ENDOCRINE SYSTEM
The endocrine system involves the release of
chemical substances known as hormones to
regulate and integrate body functions.
the kidneys produce erythropoietin, a hormone
that stimulates the bone marrow to produce red
blood cells.
the white blood cells produce cytokines
(hormonelike proteins) that actively participate in
inflammatory and immune responses.
The immune system and the nervous system have
unique relationships with the endocrine system.
Chemicals such as neurotransmitters (e.g.,
epinephrine) released by the nervous system can
also function as hormones when needed.
The immune system responds to the introduction
of foreign agents by means of chemical
messengers (cytokines), which are hormonelike
proteins, while it is also subject to regulation by
adrenal corticosteroid hormones (Porth & Matfin,
2009).
The endocrine system is composed of several
glands: the pituitary, the thyroid gland, parathyroid
glands, adrenal glands, pancreatic islets, ovaries,
and testes.
Unlike the exocrine glands, most hormones
secreted from endocrine glands are released
directly into the bloodstream. Exocrine glands,
such as sweat glands, secrete their products
through ducts onto epithelial surfaces or into the GI
tract, e.g., sweat, saliva, digestive enzymes, and
oil.
concentration decreases, the rate of production of
that hormone increases.
Hormones are classified into four categories
according to their structure:
(1) amines and amino acids (e.g., epinephrine,
norepinephrine, and thyroid hormones);
(2) peptides, polypeptides, proteins, and
glycoproteins (e.g., thyrotropinreleasing hormone,
follicle-stimulating hormone, and growth hormone);
(3) steroids (e.g., corticosteroids); and
(4) fatty acid derivatives (e.g., eicosanoid, retinoids)
Exocrine glands (sweat glands, salivary glands,
sebaceous glands). Have local effects and involved
in tasks like digestion, lubrication, and temperature
regulation.
Hormones can alter the function of the target tissue
by interacting with chemical receptors located
either on the cell membrane or in the interior of the
cell.
the endocrine glands are composed of secretory
cells arranged in minute clusters known as acini.
No ducts are present, but the glands have a rich
blood supply, so the hormones they produce enter
the bloodstream rapidly.
For example, peptide and protein hormones
interact with receptor sites on the cell surface,
resulting in stimulation of the intracellular enzyme
adenyl cyclase. This causes increased production
of cyclic 3’,5’-adenosine monophosphate (cyclic
AMP). The cyclic AMP inside the cell alters enzyme
activity. Thus, cyclic AMP is the “second
messenger” that links the peptide hormone at the
cell surface to a change in the intracellular
environment. Some protein and peptide hormones
Negative feedback is the mechanism for
regulating hormone concentration in the
bloodstream. When the hormone concentration
increases, further production of that hormone is
inhibited. Conversely, when the hormone
also act by changing membrane permeability and
act within seconds or minutes.
The mechanism of action for amine hormones is
similar to that for peptide hormones. Steroid
hormones, because of their smaller size and higher
lipid solubility, penetrate cell membranes and
interact with intracellular receptors. The steroid–
receptor complex modifies cell metabolism and the
formation of messenger ribonucleic acid (mRNA)
from deoxyribonucleic acid (DNA). The mRNA then
stimulates protein synthesis within the cell. Steroid
hormones require several hours to exert their
effects, because they exert their action by the
modification of protein synthesis.
Although most hormones released by endocrine
glands can be transported to distant target sites for
action, some hormones and hormonelike
substances never enter the bloodstream.
Some hormones act locally in the area where they
are released; this is called paracrine action (e.g.,
the effect of sex hormones on the ovaries). When
sex hormones are released by certain glands near
the ovaries, they exert their effects specifically
within the ovarian tissue, influencing processes like
ovulation and reproductive function.
Others may act on the actual cells from which they
were released; this is called autocrine action (e.g.,
the effect of insulin from pancreatic beta cells on
those cells). When beta cells release insulin, the
insulin binds to receptors on the surface of the beta
cells themselves.
