Hyperthyroidism; Defination, Causes, Symptoms, Diagnosis, Treatment, Complication, Preventions

Hyperthyroidism is the condition that occurs due to excessive production of thyroid hormone by the thyroid gland. Thyrotoxicosis is the condition that occurs due to excessive thyroid hormone of any cause and therefore includes hyperthyroidism. Some, however, use the terms interchangeably. Signs and symptoms vary between people and may include irritability, muscle weakness, sleeping problems, a fast heartbeat, heat intolerancediarrhea, enlargement of the thyroid, and weight loss. Symptoms are typically less in the old and during pregnancy. An uncommon complication is thyroid storm in which an event such as an infection results in worsening symptoms such as confusion and a high temperature and often results in death. The opposite is hypothyroidism, when the thyroid gland does not make enough thyroid hormone

Causes of Hyperthyroidism

The major causes in humans are

  • Graves’ disease. An autoimmune disease (usually, the most common etiology with 50-80% worldwide, although this varies substantially with location- i.e., 47% in Switzerland (Horst et al., 1987) to 90% in the USA (Hamburger et al. 1981)). Thought to be due to varying levels of iodine in the diet. It is eight times more common in females than males and often occurs in young females, around 20 – 40 years of age.
  • Toxic thyroid adenoma (the most common etiology in Switzerland, 53%, thought to be atypical due to a low level of dietary iodine in this country)
  • Toxic multinodular goiter

High blood levels of thyroid hormones (most accurately termed hyperthyroxinemia) can occur for a number of other reasons

  • Inflammation of the thyroid is called thyroiditis. There are several different kinds of thyroiditis including Hashimoto’s thyroiditis (Hypothyroidism immune-mediated), and subacute thyroiditis (de Quervain’s). These may be initiallyassociated with secretion of excess thyroid hormone but usually progress to gland dysfunction and, thus, to hormone deficiency and hypothyroidism.
  • Oral consumption of excess thyroid hormone tablets is possible (surreptitious use of thyroid hormone), as is the rare event of consumption of ground beef contaminated with thyroid tissue, and thus thyroid hormone (termed “hamburger hyperthyroidism”). Pharmacy compounding errors may also be a cause.
  • Amiodarone, an antiarrhythmic drug, is structurally similar to thyroxine and may cause either under- or overactivity of the thyroid.
  • Postpartum thyroiditis (PPT) occurs in about 7% of women during the year after they give birth. PPT typically has several phases, the first of which is hyperthyroidism. This form of hyperthyroidism usually corrects itself within weeks or months without the need for treatment.
  • A struma ovarii is a rare form of monodermal teratoma that contains mostly thyroid tissue, which leads to hyperthyroidism.
  • Excess iodine consumption notably from algae such as kelp.

Thyrotoxicosis can also occur after taking too much thyroid hormone in the form of supplements, such as levothyroxine (a phenomenon known as exogenous thyrotoxicosis, alimentary thyrotoxicosis, or occult factitial thyrotoxicosis).

Hypersecretion of thyroid stimulating hormone (TSH), which in turn is almost always caused by a pituitary adenoma, accounts for much less than 1 percent of hyperthyroidism cases.

Symptoms of Hyperthyroidism

Constitutional Weight loss, heat intolerance, perspiration
Cardiopulmonary Palpitations, chest pain, dyspnea
Neuropsychiatric Tremor, anxiety, double vision, muscle weakness
Neck Fullness, dysphagia, dysphonia
Musculoskeletal Extremity swelling
Reproductive Irregular menses, decreased libido, gynecomastia

Signs of Hyperthyroidism

Vital signs Tachycardia, widened pulse pressure, fever
Cardiovascular Hyperdynamic precordium, CHF, atrial fibrillation, systolic flow murmur
Ophthalmologic Widened palpebral fissure, periorbital edema, proptosis, diplopia, restricted superior gaze
Neurologic Tremor, hyperreflexia, proximal muscle weakness
Dermatologic Palmar erythema, hyperpigmented plaques or non-pitting edema of tibia
Neck Enlarged or nodular thyroid

Thyroid Storm 

Essentially an exaggeration of thyrotoxicosis featuring marked hyperthermia (104-106°F), tachycardia (HR > 140bpm), and altered mental status (agitation, delirium, coma).

