ENDOCRINE SYSTEM

Endocrine glands include:

- Hypothalamus
- Pituitary gland
- Adrenal glands
o On top of each kidney
o Have and outer cortex and inner medulla
- Thyroid glands
- Islet cells of the pancreas
- Parathyroid glands
- Gonads
o Are the male and female reproductive endocrine glands.
o Male gonads are the Testes
o Female gonads are the ovaries

Endocrine glands secrete hormones which are natural chemicals that exert their functions
on target tissues by binding to receptors. Each receptor is specific to 1 hormone “lock and
key”

Disorders of the endocrine system usually are related to:

- An excess/ deficiency of a specific hormone
- A receptor defect

Principal hormones of Endocrine Glands

- Anterior pituitary
o Adrenocorticotrophic hormone (ACTH)
o Thyroid-stimulating hormone (TSH)
o Luteinizing hormone (LH)
o Follicle-stimulating hormone (FSH)
o Prolactin (PRL)
o Growth hormone (GH)
o Melanocyte-stimulating hormone (MSH)

- Posterior pituitary
o Anti-diuretic hormone (ADH)
o Oxytocin

- Thyroid
o Triiodothyronine (T3)
  Is the most active hormone
o Thyroxine (T4)
 T4 is converted to T3
o Calcitonin
 Control of Ca and Phosphorus balance
  serum Ca & Phosphorus suppress the
release of calcitonin and vice.
If thyroid level hormones are  TSH
release is inhibited and vice versa.
Always palpate the thyroid gently
because vigorous palpation can
stimulate a thyroid storm in a
person who has or is suspected to
have hyperthyroidism.

- Parathyroid
Consist of 4 small glands close or within the back of the thyroid.
o Parathyroid hormone (PTH)
 Regulates Ca and Phosphorus metabolism, by acting on bones, kidneys and
GI.
 Bone is the main storage of Ca. PTH  bone resorption (bone release of Ca
into the blood) thus  serum Ca
 In the kidneys PTH activates vit D which  absorption of Ca and Phosphorus
from the intestines.
 If Ca is  PTH 

- Adrenal cortex
o Glucocorticoids (Cortisol)
 Cortisol affects the body response to stress
 Carbohydrate, protein and fat metabolism
 Emotional stability
 Immune function
 Sodium and water balance.
 Cortisol prepares the body for a fight-or-flight response by flooding it with
glucose, supplying an immediate energy source to large muscles.
 Cortisol inhibits insulin production in an attempt to prevent glucose from
being stored, favoring its immediate use.
 Cortisol narrows the arteries while the epinephrine increases heart rate,
both of which force blood to pump harder and faster

o Mineralocorticoids (Aldosterone)
 Aldosterone promotes Na and H2O reabsorption and K excretion.
 Aldosterone secretion is regulated by Renin-Angiotensin system
 Renin release is triggered by a decreased in ECF volume from blood loss,
sodium loss or posture changes.
  K levels also controls aldosterone secretion. If serum K levels  aldosterone
enhances kidney excretion of potassium to have levels back to normal.

- Ovary
o Estrogen
o Progesterone

- Testes
o Testosterone

- Pancreas
o It has exocrine and endocrine functions.
o The exocrine function involves secretion of digestive enzymes that empty in the
duodenum
o Endocrine functions are the cells in the islets of Langerhans
o Alpha cell secretes glucagon
o Beta cells secrete insulin
o Delta cells secrete somatostatin (to inhibit release of glucagon and insulin.)
- Hypothalamus
 o Gonadotropin - releasing hormone – GnRH
o Thyrotropin - releasing hormone – TRH
o Corticotropin - releasing hormone – CRH
o Growth hormone-releasing hormone (GHRH)
o Somatostatin

DISORDERS OF ANTERIOR PITUITARY

The anterior pituitary regulates growth, metabolism and sexual development.

1. Hypopituitarism

 General concepts
- The cause of hypopituitarism varies. Benign or malignant pituitary tumors can compress
and destroy pituitary tissue. Malnutrition or rapid body fat loss. Shock or severe
hypotension blood flow to the pituitary gland, leading to hypoxia and infarction. Other
causes can be head trauma, brain tumors, infection and AIDS.
- Postpartum hemorrhage is the most common cause of pituitary infarction which results
in decreased hormone secretion. This clinical problem is known as Sheehan’s syndrome.
The pituitary gland normally enlarges during pregnancy, and when hypotension results
from hemorrhage, ischemia and necrosis of the gland occur. Usually this condition
develops immediately after delivery, although some cases have occurred several years
later.
- Neurologic manifestations of hypopituitarism as a result of tumor growth often first
occur as changes in vision. Assess the patient’s visual acuity, especially peripheral vision,
for changes or loss. Temporal headaches are a common finding. Other manifestations
may include diplopia (double vision) and ocular muscle paralysis, limiting eye
movement.

