Download Thyroid Disorders

Thyroid Disorders
Eric J Milie, D.O.
Objectives
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Understand basic interactions of the
hypothalamic-pituitary-thyroid axis
Recognize the various causes of hypo- and
hyperthyroid
Differentiate between acute, subacute, and
chronic thyroiditis in terms of clinical picture
and treatment
Explain the work-up required for a patient
with a solitary thyroid nodule
Thyroid Anatomy
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Small gland located in anterior portion of
neck
Attached to larynx
Two halves (lobes) connected by isthmus
Resembles a butterfly or bow-tie
From Greek word meaning shield
Each lobe roughly 4cm long, 1-2cm wide
Cannot normally be seen, barely palpable in
healthy adult
Thyroid Anatomy continued
Function of Thyroid Gland
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Secretes thyroid hormones, which regulate
metabolism throughout the body
Two hormones secreted: Thyroxine (T4) and
Triiodothyronine (T3)
Thyroid Hormones
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T4, the major hormone produced by the
thyroid, has only slight effect on controlling
body’s metabolism
T4 converted to T3 (active thyroid hormone)
mainly in the liver and kidney
Many factors effect conversion rate, including
body’s need from moment to moment and
presence or absence of illness
Chemical Structure
Thyroid Hormones continued
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T4 de-iodinated in liver and kidney, resulting
in T3 and reverse T3 (inactive)
Thyroid hormones poorly soluble in water, so
99% protein bound
Principle carrier is thyroxine binding globulin,
a glycoprotein synthesized by the liver
Some Thyroid Hormone
Responsibilities
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Heart rate
Respiratory rate
Rate of caloric consumption
Skin maintenance
Growth
Fertility
Digestion
Heat regulation
Role of Iodine
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Chief component of thyroid hormones, essential for
their production
Iodine concentrated from blood via the Sodiumiodide symporter, so-called “iodine trap”
In areas where there is not sufficient levels of iodine
(Great Lakes, Swiss Alps, Tasmania), iodine must
be supplimented
In U.S., salt iodized, so iodine deficiency is rare
Sodium-Iodine Symporter
Thyroid Stimulating Hormone
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Chief stimulator of thryoid hormone synthesis
is TSH (Thyroid Stimulating Hormone),
released from anterior pituitary
Most important controller of TSH secretion is
Thyrotropin Releasing Hormone (TRH) from
hypothalamic neurons
Secretion of TRH, and hence TSH, inhibited
by high blood levels of thyroid hormones
(negative feedback loop)
TRH-TSH-Thyroid Hormone
Feedback Loop
Hypothalamic-Pituitary Axis
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Feedback loop pat of so-called “hypothalamic
pituitary axis”
As thyroid hormone levels in blood increase,
negative feedback to hypothalamus and pituitary
Leads to shut-down of thyroid producing follicles
When circulating levels of thyroid hormone stabilize,
process begins anew
Axis influenced by other factors, including
environmental factors (cold exposure leads to
increase in thyroid hormone production in rodent
models)
Hypothalamic-Pituitary-Thyroid Axis
Goiter Formation as Dysfunction
of Hypothalmic-Pituitary-Thyroid
Axis
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Insufficient dietary intake of iodine leads to
insufficient production of T3 and T4
Hypothalamus responds with increasing
levels of circulating TRH
Causes pituitary to release more TSH
Secondary function of TSH is thyroid cell
growth
Prolonged exposure to high levels of TSH
results in goiter
Goiter
Thyroid Gland- Diagnostic
Studies
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No single test is 100% accurate in diagnosing
thyroid disease, so usually combination of
two or more tests ordered
TSH level is most common test ordered for
monitoring of thyroid function
High levels of TSH usually indicative of under
active thyroid gland (hypothyroid)
Low levels usually indicative of over active
thyroid gland (hyperthyroid)
Diagnostic Tests continued
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Measurement of T4 by radioimmunoassay
(RIA) reflects the amount of T4 circulating in
the blood.
Usually combined with T3 uptake to give a
“free T4 level,” which corrects for other
medications which influence the routine T4
test
Diagnostic Tests continued
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Thyroid Binding Globulin may be ordered for
patients with unexplained elevations or
deficiency of T4 and T3
Excess or deficiency of TBG will alter the
measurement of T3 and T4, but not the
