HYPERTHYROIDISM  large amounts of tetraiodothyronine
taken through dietary supplements or
Hyperthyroidism (overactive thyroid)
occurs when your thyroid gland produces
too much of the hormone thyroxine.
Hyperthyroidism can accelerate your body's
metabolism.
SIGNS & SYMPTOMS
 Unintentional weight loss
 Rapid heartbeat (tachycardia)
 Irregular heartbeat (arrhythmia)
 Pounding of your heart (palpitations)
 Increased appetite
 Nervousness, anxiety and irritability
 Tremor — usually a fine trembling in
your hands and fingers
 Sweating
 Changes in menstrual patterns
 Increased sensitivity to heat
 Changes in bowel patterns, especially
more frequent bowel movements
 An enlarged thyroid gland (goiter),
which may appear as a swelling at the
base of your neck
 Fatigue, muscle weakness
 Difficulty sleeping
 Skin thinning
 Fine, brittle hair
CAUSES
 Grave’s Disease - An autoimmune
disorder, is the most common cause
of hyperthyroidism. It causes
antibodies to stimulate the thyroid to
secrete too much hormone. Graves’
disease occurs more often in women
than in men. It tends to run in
families, which suggests a genetic
link.
 Excess iodine, a key ingredient in T4
and T3
 Thyroiditis, or inflammation of the
thyroid, which causes T4 and T3 to
leak out of the gland
 tumors of the ovaries or testes
 benign tumors of the thyroid or
pituitary gland
medication
ANATOMY AND PHYSIOLOGY
Thyroid gland
Hyperthyroidism can be caused by a number
of conditions, including Graves' disease,
Plummer's disease and thyroiditis. Your
thyroid is a small, butterfly-shaped gland at
the base of your neck, just below your
Adam's apple. The thyroid gland has an
enormous impact on your health. Every
aspect of your metabolism is regulated by
thyroid hormones.
Your thyroid gland produces two main
hormones, thyroxine (T4) and
triiodothyronine (T3), that influence every
cell in your body. They maintain the rate at
which your body uses fats and
carbohydrates, help control your body
temperature, influence your heart rate, and
help regulate the production of protein. Your
thyroid also produces a hormone that helps
regulate the amount of calcium in your blood
(calcitonin).
A butterfly-shaped organ, the thyroid gland
is located anterior to the trachea, just
inferior to the larynx. The medial region,
called the isthmus, is flanked by wing-
shaped left and right lobes. Each of the
thyroid lobes are embedded with
parathyroid glands, primarily on their
posterior surfaces. The tissue of the thyroid
gland is composed mostly of thyroid
follicles. The follicles are made up of a
central cavity filled with a sticky fluid called
colloid. Surrounded by a wall of epithelial
follicle cells, the colloid is the center of
thyroid hormone production, and that
production is dependent on the hormones’
essential and unique component: iodine. It
narrows at its center, just under the thyroid
cartilage of the larynx. This narrow area is
called the isthmus of the thyroid. Two large
arteries, the common carotid arteries, run
parallel to the trachea on the outer border of
the thyroid. A small artery enters the
superior edge of the thyroid, near the
isthmus, and branches throughout the two
“wings” of the thyroid. Part B of this figure is
a posterior view of the thyroid. The posterior
view shows that the thyroid does not
completely wrap around the posterior of the
trachea. The posterior sides of the thyroid
wings can be seen protruding from under the
cricoid cartilage of the larynx. The posterior
sides of the thyroid “wings” each contain two
small, disc-shaped parathyroid glands
embedded in the thyroid tissue. Within each
wing, one disc is located superior to the
other. These are labeled the left and right
parathyroid glands. Just under the inferior
parathyroid glands are two arteries that
bring blood to the thyroid from the left and
right subclavian arteries. Part C of this figure
is a micrograph of thyroid tissue. The
thyroid follicle cells are cuboidal epithelial
cells. These cells form a ring around
irregular-shaped cavities called follicles. The
follicles contain light colored colloid. A
larger parafollicular cell is embedded
between two of the follicular cells near the
edge of a follicle.
Synthesis and Release of Thyroid
Hormones
Hormones are produced in the colloid when
atoms of the mineral iodine attach to a
glycoprotein, called thyroglobulin, that is
secreted into the colloid by the follicle cells.
The following steps outline the hormones’
assembly:
Binding of TSH to its receptors in the follicle
cells of the thyroid gland causes the cells to
actively transport iodide ions (I–) across their
cell membrane, from the bloodstream into
the cytosol. As a result, the concentration of
iodide ions “trapped” in the follicular cells is
many times higher than the concentration in
the bloodstream.