ASSESSMENT: HEALTH HISTORY


 Ask what’s the aggravating factor (what
triggers it), alleviation (what actions you do
to make the symptoms alleviated).
 Onset
General manifestations may also occur rather than
specific clinical symptoms.
Some common signs and symptoms of endocrine
imbalances include changes in energy level,
tolerance to heat or cold, weight, fat and fluid
distribution, secondary sexual characteristics,
sexual dysfunction, memory, concentration,
sleep patterns, and mood.
The health history should include information
regarding (1) the severity of these changes, (2) the
length of time the patient has experienced these
changes, (3) the way in which these changes have
affected the patient’s ability to carry out activities of
daily living, and (4) the effect of the changes on the
patient’s self-perception.
PHYSICAL ASSESSMENT
The physical examination should include vital signs,
a visual head-to-toe assessment, and tactile
examination. Findings should be compared with
previous findings if available.


Nursing health history- purely subjective by
patient.
Physical assessment- confirmation of the
nursing health history. Taking the VS of
patient.
HEALTH HISTORY- always do this first. Never
touch the patient without taking their health history.
 Ask what the complaint (chief complaint) is.
 If there is hyposecretion, there will be
decrease in metabolism.
 Hypoglycemic- cold and clammy skin,
nauseous, dizziness.
 Ask when it started.
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Changes in physical characteristics such as
appearance of facial hair in women, “moon
face,” “buffalo hump,” exophthalmos,
edema, thinning of the skin, obesity of the
trunk, thinness of the extremities, increased
size of the feet and hands, and edema may
signify disorders of the thyroid, adrenal
cortex, or pituitary gland.
Exophthalmos and other eye symptoms
may occur with hyperthyroidism and
Graves’ disease.
Alteration in skin texture is associated with
hypofunction and hyperfunction of the
thyroid gland.
Elevated blood pressure may occur with
hyperfunction of the adrenal cortex or tumor
of the adrenal medulla. Decreased blood
pressure may occur with hypofunction of the
adrenal cortex. Behavioral changes such as
agitation, nervousness, a flat affect, or a
lack of concern about personal appearance
may also be present.
DIAGNOSTICS
1. Blood tests- Blood tests are used to determine
hormone blood levels. Knowing the serum levels of
a specific hormone may provide information about
whether there is hypofunction or hyperfunction of
the endocrine system and the site of dysfunction.
If may bukol, auscultate, if may sound na
rumaragasa (Bruits), it is inflamed. This can occur
in hyperthyroidism and thyroiditis.
Radioimmunoassays are radioisotope-labeled
antigen tests used to measure the levels of
hormones or other substances.


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2. Urinalysis- Urine tests may be used to measure
the amount of hormones or the end products of
hormones excreted by the kidneys.
One-time specimens are obtained, or in some
disorders 24-hour urine specimens are collected to
measure hormones or their metabolites.
Urine tests have several disadvantages, such as
the inability of patients to urinate at scheduled
intervals and the effect of some medications or
disease states on the test results.
Stimulation tests can determine how an endocrine
gland responds to the administration of stimulating
hormones that are normally produced or released
by the hypothalamus or pituitary gland. If the
endocrine gland responds to this stimulation, the
specific disorder may be in the hypothalamus or
pituitary. Failure of the endocrine gland to respond
to this stimulation helps identify the problem as
being in the endocrine gland itself.
Suppression tests may be used to determine
whether negative feedback mechanisms that
normally control secretion of hormones from the
hypothalamus or pituitary gland are intact. They
test the effect of administration of an exogenous
dose of the hormone on the endogenous secretion
of the hormone or on the secretion of stimulation
hormones from the hypothalamus or pituitary gland.
3. Imaging studie



Radioactive scanning (fasting, allergies,
avoid strenuous activities)
MRI- gives you different angle like a 3D.