action of the hormones
Hereditary trait can cause excessive or
deficient levels of TBG
Iodine Uptake Scan
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Radioactive iodine administered to patient
Iodine concentrated in the thyroid or excreted in the
urine
Uptake measured at various time intervals
Does not measure hormone levels, merely avidity of
thyroid for iodine and clearance rate relative to
kidney function
Diseases resulting in excessive production of thyroid
hormone generally associated with increased RAIU,
diseases resulting in decreased production generally
show decreased RAIU
RAIU continued
Thyroid Scan
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Usually done at same time as RAIU
Useful in identifying nodules and defining if
they are “hot” or “cold”
Measuring size of goiter prior to treatment
Follow-up in thyroid cancer patients after
surgery
Locating thyroid tissue outside of neck, such
as at base of tongue or in the chest
Thyroid Scan
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Two types, camera scan and Computerized
Rectilinear Thyroid scan
Camera scan most common, takes 5-10
minutes
CRT developed in the 1990’s, improves
clarity, more precisely identifies nodules, and
provides information on both function and
size
Camera Scan
Camera scan images showing “hot nodule” (left) and “cold nodule” (right)
CRT
Thyroid Ultrasound
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Screening tool for suspected thyroid nodule
Can identify if nodule is cystic or solid, but
provides little help determining if it is benign
or malignant
Can detect changes in nodule’s size
Useful in assisting with needle biopsy of
thyroid
Thyroid Ultrasound
Ultrasound Characteristics
Suggesting Benign Nodule
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Sharp edges around entire nodule (well
circumscribed)
Nodule filled with fluid and not live tissue
(cystic)
Multiple nodules throughout the thyroid
No blood flowing through nodule on Doppler
(suggest cystic lesion)
Fine Needle Biopsy
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Most reliable test to determine whether “cold”
nodule cancerous or benign
Provides definitive diagnosis in up to 75% of
biopsies
Further discussion later in presentation
Euthyroid Sick Syndrome:
Definition
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Clinical condition in which patients suffering
from severe non-thyroid illness are clinically
euthyroid but biochemically dysthyroid
Euthyroid Sick Syndrome:
Precipitating Factors
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Fasting
Starvation
Anorexia nervosa
Protein malnutrition
Surgical trauma
Hyperthermia
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Myocardial infarction
Chronic renal failure
Diabetic ketoacidosis
Cirrhosis
Sepsis
Euthyroid Sick Syndrome: Lab
Findings
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T4 concentration is normal or decreased
T4-binding to TBG is decreased
T3 concentration is decreased
rT3 concentration is increased
TSH concentration is normal
Thyroid scans usually normal
Euthyroid Sick Syndrome:
Pathogenesis
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When people are sick or malnourished or have had
surgery, the thyroid hormone T4 is not converted
normally to the active T3 hormone
Large amounts of reverse T3 accumulate
Despite this abnormal conversion, the thyroid
functions normally
No treatment is necessary, as thyroid function is
preserved
Laboratory tests normalize once the underlying
illness resolves
Hyperthyroid: Definition
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Condition of excess functional activity of the
thyroid gland
Characterized by increased basal
metabolism, goiter, and disturbances of the
autonomic nervous system
Affects women 3:1 more than men
Hyperthyroid: Types
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Graves’ disease
Toxic nodular goiter (Plummer’s disease)
Toxic adenoma
Therapeutic induced hyperthyroid (Lugol’s,
amiodarone, etc.)
Thyroiditis
Primary and/or metastatic follicular carcinoma
TSH producing tumor of the hypophysis
Hyperthyroid: Common
Symptoms and Signs
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Heat intolerance, excessive sweating, and
moist skin
Hyperactivity and tenseness
Weight loss (unintentional)
Fine tremors, palpitations, and tachycardia
Infiltrative dermopathy
Ocular signs, including lid lag, exophthalmus,
and conjunctival injection
Generalized pruritis
Hyperthyroid: Diagnostic
Work-up
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History and physical
Blood chemistries, including hormone levels
and specific antibodies
Ultrasound
Thyroid scan
Fine needle biopsy (particularly with
hyperthyroidism associated with nodularity)
