ENDOCRINE DISORDERS

Anatomy and
physiology overview

Endocrine system.
Nervous System is a system of
nerve cells called neurons. It
consists of a central nervous system
(brain and spinal cord) and
peripheral nerves. Typical
responses are fast and short lasting.

Endocrine System is a system of

ductless glands that secrete
hormone into the blood. Hormones
travel to target tissues.
Typical responses are slow and long
lasting.
 Human Endocrine Glands
Ductless glands transport hormones
in the blood.

Duct glands are exocrine glands that

use tubes to carry the secretion
(salivary, tears).
Pituitary gland and Hypothalamus serve to link the nervous
system other glands and metabolic functions.
 (a) Humoral: in response to changing
levels of ions or nutrients in the
MECHANISMS OF blood
HORMONE (b) Neural: stimulation by nerves
RELEASE (c) Hormonal: stimulation received
from other hormones
Thyroid and Parathyroid help regulate
calcium metabolism
Pancreas helps regulate
blood glucose
DISORDERS OF THE
ENDOCRINE SYSTEM
 Introduction
Acromegaly
◦ An enlargement of the bones of the
hands, feet, and jaws
Addison's disease
◦ Caused by hyposecretion of the
hormones produced by the cortex of
the adrenal gland
Cretinism
◦ Condition resulting from a congenital
deficiency of thyroid secretion or
hypothyroidism
 Intro…
Cushing’s syndrome
◦ Disorder that causes hyperactivity of
the adrenal glands, which is triggered
by the over secretion of the pituitary
hormone ACTH
Diabetes insipidus
◦ From an acquired or inherited decrease
in the antidiuretic hormone secreted by
the pituitary
Diabetes mellitus
◦ A disorder of carbohydrate, fat, and
protein metabolism resulting from
insufficient insulin production by the
pancreas
Intro…
Dwarfism
◦ Results from hyposecretion of the
growth hormone of the pituitary gland,
which has been caused by a tumor,
infection, genetic factors, or trauma
Gigantism
◦ An excessive growth of the long bones
caused by hypersecretion of the
somatotropic hormone
Graves’ disease
◦ Caused by hyperthyroidism or
thyrotoxicosis
 Intro …
Hyperparathyroidism
◦ Causes hypercalcemia, an increased
calcium blood level
Hypoglycemia
◦ Results from increased insulin
production by the pancreas
Hypoparathyroidism
◦ A decreased secretion of
parathyroid hormone that causes
tetany .
 Intro…
Hypothyroidism
◦ Also called Hashimoto's disease,
results from an insufficient production
of thyroxine
Syndrome of inappropriate
antidiuretic hormone (SIAD)
◦ Involves water intoxication and the
dilution of intracellular and
extracellular body tissues, usually
resulting from lung cancer
Virilism
◦ Results from increased secretion in the
adrenal glands
PITUITARY
DISORDERS
objectives
Describe the disorders caused by
variations in the hormones of the
pituitary gland.
Explain the pathophysiology of each of
the endocrine pituitary disorders.
Discuss the etiologies, signs, and
symptoms of each of the pituitary
disorders.
Outline current therapeutic treatment
of each of the pituitary disorders.
MECHANISMS OF ENDOCRINE
DISEASE
1) Hyperactivity
Primary hyperfunction- autonomous
hypersecretion of hormone due to tumor or
hyperplasia of the gland (e.g.
hyperthyroidism, some forms of
hyperadrenocorticism).
Secondary hyperfunction- a lesion in one
organ (e.g. pituitary gland adenoma)
secretes excess tropic hormone that leads to
long-term stimulation and hypersecretion of
hormones by the target organ (e.g. adrenal
cortical hyperplasia with excess cortisol).
Hyperactivity secondary to diseases
of other organs - Hyperparathyroidism
secondary to chronic renal disease or
nutritional imbalance.
Hypersecretion of hormones or
hormone-like substances by non-
endocrine tumors - Mostly peptides that
are similar chemically and/or biologically
to the native hormone.
Iatrogenic syndromes of hormone -
Excess administration of hormones
directly or indirectly influences the activity
of target cells (e.g. corticosteroid
administration causing iatrogenic
2) Hypoactivity
Primary Hypofunction-
The subnormal hormone secretion
due to destruction of secretory cells,
failure of development or genetic
defect in biosynthesis (e.g. immune-
mediated thyroiditis or adrenalitis).
Secondary hypofunction -A
destructive lesion in one organ (e.g.
pituitary) interferes with the secretion of
trophic hormone and results in
hypofunction of the target gland (e.g.
adrenal cortex, thyroid, gonads).
Endocrine dysfunction due to failure
of target cell response -Alterations or
defects in receptors on target cells make
them less responsive to normal or
increased amounts of hormone (e.g..
insulin resistant diabetes mellitus,
nephrogenic diabetes insipidus).
 Hypopituitarism
• Hypopituitarism results when the pituitary
gland is unable to secrete a normal amount of
pituitary hormones.
• Primary causes are pituitary tumors,
inadequate blood supply to the pituitary
gland, infection, radiation therapy, or surgical
removal of a portion of the pituitary gland.
Post partum pituitary necrosis (Sheehan's
syndrome) is a common cause of failure of the
anterior pituitary. More likely to happen to
women with severe blood loss, hypovolemia,
and hypotension at the time of delivery.
• Secondary causes affect the hypothalamus,
which regulates the pituitary gland.
Pituitarytumors are usually benign,
although their location and effects on
hormone production by target organs
can cause life threatening effects.
This condition affects all other
endocrine glands.
70% to 90% of the anterior pituitary
must be destroyed before
hypopituitarism becomes clinically
evident.
PROGNOSIS
Patients require life-long treatment
and can expect a normal life span.
 SIGNS AND SYMPTOMS
They occur gradually, but it can
present as an acute and life
threatening condition.
 Fatigue caused by a decreased
production of ACTH (adrenalcorticotropic
hormone).
Lethargy and diminished cognition caused
by a decreased production of TSH
(Thyroid stimulating hormone)
Sensitivity to cold due to low TSH, which
stimulates thyroid hormone.
Decreased appetite due to TSH deficiency.
 Sign &symptoms cont…
Infertility due to lack/reduced
luteinizing hormone (LH) and follicle
stimulating hormone (FSH) production.
Short stature due to diminished
secretion of growth hormone.
Infertility, amenorrhea caused by
decreased production of FSH and LH.
Weakness, nausea, anorexia, fever,
and postural hypotension, may result
from ACTH deficiency (secondary
adrenal insufficiency)
 TEST RESULTS
• Decreased ACTH usually due to
a lesion of the pituitary.
• TSH deficiency due to a mass,
trauma, surgery, or idiopathic.
Decreased prolactin due to a
mass, causing diminished or lack
of prolactin from the anterior
pituitary.
• Presence of a pituitary tumor
shown on MRI.
 TREATMENT
• Administer replacement hormones
(estrogen,
testosterone,corticosteroids, growth
hormone, and thyroid hormone).
• Surgical removal of the pituitary
tumor if it exists.
 NURSING INTERVENTION
• Monitor weight daily because antidiuertic
hormone (ADH) and adrenocortiocotropic
hormone (ACTH), from the pituitary,
regulate fluid retention and excretion in
the body.
• Monitor intake and output to ensure the
balance is equal due to hormone
regulation.
Explain to the patient:
• The need to take medication for the rest
of the patient’s life.
• The need for frequent laboratory tests.
 Dwarfism
Isa condition in which the attained
height is well below the third
percentile or linear growth is below
normal for age and sex.
PATHOPHYSIOLOGY.
Dwarfism, also called short
stature, occurs when growth
hormone is deficient in childhood.
A deficiency of GH in adults does
not affect growth.
 ETIOLOGY.
GH deficient as a result of a pituitary
tumor or failure of pituitary to develop.
Result of infection or other trauma to
the Pituitary gland.
Deficient in some cases of neglect or
severe emotional stress, causing
psychosocial dwarfism.
Malnutrition most common cause
worldwide.
Sometimes the cause is not known.
Chromosomal abnormalities such as
Turner syndrome.
 Etiology cont…
Chronic diseases such as chronic
kidney disease and poorly controlled
diabetes mellitus.
Malabsorption syndromes.
Certain therapies like excessive
glucocorticoids administration like in
treatment of asthma.
Low birth weight. E.g. intrauterine
growth retardation
 SIGNS AND SYMPTOMS.
• Children may grow to only 3 to 4 feet in
height but have normal body proportions.
• Sexual maturation may be slowed, related
to involvement of additional pituitary
hormones.
• Dwarfism in children is sometimes
accompanied by mental retardation.
• In adults, symptoms include weakness,
hypoglycemia, sexual dysfunction, skin
changes, and increased risk for
cardiovascular and cerebrovascular disease.
• Headaches, mental slowness, and visual
disturbances may also occur.
 DIAGNOSTIC TESTS
Growth hormone levels in the
blood are measured by a routine
laboratory test.
A growth hormone stimulation test
may be done by measuring GH
response to induced hypoglycemia.
An MRI may help determine the
presence of a pituitary tumor;
radiographic studies may be used
to determine bone age.
THERAPEUTIC
INTERVENTIONS.
Treatment of dwarfism in a child is
administration of growth hormone.
In the past, GH was derived from
human pituitary glands, so treatment
was expensive.
Now GH made in a laboratory using
genetic engineering, and is more
readily available to those who need it.
It is administered by injection.
Surgery indicated if a tumor is the
cause.
HYPERPITUITARISM
(ACROMEGALY AND
GIGANTISM)
The pituitary gland produces an
excessive amount of growth hormone.
Hyperpituitarism occurring before
epiphyseal closure, the patient
(infants and children) has gigantism,
resulting in an overgrowth of all body
tissues.
Hyperpituitarism after epiphyseal
closure, which is rare, the patient has
acromegaly resulting in bone
thickening, growth in width
(transverse growth), and enlarged
organs (visceromegaly).
PROGNOSIS
Successful treatment can stop
progression of the disease; however,
physical changes that occur before
treatment begins are permanent.
 ETIOLOGY.
Excess secretion of growth hormone
can be caused by pituitary
hyperplasia, a benign pituitary tumor,
or excess if GH-releasing hormone
due to hypothalamic dysfunction.
 PATHOPHYSIOLOGY.
• Acromegaly occurs as a result of
oversecretion of GH in an adult.
• Bones increase in size, leading to
enlargement of facial features, hands,
and feet.
• Long bones grow in width but not length
because the epiphyseal disks are closed.
• Subcutaneous connective tissue
increases, causing a fleshy appearance.
• Internal organs and glands enlarge.
• Impaired tolerance of carbohydrates
leads to elevated blood glucose.
 SIGNS AND SYMPTOMS
Often the first symptom noticed is a
change in ring or shoe size.
The nose, jaw, brow, hands, and feet
enlarge
The teeth may be displaced, causing
difficulty chewing, or dentures may no
longer fit.
The tongue becomes thick, causing
difficulty in speaking and swallowing
(dysphagia).
The patient may develop sleep apnea.
Vertebral changes may lead to kyphosis.
 s/s cont…
• Visual disturbances may occur because
of tumor pressure on the optic nerve.
• Headaches are a result of tumor
pressure on the brain.
• Diabetes mellitus may develop because
GH increases blood glucose and causes
an increased workload for the pancreas.
• Osteoporosis and arthritis may occur.
• Erectile dysfunction may occur in men
and amenorrhea in women.
• With treatment, soft tissues reduce in
size, but bone growth is permanent.
 TEST RESULTS
• Increased serum growth hormone as
the pituitary gland is producing an
excess of growth hormone.
• Increased prolactin; most pituitary
tumors will cause overproduction of
one or more of the pituitary hormones.
• Increased glucose; diabetes is
common in acromegaly.
Radiographs show abnormal bone
growth
MRI is done to locate a pituitary tumor.
 TREATMENT
Administer dopamine agonists
such as bromocriptine and
cabergoline to decrease the
tumor size.
• Surgical removal of the pituitary
tumor.
If the pituitary is removed,
lifelong replacement of thyroid
hormone, corticosteroids, and sex
hormones is important to
NURSING DIAGNOSES
• Disturbed body image related to
illness or illness treatment
NURSING INTERVENTIONS
• Perform range of motion exercise
to assure joint mobility.
• Provide emotional support.
Educate the patient:
• Don’t stop taking hormone
replacement suddenly.
 DIABETES INSIPIDUS
A disorder of the posterior lobe of the pituitary gland
characterized by a deficiency of antidiuretic hormone
(ADH), or vasopresssin.
 Great thirst (polydipsia) and large volumes of dilute
urine characterize the disorder. A decrease in ADH
activity results in diabetes insipidus (DI).
 Insufficient ADH leads to excessive water loss of >
200ml/hr and a urine specific gravity of <1.005. This
results in the excretion of large amounts of diluted
urine.
 The patient then drinks large amounts of fluid to
replace the increased urine output.
PROGNOSIS
 Treatment will eliminate the symptoms of diabetes
insipidus and the patient can expect a normal life
span.
 ETIOLOGY.
The primary causes of diabetes
insipidus are tumors or trauma to
the pituitary gland (neurogenic).
Surgery in the area of the pituitary
and certain drugs, such as
glucocorticoids or alcohol, may also
cause DI.
Occasionally, the cause is
psychogenic, in which the patient
drinks large quantities of water in
 ETIOLOGY cont...
Nephrogenic DI occurs mostly in males
and may be inherited or acquired.
It is diagnosed when the kidneys do
not respond to ADH.
Can be triggered by certain drugs or
neoplasms or by damage to the
kidneys from pyelonephritis, polycystic
disease, or other causes.
Itmay also occur with infection of the
central nervous system (meningitis,
encephalitis, tuberculosis).
 PATHOPHYSIOLOGY
ADH - reabsorption of water by the
distal tubules and collecting ducts.
ADH lack, adequate reabsorption of
water prevented - diuresis.
Nephrogenic diabetes insipidus,
there is enough ADH but the kidneys
do not respond to it.
Patients may urinate from 3 to 15 L
per day ↑ serum osmolality and
dehydration.
 PATHOPHYSIOLOGY cont..
• ↑ osmolality and ↓ BP normally trigger
ADH secretion, causes water retention
and dilutes the blood; in patients with DI,
this does not occur.
• ↑ osmolality also leads to extreme thirst,
which usually causes the patient to drink
enough fluids to maintain fluid balance.
• In an unconscious patient or a patient
with a defective thirst mechanism,
however, dehydration may quickly occur
if the problem is not recognized and
corrected.
 Diabetes Insipidus
ADH is manufactured in the hypothalamus & stored ADH not
in the post. PG Produced or
Not transported

