Thyroid Goiter

The term non-toxic goiter refers to enlargement of the thyroid that is not associated with overproduction of thyroid hormone or malignancy.
The thyroid can become very large so that it can easily be seen as a mass in the neck. This picture depicts the outline of a normal size thyroid in
black and the greatly enlarged goiter in pink. There are a number of factors that may cause the thyroid gland to become enlarged. A diet
deficient in iodine can cause a goiter, but this is rarely the cause because of the readily available iodine in our diets. A more common cause of
goiter in America is an increase in thyroid stimulating hormone (TSH) in response to a defect in normal hormone synthesis within the thyroid
gland. The thyroid stimulating hormone comes from the pituitary and causes the thyroid to enlarge. This enlargement usually takes many years
to become manifest.
This picture depicts the typical appearance of a goiter in a middle aged woman. Note how her entire neck looks swollen because of the large
thyroid. This mass will compress the trachea (windpipe) and esophagus (swallowing tube) leading to symptoms such as coughing, waking up from
sleep feeling like you can't breathe, and the sensation that food is getting stuck in the upper throat. Once a goiter gets this big, surgical removal
is the only means to relieve the symptoms. Yes, sometimes they can get a lot bigger than this!

Indications for Treatment

Most small- to moderate-sized goiters can be treated with thyroid hormone in the form of a pill. By supplying thyroid hormone in this
fashion, the pituitary will make less TSH, which should result in stabilization in size of the gland. This technique often will not cause the size of the
goiter to decrease but will usually keep it from growing any larger. Patients who do not respond to thyroid hormone therapy are often referred for
surgery if it continues to grow.
A more common indication for surgical removal of an enlarged thyroid is to remove those glands that are large enough to cause compression on
other structures in the neck, such as the trachea and esophagus. These patients will typically complain of a cough, a slight change in voice, or
nighttime choking episodes because of the way that the gland compresses the trachea while sleeping.
The x-ray on the right shows how an enlarged right thyroid lobe has moved the trachea to the patient's left. The trachea (outlined in light yellow)
should be straight from the mouth down to the lungs. But in this patient, it is compressed and displaced far to the left.
The enlarged gland can even compress the blood vessels of the neck, which is also an indication for its removal. You may read more about this
on our page examining sub-sternal thyroids.

As always, the suspicion of malignancy in an enlarged thyroid is an indication for removal of the thyroid. There is often a dominant nodule within
a multinodular goiter that can cause concern for cancer. Remember, the incidence of malignancy within a multinodular goiter is usually
significantly less than 5%. If the nodule is cold on thyroid scanning, then it may be slightly higher than this. For the vast majority of patients,
surgical removal of a goiter for fear of cancer is not warranted.

Another reason (although not a very common one) to remove a goiter is for cosmetic reasons. Often, a goiter gets large enough that it can be
seen as a mass in the neck. When other people begin to notice the mass, it is usually big enough to begin causing compression of other vital neck
structures—but not always. Sometimes, the large goiter causes no symptoms other than being a cosmetic problem. But if it's big enough to be
seen by your neighbors, you will need medications or surgery, or it will most likely continue to get bigger.

Goiter

Introduction

Background
In 1656, Thomas Wharton described the distinct nature of what he termed the thyroid gland, distinguishing it from the larynx, as this structure
had been considered a laryngeal gland from the time of Andreas Vesalius in the 16th century. It was nearly 200 more years before the function of
the thyroid was elucidated. The normal adult thyroid gland weighs 10-25 g and has 2 lobes connected by an isthmus. Nearly 50% of thyroid
glands exhibit a pyramidal lobe arising from the center of the isthmus. Longitudinal dimensions of the lobes of the thyroid range up to 5 cm, as
shown in the image below.
A goiter is an enlarged thyroid gland, and it may be diffuse or nodular. A goiter may extend into the retrosternal space, with or without
substantial anterior enlargement. Because of the anatomic relationship of the thyroid gland to the trachea, larynx, superior and inferior laryngeal
nerves, and esophagus, abnormal growth may cause a variety of compressive syndromes. Thyroid function may be normal (nontoxic goiter),
overactive (toxic goiter), or underactive (hypothyroid goiter).

Pathophysiology
The thyroid gland is controlled by thyroid-stimulating hormone (TSH; also known as thyrotropin), secreted from the pituitary gland, which in turn
is influenced by the thyrotropin-releasing hormone (TRH) from the hypothalamus. TSH permits growth, cellular differentiation, and thyroid
hormone production and secretion by the thyroid gland. Thyrotropin acts on TSH receptors located on the thyroid gland. Serum thyroid hormones
levothyroxine and triiodothyronine feed back to the pituitary, regulating TSH production. Interference with this TRH-TSH thyroid hormone axis
causes changes in the function and structure of the thyroid gland. Stimulation of the TSH receptors of the thyroid by TSH, TSH-receptor
antibodies, or TSH receptor agonists, such as chorionic gonadotropin, may result in a diffuse goiter. When a small group of thyroid cells,
inflammatory cells, or malignant cells metastatic to the thyroid is involved, a thyroid nodule may develop.
A deficiency in thyroid hormone synthesis or intake leads to increased TSH production. Increased TSH causes increased cellularity and
hyperplasia of the thyroid gland in an attempt to normalize thyroid hormone levels. If this process is sustained, a goiter is established. Causes of
thyroid hormone deficiency include inborn errors of thyroid hormone synthesis, iodine deficiency,1 and goitrogens.
A goiter may result from a number of TSH receptor agonists. TSH receptor stimulators include TSH receptor antibodies, pituitary resistance to
thyroid hormone, adenomas of the hypothalamus or pituitary gland, and tumors producing human chorionic gonadotropin.

Frequency

United States
Autopsy studies suggest a frequency of greater than 50% for thyroid nodules; with high-resolution ultrasonography, the value approaches 40% of
patients with nonthyroidal illness. In the Wickham study from the United Kingdom, 16% of the population had a goiter.2 In the Framingham study,
ultrasonography revealed that 3% of men older than 60 years had thyroid nodules, while 36% of women aged 49-58 years had thyroid nodules.3
In the United States, most goiters are due to autoimmune thyroiditis (ie, Hashimoto disease).

International
Worldwide, the most common cause of goiter is iodine deficiency.1 It is estimated that goiters affect as many as 200 million of the 800 million
people who have a diet deficient in iodine.

In a German study, 635 people underwent ultrasonographic thyroid screening, as well as basal TSH measurement, during a preventive-health
checkup.4 Thyroid nodules were detected in 432 (68%) of the persons screened; in a previous German study, ultrasonographic screening of more
than 90,000 people detected thyroid nodules in 33% of the normal population. The authors of the latter report attributed this difference to the
fact that patients in their study were screened using 13 MHz ultrasonographic scanners, which were more sensitive than the 7.5 MHz scanners
used in the previous study. According to the investigators, their results indicated that the question of routine iodine supplementation requires
renewed attention.

Mortality/Morbidity
Most goiters are benign, causing only cosmetic disfigurement. Morbidity or mortality may result from compression of surrounding structures,
thyroid cancer, hyperthyroidism, or hypothyroidism.

Race
No racial predilection exists.

Sex
The female-to-male ratio is 4:1.

• In the Wickham study, 26% of women had a goiter, compared to 7% of men.2

• Thyroid nodules are less frequent in men than in women, but when found, they are more likely to be malignant.

Age
The frequency of goiters decreases with advancing age. The decrease in frequency differs from the incidence of thyroid nodules, which increases
with advancing age.