Grave’s Disease
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Autoimmune disease associated with the
production of antibodies that bind to TSH
receptors in the follicular cells of the thyroid
and activate these cells to produce T4 and
T3.
These antibodies therefore simulate TSH TSH has no part in this hyperfunctioning
Graves’ Disease:
Pathophysiology
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Most common form of adult hyperthyroidism
Peaks in 3rd and 4th generations
Clinical presentation includes all
aforementioned signs and symptoms; ocular
and dermatological signs pathognomonic
Bilateral exophthalmos occurs in 40-50% of
Graves’ patients- unilateral involvement is
rare
Graves’ Disease continued
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T3 and T4 concentrations increased
TSH level decreased
Autoimmune antibodies to TSH receptors
RAI and Tc-99m studies are increased
Scans usually show mildly enlarged thyroid
which concentrates isotope evenly and
intensely
Graves’ Disease- Therapy
(Conservative)
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Treatment with antithyroid drugs
(Propranolol, propylthiouricil, methimazole)
Long term remission rate with conservative
treatment is low (30-50%)
Propranolol β-blocker; makes patient
eumetabolic but not euthyroid
Other drugs block iodothyronine hormone
synthesis
Graves’ Disease- Therapy:
Surgery
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Treatment of choice if patient younger than
21 years of age, is sensitive to iodine, or who
have very large goiters
In good hands, recurrence rate is low (29%)with a 3% incidence of hypothyroidism
Side effects: vocal cord paralysis and
hypoparathyroidism
Graves’ Disease- Therapy:
Radioactive Iodine-131
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Therapy of choice for women past
childbearing years and adult males
No proven increase in incidence of
carcinoma, leukemia, etc.
25% of patients will be hypothyroid one year
after treatment; incidence increases 2%/year
for the next 20 years
Graves’ Ophthalmopathy
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Most frequent extrathyroidal manifestationof
Graves’ disease
Fortunately, most patients with only minor
involvement, amenable to non-aggressive
treatment
Graves’ Exophthalmos: Picture
Management of Nonsevere
Exophthalmos
Management of nonsevere Graves’ ophthalmopathy13
Sign and/or symptom
Therapeutic measure
Photophobia
Foreign body sensation
Eyelid retraction; increased
intraocular pressure
Lag ophthalmos
Mild diplopia
Sunglasses
Artificial tears and ointments
ß-Blocking eyedrops
Nocturnal taping of the eyes
Prisms
Correction of hyper- or
hypothyroidism
Elimination of risk factors (smoking)
Reassurance on the natural history
of the disease
Management of Severe
Exophthalmos
Management of severe Graves’ ophthalmopathy13
Established methods
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Glucocorticoids
a. Oral
b. Intravenous
c. Local
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Supervoltage orbital radiotherapy
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a. Rehabilitative surgery
b. Orbital decompression
c. Extraocular muscle surgery
d. Eyelid surgery
4.
Novel treatments under investigation
1. Somatostatin Analogues
2. Octreotide
3. Lanreotide
4. Intravenous immunoglobulins
5. Nonestablished methods
6. Cyclosporinea
7. Plasmapheresis
8. Anecdotal treatments
9. Cyclophosphamide
10. Bromocriptine
11. Metradinazole
Infiltrative Dermopathy of
Graves’ Disease
Toxic Adenoma: Definition
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Autonomous hyperfunctioning nodule
surrounded by normal functioning tissue
Rarely two or more adenomas exist in
normally functioning thyroid
No clear cause; neither antibodies nor TSH
involved
Nodule must be 2.5-3cm in size to produce
hyperthyroidism
Toxic Adenoma: Presentation
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Symptoms and signs of hyperthyroidism.
No exophthalmos.
No infiltrating dermopathy.
The thyroid gland may be enlarged, but is
generally of normal size.
On palpation, a non-tender, mildly firm nodule
is palpable.
Toxic Adenoma: Diagnosis
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T3 and T4 levels are elevated.
The TSH concentration is decreased.
Specific antibodies are absent.
On Radioisotope scan, the thyroid gland is
usually of normal size.
One hot nodule - rest of the gland is cool
Toxic Adenoma: Treatment
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Unless contraindicated, radioactive iodine
(131I) - higher doses are usually necessary.
Production of hypothyroidism is rare.
Toxic Adenoma: Imaging
Toxic Multinodular Goiter
(Plummer’s Disease)
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enlarged multinodular goiter commonly found in