 Deficient hormones
- Growth hormone (GH)
o Deficiency in children leads to short stature and general growth retardation
o Deficiency in adults doesn’t affect height but  the rate of bone destruction, leading
to thinner bone (osteoporosis) and  risk for fractures.
o Decreased bone density
o Pathologic fractures
o Decreased muscle strength
o Increased serum cholesterol levels

- Gonadotropins (luteinizing hormone [LH], follicle- stimulating hormone [FSH])

LH and FSH deficiencies leads to loss or change in secondary sex characteristics
 o Women:
• Amenorrhea (absence of menstrual periods)
• Anovulation
• Low estrogen levels
• Breast atrophy
• Loss of bone density
• Decreased axillary and pubic hair
• Decreased libido
• Dyspareunia (painful intercourse)
• Infertility

o Men:
• Decreased facial hair
• Decreased ejaculate volume
• Reduced muscle mass
• Loss of bone density
• Decreased body hair
• Decreased libido
• Impotence

- Thyroid-stimulating hormone (thyrotropin) (TSH)

o Decreased thyroid hormone levels
o Weight gain
o Intolerance to cold
o Scalp alopecia
o Hirsutism
o Menstrual abnormalities
o Decreased libido
o Slowed cognition
o Lethargy

- Adrenocorticotropic hormone (ACTH)

o Decreased serum cortisol levels
o Pale, sallow complexion
o Malaise and lethargy
o Anorexia
o Postural hypotension
o Headache
o Hypoglycemia
o Hyponatremia
 o Decreased axillary and pubic hair (women)

 RN Interventions
- Management focuses on replacement of deficient hormones
- Men
o who have gonadotropin deficiency receive sex steroid replacement therapy with
androgens (testosterone). The most effective route of androgen replacement is
I'M. Therapy begins with high-dose testosterone and is continued until
virilization (presence of male secondary sex characteristics) is achieved. Maximal
effects of treatment include increases in penis size, libido, muscle mass, bone
size, and bone strength. Chest, facial, pubic, and axillary hair growth also
increases, and the voice deepens. This therapy is avoided in men with prostate
cancer. Main side effect is gynecomastia (male breast tissue development)
- Women
o who have gonadotropin deficiency receive hormone replacement with a
combination of estrogen and progesterone. The risk for hypertension or
thrombosis (formation of blood clots in deep veins) is increased with estrogen
therapy, especially among women who smoke.

- Adults with  GH
o May be treated with subcutaneous injections of human GH (hGH). Injections are
given at night to mimic normal GH release

2. Hyperpituitarism

 General concepts
- The most common hormones produced in excess with hyperpituitarism are PRL, ACTH,
GH.
- The most common cause of hyperpituitarism is a hormone secreting benign tumor aka
adenoma (a benign tumor of one or more tissues within the anterior pituitary).
Adenomas are classified by size, invasiveness, and the hormone secreted. As the
adenoma gets larger and compresses brain tissue, neurologic changes as well as
endocrine problems, may occur. Main S/S are:
o Visual disturbances
o Headache
o  ICP

- Prolactin secreting tumors are the most common type of pituitary adenoma. Excessive
PRL inhibits the secretion of gonadotropins and sex hormones in men and women,
resulting in galactorrhea (breast milk production), amenorrhea, and infertility
 - Overproduction of GH in adults results in acromegaly
o Overproduction of growth hormone causes excessive growth. In children, the
condition is called gigantism. In adults, it is called acromegaly.
o The onset may be gradual with slow progression, and changes may remain
unnoticed for years before diagnosis of the disorder. Early detection and
treatment are essential to prevent irreversible changes in the soft tissues, such
as those of the face, hands, feet, and skin. Other changes include increased
skeletal thickness, hypertrophy of the skin, and enlargement of many organs,
such as the liver and heart. Some changes may be reversible after treatment,
but skeletal changes are permanent.
o Bone thinning and bone cell overgrowth occur slowly. Degeneration of joint
cartilage and hypertrophy of ligaments, vocal cords, and eustachian tubes are
common. Because GH blocks the action of insulin, hyperglycemia (elevated
blood glucose levels) is also common.

- Excess ACTH overstimulates the adrenal cortex. The result is excessive production of
glucocorticoids, mineralocorticoids, and androgens, which leads to the development of
Cushing’s disease

 Deficient hormones
- Prolactin (PRL)
o Hypogonadism (loss of secondary sexual characteristics)
o Decreased gonadotropin levels
o Galactorrhea (breast milk production)
o Increased body fat
o Increased serum prolactin levels
o RN should ask about menstrual changes,  libido, painful intercourse and any difficulty
becoming pregnant.

- Growth Hormone (GH)

o Acromegaly
o Thickened lips
o Coarse facial features
o Increasing head size
o Protrusion of the lower jaw
o Enlarged hands and feet
o Jointpain
o Backache
o Barrel-shaped chest
o Excessive sweating
o Hyperglycemia
o Sleep apnea
o Enlarged heart, lungs, and liver
o RN should ask about headache and vision changes

- Adrenocorticotropic Hormone (ACTH)Cushing’s Disease (Pituitary)

o Elevated plasma cortisol levels
o Weight gain
o Truncal obesity
o “Moon face”
o Extremity muscle wasting
o Loss of bone density
o Hypertension
o Hyperglycemia
o Purple striae
o Acne
o Thin, easily damaged skin
o Hyperpigmentation

- Thyrotropin (Thyroid- Stimulating Hormone [TSH])

o Elevated plasma TSH levels
o Elevated plasma thyroid hormone levels
o Weight loss
o Tachycardia and dysrhythmias
o Heat intolerance
o Increased GI motility
o Fine tremors

