Thyroid gland produces, stores, and releases thyroid hormones, thyroxine (T3) and triiodothyronine (T4), whose main purpose is to regulate the body’s physiological functions.

The thyroid gland is constructed of thyroid follicles, each filled with the protein thyroglobulin.

The thyroid hormones are attached to thyroglobulin protein and stored as colloid in the gland, and T3 and T4 are stored in a ratio of 15:1, respectively.

The release of thyroid hormones is regulated by thyroid stimulating hormone (TSH), an anterior pituitary hormone, which is produced in the hypothalamus.

Release of the thyroid hormones is achieved through proteolysis from thyroglobulin and eventual diffusion into the circulation.

Once released from the gland, majority of T3 and T4 are bound to various carrier proteins such as thyroid-binding globulin (TBG).

T3 is mostly produced by conversion from T4 in liver and kidney; 80% of T3 is produced in this manner by deiodination of T4 by the converting enzyme deiodinase (I, II, or III), whereas only 20% is produced directly by secretion from thyroid gland.

T3 is much more potent than T4, due to its higher receptor affinity at various tissue receptors, and thus mediates most of the body’s systemic effects. However, only the unbound form of T3 is active [1–3].

The standard testing for thyroid function includes the measurement of T3, T4, and TSH levels.

The T4 assay, also known as thyroxine test, is elevated in 90% of patients with hyperthyroidism, and depressed in 85% of patients with hypothyroidism.

The T3 test checks for levels of triiodothyronine and an abnormally high level usually indicates Graves’ disease.

T3 is used predominantly to detect hyperthyroidism if T4 is measured to be normal, as T3 may be the only hormone in excess. T3 however can be low due to various factors that impair the peripheral conversion of T4 to T3 such as seen in euthyroid sick syndrome (ESS).

TSH test is the gold standard for the diagnosis and treatment of thyroid dysfunction and is most useful in detecting hypothyroidism. The normal TSH level is between 0.4 and 4.0 mIU/L. Often in primary hypothyroidism, levels are greater than 20 mIU/L. During the treatment of hypothyroidism, the goal of thyroid replacement therapy is to normalize TSH levels [1].

Hyperthyroidism is a condition in which the thyroid gland is overactive and exposes the body tissues to excessive amounts of thyroid hormone. The most common etiologies are multinodular diffuse goiter and Graves’ disease.

Manifestation of hyperthyroidism includes warm skin, sweating, increased ventricular contractility, tachycardia, elevated systolic blood pressure, weight loss despite hyperphagia, diarrhea, palpitations, emotional lability, skeletal muscle weakness, restlessness, and heat intolerance. Graves’ disease patients might also exhibit exophthalmos from increased volume of retro-orbital fat [1, 2].

Autoimmune condition, which results in hyperstimulation of TSH receptors from autoantibodies produced by the immune system.

It is the most common cause of hyperthyroidism.

The defining features of the disease, in addition to the usual manifestation of hyperthyroidism, include goiters, exophthalmos and pretibial myxedema. These last two signs are truly “diagnostic” of Graves’ disease.

Treatment of Graves’ disease includes antithyroid drugs, which reduce the production of thyroid hormone. Other treatment modalities include radioiodine therapy and thyroidectomy.

Also known as Plummer’s disease, is a condition where the thyroid contains autonomously functioning thyroid nodules, with resulting hyperthyroidism.

It is another common cause of thyrotoxicosis; however, symptoms associated with the disease are considered less severe than those with Graves’ disease.

It occurs most often in older adults, with risk especially high in females over 55 years old.

It has typical symptoms of hyperthyroidism, but the exophthalmos and pretibial myxedema seen in Graves’ do not occur.

The disease is usually treated with beta-blockers such as propranolol, radioiodine therapy, and thyroidectomy.

Also called granulomatous thyroiditis or De Quervain thyroiditis, is a less common variant of thyroiditis, which can cause hyperthyroidism in its initial stage, followed by a transient period of hypothyroidism.

Etiology is thought to be from viral infections, especially ones affecting the ear, sinus, or throat. The viral infection induces tissue damage of the thyroid gland to release thyroid hormone into the circulation.

The disease usually affects women aged 30–50 years.

Since thyroiditis is a form of inflammation, the thyroid often presents with pain and discomfort in the thyroid, however the presentation can be insidious. Other symptoms include myalgia, fever, fatigue, malaise, palpitations, sweating, and heat intolerance.

Laboratory work up includes TSH, T3, T4, and ESR. Patients will usually have suppressed TSH, elevated T4 and T3, and high ESR.

During the initial phase of illness, T4 and T3 are elevated in almost all patients. In contrast to Graves, total T3:T4 ratio usually is less than 20, and radioiodine uptake in the acute stage of the disease is low [1, 4–6].

Therapy for most forms of hyperthyroidism include antithyroid drugs which include propylthiouracil and methimazole. These medications prevent production of T4 and conversion of T3 from T4.

Beta-adrenergic antagonist can also be used to control symptoms of sympathetic activation such as palpitations, trembling, and anxiety until thyroid hormones level normalizes. Beta-adrenergic antagonists often obtain immediate temporary relief but do not treat hyperthyroidism or any of its long-term effects (e.g., propranolol).

Radioactive iodine-131 is used as an ablative treatment and is given orally.

Total thyroidectomy is rarely indicated except for thyroid adenomas or malignancy. It is uncommonly used for treatment of hyperthyroidism since most common forms of hyperthyroidism are very effectively treated with radioactive iodine [2].

An acute exacerbation of hyperthyroidism that is life threatening, and occurs most commonly in undiagnosed or undertreated hyperthyroid patient.

Common triggers are stress of surgery or non-thyroid illness. During thyroid storm, patient will be induced into a hypermetabolic state caused by excessive release of thyroid hormones.

Symptoms: dysrhythmias, myocardial ischemia, congestive heart failure, hyperthermia, shaking, change in consciousness, nausea, vomiting, diarrhea, and tachycardia. Heart failure and pulmonary edema can rapidly occur and cause death. An early sign is often very elevated systolic pressure and low diastolic pressure.

Treatment: Less severe forms can be managed with supportive measures such as cooling blankets, IV fluids, electrolyte correction, EKG monitoring, oxygen supplementation, and medicine to manage agitation. Severe forms may require further medication with sodium iodide (blocks the release of stored thyroid hormone), propylthiouracil, hydrocortisone (prevents conversion of T4 to T3), and propranolol [1, 2, 4].

Hyperthyroidism, if unmanaged, has a high risk for cardiac dysrhythmias or heart failure. Thus one of the primary goals in the management of patients with hyperthyroidism is to attempt to have the patient reach a euthyroid state with normalized thyroid levels prior to elective surgery. Preoperative assessment should aim for goals of resting heart rate of less than 85 bpm and normal thyroid function tests.

In the case of emergency surgeries, beta-sympathetic antagonists can be used to attenuate sympathetic symptoms acutely and should be used in all hyperthyroid patients unless contraindicated. β-Adrenergic blockade such as propranolol given over 12–24 hours decreases sympathetic manifestations such as tachycardia, anxiety, heat intolerance, and tremor.

Glucocorticoids should be administered to decrease hormone release and reduce the peripheral conversion of T4 to T3.

Titrate doses on non-depolarizing muscle relaxers as there is a percentage of these patients that also have myasthenia gravis as a comorbidity.

Avoid sympathomimetic agents such as ketamine, epinephrine, atropine, and ephedrine.

Ocular protection with lubricants and tape in cases of ophthalmopathy.

Monitor EKG for dysrhythmias.

Postoperative period: Beta -sympathetic antagonist should be continued until the antithyroid drugs have taken effect. In the morning of surgery, all antithyroid medications should be continued. Antithyroid drugs such as propylthiouracil and methimazole prevent the thyroid from producing excess amounts of the hormone. However it takes at least 8 weeks for the effect of medication to take place, and thus should be started several months prior to elective surgery.

Hypothyroidism (also known as myxedema) is a common condition where the thyroid gland has decreased production of thyroid hormone resulting in inadequate circulating levels of T4 or T3, or both. Disease development can be insidious and patients often have no or only mild symptoms, making the clinical diagnosis difficult.

Signs and Symptoms: The disease can manifest with generalized reduction in metabolic activity, cardiac and respiratory depression, fatigue, slow mental functioning, hyponatremia, constipation, cold intolerance, slow movements, depression, constipation, thinning of hair, hair loss, weight gain, thickened tongue, thyroid nodule, periorbital edema, and bradycardia [1, 2, 4, 7, 8].

Primary failure of the thyroid gland is responsible for 95% of cases of hypothyroidism, and is due to decreased production of thyroid hormone, despite adequate TSH production. Etiologies of primary hypothyroidism include thyroiditis (Hashimoto’s disease), medications (iodine, propylthiouracil, methimazole), iodine deficiency, irradiation to neck, hereditary defects in biosynthesis, previous treatment with radioactive iodine, and previous thyroidectomy.

Secondary hypothyroidism is responsible for the remaining incidence and is caused by either hypothalamic or pituitary disease.

The most common cause of hypothyroidism in countries with populations that have normal amount of dietary iodine.

The disease is caused by an autoimmune process, which gradually leads to destruction of the thyroid gland. The thyroid gland exhibits atrophy of thyroid follicles and depletion of thyroid epithelial cells due to large infiltrates of lymphatic germinal centers. This leads to a decrease in thyroid hormone production despite normal levels of TSH.

It is most commonly seen in women between 45 and 65 years old.

Patients often present with painless, non-tender, diffuse enlargement of the thyroid gland and feeling of discomfort and tightness in the throat.

Lab values usually show low T4 and T3, high TSH, and presence of antibodies against thyroid peroxidase (TPO). A normal level of TSH reliably excludes hypothyroidism [1, 2, 4, 7, 8].

Treatment: Treatment of symptomatic hypothyroidism is with hormone replacement therapy such as levothyroxine [1].