areas of iodine deficiency in which patients with
long-standing non-toxic goiter develop thyrotoxicosis
One or more of the nodules begin to hyperfunction
autonomously
Encompasses a spectrum of different clinical entities
ranging from a single hyperfunctioning nodule within
an enlarged thyroid gland having additional nonfunctioning nodules to multiple hyperfunctioning
areas (nodules) scattered throughout the gland
barely distinguishable from non-functioning nodules
and ordinary thyroid tissue
Plummer’s Disease: Clinical
Presentation
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A middle-aged person with 10 - 15 years
history of an enlarged gland.
The general symptoms and signs of
hyperthyroidism.
Exophthalmos is absent.
Infiltrative dermopathy is absent.
The gland is enlarged and multinodular.
Plummer’s Disease: Diagnosis
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The serum T3 and T4 levels are raised.
The TSH concentration is decreased.
No auto-immune antibodies are present
Scan shows an enlarged, multinodular gland.
One, two or more nodules are hot
(overactive) and in between cool and cold
nodules
Plummer’s Disease: Treatment
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Similar to treatment for Grave’s disease
Plummer’s disease is more resistant to 131I
therapy than Graves’ - apparently because
the areas (nodules) of low activity at the time
of therapy become active as the hyperactive
nodules are destroyed and more TSH is
released.
Induction of hypothyroidism is rare
Plummer’s Disease: Imaging
Thyrotoxicosis Factitiae
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syndrome of hyperthyroidism that results
from an overdosage of thyroid hormone - T3
or T4.
Clinical signs and symptoms similar to other
causes of hyperthyroidism
No exophthalmos or dermopathy
Thyrotoxicosis Factitiae:
Diagnosis
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T3 therapy: serum concentration of T3 is
increased, serum T4 is decreased, and TSH
concentration is decreased.
T4 therapy: serum T3 concentration is
increased, T4 concentration is increased,
TSH level is decreased.
RAI uptake by thyroid is decreased
The thyroid gland is not enlarged.
Scan image shows a cool thyroid
Thyrotoxicosis Factitiae:
Treatment
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Reduce or suspend T4 therapy.
Normalization may take 6 weeks or longer
Hamburger Thyrotoxicosis
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Several outbreaks of thyrotoxicosis have been attributed to a
practice, now banned in the US, called "gullet trimming”
Meat in the neck region of slaughtered animals is ground into
hamburger
Thyroid glands are reddish in color and located in the neck, it's
not unusual for gullet trimmers to get thyroid glands into
hamburger or sausage
Outbreak of thyrotoxicosis in Minnesota and South Dakota that
was traced to thyroid-contaminated hamburger. A total of 121
cases were identified in nine counties, with the highest incidence
in the county having the offending slaughter plant. The patients
complained of sleeplessness, nervousness, headache, fatique,
excessive sweating and weight loss
Iodine-precipitated
Hyperthyroidism
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With iodine deficiency production of T4 and T3 decreases, so
more TSH is released and thyroid stimulation increases, resulting
in enlargement of the thyroid (goiter)
If iodine intake is increased in such a patient the enlarged gland
may produce excess amounts of T3 and T4, and hyperthyroidism
develops.
Excess iodine intake by euthyroids and hyperthyroids may
suppress TSH secretion and thus produce hypothyroidism or it
may produce hyperthyroidism by activating hormogenesis in
patients with deranged special thyroidal systems, so-called JodBasedow phenomenon
Lastly, it may elicit hyperactivity in normal thyroid glands by
deranging the function of the cells
Secondary Hyperthyroidism
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This term refers to hyperthyroidism precipitated by
excess TSH secretion by a pituitary tumour or by
other tumours (e.g. choriocarcinoma, struma ovarii,
etc.)
Clinical signs and symptoms same as other causes
of hyperthyroidism, without exophthalmos
The T3, T4 and TSH concentrations are raised
The thyroid is enlarged and the isotope uptake is
diffusely increased.
Hypothyroidism
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condition where insufficient thyroid hormones
are produced
Two main types are distinguished,. primary
and secondary hypothyroidism
Primary hypothyroidism by far more common
Primary Hypothyroidism can be subdivided
into hypothalamic-pituitary causes vs.
thyroidal causes
Hypothyroidism: Causes
Primary
