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

15 to 20 grams

Most commonly diseased of the endocrine
glands

TRHTSHthyroid hormone production

Releases two forms of thyroid hormone

T4 and T3

14:1 molar ratio

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

Inspection

Patient seated and in good light

Cup of water to facilitate swallowing

Inspect from front/side with neck extended and
patient swallowing

Thyroid moves with swallowing
Examination of the Thyroid Gland
Palpation

Behind the seated patient

Palpating with the fingertips

Find cricoid cartilage

Isthmus lies just below this

Face the seated patient

Thumb to locate the isthmus

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
hyperthyroidism

Effects 0.5% of population

Female to male ratio between 5:1 and 10:1

Peak incidence between 40 and 60 years
of age

Circulating IgG antibodies bind and activate
the G-protein coupled TSH receptor

Follicular hypertrophy and hyperplasia

Thyroid enlargement

Increases in thyroid hormone production

Increases in fraction of triiodothyronine (T3)
relative to thyroxine (T4)

Graves’ Disease Graves’ Treatment

Ophthalmopathy apparent in 30 to 50%

Rare findings (<1%) include dermopathy
(pretibial myxedema) and thyroid
acropachy (clubbing)

Antithyroid drugs (Thionamides)

Proplythiouracil (PTU) 300-400 mg daily

Methimazole 30-40 mg daily

Decrease synthesis of hormone
PTU decreases conversion of T4 to T3

Permanent remission in 20-30% of treated patients

Risk of agranulocytosis, elevated LFTs,

PTU used in pregnancy

Beta-Blockers for symptoms

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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)

Converted to T3 in the body

Studies vary on utility of using T3

Typical replacement dose is 1.6
micrograms/kg (100-150 mcg typical)

Start with reduced dose in elderly and
patients with history of heart disease

Target TSH ~2.0

Severe untreated hypothyroidism

Hypothermia, hypoglycemia, shock,
hypoventilation, ileus

50% mortality

Treat with IV levothyroxine

Steroids until rule out AI

Central hypothyroidism—other pituitary defects

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?

TPO antibodies

Tg level

TSH immunoglobulins (TSI)

Empiric trial of antithyroid drugs

RAI uptake and scan
TSH receptor antibodies (TSI)

Postpartum thyrotoxicosis

Differential includes Graves vs postpartum
thyroiditis

TSI present in >90% pts with Graves

RAI uptake and scan contraindicated b/c of
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