Precipitants
Medical: Sepsis, MI, CVA, CHF, PE, visceral ischemia
Trauma: Surgery, blunt, penetrating
Endocrine: DKA, HHS, hypoglycemia
Drugs: Iodine, amiodarone, inhaled anesthetics
Pregnancy: post-partum, hyperemesis gravidarum

Scoring (Burch, Wartofsky)

FEVER
99-100 5
100-101 10
101-102 15
102-103 20
103-104 25
>104 30
TACHYCARDIA
90-110 5
110-120 10
120-130 15
130-140 20
>140 25
MENTAL STATUS
Normal 0
Mild agitation 10
Extreme lethargy 20
Coma, seizure 30
CHF
Absent 0
Mild (edema) 5
Moderate (rales, atrial fibrillation) 10
Pulmonary edema 15
GI
None 0
Nausea/vomiting, abdominal pain 10
Jaundice 20
PRECIPITATING EVENT
None 0
Present 10
  • >45: thyroid storm
  • 25-44: impending thyroid storm
  • <25: unlikely thyroid storm

Treatment

Supportive measures
Volume resuscitation and cooling
Benzodiazepines for agitation
Beta-blockade
Propranolol 60-80mg PO q4h
Propranolol 0.5-1.0mg IV, repeat q15min then 1-2mg q3h
Esmolol continuous infusion
Endocrinology consultation
PTU, SSKI

Antithyroid drugs

Thyrostatics (antithyroid drugs) are drugs that inhibit the production of thyroid hormones, such as carbimazole (used in the UK) and methimazole (used in the US, Germany and Russia), and propylthiouracil. Thyrostatics are believed to work by inhibiting the iodination of thyroglobulin by thyroperoxidase and, thus, the formation of tetraiodothyronine (T4). Propylthiouracil also works outside the thyroid gland, preventing the conversion of (mostly inactive) T4 to the active form T3. Because thyroid tissue usually contains a substantial reserve of thyroid hormone, thyrostatics can take weeks to become effective and the dose often needs to be carefully titrated over a period of months, with regular doctor visits and blood tests to monitor results.

Beta-blockers

Many of the common symptoms of hyperthyroidism such as palpitations, trembling, and anxiety are mediated by increases in beta-adrenergic receptors on cell surfaces. Beta blockers, typically used to treat high blood pressure, are a class of drugs that offset this effect, reducing rapid pulse associated with the sensation of palpitations, and decreasing tremor and anxiety.

Some minimal effect on thyroid hormone production however also comes with Propranolol – which has two roles in the treatment of hyperthyroidism, determined by the different isomers of propranolol. L-propranolol causes beta-blockade, thus treating the symptoms associated with hyperthyroidism such as tremor, palpitations, anxiety, and heat intolerance. D-propranolol inhibits thyroxine deiodinase, thereby blocking the conversion of T4 to T3, providing some though minimal therapeutic effect. Other beta-blockers are used to treat only the symptoms associated with hyperthyroidism. Propranolol in the UK, and metoprolol in the US, are most frequently used to augment treatment for hyperthyroid patients.

Diet

People with autoimmune hyperthyroidism should not eat foods high in iodine, such as edible seaweed and kelps.

From a public health perspective, the general introduction of iodized salt in the United States in 1924 resulted in lower disease, goiters, as well as improving the lives of children whose mothers would not have eaten enough iodine during pregnancy which would have lowered the IQs of their children.

Surgery

Surgery (thyroidectomy to remove the whole thyroid or a part of it) is not extensively used because most common forms of hyperthyroidism are quite effectively treated by the radioactive iodine method, and because there is a risk of also removing the parathyroid glands, and of cutting the recurrent laryngeal nerve, making swallowing difficult, and even simply generalized staphylococcal infection as with any major surgery. Some people with Graves’ may opt for surgical intervention. This includes those that cannot tolerate medicines for one reason or another, people that are allergic to iodine, or people that refuse radioiodine.

If people have toxic nodules treatments typically include either removal or injection of the nodule with alcohol.