- Gonadotropins (Luteinizing Hormone [LH], Follicle- Stimulating Hormone [FSH])

Men:

o Elevated LH and FSH levels

o Hypogonadism or hypergonadism

Women:

o Normal LH and FSH levels (The most common clinical manifestations in men and women
are related to the physical presence of a tumor rather than to excessive hormone
secretion.)
  RN Interventions
- The expected outcomes of management for the patient who has hyperpituitarism are to
return hormone levels to normal or near normal, reduce or eliminate headache and
visual disturbances, prevent complications
- Drug therapy: - This drugs stimulate dopamine receptors and
o Bromocriptine mesylate (Parlodel) inhibit release of GH and PRL.
o cabergoline (Dostinex) - S/E: Orthostatic Hypotension, GI irritation, abd
cramps, constipation.
- Admin w/ food
- Surgical removal of the pituitary gland
- If chest pain/ dizziness develops while taking
and tumor (hypophysectomy) is the Bromocriptine seek medical attention.
most common Tx for hyperpituitarism.
Successful surgery  hormone levels,  headaches, and may reverse changes in sexual
functioning

- Hypophysectomy Care.

o Preoperative
 Explain that because nasal packing is present for 2 to 3 days after surgery, it will be
necessary to breathe through the mouth, and a “mustache” dressing (“drip” pad) will be
placed under the nose. Instruct the patient not to brush teeth, cough, sneeze, blow the
nose, or bend forward after surgery. These activities can increase intracranial pressure
(ICP) and delay healing.

o Postoperative Care.
 Monitor the patient’s neurologic response, and document any changes in vision or
mental status, altered level of consciousness, or decreased strength of the extremities.
Observe the patient for complications such as transient diabetes insipidus, CSF leakage,
infection, and increased ICP.
 Teach the patient to report any postnasal drip or increased swallowing, which might
indicate leakage of CSF.
 Keep the head of the bed elevated after surgery.
 Assess nasal drainage for quantity, quality, and the presence of glucose (which
indicates that the fluid is CSF).
 A light yellow color at the edge of the clear drainage on the dressing is called the “halo
sign” and indicates CSF.
 If the patient has persistent, severe headaches, CSF fluid may have leaked into the sinus
area. Most CSF leaks resolve with bedrest.
 Teach the patient to avoid coughing early after surgery because it increases pressure in
the incision area and may lead to a CSF leak

 Instruct the patient to use dental floss and oral mouth rinses, because brushing the
 teeth is not permitted until the incision heals sufficiently.

 Infection can occur after surgery. Specifically assess for manifestations of meningitis,
such as headache, fever, and nuchal (neck) rigidity. The surgeon may prescribe
antibiotics, analgesics, and antipyretics.
 Hormone replacement with vasopressin may be needed to maintain fluid balance.

DISORDERS OF POSTERIOR PITUITARY

- The posterior pituitary gland secretes vasopressin (Antidiuretic hormone ADH).

Problems in this gland results in changes in fluid and electrolyte balances
- Disorders of the posterior pituitary gland (neurohypophysis) are related to a deficiency
or excess of the hormone vassopressin (antidiuretic hormone [ADH]) and usually occur
independently from anterior pituitary problems.
- Diabetes insipidus occurs with ADH deficiency
- Syndrome of inappropriate antidiuretic hormone (SIADH) occurs with ADH excess.

1. Diabetes Insipidus

 General Concepts
Diabetes insipidus (DI) is a water metabolism problem caused by:
- an ADH deficiency or
- an inability of the kidneys to respond to ADH.

This results in the excretion of large volumes of dilute urine because the distal kidney tubules
and collecting ducts do not reabsorb water, leading to polyuria (excessive water loss through
urination) and dehydration, and disturbed fluid and electrolyte balance. Most common
electrolyte imbalance is  serum Na levels.
Dehydration caused by this massive water loss plasma osmolarity, which stimulates a
sensation of thirst. Thirst promotes  fluid intake and aids in maintaining water homeostasis. If
the thirst mechanism is poor or absent or if the person is unable to obtain water, dehydration
becomes more severe and can lead to death.

Critical Note: Ensure that no patient suspected of having DI is deprived of fluids for more than
4 hours, because he or she cannot reduce urine output and severe dehydration can result.
Drug related Diabetes Insipidus is usually caused by lithium carbonate (Eskalith) and
demeclocycline (Declomycin) affecting how the drug interfere with the response of the kidneys
to ADH.

 Assessment

- Most manifestations of DI are related to dehydration. The key manifestations are an

increase in the frequency of urination and excessive thirst.
- Water loss produces changes in blood and urine tests. The first step in diagnosis is to
measure a 24-hour fluid intake and output without restricting food or fluid intake.
- DI is considered if urine output is more than 4 L during this period and is greater than
the volume ingested. The amount of urine excreted in 24 hours may vary from 4 to 30
L/day. Urine is dilute with a low specific gravity (less than 1.005) and low osmolarity (50
to 200 mOsm/kg).