1. Primary (thyroidal) hypothyroidism
1. Loss of functional thyroid tissue
1. chronic autoimmune thyroiditis
2. reversible autoimmune hypothyroidism (silent and postpartum
thyroiditis, cytokine-induced thyroiditis).
3. surgery and irradiation (131I or external irradiation)
4. infiltrative and infectious diseases, subacute thyroiditis
5. thyroid dysgenesis
2. Functional defects in thyroid hormone biosynthesis and release
1. congenital defects in thyroid hormone biosynthesis
2. iodine deficiency and iodine excess
3. drugs: antithyroid agents, lithium, natural and synthetic goitrogenic
chemicals
Hypothyroidism: Causes
Secondary
2. Central (hypothalamic/pituitary) hypothyroidism
1. Loss of functional tissue
1. tumors (pituitary adenoma, craniopharyngioma, meningioma,
dysgerminoma, glioma, metastases)
2. trauma (surgery, irradiation, head injury)
3. vascular (ischemic necrosis, hemorrhage, stalk interrruption,
aneurysm of internal carotid artery)
4. infections (abcess, tuberculosis, syphilis, toxoplasmosis)
5. infiltrative (sarcoidosis, histiocytosis, hemochromatosis)
6. chronic lymphocytic hypophysitis
7. congenital (pituitary hypoplasia, septooptic dysplasia, basal
encephalocele)
2. Functional defects in TSH biosynthesis and release
1. mutations in genes encoding for TRH receptor, TSHß, or Pit2. drugs: dopamine; glucocorticoids; L-thyroxine withdrawal
3. "Peripheral" (extrathyroidal) hypothyroidism
1. Thyroid hormone resistance
2. Massive infantile hemangioma
Hypothyroidism: Signs and
Symptoms
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A dull facial expression, a hoarse voice, slow speech, a puffed
face with swollen periorbital tissues. These changes are the
result of mucopolysaccharide (hyaluronic acid and chondroitin
sulphate) infiltration of the tissues.
The patient is cold-intolerant due to low metabolic rate.
Drooped eyelids and the hair is sparse; the skin is coarse, dry,
scaly and thick.
Modest weight gain.
Signs of intellectual impairment - frank psychosis (myxoedema
madness) may develop.
A yellowish colour of the skin due to carotenaemia, and
pruritis.11
Bradycardia, cardiac arrhythmia, etc.
Hypothyroid: Lab Studies
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Anemia: normo-/micro-/macrocytic.
T4 and T3 concentrations are low, and TSH
concentration is high in the primary type.
T4, T3 and TSH are low in the secondary
type.
TRH and/or TSH tests differentiate between
primary and secondary hypothyroidism.
Thyroiditis
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Inflammation of the thyroid gland
Classified as chronic, subacute, and acute
Can initially present as hyperthyroidism,
ramification may result in hypothyroidism
Hashimoto’s Thyroiditis
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A chronic inflammation of the thyroid with
lymphocytic infiltration of the gland caused by
autoimmune factors
Most common cause of primary hypothyroidism in
North America
Women to men 8:1, rate increases in both sexes
with age
A family history of thyroid disorders is common, and
incidence is increased in patients with chromosomal
disorders, including Turner's, Down, and Klinefelter's
syndromes
Hashimoto’s: Signs and
Symptoms
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Painless enlargement of the thyroid gland
Examination reveals a nontender goiter, smooth or
nodular, firm, and more rubbery than the normal
thyroid; many patients have hypothyroidism when
first seen
Other forms of autoimmune disease are common
There may be an increased incidence of thyroid
neoplasia, particularly papillary carcinoma and
thyroid lymphoma
Hashimoto’s: Diagnosis
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Laboratory findings early in the disease consist of
normal T4 and TSH levels and high titers of thyroid
peroxidase antibodies and less commonly antithyroglobulin antibodies
The thyroid radioactive iodine uptake may be
increased, perhaps because of a defect in
organification of iodide in conjunction with a gland
that continues to trap iodine
Later in the disease, the patient develops
hypothyroidism with decreased T4, decreased
thyroid radioactive iodine uptake, and increased
TSH
Hashimoto’s: Treatment
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usually requires lifelong replacement therapy
with thyroid hormone to decrease goiter size
and treat the hypothyroidism
Occasionally, the hypothyroidism is transient
The average oral replacement dose with Lthyroxine is 100-120 µg/day
Hashimoto’s
Subacute Thyroiditis (de
Quervain’s Thyroiditis)
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Acute inflammatory disease of the thyroid,
probably caused by a virus
Frequently a history of mumps
The gland shows giant cell infiltration but
lymphocyte infiltration is absent
