Hypothyroidism can result from radiation therapy for cancer of the larynx or Hodgkin lymphoma. The incidence of permanent hypothyroidism after radiation therapy is high, and thyroid function through measurement of serum TSH should be evaluated at 6- to month intervals. Secondary hypothyroidism occurs when the hypothalamus produces insufficient thyrotropin -releasing hormone TRH or the pituitary produces insufficient TSH.
Subclinical hypothyroidism is elevated serum TSH in patients with absent or minimal symptoms of hypothyroidism and normal serum levels of free thyroxine T4. These patients are also more likely to have hypercholesterolemia and atherosclerosis. They should be treated with L-thyroxine, even if they are asymptomatic. For patients with TSH levels between 4. L-Thyroxine therapy is also indicated in pregnant women and in women who plan to become pregnant to avoid deleterious effects of hypothyroidism on the pregnancy and fetal development.
Patients should have annual measurement of serum TSH and free T4 to assess progress of the condition if untreated or to adjust the L-thyroxine dosage. Symptoms and signs of primary hypothyroidism are often subtle and insidious. Various organ systems may be affected. Metabolic manifestations: Cold intolerance, modest weight gain due to fluid retention and decreased metabolism , hypothermia.
Neurologic manifestations: Forgetfulness, paresthesias of the hands and feet often due to carpal tunnel syndrome caused by deposition of proteinaceous ground substance in the ligaments around the wrist and ankle ; slowing of the relaxation phase of deep tendon reflexes. Psychiatric manifestations: Personality changes, depression, dull facial expression, dementia or frank psychosis myxedema madness. Dermatologic manifestations: Facial puffiness; myxedema; sparse, coarse and dry hair; coarse, dry, scaly and thick skin; carotenemia, particularly notable on the palms and soles caused by deposition of carotene in the lipid-rich epidermal layers ; macroglossia due to deposition of proteinaceous ground substance in the tongue.
Ocular manifestations: Periorbital swelling due to infiltration with the mucopolysaccharides hyaluronic acid and chondroitin sulfate, droopy eyelids because of decreased adrenergic drive. Cardiovascular manifestations: Slow heart rate a decrease in both thyroid hormone and adrenergic stimulation causes bradycardia , enlarged heart on examination and imaging partly because of dilation but chiefly because of pericardial effusion; pericardial effusions develop slowly and only rarely cause hemodynamic distress.
Other manifestations: Pleural or abdominal effusions pleural effusions develop slowly and only rarely cause respiratory or hemodynamic distress , hoarse voice, and slow speech.
Symptoms Geriatrics Essentials Hypothyroidism is thyroid hormone deficiency. It is diagnosed by clinical features such as a typical facial appearance, hoarse slow speech, and dry skin and by low levels of thyroid hormones Although secondary hypothyroidism is uncommon, its causes often affect other endocrine organs controlled by the hypothalamic-pituitary axis Hypothalamic-Pituitary Relationships The endocrine system coordinates functioning between different organs through hormones, which are chemicals released into the bloodstream from specific types of cells within endocrine ductless In a woman with hypothyroidism, indications of secondary hypothyroidism are a history of amenorrhea rather than menorrhagia and some suggestive differences on physical examination.
Secondary hypothyroidism is characterized by skin and hair that are dry but not very coarse, skin depigmentation, only minimal macroglossia, atrophic breasts, and low blood pressure. Also, the heart is small, and serous pericardial effusions do not occur. Hypoglycemia is common because of concomitant adrenal insufficiency or growth hormone deficiency. Myxedema coma is a life-threatening complication of hypothyroidism, usually occurring in patients with a long history of hypothyroidism.
Severe hypothermia may be missed unless low-reading thermometers are used. Rapid diagnosis based on clinical judgment, history, and physical examination is imperative, because death is likely without rapid treatment. Precipitating factors include illness, infection, trauma, drugs that suppress the central nervous system, and exposure to cold. Serum thyroid-stimulating hormone measurement is the most sensitive test for diagnosing hypothyroidism.
In primary hypothyroidism, there is no feedback inhibition of the intact pituitary, and serum TSH is always elevated, whereas serum free T4 is low.