(remove metals, remain still during scan to
ensure metal components, inform technician
if you have metal implants).
CT scan- gives you a clear picture but
one angle only. (fasting, contrast-dye

administration, inform technician if you have
allergies or pregnant, metal implants are not
allowed)
Ultrasonography- for abdomen, not for
brain. (pelvic ultrasound- drink water, avoid
applying lotions, inform if you have metal
implants).
Positron emission tomography (PET)
(fasting, inform HCP if you have diabetes or
pregnant, avoid strenuous activities before
scan, inform if you have allergies).
Dual-energy x-ray absorptiometry
(DEXA) (fasting, inform if you are pregnant,
avoid taking calcium supplements or
calcium containing meds before scan,
inform if you had recent imaging studies
involving contrast dye).
X-ray- black and white, depends on density.
4. Genetic screening
PITUITARY GLAND
The pituitary gland, or hypophysis, is commonly
referred to as the master gland because of the
influence it has on secretion of hormones by other
endocrine glands. The round structure, about 1.27
cm (1/2 inch) in diameter, is located on the inferior
aspect of the brain. The pituitary gland is divided
into anterior and posterior lobes. It is controlled by
the hypothalamus, an adjacent area of the brain
that is connected to the pituitary by the pituitary
stalk.
ANTERIOR PITUITARY
The major hormones of the anterior pituitary gland
are: The secretion of these major hormones is
controlled by releasing factors secreted by the
hypothalamus. These releasing factors reach the
anterior pituitary by way of the bloodstream in a
special circulation called the pituitary portal blood
system.
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follicle-stimulating hormone (FSH)- has
effect on gonads.
luteinizing hormone (LH)- has effect on
gonads.
prolactin- acts on the breast to stimulate
milk production.
adrenocorticotropic hormone (ACTH)- has
effect on adrenal glands.
thyroid-stimulating hormone (TSH)- has
effect on thyroid.

growth hormone (GH) (also referred to as
somatotropin)- is a protein hormone that
increases protein synthesis in many tissues,
increases the breakdown of fatty acids in
adipose tissue, and increases the glucose
level in the blood. LARGELY INACTIVATED
IN LIVER. Stress, exercise, and low blood
glucose levels increase the secretion of GH.
Other hormones include melanocyte-stimulating
hormone and beta-lipotropin; the function of
lipotropin is poorly understood.
Oversecretion (hypersecretion) of the anterior
pituitary gland most commonly involves ACTH or
GH and results in Cushing’s syndrome or
acromegaly, respectively.
Acromegaly, an excess of GH in adults, results in
bone and soft tissue deformities and enlargement
of the viscera without an increase in height. It
occurs in approximately 3 cases per 1 million
people per year (Melmed, 2006).
Over secretion of GH results in gigantism in
children; a person may be 7 or even 8 feet tall.
Conversely, insufficient secretion of GH during
childhood results in generalized limited growth
and dwarfism (Porth & Matfin, 2009).
Under secretion (hyposecretion) commonly
involves all of the anterior pituitary hormones and is
termed panhypopituitarism. In this condition, the
thyroid gland, the adrenal cortex, and the gonads
atrophy (shrink) because of loss of the trophicstimulating hormones.
Hypopituitarism may result from destruction of the
anterior lobe of the pituitary gland.
Postpartum pituitary necrosis (Sheehan’s
syndrome) is another uncommon cause of failure
of the anterior pituitary. It is more likely to occur in
women with severe blood loss, hypovolemia, and
hypotension at the time of delivery.
POSTERIOR PITUITARY
The important hormones secreted by the posterior
lobe of the pituitary gland are:

Vasopressin, also called antidiuretic
hormone (ADH)- they have direct
vasoconstriction effect on heart
(vasopressin).

- Vasopressin controls the excretion of
water by the kidney; its secretion is
stimulated by an increase in the osmolality
of the blood or by a decrease in blood
pressure.
