cushing’s syndromeooo
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CUSHING·S SYNDROME
Reported by: Group 4
Mariel FortunaDiane Ellisson AguinaldoSharmaine FajardoGlairievy BeltranMarie Joy VillaquidanJennifer Marie ManaloMary Christ LacadenKristine Bautista
Christopher Reglos
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CUSHING·S SYNDROME
--(also called hyperadrenocorticism orhypercorticism) is a hormone (endocrine) disorder
caused by high levels of cortisol (hypercortisolism) in
the blood. This can be caused by taking glucocorticoid
drugs, or by tumors that produce cortisol or
adrenocorticotropic hormone (ACTH).--Cushing's disease refers to one specific cause, a tumor
(adenoma
) in the pituitary gland that produces large
amounts of ACTH, which in turn elevates cortisol. It
can usually be cured by surgery. It was described byHarvey Cushing in 1932.
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CUSHING·S SYNDROME
--is a hormonal disorder caused by prolonged exposureof the body·s tissues to high levels of the hormone
cortisol. Sometimes called hypercortisolism, Cushing·s
syndrome is relatively rare and most commonly affects
adults aged 20 to 50. People who are obese and have
type 2 diabetes, along with poorly controlled blood
glucose³also called blood sugar³and high blood
pressure, have an increased risk of developing the
disorder
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CAUSES
Other people develop Cushing·s syndrome becausetheir bodies produce too much cortisol. Normally, the
production of cortisol follows a precise chain of events.
First, the hypothalamus, a part of the brain about the
size of a small sugar cube, sends corticotropin-
releasing hormone (CRH) to the pituitary gland. CRH
causes the pituitary to secrete adrenocorticotropin
hormone (ACTH), which stimulates the adrenal
glands. When the adrenals, which are located just
above the kidneys, receive the ACTH, they respond byreleasing cortisol into the bloodstream.
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CAUSES
�
Cortisol performs vital tasks in the body including>helping maintain blood pressure and cardiovascular function
>reducing the immune system·s inflammatory response
>balancing the effects of insulin, which breaks down glucosefor energy
>regulating the metabolism of proteins, carbohydrates, andfats
The hypothalamus sends CRH to the pituitary, whichresponds by secreting ACTH. ACTH then causes theadrenals to release cortisol into the bloodstream.
� One of cortisol·s most important jobs is to help the bodyrespond to stress. For this reason, women in their last 3months of pregnancy and highly trained athletes normallyhave high levels of the hormone. People suffering fromdepression, alcoholism, malnutrition, or panic disordersalso have increased cortisol levels.
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CAUSES
� Pituitary Adenomas
Pituitary adenomas cause 70 percent of Cushing·s
syndrome cases,excluding those caused by
glucocorticoid use. These benign, or noncancerous,
tumors of the pituitary gland secrete extra ACTH.Most people with the disorder have a single adenoma.
This form of the syndrome, known as Cushing·s
disease, affects women five times more often than
men.
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CAUSES
� Ectopic ACTH SyndromeSome benign or, more often, cancerous tumors that
arise outside the pituitary can produce ACTH. This
condition is known as ectopic ACTH syndrome. Lung
tumors cause more than half of these cases, and men
are affected three times more often than women. The
most common forms of ACTH-producing tumors are
small cell lung cancer, which accounts for about 13
percent of all lung cancer cases, and carcinoid
tumors³small, slow-growing tumors that arise fromhormone-producing cells in various parts of the body.
Other less common types of tumors that can produce
ACTH are thymomas, pancreatic islet cell tumors, and
medullary carcinomas of the thyroid.
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CAUSES
Adrenal TumorsIn rare cases, an abnormality of the adrenal glands, most
often an adrenal tumor, causes Cushing·s syndrome.
Adrenal tumors are four to five times more common in
women than men, and the average age of onset is about 40.
Most of these cases involve noncancerous tumors of adrenaltissue called adrenal adenomas, which release excess
cortisol into the blood.
Adrenocortical carcinomas³adrenal cancers³are the least
common cause of Cushing·s syndrome. With adrenocortical
carcinomas, cancer cells secrete excess levels of severaladrenocortical hormones, including cortisol and adrenal
androgens, a type of male hormone. Adrenocortical
carcinomas usually cause very high hormone levels and
rapid development of symptoms.
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CAUSES
F amilial Cushing·s Syndrome
Most cases of Cushing·s syndrome are not inherited.
Rarely, however, Cushing·s syndrome results from an
inherited tendency to develop tumors of one or more
endocrine glands. Endocrine glands release hormones
into the bloodstream. With primary pigmentedmicronodular adrenal disease, children or young adults
develop small cortisol-producing tumors of the adrenal
glands. With multiple endocrine neoplasia type 1
(MEN1), hormone-secreting tumors of the parathyroid
glands, pancreas, and pituitary develop; Cushing·s
syndrome in MEN1 may be due to pituitary, ectopic, or
adrenal tumors.