 RN Interventions
- Management focuses on controlling manifestations with drug therapy
- Management focuses on early detection of dehydration and maintaining adequate
hydration. Interventions include accurately measuring fluid intake and output, checking
urine specific gravity, and recording the patient’s weight daily.
- Urge the patient to drink fluids in an amount equal to urine output. If uids are given IV,
ensure the patency of the access catheter and accurately monitor the amount infused
hourly.
 - Preferred drug is Desmopressin acetate (DDAVP) a synthetic form of vasopressin given
PO or intranasal in a metered spray. Teach pt the may need 1 or 2 doses in 24 hrs in
cases of mild DI
- Vasopressin  urine output and  osmolality in diabetes insipidus.
o Drugs for DI induce water retention and can cause fluid overload. Teach all
patients taking these drugs to weigh themselves daily to identify weight gain.
o Stress the importance of using the same scale and weighing at the same time of
day while wearing a similar amount of clothing.
o If weight gain or other signs of water toxicity occur (persistent headache, acute
confusion), instruct the patient must go to the emergency department or call
911.
o Instruct the patient to wear a medical alert bracelet identifying the disorder and
drugs.

- For more severe DI, one or two metered doses two or three times daily may be needed.
- During severe dehydration, ADH may be given IV or IM.
- Ulceration of the mucous membranes, allergy, a sensation of chest tightness, and lung
inhalation of the spray may occur with use of the intranasal preparations. If side effects
occur or if the patient has an upper respiratory infection, oral or subcutaneous
vasopressin is used.

Critical Note: The parenteral form of desmopressin is 10 times stronger than the oral and
intranasal forms, and the dosage must be reduced.

2. Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

 General Concepts

- The syndrome of inappropriate antidiuretic hormone (SIADH) is a problem in which

vasopressin (antidiuretic hormone [ADH]) is secreted even when plasma osmolarity
(concentration of electrolytes, like Na) is low or normal.
- A decrease in plasma osmolarity normally inhibits ADH production and secretion.
- SIADH is also known as the Schwartz-Bartter syndrome. SIADH occurs with many
pathologic conditions (e.g., cancer therapy) and with specific drugs, including SSRI.
- In SIADH, ADH continues to be released even when plasma is hypo-osmolar. Water is
retained, which results in dilutional hyponatremia (a decreased serum sodium level) and
fluid overload.
- The  in blood volume  the kidney filtration and inhibits the release of renin and
aldosterone which  Na loss in urine, leading to greater hyponatremia
  Assessment
- The early manifestations of SIADH are related to water retention. GI disturbances, such
as loss of appetite, nausea, and vomiting, may occur first. Weigh the patient, and
document any recent weight gain
- Water retention, hyponatremia, and fluid shifts affect central nervous system function,
especially when the serum sodium level drops below 115 mEq/L. The patient may have:
o lethargy, headaches, hostility, disorientation, and a change in LOC.
Manifestations can progress from lethargy and headaches to decreased
responsiveness, seizures, and coma. Assess deep tendon re exes, which are
usually decreased
- Vital sign changes include a full and bounding pulse (caused by the increased fluid
volume) and hypothermia (caused by central nervous system disturbance)

 RN Interventions
- Medical interventions for SIADH focus on restricting fluid intake, because fluid intake
further dilutes plasma sodium levels. In some cases, fluid intake may be kept as low as
500 to 1000 mL/24 hr.
- Measure intake, output, and daily weights to assess the degree of fluid restriction
needed. A weight gain of 2.2 lb is cause of concern. (1kg=1L)
- Monitor for fluid overload (bounding pulses,  neck vein distention, crackles in lungs,
peripheral edema,  urine output)
- Pulmonary edema can occur very quickly and lead to death
 - Provide a safe environment if Na level fall below 120 mEq/L due to  risk for seizures.

- Drug Therapy
o Tolvaptan (Samsca)
o Conivaptan (Vaprisol)
o Diuretics may be used to manage SIADH when Na levels are near normal and

These 2 drugs are vasopressin antagonists that promote H2O excretion without causing Na
loss

Admin these drugs ONLY in hospital setting to monitor Na levels closely.

Tolvaptan has a black box warning
-Rapid  Na (> than 12) in 24 associated w/ CNS complications and death
-Also associated w/ liver failure and death is used for more than 30 days.

heart failure is present. Be aware of the potential Na loss which can potentiate
SIADH.
o Hypertonic saline (3% NaCl) may be used.

DISORDERS OF ADRENAL GLANDS p.1273

1. Adrenal Gland Hypofunction aka “Addison Disease”

- Production of adrenocortical steroids may decrease as a result of inadequate secretion of

adrenocorticotropic hormone (ACTH), dysfunction of the hypothalamic-pituitary control
mechanism, or direct dysfunction of adrenal gland tissue. Manifestations may develop gradually
or occur quickly with stress. In Acute adrenocortical insufficiency (adrenal crisis), life-
threatening manifestations may appear without warning.
- Insufficiency of adrenocortical steroids causes problems through the loss of aldosterone and
cortisol action:
o  cortisol levels result in poor glucose regulation leading to hypoglycemia
o Glomerular filtration and gastric acid production , leading to reduced urea nitrogen
excretion, causing anorexia and weight loss.
o  aldosterone secretion causes potassium, sodium, and water imbalances.
o Potassium excretion is , causing hyperkalemia. Potassium retention also promotes
reabsorption of hydrogen ions, which can lead to acidosis.
o Sodium and water excretion are , causing hyponatremia and hypovolemia.

- Acute adrenal insufficiency aka Adrenal Crisis

o is a life-threatening event in which the need for cortisol and aldosterone is greater than
the available supply. Often, it occurs in response to a stressful event (e.g., surgery,
 trauma, severe infection), especially when the adrenal hormone output is already
reduced.
o Unless intervention is initiated promptly, however, sodium levels fall and potassium
levels rise rapidly. Severe hypotension results from the blood volume depletion that
occurs with the loss of aldosterone.

o Adrenal insufficiency (Addison’s disease) is classified as primary or secondary.

o A common cause of secondary adrenal insufficiency is the sudden cessation of
longterm glucocorticoid therapy. This therapy suppresses production of
glucocorticoids through negative feedback by causing atrophy of the adrenal cortex.
Glucocorticoid drugs must be withdrawn gradually to allow for pituitary production of
ACTH and activation of adrenal cells to produce cortisol

CAUSES OF ADRENAL INSUFFICIENCY

PRIMARY SECONDARY

Autoimmune disease (most common) Pituitary tumors

Tuberculosis Postpartum pituitary necrosis

Metastatic cancer Hypophysectomy

AIDS

Hemorrhage

Drugs (mititane) and toxins.

Abdominal radiation therapy

 Assessment
- In patients with primary insufficiency ACTH and Melanocyte Stimulating Hormone (MSH) is
.
-  MSH results in areas of  pigmentation. But in primary autoimmune disease patchy areas
of decrease pigmentation may occur due to destruction of skin melanocytes. Body hair
may be decreased
- Check for abnormal glucose regulation, mainly hypoglycemia (sweating, headaches,
tachycardia, tremors)
- Check for fluid depletion (postural hypotension and dehydration)
- Hyperkalemia can cause dysrhythmias
o Tx of hyperkalemia!!!
 Hyperkalemia can be effectively treated by administering insulin and dextrose 50%
 Insulin will shift potassium from the extracellular space to the intracellular space and
dextrose 50 % will prevent the patient from becoming hypoglycemic when given insulin.
- Check neuro status, which may change due to the imbalances (lethargic,
depressed, confused, altered LOC)
 RN Interventions
- Nursing interventions focus on promoting fluid balance, monitoring for fluid deficit, and
preventing hypoglycemia. Assess cardiac function due to hyperkalemia. Weigh the
patient daily, and record intake and output. Assess vital signs every 1 to 4 hours,
depending on the patient’s condition and the presence of dysrhythmias or postural
hypotension
- Drug therapy:
o Prednisone (most common drug use) two doses given early in the morning and
late afternoon to mimic the normal release of this hormone.
o Fludocortisone (florinef) is a mineralocorticoid to maintain electrolyte balance
 2. Adrenal Gland Hyperfunction
Divided in:
- Cushing’s disease
- Hyperaldosteronism
- Pheochromocytoma (tumor)

 General concepts
-The adrenal gland may oversecrete just one hormone or all adrenal hormones.
-Hypersecretion by the adrenal cortex results in:
o Hypercortisolism (e.g., Cushing’s disease or Cushing’s syndrome)
o Hyperaldosteronism (excessive mineralocorticoid production), or excessive
androgen production.
-Hyperstimulation of the adrenal medulla is caused by:
o a tumor (PHEOCHROMOCYTOMA) results in excessive secretion of catecholamines
(epinephrine and norepinephrine) = HTN.
o Is a tumor that arises in the adrenal medulla.
o The tumor produce, stores, and release epinephrine and NE which mimic the action
of the Sympathetic NS.
o The pt has intermittent episodes of HTN (headaches, palpitations, diaphoresis,
flushing, apprehension or a sense of impending doom.)
o Surgery is the main treatment for pheochromocytoma. One or both adrenal glands
are removed.
o Hypertension is the hallmark of this disease and the most common serious
complication after surgery.
 Monitor BP regularly and place the cuff consistently in the same arm in the
lying and standing position.
o DO NOT PALPATE THE ABDOMEN OF A PATIENT WITH A PHEOCHROMOCYTOMA.
This action could stimulate a sudden release of catecholamines and trigger severe
HTN