smoreceptors in the hypothalamus are stimulated by

increased plasma osmolality
Neurogenic
DI

Osmoreceptors stimulate the release of ADH

from the post PG ADH not
released

Nephrogenic DI: ADH travels to the kidneys, where

Kidneys do it acts upon the collecting ducts &
not respond to loop of Henle to increase reabsorption of water
ADH
As plasma osmolality returns to normal,
the osmoreceptor cells slow
the release of ADH
SIGNS AND SYMPTOMS
• The patient urinates frequently (polyuria), and
nighttime urination (nocturia) .
Urine specific gravity is decreased of 1.001 to
1.005, urine dilute and light in color and
contains no abnormal substances such as
glucose and albumin.
Patient has extreme thirst (polydipsia), takes
large volumes of water 2 to 20 liters.
Often patients crave ice-cold water.
The disease cannot be controlled by limiting
fluid intake because the high volume loss of
urine continues even without fluid replacement.
Attempt to restrict fluid causes the patient to
experience insatiable craving for fluid and to
develop hypernatremia and severe dehydration.
SIGNS AND SYMPTOMS Cont….
• If urine output exceeds fluid intake,
dehydration occurs, with characteristic
symptoms of hypotension, poor skin turgor,
and weakness.
• Hypovolemic shock occurs if fluid balance is
not restored.
• Dehydration and electrolyte imbalances
result in a decrease in level of
consciousness and death if the problem is
not corrected.
• The patient with DI may develop an
enlarged bladder and kidney damage from
constantly trying to “hold” too much urine.
 TEST RESULTS
Normal blood glucose indicating that diabetes
insipidus isn’t a complication of diabetes mellitus.
The fluid deprivation test- carried out by withholding
fluids for 8-12 hours or until 3% to 5% of the body
weight is lost. pt weighed frequently during the test.
Plasma and urine osmolality studies are performed at
the beginning and end of test. Inability to increase
the specific gravity and osmolarity of the urine is
characteristic of diabetes inspidus.
Pt continues to excrete large volumes of urine with
low specific gravity experiences weight loss, rising
serum osmolarity, and elevated serum sodium levels.
Pts condition needs to be monitored frequently during
the test, and test terminated if tachycardia, excessive
weight loss, or hypotension develops.
TEST RESULTS cont…
 Low specific gravity in urine due to increased
fluid in the urine.
 Increased BUN, indicating dehydration because
the concentration of solutes to fluid is rising.
Vasopressin challenge test.