Clinical

History
A goiter may present in various ways, including the following:
• Incidentally, as a swelling in the neck discovered by the patient or on routine physical examination
• A finding on imaging studies performed for a related or unrelated medical evaluation
• Local compression causing dysphagia, dyspnea, stridor, plethora or hoarseness
• Pain due to hemorrhage, inflammation, necrosis, or malignant transformation
• Signs and symptoms of hyperthyroidism or hypothyroidism
• Thyroid cancer with or without metastases
Physical
The general examination for hyperthyroidism, hypothyroidism, and autoimmune stigmata is followed by systematic examination of the goiter.
A retrosternal goiter may not be evident on physical examination.
Examination of the goiter is best performed with the patient upright, sitting or standing. Inspection from the side may better outline the thyroid
profile, as shown below. Asking the patient to take a sip of water facilitates inspection. The thyroid should move upon swallowing. See the image
below.
Palpation of the goiter is performed either facing the patient or from behind the patient, with the neck relaxed and not hyperextended. Palpation
of the goiter rules out a pseudogoiter, which is a prominent thyroid seen in individuals who are thin. Each lobe is palpated for size, consistency,
nodules, and tenderness. Cervical lymph nodes are then palpated. The oropharynx is visualized for the presence of lingular thyroid tissue.
The size of each lobe is measured in 2 dimensions using a tape measure. Some examiners make tracings on a sheet of paper, which is placed in
the patient's chart. Suitable landmarks are used and documented to ensure consistent measurement of the thyroid gland.
The pyramidal lobe often is enlarged in Graves disease.
A firm rubbery thyroid gland suggests Hashimoto thyroiditis, and a hard thyroid gland suggests malignancy or Riedel struma.
Multiple nodules may suggest a multinodular goiter or Hashimoto thyroiditis. A solitary hard nodule suggests malignancy, whereas a solitary firm
nodule may be a thyroid cyst.
Diffuse thyroid tenderness suggests subacute thyroiditis, and local thyroid tenderness suggests intranodal hemorrhage or necrosis.
Cervical lymph glands are palpated for signs of metastatic thyroid cancer.
Auscultation of a soft bruit over the inferior thyroidal artery may be appreciated in a toxic goiter. Palpation of a toxic goiter may reveal a thrill in
the profoundly hyperthyroid patient.
Goiters are described in a variety of ways, including the following:
• Toxic goiter: A goiter that is associated with hyperthyroidism is described as a toxic goiter. Examples of toxic goiters include diffuse toxic
goiter (Graves disease), toxic multinodular goiter, and toxic adenoma (Plummer disease).
• Nontoxic goiter: A goiter without hyperthyroidism or hypothyroidism is described as a nontoxic goiter. It may be diffuse or multinodular,
but a diffuse goiter often evolves into a nodular goiter. Examination of the thyroid may not reveal small or posterior nodules. Examples
of nontoxic goiters include chronic lymphocytic thyroiditis (Hashimoto disease), goiter identified in early Graves disease, endemic goiter,
sporadic goiter, congenital goiter, and physiologic goiter that occurs during puberty.
Autonomously functioning nodules may present with inability to palpate the contralateral lobe. Unilobar agenesis may also present like a single
thyroid nodule with hyperplasia of the remaining lobe.
The Pemberton maneuver raises a goiter into the thoracic inlet when the patient elevates the arms. This may cause shortness of breath, stridor,
or distention of neck veins.

Causes
The different etiologic mechanisms that can cause a goiter include the following:

• Iodine deficiency1
• Autoimmune thyroiditis - Hashimoto or postpartum thyroiditis
• Excess iodine (Wolff-Chaikoff effect)5 or lithium ingestion, which decrease release of thyroid hormone
• Goitrogens
• Stimulation of TSH receptors by TSH from pituitary tumors, pituitary thyroid hormone resistance, gonadotropins, and/or thyroid-
stimulating immunoglobulins
• Inborn errors of metabolism causing defects in biosynthesis of thyroid hormones
• Exposure to radiation
• Deposition diseases
• Thyroid hormone resistance
• Subacute thyroiditis (de Quervain thyroiditis)
• Silent thyroiditis
• Riedel thyroiditis
• Infectious agents
○ Acute suppurative - Bacterial
○ Chronic - Mycobacteria, fungal, and parasitic
• Granulomatous disease
• Thyroid malignancy

Differential Diagnoses
Lipomas Thyroid, Papillary
Carcinoma

Thyroid Lymphoma Thyroiditis, Subacute

Thyroid Nodule
Thyroid, Anaplastic
Carcinoma

Thyroid, Medullary
Carcinoma

Other Problems to Be Considered

Branchial cleft cyst
Thyroglossal duct cyst
Cystic hygroma
Pseudogoiter
Lymphadenopathy
Carotid artery aneurysm
Parathyroid cyst
Parathyroid adenoma
Sarcoma
Fibroma
Thyroid abscess
Granulomatous disease of the thyroid
Infectious thyroiditis
Thyrotoxicosis

Workup

Laboratory Studies
• Initial screening should include TSH. Given the sensitive third-generation assays in the absence of symptoms of hyper or hypothyroidism
further testing is not required. An assessment of free thyroxine index or direct measurement of free thyroxine would be the next step in
the evaluation.
• Further laboratory testing is based on presentation and results of screening studies and may include thyroid antibodies (antithyroid
peroxidase formerly the antimicrosomal antibodies and antithyroglobulin), thyroglobulin, sedimentation rate and calcitonin in an
individual at high risk for medullary carcinoma of the thyroid.

Imaging Studies
Ultrasonography

Establish and follow goiter size, consistency, and nodularity.4

Localize nodules for ultrasonographically guided biopsy.
Roentgenography
Roentgenography is used to assess extent of a goiter and presence of calcification. Ultrasonography has replaced this modality.
Roentgenography is used to visualize calcifications within a goiter and regional lymph glands.
Computed tomography (CT) scanning

CT scanning is more precise than roentgenography.

CT scanning can be used to delineate size and goiter extent. Due to the superficial placement of the thyroid gland, ultrasonography is more
useful in following size. CT scanning does a much better job of determining the effect of the thyroid gland on nearby structures. It also may be
useful in the follow-up of patients with thyroid cancer that shows evidence of recurrence.
CT scanning can be used to guide biopsy of the thyroid.

MRI
Magnetic resonance imaging has the same indications as CT scanning (see above).
Radionuclide uptake and radionuclide scanning are used to assess thyroid function and anatomy in hyperthyroidism, as shown below.
Additionally, thyroid scanning may be useful in the patient with neck or superior mediastinal masses. Radionuclide scanning allows determination
of the function of a nodule. Function of a thyroid nodule has value both diagnostically and therapeutically. See the image below.
Other

Barium swallow is used to assess esophageal obstruction.

Spirometry: The flow-volume loop is useful in determining the functional significance of compressive goiters.
Perchlorate discharge test is used in individuals with inborn errors of thyroid hormone synthesis. It is used rarely today to determine the ability to
trap and organify iodine.

Procedures

• Fine-needle aspiration biopsy is used for cytologic diagnosis.6 Fine-needle aspiration of the thyroid is used to determine the cause of an
enlarged gland. In general, the procedure is not used in the workup of autonomously functioning nodules. The procedure has little
morbidity and can be tailored to the situation.
• Core biopsy, or large-needle biopsy, of the thyroid uses a larger gauge needle providing a fragment of tissue. This procedure also carries
with it a higher morbidity. Core biopsy has the advantage of more complete sampling.
• Partial thyroidectomy may be used as a first-line procedure for patients with a high probability of cancer. It is reserved mostly if the
result of a fine-needle aspiration is suspicious or if the patient/physician prefers it.
 • Total thyroidectomy is performed for malignant goiters.