CUSHING’S DISEASE
-Cushing’s disease is the excess secretion of cortisol from the adrenal cortex. It is caused by
either a problem in the adrenal cortex itself, a problem in the anterior pituitary gland, or a
problem in the hypothalamus. In addition, glucocorticoid therapy can also lead to problems
of hypercortisolism.
-The presence of excess glucocorticoids, regardless of the cause, affects metabolism and all
body systems.
o An increase in total body fat results from slow turnover of plasma fatty acids. This fat is
 redistributed, producing truncal obesity, “buffalo hump,” and “moon face”
o Increases in the breakdown of tissue protein and an increase in urine nitrogen excretion
also occur, resulting in decreased muscle mass and muscle strength, thin skin, and fragile
capillaries. The effects on minerals lead to bone density loss.
o High levels of corticosteroids kill lymphocytes and shrink organs containing lymphocytes,
such as the spleen and the lymph nodes. WBC production is  leading to reduced
protection of the inflammatory and immune responses.
o Androgen production  causing hirsutism ( body hair) and oligomenorrhea (scant or
infrequent menses)
-Cushing’s Disease vs Cushing’s Syndrome
o If the anterior pituitary gland oversecretes adrenocorticotropic hormone (ACTH), this
hormone causes hyperplasia of the adrenal cortex in both adrenal glands and an excess
of most hormones secreted by the adrenal cortex. This problem is known as pituitary
Cushing’s disease because the tissue causing the problem is the pituitary.
o When the excess glucocorticoids are caused by a problem in the actual adrenal cortex,
usually a benign tumor (adrenal adenoma), the problem is called adrenal Cushing’s
disease and usually occurs in only one adrenal gland.
o When glucocorticoid excess results from drug therapy for another health problem, it is
known as Cushing’s syndrome.

 Assessment
- In women hirsutism and clitoral hypertrophy
- Cardiac changes due to:
o H2O and Na are reabsorbed leading to hypervolemia, edema,  BP, bounding
pulses.
o  K due to excretion
o  Ca
- Glucose levels are high
- Emotional instability
o Mood swings
o Confusion
o Depression
  RN Interventions
- Monitor for indicators of fluid overload (neck distention, crackles, peripheral edema, 
urine output)
- Weight the pt daily
- No “added salt” and restriction of fluid are indications for nutrition therapy.
- Drug Therapy:
o Include drugs that interfere with ACTH production or adrenal hormone synthesis.
o metyrapone (Metopirone) use different pathways to decrease cortisol
production.
o cyproheptadine (Periactin) interferes with ACTH production.
o Mifepristone (korlym) blocks glucocorticoids receptors

Mifepristone (korlym) CAN’T be used during pregnancy bc blocks progesterone

receptors and can cause termination of the pregnancy.

- Surgical Management (depends of the cause)

o If Adrenal Hyperfunction is due to  pituitary secretion of ACTH, then removal of
pituitary adenoma is attempted. Also a hypophysectomy (removal of pituitary
gland) can be performed.
 o If Hypercortisolism is due to adrenal tumor, then adrenalectomy (removal of
adrenal gland) is performed. If is bilateral adrenalectomy, glucocorticoid and
mineralocorticoid therapy is lifelong. If is unilateral, hormone replacement therapy
continues until the remaining adrenal gland  production of hormones. Usually
takes 2 years.

HYPERALDOSTERONISM

- Hyperaldosteronism is an increased secretion of aldosterone with mineralocorticoid excess.

- Primary hyperaldosteronism (Conn’s syndrome) results from excessive secretion of
aldosterone from one or both adrenal glands, usually caused by a benign adrenal adenoma.
- In secondary hyperaldosteronism, excessive secretion of aldosterone is caused by high levels of
angiotensin II that are stimulated by high plasma renin levels. Causes of high renin levels
include kidney hypoxemia and the use of thiazide diuretics.
-  aldosterone levels affect the kidney tubules and cause:
o Na retention with potassium and hydrogen ion excretion.
o Hypernatremia, hypokalemia, and metabolic alkalosis result.
o Sodium retention increases blood volume, which raises blood pressure but usually does
not cause peripheral edema. The elevated blood pressure may cause strokes, heart
attacks, and kidney damage.
- Hypokalemia and  BP are the most common problems of the patient with hyperaldosteronism.
- Pt may have:
o headache, fatigue, muscle weakness
o nocturia (excessive urination at night), and loss of stamina.
 o Polydipsia (excessive fluid intake) and polyuria (excessive urine output) occur less
frequently.
o Paresthesias (sensations of numbness and tingling) may occur if K depletion is severe

 RN Interventions
- Surgery is the most common treatment for early-stage hyperaldosteronism. One or both
adrenal glands may be removed. Surgery is not performed, however, until the patient’s
potassium levels are normal.
- Drug Therapy used to increase potassium levels include:
o spironolactone (Aldactone, Spirono, Sincomen), a potassium-sparing diuretic and
aldosterone antagonist. Potassium supplements may be prescribed to increase
potassium levels before surgery.
o Teach patients to report any additional side effects of spironolactone therapy, including
gynecomastia, diarrhea, drowsiness, headache, rash, urticaria (hives), confusion,
erectile dysfunction, hirsutism, and amenorrhea.
 THYROID DISORDERS

1. HYPERTHYROIDISM

 General Concepts
- Hyperthyroidism is excessive thyroid hormone secretion from the thyroid gland
- In hyperthyroidism the excessive thyroid hormones stimulate most body systems, causing
hypermetabolism and increased sympathetic nervous system activity.
- Thyroid hormones stimulate the heart, increasing both heart rate and stroke volume. These
responses increase cardiac output, systolic blood pressure, and blood flow
- Elevated thyroid hormone levels affect protein, lipid, and carbohydrate metabolism. Protein
synthesis (buildup) and degradation (breakdown) are increased, but breakdown exceeds
buildup, causing a net loss of body protein known as a negative nitrogen balance.
- Glucose tolerance is decreased, and the patient has hyperglycemia (elevated blood glucose
levels).
- Fat metabolism is , and body fat . Although the patient has an increased appetite, the
increased metabolism causes weight loss and nutritional deficiency.
- Women and men have  libido (sexual interest)
- The most common form of this disease is Grave’s Disease aka “toxic diffuse goiter”

GRAVE’S DISEASE

- Grave’s disease is an autoimmune disorder resulting from Hashimoto’s Thyroiditis (HT).