Oxytocin- it has effect on contract on
uterus to prevent uterine atony, it is also
needed for prolactin to be produced.
- Oxytocin secretion is stimulated during
pregnancy and at childbirth. It facilitates milk
ejection during lactation and increases the
force of uterine contractions during labor
and delivery.
These hormones are synthesized or produced in
the hypothalamus and travel from the
hypothalamus to the posterior pituitary gland for
storage.
The most common disorder related to posterior
lobe dysfunction is diabetes insipidus, a condition
in which abnormally large volumes of dilute urine
are excreted as a result of deficient production of
vasopressin.
DIABETES INSIPIDUS
-Diabetes insipidus (DI) is a disorder of the
posterior lobe of the pituitary gland that is
characterized by a deficiency of ADH (vasopressin).
HYPOSECRETION OF ADH.
-Excessive thirst (polydipsia) and large volumes of
dilute urine characterize the disorder.
CLINICAL MANIFESTATIONS: Polyuria,
polydipsia, polyphagia. (same symptoms with
diabetes mellitus), Weight loss, hyponatremia
(tremors, hyperactivity).
-There will be activation of hypothalamus, leading
to activation of thirst center.
- Another cause of DI is failure of the renal
tubules to respond to ADH; this nephrogenic form
may be related to hypokalemia, hypercalcemia, and
a variety of medications (e.g., lithium,
demeclocycline).
- The disease cannot be controlled by limiting
fluid intake, because the high-volume loss of urine
continues even without fluid replacement.
Attempts to restrict fluids cause the patient to
experience an insatiable craving for fluid and to
develop hypernatremia and severe dehydration.
ASSESSMENT AND DIAGNOSTIC FINDINGS:
- The fluid deprivation test is carried out by
withholding fluids for 8 to 12 hours or until 3% to
5% of the body weight is lost.
- The patient’s condition needs to be monitored
frequently during the test, and the test is terminated
if tachycardia, excessive weight loss, or
hypotension develops.
- The patient is weighed frequently during the test.
(must be same time of day, same weighing scale).
- Plasma and urine osmolality studies are
performed at the beginning and end of the test.
- a trial of desmopressin (synthetic vasopressin)
therapy
-intravenous (IV) infusion of hypertonic saline
solution.
-Abdominal cramps are a side effect of this
medication. Rotation of injection sites is necessary
to prevent lipodystrophy.
3. Clofibrate (Atromid-S), a hypolipidemic agent,
has been found to have an antidiuretic effect on
patients with DI who have some residual
hypothalamic vasopressin.
-Chlorpropamide (Diabinese) and thiazide
diuretics are also used in mild forms of the disease
because they potentiate the action of vasopressin.
Hyperglycemia is possible.
-If the DI is renal in origin, the previously described
treatments are ineffective. Thiazide diuretics, mild
salt depletion, and prostaglandin inhibitors
(ibuprofen [Advil, Motrin], indomethacin [Indocin],
and aspirin) are used to treat the nephrogenic form
of DI.
NURSING MANAGEMENT:
MEDICAL MANAGEMENT
1. Desmopressin (DDAVP)- a synthetic
vasopressin n without the vascular effects of
natural ADH, is particularly valuable because it has
a longer duration of action and fewer adverse
effects than other preparations previously used to
treat the disease.
- It is administered intranasally; the patient sprays
the solution into the nose through a flexible
calibrated plastic tube.
- One or two administrations daily (e.g., every 12 to
24 hours) usually control the symptoms. Should be
administered at specific time and shouldn’t be
missed.
- Vasopressin causes vasoconstriction; thus, it must
be used cautiously in patients with coronary artery
disease.
1. the nurse should advise wearing a medical
identification bracelet and carrying
medication and information about DI at all
times.
SYNDROME OF INAPPROPRIATE
ANTRIDIURETIC HORMONE SECRETION
(SIADH)
- includes excessive ADH secretion from the
pituitary gland even in the face of subnormal serum
osmolality. Patients cannot excrete a dilute urine,
retain fluids, and develop a sodium deficiency
known as dilutional hyponatremia.
