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Diagnostic Tests for Resistance to thyroid stimulating hormone

Resistance to thyroid stimulating hormone Tests: Book Excerpts

Home Diagnostic Testing

These home medical tests may be relevant to Resistance to thyroid stimulating hormone:

Resistance to thyroid stimulating hormone Diagnosis: Book Excerpts

Diagnostic Tests for Resistance to thyroid stimulating hormone: Online Medical Books

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Thyrotoxicosis/Hyperthyroidism: Physical examination (PE)
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

 A. Observation. Clothing may be loose because of weight loss. Clothing choices may suggest inappropriate heat intolerance, whereas the welcoming handshake may present warm moist hands with a fine tremor. Other possible observations include nervousness or restlessness, a characteristic stare with widened palpebral fissures, lid lag and infrequent blinking, and silky fine hair.

 B. General examination. Vital sign abnormalities commonly include weight loss, sinus tachycardia, arrhythmias, and systolic hypertension with a widened pulse pressure. Systolic murmurs, cardiac enlargement, and, occasionally, overt heart failure may be found on cardiovascular examination (Chapters 7.4, 7.5 and 7.7). Besides the classic stare noted above, Graves’ disease can also present with proptosis (which may be asymmetric), ophthalmoplegia (with impaired conjugate eye movement and strabismus), orbital congestion (with periorbital edema and potential compression of the optic nerve), and inflammation of the conjunctiva and cornea. Pretibial myxedema, an unusual but pathognomonic finding in Graves’disease, is a painless raised thickening of the subcutaneous tissue, most often found in the anterior lower leg or dorsal foot. It produces a peau d’orange texture, which can be pruritic and hyperpigmented. Clubbing of the fingers and toes is also found in Graves’disease, but is very rare. An ovarian mass, usually unilateral, may indicate struma ovarii. Thyrotoxicosis (but not hyperthyroidism) can result from this teratoma, which infrequently produces thyroid hormone.

 C. Thyroid examination. Inspect the neck below the thyroid cartilage from the front and side. During palpation, approach the patient from the front or from behind and palpate using the fingers or thumbs. Having the patient swallow during both inspection and palpation causes the thyroid to move and aids in developing a three-dimensional impression of the gland. The size, consistency, and tenderness of the gland are important, as are the presence and characteristics of any nodules. Auscultation of a bruit over the gland correlates with increased vascularity, usually indicative of Graves’disease.

Testing

 A. Laboratory testing. A sensitive assay for thyroid-stimulating hormone (sTSH) is the best test for detecting thyrotoxicosis. Thyrotoxicosis from any cause, except the extremely rare instance of excess TSH production, results in a suppressed sTSH. Thyrotoxicosis is confirmed by an elevated free thyroxine index (FTI) or an elevated free thyroxine (fT4), measured directly. If the FTI or fT4 is normal, T3 should be measured to evaluate for T3 toxicosis. Assays for thyroid autoantibodies, including TSH receptor antibodies, are usually not required. However, they can be helpful in selected cases (e.g., pregnancy, where levels correlate with risk to the fetus).

 B. Diagnostic imaging. Radioactive iodine uptake (RAIU) can help clarify the cause of thyrotoxicosis. A diffuse increase in RAIU is consistent with Graves’ disease, whereas nodular concentration is consistent with toxic adenoma (a single increased area) or multinodular goiter (multiple areas of increased uptake) (3). A decrease in RAIU is consistent with exogenous (iatrogenic or factitious) thyrotoxicosis, thyroiditis, iodine-induced thyrotoxicosis, or struma ovarii.

Diagnostic assessment

 Accurate diagnosis depends on the appropriate combination and interpretation of history, PE, and testing.

A. Graves’ disease. If ophthalmopathy is present, the diagnosis of Graves’ disease is usually obvious. Typically, the thyroid gland is increased in size, smooth, and nontender. A bruit is present in 50% of patients. The RAIU is homogeneously increased and pretibial myxedema may be present.

B. Toxic nodular goiter is the most common cause of thyrotoxicosis in those aged more than 40 years. The thyroid gland is typically increased in size, nontender, but with multiple nodules. The RAIU is increased in a heterogeneous pattern. A single toxic nodule is more common in younger people and has the RAIU concentrated in one spot, with suppression of the remaining gland.

C. Exogenous (iatrogenic or factitious) thyrotoxicosis is associated with a gland that is small or normal sized and a low or absent RAIU. A psychiatric evaluation should be considered in factitious thyrotoxicosis.

 D. Thyroiditis. Thyrotoxicosis can be produced as hormone leaks from an inflamed gland. Typically, the symptoms of the diverse thyroiditis entities are of recent onset and have escalated rapidly. The gland is enlarged and either tender (subacute thyroiditis) or nontender (painless thyroiditis or postpartum thyroiditis). RAIU is very low or absent. Transient hypothyroidism often follows as the intrathyroidal stores of hormone are depleted. Acute suppurative thyroiditis is a rare infectious disorder, usually caused by pyogenic organisms (5).

 E. Other diagnoses. Thyrotoxicosis with hyperthyroidism and an inappropriately elevated sTSH suggests a TSH-secreting pituitary tumor. Thyrotoxicosis without hyperthyroidism and an increased RAIU over the pelvis suggests struma ovarii. A low sTSH with normal T3 and FTI or fT4 indicates subclinical hyperthyroidism or TSH suppression by nonthyroidal factors (e.g., corticosteroid administration or starvation).


References

1. Helfand M, Redfern CC. Screening for thyroid disease: an update. Ann Intern Med 1998;129:144–158.

2. Hennessey JV. Diagnosis and management of thyrotoxicosis. Am Fam Physician 1996;54:1315–1324.

3. Thyroid Guidelines Task Force of the American Association of Clinical Endocrinologists and the American College of Endocrinology. AACE Clinical Practice Guidelines for the Evaluation and Treatment of Hyperthyroidism and Hypothyroidism. Endocrine Prac 1995;1:54–62.

4. Trivalle C, Doucet J, Chassagne P, et al. Differences in the signs and symptoms of hyperthyroidism in older and younger patients. J Am Geriatr Soc 1996;44:50–53.

5. Sakiyama R. Thyroiditis: a clinical review. Am Fam Physician 1993;48:615–621.

» READ BOOK EXCERPT ONLINE »

Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000


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