Female patients outnumbered male patients
in a ratio of 3-6:1
Although the disease has been described at
all ages, it is rare in children
Subacute Thyroiditis:
Presentation
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Condition is characterized by sudden onset of sore
throat, tenderness of the neck and low grade fever
Disease may reach its peak within 3 to 4 days and
subside and disappear within a week, but more
typically, a gradual onset extends over 1 to 2 weeks
and continues with a fluctuating intensity for 3 to 6
weeks
Thyroid gland is typically enlarged two or three times
the normal size or larger and is tender to palpation
The condition is often confused with pharyngitis or
otitis media
Subacute Thyroiditis:
Presentation continued
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Approximately one-half of the patients present
during the first weeks of the illness, with symptoms
of thyrotoxicosis, including nervousness, heat
intolerance, palpitations, tremulousness, and
increased sweating
As the disease process subsides, transient
hypothyroidism occurs in about one-quarter of the
patients
Ultimately thyroid function returns to normal and
permanent hypothyroidism occurs in less than 10
percent of the cases
Subacute Thyroiditis:
Diagnosis
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History and clinical examination.
An elevated erythrocyte sedimentation rate.
The T4 level is elevated, the TSH is down.
The 131I-uptake is down in the presence of
elevated T4, and a radioisotope scan
(99mTcO4-) shows a cool thyroid or the
thyroid is not visualized.
Subacute Thyroiditis:
Treatment
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In some instances, no treatment is required
Mainstay of treatment is analgesia
Initial therapy with Aspirin or NSAIDs
May need to treat with corticosteroids (Typically, Prednisone 40mg
daily to begin with, followed by a long taper of up to six weeks)
Relief of symptoms with treatment almost diagnostic
Alternatively oral cholecystographic agents (such as sodium ipodate
or sodium iopanoate) may be used safely and effectively for the
management of hyperthyroidism in these patients even when they
have relapsed after corticosteroid therapy
The recurrent rate of subacute thyroiditis after cessation of
prednisone therapy is about 20% but no difference has been found
in routine laboratory data between recurrent and non-recurrent
groups of patients
Levothyroxine administration may be useful in situations where the
patient is not already hyperthyroid due to the release of thyroidal
contents into the circulation
Subacute Thyroiditis:
Prognosis
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In 90% or more of patients, there is a complete and
spontaneous recovery and a return to normal thyroid
function
However, the thyroid glands of patients with
subacute thyroiditis may exhibit irregular scarring
between islands of residual functioning parenchyma,
although the patient has no symptom
Up to 10% of the patients may become hypothyroid
and require permanent replacement with
levothyroxine
Acute (Infectious) Thyroiditis
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Thyroid extremely resistant to infection,
therefore infectious thyroiditis rare
However, in certain situations, particularly in
children a persistent fistula from the pyriform
sinus may make the left lobe of the thyroid
particularly susceptible to abscess formation
Occasionally, acute bacterial supporative
thyroiditis occurs in children receiving cancer
chemotherapy
Acute Thyroiditis: Etiology
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Virtually any bacteria can infect the thyroid
Strep, Staph, pneumococcus, salmonella,
bacteroides, t. pallidum, pasturella, and
mycobacterium all documented
In addition, fungal infections, including
cryptococcus, have been reported
Most commonly, however, especially in children,
infection of the thyroid gland is a result of direct
extension from an internal fistula from the pyriform
sinus
Acute Thyroiditis: Etiology
Acute Thyroiditis:
Presentation
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The dominant clinical symptom is pain in the region of the thyroid
gland which may subsequently enlarge and become hot and
tender
The patient is unable to extend the neck and often sits with the
neck flexed in order to avoid pressure on the thyroid gland
Swallowing is painful
There are usually signs of infection in structures adjacent to the
thyroid, local lymphadenopathy as well as temperature elevation
and, if bacteremia occurs, chills
Gas formation has been noted with suppurative thyroiditis
Pediatric presentation more typical than adult
In general, no sign of hypo- or hyperthyroidism
Acute Thyroiditis: Diagnosis





