INTRODUCTION

Toxic goiter, also called exophthalmic goiter, hyperthyroidism, thyrotoxicosis, or

Graves' disease, for the Irish physician Robert James Graves, is caused by an excess of
thyroxine secretion. The cause of the excessive secretion is obscure. In some cases it may
result from excessive stimulation by the pituitary gland. The symptoms of toxic goiter
may include a rapid heartbeat, tremor, increased sweating, increased appetite, weight
loss, weakness, and fatigue. Some patients have eye problems, such as staring or
protrusion. Toxic goiter is commonly treated with radioactive iodine, which is taken up
by the gland and destroys the cells by irradiation. Drugs also can be used to suppress
hormone production, or most of the toxic goiter can be removed surgically.

Thyroid hormones stimulate the metabolism of cells. They are produced by the
thyroid gland. The thyroid gland is located in the lower part of the neck, below the
Adam's apple. The gland wraps around the windpipe (trachea) and has a shape that is
similar to a butterfly formed by two wings (lobes) and attached by a middle part
(isthmus).

The thyroid gland removes iodine from the blood (which comes mostly from a
diet of foods such as seafood, bread, and salt) and uses it to produce thyroid hormones.
The two most important thyroid hormones are thyroxine (T4) and triiodothyronine (T3)
representing 99.9% and 0.1% of thyroid hormones respectively. The hormone with the
most biological activity (for example, the greatest effect on the body) is actually T3.
Once released from the thyroid gland into the blood, a large amount of T4 is converted to
T3 - the more active hormone that affects the metabolism of cells.

Diet must include caloric intake to meet the energy expenditure of the
hypermetabolism. High iodine-containing substances, such as kelp, should be avoided.

Toxic goiter can occur in all ages, but it is rare in children younger than 10
years and unusual in elderly persons. The peak incidence is in third and fourth decades.

1
In late childhood, the incidence rate is 3 per 100,000 in girls and 0.5 per 100,000 in boys.
Prevalence studies show a rate of 2.7% in women and 0.23% in men.

Our group chose Mrs. X as our patient who has Toxic Goiter because we want to
recognize the pathophysiology and the course of the disease in general. The group
believes that this case will enable us to broaden our knowledge regarding this unfamiliar
case and be able to provide each member sufficient data regarding Toxic Goiter, its signs
and symptoms and treatment process; this will also enable us to familiarize our selves
with the different nursing interventions related to this disease in order to enhance our
skills as future nurses.

This case study will serve as a learning experience for us and our patient because
this will help us to further understand how the disease works and the different nursing
interventions that we can apply. The importance of this study is to develop nursing
actions that will surely give us a background which will help us in the future; this will
also lead us to a broader understanding of the case that will enhance our knowledge
further.

2
 1. PERSONAL DATA
a. Demographic data

Name: Mrs. X
Age: 37 y/o
Sex: Female
Civil Status: Married
Religion: Roman Catholic
Occupation: Housewife
Address: Santo Nino, Concepcion, Tarlac
Date of Birth: September 16, 1971
Nationality: Filipino
Usual Source of Medical Care: Traditional hilot and Hospital
Chief Complaint:
Admitting Diagnosis:

b. Environmental status

According to the patient, she is residing at Sto. Nino, Concepcion, Tarlac.

Their community is set in a rural environment where peace and order is well maintained
by the barangay.
The patient said, as she asked by the group to describe the house that she lives in
“gawa sa bungalow na yari sa concreto ang aming bahay pero sa banding kusina ay gawa
lamang sa kawayan”. May isang kwarto at may dalawang bintana.
As she continued, “ang sukat ng lote na kinatatayuan ng bahay namin ay humigit
kumulang seventy-two square meters.” The patient is the one who maintains the
cleanliness of their house which she does religiously every morning after breakfast. They
use mosquito nets as deterrent for mosquitoes.
They don’t have their own toilet and bathroom. Instead, they share with her
husband’s parents near their house. As with the water pump, they have it at the back of
their house located approximately 10 feet away.

