Toxic multinodular goiter overview: Difference between revisions
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===Physical Examination=== | ===Physical Examination=== | ||
The clinical features of toxic multinodular hyperthyroidism includes flushing,[[diaphoresis]], smooth skin, onycholysis, hyperpigmentation, thinning of the hair, [[thyromegaly]],[[lymphadenopathy]], lid lag, shortness of breath on exertion, hypoxemia, hypercapnia, tachycardia, atrial fibrillation, weight loss, increased appetite anorexia, dysphagia, increased urinary frequency, enuresis, gynecomastia, reduced libido, erectile dysfunction, psychosis, agitation, and depression,anxiety, restlessness, irritability, and emotional lability, insomnia, confusion, poor orientation and immediate recall, amnesia, and constructional difficulties, peripheral neuropathy, carpal tunnel syndrome, tremors, myopathy, muscle weakness, proximal and distal weakness, deep tendon reflexes are usually normal or increased, osteoporosis and an increased fracture probability. | |||
===Laboratory Findings=== | ===Laboratory Findings=== | ||
Revision as of 21:15, 9 October 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Historical Perspective
In the year 40 BC, Pliny, Vitruvius, and Juvenal were the first who documented the prevalence of goiter in the Alps. In 1500, Leonardo da Vinci was the first who recognized and drew the thyroid gland. In 1913, Henry Plummer, an American physician was the first to describe toxic multinodular goiter or Plummer's disease. In 1947, Cope, Rawson, and McArthur were the first who described the usage of radioactive iodine to demonstrate a "hot" thyroid nodule.
Classification
Pathophysiology
The progression to Toxic multinodular goiter usually involves the somatic gain-of-function mutations in the TSH receptor in autonomously functioning thyroid nodules.
Causes
The progression to Toxic multinodular goiter usually involves the somatic gain-of-function mutations in the TSH receptor gene.
Differentiating ((Page name)) from Other Diseases
Epidemiology and Demographics
The incidence of toxic multinodular goiter is estimated to be 4.8 cases per 100,000 population per year. The prevalence of toxic multinodular goiter is 100 cases per 100,000 population and accounts for 5% of all patients with hyperthyroidism. Toxic multinodular goiter commonly affects individuals older than 60 years of age. The frequency of toxic multinodular goiter increases with age. Females are more commonly affected by toxic multinodular goiter than men.
Risk Factors
Common risk factors in the development of multinodular goiter include female sex,age over 50 years,areas with decreased iodine intake,iodine supplementation, natural goitrogens,vitamin A and iron deficiency,selenium deficiency.
Screening
Toxic multinodular goiter is diagnosed with a physical examination which shows nodules in the throat and rapid heart rate, among other signs such as diaphoresis and tremors. Blood screening includes tests for elevated T3 and T4 hormone levels that indicate hyperthyroidism. TSH assays are the best initial screening tool for hyperthyroidism.
Natural History, Complications, and Prognosis
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
The clinical features of toxic multinodular hyperthyroidism includes flushing,diaphoresis, smooth skin, onycholysis, hyperpigmentation, thinning of the hair, thyromegaly,lymphadenopathy, lid lag, shortness of breath on exertion, hypoxemia, hypercapnia, tachycardia, atrial fibrillation, weight loss, increased appetite anorexia, dysphagia, increased urinary frequency, enuresis, gynecomastia, reduced libido, erectile dysfunction, psychosis, agitation, and depression,anxiety, restlessness, irritability, and emotional lability, insomnia, confusion, poor orientation and immediate recall, amnesia, and constructional difficulties, peripheral neuropathy, carpal tunnel syndrome, tremors, myopathy, muscle weakness, proximal and distal weakness, deep tendon reflexes are usually normal or increased, osteoporosis and an increased fracture probability.