CUSHING’S SYNDROME and ADDISON’S DISEASE

NURSING COMPETENCY AUDIT 2

(BSN-4B) | PROF. | SEM II I SEMIFINALS l JEH

HYPOTHALAMUS
HORMONES: FUNCTION
↓
RELEASES CORTICOTROPIN-RELEASING Cortisol Sugar Glucocorticoi
HORMONE (CRH) Zona - Regulation d
↓ Fasciculata of blood
ANTERIOR PITUITARY GLAND glucose thru
↓ gluconeoge
nesis
ADRENOCORTICOTROPIC HORMONE (ACTH)
- Anti-inflam
↓ matory
ADRENAL CORTEX (steroid)
↓ - Protects the
MINERALOCORTICOID, GLUCOCORTICOID body from
stress
- Stress
ADRENAL GLANDS hormone:
needed in
times of
emotional
and
physical
stress

Aldosterone Salt Mineralocorti

Zona - Maintains coid
Glomerulosa extracellular
fluid volume
and
electrolyte
➔ A small gland that makes steroid hormones, balance
- Renal
adrenaline, and noradrenaline. These hormones
reabsorptio
help control heart rate, blood pressure, and n of Sodium
other important body functions. There are two and
adrenal glands, one on top of each kidney. Also excretion of
called suprarenal gland. Potassium
➔ Located on top of each kidneys in the distal
➔ Regulates sodium and electrolyte balance, renal
tubules
affects carbohydrate, fat, and protein
metabolism Androgens Sex Androgens
➔ Influences the development of sexual Zona - Converted
characteristics Reticularis to sex
➔ Sustains the fight-or-flight response steroids:
➔ Activated by Adrenocorticotropic Hormone testosteron
e and
(ACTH)
estrogen
PARTS:
1. ADRENAL CORTEX
- outer shell of the adrenal gland; synthesizes 2. ADRENAL MEDULLA
glucocorticoids, mineralocorticoids, and secretes Hormone:
small amounts of sex hormones ❖ Epinephrine (Adrenaline)
❖ Norepinephrine (Noradrenaline)
❖ Dopamine
➔ Collective known as Catecholamines
CUSHING’S SYNDROME and ADDISON’S DISEASE
NURSING COMPETENCY AUDIT 2
(BSN-4B) | PROF. | SEM II I SEMIFINALS l JEH

➔ Essential in the “fight or flight” response to ★ The excess ACTH overstimulates zona
stress fasciculata of both adrenal glands,
which grows larger, and secrete excess
cortisol.
- ACTH secreting tumors (most often in the lung,
pancreas, or GI tract, pancreas
- Tumor of the adrenal gland or cortex
★ which makes excess cortisol
★ Adrenal adenoma: benign
★ Adrenal Carcinoma: malignant
in both adenoma and carcinomas, the cells of zona
fasciculata within the adrenal cortex start dividing and
secrete excess cortisol
↓
Suppressing CRH and ACTH production
↓
No effect on involved zona fasciculata but since the
neoplastic cells are autonomous, meaning they have
grown independent from any stimulatory signals
↓
The zona fasciculata of the UNINVOLVED, the normal
adrenal glands shrinks and produces less than the
standard amount of cortisol
DIFFERENCE:
Syndrome is due to external sources (especially long
term medications)
CUSHING SYNDROME Disease is due to internal sources (abnormalities of
organs, ectopic ACTH secreting hormones)
○Cortisol levels are constantly HIGHER
than normal CLINICAL MANIFESTATIONS DUE TO EXCESS
○ From administration of glucocorticoids GLUCOCORTICOIDS= STRESSED
(steroids) in large doses for several (↑stress = ↑CORTISOL)
weeks or longer S- Skin fragile, bruises easily
○ Exogenous or iatrogenic (Outside - due to decreased collagen production
source) Glucocorticoid therapy (such as T- Truncal obesity
prednisone for asthma, rheumatoid - altered fat distribution
arthritis, lupus and other inflammatory R- Round face (moon face), Risk for fractures due to
diseases, or for immunosuppression brittle bones
after transplantation) - Due to inc gluconeogenesis, and increased
CUSHING DISEASE: insulin resistance leading to activation of
○ Characterized by abnormally increased Lipoprotein Lipase helping adipose accumulate
secretion (endogenous) of cortisol, fats
caused by increased amounts of ACTH - Too much glucocorticoid, calcium decreases
secreted by the pituitary gland leading to brittle bones, or osteoporosis
○ Endogenous (Inside source) E- Elevated BP, Ecchymosis
- RAAS stimulation
- Tumors/cancer on pituitary gland (70% of - Amplified effects of catecholamines on blood
Cushing's Syndrome) vessels
★ The Pituitary adenoma simply grows in - Cortisol start cross reacting with
size and secretes too much ACTH mineralocorticoid
CUSHING’S SYNDROME and ADDISON’S DISEASE
NURSING COMPETENCY AUDIT 2
(BSN-4B) | PROF. | SEM II I SEMIFINALS l JEH