3
 According to her, she cooks their food in a clay furnace using charcoal as fuel.
They do not have a refrigerator; instead, they buy their food daily from the market. Her
husband usually does the marketing because their location is quite far from the market
and other facilities. The patient also does their laundry by hand. According to her, they
have 2 cats and a dog as a pet and they keep outside their house. Their house is not gated
and fenced.
According to the patient, she is contented with the security that the barangay
officials are providing ion their community and the environment where she is currently
residing.

c. Lifestyle

The patient usually wakes at around six to seven o’clock in the morning. She
prepares the family’s breakfast and goes straight with her household chores. The patient
considers her household chores as her main form of exercise.

According to her, during her freetime, she enjoys watching her favorite noontime
show and sinenovelas i.e wowowee and una kang naging akin, rather than taking her
siesta. She is also fond of chatting and socializing with neighbors.

The patient as she claimed is omnivorous. She likes to drink coffee right after
meal. She loves to cook her favorite dish, as verbalized is “chopsuey”. She is also fond of
eating salty and sweet foods like, as verbalized, salted peanuts, seafoods, junkfoods,
noodles, kakanin, and drink pop cola.

As verbalized, “Hindi ako naninigarilyo at umiinom ng alak. Wala akong bisyo

magmula ng bata pa ako.”

The patient usually sleeps at around 9 o’clock in the evening after watching
television.

4
d. Social
The patient is happily married to her husband for ten years and they were blessed
by three children. The youngest was said to be under normal in terms of weight. She is
well accepted by her in-laws as well as their relatives. That is evident during the day of
their discharge because according to her, there are relatives outside the hospital waiting
for them together with her in-laws.

Their family’s main source of income is from her husband who works as a
boundary tricycle driver.

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 2. FAMILY HISTORY OF HEALTH AND ILLNESS

7
2 76

T.G. DM

5 60
6

Breast CA HPN

5
55
0

HPN ASTHMA

56 54
HPN HPN

3
51
7

Asthma,T.G,DM A&W

6 1
5yr
d/o 0

A&W A&W A&W

LEGEND:

*HPN-Hypertension
-living female *DM- Diabetes
*Ca- Cancer
*ASTHMA
-living male *T.G.-Toxic Goiter
* d/o – day old
-deceased female *A&W- Alive and Well

-deceased male - It can be deduced from the patient’s genogram that her disease
may be genetically acquired.

-points to patient

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3. HISTORY OF PAST ILLNESS

The client claimed that her childhood immunization was complete. Her first
hospitalization was at the age of seven years old due to severe diarrhea. At the age of
thirteen, she had chicken pox. During her childhood years she also experienced common
colds, cough and fever. She recalled that her mother used to bring her to the
“manghihilot” when ever she had fever and if she had colds and cough her mother used to
prepare oregano decoction. The client also told us that she has no allergic reaction to any
food or drug.
According to the patient, in the year 1997, she was convinced by her friends to
seek for medical advice because of her noticeable enlarged neck. It was also this year
when she experienced excessive sweating, rapid heart rate, weight loss, and easy
fatigability. She told us that her Doctor back then gave prescription drugs for her heart
condition. Unfortunately, she was not able to follow the given dosage because they were
financially challenged. Instead of taking 2 tablets every after meal, she only took one.

4. History of Present Illness

The patient’s symptoms started last 1997. She experienced difficulty of breathing,
palpitations, increased sweating and blurry visions. At first she ignored it but as she
experiences it more often she worried for her health condition. Even her relatives noticed
the enlargement of her neck. The patient said that the palpitations occurs everyday and
she had a difficulty of sleeping at night. She was just at home cleaning the house when
she first experienced the symptoms of her illness. She told us that whenever she
experience difficulty of breathing she stopped in her activity and take a rest because she
doesn’t know what to do. She did not take any medication during the onset of symptoms.
The client told us that approximately 2 hours of bed rest the client will be relieved from
the difficulties because of the frequency of the symptoms. She decided to consult the
doctor so by then she is taking her medicine but every time she had her pregnancy she
stopped taking her medicines without consulting the doctor because she thinks that it
would be harmful for her baby’s health.

