Case Study-- Toxic Goiter

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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 1

Transcript of Case Study-- Toxic Goiter

Page 1: Case Study-- Toxic Goiter

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.

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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.

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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.

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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.

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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

T.G. DM

Breast CA HPN

HPN ASTHMA

HPN HPN

Asthma,T.G,DM A&W

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

6

50

72

76

55

5456

37

56

60

51

10

6d/o

5yr

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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

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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.

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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

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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.

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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

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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.

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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 risksPrecautions: 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.

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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 T4 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

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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.

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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

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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 HyperthyroidismBasal metabolic rate Decreased DecreasedSensitivity to catecholamines

Decreased Decreased

General features Myxedematous featuresDeep voiceImpaired growth (child)

ExopthalmosLid lagDecreased blinking

Blood cholesterol levels Increased DecreasedGeneral behavior Mental retardation (infant) Restlessness, irritability,

anxiety

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Mental and physical sluggishnessSomnolence

Hyperkinesis

WakefulnessCardiovascular function Decreased cardiac output

BradycardiaIncreased cardiac outputTachycardia and palpitations

Gastrointestinal function ConstipationDecreased appetite

DiarrheaIncreased appetite

Respiratory function Hypoventilation DyspneaMuscle tone and reflexes Decreased Increased, with tremor and

fibrillatory twitchingTemperature tolerance Cold intolerance Heat intoleranceSkin and hair Decreased sweating

Coarse dry hairIncreased sweatingThin and silky skin and hair

Weight Gain Loss

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