Hypothyroidism
Hypothyroidism: Excerpt from The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
Stephen F. Wheeler and David E. Bybee
Hypothyroidism is the clinical syndrome resulting from deficient thyroid hormone action. Overt hypothyroidism is found in 2% of women aged more than 70 years and in 0.5% of women aged 40 to 60 years. Hypothyroidism is present in 0.8% of men older than 60 years and is rare in women younger than 40 years and men younger than 60 years (1).
Approach
Mild to moderate hypothyroidism often exhibits subtle, nonspecific signs and symptoms of insidious onset. Severe disease tends to have more characteristic findings. The key diagnostic tasks are to suspect and confirm the presence of hypothyroidism and consider the level of disease.
A. Hypothalamic-pituitary-thyroid axis. Thyrotropin-releasing hormone, secreted by the hypothalamus, stimulates the anterior pituitary to produce thyroid-stimulating hormone (TSH). The major hormone produced by the pituitary in response to TSH is thyroxine (T4). The most sensitive indicator of thyroid status is the level of TSH, which is controlled in classic negative-feedback fashion by the concentration of active thyroid hormones.
B. Level of disease. Primary hypothyroidism, by far the most common type, is the result of thyroid gland failure. Hypothyroidism caused by pituitary or hypothalamic disease is termed secondary or tertiary, respectively.
C. Special concerns. Myxedema refers to the hypothyroidism-associated, nonpitting edema caused by glycosaminoglycan accumulation in the skin, subcutaneous tissues, and other organs. Subclinical hypothyroidism is distinguished by an elevated sensitive test for thyroid-stimulating hormone (sTSH), normal thyroid hormone levels, and few, if any, symptoms. Transient hypothyroidism can follow the initial thyrotoxic phase of subacute or postpartum thyroiditis.
History
Symptoms generally correspond directly to the duration and severity of disease.
A. Present illness
1. The probability of thyroid disease is directly related to the number of typical symptoms manifested by the patient (2), including weakness, lethargy, skin changes (dry, coarse, cold, yellow), coarseness or loss of hair, cold intolerance, weight gain, constipation, memory or concentration impairment, depression, hoarseness, goiter, menstrual abnormalities (most commonly menorrhagia), and fluid infiltration of tissues (eyelids, face, peripheral) (3).
2. Loss of axillary or pubic hair, headaches, visual field defects, amenorrhea, galactorrhea, and symptoms of postural hypotension are suggestive of secondary or tertiary hypothyroidism.
B. Past and family history
1. Chronic autoimmune thyroiditis (Hashimoto’s disease), previous radioactive iodine therapy, and prior thyroid surgery are the most common causes of primary hypothyroidism. Other groups with an increased risk for this type include women 4 to 8 weeks postpartum; women aged more than 50 years; patients with immunologically mediated diseases such as diabetes mellitus type 1, pernicious anemia, vitiligo, Addison’s disease, and rheumatoid arthritis; and persons with a family history of thyroid disease. Screening these patients for hypothyroidism using sTSH may be appropriate (1).
2. A pituitary tumor is the most common cause of secondary hypothyroidism. Other historical diagnoses that increase the likelihood of secondary or tertiary disease include pituitary surgery, cranial radiation therapy, postpartum hemorrhage (Sheehan’s syndrome), head trauma, granulomatous diseases, metastatic disease (breast, lung, colon, prostate, others), and infectious diseases (tuberculosis, others) (4).
Physical examination (PE)
The features frequently found in hypothyroidism should be sought.
A. Observation. A welcoming handshake may reveal cold skin and further observations uncover altered affect, hoarseness, facial or eyelid edema, hair loss (scalp, eyebrows), and physical or mental slowing.
B. General examination. Vital sign abnormalities commonly include weight gain, diastolic hypertension, and bradycardia. All major organ systems are affected by thyroid hormone deficiency. The heart may be enlarged, because of both dilation and pericardial effusion, which is indicated by a cardiac rub or distant heart sounds. Adynamic ileus, rarely, can result in megacolon or intestinal obstruction. Tissue glycosaminoglycan accumulation and reduced lymphatic clearance of interstitial proteins can produce carpal tunnel syndrome. The relaxation phase of deep tendon reflexes is prolonged, creating the characteristic “hung-up reflex.” Orthostatic hypotension suggests secondary or tertiary disease, as do visual field defects and galactorrhea.