Histologic Findings
Simple nontoxic goiters show hyperplasia, colloid accumulation, and nodularity. Nodular hyperplasia is commonly seen in multinodular goiter.
Cytologic findings include benign appearing follicular cells, abundant colloid, macrophages, and, sometimes, Hürthle cells. Inflammatory disorders
of the thyroid, such as chronic lymphocytic (Hashimoto) thyroiditis, contain a mixed population of lymphocytes mixed with benign appearing
follicular cells. Malignant nodules may be follicular cell in origin, ie, papillary (most common), follicular, Hürthle cell, or anaplastic. They also may
be from parafollicular cells, medullary carcinoma or lymphoma, or other categories.

Treatment

Medical Care
Small benign euthyroid goiters do not require treatment. The effectiveness of medical treatment using thyroid hormone for benign goiters is
controversial. Large and complicated goiters may require medical and surgical treatment. Malignant goiters require medical and surgical
treatment.

• The size of a benign euthyroid goiter may be reduced with levothyroxine suppressive therapy. The patient is monitored to keep serum
TSH in a low but detectable range to avoid hyperthyroidism, cardiac arrhythmias, and osteoporosis. The patient has to be compliant with
monitoring. Some authorities suggest suppressive treatment for a definite time period instead of indefinite therapy. Patients with
Hashimoto thyroiditis respond better.
• Treatment of hypothyroidism or hyperthyroidism often reduces the size of a goiter.
• Thyroid hormone replacement is often required following surgical and radiation treatment of a goiter. Use of radioactive iodine for the
therapy of nontoxic goiter has been disappointing and is controversial.
• Medical therapy of autonomous nodules with thyroid hormone is not indicated.
• Ethanol infusion into benign thyroid nodules has not been approved in the United States, but it is used elsewhere.

Surgical Care
Surgery is reserved for the following situations:
• Large goiters with compression
• Malignancy
• When other forms of therapy are not practical or ineffective

Consultations
An endocrinologist should assess a patient at least once, and assessment should be even more frequent if the goiter is complicated by thyroid
dysfunction or malignancy or if the patient is being considered for surgical management.

Diet
Nutrition plays a role in the development of endemic goiters. Dietary factors include iodine deficiency, goitrogens, protein malnutrition, and
energy malnutrition. Often these factors occur concurrently.

• Iodine: If it is practical, treat endemic goiters in iodine-deficient regions with iodine supplementation in the diet and avoidance of
goitrogens. Treatment with iodine supplementation or levothyroxine may reduce goiter size.1
• Goitrogens: Cyanoglucosides are naturally occurring goitrogens that are digested to release cyanide, which is converted to thiocyanate.
Thiocyanate inhibits iodide transport in the thyroid and, at higher levels, inhibits organification. Foods that contain cyanoglucosides
include cassava, lima beans, maize, bamboo shoots, and sweet potatoes. Thioglucosides are natural goitrogens found in the Cruciferae
family of vegetables and weeds eaten by animals. When digested, they release thiocyanate and isothiocyanate, which have
thionamidelike properties and are passed to humans via milk ingestion.

Medication
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Thyroid hormone replacements

Benign goiters can be treated with thyroid hormone. The most widely used thyroid hormone is levothyroxine sodium, administered once a day.
Liothyronine sodium requires more frequent administration. Desiccated thyroid powder, thyroglobulin, and liotrix are less predictable following
ingestion.

Levothyroxine sodium (Synthroid, Levoxyl, Levothroid)

Synthetic thyroxine is converted to the active form, triiodothyronine, in the pituitary by 5'-deiodinase. Inhibits production of thyrotropin, which is
the main growth factor for the thyroid gland.

Follow-up

Further Inpatient Care

Preoperatively, establish euthyroid state prior to surgical treatment. Evaluation must include the stability of the airway. This must be secured
immediately if ventilatory status appears tenuous. Emergency surgical treatment of a goiter in a patient with hypothyroidism requires
intravenous levothyroxine and glucocorticoids at stress doses.
Emergency surgical treatment of a goiter in a thyrotoxic patient requires antithyroid medications, beta-blockers, and glucocorticoids at stress
doses. Suppressive doses of iodine are helpful.
Intraoperative and postoperative management includes hemodynamic monitoring, which is important in patients with preoperative
hyperthyroidism or hypothyroidism.
Postoperative management also includes monitoring of serum calcium.

Further Outpatient Care

Patients are monitored for hypothyroidism by history, examination, and TSH measurements. Initially, monitoring occurs every 6-8 weeks.

Inpatient & Outpatient Medications

Benign euthyroid goiters do not require any medication. Goiters with primary thyroid malignancy require levothyroxine replacement after surgery
and radioactive iodine ablation. Metastatic lesions to the thyroid gland require treatment of the primary malignancy. Granulomatous and
infectious etiologies for goiter require specific treatment depending on the underlying cause.

Deterrence/Prevention
Goiter prevention is based on etiology.

Correct iodine deficiency1 and avoid dietary or iatrogenic goitrogens if practical. In the United States, it is difficult to find iodine deficiency, given
the supplementation of table salt with iodine, iodine in cattle feed, and the use of iodine as a dough conditioner. Judicious use of levothyroxine is
helpful in patients with a previous diagnosis of nodular hyperplasia who have had a lobectomy to prevent occurrences in the contralateral lobe.

Goiters due to autoimmune thyroiditis may be controlled with careful use of levothyroxine and, when indicated, anti-inflammatory medication.

Congenital goiters due to inborn errors of metabolism may be reduced or prevented by careful use of levothyroxine during the postpartum
period. Newborns are screened for congenital hypothyroidism.

Complications
• Large goiters may cause compression of the trachea, with tracheomalacia and asphyxiation.
• Hyperthyroidism occurs in some patients exposed to iodine (ie, Jodbasedow phenomenon).
• A patient with autoimmune goiters may develop lymphoma. Multinodular goiters may undergo malignant transformation.
• Nodular goiters may cause pain, intranodular necrosis, or hemorrhage.
• Thyroid abscess may be associated with pain, fever, bacteremia, or sepsis.

Prognosis
• Benign goiters have a good prognosis. However, all goiters should be monitored by examination and biopsy for possible malignant
transformation, which may be signaled by a sudden change in size, pain, or consistency. Fortunately, the risk of this is low. In patients
exposed to low levels of radiation the risk rises.
• Based on the Wickham study, a few of the goiters increased in size.2
• A small percentage of multinodular goiters do cause hyperthyroidism. Lifelong surveillance is necessary.
• Patients with chronic lymphocytic thyroiditis generally have glands that become atrophic.

Patient Education
• Educate a patient about potential etiologies, eg, adequate dietary iodine intake, avoidance of goitrogens, regular personal neck
examination, and physician examination.
• For patients on medical therapy, reinforce the need to take medications on a regular basis. Review symptoms of hyperthyroidism.
• For excellent patient education resources, visit eMedicine's Endocrine System Center. Also, see eMedicine's patient education article
Thyroid Problems.