If urine output decreases and urine specific
gravity increases, then the problem is with the
pituitary gland and kidneys are normal.

If urine output remains unchanged and urine
specific gravity remains low, then the pituitary
gland is normal and the kidneys are the
problem.
• Presence of a pituitary tumor or hypothalamus
tumor appear on an MRI.
 TREATMENT
• Objective of therapy is:
1. To replace ADH (which is usually long-term therapy
program)
2. To ensure adequate fluid replacement
3. To identify and correct the underlying intracranial
pathology.
Treatment of DI involves replacement of ADH.
In acute cases, vasopressin, a synthetic form of ADH,
is given by the intravenous or subcutaneous route or
desmopressin through the nasal route, along with
intravenous fluid replacement.
 Increase fluid intake until urination returns to normal.
Hypotonic intravenous (IV) fluids such as 0.45% saline
may be ordered to replace intravascular volume
without adding excessive sodium. IV fluids are
especially important if the patient is unable to take
TREATMENT cont..
• Place the patient on a low-salt diet to reduce
urine production in the kidneys.
• In patients who require long-term therapy,
synthetic ADH (desmopressin, or DDAVP) in the
form of a nasal spray is used, usually twice a day.
• Other drugs, such as chlorpropamide
(Diabinese), help the kidneys respond better to
ADH.
• Thiazide diuretics may decrease urine flow in the
absence of ADH (even though they usually are
used to increase urine output!).
• If a pituitary tumor is involved, treatment usually
involves removal of the pituitary gland
(hypophysectomy).
NURSING DIAGNOSES
• Risk for impaired urinary elimination.
• Impaired oral mucous membrane related to
inadequate oral secretions
• Deficient fluid volume related to excessive fluid
loss or inadequate fluid intake
NURSING INTERVENTION
• Maintain fluid and electrolyte balance.
• Monitor intake and output.
• Weigh the patient each day using the same scale,
at the same time of day, wearing similar clothing.
• Explain to the patient:
• Medication must be taken every day.
• Wear a medical alert necklace/bracelet to alert
health care providers that you have diabetes
insipidus.
Syndrome of Inappropriate
Antidiuretic
Hormone
SIADH is Secretion
caused by too (SIADH)
much ADH being
secreted by the posterior pituitary gland,
stimulating the kidneys to retain water
resulting in water intoxication.
ADH is responsible for controlling the
amount of water reabsorbed by the kidney;
it prevents the loss of too much fluid.
When too much water is detected, ADH
production or secretion is halted.
An increase in ADH activity is called
syndrome of inappropriate antidiuretic
hormone (SIADH).
 ETIOLOGY.
Neoplasms: lung, lymph, pancreas,
prostate, thymus and duodenum (these
cells produce a hormone identical to
ADH)
Neurologic: hemorrhage, infection,
trauma
Pulmonary: COPD, Acute resp failure,
lung abscess, TB, pneumonia (stimulates
ADH release as a result of hypoxia)
Medications: nicotine, morphine,
antineoplastic agents, haloperidol,
thiazide diuretics (either increase ADH
secretion or potentiate its action)
 PATHOPHYSIOLOGY
• SIADH results from too much ADH in the
body.
• This causes excess water to be reabsorbed
by the kidney tubules and collecting ducts,
leading to decreased urine output and fluid
overload.
• As fluid builds up in the bloodstream,
osmolality decreases and the blood becomes
diluted.
• Normally, a decreased serum osmolality
inhibits release of ADH.
• In SIADH, however, ADH continues to be
released, adding to the fluid overload.
 Pathophysiology of SIADH

Increased ADH secretion

eased permeability in the renal tubule

eased water retention

↓↓eased Plasma Dilutional Decreased Elevated

osmolality hyponatremia Aldosterone GFR
secretion

↓↓eased Na reabsorption in proximal tubule

eased Na secretion

Hyponatremia
SIGNS AND SYMPTOMS
Neurologic: headache, decreased
LOC, disorientation, hostile, irritability
(early signs of water intoxication),
lethargy, seizures ( as a result of
rapid onset of hyponatremia)
CVS: hypertension, tachycardia,
increased CVP, CHF, Personality
changes, confusion due to
hyponatremia
Renal: decreased urine output with
increased urine osmolality
GI: nausea, vomiting, diarrhoea
• Symptoms of fluid overload, such as
weight gain (usually without edema)
and dilutional hyponatremia
electrolyte imbalance.
• Because the osmolality of the blood is
low, fluid may leak out of the vessels
and cause brain swelling.
• If untreated, this results in lethargy,
confusion, seizures, coma, and death.
Manifestations of Dilutional
Hyponatremia

