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THYROID DIAGNOSTIC
PROCEDURES,
TREATMENT AND
PREVENTION
Jassin M. Jouria, MD
Dr. Jassin M. Jouria is a medical doctor,
professor of academic medicine, and
medical author. He graduated from Ross
University School of Medicine and has
completed his clinical clerkship training in
various teaching hospitals throughout New
York, including King’s County Hospital
Center and Brookdale Medical Center,
among others. Dr. Jouria has passed all
USMLE medical board exams, and has served as a test prep tutor and instructor for
Kaplan. He has developed several medical courses and curricula for a variety of
educational institutions. Dr. Jouria has also served on multiple levels in the academic
field including faculty member and Department Chair. Dr. Jouria continues to serves
as a Subject Matter Expert for several continuing education organizations covering
multiple basic medical sciences. He has also developed several continuing medical
education courses covering various topics in clinical medicine. Recently, Dr. Jouria
has been contracted by the University of Miami/Jackson Memorial Hospital’s
Department of Surgery to develop an e-module training series for trauma patient
management. Dr. Jouria is currently authoring an academic textbook on Human
Anatomy & Physiology.
Abstract
Management of the common forms of thyroid disease has undergone
significant study and development, as evidenced by the latest
guidelines to diagnose and treat the thyroid. Because the thyroid
gland’s role is so pervasive in the body, it is important for clinicians to
understand the symptoms of various thyroid diseases. The diagnosis
and treatment of thyroid conditions are discussed.
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Policy Statement
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the policies of NurseCe4Less.com and the continuing nursing education
requirements of the American Nurses Credentialing Center's
Commission on Accreditation for registered nurses. It is the policy of
NurseCe4Less.com to ensure objectivity, transparency, and best
practice in clinical education for all continuing nursing education (CNE)
activities.
Continuing Education Credit Designation
This educational activity is credited for 3.5 hours. Nurses may only
claim credit commensurate with the credit awarded for completion of
this course activity. Pharmacology content is 0.5 hours (30 minutes).
Statement of Learning Need
The thyroid gland is active in virtually every cell of the body,
regulating cellular respiration, energy expenditure, overall metabolism,
growth and development of cells and tissues. It is important to
understand the symptoms of thyroid diseases, and to know the
management and treatment of these conditions.
Course Purpose
To provide advanced learning for clinicians interested in the diagnosis,
management and treatment of thyroid diseases.
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Target Audience
Advanced Practice Registered Nurses and Registered Nurses
(Interdisciplinary Health Team Members, including Vocational Nurses
and Medical Assistants may obtain a Certificate of Completion)
Course Author & Planning Team Conflict of Interest Disclosures
Jassin M. Jouria, MD, William S. Cook, PhD, Douglas Lawrence, MA,
Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures
Acknowledgement of Commercial Support
There is no commercial support for this course.
Please take time to complete a self-assessment of knowledge,
on page 4, sample questions before reading the article.
Opportunity to complete a self-assessment of knowledge
learned will be provided at the end of the course
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1. ______________ or T4 (containing four iodine atoms) is the
primary thyroid hormone secreted by the thyroid gland.
a.
b.
c.
d.
Thyroid stimulating hormone
Thyroxine
Triiodothyronine
Thyroglobulin
2. True or False: The thyroid stimulating hormone (TSH) test is
often the only test ordered by clinicians when thyroid
disease is suspected, and this can lead to misdiagnosis.
a. True
b. False
3. Thyroid stimulating hormone (TSH) is released by the
a.
b.
c.
d.
parathyroid.
thymus.
pituitary gland.
thyroidea ima.
4. What is the consensus regarding the diagnostic limits for
thyroid stimulating hormone (TSH) that would indicate
thyroid failure and hypothyroidism?
a.
b.
c.
d.
TSH >10 mIU/L
TSH ≥ 4 mIU/L
TSH ≥ 3 mIU/L
None of the above
5. Decreased thyroid stimulating hormone (TSH) levels are
seen in
a.
b.
c.
d.
primary hypothyroidism.
TSH-producing tumors.
Hashimoto’s thyroiditis.
primary hyperthyroidism.
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Introduction
Laboratory testing to diagnose thyroid disease makes use of a number
of blood test and imaging procedures to hopefully early identify and
manage medical treatment. Many tests utilize direct measurement of
specific analytes while others are calculated values. Thyroxine or T4
(containing four iodine atoms) is the primary thyroid hormone
secreted by the thyroid gland. Thyroid stimulating hormone (TSH) is
released by the pituitary gland depending on the level of T4 recognized
by the pituitary; the more T4 the less the TSH level and the less the
T4 the higher the TSH level. While the TSH level has been the gold
standard to diagnose and treat thyroid disease, there are other
diagnostic tests that help guide treatment. Often clinicians will rely
solely on the TSH, which can lead to misdiagnosis. The varied tests for
thyroid disease and treatment recommendations are emphasized in
the initial sections of this course.
Thyroid Hormones And Testing: A Review
The major thyroid hormone secreted by the thyroid gland is thyroxine.
Thyroxine is called T4 because it contains four iodine atoms. Thyroxine
converts to triiodothyronine (T3) by the removal of one iodine atom. It
is this conversion process (T4 to T3) that makes thyroxine
effective. Thyroxine (T4) circulates in the blood in two forms: bound or
free. When T4 is bound to proteins, i.e., thyroglobulin, it cannot enter
the various tissues that need thyroid hormone. Free T4 (fT4), on the
other hand, does enter the various target tissues to exert its effects.
This section identifies and explains the role of varied thyroid hormones
and known disease, drug and other chemical interactions affecting
thyroid processes and health.1-3,42-47,106,107
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Thyroid Stimulating Hormone
The thyroid-stimulating hormone (TSH) is commonly the first — and
often only — test ordered when thyroid disease is suspected. In most
labs, normal adult values range from 0.4-5mIU/L. By day 3, neonatal
ranges are 3-20μIU/L. TSH (thyrotropin) is secreted diurnally. In
addition, TSH secretion can be affected by age, gender, ethnic
background and overall health. Third generation TSH assays can
detect TSH with a coefficient of variation of 20% down to a level of
approximately 0.01 mIU/L. It should be noted that TSH levels will
begin to increase before fT4 levels begin to decrease.2
There is some disagreement regarding diagnostic limits for TSH. For
many years and for many clinicians, TSH >10 mIU/L was indicative of
thyroid failure and hypothyroidism. The National Academy of Clinical
Biochemistry has, however, recommended 4 mIU/L as an upper limit,
while the American Association of Clinical Endocrinologists has set the
upper limit at 3 mIU/L. Other professional groups have suggested
even lower values such as 2.5 mIU/L.
There is a growing consensus that ‘one size does not fit all’ and that
individual patient responses must be taken into account during
treatment. In addition, there is currently no accepted reference
measurement procedure (RMP) for the TSH assay, meaning there are
significant variations from lab to lab and between different assay
manufacturers. Increased TSH levels are seen in the table below.
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Various Upper Levels of Normal for TSH
National Academy of Clinical
Biochemists (NACB)
Upper Level of Normal
2.5 mIU/L with no evidence of thyroid
disease
National Health and Nutrition
Examination Survey III, NHANES
(Disease Free)
4.5 mIU/L with no evidence of thyroid
disease (self-reported)
National Health and Nutrition
Examination Survey III, NHANES
(Reference Population)
4.12 mIU/L with no evidence of thyroid
disease (self-reported), negative for antithyroid antibodies, not pregnant or using
estrogen contraceptives, androgens or
lithium
Hanford Thyroid Disease Study
4.10 mIU/L with no evidence of thyroid
disease, negative for anti-thyroid
antibodies, normal US (no nodules or
evidence of thyroiditis)
Pregnancy, 1st trimester
2.0-2.5 mIU/L
Pregnancy, 2nd trimester
3.0 mIU/L
Pregnancy, 3rd trimester
3.5 mIU/L
Increased TSH levels may be found in the following conditions:

Adults, children and neonates with primary hypothyroidism

TSH-producing tumors

Hashimoto’s thyroiditis

Thyrotoxicosis due to a pituitary tumor

TSH antibodies

Hypothyroid patients receiving insufficient replacement hormone
or hyperthyroid patients receiving excessive replacement
hormone

Hypothermia in infants and children
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Decreased TSH levels are seen in:

Primary hyperthyroidism

Secondary, tertiary hypothyroidism

Euthyroid Sick Syndrome

Hypothyroid patients receiving excessive replacement hormone
or insufficient replacement hormone in those treated for
hyperthyroidism
Drugs, pregnancy, estrogen levels, liver disease, non-thyroidal
diseases and resistance to thyroid hormones can also affect thyroid
stimulating hormone levels. The effects of varied drugs on the function
of the thyroid gland are highlighted in the table below.
Drug Effects on Thyroid Function
In Euthyroid Individuals
Inhibition of T4 Synthesis
Inhibition of T4/T3 secretion which
can be exacerbated by an
underlying lymphocytic thyroiditis
Thyroiditis may be induced
Hyperthyroidism-induced
TSH suppression
TSH elevation
Displacement from thyroxine
binding globulin causing laboratory
artifacts
Propylthiouracil
Methimazole
Lithium
Iodide
Amiodarone
Aminoglutethimide
Interferon
Interleukin-2
Amiodarone
Sunitinib
Iodide
Amiodarone
Glucocorticoids
Dopamine agonists
Somatostatin analogs
Rexinoids
Carbemazepine/Oxcarbemazepine
Metformin
Metyrapone
Furosemide
Phenytoin
Probenecid
Heparin
Nonsteroidal anti-inflammatory
medications (NSAIDs)
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Free T4
The T4 is normally bound to thyroglobulin with only a small fraction
unbound, or free (fT4). The normal range of fT4 is generally
considered to be 10-26pmol/L. (0.7-2.0ng/dL). The fT4 test — as
opposed to the total T4 test, is believed to more accurately represent
thyroid hormone functional levels. The assay is an RIA and may be
corrected for medications via a resin T3 uptake test.1-3,20
Elevated fT4 levels are seen in:

Graves’ disease

Hypothyroidism treated with replacement hormone

Euthyroid sick syndrome

High altitude
Depressed fT4 levels are seen in:

Primary, secondary or tertiary hypothyroidism

Hypothyroidism treated with T3
Free T3
The free T3 (fT3) test is commonly used to aid in the diagnosis of
hyperthyroidism and to monitor treatment. Most T3 is intracellular and
therefore only a very small portion is found in the serum. Normal
levels are generally between 260-480pg/dL (4.0-7.4pmol/L; 0.26-0.48
ng/dL).
Elevated fT3 levels are seen in:

Hyperthyroidism

T3 toxicosis
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
High altitudes
Depressed fT3 levels are seen in:

Primary or secondary hypothyroidism

3rd trimester of pregnancy

Deiodinase deficiency or insufficiency
TSH, fT4 and fT3 Levels in Thyroid Disease
TSH
fT4
Normal
fT3
Normal
Normal or
Interpretation
Subclinical hypothyroidism
Hypothyroidism
Normal
Normal or
Normal
Normal or
Subclinical hyperthyroidism
Hyperthyroidism
Normal or
Normal or
Rarely, 2o hypothyroidism. More
commonly, non-thyroidal chronic
disease
Thyroid hormone resistance
Normal
Assessing Thyroid Hormone in Pregnancy
FT4I (calculated)
Direct assay of fT4
Usually normal values in pregnancy
Usually decreased in pregnancy. May be normal
with alterations in TBG binding assays.
Other Laboratory Tests To Diagnose Thyroid Disease
Clinicians often do not rely on a full thyroid blood screen to diagnose a
thyroid condition. This section reviews thyroid tests that can help
clinicians develop a clear and more accurate diagnosis of an existing
thyroid disease.57,72,83,107
The human body depends on thyroid hormones to function at an
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optimal healthy state. Because no test can fully measure how thyroid
hormone is utilized once it enters the bloodstream, it is important for
clinicians to understand the varied tests and measures that inform how
each unique individual responds to thyroid hormone imbalances.
Thyroglobulin Test
Thyroglobulin (Tg) binds T4 in the thyroid. The thyroglobulin test is
used primarily as a tumor marker to follow the effectiveness of thyroid
cancer treatment, primarily the well-differentiated thyroid cancers, and
to monitor disease-free progression. Other reasons for testing for
thyroglobulin are to monitor the treatment of Graves’ disease. Rarely,
it may be used to try and determine the underlying cause of congenital
hypothyroidism or to help differentiate between subacute thyroiditis
and thyrotoxicosis factitia.
Thyroglobulin is normally primarily found in the thyroid within thyroid
follicles. Normal levels for adults are 3-42 ng/mL(3-42μg/L) and for
newborns (at 48 hours), 36-48 ng/mL(36-48μg/L).
Increased thyroglobulin levels are seen with:

Untreated or metastatic well-differentiated thyroid cancer
(Thyroglobulin levels are not diagnostic of thyroid cancer)

Subacute thyroiditis, thyrotoxicosis

Hyperthyroidism
Depressed levels of thyroglobulin may be seen with:

Thyrotoxicosis factitia

Newborns and infants with goiter and hypothyroidism
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Thyroxine-Binding Globulin
Often confused with thyroglobulin, thyroxine binding globulin (TBG) is
the main serum carrier protein for T4. Serum levels of TBG can have
significant effect on the T4 levels. TBG measurement is most useful to
distinguish between hyperthyroidism and euthyroidism with increased
binding, increased versus functionally normal T4 levels, and to identify
hereditary deficiency of TBG.
Normal levels of TBG in infants are 3-6 mg/dL (30-60mg/L). In adult
males, the normal range is 1.2-2.5 mg/dL (12-25mg/L) while in adult
females, the normal range is 1.4-3.0 mg/dL (14-30mg/L). Women on
oral contraceptives and in the 3rd trimester of pregnancy may have
elevated TBG values.
Elevated TBG levels are seen in:

Genetic hyperexpression of TBG

Some cases of hypothyroidism

Infectious hepatitis

Acute intermittent porphyria

Estrogen-producing tumors

Late-stage HIV

Heroin, methadone use
Depressed TBG levels are seen in:

Genetic defect in TBG gene

Nephrotic syndrome

Trauma, stress, major illness, chronic liver disease
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
Ovarian hypofunction

Acromegaly

Anabolic steroid use

Hypoproteinemia

Malnutrition
Triiodothyrodine Uptake Test
The triiodothyrodine uptake (T3U) test is an indirect measurement of
the amount of unsaturated TBG available and is inversely proportional
to the TBG levels. This test is usually done along with the T4 test
(resulting in the calculated “T7” test). Normal levels (as compared to
controls) should be 0.9-1.0 and 25-35%.
The T3U test can be done to correct for drugs that may interfere with
the T4 assay. T7 is also known as the Free Thyroxine Index (FTI) and
is a calculated result —the product of the T5 value and the T3U. The
FTI can give a clearer picture of the totality of thyroid function in both
suspected hypothyroidism and hyperthyroidism as well in patients who
are pregnant or with suspected abnormalities in TBG levels.
Decreased T3U levels occur in a normal pregnancy, with a variety of
drugs such as estrogens, methadone and heparin. Increased T3U
levels can occur with heparin, salicylates and anabolic steroids.
Thyroid Antibodies Testing
One of the primary ways of diagnosing autoimmune thyroid disease is
by testing for antibodies. The most commonly found antibody is
thyroid peroxidase (TPO antibodies/TPOAb). These have been referred
to in the past as anti-microsomal antibodies. Other antibodies include
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anti-thyroglobulin (Tg antibodies/TgAb), and TSH receptor (TSH-R
antibodies/TSH-RAb) antibodies. These antibodies are persistent, even
with treatment.
In the NHANES III survey, approximately 10% of participants were
TgAb positive while approximately 11% of participants were TPOAb
positive, though only those positive with TPOAb were associated with
progression to hypothyroidism. These antibodies should be assessed
for anyone with a goiter who may be at risk for autoimmune thyroiditis
as well as any patients with signs and symptoms of hypothyroidism
and in screening patients for thyroid disease.
These antibodies can variously act as either agonists or antagonists,
particularly TSH-RAb. Stimulating antibodies (TSI) promote thyroid
hormone production leading to hyperthyroidism while inhibiting
antibodies (TBII) inhibit production and lead to hypothyroidism,
though this is not routinely tested.
Antibodies to TSH should be assessed particularly in euthyroid and
thyroid hormone treated pregnant women or those with a history of
hyperthyroidism, as these antibodies are predictors of fetal and
neonatal thyrotoxicosis. TPO-Ab can be positive in both Hashimoto’s
thyroiditis and in Graves’ disease.
Radioactive Iodine Uptake Test
The Radioactive Iodine Uptake test (RAIU) is a direct measurement of
the ability of the thyroid gland to concentrate inorganic iodine. The
test measures the rate of accumulation, incorporation and release of
iodine. In order to minimize exposure to the patient, this test is often
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done in conjunction with thyroid imaging such as scintigraphy (thyroid
scan).
The patient may be asked to use a low-iodine diet for 7-10 days before
the test and may be asked to fast. The first scan is usually done at two
hours, then 4-6 hours after ingesting the radiotracer (either
131I)
123I
or
with a second scan within 24 hours. Normal values are 1-13%
after 2 hours, 5-30% after 6 hours, and 15-40% after 24 hours.
Increased uptake is associated with hyperthyroidism. Decreased
uptake is associated with hypothyroidism. Neither is diagnostic and
may be affected by malabsorption, diarrhea, rapid diuresis and renal
insufficiency.
Calcitonin Testing
Calcitonin, produced by the parafollicular or C cells of the parathyroid
gland may be used to diagnose medullary thyroid cancer. Stimulation
tests, using intravenous calcium or pentagastrin are more sensitive
than direct measurement in the blood.
Agents Affecting Thyroid Laboratory Tests And Treatment
There are a large number of substances that can significantly affect all
aspects of thyroid function, metabolism, laboratory tests, treatment
outcomes and other clinical parameters.5,34-49,107
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Agents that
block iodide
transport into
the thyroid
gland
Agents that
impair TG
iodination and
iodotyrosine
coupling

Monovalent anions (SCN–, Cl04–, N03–)

Dietary

Minerals (Bromine, Chloride)

Exogenous iodine supplements including
kelp

Minerals: Lithium, fluoride

Drugs: ethionamide

Drugs:

Thionamides and thiourylenes,
(PTU,methimazole, carbimazole)

Sulfonamides (acetazolamide, sulfadiazine,
sulfisoxazole)

Sulfonylureas (carbutamide, tolbutamide,
metahexamide, chloropropamide)

Salicylamides (p-aminosalicylic acid, paminobenzoic acid)

Others: Resorcinol, amphenone,
aminoglutethimide, Antipyrine (phenazone),
amphenidone, ketoconazole

Dietary thiocyanates
Agents that
inhibit thyroid
hormone
secretion

Drugs: amiodarone, iodide (as topical antiseptics
as well), lithium
Agents that
can induce
thyroiditis

Drugs: amiodarone, IL-2, γ-IFN, Sunitinab,
sarafenib. Ipilmumab, pembrolizumab, nivolumab,
tyrosine kinase inhibitors
Agents that
can induce
Graves’
disease

Drugs: α-IFN, HAART (highly active antiretroviral
therapy)
Agents that
can affect
thyroid
function via
unknown
mechanisms

Drugs: p-bromdylamine maleate, phenylbutazone,
thalidomide

Minerals: calcium, rubidium, cobalt
Agents that

Drugs: Estrogen, opiates, clofibrate, 5-fluorouracil,
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perpneazine
increase TBG
levels
Agents that
decrease TBG
levels

Drugs: Androgens, metabolic steroids,
glucocorticoids, l-asparaginase, nicotinic acid
Agents that
interfere with
TBG-binding

Drugs: salicylates, diphenylhydantoin, furosemide,
sulfonylureas, heparin, dinitrophenol, free fatty
acids, phenylbutazone, halofenate, orphenadrine,
thyroid hormone analogs
Agents that
inhibit
deiodinases

Drugs: Propylthiouracil (PTU), glucocorticoids,
propranolol, iodinated contrast agents,
amiodarone, clomipramine
Agents that
stimulate
degradation or
excretion

Drugs: Diphenylhydantoin, carbamazepine,
phenobarbital. Cholestyramine, colestipol,
rifampin, sucralfate, imatinib, bexarotene,
sevelemer. Colesevelam

Diet: soy, caffeine

Mineral salts: aluminum hydroxide, ferrous sulfate
Agents that
increase TSH
secretion or
response to
TRH

Drugs: iodine-containing drugs, lithium, dopamine
blocking agents, decarboxylase inhibitors, L-dopa
inhibitors, cimetidine, dlomifene, spironolactone,
amphetamines
Agents that
decrease TSH
secretion or
response to
TRH

Drugs: Thyroid hormone replacement therapy,
Thyroid hormone analogs, Dopaminergic agents,
Dopamine, L-Dopa, serotonin agonists, dopamine
antagonists, serotonin anatagonists,
glucocorticoids, acetylsalicylic acid, growth
hormone, somatastatin, opiates, fenclofenac,
clofibrate, bexarotene, metformin, ipilmumab,
pembrlizumab, nivolumab

Vitamins: Pyridoxine

Drugs:
Agents that
interfere with
absorption of
levothyroxine

Bile acid sequestrants

Cation exchange resins (Kayexelate)

Oral bisphosphonates

Proton pump inhibitors

Raloxifene
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Medical
conditions
that interfere
with
absorption of
levothyroxine

Orlistat

Ciprofloxacin

H2 receptor antagonists

Multivitamins (containing ferrous sulfate or
calcium carbonate)

Minerals: Ferrous sulfate, Chromium picolinate,
Calcium salts (carbonate, citrate, acetate)

Phosphate binders (sevelamer, aluminum
hydroxide)

Charcoal

Dietary

Ingestion with a meal

Grapefruit juice

Espresso coffee

High fiber diet

Soybean formula (infants)

Soy
Malabsorption syndromes
 Celiac disease

Jejunoileal bypass surgery

Cirrhosis (biliary)

Achlorhydria
Neonatal Testing for Thyroid Disease
Neonatal screening for congenital hypothyroidism that, in the U.S.,
occurs at a rate of between 1 of 3600 and 1 of 5000, has been a
success story to a very large degree. TSH screening is more specific,
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but T4 screening is more sensitive, though with a high rate of false
positives, particularly for low birth weight and premature infants. In
general, these should be done after the first 24 hours to minimize the
falsely positive TSH that is due to the physiological increase in TSH, T4
and T3 immediately after birth.82,103
By the third day, neonatal TSH should be < 20μU/mL (20mU/L).
Neonatal T4 peaks during the first 24 hours and then decreases to 1222μg/dL (152-292mmol/L) within 1-3 days, dropping further to 1017μg/dL (126-214mmol/L) within two weeks.
Low T4 with a normal TSH, hypothyroxinemia is found in 50% of
babies born less than 30 weeks gestation — these will be missed if
only TSH is screened in this population. Premature babies have
hypothalamo-pituitary immaturity, low TBG levels and decreased
conversion rate of T4 to T3. In addition, hypothyroxinemia may be
seen in euthyroid sick syndrome in newborns.
Isolated hyperthyrotropinemia with normal T4 and elevated TSH levels
can also occur, indicating the inadequate production of T4. It is most
common in premature babies. The hyperthyrotropinemia can be a
transient finding due to goitrogens, iodine deficiency, or certain
medications, genetic defects of hormone biosynthesis and also
dysgenesis, especially ectopia, could be the causes.
Elevated TSH levels with normal T4 levels can persist for years. Iodine
excess, particularly from the use of iodine-containing antiseptics may
also cause transient hypothyroxinemia in preterm babies.
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Screening Recommendations
Different organizations have recommended somewhat different
screening plans, as listed below, while the U.S. Preventive Services
Task Force and the Royal College of Physicians (London) find there is
insufficient evidence for screening any specific population. The
screening recommendations for pregnant women and newborns have
been covered above.62-64,88,104

The American Thyroid Association recommend that both women
and men over the age of 35 should be screened every 5 years

The American Association of Clinical Endocrinologists
recommends that older patients, particularly older women,
should be screened.

The American Academy of Family Physicians recommends that
all patients over the age of 60 should be screened.

American College of Physicians recommends that women over
the age of 50 years with an incidental finding suggestive of
symptomatic thyroid disease should be evaluated.
Thyroid Scans
Thyroid imaging utilizes I-123 or I-131 (and sometimes Technetium
pertechnetate-99m) to visualize and evaluate the size, position,
function and the presence of “hot” or “cold” spots in the thyroid. The
radioactive iodine uptake test (RAIU), also known as a thyroid uptake
test, is a measurement of thyroid function, and does not involve
imaging. “Hot” spots, indicating increased uptake of iodine are
generally nonmalignant while “cold” spots generally need further
evaluation, with a greater possibility that these represent
malignancies.
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The
123I
or
131I
(tracer) can be given as an IV, a pill, or as a liquid. A
waiting period of 24 hours is needed before the actual scan with a
probe positioned over the thyroid gland. If there is a suspicion of the
ectopic presence of thyroid tissue, the probe can be moved, for
example, to the mediastinum. The actual scan is likely to take less
than 10 minutes. Inorganic iodine is also concentrated in fetal iodine
and in breast milk, so pregnant and lactating women should not
ordinarily be tested with radioactive iodine.
As mentioned, thyroid cancer commonly appears as “cold” areas.
Areas of diffuse “hotness” or increased uptake represent hyperthyroid
disease such as Graves’ disease, while areas of diffuse “coldness”
represent hypothyroid disease. Hashimoto’s thyroiditis is often
characterized by a “mottled” appearance.
A Computerized Rectilinear Thyroid (CRT) scanner in some areas is
replacing the gamma camera scan. More commonly, nuclear labs use a
scintillation camera. The CRT scanner uses computer technologies to
enhance the clarity of the scans and can provide information on the
size and function of the thyroid. Indications for a thyroid scan are
highlighted below.

Hyperthyroid patients with or without a goiter (diffuse or nodular):
These can be used to determine the functionality of a palpable
nodule, to detect unsuspected or nonpalpable nodules, to
differentiate between Graves’ disease, toxic nodular goiter and
other causes of thyrotoxicosis. The scan can also be used to
estimate the volume of the thyroid before

131I
therapy.
Euthyroid patients with a solitary nodule or multiple nodules:
These can be used to determine if the nodule(s) are
hyperfunctioning, to identify nodules for fine needle aspiration
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biopsies, and to estimate the volume of functional tissue for future
surgery.

Patients with suspected ectopic thyroid tissue.

Patients who has had thyroid cancer to follow remaining thyroid
tissue.
The I-131 has a half-life of 8 days and can be used for whole body
scintigraphy, post cancer treatment. I-123 has a shorter half-life of 13
hours and is commonly used for thyroid scintigraphy. Tc-99m
pertechnetate and Tc-99m sestamibi each have half-lives of 6 hours
with the former being useful for thyroid scans and the latter useful in
the localization of thyroid metastases. TI-210-Cl- has a much longer
t1/2 (77hours) and can be used to localize metastases. Finally, F-18
fluorodeoxyglucose, a positron emitter with a t1/2 of 110 minutes can
be used in PET scans.
Patients do not need to fast before thyroid scintigraphy, but should be
on low iodine diet for 7-10 days preceding the scan.
Non-isotopic imaging comprises ultrasonography (US), CT and MRIs.
US is commonly used to clarify results from puzzling physical finding,
for guiding fine needle aspiration (FNA) biopsies, detect small nodules,
identify individual nodules that may be at greater risk of neoplastic
transformation and to evaluate the recurrence of thyroid cancer after
surgery, particularly in the cervical lymph nodes. In US, a normal
thyroid has a relatively homogenous appearance, sometimes
compared to “ground glass”. In goiter, US may be able to locate a
specific region where the echo pattern is distinct from the rest of the
thyroid, though US cannot identify specific disorders.
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Focal lesions are often surrounded by a distinctive halo or rim, but the
greatest use of US may be to guide FNA biopsies. Hypothyroid patterns
often have low echogenicity, particularly in Hashimoto’s thyroiditis. In
pediatric patients, an additional sign, with 98% sensitivity and 100%
specificity appears to be in the lymph nodes adjacent to the lower part
of the thyroid lobes. A sonographic classification system has been
proposed based on real-time sonography that may be a useful tool for
the differentiation of asymptomatic diffuse thyroid disease. Diffuse
thyroid disease versus normal thyroid has been differentiated in the
literature based on differences in echogenicity, echotexture, AP
(anterior posterior) diameter, vascularity, a glandular margin, and the
presence of scattered microcalcifications. Micronodulation has been
described as a sonographic sign of Hashimoto’s thyroiditis and a
“thyroid inferno” has been described as a sonographic sign of Graves’
disease.
Ultrasonography can be somewhat correlated with an increased or
decreased risk of thyroid cancer.
Increased risk of thyroid cancer is associated with the following
features: hypoechoic, microcalcifications, central vascularity, irregular
margins, incomplete haloes, a nodule that is taller than it is wide,
documented enlargement and associated rounded adenopathy,
particularly when associated with cystic spaces. Decreased risk of
thyroid cancer is associated with the following features: hyperechoic,
large and coarse calcifications (with the exception of medullary
cancer), peripheral vascularity, a lesion that looks like a “puff pastry”
(wider than taller) and “comet-tail shadowing”.
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Sonography is often used in conjunction with a FNA biopsy, though it
may be reserved for very deep or very small nodules, for nonpalpable
nodules, nodules suspicious for cancer and in nonpalpable adenopathy.
The success rate is low for nodules smaller than 8 mm.
Computed tomography and MRIs are sometimes used, but because of
the cost, these are generally thought not to be cost-effective and
usually not required. PET scans are sensitive and specific for
monitoring recurrent or persistent thyroid cancer post-surgically when
using a biochemical indicator such as thyroglobulin. Multimodality
scanning (using PET, CT and MRI scans simultaneously) can
superimpose function and anatomy and are currently in development.
Thyroid scans utilizing radioactive tracers are commonly done along
with the RAIU tests.
Fine Needle Aspiration Biopsy
The fine needle aspiration biopsy (FNAB) of the thyroid is commonly
performed with US guidance. The basic procedure itself dates from the
mid-1800s. The medical literature reported the first needle aspiration
in the diagnosis of infectious disease during 1904 (study by Grieg and
Gray), where needle aspiration of the lymph nodes on patients with
sleeping sickness revealed motile trypanosomes. In their report, the
authors suggested FNA might be more effective at diagnosing cases of
sleeping sickness than blood testing. In the 1930s, at the Memorial
Sloan Kettering Cancer Center in New York and later during World War
II refinement of the FNA procedure developed.104 Since those early
years, FNAB has become a very well accepted, cost-effective safe and
efficient method to evaluate the histology of the aspirated cells.
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However, it should be noted that false-positives and false-negatives
are common and reliance on FNAB solely is not advisable.
Advantages of the FNAB include cost, convenience, outpatient status
and that it is a relatively painless procedure not leaving any scar. On
the other hand, the number of false positives and false negatives,
likely due to sampling errors, limits FNAB. The procedure requires
specialized training, though it can be done in an office setting.
Currently, the best evidence suggests that US or CT guidance provides
the best and most reliable results. In adults, research has indicated a
97% positive predictive value with a 92% negative predictive value for
malignancy. It does not appear that there are significant differences in
nodules based on size. Further, studies have shown that the reliability
of FNAB as a diagnostic tool is not affected by the size of the nodules
and size alone should not be used as the primary independent factor
for determining candidacy for surgery.
Papillary thyroid carcinoma can commonly be diagnosed by FNAB, but
the same is not true for follicular adenomas, which can be difficult to
differentiate from follicular carcinomas in most samples. The presence
of a follicular neoplasm in the FNAB sample is considered an indication
for thyroid surgery.
In the pediatric population, there are fewer studies. Pediatric patients
are more likely than adult patients to have reactive lymphadenopathy,
limiting the utility of the biopsy. Research on the use of FNAB in
pediatric patients has shown that FNAB is a sensitive test in this
population, particularly for excluding the possibility of a thyroid tumor.
Similarly, smaller studies of pediatric patients have shown that FNAB
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had a diagnostic sensitivity of 100%, positive-predictive value of
93.3%, and accuracy of 94.5% for diagnosing pediatric cervical
lymphadenopathy.
Genetic markers and gene panels are becoming more widely used in
assessing the potential for malignant thyroid tumors. A number of
different alterations in gene expression, the expression of micro RNA
(miRNA) and in the methylation of gene promotors has been
described. In papillary thyroid cancer, the best-described are point
mutations of the BRAF and the RAS genes. In addition, RET/PTC and
TRK rearrangements have been detected in papillary thyroid cancers —
these activate the mitogen-activated protein kinase (MAPK) pathway
and are found in over 70% of papillary thyroid tumors.
The BRAF mutation is the most common mutation found in papillary
tumors. Follicular thyroid cancer has been studied for genetic markers
as well; these tumors have been shown to contain RAS mutations or a
PAX8/PPARγ rearrangement. These markers are mutually exclusive as
are those described for papillary tumors, and are also found in more
than 70% of follicular thyroid tumors. In both familial and in sporadic
medullary thyroid tumors, point mutations are commonly found in the
RAS or the RET genes. In poorly differentiated and anaplastic
carcinomas, markers involve the TP53 and CTNNB1.
Treatment Of Hypothyroidism And Hyperthyroidism
The pillar of the treatment of hypothyroidism has long been Lthyroxine (Levothyroxine). The dosage should be titrated, leaving a
minimum of 6-8 weeks between changes in dosage, to allow TSH to
fall within the normal range. High doses of levothyroxine will likely
result in significant changes in TSH within 4 weeks, but subsequent
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changes in dosage generally take longer to be effective. However,
since the normal range varies among different labs and because there
is still a lack of consensus regarding the value above which to assign
the label hypothyroid, patient feedback regarding their symptoms and
energy levels can be an important part of assessing the overall ideal
dosage. In this context, it is important to remember that some
symptoms will respond more slowly (i.e., skin or hair changes) than
will others (i.e. energy level, change in weight, menstrual symptoms).
Women have been shown to require higher doses, on average, but age
does not appear to be an independent predictor of dosage. The
medical and surgical treatment of hypo- and hyperthyroidism is
discussed in this section.9,57,88,105-107
Medical Treatment of Thyroid Disease
Starting dosage in those with little thyroid function can be estimated
based on weight (1.6μg/kg body mass daily). Those patients who have
undergone a total thyroidectomy may require a higher dose while
those with subclinical hypothyroidism or those who have undergone
treatment for Graves’ disease may require less replacement hormone.
It is not clear which dosing schedule is better, i.e., within 2 hours of
the last meal of the day versus 20 minutes before breakfast. This may
also be “titrated” though ease of compliance should be considered a
factor. Central hypothyroidism measurement of T4 is considered a
better measure of effectiveness than the measurement of TSH.
Once a euthyroid state has been achieved, generally the
recommendation is for follow-up every 6 months for 2-3 years unless
otherwise clinically indicated. After 2-3 years, most recommend yearly
follow-ups. It should be noted that major life changes may be an
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indication for follow-up. These changes can include trauma, injury,
perimenopause, the diagnosis of an autoimmune disorder or the
appearance or re-appearance of symptoms.
It is possible that while the TSH levels (and therefore the T4 levels)
are in the normal range, the T3 levels may be subnormal if the patient
is not converting T4 to T3 efficiently, i.e., in the case of the
aforementioned D2 polymorphisms. The latest trends in personalized
medicine would support this concept — that once the TSH (and, by
extension, the T4 levels) have reached normal ranges — and
remembering that ranges are just that (some patients report feeling
improvement in hypothyroid symptoms with low-end normal TSH
levels) at that point, it may be useful if selected patients undergo trials
of additional T3. The dose of T3 can be problematic given its short
half-life of one day, and many clinicians recommend 3 daily doses to
achieve approximately physiologic levels of T3.
Several studies have been undertaken in an effort to establish more
physiologic levels of both T4 and T3 by using combination therapy.
Brain function may benefit the most from T3 therapy; functional PET
and MRIs indicate that the hippocampus and amygdala are particularly
sensitive to fluctuations in T3, as is the frontal lobe and executive
function. Treatment with T4 only may not allow for sufficient recovery
of T3 levels and may therefore be most critical for those patients with
cognitive difficulties, mood swings, depression and other symptoms of
neuropsychological function.
A recent review of studies combining T4 with T3 therapy suggested
that certain patients might benefit from combined therapy. These
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patients include those in whom normal TSH/T4 levels have been
achieved yet who still experience cognitive difficulties, depression,
mood swings, patients with autoimmune thyroiditis, some
thyroidectomized patients, those patients with known or suspected
deiodinase deficiencies and those for whom hypothyroid symptoms
appear to be resistant to T3 therapy. Three meta-analyses of
combination therapy have been done, with somewhat variable results:
two found no significant differences between combined and
monotherapy. A third study found improvements in both physical and
psychological wellbeing. Each study had methodological limitations
including small sample size, a lack of homogeneity in the patient
populations, large variations in the dosages of T4/T3 and lack of clarity
in outcomes measured.
More recent investigations have identified that substitution of l-T3 for
l-T4 at equivalent doses (relative to the pituitary) reduced body weight
and resulted in greater thyroid hormone action on the lipid
metabolism, without detected differences in cardiovascular function or
insulin sensitivity. On the other hand, a recent systematic review of
clinical practice guidelines did not support the use of combination
therapy. There may be increased risk of cardiovascular effects,
particularly in the elderly and those with pre-existing cardiovascular
conditions.
Combinations of T4 and T3 exist that attempt to mimic the purported
physiological ratio of 80/20%. These include Thyrolar (Liotrix), which
is a 4:1 combination of synthetic T4/T3. Combination therapeutic
dosing can also be supplied by compounding pharmacies that can
provide at 4:1 combination of levothyroxine and triiodothyronine.
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Glandular preparations are generally eschewed by mainstream
medicine due to the lack of standardization and substantiation, though
these were the mainstay of hypothyroidism treatment for over a
century. Many patients, however, are looking for more natural
approaches to treating hypothyroidism and may request information
regarding these products, which can include Armour (Erfa in Canada)
and other dessicated thyroid products. These are generally derived
from porcine thyroid glands. Three dosage forms are usually available:
30mg (1/2 grain), 60mg (1 grain) and 125mg (2 grains); 1 grain of
Armour contains 30μg of T4 and 9 μg of T3 and is roughly equivalent
to 74 μg of levothyroxine. Patients are usually started at ¼ to ½ grain
daily and titrated as done with levothyroxine.
Anecdotally, it has been noted by some that certain patients do better
with glandular preparations than others. Recently, it was reported that
in those patients with persistant subjective complaints while on T4
monotherapy, 78% reported a preference for Armour thyroid
treatment when switched. Other reports suggested while there were
no significant differences in symptoms or in neurocognitive
measurements, patients switched from synthetic T4 therapy realized
modest weight loss and 48.6% reported preference for the Armour
thyroid treatment.
The most common treatment for hyperthyroidism in the U.S. is
treatment with I-131. Antithyroid medications are also commonly
used, which include methimazole and propylthiouracil. In general, the
antithryoid medications are used in the pediatric population while in
adults, the antithyroid medications are used prior to therapy with I-
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131. Medications should be titrated until indications of thyroid
normalization.
Both methimazole and propylthiouracil (PTU) are thiomides and
interfere with the production of T4. PTU prevents thyroid hormone
synthesis by inhibiting the thyroid peroxidase-catalyzed reactions,
blocking iodine organification, blocking the coupling of iodotyrosinases
and inhibition of D2. PTU may take up to 3-4 weeks before stores of
T4 are depleted. Adverse effects include rash, rare agranulocytosis,
hepatitis and cholestatic jaundice. PTU is pregnancy risk category D.
However, since more PTU is protein-bound, it is preferred to
methimazole in the first trimester. Very low amounts of PTU are
secreted into breast milk. PTU is also used to treat thyroid storm, often
along with potassium iodide and propranolol.
Methimazole shares the mechanism of action with PTU but is
considered significantly more potent. Methimazole does not inhibit the
D2 deiodinase. In non-pregnant adults, methimazole is the primary
drug used to treat Graves’ disease. Methimazole has a longer duration
of action and its use can result in a euthyroid state more rapidly.
Methimazole is also pregnancy risk category D and is contraindicated
in pregnancy and during lactation. Adverse effects include a
maculopapular rash, rare agranulocytosis, hepatitis and cholestatic
jaundice.
Potassium iodide inhibits thyroxine release by the thyroid as well as
inhibiting thyroid peroxidase-catalyzed reactions. Indications include
thyroid storm, Graves’ disease, toxic adenoma, goiter and thyroiditis,
but it is rarely used alone.
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The I-131 is a beta emitter with an effective half-life of about 56 days
in the thyroid. It is contraindicated in pregnancy or lactation with a
potential adverse effect of delayed hyperthyroidism. Its effects are
much less rapid than treatment with antithyroid drugs or with a
thyroidectomy, but it is safe, effective and does not require a stay in
the hospital. In addition, it has been suggested that treatment with
radioactive iodine has a higher cure rate for Graves’ disease and is
associated with a lower recurrence rate. However, it should be noted
that treatment with radioactive iodine is also associated with an
increased risk of development or worsening of ophthalmologic
symptoms and disorders as well as an increased risk of
hypothyroidism.
The American Thyroid Association recently provided recommendations
for I-131 therapy in compliance with the Nuclear Regulatory
Commission regulations. Contraindications include pregnancy and
breastfeeding. In general, the dose of
131I
is between 75-200 μCi/g of
the estimated mass of thyroid tissue divided by the percent uptake of
I-123 in 24 hours previously determined by RAI testing. For doses
over 200 μCi/g, hospitalization along with proper radiation safety
measures should be considered.
The I-131 should be administered as a single dose. The iodine is
selective for thyroid tissue and the treatment is therefore associated
with few adverse effects. There is no credible evidence that I-131
therapy is associated with increased risk of thyroid carcinoma,
increased mortality or any other form of cancer, including leukemias.
I-131 treatment is not recommended for children under the age of 5.
In those children between the ages of 5 to 10 years, I-131 therapy can
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be used if the calculated activity of administered I-131 is less than 10
mCi. In any child older than 10, I-131 can be undertaken as long as
the activity is greater than 150 µCi/g of thyroid tissue.
Surgical Treatment of Thyroid Disease
Thyroidectomy
Thyroidectomy, while once the most common treatment for
hyperthyroidism, is now generally reserved for specific cases including:

In children with severe hyperthyroidism

In pregnant women who are noncompliant with or intolerant of
antithyroid pharmacotherapy

In those patients with very large goiters or severe
ophthalmopathy

In those patients who refuse radioactive iodine therapy

In those patients with refractory amiodarone-induced
hyperthyroidism

In those patients who require rapid normalization of thyroid
functions. This can include pregnant women, women who desire
pregnancy in the next 6 months, or patients with unstable or
otherwise dangerous cardiac conditions.
Pre-thyroidectomy treatment generally involves antithyroid
medication, treatment with iodine salts (SSKI: 2 drops bid for 10-14
days) and beta blockers until euthyroid biochemical status and pulse
<80bpm is achieved. Excess iodine in the diet or as supplements
should be avoided. Thyroid storm can generally be avoided with this
procedure, but adverse effects include hypoparathyroidism and
damage to the recurrent laryngeal nerve.
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Treatment of Thyroid Disease Complications
Ophthalmopathy
Up to half of Graves’ disease patients have signs and symptoms of
thyroid eye disease, but approximately 5% can develop severe
ophthalmopathy including diplopia, visual-field deficits, or blurred
vision. The less serious eye symptoms, which can include photophobia,
tearing and irritation are often treated with sunglasses and saline
drops as needed. If more serious ophthalmopathy is suspected, an
ophthalmologist should monitor patients regularly. Emergency
symptoms that the patient should be made aware of included loss of
color vision or orbital pain.
Dermopathy
Graves’ disease can result in an infiltrative dermopathy over the lower
legs. The dermopathy includes a non-pitting and erythematous edema
on the shins. The dermopathy commonly accompanies
ophthalmopathy and is characterized by an accumulation of
glycosaminoglycans and inflammatory cells in the skin. There is no
effective treatment; topical steroid creams are often used for
symptomatic relief.
Neurological and Cardiovascular Symptoms
Symptomatic relief for neurologic and cardiovascular symptoms may
be necessary. Beta-blockers are the drug of choice unless
contraindicated in which case calcium channel blockers may be used.
These medications can usually be stopped once a euthyroid state has
been attained.
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Thyroid Nodules
Fine needle aspiration biopsy (FNAB) is most commonly used to
evaluate thyroid nodules. The Bethesda System for Reporting Thyroid
Cytopathology is used to classify thyroid nodules into a number of
categories: benign, atypia of undetermined significance (AUS),
follicular neoplasm, suspicious for malignancy, malignancy, and
nondiagnostic. The benign category has a less than 1% risk of
malignancy. AUS has a 5-10% risk, follicular neoplasm has a 20-30%
risk, suspicious for malignancy has a 50-75% risk, and malignant has
100% risk. Hypocellular aspirates are a significant problem and may
either be related to poor technique or the presence of cystic nodules.
Benign nodules should be observed and re-evaluated at 6-18 month
intervals. If the patient is experiencing significant distress, such as
dysphagia or discomfort a surgical consult should be obtained.
Indeterminate samples should be repeated at regular intervals.
For AUS, the FNAB can be repeated in 3-6 months, with surgical
consult as needed. If there are atypical findings on US such as
hypoechogenicity, irregular borders, calcifications, or hypervascularity,
a surgical consult should also be sought. Bethesda categories of
follicular neoplasm, suspicious for malignancy, and malignant
classifications each warrant surgical consultation.
Prevention Of Thyroid Disease
Screening and prevention of thyroid disease is an evolving field of
research and medical management. This section covers considerations
of family and personal history, and prevention, including
supplementation and diet. More could be said on this topic, however a
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brief highlight of its significance in the treatment plan is offered
here.93-102
Individuals who are at risk for thyroid disease include those with family
members with a history of thyroid disease, a family history of
autoimmune disease, a personal history of thyroid or autoimmune
disease, live in a region with either an excess or deficiency of iodine or
take a variety of multi-mineral, herbal or nutraceutical supplements
which contain iodine, are taking medications such as Interferon Beta1b, Interleukin-4, immunosuppressants, antiretrovirals, some
monoclonal antibodies, Lithium, and amiodarone, have been exposed
to radiation in the region of the thyroid or have been exposed to
radioactive contrast agents that contain iodine.
The only currently accepted prevention of thyroid disease is avoiding
as much as possible the risk factors such as those listed above. Some
of these risk factors are obviously unavoidable. Others, such as the
intake of excess amounts of goitrogenic foods (including cabbage,
Brussels sprouts, broccoli, turnips, rutabagas, kohlrabi, radishes,
cauliflower, African cassava, millet, kale and soy products) should be
avoided. However, it should be noted that an individual would likely
need to ingest very large quantities of these foods before any
significant risk is incurred and these are generally very healthy foods
and should overall be encouraged.
On the other hand, the intake of iodine in amounts significantly
exceeding recommended daily limits is likely to be quite common,
particularly in individuals who are interested in health and wellness.
Many websites and social media sites tout the benefit of iodine and
selenium. While adequate amounts of these minerals are crucial to a
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healthy and functioning thyroid, the levels of iodine for example often
far exceed the Recommended Daily Allowance (RDA) of 150μg for
adults over the age of 19. A quick survey of supplements shows that
iodine is available in amounts many-fold more than the recommended
daily allowance, i.e., at 225 μg, 1000 μg and even 12.5 mg doses.
Kelp products often contain large amounts of iodine as well. With
selenium, the situation is similar; multimineral supplements or
selenium supplements often exceed the recommended daily allowance
of 55 μg. While there are differences in how much selenium is
bioavailable (sodium selenite is completely absorbed but is excreted
rapidly while sodium selenite is more poorly absorbed but more
efficiently incorporated into selenoproteins), the tolerable upper limit
(UL) for selenium is 400 μg and in areas of China where selenium
deficiencies are common, evidence of selenium toxicity (selenosis)
such as gastrointestinal disturbances, skin rashes, a garlic breath odor,
fatigue, irritability, and neurologic disorders begin to occur when blood
selenium levels correspond to intakes of 850 μg/day.
Supplements with 200 μg of selenium representing 286% of the daily
value (DV) are common. Selenium is required for deiodinase activity
and in individuals with Hashimoto’s thyroiditis as well as in pregnant
women with anti-TPO antibodies, selenium supplementation has been
shown to decrease antibody levels and improves the normalcy of US.
In pregnant women supplementation with selenium significantly
decreases the percentage of those suffering postpartum thyroiditis and
definitive hypothyroidism. In Graves’ disease, selenium
supplementation results in a more rapid return to euthyroidism and a
beneficial effect on mild instances of inflammatory orbitopathy.
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Vitamin D deficiency is a risk factor for Graves’ disease and other
autoimmune diseases, though there are some contradictory results.
Sufficient Vitamin D levels, particularly in those individuals at higher
latitudes, those patients who practice sun-safety measures, those
patients who for cultural or religious reasons get little sun-exposure,
those with a darker complexion, older individuals or any patient at risk
for Vitamin D deficiency may benefit from Vitamin D supplementation.
Supplementations with either Vitamin D2 (ergocalciferol) or D3
(cholecalciferol) appear to be of equal effectiveness.
The Arthritis Foundation recommends the anti-inflammatory diet for
symptoms relief. A recent review of the role of the “Western diet”
consisting of high-fat and cholesterol, high-protein, high-sugar, and
excess salt intake, as well as frequent consumption of processed and
‘fast foods’, otherwise known as too much, too fatty, too salty and too
sugary is known to promote cardiovascular disease, obesity,
prediabetes and diabetes, metabolic syndrome and worsen those
conditions where they exist.
These same dietary trends increase the risk of autoimmune diseases.
It has been suggested that the body of studies so far addressing
nutrition as an etiological factor in inflammatory autoimmune diseases
has not firmly verified functional links between dietary macronutrients
and a risk for developing disease. However, the inconclusive results of
epidemiologic studies do not justify omitting nutrients as influential
factors, but rather illustrate the challenge to detect these on the level
of otherwise heterogeneous populations.
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Subjects prone to autoimmunity have complex individual risk profiles
comprised of genetic and environmental determinants that make their
response to nutritional cues diverse. The Western diet or the Standard
American Diet (SAD) has been associated with the increase in chronic
diseases in developed and developing nations.
The anti-inflammatory diet is similar in many ways to the betterknown Mediterranean diet and emphasizes whole grains, vegetables,
fruit, lean meats, nuts, seeds and oily fish while de-emphasizing
processed or prepared foods, foods with added salt and sugar, fatty
meats and dairy products. While final confirmation that either the antiinflammatory diet or the Mediterranean diet can prevent autoimmune
disease or more specifically thyroid disease awaits further studies, the
nutritional value of these diets and the benefit in preventing disease
make these nutritional approaches viable clinical recommendations.
Summary