Miscellaneous

Medicolegal Pitfalls
• Autoimmune thyroiditis goiters have a higher association with lymphoma.
• A nodular goiter with hypertension may be associated with a pheochromocytoma.
• A "thyroid nodule" could be a parathyroid tumor.
• Pain and enlargement of a nodule may be due to hemorrhage or anaplastic carcinoma.
• Rapid growth of the thyroid in a patient with extrathyroidal cancer may signal metastasis to the thyroid.
• A goiter with prior radiation exposure may develop lymphoma.
• Levothyroxine use for goiter control warrants close monitoring to avoid hyperthyroidism, arrhythmias, and osteoporosis.
• Hyperthyroidism does not exclude presence of a papillary carcinoma. Follicular carcinomas can retain enough function to result in
hyperthyroidism.
• Thyroid fine-needle aspiration becomes less reliable in large goiters because of sampling bias. Likewise, very small nodules may be
missed. Thyroid cysts should not be left without first detecting the underlying cause. Nondiagnostic biopsy findings should precipitate
further investigation, which may include performing an additional biopsy or more invasive procedures, depending on the clinical
situation.
Special Concerns
• Withhold treatment of a benign euthyroid goiter in patients who are pregnant until after delivery.
• Thyroidectomy, if necessary, can be more safely performed in the second trimester.
Pathophysiology, Complications and Management of Goiter
Patients that are not responding well with levothyroxine may undergo thyrodectomy procedure. Depending on the size of the goiter and how
much the thyroid gland should be removed or destroyed, thyrodectomy may destroy sufficient thyroid tissue which helps produce
hypothyroidism. This requires a life-long treatment together with thyroid hormonal pills.

This disease, an autoimmune disorder, is the most common cause of an overactive thyroid (hyperthyroidism). In Graves' disease, antibodies
produced by your immune system stimulate the thyroid to produce too much thyroxine. Normally, your immune system uses antibodies to help
protect against viruses, bacteria and other foreign substances that invade the body. In Graves' disease, antibodies mistakenly attack your thyroid
gland and occasionally the tissue behind your eyes and the skin of your lower legs. The overstimulation of your thyroid in Graves' disease results
in uniform and nonpainful swelling of the gland," said the Mayo Clinic.

Small doses of iodine may offer temporary relief and are usually given in preparation for thyroid surgery. Certain drugs may correct thyroid gland
overactivity.

Goiter can also be caused by hereditary factors and excessive intake of iodine. Symptoms include thyroid enlargement which vary from single
small nodule to massive enlargement or a neck lump. One experiences swallowing difficulties due to compression of the esophagus. Breathing
difficulties are experienced, neck vein distention and dizziness when arms are raised above the head. Goiter can be detected through thyroid
scan, ultrasound of thyroid, low urinary excretion of iodine, high or normal thyroid stimulating hormone, normal or increased radioactive iodine
uptake and others.

Goiter can be treated and prevented through various ways. Moderate goiters can be treated by providing a thyroid hormone pill. This makes the
pituitary secrete less thyroid hormone which results in well stabilized size of the gland. Hence this will not decrease the size of the goiter but will
inhibit further growth. Surgical operation is also performed to remove those glands that are enlarged enough to cause compression on other vital
pars in the neck i.e. trachea and esophagus. Prevent goiter by taking iodized table salt and eat limited gotrogenic food and drugs to prevent
sporadic goiter.

One may think that if the thyroid gland is enlarged, there should be a corresponding increase in the production of thyroid hormones. But that is
not always so, although in some of the cases, the gland may turn toxic or hyperactive, or underactive, and yet in some other cases, malignancy
may develop, as in cases of multinodular goiter. Hence the size of the thyroid gland may not indicate the true pathology developing in the gland.

Deficiency of iodine or any of the other causes of goiter leads to interference in the synthesis of thyroxine. This disturbance leads to thyroxine
deficiency. Thyroxine deficiency stimulates the thyroid gland to produce excess thyrotrophin which subsequently leads to hypertrophy and
hyperplasia of thyroid cellular tissue. This brings about goiter or thyroid adenoma which manifest as swelling in the neck.
Diagnosis
Diagnosis is usually by presenting signs (swelling in the neck) and radio active iodine test to confirm the goiter of iodine deficiency which usually
takes up excessive amounts of 131I radio active iodine.
Complications of goiter
1. Venous engorgement: As a result of pressure on the neck, venous return is obstructed leading to engorgement in the veins of the neck.
2. Respiratory obstruction: pressure on the neck could also obstruct respiratory apparatus leading to respiratory distress.
3. Difficulty in swallowing: The pressure also obstructs the oesophagus thereby producing difficulty in swallowing.
4. Toxicity: Goiter may also progress to become Grave's disease (excessive activity of the thyroid gland otherwise known as hyperthyroidism)
Management
Goiter can only be properly managed if the actual cause is known otherwise treatment may provoke further complications. An attempt to reduce
the hyperplasia may lead to a suppression of the function of the thyroid gland, and haemorrhage may occur and increase its size further.
Nevertheless, the following can be done to help the patient:
a. In case of iodine deficiency, thyroid hormone should be given to suppress the goiter.
b. Goitrogens should be eliminated from the patient's food if he has been on foods that are goitrogenic.
c. Surgery: A partial thyroidectomy is carried out to reduce the size of the growth, and relieve the symptoms. The surgery is also performed for
cosmetic reasons.
Prevention
The nurse at the community level should help to bring endemic goiter under control. The dietary habit of the people should be investigated to
determine the quantity of iodine they consume.
History should be taken from parents and children to find out the type of food available in their areas. Possibly soil samples can be analysed to
determine their iodine levels.