• Bounding pulse
• Elevated or normal blood pressure
• Muscle weakness
• Headache
• Personality changes
• Nausea
• Diarrhea
• Convulsions
• Coma
DIAGNOSTIC FINDINGS
• Serum and urine sodium levels and
osmolality are measured.
Serum ADH is high.
Additional testing may be done to
diagnose and locate an ADH
secreting tumor.
 Treatment
• Treatment aimed at eliminating the cause.
• A tumor secreting ADH, surgical removal
may be indicated.
• Symptoms may be alleviated by restricting
fluids to 800 to 1000 mL per 24 hours.
• Hypertonic saline fluids may be administered
intravenously, and oral salt may be
encouraged to maintain the serum sodium
level.
• With severe hyponatremia (<120mEq/l) or
when pt develops seizures, hypertonic saline
may be ordered. Use of hypertonic saline
(3%), caution, avoid rapid infusions!! Cause
 Treatment cont…
If the cause is inoperable cancer,
drugs such as furosemide (Lasix) and
demeclocycline (Declomycin) may be
used to block the action of ADH in
the kidney.
• To monitor fluid balance, assess vital
signs, weight, intake and output,
urine specific gravity, skin turgor,
and edema.
• Auscultate lung sounds for crackles,
a sign of fluid overload.
 Treatment cont…
• Determine the patient’s ability to
maintain a fluid restriction. Initiate
measures to alleviate thirst and dry
mouth by providing good oral care &
chilled beverages Instruct pt/ family on
the importance of water restriction.
• Assess level of consciousness and
neuromuscular function.
• Monitor laboratory tests, including
serum sodium level.
• Assess the patient’s understanding of
the disease process and treatment.
NURSING DIAGNOSES
• Risk for imbalanced fluid volume
• Excess fluid volume
NURSING INTERVENTION
• Monitor electrolytes to determine
sodium levels.
• Restrict fluid because excess fluid
dilutes sodium levels.
Weigh the patient daily using the
same scale, at same time of day
with similar clothing.
• Monitor intake and output.
ADRENAL DISORDERS
 Outline
Causes, clinical manifestations,
management, and nursing
interventions of:
◦Pheochromocytoma
◦ Addison’s Disease
◦Cushings syndrome
INTODUCTION
• Adrenal disorders may involve the adrenal
medulla or the adrenal cortex.
• A rare tumor of the adrenal medulla,
called a pheochromocytoma, causes
hypersecretion of epinephrine and
norepinephrine.
• Hyposecretion of epinephrine is rare and
generally causes no symptoms.
• Hypersecretion of cortisol from the
adrenal cortex results in Cushing’s
syndrome.
• Hypofunction of the adrenal cortex results
in Addison’s disease.
 Pheochromocytoma
Pathophysiology
• A pheochromocytoma is an uncommon tumor
that arises from the chromaffin cells of the
adrenal medulla.
• May occur outside the adrenal gland.
• The tumor autonomously secretes
catecholamines in excessive amounts.
• Ninety (90)percent of pheochromocytomas
are benign.
In the remaining patients(10%), it occurs in
the extra-adrenal chromaffin tissue located in
or near the aorta, ovaries, spleen, or other
organs.
Etiology
• The cause of pheochromocytoma is unknown.
• About 5% of cases are hereditary.
May occur at any age, but its peak incidence is
between ages 40 and 50 years
10% of the tumors are bilateral, and 10% are
malignant.
Signs and Symptoms
• Patients exaggerated fight or- flight symptoms
which might be constant, or occur in “attacks.”
• Manifestations include hypertension,
tachycardia (heart rate > 100), palpitations,
tremor, diaphoresis, feeling of apprehension,
and severe pounding headache.
 Signs and Symptoms cont..
Nausea and vomiting occasionally
present.
Blood glucose may increase
catecholamines inhibit insulin release
Constipation may occur because
catecholamines relax the bowel.
Most prominent characteristic is
intermittent unstable hypertension.
Diastolic pressure may be greater than
115 mm Hg.
Signs and Symptoms cont…
• Hypertension uncontrolled , the patient is at risk
for stroke, vision changes, and organ damage.
• About 0.2% of cases of hypertension caused by
pheochromocytoma.
Diagnosis
Pheochromocytoma is suspected if signs of
sympathetic nervous system overactivity occur
in association with marked elevation of blood
pressure. This signs can be associated with the
“five Hs”: hypertension, headache, hyperhidrosis
(excessive sweating), hypermetabolism, and
hyperglycemia.the presence of these signs has a
93.8% specificity an a 90.9% sensitivity for
pheochromocytoma with a 99% certinity.
Diagnostic Tests cont..
Measures of urine and plasma levels of
catecholamines are the most direct and conclusive
tests for overativity of the adrenal medulla.
Measurement of urine catecholamine metabolites
(metanephrines[MN] and vanillylmandelic acid [VMA])
or free catecholamines are the stardard diagnostic
tests used in the diagnosis of pheochromocytoma.
The levels can be as high as three times the normal
limits. A 24-hour specimen of urine is collected for
determining free catecholamine .
The patient should avoid caffeine and medications for
2 days before and during the test. (coffee, tea,
bananas, chocolate, vanilla, aspirin)
Check institution policy for other dietary restrictions.
 If results are elevated, a CT scan or MRI is done to
locate the tumor.
 Therapeutic Interventions
• Treatment for pheochromocytoma is surgical removal
of one or both adrenal glands (adrenalectomy).
• Pt may be nursed in ICU for monitoring of ECG changes
and careful administration of alpha adrenergic blocking
agents (e.g. phentolamine) or smooth muscle
relaxants (e.g. sodium nitroprusside) to lower the
blood pressure quickly.
• NB, the patient must be stabilized before surgery.
• Alpha-blocking medications such a phenoxybenzamine
(Dibenzyline) may be used when the blood pressure is
stable to prepare the patient for surgery, (dilate blood
vessels to control acute hypertension. )
• Beta-blocking medication e.g. propranolol (inderal)
may be added to block beta-adrenergic receptors in
the heart and lungs, reducing other fight-or-flight
symptoms.
 Nursing care
Monitor vital signs and report elevated pulse
and blood pressure promptly.
Prompt treatment helps prevent complications.
Approach the patient calmly and maintain a
quiet environment.
Stress may precipitate a hypertensive episode.
Administer alpha and beta blockers as ordered
to control symptoms.
During an episode or attack of hypertension,
tachycardia, anxiety, and the other symptoms
of pheochromocytoma, the patient I placed on
bed rest with the head of the bed elevated to
promote an orthostatic decrease in blood
pressure.
 Nursing care cont…
Teach the patient how the
medications will reduce symptoms,
and the importance of avoiding
foods and beverages containing
caffeine, so the patient can
participate in self-care.
• If patient has surgery, continue
careful monitoring as manipulation
of tumor can increase catecholamine
release.
Find nursing diagnosis for this client.
 Adrenocortical Insufficiency/
Addison’s Disease

Adrenocortical insufficiency (AI) is

the insufficient production of the
hormones of the adrenal cortex.
Primary AI is called Addison’s
disease.
Results when adrenal cortex function
is inadequate to met the patient’s
needs for the cortical hormones.
 Pathophysiology
• Adrenal insufficiency is associated with reduced
levels of cortisol, aldosterone, or both
hormones.
• A deficiency in androgens may exist.
• primary disease, ACTH levels from the
pituitary may be elevated in an attempt to
stimulate the adrenal cortex to synthesize more
hormone.
• Secondary disease, deficient ACTH fails to
stimulate adrenal steroid synthesis.
• In most cases, the adrenal glands are atrophied,
small, and misshapen and are unable to produce
adequate amounts of hormone.
Primary Adrenal Secondary Adrenal
Insufficiency Insufficiency
Is caused by destruction of Is caused by inadequate
the adrenal cortex, causing secretion of ACTH by the
decreased secretion of APG, resulting in secretion
aldosterone & of glucocorticoids (but
glucocorticoids. secretion of
-80% is autoimmune mineralocorticoids remains
disease unaffected). Due to;
-TB is 2nd most common -Hypothalamic or pituitary
cause dse
-Adrenalectomy -Suppression of HPA axis
-Sepsis by steroids therapy then
-Cancer abrupt discontinuation of
-Infections that therapy
-Drugs
05/22/2025 86
Etiology

Addison’s disease is thought to be

autoimmune; that is, the gland destroys itself
in response to conditions such as
tuberculosis, fungal infection, infection
related to acquired immunodeficiency
syndrome (AIDS), or metastatic cancer.
May be associated with other autoimmune
diseases, such as Hashimoto’s thyroiditis.
Surgical removal of both adrenal glands.
Inadequate secretion of ACTH from the
pituitary gland also results in adrenal
insufficiency because of decreased
stimulation of the adrenal cortex.
 Etiology cont..
• Adrenalectomy also results in adrenal
insufficiency.
• Secondary AI due to dysfunction of the
pituitary or hypothalamus.
• Prolonged use of corticosteroids may
depress ACTH and corticotropin
releasing hormone production, in turn
reduces hormone production.
• long-term corticosteroid therapy is
particularly at risk for AI if the drugs are
abruptly discontinued.
Signs and Symptoms

Most significant sign of Addison’s

disease is hypotension.
This is related to the lack of
aldosterone.
Low cortisol levels cause
hypoglycemia, weakness, fatigue,
weight loss, confusion, and
psychosis.
Mental status changes such as
depression, emotional lability,
apathy, and confusion are present in
 Signs and Symptoms

cont…
In primary AI, increased ACTH may
produce hyperpigmentation of the
skin, causing the patient to have a
tanned or bronze appearance.
Anorexia, nausea, and vomiting may
also occur, possibly as the result of
electrolyte imbalances.
Women may have decreased body
hair because of low androgen levels.
 Complications

Ifa patient is exposed to stress, such

as infection, trauma, or psychological
pressure, the body may be unable to
respond normally with secretion of
cortisol and an adrenal crisis can
occur.
Loss of large amounts of sodium and
water and the resulting fluid volume
deficit cause profound hypotension,
dehydration, and tachycardia.
Potassium retention can cause
 Addisonian crisis
Characterized by cyanosis and classic
signs of circulatory shock: pallor,
apprehension, rapid and weak pulse,
rapid respirations, and low BP.
Patient may complain of headache,
nausea, abdominal pain, diarrhea and
show signs of confusion and restlessness.
Even slight overexertion, exposure to
cold, acute infections, or a decrease in
salt intake may lead to circulatory
collapse, shock, and death if untreated.
 Complications cont…
• Hypoglycemia may be severe.
• Coma and death result if treatment is
not initiated.
• Treatment of adrenal crisis involves
rapidly restoring fluid volume and
cortisol levels.
• Intravenous fluids (containing glucose)
and large doses of glucocorticoids are
administered.
• Electrolytes are replaced as needed.
• The cause of the crisis should be
identified and treated.
 Diagnostic Tests
Laboratory findings include decreased blood
glucose (hypoglycemia)and sodium
(hyponatremia) levels, an increased serum
potassium(hyperkalemia) level, and an
increased white blood cell
count(leukocytosis).
Diagnosis is confirmed by low levels of
adrenocortical hormones in the blood or urine
and decreased serum cortisol levels.
Blood urea nitrogen (BUN) and hematocrit
levels may appear to be elevated because of
dehydration.
An ACTH stimulation test may help determine
whether the adrenal glands are functioning.
 Therapeutic Interventions
Immediate treatment to combat circulatory
shock: restoring blood circulation,
administer fluids and corticosteroids,
monitoring vital signs, and placing the
patient in a recumbent position with the
legs elevated.
Hydrocortisone is administered IV, followed
with 5% dextrose in normal saline.
Vasopressor amines if hypotension persists.
Antibiotics if infection has precipitated
adrenal crisis in a patient with chronic
adrenal insufficiency.
 Therapeutic Interventions

