Outline
Disorders of the Review thyroid physiology
Discuss examination of the thyroid gland
Thyroid Review thyroid testing
Resident Core Conference Discuss the evaluation and management
September 25th, 2008 Hyperthyroidism
Hypothyroidism
Leigh M. Eck, MD
Thyroid nodules
Thyroid Thyroid Physiology
One of the largest of the endocrine glands TRHTSHthyroid hormone production
15 to 20 grams Releases two forms of thyroid hormone
T4 and T3
Most commonly diseased of the endocrine 14:1 molar ratio
glands T4T3 peripheral conversion
Propranolol, corticosteroids, PTU, iopanoic acid,
amiodarone
Acutely downregulated in nonthyroid illness
T3 affects physiologic function of all tissues in the
body
Thyroid Physiology
T4 and T3 extensively protein bound
Prevents excessive tissue uptake
Maintains accessible reserve
TBG, albumin, transthyretin
Estrogen, 5-FU, methadone ↑ TBG
Androgens, steroids, L-asparginase, niacin ↓ TBG
T3 half life 1 to 1.5 days
T4 half life 8 days
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Examination of the Thyroid Gland Examination of the Thyroid Gland
Inspection Palpation
Behind the seated patient
Patient seated and in good light Palpating with the fingertips
Cup of water to facilitate swallowing Find cricoid cartilage
Inspect from front/side with neck extended and Isthmus lies just below this
patient swallowing Face the seated patient
Thumb to locate the isthmus
Thyroid moves with swallowing Right thumb then moved laterally without releasing
pressure
Same procedure with left thumb
Normal lobe same size as patient’s thumb
Tests of Thyroid Function
Examination of the Thyroid Gland Test Indication Comment
TSH Suspect Thyroid Dysfunction Misleading if central dysfunction
Auscultation
Thyroid bruit suggestive of hyperthyroidism FT4 Suspect Thyroid Dysfunction
Differentiate from transmitted murmur TT3/FT3 Suppressed TSH but normal
FT4
Pemberton’s sign Thyroglobulin Thyroid cancer surveillance
If retrosternal goiter, arm raising narrows thoracic
Thyroid Stimulating Suspect Grave’s Disease; Expensive but useful if patient
inlet causing venous engorgement and even Immunoglobulin Euthyroid Ophthalmopathy cannot due RAI testing—
pregnancy/breast feeding
respiratory distress Thyroid Peroxidase Antibodies Suspect Hashimoto’s Thyroiditis
Radioacitve Iodine Uptake Determine etiology of Contraindicated in
hyperthyroidism pregnancy/breastfeeding
Thyrotoxicosis
Any cause of thyroid hormone excess
Excessive thyroid hormone production and release
Hyperthyroidism
Increased thyroid uptake of iodide
Graves’ Disease
Autonomous thyroid nodule
Toxic multinodular goiter
Thyroid Destruction
Decreased thyroid uptake of iodide
Subacute thyroiditis
Postpartum thyroiditis
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CONDITION UPTAKE and ADDITIONAL
PATTERN STUDIES
Hyperthyroidism Signs/Symptoms
Anxiety/irritability Fatigue Graves Elevated-Diffuse TSI
Weakness Weight loss
Painless thyroiditis Low TPO
Tremors Hyperkinetic
Difficulty sleeping movements Toxic MNG Elevated-Patchy Neg. antibodies
Palpitations Heat intolerance Solitary nodule Elevated-Focal Neg. antibodies
Increased bowel
Iodine induced Variable
movements
Exogenous T4 Low Thyroglobulin low
Graves’ Disease Graves’ Disease
Etiology of 50-80% cases of Circulating IgG antibodies bind and activate
hyperthyroidism the G-protein coupled TSH receptor
Effects 0.5% of population Follicular hypertrophy and hyperplasia
Female to male ratio between 5:1 and 10:1 Thyroid enlargement
Increases in thyroid hormone production
Peak incidence between 40 and 60 years
of age Increases in fraction of triiodothyronine (T3)
relative to thyroxine (T4)
Graves’ Disease Graves’ Treatment
Ophthalmopathy apparent in 30 to 50% Antithyroid drugs (Thionamides)
Proplythiouracil (PTU) 300-400 mg daily
Rare findings (<1%) include dermopathy Methimazole 30-40 mg daily
(pretibial myxedema) and thyroid Decrease synthesis of hormone
PTU decreases conversion of T4 to T3
acropachy (clubbing)
Permanent remission in 20-30% of treated patients
Risk of agranulocytosis, elevated LFTs,
PTU used in pregnancy
Beta-Blockers for symptoms
3
Graves’ Treatment Multinodular Goiter
Thyroidectomy Less common than Graves and effects
Rapid cure but requires thyroid replacement older individuals
Radioactive Iodine Discrete nodules become autonomous and
hyperfunction
I131 is given
Effect is typically seen in 3-6 months Treatment with thyroidectomy, radioactive
iodine, thionamides
Hypothyroidism often develops
Thyroiditis Hyperthyroidism Summary
Silent = painless Suspect hyperthyroidism
Thyrotoxicosis phase of hashimoto’s
Postpartum Obtain TFTs
Subacute/De Quervain’s = painful If TSH is suppressed, proceed with RAI
Etiology is typically viral uptake and scan
Thyroid is often enlarged, tender, painful
Very low radioactive iodine uptake
Self-resolving within weeks to months
Treatment with NSAIDS, steroids, beta-blockers
Signs and Symptoms
Weakness
Fatigue
Hypothyroidism
Lethargy, sleepiness
Slowness of speech and thought
“Puffy” appearance
Dry skin, coarse hair
Cold intolerance
Constipation
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Causes of Hypothyroidism Hashimotos Thyroiditis