PATOFISIOLOGI GOITER / GONDOK

2.1 Definisi
Goiter adalah pembesaran pada kelenjar tiroid. Pembesaran ini dapat memiliki fungsi kelenjar yang normal (eutirodisme), pasien tyroid
(hipotiroidisme) atau kelebihan produksi hormon (hipetiroidisme). Terlihat pembengkakan atau benjolan besar pada leher sebelah depan (pada
tenggorokan) dan terjadi akibat pertumbuhan kelenjar tiroid yang tidak normal.
2.2 Anatomi dan Fisiologi Kelenjar Tiroid
Kelenjar tiroid ialah organ endokrin yang terletak di leher manusia. Fungsinya ialah mengeluarkan hormon tiroid. Hormon yang terpenting ialah
Thyroxine (T4) dan Triiodothyronine (T3).
Kelenjar tiroid terdiri dari dua lobus, satu di sebelah kanan dan satu lagi disebelah kiri. Keduanya dihubungkan oleh suatu struktur ( yang
dinamakan isthmus atau ismus). Setiap lobus berbentuk seperti buah pir. Kelenjar tiroid mempunyai satu lapisan kapsul yang tipis dan
pretracheal fascia. Pada keadaan tertentu kelenjar tiroid aksesoria dapat ditemui di sepanjang jalur perkembangan embriologi tiroid.
Sel tiroid adalah satu-satunya sel dalam tubuh manusia yang dapat menyerap iodin atau yodium yang diambil melalui pencernaan makanan.
Iodin ini akan bergabung dengan asam amino tirosin yang kemudian akan diubah menjadi T3 (triiodotironin) dan T4 (tiroksin). Dalam keadaan
normal pengeluaran T4 sekitar 80% dan T3 15%. Sedangkan yang 5% adalah hormon-hormon lain seperti T2.
T3 dan T4 membantu sel mengubah oksigen dan kalori menjadi tenaga (ATP = adenosin tri fosfat). T3 bersifat lebih aktif daripada T4. T4 yang
tidak aktif itu diubah menjadi T3 oleh enzim 5-deiodinase yang ada di dalam hati dan ginjal. Proses ini juga berlaku di organ-organ lain seperti
hipotalamus yang berada di otak tengah.
Hormon-hormon lain yang berkaitan dengan fungsi tiroid ialah TRH (thyroid releasing hormon) dan TSH (thyroid stimulating hormon). Hormon-
hormon ini membentuk satu sistem aksis otak (hipotalamus dan pituitari)- kelenjar tiroid. TRH dikeluarkan oleh hipotalamus yang kemudian
merangsang kelenjar pituitari mengeluarkan TSH. TSH yang dihasilkan akan merangasang tiroid untuk mengeluarkan T3 dan T4. Oleh kerena itu
hal yang mengganggu jalur di atas akan menyebabkan produksi T3 dan T4.
Adapun struktur tiroid terdiri atas sejumlah besar vesikel-vesikel yang dibatasi oleh epitelium silinder disatukan oleh jaringan ikat sel-selnya
mengeluarkan sera. Adapun fungsi kelenjar tiroid adalah:
1. Bekerja sebagai perangsang proses oksidasi
2. Mengatur pengguanaan oksidasi
3. Mengatur pengeluaran karbondioksida
4. Metabolik dalam hal pengaturan susunan kimia dalam jaringan
5. Pada anak mempengaruhi perkembangan fisik dan mental.
2.3 Etiologi
a. Defisiensi Yodium.
Yodium sendiri dibutuhkan untuk membentuk hormon tyroid yang nantinya akan diserap di usus dan disirkulasikan menuju bermacam-macam
kelenjar. Kelenjar tersebut diantaranya:
1. Choroid
2. Ciliary body
3. Kelenjar susu
4. Plasenta
5. Kelenjar air ludah
6. Mukosa lambung
7. Intenstinum tenue
8. Kelenjar gondok
Sebagaian besar unsur yodium ini dimanfaatkan di kelenjar gondok. Jika kadar yodium di dalam kelenjar gondok kurang, dipastikan seseorang
akan mengidap penyakit gondok.
1. Tiroiditis Hasimoto’s
Ini adalah kondisi autoimun di mana terdapat kerusakan kelenjar tiroid oleh sistem kekebalan tubuh sendiri. Sebagai kelenjar menjadi lebih
rusak, kurang mampu membuat persediaan yang memadai hormon tiroid.
1. Penyakit Graves
Sistem kekebalan menghasilkan satu protein, yang disebut tiroid stimulating imunoglobulin (TSI). Seperti dengan TSH, TSI merangsang kelenjar
tiroid untuk memperbesar memproduksi sebuah gondok.
1. Multinodular Gondok
Individu dengan gangguan ini memiliki satu atau lebih nodul di dalam kelenjar tiroid yang menyebabkan pembesaran. Hal ini sering terdeteksi
sebagai nodular pada kelenjar perasaan pemeriksaan fisik. Pasien dapat hadir dengan nodul tunggal yang besar dengan nodul kecil di kelenjar,
atau mungkin tampil sebagai nodul beberapa ketika pertama kali terdeteksi.
1. Kanker Tiroid
Thyroid dapat ditemukan dalam nodul tiroid meskipun kurang dari 5 persen dari nodul adalah kanker. Sebuah gondok tanpa nodul bukan
merupakan resiko terhadap kanker.
f. Kehamilan
Sebuah hormon yang disekresi selama kehamilan Chorionic manusia (gonadotropin) dapat menyebabkan pembesaran kelenjar tiroid.
1. Tiroiditis
Peradangan dari kelenjar tiroid sendiri dapat mengakibatkan pembesaran kelenjar tiroid. Hal ini dapat mengikuti penyakit virus atau kehamilan.
2.4 Klasifikasi Goiter
1. Goiter kongenital
Hampir selalu ada pada bayi hipertiroid kongenital, biasanya tidak besar dan sering terjadi pada ibu yang memiliki riwayat penyakit graves.
2. Goiter endemik dan kretinisme
Biasa terjadi pada daerah geografis dimana detistensi yodium berat, dekompensasi dan hipotiroidisme dapat timbul karenanya, goiter endemik
ini jarang terjadi pada populasi yang tinggal disepanjang laut.
3. Goiter sporadis
Goiter yang terjadi oleh berbagai sebab diantaranya tiroiditis fositik yang terjadi lazim pada saudara kandung, dimulai pada awal kehidupan dan
kemungkinan bersama dengan hipertiroidisme yang merupakan petunjuk penting untuk diagnosa. Digolongkan menjadi 3 (tiga) bagian yaitu :
1. a. Goiter yodium
Goiter akibat pemberian yodium biasanya keras dan membesar secara difus, dan pada beberapa keadaan, hipotirodisme dapat berkembang.
b. Goiter sederhana (Goiter kollot)
Yang tidak diketahui asalnya. Pada pasien bistokgis tiroid tampak normal atau menunjukan berbagai ukuran follikel, koloid dan epitel pipih.
c. Goiter multinodular
Goiter keras dengan permukaan berlobulasi dan tunggal atau banyak nodulus yang dapat diraba, mungkin terjadi perdarahan, perubahan kistik
dan fibrosis.
4. Goiter intratrakea
Tiroid intralumen terletak dibawah mukosa trakhea dan sering berlanjut dengan tiroid ekstratrakea yang terletak secara normal.
Klasifikasi Goiter menurut WHO :
1. Stadium O – A: tidak ada goiter.
2. Stadium O – B: goiter terdeteksi dari palpasi tetapi tidak terlihat walaupun leher terekstensi penuh.
3. Stadium I : goiter palpasi dan terlihat hanya jika leher terekstensi penuh.
4. Stadium II: goiter terlihat pada leher dalam Potersi.
5. Stadium III : goiter yang besar terlihat dari Darun.
2.5 Patofisiologi
Aktifitas utama kelenjar tiroid adalah untuk berkonsentrasi yodium dari darah untuk membuat hormon tiroid. Kelenjar tersebut tidak dapat
membuat hormon tiroid cukup jika tidak memiliki cukup yodium. Oleh karena itu, dengan defisiensi yodium individu akan menjadi hipotiroid.
Akibatnya, tingkat hormon tiroid terlalu rendah dan mengirim sinyal ke tiroid. Sinyal ini disebut thyroid stimulating hormone (TSH). Seperti
namanya, hormon ini merangsang tiroid untuk menghasilkan hormon tiroid dan tumbuh dalam ukuran yang besar Pertumbuhan abnormal dalam
ukuran menghasilkan apa yang disebut sebuah gondok
Kelenjar tiroid dikendalikan oleh thyroid stimulating hormone (TSH) yang juga dikenal sebagai thyrotropin. TSH disekresi dari kelenjar hipofisis,
yang pada gilirannya dipengaruhi oleh hormon thyrotropin releasing hormon (TRH) dari hipotalamus. Thyrotropin bekerja pada reseptor TSH
terletak pada kelenjar tiroid. Serum hormon tiroid levothyroxine dan triiodothyronine umpan balik ke hipofisis, mengatur produksi TSH.
Interferensi dengan sumbu ini TRH hormon tiroid TSH menyebabkan perubahan fungsi dan struktur kelenjar tiroid. Stimulasi dari reseptor TSH
dari tiroid oleh TSH, TSH reseptor antibodi, atau agonis reseptor TSH, seperti chorionic gonadotropin, dapat mengakibatkan gondok difus. Ketika
sebuah kelompok kecil sel tiroid, sel inflamasi, atau sel ganas metastasis untuk tiroid terlibat, suatu nodul tiroid dapat berkembang.
Kekurangan dalam sintesis hormon tiroid atau asupan menyebabkan produksi TSH meningkat. Peningkatan TSH menyebabkan peningkatan
cellularity dan hiperplasia kelenjar tiroid dalam upaya untuk menormalkan kadar hormon tiroid. Jika proses ini berkelanjutan, maka akan
mengakibatkan gondok. Penyebab kekurangan hormon tiroid termasuk kesalahan bawaan sintesis hormon tiroid, defisiensi yodium, dan
goitrogens.
Gondok dapat juga terjadi hasil dari sejumlah agonis reseptor TSH. Pendorong reseptor TSH termasuk antibodi reseptor TSH, resistensi terhadap
hormon tiroid hipofisis, adenoma kelenjar hipofisis hipotalamus atau, dan tumor memproduksi human chorionic gonadotropin.
Pemasukan iodium yang kurang, gangguan berbagai enzim dalam tubuh, hiposekresi TSH, glukosil goitrogenik (bahan yang dapat menekan
sekresi hormone tiroid), gangguan pada kelenjar tiroid sendiri serta factor pengikat dalam plasma sangat menentukan adekuat tidaknya sekresi
hormone tiroid. Bila kadar – kadar hormone tiroid kurang maka akan terjadi mekanisme umpan balik terhadap kelenjar tiroid sehingga aktifitas
kelenjar meningkat dan terjadi pembesaran (hipertrofi).
Dampak goiter terhadap tubuh terletak pada pembesaran kelenjar tiroid yang dapat mempengaruhi kedudukan organ-organ lain di sekitarnya. Di
bagian posterior medial kelenjar tiroid terdapat trakea dan esophagus. Goiter dapat mengarah ke dalam sehingga mendorong trakea, esophagus
dan pita suara sehingga terjadi kesulitan bernapas dan disfagia yang akan berdampak terhadap gangguan pemenuhan oksigen, nutrisi serta
cairan dan elektrolit. Penekanan pada pita suara akan menyebabkan suara menjadi serak atau parau.
Bila pembesaran keluar, maka akan memberi bentuk leher yang besar dapat simetris atau tidak, jarang disertai kesulitan bernapas dan disfagia.
Tentu dampaknya lebih ke arah estetika atau kecantikan. Perubahan bentuk leher dapat mempengaruhi rasa aman dan konsep diri klien.
2.6 Manifestasi klinis
Gejala utama :