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 Due to her present illness the physician’s ordered not to breastfeed her baby
because of her condition.

ANATOMY AND PHYSIOLOGY

The thyroid gland consists of two lobes connected in a smaller band called the isthmus.
The lobes are situated on the right and left sides of the trachea and thyroid cartilage just
below the larynx. It is a highly vascular, large endocrine gland covered with a capsule of
connective tissue. It is made up of spheres of cells called follicles. These follicles are
composed of simple cuboidal epithelium, which produce and secrete thyroid hormones.
Thyroid output is regulated by the hypothalamus, which signals the pituitary to release
TSH to increase thyroid production.
The thyroid gland requires iodine to function properly. In the United States
iodized salt is used as a way to ensure the intake of adequate amounts of iodine in the
diet. In countries with adequate amounts of in the diet, the thyroid gland enlarges forming
goiter. However, proper amounts of iodine cause the thyroid hormone to effectively
produce its hormones. One hormone is thyroxine, also known as tetraiodothyronine,
which contains four iodine atoms and is abbreviated as T4. The other hormone is
triiodothyronine, which contains three iodine atoms and is abbreviated as T3.
These hormones regulate the metabolism of carbohydrates, fats and proteins.
These hormones are necessary for normal growth and development as well as for nervous
system maturation. They cause an increase in the rate of carbohydrate and lipid
breakdown into energy molecules as well as in increasing the rate of protein synthesis. A
lack or low level of thyroid hormones is called hypothyroidism. Too much secretion of
thyroid hormone causes hyperthyroidism. This results in extreme nervousness, fatigue
and an elevated rate of body metabolism.
Thyroid hormone secretion is controlled by TSH produced by anterior pituitary
gland. Increased levels of thyroid hormones, through the negative feedback mechanism,
inhibit the anterior pituitary gland from releasing more TSH and the hypothalamus from

8
secreting TSH-stimulating hormone. Because of negative-feedback, the thyroid hormones
fluctuate daily within a narrow range of concentration in the blood.

Hyperthyroidism
Hyperthyroidism is the second most prevalent endocrine disorder, after diabetes mellitus.
Grave’s 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. It affects women eight times more frequently than men,
with onset usually between the second and fourth decades (Tierney et al., 2005). It may
appear after an emotional shock, stress, or an infection, but the exact significance of these
relationships is not understood. Other common cases of hyperthyroidism include
thyroiditis and excessive ingestion of thyroid hormone.

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,
anmd is likely rto be warm, soft, and moist. However, elderly patients may report dry
skin and diffuse pruritus. A fine tremor of the hands may be observed. Patients may
exhibit exopthalmos (bulging eyes), which produces a startled facial expression.

9
 Other manifestations include an increase appetite and dietary intake, progressive
weight loss, abnormal muscular fatigability and weakness (difficulty in climbing stairs
and rising from a chair), amenorrhea, and changes in bowel function. The pulse rate
ranges constantly between 90 and 160 bpm; the systolic, but characteristically not the
diastolic, blood pressure is elevated; are atrial fibrillation may occur; and cardiac
decompensation in the form of heart failure is common, especially in elderly patients.
Osteoporosis and fracture are also associated with hyperthyroidism.
Cardiac effects may include sinus, tachycardia or dysrhythmias, increased pulse
pressure, and palpitations; it has been suggested that these changes may be related to
increased sensitivity to cathecolamines or to changes in neurotransmitter turnover.
Myocardial hypertrophy and heart failure may occur if the hyperthyroidism is severe and
untreated.
The course of the disease may be mild, characterized by remissions and
exacerbations and terminating with spontaneous recovery in a few months or years.
Conversely, it may progress relentlessly, with the untreated person becoming emaciated,
intensely nervous, delirious, and even disoriented; eventually, the heart fails.
Symptoms of hyperthyroidism may occur with the release of excessive amounts
of thyroid hormones as a result of inflammation after irradiation of the thyroid or
destruction of thyroid tissue by tumor. Such symptoms may also occur with excessive
administration of thyroid hormone for treatment of hypothyroidism. Long-standing use of
thyroid hormone in the absence of close monitoring may be a cause of symptoms of
hyperthyroidism. It is also likely to result in a premature osteoporosis, particularly in
women.
Assessment and Diagnostic Findings
The thyroid gland invariably is enlarged to some extent. It is soft and may pulsate; a thrill
often can be palpated, and a bruit is heart over the thyroid arteries. These are signs of
greatly increased blood flow through the thyroid gland. In advanced cases, the diagnosis
is made on the basis of the symptoms, a decrease in serum TSH, increased free T4, and
an increase in radioactive iodine uptake.
Medical Management