History, physical, and clinical suspicion most
important
Patient more ill appearing than in subacute
The T3, T4 and TSH levels are usually
normal, and the rT3 is increased
A radioisotope scan shows an enlarged gland
with diffusely increased isotope uptake
If lesion localized on ultrasound or scan,
needle biopsy diagnostic
Acute Thyroiditis: Treatment



Surgical removal of fistulous tract in pediatric
patients with communication with pyriform
sinus
Systemic antibiotics with broad spectrum
coverage needed for some patients
Must add fungal coverage in
immunocompromised patients
Acute Thyroiditis: Prognosis



some patients with thyroiditis, the destruction
may be sufficiently severe that
hypothyroidism results
Patients with a particularly diffuse thyroiditis
should have follow-up thyroid function studies
performed to determine that this has not
occurred
Surgical removal of a fistula or branchial
pouch sinus is required to prevent recurrence
when this is present
Clinical Differences Between
Thyroiditis Types
Subtype
Etiology
Neck
Pain
RAIU
TSH
T4
Autoantibodies
Chronic lymphocytic
(Hashimoto's disease)
Autoimmu
ne
No
±
±
±
Present
Subacute granulomatous
Viral
Yes
↓
↓
↑
Absent
Microbial inflammatory
Bacterial,
fungal,
parasitic
Yes
±
Normal
Normal
Absent
Amiodarone and Thyroid




Amiodarone used to treat cardiac arrythmias
Structurally similar to thyroid hormone,
comprised of 39% iodine
Patients on amiodarone may become hypoor hyperthyroid
If hypothyroid, stop amiodarone and give T4
Amiodarone Induced
Hyperthyroid





Two Types: Type I and Type II
Type 1: In this type underlying thyroid pathology is present, for
example multinodular or diffuse goiter (thyroid enlarged) and in
these patients amiodarone precipitates typical Jod-Basedow with
increased blood T4 and T3 levels and a decreased blood TSH
level
Radioisotope studies show a diffusely or multinodular enlarged
gland (goiter) with normal or increased 131I or 99mTc uptake
Ultrasound shows a nodular or enlarged thyroid gland
Improves with use of perchlorate, which promotes iodine
expulsion from thyroid
Amiodarone Induced
Hyperthyroid continued






Type II: In this type there is no evidence of
underlying thyroid pathology
The gland is small and it may be tender
Radioisotope studies (131I or 99mTc) show a small
gland with low or absent radioisotope uptake
Ultrasound images are normal
The onset of the condition is often explosive
The condition is treated by steroids, in addition to
perchlorate
Thyroid Nodule









One in 12 to 15 young women has a thyroid nodule
One in 40 young men has a thyroid nodule
More than 95 percent of all thyroid nodules are benign (noncancerous growths)
Some are actually cysts which are filled with fluid rather than
thyroid tissue
Most people will develop a thyroid nodule by the time they are 50
years old
The incidence of thyroid nodules increases with age
50% of 50 year olds will have at least one thyroid nodule
60% of 60 year olds will have at least one thyroid nodule
70% of 70 year olds will have at least one thyroid nodule
Thyroid Nodule continued




Ninety-five percent of solitary thyroid nodules are
benign
Thyroid cancers typically present as a dominant
solitary thyroid nodule, cold nodule on scan
Papillary carcinoma accounts for 60 percent,
follicular carcinoma accounts for 12 percent, and the
follicular variant of papillary carcinoma accounting
for six percent
Fine needle biopsy is a safe, effective, and easy
way to determine if a nodule is cancerous
Features Favoring Benign
Nodule

Family history of Hashimoto's thyroiditis

Family history of benign thyroid nodule or goiter

Symptoms of hyperthyroidism or hypothyroidism

Pain or tenderness associated with a nodule

Soft, smooth, mobile nodule

Multinodular goiter without a predominant nodule (lots of nodules,
not one main nodule)

“Warm" nodule on thyroid scan (produces normal amount of
hormone)