Iodide ions then move to the lumen of the
follicle cells that border the colloid. There,
the ions undergo oxidation (their negatively
charged electrons are removed). The
oxidation of two iodide ions (2 I–) results in
iodine (I2), which passes through the follicle
cell membrane into the colloid.
In the colloid, peroxidase enzymes link the
iodine to the tyrosine amino acids in
thyroglobulin to produce two intermediaries:
a tyrosine attached to one iodine and a
tyrosine attached to two iodines. When one
of each of these intermediaries is linked by
covalent bonds, the resulting compound is
triiodothyronine (T3), a thyroid hormone
with three iodines. Much more commonly,
two copies of the second intermediary bond,
forming tetraiodothyronine, also known as
thyroxine (T4), a thyroid hormone with four
iodines.
These hormones remain in the colloid center
of the thyroid follicles until TSH stimulates
endocytosis of colloid back into the follicle
cells. There, lysosomal enzymes break apart
the thyroglobulin colloid, releasing free T3
and T4, which diffuse across the follicle cell
membrane and enter the bloodstream.
In the bloodstream, less than one percent of
the circulating T3 and T4 remains unbound.
This free T3 and T4 can cross the lipid
bilayer of cell membranes and be taken up
by cells. The remaining 99 percent of
circulating T3 and T4 is bound to specialized
transport proteins called thyroxine-binding
globulins (TBGs), to albumin, or to other
plasma proteins. This “packaging” prevents
their free diffusion into body cells. When
blood levels of T3 and T4 begin to decline,
bound T3 and T4 are released from these
plasma proteins and readily cross the
membrane of target cells. T3 is more potent
than T4, and many cells convert T4 to T3
through the removal of an iodine atom.
RISK FACTORS:
 A family history, particularly of
Graves' disease
 Female sex
 A personal history of certain chronic
illnesses, such as type 1 diabetes,
pernicious anemia and primary
adrenal insufficiency
PHARMACOTHERAPY
 The objective of pharmacotherapy is
to inhibit hormone synthesis or
release and reduce the amount of
thyroid tissue.
  The most commonly used
medications are propylthiouracil
(Propacil, PTU) and methimazole
(Tapazole) until patient is euthyroid.
 Maintenance dose is establish,
followed by gradual withdrawal of the
medication over the next several
months.
 Antithyroid drugs are contraindicated
in late pregnancy because of a risk for
goiter and cretinism in the fetus.
 Thyroid hormone may be
administered to put the thyroid to
rest.
COMPLICATIONS:
 Heart problems. Some of the most
serious complications of
hyperthyroidism involve the heart.
These include a rapid heart rate, a
heart rhythm disorder called atrial
fibrillation that increases your risk of
stroke, and congestive heart failure —
a condition in which your heart can't
circulate enough blood to meet your
body's needs.
 Brittle bones. Untreated
hyperthyroidism can also lead to
weak, brittle bones (osteoporosis).
The strength of your bones depends,
in part, on the amount of calcium and
other minerals they contain. Too
much thyroid hormone interferes
with your body's ability to incorporate
calcium into your bones.
 Eye problems. People with Graves'
ophthalmopathy develop eye
problems, including bulging, red or
swollen eyes, sensitivity to light, and
blurring or double vision. Untreated,
severe eye problems can lead to vision
loss.
 Red, swollen skin. In rare cases,
people with Graves' disease develop
Graves' dermopathy. This affects the
skin, causing redness and swelling,
often on the shins and feet.
 Thyrotoxic crisis. Hyperthyroidism
also places you at risk of thyrotoxic
crisis — a sudden intensification of
your symptoms, leading to a fever, a
rapid pulse and even delirium. If this
occurs, seek immediate medical care.
HOW TO DIAGNOSE HYPERTHYROIDISM
Cholesterol test
- Your doctor may need to check your
cholesterol levels. Low cholesterol can
be a sign of an elevated metabolic
rate, in which your body is burning
through cholesterol quickly.
T4, free T4, T3
- These tests measure how much
thyroid hormone (T4 and T3) is in
your blood.
Thyroid stimulating hormone level test
- Thyroid stimulating hormone (TSH) is
a pituitary gland hormone that
stimulates the thyroid gland to
produce hormones. When thyroid
hormone levels are normal or high,
your TSH should be lower. An
abnormally low TSH can be the first
sign of hyperthyroidism.
Triglyceride test
- Your triglyceride level may also be
tested. Similar to low cholesterol, low
triglycerides can be a sign of an
elevated metabolic rate.
Thyroid scan and uptake
- This allows your doctor to see if your
thyroid is overactive. In particular, it
can reveal whether the entire thyroid
or just a single area of the gland is
causing the overactivity.