• Patient also assessed to identify other factors,

stressors, or illnesses that led to the acute
episode.
• Long-term treatment consists of replacement
of glucocorticoids (hydrocortisone) and
mineralo-corticoids (fludrocortisone).
• Patients will need hormone replacement
therapy for the rest of their lives.
• Hormones are given in divided doses, with
two-thirds of the daily dose given in the
morning and one-third in the evening to
mimic the body’s own diurnal rhythm.
• The patient may also be placed on a high-
sodium diet.
 Nursing Process for the Patient
with Addison’s Disease

ASSESSMENT/DATA COLLECTION.
• The patient with Addison’s disease should be
assessed for understanding of and compliance with
the treatment regimen.
• Monitor daily weights or intake and output to track
fluid status.
• Monitor serum glucose levels and symptoms of
hyperkalemia and hyponatremia.
• Report changes in mental status.
• If the patient is in crisis, monitor vital signs closely
and report any signs of fluid volume deficit such as
orthostatic hypotension or poor skin turgor, check the
mucous membranes for dryness, weigh the patient
and instruct the patient to report increased thirst,
which may indicate impending fluid imbalance.
 NURSING DIAGNOSIS, PLANNING,
AND IMPLEMENTATION
Risk for deficient fluid volume related to
deficient adrenal cortical hormones
EXPECTED OUTCOME: Fluid volume will
be stable as evidenced by stable
weights and vital signs, and skin turgor
within normal limits.
Monitor fluid status and report changes
promptly so treatment can be initiated.
• Administer steroid replacements as
ordered to maintain fluid and electrolyte
balance.
• Risk for ineffective health maintenance
related to deficient knowledge about self-
care of Addison’s disease
• EXPECTED OUTCOME: The patient will
verbalize understanding of self-monitoring
and self-medication at home.
• Assess patient’s understanding of his or
her disease process and treatment.
• Teaching should build on baseline
knowledge.
• Teach the patient the importance of
hormone replacement.
• Doses are generally taken two-thirds in the
morning and one-third in the evening.
The patient who does not secrete
endogenous adrenocortical hormones
must rely on replacements.
Help the patient identify the causes and
symptoms of stress, and explain the
need to increase medication
Advise patient he or she may need to
increase salt intake in hot weather
because of fluid and salt losses.
Recommend medical alert identification
to the patient.
Teach the patient and significant other
how to use an emergency intramuscular
hydrocortisone injection kit.
EVALUATION.
If nursing care is effective, the
patient’s fluid status will be stable,
and the patient and family will be
able to describe proper self-care of
Addison’s disease.
 Cushing’s Disease/ Syndrome
Cushing’s disease is
characterized by excess cortisol
secretion resulting from
secretion of too much
adrenocorticotropic hormone
(ACTH) by the pituitary.
Cushing’s syndrome also refers
to symptoms of cortisol excess
caused by other factors.
 Pathophysiology
• Cortisol, aldosterone, and androgens are the
steroid hormones secreted by the adrenal
cortex.
• Cortisol essential for survival - normally
secreted in a diurnal rhythm, levels increasing
in the early morning.
• Cortisol affects sugar (carbohydrate)
metabolism.
• Secretion is increased during times of stress.
• In Cushing’s syndrome, cortisol is hypersecreted
without regard to stress or time of day.
• When levels of cortisol are very high, effects
related to excess aldosterone and androgens
are also seen.
Etiology
• Cushing’s disease is caused by the
hypersecretion of ACTH by the pituitary. This
is most often the result of a pituitary adenoma.
• Sometimes ACTH is produced by a tumor in
the lungs or other organs.
• The high levels of ACTH cause adrenal
hyperplasia, which in turn increases production
and release of cortisol.
• The most common cause of Cushing’s
syndrome is prolonged use of glucocorticoid
medication (e.g., prednisone) for chronic
inflammatory disorders such as rheumatoid
arthritis, chronic obstructive pulmonary
disease, and Crohn’s disease.
Signs and Symptoms
• Related to excess cortisol levels. Weight gain,
truncal obesity with thin arms and legs, buffalo
hump, and moon face result from deposits of
adipose tissue at these sites.
• Cortisol also causes insulin resistance and
stimulates gluconeogenesis, which result in
glucose intolerance.
• Some patients develop secondary diabetes
mellitus.
• Muscle wasting and thin skin with purple striae
occur as a result of cortisol’s catabolic effect on
tissues.
• Catabolic effects on bone lead to osteoporosis,
pathological fractures, and back pain from
compression fractures of the vertebrae.
Signs and Symptoms
• Because cortisol has anti-inflammatory and
immunosuppressive actions, the patient is at
risk for infection.
• Hyperpigmentation of the skin may occur.
• Approximately 50% of patients experience
mental status changes from irritability to
psychosis (sometimes referred to as steroid
psychosis).
• Sodium and water retention are related to the
mineralocorticoid effect.
• As sodium is retained, potassium is lost in the
urine, causing hypokalemia.
• Androgen effects include acne, growth of facial
hair, and amenorrhea in women.
Cushing’s syndrome
• Cushing’s Syndrome
– Characterized by:
• truncal obesity
• moon face
• buffalo hump
• acne, hirsutism
• abdominal striae
• hypertension
• psychiatric disturbances
• osteoporosis
• Amenorrhea
• Diabetes
Frequency of signs and symptoms in
Cushing’s syndrome
Sign Occurrenc Sign Occurrence
e% %
or or
symptom symptom

Central obesity 94 Easy bruisability 60

Hypertension 82 Osteoporosis 60
Glucose intolerance 80 Personality changes 55

Hirsutism 75 Acne 50
Amenorrhea or impotency 75 Edema 50

Purple striae 65 Headache 40

Plethoric faces 60 Poor wound healing 40
Diagnostic Tests
• Indicators of Cushing's syndrome include an
increase in serum sodium and blood glucose
levels and a decreased serum concentration of
potassium, a reduction in the number of blood
eosinophils and disappearance of lymphoid
tissue.
• Suspicion of Cushing’s disease or syndrome may
initially be based on a cushingoid appearance.
• Plasma and urine cortisol and plasma ACTH are
measured. Several blood samples may be
collected to determine whether the normal
diurnal variation in plasma levels is present, this
variation is frequently absent in adrenal
dysfunction.
• A 24-hour urine test for cortisol may be collected.
• An overnight dexamethasone
suppression test may be done to
diagnose for pituitary and adrenal causes
of Cushings syndrome. Dexamethasone 1
mg is administered orally at 11pm, ad
plasma cortisol level is obtained at 8 the
next morning. Suppression of corisol to
less than 5 mg/dL indicates that the
hypothalamic-pituitary-adrenal axis is
functioning properly
• Serum potassium is measured.
• Additional tests to locate the cause of
excess endogenous cortisol may be done.
Therapeutic Interventions
• If a pituitary or other ACTH-secreting tumor is
present, surgical removal or radiation therapy
to the pituitary may be employed.
• If the adrenals are the primary cause of the
problem, radiation or removal of the adrenal
gland or glands maybe performed.
• Drugs such as adrenal enzyme inhibitors (e.g.
ketoconazole, metyrapone, aminoglutethimide,
mitotane) block production of adrenal steroids.
• If the cause of Cushing’s syndrome is
administration of steroid medication, an
attempt is made to reduce or taper the
medication to the minimum dosage needed to
treat the underlying disease process.
Therapeutic Interventions
Usually steroids are prescribed as a
last resort for chronic disorders that are
unresponsive to other treatment.
The patient and physician must weigh
the risks and benefits of continuing the
medication.
a high-potassium, low-sodium, high-
protein diet may be ordered. Potassium
supplements may be ordered.
If the patient has high blood sugar,
appropriate therapy for diabetes
should be instituted.
Pre treatment Post treatment
Nursing Process for the Patient
With Cushing’s Disease