S - Striae on the extremities (purplish pink stretch marks

during puberty
on abdomen, breast, buttocks and thighs) and abdomen,
Slow wound healing Secondary sex ↑sex drive in adulthood
S- Sugar extremely high (hyperglycemia), Sodium characteristics (facial hair,
elevation Adam’s apple)
E - Excessive body hair esp. in women (hirsutism), MANIFESTATIONS CAUSED BY EXCESS
amenorrhea, gynecomastia in men ANDROGENS
- Inhibits Gonadotropin- Releasing Hormone ● Women experience virilism (masculinization).
(GRH) ● Hirsutism excessive growth of hair on the face
- Decreased Estrogen and Testosterone levels and midline of the trunk.
D - Dorsocervical fat pad (Buffalo hump). Depression ● Breasts atrophy.
● Clitoris enlargement
● Voice becomes masculine.
● If exposed in utero - possible hermaphroditism
● Males - loss of libido.
● Male: gynecomastia

Additionals:
● Muscle weakness, proximal muscle wasting,
fatigue
- excessive catabolism, inc proteolysis Increased
Protein Synthesis
● Mental status changes and mood swings,
- reduces brain functions DIAGNOSIS:
● Diminished libido 1. 24 hour urine sample
● Osteoporosis (inhibition of bone formation, - Assess the total amount of cortisol
suppression of calcium absorption) excreted in the urine over a 24-hour
MANIFESTATIONS CAUSED BY EXCESS period.
MINERALOCORTICOIDS - This is the most specific diagnostic test.
● Hypertension - The patient's urine is collected over a
● Hypernatremia, hypokalemia. 24-hour period and tested for the
● Weight gain amount of cortisol.
● Edema. - Levels higher than 50-100 micrograms a
day for an adult suggest Cushing's
syndrome.
TESTOSTERONE 2. Blood or Saliva test late at night
- Help check the daily rise and fall of
Men Women
cortisol levels
Development of MALE Growth spurt in 3. Dexamethasone suppression
reproductive tissue development - A person is given a low dose of
Underarm and pubic hair dexamethasone, which is an exogenous
CUSHING’S SYNDROME and ADDISON’S DISEASE
NURSING COMPETENCY AUDIT 2
(BSN-4B) | PROF. | SEM II I SEMIFINALS l JEH