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SIGNS AND SYMPTOMS
1. Rapid weight gain2. Hyperhidrosis (excess sweating)
3. Telangiectasia ( dilation of capillaries)
4. Thinning of the skin
5. Hirsutism
6. Baldness and/or cause hair to become extremely dry
and brittle
7. Bufallo hump
8. Moon face
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SIGNS AND SYMPTOMS
9. Reduced libido10. Impotence, amenorrhea/ oligimenorrhea, infertility
OTHER COMMON SIGNS AND SYMPTOMS
INCLUDE
severe fatigue
weak muscles
high blood pressure
high blood glucose
increased thirst and urination
irritability, anxiety, or depression
a fatty hump between the shoulders
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K EY FEATURES OF HYPERCOTISOLISM
(CUSHING·S SYNDROME/DISEASE)
GENERAL APPERANCE
1. Fat redistribution
Moon face Buffalo hump
Truncal obesity
2. Weight Gain
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K EY FEATURES OF HYPERCOTISOLISM
(CUSHING·S SYNDROME/DISEASE)
CARDIOVASCULAR MANIFESTATIONS
1. Hypertension
2. Increased risk for thromboembolic events
3. Frequent dependent edema
4. Capillary fragility
Bruising
Petechiae
MUSCULOSK ELETAL MANIFESTATIONS
1. Muscle Atrophy ( most apparent in extremities)
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K EY FEATURES OF HYPERCOTISOLISM
(CUSHING·S SYNDROME/DISEASE)
2. Osteoporosis ( bone density loss)
Pathologic fractures
Decreased height with vertebral collapse
Aseptic necrosis of the femur head Slow or poor healing of bone fractures
SK IN MANIFESTATIONS
1.
Thinning of skin ( ´paper-likeµ appearance, esp.on the back of the hands)
2. Striae
3. Increase pigmentation ( with ectopic orpituitary production of ACTH)
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K EY FEATURES OF HYPERCOTISOLISM
(CUSHING·S SYNDROME/DISEASE)
IMMUNE SYSTEM MANIFESTATIONS
1. Increased risk for infection
2. Decreased immune functions
Decreased circulating lymphocytes
Decreased production of immunoglobulins(antibodies)
3. Decreased inflammatory responses
Decreased eosinophil count
Slight increased in neutrophil count but activity is
reduced4. Decreased production of proinflammatory cytokines,
histamine, & prostaglandines
5. Manifestations of infections/inflammations may bemasked
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IF LEFT UNTREATED:
1. Heart Disease2. Pathologic Fractures
3. Skin Breakdown
4. GI Bleeding
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RISK FACTORS
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NURSING INTERVENTION
Goals of treatment for Cushing·s syndrome are the
reduction of plasma cortisol levels, removal of tumors,
prevention of complications, and restoration of normalacceptable body apperance
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NURSING INTERVENTIONS
NON SURGICAL MANAGEMENT
Weigh the ct. daily and monitor intake and output.
Drug Therapy. Drugs that interfere with ACTH
production or adrenal hormone synthesis, however,may be used for temporary relief. ( cyproheptadine
[periactin])
Radiation Therapy. Radiation may be use to treat
hypercorticolism caused by pituitary adenomas.However, radiation is not always effective and
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NURSING INTERVENTIONS
and often destroys normal tissue.
SURGICAL MANAGEMENT
Preoperative Care. Electrolyte imbalances are
corrected before surgery. Continue to monitor blood
potassium, sodium, and chloride levels, dysrhythmias
from potassium imbalance may occur, and cardiac
monitoring is needed. Hyperglycemia is controlled
before surgery and blood glucose levels are monitored.
Prevent infection with hand washing and aseptic technique. Decrease risk for
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NURSING INTERVENTIONS
falls by raising bed siderails and encouraging the client to ask for assistance when getting out
of bed. A high-calorie, high-protein diet is prescribed
before surgery.
The client continues to receive glucocorticoids during
surgery to prevent adrenal crisis because the removal
of the tumor results in a sudden drop of cortisol levels.
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NURSING INTERVENTIONS
Post Operative Care. After an adrenalectomy, aclient is usually sent to critical care unit. Immediately
after surgery, assess the client every 15 min for
shock (e.g., hypotension, a rapid, weak pulse,
and decreasing urine output) due to possible
insufficient glucocorticoid replacement. Monitor
ongoing V/S and other hemodynamic variables
(central venous pressure, pulmonary wedge
pressure), I & O, daily weight and serum
electrolytes levels.
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DX PROCEDURES/ TEST
Midnight plasma cortisol and late-night salivary cortisol measurements. The midnight plasma
cortisol test measures cortisol concentrations in theblood. Cortisol production is normally suppressed atnight, but in Cushing·s syndrome, this suppression
doesn·t occur. If the cortisol level is more than 50nanomoles per liter (nmol/L), Cushing·s syndrome issuspected. The test generally requires a 48-hourhospital stay to avoid falsely elevated cortisol levelsdue to stress.