• ASSESSMENT/DATA COLLECTION.
• When caring for the patient with Cushing’s
disease or syndrome, assess the patient’s
drug history.
• Monitor vital signs and complications
related to fluid and sodium excess.
• Auscultate the lungs for crackles, and
assess extremities for edema.
• Assess skin integrity, and monitor capillary
glucose as ordered by the physician.
• Watch for signs of infection.
Possible nursing diagnosis
 Risk for injury related to weakness
 Risk for infection related to altered protein
metabolism and inflammatory response.
 Self care deficit related to weakness,
fatigue, muscle wasting and altered sleep
patterns.
 Impaired skin integrity related to edema,
impaired healing, and thin and fragile skin.
 Disturbed body image related to altered
physical appearance, impaired sexual
functioning, and decreased activity level.
 Disturbed thought process related to
mood swings, irritability, and depression.
Nursing Care of the Patient
Undergoing Adrenalectomy
Preoperative Care
• Monitor the patient for electrolyte
imbalance and hyperglycemia.
• Abnormalities must be corrected before
surgery.
• To prevent adrenal crisis, glucocorticoids
are administered because removal of the
adrenals causes a sudden drop in adrenal
hormones.
• Prepare the patient for adrenalectomy or
hypophysectomy, depending on which
surgery will be performed.
Postoperative Care
• Following adrenalectomy, the patient
receives routine postoperative care.
• In addition, the patient is closely
monitored for changes in fluid and
electrolyte balance and adrenal crisis.
• Patients who undergo bilateral
adrenalectomy must take replacement
glucocorticoid and mineralocorticoid
hormones for the remainder of their life.
• If only one adrenal gland is removed, the
remaining gland should eventually produce
enough hormone to enable the patient to
discontinue replacement hormone.
DISORDERS OF THE
THYROID GLAND
 Introduction
Triiodothyronine (T3) and thyroxine
(T4) are thyroid hormones secreted
by the thyroid gland.
These hormones may be
collectively referred to as thyroid
hormone (TH).
Deficient secretion of TH results in
hypothyroidism; excess TH results
in hyperthyroidism.
 Introduction cont…
Thyroid disorders are difficult to
detect because symptoms are vague
until the disease advances to a
severe level.
Treatment often is long term, and the
client requires periodic follow-up to
monitor response.
Thyroid disorders include
hyperthyroidism, thyrotoxic crisis,
hypothyroidism, thyroid tumors, and
endemic and multinodular goiters.
 Hypothyroidism
Hypothyroidism occurs primarily in
women 30 to 60 years old.
If hypothyroidism occurs in an
infant, the result is cretinism.
Hypothyroidism that develops in an
adult is called myxedema.
 Pathophysiology