-INTERVENTIONS include:


2. Intramuscular administration of ADH,
vasopressin tannate in oil, is used if the
intranasal route is not possible.
-The medication is administered every 24 to 96
hours.
-The vial of medication should be warmed or
shaken vigorously before administration. The
injection is administered in the evening so that
maximum results are obtained during sleep.


the elimination of the underlying cause
if possible, and restricting fluid intake.
Because retained water is excreted
slowly through the kidneys, the
extracellular fluid volume contracts and
the serum sodium concentration
gradually increases toward normal.
Diuretics such as furosemide (Lasix)
may be used along with fluid restriction
if severe hyponatremia is present.
Close monitoring of fluid intake and
output, daily weight, urine and blood
chemistries, and neurologic status is
indicated for the patient at risk for
SIADH.

-a butterfly-shaped organ located in the lower neck,
anterior to the trachea.
-TSH controls the rate of thyroid hormone
release through a negative feedback
mechanism. In turn, the level of thyroid hormone in
the blood determines the release of TSH. If the
thyroid hormone concentration in the blood
decreases, the release of TSH increases, which
causes increased output of T3 and T4.
-It consists of two lateral lobes connected by an
isthmus.
-The term euthyroid refers to thyroid hormone
production that is within normal limits.
-The gland is about 5 cm long and 3 cm wide and
weighs about 30 g.
-Thyrotropin-releasing hormone (TRH), secreted
by the hypothalamus, exerts a modulating influence
on the release of TSH from the pituitary.
Environmental factors, such as a decrease in
temperature, may lead to increased secretion of
TRH, resulting in elevated secretion of thyroid
hormones.
Supportive measures and explanations
of procedures and treatments assist the
patient in managing this disorder.
THYROID GLAND
-The blood flow to the thyroid is very high (about 5
mL/min per gram of thyroid tissue), approximately
five times the blood flow to the liver. This reflects
the high metabolic activity of the thyroid gland.
-The thyroid gland produces three hormones:
thyroxine (T4), triiodothyronine (T3), and
calcitonin.
THYROID HORMONE:
-T4, a relatively weak hormone, maintains body
metabolism in a steady state.
-T4 and T3, which are referred to collectively as
thyroid hormone, are two separate hormones
produced by the thyroid gland.
-T3 is about five times as potent as T4 and has a
more rapid metabolic action.
-Both are amino acids that contain iodine molecules
bound to the amino acid structure; T4 contains four
iodine atoms in each molecule, and T3 contains
three.
-Calcitonin, it is secreted in response to high
plasma levels of calcium, and it reduces the plasma
level of calcium by increasing its deposition in
bone.
-These hormones are synthesized and stored
bound to proteins in the cells of the thyroid gland
until needed for release into the bloodstream. About
75% of bound thyroid hormone is bound to
thyroxine-binding globulin (TBG); the remaining
bound thyroid hormone is bound to thyroid-binding
prealbumin and albumin.
PATHOPHYSIOLOGY
IODINE
Iodine is essential to the thyroid gland for synthesis
of its hormones.
-The thyroid gland is extremely efficient at taking up
iodide from the blood and concentrating it within the
cells, where iodide ions are converted to iodine
molecules, which react with tyrosine (an amino
acid) to form the thyroid hormones.
-The hypothalamic–pituitary–thyroid axis. Thyroid
releasing hormone (TRH) from the hypothalamus
stimulates the pituitary gland to secrete thyroidstimulating hormone (TSH). TSH stimulates the
thyroid to produce thyroid hormone
(triiodothyronine [T3] and thyroxine [T4]). High
circulating levels of T3 and T4 inhibit further TSH
secretion and thyroid hormone production through
a negative feedback mechanism (dashed lines).