Ultrasound
- Ultrasounds can measure the size of
the entire thyroid gland, as well as any
masses within it. Doctors can also use
ultrasounds to determine if a mass is
solid or cystic.
CT or MRI scans
- A CT or MRI can show if a pituitary
tumor is present that’s causing the
condition.
PATHOPHYSIOLOGY In Graves disease, a circulating autoantibody
against the thyrotropin receptor provides
Normally, the secretion of thyroid hormone continuous stimulation of the thyroid gland.
is controlled by a complex feedback This stimulatory immunoglobulin has been
mechanism involving the interaction of called long-acting thyroid stimulator (LATS),
stimulatory and inhibitory factors (see the thyroid-stimulating immunoglobulin (TSI),
image below). Thyrotropin-releasing thyroid-stimulating antibody (TSab), and
hormone (TRH) from the hypothalamus TSH-receptor antibody (TRab). [5] These
stimulates the pituitary to release TSH. antibodies stimulate the production and
release of thyroid hormones and
Binding of TSH to receptors on the thyroid thyroglobulin; they also stimulate iodine
gland leads to the release of thyroid uptake, protein synthesis, and thyroid gland
hormones—primarily T4 and to a lesser growth. Anti–thyroid peroxidase (anti-TPO)
extent T3. In turn, elevated levels of these antibody is assessed in a nonspecific test for
hormones act on the hypothalamus to autoimmune thyroid disease. Although the
decrease TRH secretion and thus the anti-TPO antibody is not diagnostic for
synthesis of TSH. Graves disease, it is present in 85% of
Synthesis of thyroid hormone requires patients with the disorder and can be quickly
iodine. Dietary inorganic iodide is measured in local laboratories
transported into the gland by an iodide
transporter, converted to iodine, and bound
to thyroglobulin by the enzyme thyroid
peroxidase through a process called
organification. This results in the formation
of monoiodotyrosine (MIT) and
diiodotyrosine (DIT), which are coupled to
form T3 and T4; these are then stored with
thyroglobulin in the thyroid’s follicular
lumen. The thyroid contains a large supply
of its preformed hormones.
Thyroid hormones diffuse into the
peripheral circulation. More than 99.9% of T4
and T3 in the peripheral circulation is bound
to plasma proteins and is inactive. Free T3 is
20-100 times more biologically active than
free T4. Free T3 acts by binding to nuclear
receptors (DNA-binding proteins in cell
nuclei), regulating the transcription of
various cellular proteins.
Any process that causes an increase in the
peripheral circulation of unbound thyroid
hormone can cause thyrotoxicosis.
Disturbances of the normal homeostatic
mechanism can occur at the level of the
pituitary gland, the thyroid gland, or in the
periphery. Regardless of etiology, the result
is an increase in transcription in cellular
proteins, causing an increase in the basal
metabolic rate. In many ways, signs and
symptoms of hyperthyroidism resemble a
state of catecholamine excess, and
adrenergic blockade can improve these
symptoms.
TREATMENT NURSING INTERVENTIONS
 Provide adequate rest.
Medication  Administer sedatives as prescribed.
Antithyroid medications, such as  Provide a cool and quiet environment.
methimazole (Tapazole), stop the  Obtain weight daily.
thyroid from making hormones. They  Provide a high-calorie diet.
are a common treatment.  Avoid the administration of
stimulants.
Radioactive iodine  Administer antithyroid medications
(propylthiouracil [PTU]) that block
Radioactive iodine is given to over 70 thyroid synthesis, as prescribed.
percent of U.S. adults with  Administer iodine preparations that
hyperthyroidism. It effectively inhibit the release of thyroid hormone
destroys the cells that produce as prescribed.
hormones. Common side effects  Administer propranolol (INderal) for
include dry mouth, dry eyes, sore tachycardia as prescribed.
throat, and changes in taste.  Prepare the client for radioactive
Precautions may need to be taken for iodine therapy, as prescribed, to
a short time after treatment to destroy thyroid cells.
prevent radiation spread to others.  Prepare the client for thyroidectomy if
prescribed.
Surgery

A section or all of your thyroid gland

may be surgically removed. You will
then have to take thyroid hormone
supplements to prevent
hypothyroidism, which occurs when
you have an underactive thyroid that
secretes too little hormone. Also,
beta-blockers such as propranolol can
help control your rapid pulse,
sweating, anxiety, and high blood
pressure. Most people respond well to
this treatment.

NURSING DIAGNOSIS

1. Risk for Decreased Cardiac Output

2. Fatigue
3. Risk for Disturbed Thought Processes
4. Risk for Imbalanced Nutrition: Less
Than Body Requirements
5. Anxiety
6. Risk for Impaired Tissue Integrity
7. Deficient Knowledge