• Primary hypothyroidism occurs when the thyroid gland

fails to produce enough TH even though there is enough
(TSH).
• The pituitary responds to the low level of TH by
producing more TSH.
• Secondary hypothyroidism is caused by low levels of
TSH, which fail to stimulate release of TH.
• Tertiary hypothyroidism results from inadequate release
of thyrotropin-releasing hormone (TRH), secreted by the
hypothalamus.
• Thyroid hormones responsible for metabolism, low levels
result in a slowed metabolic rate, which causes many of
the characteristic symptoms of hypothyroidism.
• Other symptoms related to myxedema, which refers to a
nonpitting type of edema that occurs in connective
tissues throughout the body.
 Etiology
• Primary hypothyroidism may be a result of a
congenital defect, inflammation of the thyroid
gland, or iodine deficiency.
• Hashimoto’s thyroiditis - autoimmune
disorder that eventually destroys thyroid
tissue, leading to hypothyroidism.
• Secondary or tertiary hypothyroidism may be
caused by a pituitary or hypothalamic lesion or
by postpartum pituitary necrosis, a rare disorder
in which the pituitary is destroyed following
pregnancy and delivery.
• Treatment of hyperthyroidism with medication
or thyroidectomy, can lead to secondary
hypothyroidism.
• Peripheral resistance to TH may also occur.
 Signs and Symptoms
• Manifestations include fatigue, weight
gain, bradycardia, constipation, mental
dullness, feeling cold, shortness of breath,
decreased sweating, dry skin and hair.
• Heart failure may occur because of
decreased pumping strength of the heart.
• Altered fat metabolism causes
hyperlipidemia.
• Myxedema causes water retention, with
puffiness in the face, eye area, and feet.
• Fluid may also accumulate around the
heart, causing altered cardiac function.
 Complications
• If the metabolic rate drops so low
that it becomes life threatening, the
result is myxedema coma.
• Usually occurs in patients with
longstanding, untreated
hypothyroidism and can be triggered
by stress, such as infection, trauma,
or exposure to cold.
• The patient becomes hypothermic,
with a temperature less than 95F
(35C) and a decreased respiratory
rate.
• Depressed mental function and lethargy may
occur.
• Blood glucose drops.
• Cardiac output drops, which in turn can
reduce perfusion of kidneys.
• Nonpitting edema of the hands and feet may
develop.
• Death may occur as a result of respiratory
failure.
• Note changes in mental status or vital signs,
take immediate action.
• Treatment involves intubation and mechanical
ventilation, patient rewarmed with blankets.
• Intravenous levothyroxine (Synthroid) is
given, and any underlying cause is treated.
 Diagnostic Tests
• T3 and T4 levels are low, and TSH
may be high or low, depending on the
cause.
• If the pituitary is functioning normally,
TSH is elevated in an attempt to
stimulate an increase in TH.
• Serum cholesterol and triglycerides
are elevated.
• Antibodies are usually present in
autoimmune disease.
 Therapeutic Interventions
Primary hypothyroidism is
treated with oral thyroid
replacement hormone.
Main treatment synthetic thyroid
hormone(levothyroxine).
Doses are started low and are
slowly increased to prevent
symptoms of hyperthyroidism or
cardiac complications.
 Nursing Diagnosis
Activity intolerance related to
fatigue
Constipation related to slowed
gastrointestinal motility
Impaired skin integrity related to
dry skin, inactivity
Imbalanced nutrition, more than
body requirements, related to
decreased metabolic rate
 Hyperthyroidism
Hyperthyroidism is most often
diagnosed in young women.
Graves’ disease, which is one cause of
hyperthyroidism, is more common in
young women.
Multinodular goiter more common in
older women.
Pathophysiology
Hyperthyroidism results in excessive
amounts of circulating thyroid hormone
(thyrotoxicosis).
• Primary hyperthyroidism occurs when a
problem within the thyroid gland causes
excess hormone release.
• Secondary hyperthyroidism due to excess TSH
release from the pituitary, causing
overstimulation of the thyroid gland
• Tertiary hyperthyroidism caused by excess
TRH from the hypothalamus.
• A high level of thyroid hormone increases the
metabolic rate.
• It is also believed to increase the number of
beta-adrenergic receptor sites in the body,
which enhances the activity of norepinephrine.
• Resulting fight-or-flight response the cause of
many of the symptoms of hyperthyroidism.
 Etiology
• A variety of disorders can cause
hyperthyroidism.
• Graves’ disease the most common cause;
thought to be an autoimmune disorder as
thyroid-stimulating antibodies are present
in the blood of affected patients.
• Multinodular goiter, in which thyroid
nodules secrete excess TH, is also
sometimes associated with
hyperthyroidism.
• A pituitary tumor may secrete excess TSH,
which over stimulates the thyroid gland. A
thyroid tumor may secrete TH.
 Etiology
• Patients taking thyroid hormone for
hypothyroidism may take too much.
• Each of these problems can cause
excess circulating TH and symptoms
of hyperthyroidism.
• Radiation exposure may predispose
a patient to develop
hyperthyroidism.
• Heredity may also play a role in
autoimmune hyperthyroidism.
 Signs and Symptoms
• Many signs and symptoms related to the
hypermetabolic state, such as heat
intolerance, increased appetite with weight
loss, and increased frequency of bowel
movements.
• Nervousness, tremor, tachycardia, and
palpitations are caused by the increase in
sympathetic nervous system activity, more
common in younger patients.
• Heart failure may occur because of
tachycardia and the resulting inefficient
pumping of the heart.
• If treatment is not begun, the patient may
become manic or psychotic.
 Signs and Symptoms cont..
• Additional signs that occur only with
Graves’ disease include thickening of the
skin on the anterior legs and exophthalmos
(bulging of the eyes; caused by swelling of
the tissues behind the eyes. Other eye
changes include photophobia and blurred
or double vision.
• Elderly patients may not exhibit the typical
signs and symptoms of hyperthyroidism so
be especially alert for this.
• These patients may present with heart
failure, atrial fibrillation, fatigue, apathy,
and depression.
 Complications
THYROTOXIC CRISIS (thyroid storm)
is a severe hyperthyroid state that
can occur in hyperthyroid individuals
who are untreated or who are
experiencing another illness or
stressor.
May also occur following thyroid
surgery in patients who have been
inadequately prepared with
antithyroid medication.
Thyrotoxic crisis can result in death in
as little as 2 hours if untreated.
 Thyrotoxic crisis cont…
Symptoms include tachycardia, high
fever, hypertension (with eventual
heart failure and hypotension),
dehydration, restlessness, and delirium
or coma.
If thyrotoxic crisis , treatment first
directed toward relieving the life-
threatening symptoms.
Acetaminophen is given for the fever
(Aspirin is avoided binds with the same
serum protein as T4, freeing additional
T4 into the circulation
 Complications cont..
• Intravenous fluids and a cooling
blanket may be ordered to cool the
patient.
• A beta-adrenergic blocker, such as
propranolol, is given for tachycardia.
• Oxygen is administered and the head
of the bed is elevated because the
high metabolic rate requires more
oxygen.
• Once symptoms are controlled and the
patient is safe, the underlying thyroid
problem is treated.
 Complications cont…
HYPOTHYROIDISM.
• This can occur as a result of long-
term disease or as a result of
treatment.
• Patients with a history of
hyperthyroidism should be
monitored for recurrent
hyperthyroidism or the onset of
hypothyroidism.
 Diagnostic Tests
• Serum levels of T3 and T4 are elevated.
• TSH is low in primary hyperthyroidism or
high if the cause is pituitary.
• A thyroid scan can be done to locate a
tumor.
• The thyroid gland may be enlarged;
palpation of the thyroid in a patient
suspected to be hyperthyroid should only
be performed by a physician.
• TSI (thyroid-stimulating immunoglobulin)
is present in Graves’ disease.
 Therapeutic Interventions
• Propylthiouracil and methimazole inhibit the
synthesis of TH.
• Propranolol (Inderal) is a beta-blocking
medication that relieves the sympathetic
nervous system symptoms.
• Oral iodine suppresses the release of thyroid
hormone.
• Radioactive iodine (131I or RAI) may be used
to destroy a portion of the thyroid gland.
• Dietary iodine normally goes to the thyroid
gland, where it is used to make thyroid
hormone. When RAI is given, the radioactivity
destroys some of the cells that make thyroid
hormone.
 Therapeutic interventions cont…
• Sometimes medications alone control
hyperthyroidism.
• If medications do not control
hyperthyroidism, surgery is planned.
• Antithyroid medications are given to calm
the thyroid before surgery.
• Iodine also reduces the vascularity of the
thyroid gland, decreasing the risk of
bleeding during surgery.
• Adequate preparation of the patient is
important because a euthyroid state helps
prevent a postoperative thyrotoxic crisis.
 Goiter
Pathophysiology and Etiology
• Enlargement of the thyroid gland.
• The thyroid gland may enlarge in
response to increased TSH levels.
• TSH is elevated in response to low TH,
iodine deficiency, pregnancy, or viral,
genetic, or other conditions.
• Goiter caused by iodine deficiency or
other environmental factors, is called
an endemic goiter.
• Some foods and medications are
goitrogens.
• These interfere with the body’s use of
iodine and include such foods as turnips,
cabbage, broccoli, horseradish, cauliflower,
and carrots.
• Medications include propylthiouracil,
sulfonamides, lithium, and salicylates
(aspirin).
• A goiter may be associated with a
hyperthyroid, hypothyroid, or euthyroid
state.
• Goiter that occurs with hyperthyroidism is
sometimes called a toxic goiter.
• Once the cause of the goiter is removed,
the gland usually returns to normal size.
Signs and Symptoms
• The thyroid gland is enlarged, and
swelling may be apparent at the
base of the neck.
• Alternatively, it may enlarge
posteriorly, which can interfere with
swallowing or breathing.
• The patient may have a full
sensation in the neck.
• Symptoms of hypothyroidism or
hyperthyroidism may be present.
Diagnostic Tests
A thyroid scan shows an
enlarged thyroid gland.
Serum T3 and T4 levels are
measured to determine
thyroid function.
Additional diagnostic studies
may be done to determine
the cause or evaluate the size
of the gland.
Therapeutic Interventions
• Treatment is aimed at the cause.
• If goitrogens are suspected, the patient is
given a list of foods to be avoided.
• If iodine deficiency is a problem, it is
added to the diet with supplements or
iodized salt.
• Hypothyroidism or hyperthyroidism is
treated if indicated.
• Levothyroxine (Synthroid) may be given to
reduce TSH levels via negative feedback.
• A thyroidectomy may be necessary if the
gland is interfering with breathing or
swallowing.
Nursing Care
• Be careful to assess the effect of the goiter on
breathing and swallowing.
• Stridor, a whistling sound, may be heard if the
airway is obstructed.
• Stridor is an ominous sign and should be
reported immediately.
• If the patient experiences difficulty
swallowing, liaise with the physician and
collaborate with the dietitian to provide soft
foods or liquid nutrition.
• A swallowing study might be ordered, which
can assist a speech pathologist or other
expert to make specific recommendations for
safe swallowing.
 Cancer of the Thyroid Gland
Though rare, it is the most common cancer
of the endocrine system.
Women more often than men.
Most tumors of the thyroid gland are not
malignant.
Etiology
• Thyroid hyperplasia may lead to thyroid
cancer.
• Other causes include exposure to radiation,
iodine deficiency, and prolonged exposure to
goitrogens.
• Tendency to develop some forms of thyroid
cancer is inherited.
Signs and Symptoms
• A hard, painless nodule palpable on the
thyroid gland.
• Difficulty breathing or swallowing or changes
in the voice may occur if the tumor is near the
esophagus and trachea.
• Most patients with thyroid cancer have
normal TH levels.
Diagnostic Tests
• A thyroid scan shows a “cold” nodule because
malignant tumors of the thyroid do not take
up the radioactive iodine administered for the
scan.
• A fine-needle aspiration biopsy confirms the
diagnosis.
Diagnostic Tests
• A thyroid scan shows an enlarged thyroid
gland.
• Serum T3 and T4 levels are measured to
determine thyroid function.
• Additional diagnostic studies may be done
to determine the cause or evaluate the
size of the gland.
Therapeutic Interventions
• A partial or total thyroidectomy may be
done.
• Chemotherapy, radioactive iodine
therapy, or external beam radiation may
also be used, alone or following surgery.
Nursing Process for the Patient
Undergoing Thyroidectomy

• Patients may undergo thyroidectomy for

cancer of the thyroid, hyperthyroidism, or
a goiter that is causing dyspnea or
dysphagia.
• A total thyroidectomy is usually
performed if cancer is present.
• After a total thyroidectomy, lifelong
replacement hormone must be taken.
• A subtotal (partial) thyroidectomy may be
done for hyperthyroidism, leaving a
portion of the thyroid gland to secrete TH.
 Preoperative Care
• Before undergoing a thyroidectomy, the
patient should be in a euthyroid state
accomplished with the use of antithyroid
medication.
• Saturated solution of potassium iodide (SSKI)
may also be administered to decrease the
size and vascularity of the gland, reducing
the risk of bleeding during surgery.
• A baseline assessment of vital signs and
voice quality, so you can compare findings
postoperatively.
• Explain what the patient can expect before,
during, and after surgery and clarify
misconceptions.
Preoperative teaching should include how to
perform gentle range-of-motion exercises of the
neck, how to support the neck during position
changes, and how to use an incentive
spirometer after surgery.
Postoperative Care
• Assessment/data collection.
• Monitor vital signs, oxygen saturation, drain
(if present), and dressings every 15 minutes
initially, progressing to every 4 hours, as
ordered.
• Decreased blood pressure with increased pulse
should alert you to the possibility of shock
related to blood loss.
• Tachycardia and fever, along with mental status
changes, may indicate thyrotoxic crisis.
• Check the back of the neck for pooling of
blood.
• Because of the location of the surgery,
observe for signs of respiratory distress,
including an increase in respiratory rate,
dyspnea, or stridor.
• Ask the patient to speak to detect
hoarseness of the voice, which may
indicate trauma to the recurrent laryngeal
nerve.
• Monitor the patient’s serum calcium levels
and watch for evidence of tetany.
• Report abnormal findings to the physician
immediately.
 NURSING DIAGNOSIS,
Risk for ineffective airway
clearance due to edema at
surgical site
Risk for injury (tetany, thyrotoxic
crisis) related to surgical
procedure
Pain related to surgical procedure
Risk for ineffective health
maintenance related to knowledge
deficit
EVALUATION.
Ifthe plan has been effective,
complications caused by surgery
will not occur or will be recognized
and reported early.
Pain will be prevented or controlled,
and the patient will demonstrate
understanding of dietary
modifications and postoperative
self-care.
Complications
Thyrotoxic crisis.
Thyrotoxic crisis may result from manipulation
of the thyroid gland during surgery, with the
subsequent release of large amounts of
thyroid hormone.
This is a rare complication because the use of
antithyroid drugs before surgery has become
routine.
TETANY.
• Tetany is caused by low calcium levels and is
characterized by tingling in the fingers and
perioral area (around the mouth), muscle
spasms, twitching, and cardiac dysrhythmias.
• Muscle spasms in the larynx can lead to
respiratory obstruction.
• Watch carefully for symptoms of tetany and
report them immediately if they occur
because if the problem is not recognized
quickly, death can result.
• Tetany can occur if the parathyroid glands
are accidentally removed during thyroid
surgery.
• Because of the proximity of the parathyroid
glands to the thyroid, it is sometimes
difficult for the surgeon to avoid them. In
the absence of parathyroid hormone, serum
calcium levels drop and tetany results.
• Intravenous calcium gluconate is given to
treat acute tetany.
 DISORDERS OF THE
PARATHYROID GLANDS
Parathyroid glands secrete parathyroid
hormone (PTH) in response to low
serum calcium levels.
PTH raises serum calcium levels by
promoting calcium movement from
bones to blood and by increasing
absorption of dietary calcium.
Decreased PTH activity is called
hypoparathyroidism.
Increased PTH activity is called hyper -
parathyroidism.
 Hypoparathyroidism

Pathophysiology
• A decrease in PTH causes a decrease in
bone resorption of calcium, a decrease in
calcium absorption by the GI tract, and
decreased resorption in the kidneys.
• This means that calcium stays in bones
instead of being moved into the blood, and
more calcium is excreted from the body.
• The result is a decreased serum calcium
level (hypocalcemia).
• As calcium levels fall, phosphate levels
rise.
Etiology
• The most common causes of
hypoparathyroidism are heredity and the
accidental removal of the parathyroid glands
during thyroidectomy.
• Because of the proximity of the glands to the
thyroid, it is sometimes difficult to avoid
removing them.
• Hypoparathyroidism also occurs following
purposeful removal of the parathyroid glands
for hyperparathyroidism or cancer.
• Another cause is hypomagnesemia, which
impairs secretion of PTH.
• Hypomagnesemia can occur with chronic
alcoholism or certain nutritional problems.
Signs and Symptoms
• Calcium plays an important role in nerve
cell stability.
• Hypocalcemia causes neuromuscular
irritability.
• In acute cases, tetany may occur with
numbness and tingling of the fingers and
perioral area, muscle spasms, and
twitching.
• Positive Chvostek’s and Trousseau’s signs
are early indications of tetany.
• To check Chvostek’s sign, tap on the
patient’s facial nerve just in front of the ear.
• Spasm of the face is a positive result,
indicating hypocalcemia.
• To elicit Trousseau’s sign, place a
sphygmomanometer on the patient’s arm and
pump it to above the patient’s systolic pressure.
• Spasm of the thumb and fingers occurs within 3
minutes if the patient has hypocalcemia.
• In chronic hypoparathyroidism, the patient is
lethargic and experiences muscle spasms.
• Calcifications may occur in the eyes and brain,
leading to psychosis.
• Cataracts can develop.
• Bone changes are evident on x-ray examination.
• Convulsions may occur.
• Death can result from laryngospasm if
treatment is not provided
Diagnostic Tests
• Chvostek’s and Trousseau’s signs are present.
• Laboratory studies show decreased serum
calcium and PTH levels and increased serum
phosphate.
• Radiographs show bone changes.
Therapeutic Interventions
• Acute cases of hypoparathyroidism are treated
with intravenous calcium gluconate.
• Long-term treatment includes a high-calcium
diet with oral calcium and vitamin D
supplements.
• Thiazide diuretics may also be used - reduce the
amount of calcium excreted in the urine.
• Magnesium is given if hypomagnesemia is
present.
 Hyperparathyroidism
Pathophysiology
• Overactivity of one or more of the
parathyroid glands causes an increase
in PTH, with a subsequent increase in
the serum calcium level
(hypercalcemia).
• This is achieved through movement of
calcium out of the bones and into the
blood, absorption in the small intestine,
and reabsorption by the kidneys.
• PTH also promotes phosphate excretion
by the kidneys.
Etiology
• Hyperparathyroidism is usually the result of
hyperplasia or a benign tumor of the
parathyroid glands, or it may be hereditary.
• Some cancers can also make a substance
that mimics PTH and causes hypercalcemia.
• Secondary hyperparathyroidism occurs
when the parathyroids secrete excessive
PTH in response to low serum calcium
levels.
• Serum calcium may be reduced in kidney
disease because of the kidneys’ failure to
activate vitamin D, which is necessary for
absorption of calcium in the small intestine.
Signs and Symptoms
• Signs and symptoms of hyperparathyroidism are
caused primarily by the increase in serum calcium
level, although many patients are asymptomatic.
• Symptoms include fatigue, depression, confusion,
increased urination, anorexia, nausea, vomiting,
kidney stones, and cardiac dysrhythmias.
• The increased serum calcium level also causes
gastrin secretion, resulting in abdominal pain and
peptic ulcers.
• As calcium is being removed from bones, bone
and joint pain and pathological fractures may
occur.
• With severe hypercalcemia, the result may be
coma and cardiac arrest.
Diagnostic Tests
Laboratory studies include serum
calcium, phosphate, and PTH levels.
Radiographs may show decreased
bone density.
Nuclear scanning may be used to
help locate the parathyroid glands
if surgical removal is planned.
Therapeutic Interventions
The patient is monitored for bone
changes and decline in renal
function.
Hydration with intravenous normal
saline lowers the calcium level by
dilution.
Furosemide (Lasix) is given to
increase renal excretion of calcium.
Alendronate or calcitonin may be
given to prevent calcium release
from bones.

 Therapeutic Interventions cont..
• If hypercalcemia is severe or if the patient
is at risk for bone or kidney complications,
surgery to remove the diseased
parathyroid glands (parathyroidectomy) is
performed.
• If possible, some parathyroid tissue is left
intact to continue to secrete PTH.
• Preoperative and postoperative care is
similar to that of the patient undergoing
thyroid surgery, with special attention
paid to calcium and PTH levels.
• The patient will likely be on calcium and
vitamin D supplements following surgery.
Read and make notes on:
Endocrine disorders of the ovary
and testes.
Hashmotos thyroiditis