Autoimmune thyroid destruction (Hashimoto’s) Most common type of thyroid disease
Iatrogenic
Surgery Autoimmune damage
Radioablation Lymphocytic infiltrate, fibrosis, decreased thyroid
Iodine deficiency hormone production
Drugs interfering with hormone synthesis Autoantibodies (thyroglobulin and peroxidase)
Infiltrative disease Can also be associated with polyglandular
hemochromotosis, sarcoidosis, neoplastic disease autoimmune disease
Congenital thyroid agensis or defects in
hormone synthesis
Thyroid Replacement Myxedema Coma
Synthetic levothyroxine (T4) Severe untreated hypothyroidism
Converted to T3 in the body Hypothermia, hypoglycemia, shock,
Studies vary on utility of using T3 hypoventilation, ileus
Typical replacement dose is 1.6 50% mortality
micrograms/kg (100-150 mcg typical) Treat with IV levothyroxine
Start with reduced dose in elderly and Steroids until rule out AI
patients with history of heart disease Central hypothyroidism—other pituitary defects
Target TSH ~2.0 Primary hypothyroidism—polyglandular disorder
Thyroid Nodules
THYROID
Lifetime risk of palpable nodule 5-10%
>50% of the population has a nodule on
NODULES autopsy or ultrasound
Only 1 in 20 is malignant
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Differential Diagnosis
Malignancy
Tumors of follicular cells
Papillary
Follicular
Anaplastic
Tumors of C cells
Medullary
Benign thyroid nodule
Thyroid cyst
Hegedus, L. N Engl J Med 2004;351:1764-1771
Evaluation of Nodule Fine Needle Aspiration
Measure TSH FNA is most effective way to distinguish between
If hyperthyroid (low TSH), do uptake and scan benign and malignant nodules
If “hot”not cancer Inexpensive, performed as outpatient
If “cold”proceed with FNA Ultrasound guided FNA if not palpable or less
If normal thyroid function, next step is fine needle than 1.5 cm in diameter
aspiration (FNA) What results will I see?
Benign-75% of the time
Malignant-5% of cases
Suspicious or inadequate-20%
Management of Nodules EVAL OF THYROID NODULE
Malignant Thyroid Nodule
Thyroidectomy
TSH
Suspicious
Thyroidectomy Thyroid Radionuclide Scan
If TSH suppressed
Inadequate – Repeat FNA
Benign Thyroid ultrasound
Ultrasound surveillance
FNA if suspicious
Surgery
AACE/AME Guidelines. Endocr Pract. 2006;12 (No 1)
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Which of the following is most likely
MKSAP dx?
57yo man with MNG evaluated for 4month Medullary thyroid CA
h/o progressive DOE and choking Thyroid lymphoma
sensation while supine. Substernal goiter
On exam, TM. CXR shows tracheal deviation Anaplastic thyroid cancer
to right. When asked to raise arms over his
head, marked facial plethora develops. A carotid body tumor
Lab testing shows euthyroid status
A 58-year-old woman with a 20-year history of goiter presented with a two-month history of
progressive dyspnea on exertion, occasional stridor, and a choking sensation while supine
Substernal goiter
MNG has extended downward beneath
sternum into anterior mediastinum
Narrowed thoracic inletcompression of
great veins of neckPemberton’s sign
Basaria S and Salvatori R. N Engl J Med 2004;350:1338
MKSAP Lab
27yo evaluated for palpitations and heat FT4 2.7
intolerance 3months after a successful FT3 46.22
pregnancy. She is breastfeeding TSH undetectable
On exam, she is tachycardic. She has lid lag
but no proptosis. Thyroid gland moderately
enlarged and nontender. Moist palms and
brisk DTRs.
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What is the next step in this pt’s
management? TSH receptor antibodies (TSI)
TPO antibodies Postpartum thyrotoxicosis
Tg level Differential includes Graves vs postpartum
thyroiditis
TSH immunoglobulins (TSI)
TSI present in >90% pts with Graves
Empiric trial of antithyroid drugs
RAI uptake and scan contraindicated b/c of
RAI uptake and scan breast feeding
TPO antibodies likely positive in both
states—not helpful in this situation
MKSAP Lab Studies
24yo woman with palpitations and sweating 4 TSH <0.01
wks postpartum. Occasional loose stools. FT4 3.4
Otherwise well. Nursed for 6 wks but TT3 315
stopped.
RAI Uptake <1%
On exam, BP normal, pulse 92. Thyroid
gland normal size but slightly firm.
What is the most appropriate therapy? B-blocker
RAI This pt has postpartum thyroiditis—occurs in 5-
15% pregnancies
B-blocker
75% normalizes
Prednisone 25% hypothyroidism
PTU Thyrotoxicosis, nontender gland, low RAI uptake
ASA Transient lymphocytic inflammatory process
Tx with B-blockers to reduce symptoms
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MKSAP What should we do?
75yo adx to MICU with obtundation. She is LT4, corticosteroids, emperic abx
hypothermic, BP 104/84, pulse 48/min. 4cm
LT4
transverse scar above mid-sternal notch, cold
skin, delayed DTR relaxation. LT4 and T3
Meds include digoxin and LT4 per records; no MD Await TSH
visit > 1year.
Sodium 127, cholesterol 318, digoxin level
undetectable. TSH pending. UA leukocytes
TMTC and GNR. Cx pending
LT4, steroids, abx
Myxedema coma
Infx common precipitant of myxedema
coma
Steroids given prophylactically in case
concurrent AI which may result in AI crisis
with LT4 therapy