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Appropriate treatment of hyperthyroidism depends on the underlying cause and often
consists of a combination of therapies, including antithyroid agents, radioactive iodine,
and surgery. Treatment of hyperthyroidism is directed toward reducing thyroid
hyperactivity to relieve and preventing complications. Use of radioactive iodine is the
most common form of treatment for Graves’ disease, in North America (Ginsberg, 2003).
Beta-adrenergic blocking agents are used as adjunctive therapy for symptomatic relief,
particularly in transient thyroiditis (Cooper, 2005). Surgical removal of the most of the
thyroid gl;and is a non pharmacologic alternative.
No treatment for thyrotoxicosis is without side-effects, and all three treatments
(radioactive iodine therapy, antithyroid medications, and surgery) share the same
complications: relapse or recurrent hyperthyroidism and permanent hypothyroidism. The
rate of relapse increases in patients who have had very severe disease, along history of
dysfunction, ocular and cardiac symptom, large goiter, or relapse after previous
treatment. The relapse rate after radioactive iodine therapy dependas on the dose used in
treatment. Patients receiving a lower dose of radioactive iodine are more likely to require
subsequent treatment than those being treated with a higher dose. The remission rate
achieved with a single dose of radioactive iodine is 80% (Metso, Jaatienn, Huhtala, et al.,
2004).
Although rates of relapse and the occurrence of the hyperthyroidism vary, relapse
with antithyroid medications is about 45% 1 year after completion of therapy and almost
75 % \5 years later (Larsen, Cronenberg, Melmed, et al., 2003). Discontinuation of
antithyroid medication\s before therapy is complete usually results in relapse within 6
months. The incidence of relapse within subtotal thyroidectomy is 19% at 18 months; and
incidence of hyperthyroidism of 25% has been reported at 18 months after surgery. The
risk of these complications illustrates the importance of long-term follow-up of patients
treated for hyperthyroidism.
Pharmacologic Therapy
Two forms of pharmacologic therapy are available for treating hyperthyroidism and
controlling excessive thyroid activity: (1) used of irradiation by administration of the
radioisotope iodine 131 for destructive effects on the thyroid gland and (2) antithyroid