Many patients with primary hypothyroidism have normal circulating levels of triiodothyronine T3 , probably caused by sustained TSH stimulation of the failing thyroid, resulting in preferential synthesis and secretion of biologically active T3. Therefore, serum T3 is not sensitive for hypothyroidism. Anemia is often present, usually normocytic-normochromic and of unknown etiology, but it may be hypochromic because of menorrhagia and sometimes macrocytic because of associated pernicious anemia or decreased absorption of folate.
As the hypometabolic state is corrected, anemia subsides, sometimes requiring 6 to 9 months. Serum cholesterol is usually high in primary hypothyroidism but less so in secondary hypothyroidism. In addition to primary and secondary hypothyroidism, other conditions may cause decreased levels of total T4, such as euthyroid sick syndrome Euthyroid Sick Syndrome Euthyroid sick syndrome is a condition in which serum levels of thyroid hormones are low in clinically euthyroid patients with nonthyroidal systemic illness.
Diagnosis is based on excluding Screening for hypothyroidism Laboratory Testing of Thyroid Function The thyroid gland, located in the anterior neck just below the cricoid cartilage, consists of 2 lobes connected by an isthmus. Screening is done by measuring TSH levels. Various thyroid hormone preparations are available for replacement therapy, including synthetic preparations of T4 L-thyroxine [ levothyroxine ] , T3 liothyronine , combinations of the 2 synthetic hormones, and desiccated animal thyroid extract.
L-Thyroxine is preferred; the usual maintenance dose is 75 to mcg orally once a day, depending on age, body mass index, and absorption for pediatric doses, see Hypothyroidism in Infants and Children Treatment regimens Hypothyroidism is thyroid hormone deficiency. The starting dose in young or middle-aged patients who are otherwise healthy can be mcg or 1. However, in patients with heart disease, therapy is begun with low doses, usually 25 mcg once a day. The dose is adjusted every 6 weeks until maintenance dose is achieved.
The maintenance dose may need to be increased in pregnant women. Dose may also need to be increased if drugs that decrease T4 absorption or increase its metabolic clearance are administered concomitantly.
The dose used should be the lowest that restores serum TSH levels to the midnormal range though this criterion cannot be used in patients with secondary hypothyroidism.
In secondary hypothyroidism the dose of L-thyroxine should achieve a free T4 level in the midnormal range. Liothyronine L-triiodothyronine should not be used alone for long-term replacement because of its short half-life and the large peaks in serum T3 levels it produces.
The administration of standard replacement amounts 25 to Additionally, patients receiving liothyronine are chemically hyperthyroid for at least several hours a day, potentially increasing cardiac risks. Similar patterns of serum T3 changes occur when mixtures of T3 and T4 are taken orally, although peak T3 is lower because less T3 is given. Replacement regimens with synthetic T4 preparations reflect a different pattern in serum T3 response.
Increases in serum T3 occur gradually, and normal levels are maintained when adequate doses of T4 are given. Desiccated animal thyroid preparations contain variable amounts of T3 and T4 and should not be prescribed unless the patient is already taking the preparation and has normal serum TSH. In patients with secondary hypothyroidism, L-thyroxine should not be given until there is evidence of adequate cortisol secretion or cortisol therapy is given , because L-thyroxine could precipitate adrenal crisis.
The intravenous maintenance dose of T4 is 75 to mcg once a day and of T3, 10 to 20 mcg twice a day until T4 can be given orally. Corticosteroids are also given because the possibility of central hypothyroidism usually cannot be initially ruled out. The patient should not be rewarmed rapidly, which may precipitate hypotension or arrhythmias. Hypoxemia is common, so PaO2 should be monitored. If ventilation is compromised, immediate mechanical ventilatory assistance is required. The precipitating factor should be rapidly and appropriately treated and fluid replacement given carefully, because hypothyroid patients do not excrete water appropriately.
Finally, all drugs should be given cautiously because they are metabolized more slowly than in healthy people. Hypothyroidism is particularly common among older adults. Although typically easy to diagnose in younger adults, hypothyroidism may be subtle and manifest atypically in older adults.
Older patients have significantly fewer symptoms than do younger adults, and complaints are often subtle and vague. Many older patients with hypothyroidism present with nonspecific geriatric syndromes—confusion, anorexia, weight loss, falling, incontinence, and decreased mobility. Musculoskeletal symptoms especially arthralgias occur often, but arthritis is rare. TRH stimulation tests are used in the diagnosis and result in a flat response curve.