1. Pembengkakan, mulai dari ukuran sebuah nodul kecil untuk sebuah benjolan besar, di bagian depan leher tepat di bawah Adam’s apple.
2. Perasaan sesak di daerah tenggorokan.
3. Kesulitan bernapas (sesak napas), batuk, mengi (karena kompresi batang tenggorokan).
4. Kesulitan menelan (karena kompresi dari esofagus).
5. Suara serak.
6. Distensi vena leher.
7. Pusing ketika lengan dibangkitkan di atas kepala
8. Kelainan fisik (asimetris leher)
Dapat juga terdapat gejala lain, diantaranya :
1. Tingkat peningkatan denyut nadi
2. Detak jantung cepat
3. Diare, mual, muntah
4. Berkeringat tanpa latihan
5. Goncangan
 6. Agitasi
2.7 Pemeriksaan Diagnostik

1. Pengukuran T3 (Triodothyroxin) dan T4 (Tiroksin)

Nilai normal pada orang dewasa adalah sebagai berikut :
Iodium bebas : 0,1-0,6 ml/dl
T3 : 0,2-0,3 ml/dl
T4 : 6-12 ml/dl
Nilai normal pada bayi/anak :
T3 : 180-240
Hasil pemeriksaan dengan radioisotop adalah ukuran, bentuk lokasi, dan yang utama ialah fungsi bagian-bagian tiroid. Pada pemeriksaan ini
pasien diberi NaI peroral dan setelah 24 jam secara fotografik ditentukan konsentrasi yodium radioaktif yang ditangkap oleh tiroid. Nilai
normalnya 10-35%. Jika , 10% disebut menurun (hipotiroidisme), jika .35% disebut meninggi (hipertiroidisme).Dari hasil sidik tiroid dibedakan 3
bentuk :
1. Nodul dingin bila penangkapan yodium nihil atau kurang dibandingkan sekitarnya.
2. Nodul panas bila penangkapan yodium lebih banyak dari pada sekitarnya. Keadaan ini memperlihatkan aktivitas yang berlebih.

3. Nodul hangat bila penangkapan yodium sama dengan sekitarnya. Ini berarti fungsi nodul sama dengan bagian tiroid yang lain.
4. Scintiscan yodium radio aktif dengan teknetium porkeknera, untuk melihat medulanya.
5. Sidik ultrasoud untuk mendeteksi perubahan-perubahan kistik pada medula tiroid.
Pemeriksaan ini dapat membedakan antara padat, cair, dan beberapa bentuk kelainan, tetapi belum dapat membedakan dengan pasti ganas
atau jinak. Kelainan-kelainan yang dapat didiagnosis dengan USG :
1. Kista
2. Adenoma
3. Kemungkinan karsinoma
4. Tiroiditis
5. Foto polos leher dan dada atau berguna untuk menunjukan pergeseran trakea dan esofagus.
6. Esofagogram untuk menunjukan goiter sebagai penyebab disfagia.
2.9 Penatalaksanaan
Perawatan akan tergantung pada penyebab gondok.
1. Defisiensi Yodium
Gondok disebabkan kekurangan yodium dalam makanan maka akan diberikan suplementasi yodium melalui mulut. Hal ini akan menyebabkan
penurunan ukuran gondok, tapi sering gondok tidak akan benar-benar menyelesaikan.
1. Hashimoto Tiroiditis
Jika gondok disebabkan Hashimoto tiroiditis dan hipotiroid, maka akan diberikan suplemen hormon tiroid sebagai pil setiap hari. Perawatan ini
akan mengembalikan tingkat hormon tiroid normal, tetapi biasanya tidak membuat gondok benar-benar hilang. Walaupun gondok juga bisa lebih
kecil, kadang-kadang ada terlalu banyak bekas luka di kelenjar yang memungkinkan untuk mendapatkan gondok yang jauh lebih kecil. Namun,
pengobatan hormon tiroid biasanya akan mencegah bertambah besar.
1. Hipertiroidisme
Jika gondok karena hipertiroidisme, perawatan akan tergantung pada penyebab hipertiroidisme. Untuk beberapa penyebab hipertiroidisme,
perawatan dapat menyebabkan hilangnya gondok. Misalnya, pengobatan penyakit Graves dengan yodium radioaktif biasanya menyebabkan
penurunan atau hilangnya gondok.
Tujuan pengobatan hipertiroidisme adalah membatasi produksi hormon tiroid yang berlebihan dengan cara menekan produksi (obat antitiroid)
atau merusak jaringan tiroid (yodium radioaktif, tiroidektomi subtotal).
1. Obat antitiroid
Indikasi :
1. Terapi untuk memperpanjang remisi atau mendapatkan remisi yang menetap, pada pasien muda dengan struma ringan sampai sedang
dan tirotoksikosis.
2. Obat untuk mengontrol tirotoksikosis pada fase sebelum pengobatan, atau sesudah pengobatan pada pasien yang mendapat yodium
aktif.
3. Persiapan tiroidektomi
4. Pengobatan pasien hamil dan orang lanjut usia
5. Pasien dengan krisis tiroid
Obat antitiroid yang sering digunakan :
Karbimazol 30-60 5-20
Metimazol 30-60 5-20
Propiltourasil 300-600 5-200
1. Pengobatan dengan yodium radioaktif
Indikasi :
1. Pasien umur 35 tahun atau lebih
 2. Hipertiroidisme yang kambuh
3. Gagal mencapai remisi sesudah pemberian obat antitiroid
4. Adenoma toksik, goiter multinodular toksik
1. Operasi
Tiroidektomi subtotal efektif untuk mengatasi hipertiroidisme.
Indikasi :
1. Pasien umur muda dengan struma besar serta tidak berespons terhadap obat antitiroid.
2. Pada wanita hamil (trimester kedua) yang memerlukan obat antitiroid dosis besar
3. Alergi terhadap obat antitiroid, pasien tidak dapat menerima yodium radioaktif
4. Adenoma toksik atau struma multinodular toksik
5. Pada penyakit Graves yang berhubungan dengan satu atau lebih nodul
6. Multinodular
Banyak gondok, seperti gondok multinodular, terkait dengan tingkat normal hormon tiroid dalam darah. Gondok ini biasanya tidak memerlukan
perawatan khusus setelah dibuat diagnosa yang tepat.
2.8 Pencegahan
a. Penggunaan yodium yang cukup, makan makanan yang banyak mengandung yodium, seperti ikan laut, ganggang-ganggangan dan sayuran
hijau. Untuk penggunaan garam beryodium dalam masakan perlu diperhatikan. Garam yodium bisa ditambahkan setelah masakan matang,
bukan saat sedang memasak sehingga yodium tidak rusak karena panas.
1. Pada ibu hamil dianjurkan agar tidak menggunakan obat-obatan yang beresiko untuk ketergantungan goiter kongenital.
2. Hindari mengkonsumsi secara berlebihan makanan-makanan yang mengandung goitrogenik glikosida agent yang dapat menekan
sekresi hormone tiroid seperti ubi kayu, jagung, lobak, kankung, dan kubis.

ASUHAN KEPERAWATAN PADA PENYAKIT GOITER

PENDAHULUAN
Tumor pada kelenjar tiroid diklasifikasikan berdasarkan sifat benigna atau maligna selain berdasarkan ada tidaknya tirotoksikosis dan kualitas
pembesaran kelenjar tersebut yang dapat menyebar atau ireguler. Jika pembesaran kelenjar tiroid cukup membuat kelenjar tersebut terlihat
pada leher, tumor ini dinamakan Goiter atau gondok. ( Susanne, keperawatan medikal bedah Brunner, hal.1315)

PENGERTIAN
TIPE GOITER
Goiter toksikθ
Goiter yang disertai dengan hipertiriodisme. Hipertiroidisme dapat didefenisikan sebagai respon jaringan-jaringan tubuh terhadap pengaruh
metabolik hormon tiroid yang berlebihan. Keadaan ini dapat timbul spontan atau akibat asupan hormon tiroid secara berlebihan. Ciri-ciri tiroidal
berupa goiter akibat hiperplasia kelenjar tiroid dan hipertiroidisme akibat sekresi hormon tiroid yang berlebihan.

Goiter nontoksikθ
Etiologi goiter non toksik antara lain adalah defisiensi iodium atau gangguan kimia intra tiroid oleh berbagai faktor.

Simple goiter atau Goiter koloidθ

Tipe penyakit goiter yang sering ditemukan terutama pada kawasan geografis yang kekurangan iodium. Penyakit ini disebabkan oleh defisiensi
iodium dan konsumsi sat goitrogenik dalam jumlah yang lebih besar oleh pasien dengan kelenjar tiroid yang rentan. Zat ini mencakup pemberian
iodium atau litium secara berlebihan untuk pengobatan manik-depresif.
Simpel goiter menggambarkan keadaan hipertropi kompensatoripada kelenjar tiroid yang kemungkinan disebabkan stimulasi kelenjar tiroid.
Kelenjar hipofisis menghasilkan tirotropin atau TSH, yaitu suatu hormon yang mengontrol pelepasan hormon dari kelenjar tiroid, produksinya
meningkat, jika aktivitas tioid berada dibawah normal seperti pada iodium tidak cukup untuk produksi hormon tiroid. Penyakit goiter semacam ini
biasanya tidak menimbulkan gejala kecuali pembesaran pada leher, yang terjasi secara berlebihan, dapat mengakibatkan kompressi trakea.
Apabila tindakan operatif dianjurkan, komplikasi pasca operatif dapat dikurangi dengan menempatkan keadaan ioditiroid pra operatif yang
ditimbulkan oleh pengobatan dengan preparat anti tiroid dan pemberian senyawa iodida pra operatif untuk mengurangi ukuran serta
vaskularisasi.

Goiter nodulerθ
Kelenjar tiroid tertentu bersifat noduler karena ada satu atau beberapa daerah hiperplasia (pertumbuhan berlebihan) dalam keadaan yang
tampaknya serupa dengan keadaan yang menyebabkan timbulnya simple goiter. Akibat kelainan ini tidak terdapat gejala, tetapi ukuran nodul
yang terbentuk tidak jarang meningkat secara perlahan dan kemudian turun kedalam rongga thoraks sehingga menimbulkan gejala penekanan.
Sebagian nodul berubah menjadi maligna dan sebagian lainnya disertai keadaan hipertiroid.

GOITER NON TOKSIK

Untuk menghindari kesimpangsiuran pada pembahasan penata laksanaan asuhan keperawatan, penulisan makalah ini dibatasi hanya pada
pembahasan goiter non toksik.
Goiter non toksik merupakan gangguan yang sangat sering dijumpai dan menyerang sampai 16 % wanita dan 4 % pria yang berusia antara 20-60
tahun (patofisiologi, EGC hal. 1077).

ETIOLOGI
Etiologi goiter non toksik antara lain adalah defisiensi iodium atau gangguan kimia intra tiroid oleh berbagai faktor (patofisiologi, EGC hal. 1077).

PATOFISIOLOGI
Akibat defisiensi iodium atau gangguan kimia intra tiroid kapasitas kelenjar tiroid untuk mensekresi tiroksin terganggu, mengakibatkan
peningkatan kadar TSH dan hiperplasia dan hipertropi folikel-folikel tiroid. Pembesaran kelenjar tiroid pada pasien goiter non toksik sering
bersifat eksaserbasi dan remisi disertai hiperevolusi dan involusi pada bagian-bagian kelenjar tiroid. Hiperplasia mungkin bergantian dengan
fibrosis, dan dapat timbul nodula-nodula yang mengandung folikel-folikel tiroid.

GAMBARAN KLINIS
Secara klinis pasien dapat memperlihatkan penonjolan disepertiga bagian bawah leher. Goiter yang besar dapat menimbulkan masalah kompresi
mekanik, disertai pergeseran letak trakea dan eusofagus, dan gejala-gejala obstruksi.

PENGOBATAN
Terapi goiter antara lain dengan penekanan TSH oleh hormon tiroid. Pengobatan dengan tiroksin yang lama akan mengakibatkan penekanan TSH
hifosis, dan penghambatan fungsi tiroid disertai atropi kelenjar tiroid. Goiter yang besar mungkin perlu dibedah untuk menghilangkan gangguan
mekanis dan kosmetis yang diakibatkannya. Pada masyarakat dimana goiter timbul sebagai akibat kekurangan iodium maka garam dapur harus
diberi tambahan iodium.

PENCEGAHAN
Penyakit simple goiter atau gondok endemik dapat dicegah dengan memberikan senyawa iodiumkepada anak-anak dikawasan yang kandungan
iodiumnya buruk. Jika asupan merata iodium kurang dari 40 mg/hari, kelenjar tiroid akan mengalami hipertropi . Organisasi kesehatan sedunia
(WHO) menganjurkan iodisasi garam hingga mencapai konsentrasi satu bagian dalam 100.000 yang sudah cukup untuk pencegahan goiter. Di
Amerika Serikat, garam beriodium merupakan satu-satunya cara yang paling efektif untuk mencegah penyakit goiter dalam masyarakat yang
rentan.

ASUHAN KEPERAWATAN

a. Pengkajian
Aktifitas/istirahat♣
Gejala : insomnia, sensivitas meningkat, otot lemah, gangguan koordinasi, kelelahan berat.
Tanda : atropi otot

Sirkulasi♣
Gejala : palpitasi, nyeri dada (angina)
Tanda : disritmia (vibrilasi atrium), irama gallop, murmur, peningkatan tekanan darah dengan takanan dada yang berat, takhikardi saat istirahat,
sirkulasi kolap, syok (krisis tirotoksikosis).

Eliminasi♣
Gejala : urine dalam jumlah yang banyak, perubahan dalam faeces.

Integritas ego♣
Gejala : mengalami stress yang berat baik maupun fisik
Tanda : emosi labil (euphoria sedang sampai delirium), depresi.

Makanan/cairan♣
Gejala : kehilangsn berat badan mendadak, nafsu makan meningkat, makannya sering, kehausan, mual dan muntah.
Tanda : pembesaran tiroid, goiter, edema non pitting terutama daerah pretibial.

Neurosensori♣
Tanda : bicara cepat dan parau, gangguan status mental dan perilaku, seperti bingung, disorientasi, gelisa, peka rangsang, delirium, psikosis,
stupor, koma, tremor halus pada tangan, tanpa tujuan, beberapa bagian tersentak-sentak, hiperaktif reflek tendon dalam (RTD).
Nyeri/kenyamanan
Gejala : nyeri orbital/fothopobia

Pernafasan♣
Tanda : frekwensi pernafasan meningkat, takipnea, dispnea, sumbatan jalan nafas, terjadi penekanan.

Keamanan♣
Gejala : tidak toleransi terhadap panas, keringat yang berlebihan, kebutuhan meningkat akan iodium (G), alergi etrhadap iodium (Hi).
Tanda : suhu meningkat 37,4 derajat celcius. Diaforesisi, kulit halus, hangat dan kemerahan, rambut tipis, mengkilat dan lurus, exoftalmus:
retraksi, iritasi padakonjungtiva dan berair. Puritus, lesi, eritema ( sering terjadi pada pretibial) yang menjadi sangat parah.

Seksualitas♣
Tanda : penurunan libido, hipomenorhea dan impotensi.

Penyuluhan/pembelajaran♣
Gejala : adanya riwayat keluarga mengalami masalah itroid, riwayat hipotiroidisme, terapi hormon tiroid atau pengobatan antitiroid, dihentikan
terhadap pengobatan antitiroid, dilakukan pembedahan tiroidektomi sebagian, riwayat pemberian insulin yang menyebabkan hipoglikemia,
gangguan jantung atau pembedahan jantung, penyakit yang baru terjadi (pnemonia), trauma, periksaan rontgen fhoto dengan zat kontras.

b. Diagnosa keperawatan
1. Nafas tidak efektif berhubungan dengan adanya pembesaran jaringan pada leher, penekanan trakhea.
2. Perubahan pola nutrisi berhubungan dengan adanya penekanan daerah oesofagus, penurunan nafsu makan.
3. Gangguan konsep diri (harga diri rendah) berhubungan dengan tidak efektifnya coping individu, adanya pembesaran pada leher.
4. Kurang pengetahuan berhubungan dengan tidak mengenal sumber informasi.

c. Intervensi
Diagnosa 1
Rencana tindakan :
1. Pantau frekwensi pernafasan , kedalaman, dan kerja pernafasan
2. Auskultasi suara nafas, catat adanya perubahan suara patologis
3. Waspadakan klien agar leher tidak tertekuk/posisikan semi ekstensi atau eksensi pada saat beristirahat.
4. Ajari klien latiahan nafas dalam
5. Selidiki keluhan kesulitan menelan
6. Persiapkan operasi bila diperlukan.

Diagnosa 2
Rencana tindakan :
1. Kaji adanya kesulitan menelan, selera makan, kelemahan umum dan munculnya mual dan muntah.
2. Pantau masukan makanan setiap hari dan timbang berat bada setiap hari serta laporkan adnaya penurunan.
3. Dorong klien untuk makan dan meningkatkan jumlah makan dan juga beri makanan lunak, dengan menggunakan makanan tinggi kalori yang
mudah dicerna.
4. Beri/tawarkan makanan kesukaan klien.
5. Kolaborasi : konsultasikan dengan ahli gizi untuk memberikan diet tinggi kalori, protein, karbohidrat dan vitamin.

Diagnosa 3
Rencana tindakan :
1. Kaji tingkat perubahan rentang harga diri rendah
2. Pastikan tujuan tindakan yang kita lakukan adalah realistis
3. Sampaikan hal-hal yang positif secara mutlak untuk klien, tingkatkan pemahaman tentang penerimaan anda pada pasien sebagai seorang
individu yang berharga.
4. Tentukan untuk perilaku manipulatif, identifikasi konsekensi untuk pelanggaran ini dengana cara yang berbelit-belit.
5. Diskusikan masa depan klien, bantu klien dalam menetapkan tujuan-tujuan jangka pendek dan panjang.

Diagnosa 4
Rencana tindakan :
1. Tinjau kembali proses penyakit dan harapan masa datang
2. Berikan informasi yang tepat dengan keadaan individu
3. Identifikasi sumber stress dan diskusikan faktor pencetus krisis tiroid yang terjadi, seperti orang/sosial, pekerjaan, infeksi, kehamilan
4. Berikan informasi tentang tanda dan gejala dari penyakit gondok serta penyebabnya
5. Diskusikan mengenai terapi obat-obatan termasuk juga ketaatan etrhadap pengobatan dan tujuan terapi serta efek samping obat etrsebut
6. Beri dukungan moril dapat menjalankan semua anjuran/informasi yang didapat baik oleh petugas kesehatan maupun keluarga.

PENYIMPANGAN KDM PENYAKIT GOITER

Defesiensi iodium/Gg kimia intra tiroid Perubahan litium dan iodium berlebihan
Zat goiterroenik

simple goiter/goiter koloid Goiter noduler

Gangguan kelenjar tiroid

Gangguan sekresi tiroksin

Kompensatorik stimulus kel.tiroid

Hipetropi peningkatan TSH hiperplasia

Maligna
Pembesaran pada leher kelainan kel.tiroid nodul Hipertiroid

Berlebih : kompresi trakhea turun kerongga thorax

Dan oesofagus
Penekanan daerah setempat

Obstruksi jalan nafas

Gg pernafasan Gg pola nutrisi
Nafas tidak efektif

Efektifitas coping tidak Gg konsep diri (HDR)

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