11
medications that interfere with the synthesis of the thyroid hormones and other agents
that control manifestations of hyperthyroidism.
Radioactive Iodine Therapy. 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. Over a period of several weeks, thyroid cells exposed to the
radioactive iodine are destroyed, resulting in the reduction of the hyperthyroid state and
inevitably hypothyroidism.
The patient is instructed about what to expect with this tasteless, colorless
radioiodine, which may be administered by the radiologist. Typically, a single dose is
needed (Metso et al., 2004). About 95% of patients are cured by 1 dose of radioactive
iodine. The additional 5% require 2 doses: rarely is a third dose necessary. Use of an
ablative dose of radioactive iodine initially causes an acute release of thyroid hormone
from the thyroid gland and may cause an increase of symptoms. The patient is observed
for signs of thyroid storm; propanolol (Inderal) is useful in controlling these symptoms.
After treatment with radioactive iodine, the patient is monitored closely until the
euthyroid state is reached. In three to four weeks, symptoms of hyperthyroidism subside.
Close follow-up is required to evaluate thyroid function, because the incidence of
hypothyroidism after this form of treatment is very high. Approximately 20% of patients
become hypothyroid within 2 years after treatment and another 3%-5% of patients each
year thereafter (Schori-Ahmed, 2003). Thyroid hormone replacement is necessary: small
doses are usually prescribed, with the dose gradually increased over a period of month
(up to about 1 year) until the free T4 and TSH levels within normal ranges.
Radioactive iodine has been used to treat toxic adenomas, multinodular goiter,
and most varieties of thyrotoxicosis (variety rarely with permanent success): it is
preferred for treating patients beyond the child bearing years who have diffuse toxic
goiter. Radioactive treatment is contraindicated during pregnancy (because it crosses the
placenta) and while breastfeeding (because it is secreted in breastmilk) to prevent
hypothyroidism in one infant (Blackwell, 2004). Pregnancy should be postponed for at
least 6 months after treatment.

12
 a major advantage of treatment with radioactive iodine is that it avoids many of
the side effects associated with antithyroid medications. However, some patients and
their families fear medications that are radioactive. For this reason, patients may elect to
take antithyroid medications rather than radioactive iodine.
Antithyroid Medications.

7. Anatomy and Physiology

The thyroid itself is regulated by another gland located in the brain, called the
pituitary. In turn, the pituitary is regulated in part by thyroid hormone that is circulating
in the blood (a "feedback" effect of thyroid hormone on the pituitary gland) and in part by
another gland called the hypothalamus, also a part of the brain.

The hypothalamus releases a hormone called thyrotropin releasing hormone (TRH),

which sends a signal to the pituitary to release thyroid stimulating hormone (TSH). In
turn, TSH sends a signal to the thyroid to release thyroid hormones. If overactivity of any
of these three glands occurs, an excessive amount of thyroid hormones can be produced,
thereby resulting in hyperthyroidism.
Hypothalamus - TRH

Pituitary- TSH

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 Thyroid- T4 and T3

The rate of thyroid hormone production is controlled by the pituitary gland. If there is an
insufficient amount of thyroid hormone circulating in the body to allow for normal
functioning, the release of TSH is increased by the pituitary in an attempt to stimulate the
thyroid to produce more thyroid hormone. In contrast, when there is an excessive amount
of circulating thyroid hormone, the release of TSH is reduced as the pituitary attempts to
decrease the production of thyroid hormone.

8. Pathophysiology

The thyroid gland is usually enlarged to a variable degree and is vascular and diffusely
affected. This results in a smooth, rubbery-firm consistency, and often a bruit is heard on
auscultation. Microscopically, the thyroid follicular cells are hypertrophic and
hyperplastic, and they contain little colloid (stored hormone) and show evidence of
hypersecretion. Lymphocytes and plasma cells infiltrate into the thyroid gland and may
aggregate into lymphoid follicles.

This condition is an autoimmune disorder whereby the thyroid gland is overstimulated by

antibodies directed to the thyroid-stimulating hormone (TSH) receptor on the thyroid
follicular cells. This antibody stimulates iodine uptake, thyroid hormonogenesis and
release, and thyroid gland growth. Although mainly produced within the thyroid gland,
these antibodies reach the circulation and can be measured by various assays in most, but
not all cases.

The association with another autoimmune thyroid disease, Hashimoto thyroiditis, and to a
lesser degree, with other autoimmune diseases in other endocrine glands and other
systems in the same person is high. A strong familial association exists with the same
toxic goiter or the associated disorders, especially Hashimoto thyroiditis. The presence of
Hashimoto thyroiditis, which has more of a destructive effect on the thyroid gland, or the
presence of another antibody, TSH-receptor blocking antibody, results in a variable
natural history of the course of toxic goiter.