-Inadequate secretion of thyroid hormone during
fetal and neonatal development results in stunted
physical and mental growth (cretinism) because of
general depression of metabolic activity.
REGULATION:
- In adults, hypothyroidism manifests as lethargy,
slow mentation, and generalized slowing of
body functions.
The secretion of T3 and T4 by the thyroid gland is
controlled by TSH (also called thyrotropin) from
the anterior pituitary gland.
-Oversecretion of thyroid hormones is usually
associated with an enlarged thyroid gland known as
a goiter.
-Goiter also commonly occurs with iodine
deficiency. In this latter condition, lack of iodine
results in low levels of circulating thyroid hormones,
which causes increased release of TSH; the
elevated TSH causes overproduction of
thyroglobulin (a precursor of T3 and T4) and
hypertrophy of the thyroid gland.
11.5 g/dL (58.5 to 150 nmol/L). Although
serum T3 and T4 levels generally increase
or decrease together, the T3 level appears
to be a more accurate indicator of
hyperthyroidism, which causes a greater
increase in T3 than in T4 levels. The normal
range for serum T3 is 70 to 220 ng/dL (1.15
to 3.10 nmol/L).
ASSESSMENT:
-The thyroid gland is inspected and palpated
routinely in all patients. The patient is instructed to
extend the neck slightly and swallow. Thyroid tissue
rises normally with swallowing.
-When palpable, the isthmus is perceived as firm
and of a rubber-band consistency.
-The isthmus is the only portion of the thyroid that is
normally palpable.
-If palpation discloses an enlarged thyroid gland,
both lobes are auscultated using the diaphragm of
the stethoscope. Auscultation identifies the
localized audible vibration of a bruit. This is
indicative of increased blood flow through the
thyroid gland associated with hyperthyroidism
and necessitates referral to a physician. Other
abnormal findings that require referral for further
evaluation may include a soft texture (Graves’
disease), firmness (Hashimoto’s thyroiditis or
malignancy), and tenderness (thyroiditis).
LABORATORY
-The most widely used tests are serum
immunoassay for TSH and free T4 (Tierney, et
al., 2005)



Serum thyroid-stimulating hormoneMeasurement of the serum TSH
concentration is the single best screening
test of thyroid function in outpatients
because of its high sensitivity.
Serum free T4- The test most commonly
used to confirm an abnormal TSH result is
free T4. It is a direct measurement of free
(unbound) thyroxine, the only metabolically
active fraction of T4. The range of free T4 in
serum is normally 0.9 to 1.7 ng/dL (11.5 to
21.8 pmol/L).
Serum T3 and T4- Measurement of total T3
or T4 includes protein-bound and free
hormone levels that occur in response to
TSH secretion. Normal range for T4 is 4.5 to
HYPOTHYROIDISM
-Hypothyroidism results from suboptimal levels of
thyroid hormone. Thyroid deficiency can affect all
body functions and can range from mild, subclinical
forms to myxedema, an advanced form.
-The most common cause of hypothyroidism in
adults is autoimmune thyroiditis (Hashimoto’s
disease), in which the immune system attacks the
thyroid gland.
1. Primary or thyroidal hypothyroidism, which
refers to dysfunction of the thyroid gland itself.
2. Central hypothyroidism- cause of the thyroid
dysfunction is failure of the pituitary gland, the
hypothalamus, or both, the hypothyroidism is
known as central hypothyroidism.
3. Pituitary of Secondary hypothyroidism- the
cause is entirely a pituitary disorder; it may be
referred to as pituitary or secondary
hypothyroidism.
4. Hypothalamic hypothyroidism- the cause is a
disorder of the hypothalamus resulting in
inadequate secretion of TSH due to decreased
stimulation of TRH, it is referred to as hypothalamic
or tertiary hypothyroidism.
5. If thyroid deficiency is present at birth, it is
referred to as cretinism. In such instances, the
mother may also have thyroid deficiency.