HT results in the production of autoantibodies to different substances and structures
within the thyroid gland. In Grave’s disease these antibodies (thyroid-stimulating
immunoglobulins [TSIs]) attach to the thyroid-stimulating hormone (TSH) receptors on
the thyroid tissue. The thyroid gland responds by increasing the number and size of
glandular cells, which enlarges the gland, forming a goiter, and overproduces thyroid
hormones(thyrotoxicosis).
- In Grave’s disease all the manifestations of hyperthyroidism are present plus other
manifestations specific to Graves’ disease include:
o exophthalmos (abnormal protrusion of the eyes) and
o pretibial myxedema (dry, waxy swelling of the front surfaces of the lower legs).
o Not all patients with a goiter have hyperthyroidism.

- Hyperthyroidism also can be caused by excessive use of thyroid replacement hormones.

This type of problem is called exogenous hyperthyroidism.

 Assessment
- Graves’ disease can occur at any age but is diagnosed most often in women between 20
and 40 years of age, affecting women about ten times more often than men
- A hallmark of hyperthyroidism is poor thermoregulation with heat intolerance.
o Pt may have  sweating even with normal temperatures.
- Exophtalmus is common in patients with Graves disease. Pressure on the optic nerve
 may impair vision. If the eyes fail to close completely and the eyes are unprotected, they
may become dry and corneal ulcer develops. Photophobia also occurs
- Goiter is also common in patients with Graves disease. Bruit (turbulence from  blood
flow) may be heard in the neck with sthetoscope.
- The cardiovascular problems of hyperthyroidism include:
o  systolic blood pressure
o tachycardia, and
o dysrhythmias.
o Usually the diastolic pressure is decreased, causing a widened pulse pressure.
- Inspect the hair and skin. Fine, soft, silky hair and smooth, warm, moist skin are
common.
- Muscle weakness and hyperactive deep tendon reflexes are common. Observe motor
movements of the hands for tremors. The patient may appear restless, irritable, and
fatigued.
- Mood swings are common.
- Laboratory Assessment
o Testing for hyperthyroidism involves measurement of blood values for
triiodothyronine (T3), thyroxine (T4), T3 resin uptake (T3RU), and thyroid-
stimulating hormone (TSH). Antibodies to TSH (TSH-RAb) are measured to
diagnose Graves’ disease.
- Other Dx Test:
o Thyroid scan evaluates the position, size, and functioning of the thyroid gland
o Radioactive iodine (RAI [123I]) is given by mouth, and the uptake of iodine by the
thyroid gland (radio- active iodine uptake [RAIU]) is measured. Pregnancy should
be ruled out before the scan is performed, because it crosses the placenta
o Any drug that contains iodine should be discontinued for 1 week before the scan.
  RN Interventions
- Monitoring includes:
o measuring the patient’s apical pulse, blood pressure (BP), and temperature at
least every 4 hours.
o Instruct the patient to report immediately any palpitations, dyspnea, vertigo, or
chest pain.
o Increases in temperature may indicate a rapid worsening of the patient’s
condition and the onset of thyroid storm, a life-threatening event that occurs
with uncontrolled hyperthyroidism and is characterized by high fever and severe
hypertension. Immediately report a temperature increase of even one degree
Fahrenheit. If a temperature elevation is reported, immediately assess the
patient’s cardiac status. If the patient has a cardiac monitor, check for
dysrhythmias.
-  environmental stimulation
- Drug therapy:
o Antithyroid hormones are the initial Tx. These drugs block thyroid hormone
production by preventing iodide binding in the thyroid gland
o Methimazole (tapazole)
o Propylthiouracil (PTU) Less used due to liver toxicity.

