Thyroid Disorders

THYROID
DISORDERS
PGI Agunod/Boongaling/Briones/Saplan/Rañeses
EVALUATION OF PATIENTS
CLINICAL ASSESSMENT
● Size
○ Diffuse enlargement
○ Nodular enlargement
● Function
○ Hypothyroidism
○ Hyperthyroidism
DIAGNOSTIC TEST
● Thyroid function tests
○ Measurement of hormone concentration and binding (TSH, T3, T4)
● Radioactive Iodine Uptake (RAIU)
○ To differentiate hyperthyroidism into high- and low- uptake states
○ Generally provides an accurate estimate of the thyroid gland’s functional activity
● Thyroid antibody tests
○ Anti-thyroid peroxidase
○ Anti-thyroglobulin antibodies
DIAGNOSTIC TEST
● Ultrasonography
○ Most widely used imaging study in evaluating thyroid gland masses
○ Useful for detecting non-palpable thyroid nodules, differentiating solid versus
cystic lesions and identifying cervical lymphadenopathies
● Radionucleotide Imaging/ Thyroid Scan
○ Determine the distribution, shape and position of the thyroid gland
○ Identify functional solitary nodule
○ Hot nodule vs. Cold nodule
Hypothyroidism
● May occur as a result of primary gland failure or insufficient thyroid gland stimulation by
the hypothalamus or pituitary gland
● Prevalence increases with age; F>M
● If untreated, may lead to hypertension, dyslipidemia, infertility, cognitive impairment and
neuromuscular dysfunction
1. Hashimoto’s Thyroiditis
(Autoimmune Lymphocytic Thyroiditis)
● Most common cause of hypothyroidism in iodine-sufficient areas
● Primarily affects middle-aged women
● Progresses slowly over the years causing chronic thyroid damage
● Both FT4 and Anti-Thyroid Peroxidase antibody are elevated
● FT3 are normal in 25% of patients, and therefore, not indicated
● Treatment:
○ Thyroid Replacement (Levothyroxine)
○ Re-evaluation is done after 4-6 weeks
○ TSH levels should be maintained between 0.5-3.0 mU/L
2. Subacute Thyroiditis
(De Quervain’s Thyroiditis)
● Less common than Hashimoto’s Thyroiditis
● Indirect evidence suggests that this is a viral illness, but lacks conclusive proof
● Rapid painful swelling of the thyroid gland
● Treatment:
○ Salicylates or NSAIDS to provide relief
○ Prednisone may be given for severe thyroid pain
3. Myxedema Coma
● Rare but extremely severe manifestation of hypothyroidism that most commonly occurs
in older women with history of primary hypothyroidism
● Hallmark features: Mental status changes including lethargy, cognitive dysfunction and
hypothermia
● Management:
○ Proper ventilatory, electrolyte, and hemodynamic support
○ Corticosteroids may be given
HYPERthyroidism
Hyperthyroidism: DEFINITION OF TERMS
Thyrotoxicosis vs. Hyperthyroidism
• Thyrotoxicosis – state of thyroid hormone excess
• Hyperthyroidism – result of excessive thyroid function

Graves’ Disease: ETIOLOGY/ EPIDEMIOLOGY
● 60–80% of thyrotoxicosis
● F>M
● Rarely begins before adolescence
● Usually occurs 20-50 y/o
● Also occurs in elderly
Graves’ Disease: PATHOPHYSIOLOGY
● Autoimmune
● Genetics:
○ Polymorphisms in HLA-DR; Immunoregulatory genes CTLA-4, CD25, PTPN22,
FCRL3, & CD226; Gene encoding the TSH receptor
● Environmental:
○ Stress
○ Smoking
○ Sudden 🠉 in iodine intake
○ Postpartum Period – 🠉🠉🠉 (3x)
○ Immune reconstitution phase after highly active antiretroviral therapy (HAART) or
alemtuzumab treatment
● TSI that are synthesized in the thyroid gland, bone marrow, and lymph nodes
● TPO and Tg antibodies - 80% of cases
Graves’ Disease: CLINICAL MANIFESTATIONS
● Depends on the:
○ Severity of thyrotoxicosis
○ Duration of disease
○ Individual susceptibility to excess thyroid hormone
○ Patient’s age
● Apathetic thyrotoxicosis
○ In the elderly
○ Features of thyrotoxicosis may be subtle or masked
○ (+) fatigue and weight loss
● Diffusely enlarged to 2-3x times its normal size
● Consistency: firm, but not nodular
● (+) Thrill or bruit, at the inferolateral margins of the thyroid lobes
1. Graves’ Ophthalmopathy
a. a.k.a. thyroid-associated ophthalmopathy
b. Infiltration of the EOMs by activated T cells → (+)
fibroblast & 🠉 GAGs → trap water → muscle swelling
2. Thyroid Dermopathy
a. Pretibial myxedema
b. Typical lesion: non-inflamed, indurated plaque w/ a
deep pink or purple color and an “orange🍊 skin”
c. Mimicking elephantiasis
3. Thyroid Acropachy
a. Clubbing
Graves’ Disease:
DIAGNOSTICS
Graves’ Disease: TREATMENT
1. Reducing thyroid hormone synthesis
a. Antithyroid drug → Thionamides
2. Supportive Treatment
a. Beta blockers
i. Propranolol (20–40 mg every 6 h)
ii. Longer-acting selective β1 receptor blockers (e.g. atenolol)
b. Anticoagulation
i. Warfarin → AF
3. Reducing the amount of thyroid tissue

a. Radioiodine (131 I)
b. Thyroidectomy
Subclinical
Hyperthyroidism
Subclinical Hyperthyroidism
● Low or undetectable serum thyroid-stimulating hormone level, with
normal free thyroxine and total or free triiodothyronine levels
● The prevalence of subclinical hyperthyroidism in the general
population is about 1% to 2%
○ May be higher in iodine-deficient areas
● The prevalence of subclinical hypothyroidism is about 4 to 8.5
percent
○ may be as high as 20 percent in women older than 60 years
Etiology
● In many patients who have subclinical
hyperthyroidism, careful clinical evaluation will
suggest an etiology
● Early Graves’ disease accounts for the majority of
cases, with the remainder caused by toxic
multinodular goiter, autonomous functioning nodules,
or exogenous levothyroxine (Synthroid)
Subclinical Hyperthyroidism
● Screening is recommended for high-risk populations
● Other causes of low serum TSH concentration include
○ Delayed recovery of the pituitary after treatment for
hyperthyroidism
○ Pregnancy
○ euthyroid sick syndrome
○ Medications such as dopamine (Intropin)
○ Glucocorticoids
○ Dobutamine (Dobutrex)
● Few persons with subclinical hyperthyroidism progress to overt
disease
Associated Clinical Conditions
● Atrial fibrillation
● Reduced bone mineral density,
● Cardiac dysfunction
● Progression to overt hyperthyroidism in patients with known thyroid
disease
Management
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Thyroid Disorders

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THYROID

Thyrotoxicosis vs. Hyperthyroidism

• Thyrotoxicosis – state of thyroid hormone excess

• Hyperthyroidism – result of excessive thyroid function

3. Reducing the amount of thyroid tissue

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