Radioiodine

In iodine-131 (radioiodine) radioisotope therapy, which was first pioneered by Dr. Saul Hertz, radioactive iodine-131 is given orally (either by pill or liquid) on a one-time basis, to severely restrict, or altogether destroy the function of a hyperactive thyroid gland. This isotope of radioactive iodine used for ablative treatment is more potent than diagnostic radioiodine (usually iodine-123 or a very low amount of iodine-131), which has a biological half-life from 8–13 hours. Iodine-131, which also emits beta particles that are far more damaging to tissues at short range, has a half-life of approximately 8 days. Patients not responding sufficiently to the first dose are sometimes given an additional radioiodine treatment, at a larger dose. Iodine-131 in this treatment is picked up by the active cells in the thyroid and destroys them, rendering the thyroid gland mostly or completely inactive

References

  1.  An Appraisal of Endocrinology: A Report Made to the Directors of the John and Mary R. Markle Foundation by a Special Committee of the National Research Council Consisting of Walter B. Cannon, Chairman, Earl Engle, Curt Richter, Oscar Riddle, R.G. Hoskins … with the Assistance of Milton Lee. National Academies. 1936. p. 9. Archived from the original on 8 September 2017.
  2. Fumarola, A; Di Fiore, A; Dainelli, M; Grani, G; Carbotta, G; Calvanese, A (June 2011). “Therapy of hyperthyroidism in pregnancy and breastfeeding”. Obstetrical & gynecological survey66 (6): 378–85. doi:10.1097/ogx.0b013e31822c6388PMID 21851752.
  3.  Korevaar, Tim I M; Muetzel, Ryan; Medici, Marco; Chaker, Layal; Jaddoe, Vincent W V; De Rijke, Yolanda B; Steegers, Eric A P; Visser, Theo J; White, Tonya; Tiemeier, Henning; Peeters, Robin P (2016). “Association of maternal thyroid function during early pregnancy with offspring IQ and brain morphology in childhood: A population-based prospective cohort study”. The Lancet Diabetes & Endocrinology4: 35. doi:10.1016/S2213-8587(15)00327-7.
  4. Shomon, Mary (2004). “Feline Hyperthyroidism: Frequently Asked Questions, Information About Overactive Thyroid Conditions in Cats”Archived from the original on 31 August 2009. Retrieved 24 June2009.
  5. Gussekloo, Jacobijn; Williams, Graham R.; Walsh, John P.; Jüni, Peter; Aujesky, Drahomir; Rodondi, Nicolas (26 May 2015). “Subclinical Thyroid Dysfunction and Fracture Risk”JAMA313 (20): 2055–65. doi:10.1001/jama.2015.5161PMC 4729304PMID 26010634Archived from the original on 28 May 2015.
  6. LeFevre, ML; U.S. Preventive Services Task, Force (5 May 2015). “Screening for thyroid dysfunction: U.S. Preventive Services Task Force recommendation statement.”. Annals of Internal Medicine162 (9): 641–50. doi:10.7326/m15-0483PMID 25798805.
  7. Fumarola, A; Di Fiore, A; Dainelli, M; Grani, G; Calvanese, A (Nov 2010). “Medical treatment of hyperthyroidism: state of the art”. Experimental and Clinical Endocrinology & Diabetes118 (10): 678–84. doi:10.1055/s-0030-1253420PMID 20496313.
  8. Eber O, Buchinger W, Lindner W, et al. (1990). “The effect of D-versus L-propranolol in the treatment of hyperthyroidism”. Clin Endocrinol32 (3): 363–72. doi:10.1111/j.1365-2265.1990.tb00877.x.
  9. Geffner DL, Hershman JM (July 1992). “β-Adrenergic blockade for the treatment of hyperthyroidism”. The American Journal of Medicine93 (1): 61–8. doi:10.1016/0002-9343(92)90681-ZPMID 1352658.
  10. Max Nisen (22 July 2013). “How Adding Iodine To Salt Resulted In A Decade’s Worth Of IQ Gains For The United States”Business InsiderArchived from the original on 23 July 2013. Retrieved 23 July 2013

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