The human body depends on thyroid hormones to function at an
optimal healthy state. Because no test can fully measure how thyroid
hormone is utilized once it enters the bloodstream, it is important for
clinicians to understand the varied tests and measures that inform how
each unique individual responds to thyroid hormone imbalances. While
the TSH has been the gold standard to diagnose and treat thyroid
disease, there are other diagnostic tests that help guide treatment.
Often clinicians will rely solely on the TSH test, which can lead to
misdiagnosis. Therefore, lab diagnosis of thyroid diseases makes use
of a number of tests and imaging procedures to diagnose and manage
treatment.
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Please take time to help NurseCe4Less.com course planners
evaluate the nursing knowledge needs met by completing the
self-assessment of Knowledge Questions after reading the
article, and providing feedback in the online course evaluation.
Completing the study questions is optional and is NOT a course
requirement.
1. ______________ or T4 (containing four iodine atoms) is the
primary thyroid hormone secreted by the thyroid gland.
a.
b.
c.
d.
Thyroid stimulating hormone
*Thyroxine
Triiodothyronine
Thyroglobulin
2. True or False: The thyroid stimulating hormone (TSH) test is
often the only test ordered by clinicians when thyroid
disease is suspected, and this can lead to misdiagnosis.
a. *True
b. False
3. Thyroid stimulating hormone (TSH) is released by the
a.
b.
c.
d.
parathyroid.
thymus.
*pituitary gland.
thyroidea ima.
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4. What is the consensus regarding the diagnostic limits for
thyroid stimulating hormone (TSH) that would indicate
thyroid failure and hypothyroidism?
a.
b.
c.
d.
TSH >10 mIU/L
TSH ≥ 4 mIU/L
TSH ≥ 3 mIU/L
*None of the above
5. Decreased thyroid stimulating hormone (TSH) levels are
seen in
a.
b.
c.
d.
primary hypothyroidism.
TSH-producing tumors.
Hashimoto’s thyroiditis.
*primary hyperthyroidism.
6. One of the consequences of a hypothyroid patient receiving
excessive replacement hormone may be
a.
b.
c.
d.
*decreased TSH levels.
increased TSH levels.
TSH-producing tumors.
TSH antibodies.
7. True or False: The T4 test—as opposed to the total fT4 test,
is believed to more accurately represent thyroid hormone
functional levels.
a. True
b. *False
8. The free T3 (fT3) test is commonly used to aid in the
diagnosis of _________________ and to monitor treatment.
a.
b.
c.
d.
hypothyroidism
myxedema
Hashimoto’s thyroiditis
*hyperthyroidism
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9. Elevated free T3 (fT3) levels are seen in
a.
b.
c.
d.
primary hypothyroidism.
secondary hypothyroidism.
*T3 toxicosis.
deiodinase deficiency or insufficiency.
10. Depressed free T3 (fT3) levels are seen in
a.
b.
c.
d.
hyperthyroidism.
high altitudes.
*3rd trimester of pregnancy.
T3 toxicosis.
11. The thyroglobulin test is used primarily
a. *as a tumor marker to monitor thyroid cancer treatment.
b. to monitor T3 toxicosis.
c. to determine the underlying cause of congenital
hypothyroidism.
d. to help differentiate between subacute thyroiditis and
thyrotoxicosis factitia.
12. True or False: Clinicians often do not rely on a full thyroid
blood screen to diagnose a thyroid condition.
a. *True
b. False
13. Tests that measure thyroid function are important because
they inform clinicians
a.
b.
c.
d.
about thyroid hormone utilization in the bloodstream.
if a patient has thyroid cancer.
*how each person responds to thyroid hormone imbalances.
All of the above
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14. Depressed levels of thyroglobulin may be seen with
a.
b.
c.
d.
subacute thyroiditis.
*thyrotoxicosis factitia.
thyrotoxicosis.
hyperthyroidism.
15. Thyroglobulin levels are NOT used to
a.
b.
c.
d.
*diagnose thyroid cancer.
monitor untreated, well-differentiated thyroid cancer.
monitor metastatic, well-differentiated thyroid cancer.
to monitor the treatment of Graves’ disease.
16. _______________ binding globulin is the main serum
carrier protein for T4.
a. *Thyroxine
b. Triiodothyrodine
c. T7
d. Thyroglobulin
17. True or False: The thyroglobulin test may be used to
monitor the treatment of Graves’ disease.
a. *True
b. False
18. Triiodothyrodine Uptake (T3U) is an indirect measurement
of the amount of unsaturated _________________
available.
a.
b.
c.
d.
Fatty Acids
*Thyroxine-Binding Globulin (TBG)
Linolenic acid
Natural food ingested is
19. The _____________________ test is usually done along
with the T4 test, resulting in the calculated “T7” test.
a.
b.
c.
d.
*triiodothyrodine uptake (T3U)
thyroglobulin
free T3 (fT3)
free thyroxine
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20. Free Thyroxine Index (FTI) is also known as
a.
b.
c.
d.
*T7.
T3U.
free T3 (fT3).
a full thyroid blood screen.
21. The Free Thyroxine Index (FTI) can give a clearer picture
of thyroid function in
a.
b.
c.
d.
suspected hypothyroidism and hyperthyroidism.
in patients who are pregnant.
in patients with suspected abnormalities in TBG levels.
*All of the above
22. True or False: The measurement of Triiodothyrodine
Uptake (T3U) is inversely proportional to the ThyroxineBinding Globulin (TBG) levels.
a. *True
b. False
23. Decreased T3U levels occur
a.
b.
c.
d.
with inorganic iodine.
with salicylates.
with anabolic steroids.
*in a normal pregnancy.
24. One of the primary ways of diagnosing autoimmune thyroid
disease is by testing for
a.
b.
c.
d.
inorganic iodine.
Thyroxine-Binding Globulin (TBG) levels.
*antibodies.
free thyroxine.
25. Stimulating antibodies (TSI) promotes thyroid hormone
production leading to
a.
b.
c.
d.
*hyperthyroidism.
Hashimoto's thyroiditis.
hypothyroidism.
TBII production.
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26. Elevated levels of antibodies, such as TSH-RAb, are
predictors of
a.
b.
c.
d.
suspected hypothyroidism.
Hashimoto's thyroiditis.
*fetal and neonatal thyrotoxicosis.
abnormalities in TBG levels.
27. True or False: Inhibiting antibodies (TBII) inhibit
production of thyroid hormones and lead to
hypothyroidism, and this is routinely tested for.
a. True
b. *False
28. The first thyroid imaging thyroid scan done with a
Radioactive Iodine Uptake test (RAIU) is performed
____________ after ingesting the radiotracer.
a.
b.
c.
d.
*two hours
8 hours
within 24 hours
within 12 hours
29. With the Radioactive Iodine Uptake test (RAIU), which of
the following is diagnostic of thyroid disease?
a.
b.
c.
d.
Increased uptake
Decreased uptake
Inorganic iodine concentrations
*None of the above
30. Testing calcitonin, which is produced by the parafollicular
or C cells of the parathyroid gland, may be used to
diagnose
a.
b.
c.
d.
hyperthyroidism.
Hashimoto's thyroiditis.
hypothyroidism.
*medullary thyroid cancer.
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31. The American Academy of Family Physicians recommends
that all patients over the age of ___ should be screened for
thyroid disease.
a.
b.
c.
d.
*60
35
50
45
32. True or False: The Radioactive Iodine Uptake test (RAIU) is
a direct measurement of the ability of the thyroid gland to
concentrate inorganic iodine.
a. *True
b. False
33. Thyroid imaging utilizes I-123 or I-131 (and sometimes
Technetium pertechnetate-99m) to visualize and evaluate
the size, position, function and the presence of
a.
b.
c.
d.
inorganic iodine.
*“hot” or “cold” spots in the thyroid.
thyroid tumors.
medullary thyroid cancer.
34. Thyroid imaging “hot” spots, indicating increased uptake of
iodine, are generally a sign of
a.
b.
c.
d.
malabsorption syndrome.
celiac disease.
*non-malignancy.
medullary thyroid cancer.
35. Genetic markers and gene panels are becoming more
widely used in assessing the potential for
a.
b.
c.
d.
*malignant thyroid tumors.
celiac disease.
neonatal thyrotoxicosis.
abnormalities in TBG levels.
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CORRECT ANSWERS:
1. ______________ or T4 (containing four iodine atoms) is the
primary thyroid hormone secreted by the thyroid gland.
b. Thyroxine
“Thyroxine or T4 (containing four iodine atoms) is the primary
thyroid hormone secreted by the thyroid gland.”
2. True or False: The thyroid stimulating hormone (TSH) test is
often the only test ordered by clinicians when thyroid
disease is suspected, and this can lead to misdiagnosis.
a. True
“Thyroid stimulating hormone (TSH) is released by the
pituitary gland depending on the level of T4 recognized by the
pituitary; the more T4 the less the TSH value and the less the
T4 the higher the TSH value. While the TSH has been the gold
standard to diagnose and treat thyroid disease, there are other
diagnostic tests that help guide treatment. Often clinicians will
rely solely on the TSH test, which can lead to misdiagnosis.”
3. Thyroid stimulating hormone (TSH) is released by the
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c. pituitary gland.
“Thyroid stimulating hormone (TSH) is released by the
pituitary gland depending on the level of T4 recognized by the
pituitary;…”
4. What is the consensus regarding the diagnostic limits for
thyroid stimulating hormone (TSH) that would indicate
thyroid failure and hypothyroidism?
d. None of the above
“There is some disagreement regarding diagnostic limits for
TSH. For many years and for many clinicians, TSH >10 mIU/L
was indicative of thyroid failure and hypothyroidism. The
National Academy of Clinical Biochemistry has, however,
recommended 4 mIU/L as an upper limit, while the American
Association of Clinical Endocrinologists has set the upper limit
at 3 mIU/L. Other professional groups have suggested even
lower values such as 2.5 mIU/L. There is a growing consensus
that “one size does not fit all” and that individual patient
responses must be taken into account during treatment. In
addition, there is currently no accepted reference
measurement procedure (RMP) for the TSH assay, meaning
there are significant variations from lab to lab and between
different assay manufacturers.”
5. Decreased thyroid stimulating hormone (TSH) levels are
seen in
d. primary hyperthyroidism.
“Decreased TSH levels are seen in: Primary hyperthyroidism;
Secondary, tertiary hypothyroidism; Euthyroid Sick Syndrome;
Hypothyroid patients receiving excessive replacement hormone
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or insufficient replacement hormone in those treated for