NCP

14
DRUG STUDY
Drug Name: Methimazole (Tapazole)
Description: Actively transported in thyroid gland and inhibits thyroid synthesis by
preventing oxidation of trapped iodine. Ten times more potent than PTU, and
once-a-day dose is effective. Euthyroid state is achieved in 4-6 wk, and
maintenance treatment continued for 12-24 mo. Relapse may be observed 1-6
mo after stopping therapy, occasionally later.
Less desirable than propylthiouracil in pregnancy and lactation but may be if
propylthiouracil cannot be used.

15
Adult Dose: 10-40 mg PO qd; decrease dose once euthyroid; minimize dose
needed to maintain euthyroid state
Pediatric Dose: 0.4 mg/kg/d PO divided tid initially, 0.2 mg/kg/d PO divided tid
maintenance; not to exceed 30 mg qd
Contraindications: Documented hypersensitivity
Interactions: Has activity against vitamin K; may potentiate action of oral
anticoagulants
Pregnancy: B - Usually safe but benefits must outweigh the risks
Precautions: Rashes occur in about 3%; agranulocytosis is a rare but severe
complication; measure WBC if sore throat or fever occurs; monitor TFTs during
therapy, and adjust dose once patient is euthyroid

CONTROL OF THYROID FUNCTION

The thyroid gland is a shield-shaped structure located immediately below the larynx in
the anterior middle portion of the neck. It is composed of a large number of tiny, saclike
structures called follicles. These are the functional units of the thyroid. Each follicle is
formed by a single layer of epithelial (follicular) cells and is filled with a secretory
substance called colloid, which consists largely of a glycoprotein-iodine complex called
thyroglobulin.

16
 The thyroglobulin that fills the thyroid follicles is large glycoprotein molecule
that contains 140 tyrosine amino acids. In the process of thyroid synthesis, iodine is
attached to these tyrosines. Both thyroglobulin and iodide are secreted into the colloid of
the follicle by the follicular cells.
The thyroid is remarkably efficient in its use of iodide. A daily absorption of 100
to 200 micro gram of dietary iodide is sufficient to form normal quantities of thyroid
hormone. In the process of removing it from the blood and storing it for future use, iodide
is pumped into the follicular cells against a concentration gradient. As a result, the
concentration of iodide in the normal thyroid gland is approximately 40 times that in the
blood.
Once inside the follicle, most of the iodide is oxidized by the enzyme peoxidase
in a reaction that facilitates combination with a tyrosine molecule to form
monoiodotyrosine and then diiodotyrosine. Two diiodotyrosine residues are coupled to
form thyroxine (T4), or a monoiodotyrosine and a diiodotyrosine are coupled to form a
triiodotyrosine (T3). Only T4 (90 %) and T3 (10 %) are released into the circulation. There
is evidence that T3 is the active form of the hormone and that T 4 is converted to T3 before
it can act physiologically.
Thyroid hormones are bound to thyroid-binding globulin and other plasma
proteins for transport in the blood. Only the free hormone enters cells and regulated the
pituitary feedback mechanism. Protein-bound thyroid hormone forms a large reservoir
that is slowly drawn on as free thyroid hormone is needed. There are three major thyroid-
binding proteins: thyroid hormone-binding globulin (TBG) thyroxine-binding prealbumin
(TBPA), and albumin. More than 99 % of T4 and T3; is carried in the bound form. TBG
carries approximately 70 % of T4 and T3; TBPA binds approximately 10 % of circulating
T4 and lesser amounts of T3; and albumin binds approximately 15 % of circulating T4 and
T3.
A number of disease conditions and pharmacologic agents can decrease the
amount of binding protein in the plasma or influence the binding hormone. Congenital
TBG deficiency is an X-linked trait that occurs in 1 of every 2500 live births.
Corticosteroid medications and systemic disease conditions such as protein malnutrition,
nephritic syndrome, and cirrhosis decrease TBG concentrations. Medications such as