-The term myxedema refers to the accumulation of
mucopolysaccharides in subcutaneous and other
interstitial tissues. Although myxedema occurs in
long-standing hypothyroidism, the term is used
appropriately only to describe the extreme
symptoms of severe hypothyroidism.
CLINICAL MANIFESTATIONS:
1.
2.
3.
4.
5.
Fatigue
Hair loss, brittle nails, dry skin.
Numbness, and tingling of the fingers.
Voice maybe husky (occasional).
Menstrual disturbances (Menorrhagia,
amenorrhea) + loss of libido
6. Common in women.
Severe hypothyroidism:
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
abnormal body temperature and pulse rate.
Weight gain even without an increase in
food intake.
Masklike
Complain of being cold even in a warm
environment.
Constipation
Advanced hypothyroidism:
 Personality and cognitive changes
(dementia’s characteristics).
Myxedema coma is a rare life-threatening
condition. It is the decompensated state of severe
hypothyroidism in which the patient is hypothermic
and unconscious (Kwaku & Burman, 2007)
MEDICAL MANAGEMENT:
Synthetic levothyroxine (Synthroid or Levothroid)
is the preferred preparation for treating
hypothyroidism and suppressing nontoxic goiters.
HYPERTHYROIDISM
Hyperthyroidism is the second most prevalent
endocrine disorder, after diabetes mellitus. Graves’
disease, the most common type of
hyperthyroidism, results from an excessive output
of thyroid hormones caused by abnormal
stimulation of the thyroid gland by circulating
immunoglobulins.
CLINICAL MANIFESTATIONS:
-Patients with well-developed hyperthyroidism
exhibit a characteristic group of signs and
symptoms (sometimes referred to as
thyrotoxicosis). The presenting symptom is often
nervousness. These patients are often emotionally
hyperexcitable, irritable, and apprehensive; they
cannot sit quietly; they suffer from palpitations; and
their pulse is abnormally rapid at rest as well as on
exertion. They tolerate heat poorly and perspire
unusually freely. The skin is flushed continuously,
with a characteristic salmon color, and is likely to be
warm, soft, and moist. However, patients may
report dry skin and diffuse pruritus.
-A fine tremor of the hands may be observed.
-Patients may exhibit ophthalmopathy, such as
exophthalmos (bulging eyes), which produces a
startled facial expression. Despite treatment, these
ocular changes are not always reversible. Patients
should be informed that smoking has been shown
to aggravate ocular changes.
-increase appetite, weight loss, increased systolic
but not diastolic (increased BP)
PHARMACOLOGIC:
Two forms of pharmacotherapy are available for
treating hyperthyroidism and controlling excessive
thyroid activity: (1) use of irradiation by
administration of the radioisotope iodine 131 for
destructive effects on the thyroid gland and (2)
antithyroid medications that interfere with the
synthesis of thyroid hormones and other agents
that control manifestations of hyperthyroidism.
RADIOACTIVE:
The goal of radioactive iodine therapy is to
destroy the overactive thyroid cells. Almost all the
iodine that enters and is retained in the body
becomes concentrated in the thyroid gland.
Therefore, the radioactive isotope of iodine is
concentrated in the thyroid gland, where it destroys
thyroid cells without jeopardizing other
radiosensitive tissues.
-The patient is observed for signs of thyroid storm ,
a life-threatening condition manifested by cardiac
dysrhythmias, fever, and neurologic impairment
(Harris, 2007). Propranolol (Inderal) is useful in
controlling these symptoms.
-The surgical removal of about five sixths of the
thyroid tissue (subtotal thyroidectomy) reliably
results in a prolonged remission in most patients
with exophthalmic goiter. Its use today is reserved
for patients with obstructive symptoms, for pregnant
women in the second trimester, and for patients
with a need for rapid normalization of thyroid
function.
TYPES OF GOITERS:
 Endemic goiter
 Nodular goiter
 Thyroid cancer