However, a late-night or bedtime saliva sample can beobtained at home, then tested to determine the
cortisol level. Diagnostic ranges vary, depending on
the measurement technique used.
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DX PROCEDURES/ TEST
� Low-dose dexamethasone suppression test (LDDST). In
the LDDST, a person is given a low dose of dexamethasone, a
synthetic glucocorticoid, by mouth every 6 hours for 2 days.Urine is collected before dexamethasone is administered and
several times on each day of the test. A modified LDDST uses
a onetime overnight dose.
Cortisol and other glucocorticoids signal the pituitary to release
less ACTH, so the normal response after takingdexamethasone is a drop in blood and urine cortisol levels. If
cortisol levels do not drop, Cushing·s syndrome is suspected.
The LDDST may not show a drop in cortisol levels in people with
depression, alcoholism, high estrogen levels, acute illness, or
stress, falsely indicating Cushing·s syndrome. On the otherhand, drugs such as phenytoin and phenobarbital may cause
cortisol levels to drop, falsely indicating that Cushing·s is not
present in people who actually have the syndrome. For this
reason, physicians usually advise their patients to stop taking
these drugs at least 1 week before the test.
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DX PROCEDURES/ TEST
Dexamethasone-corticotropin-releasing hormone (CRH) test. Some people have high cortisol
levels but do not develop the progressive effects of
Cushing·s syndrome, such as muscle weakness,
fractures, and thinning of the skin. These people may
have pseudo-Cushing·s syndrome, a conditionsometimes found in people who have depression or
anxiety disorders, drink excess alcohol, have poorly
controlled diabetes, or are severely obese. Pseudo-
Cushing·s does not have the same long-term effects onhealth as Cushing·s syndrome and does not require
treatment directed at the endocrine glands.
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TEST TO FIND THE CAUSE
CRH stimulation test. The CRH test, withoutpretreatment with dexamethasone, helps separate
people with pituitary adenomas from those with
ectopic ACTH syndrome or adrenal tumors. As a result
of the CRH injection, people with pituitary adenomas
usually experience a rise in blood levels of ACTH andcortisol because CRH acts directly on the pituitary.
This response is rarely seen in people with ectopic
ACTH syndrome and practically never in those with
adrenal tumors.
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TEST TO FIND THE CAUSE
high-dose dexamethasone suppression test (HDDST). The HDDST is the same as the LDDST,
except it uses higher doses of dexamethasone. This test
helps separate people with excess production of ACTH
due to pituitary adenomas from those with ectopic
ACTH-producing tumors. High doses of dexamethasone usually suppress cortisol levels in
people with pituitary adenomas but not in those with
ectopic ACTH-producing tumors.
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TEST TO FIND THE CAUSE
Petrosal sinus sampling. This test is not alwaysrequired, but in many cases, it is the best way to
distinguish pituitary from ectopic causes of Cushing·s
syndrome. Samples of blood are drawn from the
petrosal sinuses³veins that drain the pituitary³byinserting tiny tubes through a vein in the upper thigh
or groin region. A local anesthetic and mild sedation
are given, and x rays are taken to confirm the correct
position of the tubes. Often CRH, the hormone that
causes the pituitary to release ACTH, is given duringthis test to improve diagnostic accuracy.
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PREVENTING COMPLICATIONS
Skin Breakdowns
1. Assess client·s skin.
2. Instruct client to avoid activities that can result
in skin trauma.3. Reduce tissue injury.
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PREVENTING COMPLICATIONS
4. Excessive dryness can be prevented by moisturizinglotion.
Pathologic Fractures. Hypercortisolism causes bone
density loss and osteoporosis.
1.
Teach client about safety issues and dietary needs.2. The client is at risk for fractures as a result of minor
falls or bumps.
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PREVENTING COMPLICATIONS
Gastrointestinal Bleeding. Interventions aim toreduce gastric irritation, usually through drug
therapy. Drug therapy involves agents that protect the
GI mucosa and those that decrease the secretion of
HCL.
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COMMON NURSING DIAGNOSES &
COLLABORATIVE PROBLEMS
Disturbed Body Image r/t illness
Fatigue r/t sleep deprivation
Excess fluid volume r/t excess water and sodiumreabsorption
Risk for infection r/t immunosuppresion and inadequateprimary defenses
Risk for Injury r/t poor wound healing and bone densityloss
Deficient K nowledge (Illness and treatment) r/t lack of
interest in learning and unfamiliarity with informationresources
Imbalanced nutrition: More than body requirements r/texcess intake in relation to metabolic need as a result of appetite stimulation by cortisol
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MNEMONIC
C - Central obesity, Cervical fat pads, Collagen
fibre weakness, Comedones (acne)
U - Urinary free cortisol and glucose increase
S - Striae, Suppressed immunityH - Hypercortisolism, Hypertension,
Hyperglycaemia, Hirsutism
I - Iatrogenic (Increased administration of
corticosteroids)N - Noniatrogenic (Neoplasms)
G - Glucose intolerance, Growth retardation