17
phenytoin, salicylates,and diazepam can affect the binding of thyroid hormone to normal
concentrations of binding proteins.
The secretion of thyroid hormone is regulated by the hypothalamic-pituitary-
thyroid feedback system. In this system, thyrotropin-releasing hormone (TRH), which is
produced by thehypothalamus, controls the release of thyroid-stimulating hormone (TSH)
from the anterior pituitary gland. TSH increases the overall activity of the thyroid gland
by increasing thyroglobulin breakdown and the release of thyroid hormone from follicles
into the bloodstream, activating the iodine pump, increasing the iodide and the coupling
of iodide to thyrosine, and increasing the number and the size of the follicle cells. The
effect of TSH on the release of thyroid hormones occurs within approximately 30
minutes, but the other effects require days or weeks.
Increased levels of thyroid hormone act in the feedback inhibition of TRH or
TSH. High levels of iodide (e.g., from iodine-containing cough syrup or kelp tablets) also
cause a temporary decrease in thyroid activity that lasts for several weeks, probably
through a direct inhibition of TSH on the thyroid. Cold exposure is one of the strongest
stimuli for increased thyroid hormone production and probably is mediated through TRH
from the hypothalamus. Various emotional reactions also can affect the output of TRH
and TSH and therefore indirectly affect secretion of thyroid hormones.
Actions of Thyroid Hormone
All of the major organs of the body are affected by altered level of thyroid hormone.
Thyroid hormone has two major functions: it increases metabolism and protein synthesis,
and it is necessary for growth and development in children, including the mental
development and attainment of sexual maturity.
Metabolic Rate
Thyroid hormone increases the metabolism of all body tissues except the retina, spleen,
testes, and lungs. The basal metabolic rate can increase by 60% to 100% above normal
when large amounts of T4 are present. As a result of this higher metabolism, the rate of
glucose, fat, and protein use increases. Lipids are mobilized from adipose tissue, and the
catabolism of cholesterol by the liver is increased. Blood vessels of cholesterol are
decreased in hyperthyroidism. Muscle proteins are broken down and used as fuel,
probably accounting for some of the muscle fatigue that occurs with hyperthyroidism.

18
The absorption of glucose from the gastrointestinal tract is increased. Because vitamins
are essential parts of metabolic enzymes and coenzymes, an increase in metabolic rate
“speeds up” the use of vitamins and tends to cause vitamin deficiency.
Cardiovascular System
Cardiovascular and respiratory functions are strongly affected by thyroid function. With
an increase in metabolism, there is a rise in oxygen consumption and production of
metabolic end products, with an accompanying increase in vasodilation. Blood flow to
the skin, in particular, is augmented as a means of dissipating the body heat that results
from the higher metabolism. Blood volume, cardiac output, and ventilation all are
increased as a means of maintaining the needed cardiac output. On the other hand, blood
pressure is likely to change little because the increase in vasodilation tends to offset the
increase in cardiac output.
Gastrointestinal Function
Thyroid hormone enhances gastrointestinal function, causing an increase in motility and
production of gastrointestinal secretions that often results in diarrhea. An increase in
appetite and food intake accompanies the higher metabolic rate that occurs with increased
thyroid hormone levels. As the same time, weight loss occurs because of the increased
use of calories.
Neuromuscular Effects
Thyroid hormone has marked effects on neural control of muscle function and tone.
Slight elevations in hormone levels cause skeletal muscles to react more vigorously, and
a drop in hormone levels causes muscles to react more sluggishly. In the hyperthyroid
state, a fine muscle tremor is present. The cause of this tremor is unknown, but it may
represent an increased sensitivity of the neural synapses in the spinal cord that control
muscle tone.
In the infant, thyroid hormone is necessary for normal brain development. The
hormone enhances cerebration; in the hyperthyroid state, it causes extreme nervousness,
anxiety, and difficulty in sleeping.
Evidence suggests strong interaction between thyroid hormone and sympathetic
nervous system. Many of the signs and symptoms of hyperthyroidism suggest over
activity of the sympathetic division of the autonomic nervous system, such as