This condition occurs rarely and is principally seen in newborn babies of mothers who have Graves' disease. It occurs in around one out of 70 pregnancies with Graves' disease [ 17 ].
Occasionally it is seen in neonates of euthyroid mothers. Maternal TSH-receptor antibody levels may be high. Clinical features vary but may include tachycardia, pulmonary hypertension and cardiopulmonary failure.
Neonates commonly develop tachycardia and are treated with carbimazole and beta-blockers once the diagnosis is confirmed. Robert James Graves was an outstanding Irish physician and teacher. He was a prolific medical author and his paper 'Newly observed affection of the thyroid gland in females' was published in the London Medical and Surgical Journal in J Clin Endocrinol Metab.
Epub Jan 1. Epub Mar 5. J Clin Res Pediatr Endocrinol. Int J Endocrinol. Epub Aug 3. Int Med Case Rep J. Case Rep Endocrinol. Epub Mar 9. Akamizu T, Satoh T, Isozaki O, et al ; Diagnostic criteria, clinical features, and incidence of thyroid storm based on nationwide surveys. Epub Jun Tozzoli R, Bagnasco M, Giavarina D, et al ; TSH receptor autoantibody immunoassay in patients with Graves' disease: improvement of diagnostic accuracy over different generations of methods.
Systematic review and meta-analysis. Autoimmun Rev. Epub Jul 7. Akmal A, Kung J ; Propylthiouracil, and methimazole, and carbimazole-related hepatotoxicity. Expert Opin Drug Saf. Epub Aug Cochrane Database Syst Rev. Watanabe N, Narimatsu H, Noh JY, et al ; Antithyroid drug-induced hematopoietic damage: a retrospective cohort study of agranulocytosis and pancytopenia involving 50, patients with Graves' disease.
Epub Nov 2. Collet TH, Bauer DC, Cappola AR, et al ; Thyroid antibody status, subclinical hypothyroidism, and the risk of coronary heart disease: an individual participant data analysis. Batra CM ; Fetal and neonatal thyrotoxicosis. Indian J Endocrinol Metab. Bauer AJ ; Approach to the pediatric patient with Graves' disease: when is definitive therapy warranted? Eur Thyroid J. Epub Feb Case Rep Med. Epub Nov Intern Emerg Med.
Epub Oct Mirza F, Canalis E ; Management of endocrine disease: Secondary osteoporosis: pathophysiology and management. Eur J Endocrinol. Epub May Int J Clin Pract. We all have Graves Disease or overactive thyroid issues, most of us have been through RAI and are now on thyroxine. Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions.
Egton Medical Information Systems Limited has used all reasonable care in compiling the information but make no warranty as to its accuracy.
Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions. This article is for Medical Professionals. In this article Epidemiology Aetiology Presentation Differential diagnosis Investigations Management Summary approach to a patient suspected of having hyperthyroidism Secondary hyperthyroidism Subclinical hyperthyroidism Hyperthyroidism in neonates Hyperthyroidism in children Amiodarone-induced thyrotoxicosis Prognosis History.
Hyperthyroidism In this article Epidemiology Aetiology Presentation Differential diagnosis Investigations Management Summary approach to a patient suspected of having hyperthyroidism Secondary hyperthyroidism Subclinical hyperthyroidism Hyperthyroidism in neonates Hyperthyroidism in children Amiodarone-induced thyrotoxicosis Prognosis History. It can be primary or secondary: Primary hyperthyroidism is the term used when the pathology is within the thyroid gland. Secondary hyperthyroidism is the term used when the thyroid gland is stimulated by excessive thyroid-stimulating hormone TSH in the circulation.
Anatomy and physiology of the thyroid gland The thyroid gland is situated in the neck and its hormones control the metabolic rate of tissues. It is stimulated and controlled by TSH from the anterior pituitary. Greater amounts of T4 are produced than T3. T4 is inactive and needs to be converted to T3 - which occurs peripherally such as in the liver and kidney. Most T3 and T4 in the circulation are bound to protein mostly thyroglobulin ; it is only free thyroid hormone that is active.
Free thyroid hormones in the circulation act negatively on the hypothalamus and pituitary - thus reducing the release of TRH and TSH. Symptoms Signs Weight loss despite an increased appetite. Weight gain. Increased or decreased appetite. Weakness and fatigue.
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