steroid that suppresses ACTH ● Administer hydrocortisone parenteral therapy as

production in the pituitary gland. ordered; rate indicated by: fluid and electrolyte
- Normally: Should cause decrease in balance, blood sugar and blood pressure
Cortisol level but if Cushing Syndrome is ● Monitor for Addison's crisis
caused by endogenous cortisol
production, then the serum cortisol Prevent postoperative complications:
levels should remain unchanged. ● Monitor vital signs until stability is regained
- If tested POSITIVE, determine the ● Monitor BP every 15 minutes, notify physician of
cause of endogenous cortisol significant elevations in BP
production, and ACTH plasma levels ● NPO
can be checked ● Respiratory care:
- Turn, cough and deep breath
- Splint incision when coughing
● Position: semi-fowler's
● Monitor dressing for bleeding
● Ambulation as order
● Once NGT is removed - DAT
● Use meticulous skin care to avoid traumatizing
fragile skin.
● Avoid adhesive tape, which can tear and irritate
the skin.
● Assess skin and bony prominences frequently.
● Encourage and assist patients to change
positions frequently.
TREATMENT: depends on underlying cause
● Emphasize the need to keep an adequate
- Exogenous: gradual decrease of offending drugs
supply of the corticosteroid to prevent running
and eventually stopped if possible.
out or skipping a dose, because this could result
- It is important to avoid sudden steroid
in an addisonian crisis.
withdrawal, because it can cause adrenal crisis
● Stress the need for dietary modifications to
= LIFE THREATENING
ensure adequate calcium intake without
● Mitotane, an agent toxic to the adrenal cortex
increasing risk for hypertension, hyperglycemia,
(known as medical adrenalectomy.
and weight gain.
● Ketoconazole + Metyrapone (Metopirone) to
● Help the patient prevent hyperglycemia and
control steroid hypersecretion in patients who do
obesity by teaching about a low-calorie,
not respond to mitotane therapy.
low-concentrated carbohydrate and -fat diet and
- Especially for ectopic ACTH production
to increase activity as tolerated.
or adrenal carcinoma that have already
● Encourage diet high in calcium (dairy products,
spread.
broccoli) and weight-bearing activity to prevent
● Aminoglutethimide (Cytadren) effectively
osteoporosis caused by glucocorticoid
blocking cortisol production
replacement.
ADRENALECTOMY:
RADIATION THERAPY
➢ The surgical removal of the adrenal glands
➢ Given over a 6-week period, with improvement
because of tumors or uncontrolled overactivity
occurring in 40 to 50 percent of adults and up to
➢ Require a lifelong replacement therapy with the
80 percent of children indicated, stress to patient
following:
and family that stopping corticosteroid use
a. glucocorticoid - cortisone (Cortef).
abruptly and without medical supervision can
b. mineralocorticoid - fludrocortisone (Florinef).
result in adrenal insufficiency and reappearance
Post operative Care:
of symptoms.
● Promote hormonal balance
CUSHING’S SYNDROME and ADDISON’S DISEASE
NURSING COMPETENCY AUDIT 2
(BSN-4B) | PROF. | SEM II I SEMIFINALS l JEH

Decreased aldosterone causes decrease in sodium

ADDISON’S DISEASE (HYPONATREMIA), increase in potassium
(HYPERKALEMIA), and decrease in blood volume
○ Adrenal cortical insufficiency causing
(HYPOVOLEMIA) and pressure. Finally, fewer protons
deficiency in mineralocorticoid,
are lost, meaning more build up in the blood
glucocorticoid, and androgen hormones
(METABOLIC ACIDOSIS)
○ The disease is also called adrenal
insufficiency, or hypocortisolism.
○ ↓ Aldosterone and ↓ Cortisol

ETIOLOGY: ADDI
A- Adrenocortical destruction from infection,
autoimmune process
- Adrenal hypoplasia secondary to lack of pituitary
ACTH
D - DISEASE
- Cancer
- Infections
- HIV Decreased cortisol leads to inadequate glucose in times
- Tuberculosis (most common): the infection of stress leading to weak, tired, and disoriented.
spreads from the lungs to the adrenal glands,
causing inflammation and destruction adrenal
cortex
- accounts for about 20 percent of cases of
primary adrenal insufficiency in developed
countries.
D - Damage
- Adrenal hemorrhage (trauma)
I - Iatrogenic:
- bilateral adrenalectomy, sudden withdrawal of
long-term glucocorticoid therapy
- Cortisol deficiency produces abnormal fat Decreased cortisol causes overactivation of pituitary
protein, and carbohydrate metabolism glands causing producing pro-opiomelanocortin, a
precursor to adrenotropic hormone, and also a precursor
to melanocyte- stimulating hormone, the hormone that
leads to skin pigmentation production (melanin). Making
more melanocyte-stimulating hormone, resulting in
hyperpigmentation or darkening of the skin, especially in
CUSHING’S SYNDROME and ADDISON’S DISEASE
NURSING COMPETENCY AUDIT 2
(BSN-4B) | PROF. | SEM II I SEMIFINALS l JEH

