes: corticotropinsecreting pituitary tumors; a cortisol-secreting
neoplasm within adrenal glands; excess secretion of
corticotropin by carcinoma of the lung or other tissues
2.Exogenous (external) cause: prolonged
administration of high doses of corticosteroids
(most common cause) in allergies, asthma,
chemotherapy, organ transplant, auto immune
diseases
Cushings Disease is a secondary Cushings syndrome
caused by pituitary, hypothalamus or adrenal cortex
problems- excessive production of ACTH

CUSHINGS SYNDROME

Clinical manifestations affect most body systems

due to excess levels of circulating corticosteroids
marked changes in personal appearance:
weight gain, truncal obesity, pendulous
abdomen, muscle wasting of extremities,
bufallo hump, moon-face
Hypertension, hypokalemia, delayed wound
healing
insomnia, irrational behavior, and mood
disturbances such as irritability and anxiety
facial redness, purple striae on the abdomen,
breasts, buttocks, or thighs, delayed wound
healing
hirsutism, menstrual disorders, osteoporosis
especially in premenopausal women

TRUNCAL OBESITY, MOON-FACE,

BUFALLO HUMP

CUSHINGS SYNDROME

CUSHINGS
SYNDROME
Diagnostic Tests:
Abnormal laboratory findings:
polycythemia, hypokalemia, hypocalcemia,
hypernatremia, hyperglycemia,
leukocytosis, glycosuria
Elevated plasma and urine cortisol levels,
ACTH levels, chemistry, 24-hour urine collection
for cortisol, CT scan, MRI to localize tumor
Low-dose dexamethasone suppression test
Complications: DM, osteoporosis, depression, F
& E imbalance, GI bleeding, HTN, risk for
immunosuppression (susceptible to infection).
Addisons crisis after adrenalectomy and abrupt
withdrawal of medication

CUSHINGS
SYNDROME:
Remove the cause: If caused by exogenous
glucocorticoids, gradually withdraw the drug or
MANAGEMENT

lower the dose

Drug therapy: medications that suppress adrenal activity
Mitotane (Lysodren), ketoconazole (Nizoral),
aminoglutethimide (Cytadren), and metyrapone
(Metopirone). Aldosterone antagonist: potassiumsparing diuretic (spironolactone)
Risk of acute adrenal crisis can occur when on
drugs that suppresses adrenal function
Low sodium diet, high K, high protein diet,
frequent glucose checks, administer insulin as
needed, give potassium supplement, monitor I&O, daily
weights
Safe environment to prevent pathological fractures and
skin trauma/breakdown

CUSHINGS SYNDROME

Radiation: Administered externally or

internally. Observe for alopecia, irritated skin
Surgical management : surgical removal of
pituitary or adrenals: Adrenalectomy:
unilateral or bilateral
Preoperative Care of the Adrenalectomy
Patient
Correct any electrolyte imbalances
Strict hand washing and observance of aseptic
technique to prevent infections in these
susceptible patients
Preoperative education involves a discussion of
glucocorticoid replacement therapy, including
dosage, side effects, and complications

CUSHINGS SYNDROME

Postoperative Care of the Adrenalectomy

Patient
Vital signs for signs and symptoms of impending
shock (evident as hypotension), weak or
thready pulse, decreased urinary output, and
changes in level of consciousness
Pulse and blood pressure may be unstable for 24 to
48 hours after surgery; vasopressors to maintain
blood pressure in immediate postoperative period
Protect patient by using strict aseptic technique for
wound care and invasive procedures
Assess comfort at frequent intervals, and treat pain
with opioid analgesics
Instruct the patient to turn, cough, deep breathe,
or use an incentive spirometer

CUSHINGS SYNDROME: NURSING

Risk for Infection related to high serum cortisol
DIAGNOSIS
levels and immune suppression. Outcome:

normal body temperature, WBC

Excess fluid volume related sodium and water
retention. Outcome: stable body weight and
normal electrolyte levels
Risk for Impaired Skin Integrity related to
edema
Risk for Injury related to osteoporosis
Disturbed Body Image related to changes in
physical appearance. Outcome: acceptance of
self
Ineffective Therapeutic Regimen Management
or Deficient knowledge related to lack of
understanding of disease process, medications,
diet, self-care. Outcome: patient understands
disease process and follows regimen