hyperthyroidism.”
6. One of the consequences of a hypothyroid patient receiving
excessive replacement hormone may be
a. decreased TSH levels.
“Decreased TSH levels are seen in: Primary hyperthyroidism;
Secondary, tertiary hypothyroidism; Euthyroid Sick Syndrome;
Hypothyroid patients receiving excessive replacement hormone
or insufficient replacement hormone in those treated for
hyperthyroidism.”
7. True or False: The T4 test—as opposed to the total fT4 test,
is believed to more accurately represent thyroid hormone
functional levels.
b. False
“The fT4 test—as opposed to the total T4 test, is believed to
more accurately represent thyroid hormone functional levels.”
8. The free T3 (fT3) test is commonly used to aid in the
diagnosis of _________________ and to monitor treatment.
d. hyperthyroidism
“The free T3 (fT3) test is commonly used to aid in the
diagnosis of hyperthyroidism and to monitor treatment.”
9. Elevated free T3 (fT3) levels are seen in
c. T3 toxicosis.
“Elevated fT3 levels are seen in: Hyperthyroidism; T3
toxicosis; High altitudes.”
10. Depressed free T3 (fT3) levels are seen in
c. 3rd trimester of pregnancy.
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“Depressed fT3 levels are seen in: Primary or secondary
hypothyroidism; 3rd trimester of pregnancy; Deiodinase
deficiency or insufficiency.”
11. The thyroglobulin test is used primarily
a. as a tumor marker to monitor thyroid cancer treatment.
“The thyroglobulin test is used primarily as a tumor marker to
follow the effectiveness of thyroid cancer treatment, primarily
the well-differentiated thyroid cancers, and to monitor diseasefree progression.”
12. True or False: Clinicians often do not rely on a full thyroid
blood screen to diagnose a thyroid condition.
a. True
“Clinicians often do not rely on a full thyroid blood screen to
diagnose a thyroid condition.”
13. Tests that measure thyroid function are important because
they inform clinicians
c. how each person responds to thyroid hormone imbalances.
“The human body depends on thyroid hormones to function at
an optimal healthy state. Because no test can fully measure
how thyroid hormone is utilized once it enters the bloodstream,
it is important for clinicians to understand the varied tests and
measures that inform how each unique individual responds to
thyroid hormone imbalances.”
14. Depressed levels of thyroglobulin may be seen with
b. thyrotoxicosis factitia.
“Depressed levels of thyroglobulin may be seen with:
Thyrotoxicosis factitia; Newborns and infants with goiter and
hypothyroidism.”
15. Thyroglobulin levels are NOT used to
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a. diagnose thyroid cancer.
“The thyroglobulin test is used primarily as a tumor marker to
follow the effectiveness of thyroid cancer treatment, primarily
the well-differentiated thyroid cancers, and to monitor diseasefree progression. Other reasons for testing for thyroglobulin
are to monitor the treatment of Graves’ disease. Rarely, it may
be used to try and determine the underlying cause of
congenital hypothyroidism or to help differentiate between
subacute thyroiditis and thyrotoxicosis factitia.”
16. _______________ binding globulin is the main serum
carrier protein for T4.
a. Thyroxine
“Often confused with thyroglobulin, thyroxine binding globulin
is the main serum carrier protein for T4.”
17. True or False: The thyroglobulin test may be used to
monitor the treatment of Graves’ disease.
a. True
“The thyroglobulin test is used … for testing for thyroglobulin
are to monitor the treatment of Graves’ disease.”
18. Triiodothyrodine Uptake (T3U) is an indirect measurement
of the amount of unsaturated _________________
available.
b. Thyroxine-Binding Globulin (TBG)
“Triiodothyrodine Uptake (T3U): This test is an indirect
measurement of the amount of unsaturated TBG available and
is inversely proportional to the TBG levels.”
19. The _____________________ test is usually done along
with the T4 test, resulting in the calculated “T7” test.
a. triiodothyrodine uptake (T3U)
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“[Triiodothyrodine Uptake (T3U)] test is usually done along
with the T4 test (resulting in the calculated “T7” test).”
20. Free Thyroxine Index (FTI) is also known as
a. T7.
“T7 is also known as the Free Thyroxine Index (FTI)….”
21. The Free Thyroxine Index (FTI) can give a clearer picture
of thyroid function in
a.
b.
c.
d.
suspected hypothyroidism and hyperthyroidism.
in patients who are pregnant.
in patients with suspected abnormalities in TBG levels.
All of the above [correct answer]
“The FTI can give a clearer picture of the totality of thyroid
function in both suspected hypothyroidism and
hyperthyroidism as well in patients who are pregnant or with
suspected abnormalities in TBG levels.”
22. True or False: The measurement of Triiodothyrodine
Uptake (T3U) is inversely proportional to the ThyroxineBinding Globulin (TBG) levels.
a. True
“Triiodothyrodine Uptake (T3U): This test is an indirect
measurement of the amount of unsaturated TBG available and
is inversely proportional to the TBG levels.”
23. Decreased T3U levels occur
d. in a normal pregnancy.
“Decreased T3U levels occur in a normal pregnancy, with a
variety of drugs such as estrogens, methadone and heparin.
Increased T3U levels can occur with heparin, salicylates and
anabolic steroids.”
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24. One of the primary ways of diagnosing autoimmune thyroid
disease is by testing for
c. antibodies.
“One of the primary ways of diagnosing autoimmune thyroid
disease is by testing for antibodies.”
25. Stimulating antibodies (TSI) promotes thyroid hormone
production leading to
a. hyperthyroidism.
“Stimulating antibodies (TSI) promote thyroid hormone
production leading to hyperthyroidism while inhibiting
antibodies (TBII) inhibit production and lead to
hypothyroidism, though this is not routinely tested for.”
26. Elevated levels of antibodies, such as TSH-RAb, are
predictors of
c. fetal and neonatal thyrotoxicosis.
“Antibodies to TSH should be assessed particularly in euthyroid
and thyroid hormone treated pregnant women or those with a
history of hyperthyroidism as these antibodies are predictors of
fetal and neonatal thyrotoxicosis.”
27. True or False: Inhibiting antibodies (TBII) inhibit
production of thyroid hormones and lead to
hypothyroidism, and this is routinely tested for.
b. False
“Stimulating antibodies (TSI) promote thyroid hormone
production leading to hyperthyroidism while inhibiting
antibodies (TBII) inhibit production and lead to
hypothyroidism, though this is not routinely tested for.”
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28. The first thyroid imaging thyroid scan done with a
Radioactive Iodine Uptake test (RAIU) is performed
____________ after ingesting the radiotracer.
a. two hours
“The Radioactive Iodine Uptake test (RAIU) is a direct
measurement of the ability of the thyroid gland to concentrate
inorganic iodine. The test measures the rate of accumulation,
incorporation and release of iodine. In order to minimize
exposure to the patient, this test is often done in conjunction
with thyroid imaging such as scintigraphy (thyroid scan). The
patient may be asked to use a low-iodine diet for 7-10 days
before the test and may be asked to fast. The first scan is
usually done at two hours, then 4-6 hours after ingesting the
radiotracer (either 123I or 131I), with a second scan within 24
hours.”
29. With the Radioactive Iodine Uptake test (RAIU), which of
the following is diagnostic of thyroid disease?
a.
b.
c.
d.
Increased uptake
Decreased uptake
Increased uptake with thyroid imaging
None of the above [correct answer]
“Increased uptake is associated with hyperthyroidism.
Decreased uptake is associated with hypothyroidism. Neither
is diagnostic and may be affected by malabsorption, diarrhea,
rapid diuresis and renal insufficiency…. The radioactive iodine
uptake test (RAIU), also known as a thyroid uptake test, is a
measurement of thyroid function, and does not involve
imaging.”
30. Testing calcitonin, which is produced by the parafollicular
or C cells of the parathyroid gland, may be used to
diagnose
d. medullary thyroid cancer.
“Calcitonin, produced by the parafollicular or C cells of the
parathyroid gland may be used to diagnose medullary thyroid
cancer.”
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31. The American Academy of Family Physicians recommends
that all patients over the age of ___ should be screened for
thyroid disease.
a. 60
“The American Academy of Family Physicians recommends that
all patients over the age of 60 should be screened [for thyroid
disease].”
32. True or False: The Radioactive Iodine Uptake test (RAIU) is
a direct measurement of the ability of the thyroid gland to
concentrate inorganic iodine.
a. True
“The Radioactive Iodine Uptake test (RAIU) is a direct
measurement of the ability of the thyroid gland to concentrate
inorganic iodine.”
33. Thyroid imaging utilizes I-123 or I-131 (and sometimes
Technetium pertechnetate-99m) to visualize and evaluate
the size, position, function and the presence of
b. “hot” or “cold” spots in the thyroid.
“Thyroid imaging utilizes I-123 or I-131 (and sometimes
Technetium pertechnetate-99m) to visualize and evaluate the
size, position, function and the presence of “hot” or “cold”
spots in the thyroid. The radioactive iodine uptake test (RAIU),
also known as a thyroid uptake test, is a measurement of
thyroid function, and does not involve imaging.”
34. Thyroid imaging “hot” spots, indicating increased uptake of
iodine, are generally a sign of
c. non-malignancy.
“‘Hot’ spots, indicating increased uptake of iodine are generally
non-malignant while “cold” spots generally need further
evaluation, with a greater possibility that these represent
malignancies.”
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35. Genetic markers and gene panels are becoming more
widely used in assessing the potential for
a. malignant thyroid tumors.
“Genetic markers and gene panels are becoming more widely
used in assessing the potential for malignant thyroid tumors.”
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The References below include published works and in-text citations of
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