o Iodine preparations may be used for short-term therapy before surgery. They
decrease blood flow through the thyroid gland, reducing the production and
release of thyroid hormone. Improvement usually occurs within 2 weeks, but it
may be weeks before metabolism returns to normal. This treatment can result in
hypothyroidism, and the patient is monitored closely for the need to adjust the
drug regimen.
o Beta-adrenergic blocking drugs, such as propranolol (Inderal, Detensol) may be
used as supportive therapy. These drugs relieve diaphoresis, anxiety,
tachycardia, and palpitations but do not inhibit thyroid hormone production.
o Radioactive iodine (RAI) therapy is not used in pregnant women because it
crosses the placenta and can damage the fetal thyroid gland.
 The patient with hyperthyroidism may receive RAI in the oral form, dosage
depends on the thyroid gland’s size and sensitivity to radiation.
 The thyroid gland picks up the RAI, and some of the cells that produce thyroid
hormone are destroyed by the local radiation. Because the thyroid gland
stores thyroid hormones to some degree, the patient may not have complete
symptom relief until 6 to 8 weeks after RAI therapy. Additional drug therapy
for hyperthyroidism is still needed during the first few weeks after RAI
treatment.
 The radiation dose is low and is usually completely eliminated within a
month; however, the source is unsealed, and some radioactivity is present in
the patient’s body fluids and stool for a few weeks after therapy
- Surgery Tx
o Preferred management for Grave’s Disease.
o Also use when a large goiter causes tracheal or esophageal compression or
hyperthyroidism doesn’t respond to drug therapy.
o Removal of all (total thyroidectomy) or part (subtotal thyroidectomy) of the
thyroid tissue decreases the production of thyroid hormones. After a total
thyroidectomy, patients must take lifelong thyroid hormone replacement.
o Preoperative Care.
 If possible, the patient is treated with drug therapy first to have near-
normal thyroid function (euthyroid) before thyroid surgery.
 Hypertension, dysrhythmias, and tachycardia must be controlled before
surgery.
o Postoperative Care.
 Monitoring the patient for complications is the most important nursing
action after thyroid surgery. Monitor vital signs every 15 minutes until
the patient is stable and then every 30 minutes for 24 hours.
 Thyroid surgery can cause hemorrhage, respiratory distress, parathyroid
gland injury (resulting in hypocalcemia [low serum calcium levels] and
tetany [hyperexcitability of nerves and muscles]), damage to the
laryngeal nerves, and thyroid storm. Remain alert to the potential for
complications, and identify manifestations early.
 Hemorrhage is most likely to occur during the first 24 hours after
surgery. Inspect the neck dressing and behind the patient’s neck for
blood. A drain may be present, and a moderate amount of
serosanguineous drainage is normal.
 Respiratory distress can result from swelling, tetany, or damage to the
laryngeal nerve resulting in spasms. Laryngeal stridor (harsh, high-
pitched respiratory sounds) is heard in acute respiratory obstruction.
Keep emergency tracheostomy equipment in the patient’s room. When
stridor, dyspnea or other symptoms of obstruction appear after
thyroid surgery, notify the RAPID RESPONSE TEAM.
 Hypocalcemia and tetany may occur if the parathyroid glands are
 removed, damaged or their blood supply is impaired during thyroid
surgery, resulting in decreased para- thyroid hormone (PTH) levels. Ask
the patient hourly about tingling around the mouth or of the toes and
fingers. Assess for muscle twitching as a sign of calcium deficiency.
Calcium gluconate or calcium chloride for IV use should be available in
an emergency situation.
 Laryngeal nerve damage may occur during surgery. This problem results
in hoarseness and a weak voice. Assess the patient’s voice at 2-hour
intervals; Speaking is important to determine the status of the
laryngeal nerve. and document any changes. Reassure the patient that
hoarseness is usually temporary.
 Thyroid storm, or thyroid crisis or Thyrotoxic crisis, is a life-threatening
event that occurs in patients with uncontrolled hyperthyroidism and
occurs most often with Graves’ disease
 Sudden and excessive release of thyroid hormones.
 Manifestations of crisis develop quickly.
 It is often triggered by stressors such as trauma, infection,
diabetic ketoacidosis, and pregnancy. Other conditions that can
lead to thyroid storm include vigorous palpation of the goiter,
exposure to iodine, and radioactive iodine (RAI) therapy.
 Although thyroid storm after surgery is less common because
patients receive antithyroid drugs, beta blockers, and iodides
before thyroid surgery, it can still occur.
 The manifestations of thyroid storm are caused by excessive
thyroid hormone release, which dramatically increases metabolic
rate.
 Key manifestations include fever, tachycardia, and systolic
hypertension.
 The patient may have GI problems such as abdominal pain,
nausea, vomiting, and diarrhea. Often he or she is very anxious
and has tremors. As the crisis progresses, the patient may
become restless, confused, or psychotic and may have seizures,
leading to coma. Even with treatment, thyroid storm may lead to
death.
 When caring for a patient with hyperthyroidism, even after a
partial thyroidectomy, immediately report a temperature
increase of even 1° F because it may indicate an impending
thyroid crisis.

EMERGENCY CARE DURING THYROID STORM

- Maintain a patent airway and adequate ventilation.

- Give antithyroid drugs as prescribed:
o methimazole (Tapazole), up to 60 mg daily;
o propylthiouracil (PTU, Propyl-Thyracil), 300 to 900 mg daily.
- Administer sodium iodide solution, 2 g IV daily as prescribed.
- Give propranolol (Inderal, Detensol ), 1 to 3 mg IV as prescribed. Give slowly over 3 minutes.
 The patient should be connected to a cardiac monitor, and a central venous pressure
catheter should be in place.
- Give glucocorticoids as prescribed:
o hydrocortisone, 100 to 500 mg IV daily;
o prednisone, 4 to 60 mg IV daily; or
o dexamethasone, 2 mg IM every 6 hours.
- Monitor continually for cardiac dysrhythmias.
- Monitor vital signs every 30 minutes.
- Provide comfort measures, including a cooling blanket.
- Give non-salicylate antipyretics as prescribed.
- Correct dehydration with normal saline infusions.
- Apply cooling blanket or ice packs to reduce fever.

2. HYPOTHYROIDISM p.1291

PARATHYROID DISORDERS

1. HYPERPARATHYROIDISM
2. HYPOPARATHYROIDISM