Simple cyst on ultrasound
Factors Favoring Malignant
Nodule











Age less than 20
Age greater than 70
Male gender
New onset of swallowing difficulties
New onset of hoarseness
History of external neck irradiation during childhood
Firm, irregular and fixed nodule
Presence of cervical lymphadenopathy (swollen hard lymph nodes
in the neck)
Previous history of thyroid cancer
Nodule that is "cold" on scan (shown in picture above, meaning the
nodule does not make hormone)
Solid or complex on ultrasound
Thyroid Disease: Review
Condition
TSH
Free T4
Free T3
Other
Graves’ Disease
↓↓↓
↑
Usually ↑
Thyroid scan with diffuse isotope
uptake
Toxic Adenoma
↓
↑ or Normal
↑ or Normal
thyroid scan shows functioning
nodule and suppression of other
thyroid tissue
Toxic Multi-nodular
Goiter
↓
↑ or Normal
↑ or Normal
thyroid scan shows enlarged
gland with multiple active nodules
Thyroiditis
↓
Variably ↑
Variably ↑
thyroid scan shows low
radioiodine uptake, thyroglobulin
level markedly raised.
Factitious Hyperthyroidism
↓
↑
↑ or Normal
low radioiodine uptake on thyroid
scan and absent thyroglobulin
levels
Pregnancy
Normal
↑ total T4
Normal free
T4
↑ total T3
Norma free
T3
positive pregnancy test
Steroid therapy,
Severe Illness,
etc.
Normal or ↓
Normal
Normal
N/A
Question 1





A 60 year old woman comes to your clinic for examination of a
“lump” in her neck. On physical examination, a soft, smooth,
mobile nodule is palpated in the left lobe of the thyroid. Thyroid
scan ordered through your clinic shows a 1cm “hot” nodule at the
superior pole of the left thyroid lobe. Which of the following
should you tell your patient when she asks about the results of
her tests?
A. This lesion most likely represents cancer and an urgent
surgical referral must be sought
B. Lesions such as these are exceedingly rare in patients her
age
C. 95% of these lesions are benign
D. She most likely has an infection of the thyroid and will require
inpatient antibiotic therapy
Question 2






A 35 year old African American female presents to your clinic with
a two week history of palpitations, excessive sweating, and a
recent 15 pound weight loss, though she is “always eating.” Also,
she notices that the front of her neck is “fuller” than usual and her
eyes “bug-out.” She has a history of Lupus, but has otherwise
been healthy. Routine laboratory tests are ordered. Which of the
following would you expect to find?
A. Elevated level of TSH
B. Decreased level of T4
C. Decreased level of T3
D. Auto-antibodies to TSH receptors
E. Anti-thyroglobulin antibodies
Question 3






While working in the Emergency Department of a local
community hospital, a five year old boy is brought in by his
parent’s because of a “sore throat.” The child has leukemia, and
has received chemotherapy for the same two weeks prior to his
presentation. On exam, the child appears lethargic. There is a
noticeably enlarged lump in the area of the left lobe of the thyroid
gland, which elicits a painful response when palpated. Upon
further questioning, the parents state that he hasn’t eaten well
over the past 2-3 days because of “difficulty swallowing.” Which
of the following is the most likely diagnosis?
A. Acute infectious thyroiditis
B. Sick Euthyroid Syndrome
C. Hamburger Thyrotoxicosis
D. Hashimoto’s Thyroiditis
E. Plummer’s Disease
References









American Association of Clinical Endocrinologists medical guidelines for clinical
practice for the evaluation and
treatment of hyperthyroidism and
hypothyroidism. Endocr Pract. 2002 Nov-Dec;8(6):457-69
Bartalena L. Pinchera A, Macocci C. Management of Graves’ ophthalmopathy:
Reality and prespectives. Endocrine Reviews 2000; 21:168-199.
Beers, Mark MD et al. The Merck Manual of Diagnosis and Therapy Seventh
Edition. Merck, New York, 1995
Braunwald, et al. Harrison’s Principals of Internal Medicine, 15th Edition.
McGraw, New York. 2001.
Klopper JF. Diagnosis and management of amiodarone-induced
hyperthyroidism. SA Med J 1999; 89:453-454.
Murray IPC and Ell PJ. (1998) Nuclear Medicine in Clinical Diagnosis and T
reatment. 2nd Ed. Churchill Livingstone,
Edinburgh: 136-142.
O'Reilly DS; Thyroid function tests-time for a reassessment.;BMJ 2000 May
13;320(7245):1332-4.
Student BMJ . Interpreting Thyroid Function Tests.
www.emedicine.com