sun-exposed areas and joints, like knees, elbows, and

knuckles.
- dark tanning (bronze skin), covering exposed
and unexposed parts of the body (visible on
scars; skin folds; pressure points such as the
elbows, knees, knuckles, and toes; lips; and
mucous membranes)

Symptoms AND Signs: STEROID LOW

S- Sodium and sugar (low), Salt craving
T- Tired and weak
E - Electrolyte imbalances (increased K and calcium)
R- Reproductive changes
Men: does not affect men much because testes are the
lOw - BP that falls further when standing, causing
major source of male androgens
dizziness or fainting - increased, collapsing, irregular
vascular response
I - increased pigmentation of skin
D- Diarrhea, nausea, depression
SLOW
➔ Low weight - water loss
➔ Low temperature
➔ Low energy, chronic, worsening fatigue
➔ Low muscle strength
➔ Low appetite
DIAGNOSIS:
1. Adrenocorticotropic Hormone Stimulation Test
Symptoms are slowly progressive, chronic, and they are
- A small amount of synthetic ACTH is
usually missed or ignored until a major stressor, like
given
serious injury or infection suddenly causes the
- Measures the amount of cortisol and
symptoms to become really severe.
aldosterone produced which helps in
Symptoms of an addisonian crisis include:
knowing the functionality of the adrenal
➔ Profound fatigue
glands.
➔ Dehydration
TREATMENT:
➔ Low blood pressure, vasomotor collapse
Immediate treatment if addisonian (adrenal) crisis or
➔ Renal shutdown
circulatory collapse is imminent:
➔ Loss of consciousness
● I.V. sodium chloride solution to replace sodium
ions.
● Hydrocortisone (Cortef).
● Injection of circulatory stimulants, such as
atropine sulfate (Atropine), calcium chloride
(Calcium), epinephrine (Adrenalin).
MEDICAL MANAGEMENT:
● Restoration of normal fluid and electrolyte
balance: high-sodium, low-potassium diet and
fluids.
CUSHING’S SYNDROME and ADDISON’S DISEASE
NURSING COMPETENCY AUDIT 2
(BSN-4B) | PROF. | SEM II I SEMIFINALS l JEH

● Treatment of glucocorticoid deficiency with such

agents as hydrocortisone (Cortef) or prednisone
(Orasone).
■ Patients with chronic obstructive
pulmonary disease and heart
failure may require preparations
with low mineralocorticoid
activity, such as
methylprednisolone
(Solu-Medrol), to prevent fluid
retention.
● Mineralocorticoid deficiency treated with
fludrocortisone (Florine).
● Cardiovascular support if indicated.
NURSING MANAGEMENT:
● Decrease stress: environment should be quiet
and non demanding
● Diet: Acute phase - high sodium, low potassium,
high-protein, low-carbohydrate
● Force fluids to balance fluid losses
● Monitor I and O and daily weights
● Administer life-long exogenous replacement as
prescribed
HEALTH TEACHINGS
■ Take medication with food
■ Side-effects of steroid therapy
■ Need to adjust medication
dosage when stress is
increased
■ Signs and symptoms of Addison
crisis
● Prevent serious complications of addisonian
crisis:
■ CBR, avoid stimuli
■ Treat shock - IV saline
● RISK FOR DEFICIENT FLUID VOLUME:
○ Assess skin turgor and mucus for signs
and symptoms of dehydration.
■ The patient will have dry skin
and mucous membranes.
Tenting of the skin will occur.
The tongue may have
longitudinal furrows.