19
tachycardia, palpitations, and sweating. Tremor, restlessness, anxiety, and diarrhea also
may reflect autonomic nervous system imbalances. Drugs that block sympathetic activity
have proved to be valuable adjuncts in the treatment of hyperthyroidism because of their
ability to relieve some of these undesirable symptoms.
Tests of Thyroid Hormone
Various tests aid in the diagnosis of thyroid disorders. Measures of T3, T4 and TSH have
been made available through immunoassay methods. The free T4 test measures the
unbound portion of T4 that is free to enter cells to produce its effects. The resin uptake
test is an inverse to test TBG. The test involves adding radiolabeled T3 or T4 to a serum
sample and allowing it to compete with the T3 or T4 in the sample for binding sites on
TBG. The mixture is then added to a thyroid hormone-binding resin and the resin assayed
for uptake of the labeled T3 or T4. A high resin test result indicated that the serum sample
contains low amount of TBG or high T4 levels. TSH levels are used to differentiate
between primary and secondary thyroid disorders. T3, T4, and free T4 levels are low in
primary hypothyroidism, and the TSH level is elevated.
The radioiodine uptake test measures the ability of the thyroid gland to remove
and concentrate iodine from the blood. Thyroid scans can be used to detect thyroid
nodules and determine the functional activity of the thyroid gland. Ultrasonography can
be used to differentiate cystic from solid thyroid lesions, and CT and MRI scans are used
to demonstrate tracheal compression or impingement on other neighboring structures.

Alterations in Thyroid Function

An alteration in thyroid function can represent a hypofunctional or a hyperfunctional
state. Disorders of the thyroid may be due to a congenital defect in thyroid development,
or they may develop later in life, with a gradual or sudden onset.
Goiter is an increase in the size of the thyroid gland. I can occur in hypothyroid,
euthyroid, and hyperthyroid states. Goiter may be diffuse, involving in the entire gland
without evidence of nodularity, or they may contain nodules. Diffuse goiters usually
become nodular. Goiters may be toxic, producing signs of extreme hyperthyroidism, or
thyrotoxicosis, or they may be nontoxic. Diffuse nontoxic and multinodular goiters are

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the result of compensatory hypertrophy and hyperplasia of follicular epithelium from
some derangement that impairs thyroid hormone output.
The degree of thyroid enlargement usually is proportional to the extent and
duration of thyroid deficiency. Mulinodular goiters produce the largest thyroid
enlargements and often are associated with thyrotoxicosis. When sufficiently enlarged,
they may compress the esophagus and trachea, causing difficulty in swallowing, a
choking sensation, and inspiratory stridor. Such lesions also may compress the superior
vena cava, producing distention of the veins of the neck and upper extremities, edema of
the eyelids and conjunctiva, and syncope with coughing.

Manifestations of Hypothyroidism and Hyperthyroidism

Level of Organization Hypothyroidism Hyperthyroidism
Basal metabolic rate Decreased Decreased
Sensitivity to Decreased Decreased
catecholamines
General features Myxedematous features Exopthalmos
Deep voice Lid lag
Impaired growth (child) Decreased blinking
Blood cholesterol levels Increased Decreased
General behavior Mental retardation (infant) Restlessness, irritability,
anxiety

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 Mental and physical Hyperkinesis
sluggishness
Somnolence Wakefulness
Cardiovascular function Decreased cardiac output Increased cardiac output
Bradycardia Tachycardia and
palpitations
Gastrointestinal function Constipation Diarrhea
Decreased appetite Increased appetite
Respiratory function Hypoventilation Dyspnea
Muscle tone and reflexes Decreased Increased, with tremor and
fibrillatory twitching
Temperature tolerance Cold intolerance Heat intolerance
Skin and hair Decreased sweating Increased sweating
Coarse dry hair Thin and silky skin and hair
Weight Gain Loss

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