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 should be noted, as should the presence and characteristics of any nodules.
Testing
A. Laboratory tests. The most useful test is a sTSH, which is elevated (>10 ľU/ml) in the vast majority of patients with hypothyroidism (1). Primary hypothyroidism is confirmed by a low free thyroxine index (FTI) or free T4 (fT4) measured directly (5). Antithyroid antibodies are not usually necessary in the evaluation of patients with hypothyroidism.
B. Diagnostic imaging. Radionuclide scans are not commonly helpful in the evaluation of patients with hypothyroidism. Radioactive iodine uptake is typically low in hypothyroidism of any cause. Notable exceptions are the rare cases of iodine deficiency or an intrathyroidal block in thyroid hormone production or release. The underlying pathology determines the distribution of the isotope in the gland.
Diagnostic assessment
A. Pitfalls of sTSH. The sTSH is characteristically elevated in primary hypothyroidism. Starvation, corticosteroid administration, and use of dopamine can lower sTSH, even in hypothyroid patients, making the diagnosis more difficult. In patients with severe nonthyroidal illness, low peripheral thyroid hormone levels may suggest hypothyroidism. However, the sTSH is usually normal unless affected by starvation or therapies.
B. Primary hypothyroidism. Most patients have primary disease. Typical findings on history and PE, coupled with an elevated sTSH and low FTI or fT4, are sufficient for the diagnosis. Hypothyroid patients should be treated with T4, and replacement therapy monitored using sTSH (5). Retest annually or at least 6 to 8 weeks after changes in therapy.
C. Secondary or tertiary hypothyroidism. In a patient with overt hypothyroidism, a sTSH that is low, normal, or only mildly elevated suggests secondary or tertiary hypothyroidism. The historical and clinical features previously discussed support the diagnosis, and evaluation of the pituitary is necessary (4). Multiple endocrine end-organ failure caused by the autoimmune destruction of endocrine glands (Schmidt’s syndrome) is a special case of primary hypothyroidism that mimics secondary level disease.
D. Severity. Most patients will have only mild or moderate disease at the time of diagnosis. Profound hypothyroidism with hypothermia and stupor (myxedema coma) is life threatening and requires hospitalization. Factors that predispose to myxedema coma include infection, trauma, cold exposure, and central nervous system depressants.
E. Subclinical hypothyroidism. In patients with subclinical hypothyroidism not treated with thyroid hormone replacement, monitor clinical and biochemical markers for evidence of progressive thyroid dysfunction. An appropriate follow-up interval has not been firmly established, but every 2 to 5 years may be adequate (1).
References
1. Helfand M, Redfern CC. Screening for thyroid disease. Ann Intern Med 1998;129:
144–158.
2. White GH, Walmsley RN. Can the clinical assessment of thyroid function be improved? Lancet 1978;2(8096):933–935.
3. Thyroid Guidelines Task Force of the American Association of Clinical Endocrinologists and the American College of Endocrinology. ACCE Clinical Practice Guidelines for the Evaluation and Treatment of Hyperthyroidism and Hypothyroidism. Endocrine Prac 1995;1:54–62.
4. Vance ML. Medical progress: hypopituitarism. N Engl J Med 1994;330:1651–1662.
5. Lindsay RS, Toft AD. Hypothyroidism. Lancet 1997;349:413–417.
Book Source Details
- Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
- Author(s): Robert B. Taylor (editor)
- Year of Publication: 2000
- Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.
More About Hypothyroidism
More Medical Textbooks Online about Hypothyroidism
Review other book chapters online related to Hypothyroidism:
Medical Books Excerpts
- Hypothyroidism
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
- [ read ]
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
» Next page: Thyroid Enlargement/Goiter (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
Rate This Website
What do you think about the features of this website?
Take our user survey and have your say:
Website User Survey
Medical Tools & Articles:
Next articles:
Tools & Services:
Medical Articles:
Forums & Message Boards
- Ask or answer a question at the Boards:
