Hypothyroidism and Hyperthyroidism

Hypothyroidism and Hyperthyroidism



Mario Skugor, Maria Fleseriu



ANATOMY AND PHYSIOLOGY


A normal adult thyroid weighs 10-20 g and receives blood from bilateral superior and inferior thyroid arteries and a small artery called the thyroid ima. The thyroid secretes two hormones. Thyroxine (T4) makes 90% of hormone production, and triiodothyronine (T3) produces the other 10%. Peripheral tissues convert T4 to T3, and most of T3 is derived from T4. Thyroid hormone secretion is regulated by hypothalamo-pituitary-thyroid axis through actions of TRH and TSH.


Thyroid hormones are transported in serum bound to carrier proteins (0.03%-0.04% of T4 and 0.3%-0.4% of T3 are free hormone). Thyroid hormone binding globulin (TBG) is the main carrier, accounting for 75% of bound T4 and all of bound T3. Thyroxine binding prealbumin and albumin are responsible for the rest.



PHYSIOLOGIC EFFECTS


Most thyroid hormone actions (metabolic and developmental) are mediated via nuclear receptors through gene expression regulation. Thyroid hormone receptors are found in most body tissues. T3 is biologically much more active than T4. Thyroid hormones increase the basal metabolic rate by stimulating catabolic and anabolic reactions in metabolism of carbohydrates, fat, and proteins and by stimulating thermogenesis. Thyroid hormone deficiency during embryonic development leads to cretinism and dwarfism (congenital myxedema).



HYPOTHYROIDISM



Definition and Prevalence


Hypothyroidism results from reduced effects of thyroid hormone on tissues. Hypothyroidism is more common in women, has total prevalence of 1% to 2%,1 and increases with age (~10% adults >65 years). In the U.S. population, prevalence of biochemical hypothyroidism is 4.6%, but clinically evident hypothyroidism is present in 0.3%.2 Congenital hypothyroidism is among the most common congenital diseases, with an incidence of 1/4000 newborns. Higher risk of hypothyroidism is seen in persons with the conditions listed in Box 1.



Box 1 Conditions Indicating Higher Risk for Hypothyroidism



Family or personal history of autoimmune disease

Women in the postpartum period

Personal history of neck or head irradiation

Primary pulmonary hypertension

Genetic syndromes: Turner’s and Down syndromes

Patients treated with amiodarone, interferon-alpha, or lithium

Persons over 65 years of age

Hypothyroidism can be congenital or acquired, subclinical or overt, and, according to the site of abnormality, primary (thyroid level) or secondary (pituitary or hypothalamic). The most common causes (Box 2) are Hashimoto’s thyroiditis, postsurgical or postablative hypothyroidism, amiodarone-induced hypothyroidism, and postpartum thyroiditis.



Box 2 Causes of Hypothyroidism



Primary



Agenesis

Gland destruction
• Surgical removal

• Irradiation (therapeutic radioiodine, external irradiation)

• Autoimmune disease (Hashimoto’s, atrophic thyroiditis)

• Idiopathic atrophy

• Infiltrative process

Inhibition of thyroid hormone synthesis and release
• Iodine deficiency

• Excess iodide in susceptible persons

• Drugs: interferon alpha, lithium, amiodarone, aminoglutethimide, thalidomide, sunitinib, sovafenib

• Inherited enzyme defects

Transient
• After surgery or therapeutic radioiodine

• Postpartum

• Thyroiditis


Secondary



Hypothalamic disease

Pituitary disease
• Genetic forms of pituitary hormone deficiencies

• Infiltrative disorders

• Sheehan’s syndrome

• Surgery or irradiation

• Trauma

• Tumors

Resistance to thyroid hormone


Specific Syndromes



Hashimoto’s Thyroiditis


Hashimoto’s thyroiditis is an autoimmune disorder directed against thyroid antigens and is the most common cause of hypothyroidism. The incidence is 0.3 to 1.5 per 1000 person-years, and it is 4 to 10 times more common in women than in men. Hashimoto’s thyroiditis is more prevalent in areas with a high dietary iodine intake, and smoking increases the risk. Goiter can be seen on presentation, but thyroid atrophy is more common. Hashimoto’s thyroiditis is associated with other endocrine diseases in polyglandular autoimmune failure syndrome (Addison’s disease, type1 diabetes mellitus, and hypogonadism).


The diagnosis is made by clinical features, elevated TSH, low thyroid hormone, and the presence of anti–thyroid peroxidase antibodies (anti-TPO).



Amiodarone-Induced Hypothyroidism


Excess iodine from amiodarone exerts an acute, transient inhibition of iodide organification, the Wolff-Chaikoff effect, but the normal gland escapes this effect due to adaptation of the iodide transport system. In some persons, the thyroid gland is unable to escape the block, and hypothyroidism ensues. Thyroid function tests should be checked before starting amiodarone therapy, after 3 to 4 months of therapy, and 1 year after discontinuing therapy.



Postpartum Thyroiditis


Postpartum thyroiditis usually manifests with hyperthyroidism (see later) followed by a hypothyroid phase (transient or permanent).



Signs and Symptoms


Symptoms of hypothyroidism depend on pathogenesis, duration, severity, and the age of the patient. Symptoms of mild hypothyroidism are nonspecific: fatigue, cold intolerance, sleepiness, weight gain and muscle aches. These symptoms are also seen with a variety of other conditions; however, such patients should be tested for hypothyroidism. Other symptoms include bradycardia, constipation, menstrual irregularities, dry skin, coarse or brittle hair, edema (especially periorbital), and difficulty with concentration and memory. Laboratory tests might also show elevated cholesterol, prolactin, and creatine phospokinase.


Hypothyroidism is associated with impaired endothelial function, left ventricular diastolic dysfunction, and higher diastolic blood pressure due to increased systemic vascular resistance. These abnormalities are reversible with L-T4 replacement therapy.3


Myxedema coma is the most serious form of hypothyroidism; it is often precipitated by other diseases. Patients have profound hypothermia, bradycardia, and typical skin and facial changes. Mortality is 100% if not treated. Myxedema coma is seen extremely rarely today.



Diagnosis


A TSH level is the best screening test for detecting hypothyroidism. A normal TSH rules out primary hypothyroidism in asymptomatic patients. Abnormal TSH should be followed by determination of thyroid hormone levels.


Overt hypothyroidism is defined as a clinical syndrome of hypothyroidism associated with elevated TSH and decreased serum levels of T4 or T3. Subclinical hypothyroidism is defined as a condition without typical symptoms of hypothyroidism, elevated TSH (>5 µU/mL), and normal circulating thyroid hormone.


The measurement of thyroid autoantibodies helps in diagnosing autoimmune process. However, this test should be ordered only if it will influence the decision to treat.



Treatment


Treatment is with thyroid hormone supplementation. Levothyroxine (L-T4) is acceptable therapy for most patients. The starting dose should be 1.6 µg/kg of body weight. In elderly patients and patients with cardiac disease, we recommend starting at a lower dose (25-50 µg/day) and increase by 25 µg/d until the patient is clinically and biochemically euthyroid. The dose should be adjusted about 6 to 8 weeks after treatment is initiated (unless symptoms of overtreatment occur). Once the patient is euthyroid and TSH is stable, an annual follow-up with TSH measurement should suffice. During pregnancy, more-frequent TSH determination are needed because of increasing needs secondary to an increase in binding protein levels. TSH should be checked 2 months after the start or discontinuation of HRT.


The patient should be advised to take the T4 preparation 2 to 4 hours before or after meals or using preparations known to impede T4 absorption: calcium, magnesium, iron, sucralfate, and aluminum hydroxide.


If any signs or symptoms suggest adrenal insufficiency, this should be investigated and, if confirmed, glucocorticoids should be given before starting T4. Failure to do so can precipitate adrenal crisis.


In selected circumstances, T3 may also be used to treat hypothyroidism. Drawbacks to routine use of T3 include short half-life, requiring multiple daily doses, and fluctuating symptoms when doses are missed.


Combination therapy using both T4 and T3 (dessicated thyroid extract, compounded T4-T3 preparation) has been proposed to improve mood and quality of life, but most studies did not show benefit.4 We do not recommend routine use of combination therapy except in cases where fast improvements in clinical condition are required (profound hypothyroidism).


Myxedema coma requires aggressive treatment with intravenous T4 (≤500 µg/day), and some authors recommend addition of T3.5


Consultation with an endocrinologist should be sought in hypothyroid patients who are 18 years old or younger, unresponsive to therapy, or pregnant; who have cardiac disease, goiter, nodule, or other structural abnormality of thyroid gland; or who have another coexisting endocrine disease



HYPERTHYROIDISM



Definition and Prevalence


Thyrotoxicosis is a clinical condition resulting from the action of excess thyroid hormone on tissues. The term hyperthyroidism is usually reserved for thyrotoxicosis caused by excessive production of thyroid hormone (Boxes 3 and 4). Other forms of thyrotoxicosis include thyrotoxicosis factitia and those associated with different forms of thyroiditis. Overt thyrotoxicosis is defined as the syndrome of hyperthyroidism associated with suppressed TSH and elevated serum levels of T4 or T3. Subclinical thyrotoxicosis is devoid of symptoms, but TSH is suppressed although there are normal circulating levels of thyroid hormone.



Box 3 Causes of Thyrotoxicosis



Thyroid hormone overproduction



• Graves’ disease

Related posts:

  1. Anaphylaxis
  2. Sleep-Disordered Breathing
  3. Nontuberculous Mycobacterial Disorders
  4. Systemic Scleroderma

Stay updated, free articles. Join our Telegram channel
Tags:
Jul 18, 2017 | Posted by in GENERAL SURGERY | Comments Off on Hypothyroidism and Hyperthyroidism

Full access? Get Clinical Tree
Get Clinical Tree app for offline access