Chapter 10 Thyroid disorders

CHAPTER CONTENTS

Introduction137

Relevant anatomy and physiology137

Thyroid disorders139

Incidence139

Aetiology of thyroid disease140

Physiological changes in pregnancy142

Thyroid function tests in pregnancy142

Hyperthyroidism in pregnancy143

Hypothyroidism in pregnancy144

References146

INTRODUCTION

Thyroid disease is one of the most common endocrine diseases likely to occur in women of childbearing age. Within the general population, thyroid disease is more likely to occur in the young adult woman, although both sexes may be affected. Thyroid disorders are among the most prevalent of medical conditions and increase with age. Overactivity, known as hyperthyroidism or thyrotoxicosis may be caused by a variety of disorders, for example, Graves’ disease, thyroiditis, toxic multinodular goitre. Underactivity, known as hypothyroidism or myxoedema is considered to be an autoimmune disorder. Although normally already diagnosed and treated, the thyroid hormones may be affected by the process of childbirth and thus the midwife must have a clear knowledge of the implications for pregnancy, labour and the puerperium.

RELEVANT ANATOMY AND PHYSIOLOGY

The thyroid gland is an endocrine gland, responsible for producing, storing and secreting the thyroid hormones. The gland is located anteriorly to the trachea, just below the level of the thyroid cartilage, which forms the anterior surface of the larynx, and superior to the cricoid cartilage (Fig. 10.1).

Figure 10.1 Anterior view of the thyroid gland.

The thyroid gland is shaped like a ‘butterfly’, having a right and left lobe joined by a narrow isthmus; normal weight in adults is 15–25 g. The thyroid gland has an extensive blood supply from the superior and inferior thyroid arteries, which are branches of the subclavian and external carotid arteries. Venous blood drains into three veins – superior and middle thyroid veins drain into the internal jugular vein. The inferior thyroid veins anastomose with each other and drain into the left brachiocephalic vein in the thorax. Four parathyroid glands are located behind the thyroid gland on its posterior aspect (Fig. 10.2)

Figure 10.2 Location of parathyroid glands.

Each lobe of the gland is divided into follicles, and each follicle is lined with a single spherical layer of cuboidal epithelium, surrounding a noncellular centre. The central follicular cavitycontains a viscous gelatinous protein type material in suspension, referred to as a colloid (Fig. 10.3).

Figure 10.3 Microstructure of thyroid tissue.

The glycoprotein that is secreted by the follicular cells is known as thyroglobulin. Iodine circulating in the bloodstream is removed and follicular cells trap and oxidize the element. At the apical surface of each follicular cell iodide ions are converted to an activated form of iodide (I⁺) by the enzyme thyroid peroxidase.

Simultaneously, one or two iodide ions are attached to tyrosine molecules in thyroglobulin. Tyrosine–iodide ion molecules are paired forming molecules of thyroid hormones, resulting in the formation of the hormone thyroxine, T₄ containing 4 iodide ions, and the hormone tri-iodothyronine, or T₃ containing 3 ions (Martini 2005).

Thyroid hormones are released in response to hormonal signals from the hypothalamus and pituitary gland. Thyrotrophin releasing hormone (TRH) is secreted into the blood in response to low circulating concentrations of thyroid hormones. This in turn acts on the anterior pituitary which stimulates the secretion of thyroid stimulating hormone (TSH) and as the concentration of thyroid hormones rise, the production rates of TRH and TSH decrease. Therefore, the release of thyroid hormones is controlled by the level of thyroid stimulating hormone in the blood, and control is by a negative feedback system (Box 10.1).

Box 10.1 Negative feedback systems

Feedback systems are essential within the body to ensure a constant supply of components vital to physiology such as hormones, blood sugar levels, etc. A feedback system is any circular situation in which information regarding the status of something is fed back to a central point. In the human body, the central point is commonly the central nervous system.

The most common feedback system in the body is a negative feedback system. A substance is released from a gland in response to a stimulus from the brain. Once this substance reaches a certain level, this information is fed back to the brain which then turns off the original stimulus. In the case of the thyroid gland low levels of thyroid hormones are detected by the hypothalamus which stimulates the pituitary gland via thyroid releasing hormone (TRH) to release thyroid stimulating hormone. Thyroid hormone levels rise and as they reach normal levels, TRH is inhibited.

One of the few positive feedback systems is seen in childbirth. Oxytocin is released from the hypothalamus via the pituitary gland and stimulates uterine contractions. As the cervix becomes dilated, this information is fed back to the hypothalamus, which releases increasing levels of oxytocin. This cycle is only interrupted by birth.

The levels of T₄ (thyroxine) and T₃ (tri-iodothyronine) circulating in the blood are quite different. The thyroid gland makes more T₄ than T₃, and T₄ has a longer half-life, but significantly, T₄ is less active and is used more as a storage form. In the peripheral circulation and at cell level T₄ can be converted to T₃ (de Swiet et al 2002).

Most of the thyroid hormones entering the bloodstream become attached to thyroid binding globulins, and only very small amounts remain unbound and are free to diffuse into peripheral tissues. Thyroid hormones readily cross cell membranes and they activate receptors involved with energy transformation and utilization; in other words, they regulate the metabolism of nearly all body cells. The critical effects from a midwifery perspective are that the thyroid hormones regulate carbohydrate, lipid and protein metabolism and the normal development of the nervous system in fetus and infant. They also promote normal growth and the hydration and secretory activity of the skin (Table 10.1). Female reproduction and lactation are also influenced (Marieb & Hoehn 2007).

Table 10.1 Effects of thyroid hormones on body organs and tissues

• Increases the heart rate and force of the contraction, promoting normal function of the heart • Promotes normal adult nervous system function; enhances the effects of the sympathetic nervous system • Maintains normal sensitivity of respiratory centres to changes in oxygen and carbon dioxide concentrations • Stimulates the formation of red blood cells and thereby enhances oxygen delivery • Stimulates the activity of other endocrine tissues • Accelerates the utilization of minerals in bones • Regulates metabolic rate and heat production through glucose oxidization

Marieb & Hoehn 2007, Martini 2005, Jordan 2002.

Other larger endocrine cells are also found within the thyroid gland interspersed between the follicle cells. These are known as para-follicular or clear cells and produce the hormone calcitonin, which combined with parathyroid hormones coordinates the storage, absorption and excretion of calcium ions and phosphorus.

Calcitonin acts primarily on bone. Bone is in a constant state of remodelling, whereby old bone is removed by osteoclasts, and new bone is laid down by osteoblasts. Calcitonin inhibits bone removal by osteoclasts, and promotes bone formation by osteoblasts. In the kidney, calcium and phosphorus are conserved by reabsorption in the kidney tubules. Calcitonin inhibits tubular reabsorption of these two ions, leading to increased rates of their loss in urine. Thus, calcium ion balance is also maintained by a negative feedback system.

THYROID DISORDERS

Incidence

Thyroid disease is common in the general population and prevalence increases with age. Hypo-thyroidism is by far the most common disorder and is more common in older women. It is frequently the result of autoimmune disease, or may arise following radioactive iodine therapy or thyroid surgery for hyperthyroidism. Hyperthyroidism is much less common, with a female to male ratio of 9:1. Graves’ disease is the most common cause and mainly affects young adults. Toxic multinodular goitres tend to affect older age groups.

Aetiology of thyroid disease

Hyperthyroidism

Graves’ disease

This is the most common cause of hyperthyroidism. It is thought to be an autoimmune disease triggered by an infection or other stressor which leads to destruction of thyroid cells in susceptible individuals. It predominately affects females between 20–50 years, but can affect both sexes at any age. It is characterized by an enlargement of the gland (goitre) and ophthalmic features, e.g. lid-lag, lid-retraction with limited upward gaze (staring), exophthalmia, and retro-orbital inflammation leading to periorbital oedema.

Thyroiditis

This is rare condition, often referred to as subacute thyroiditis as frequently it occurs as a result of an upper respiratory tract infection. It is thought to be the major cause of pain in the thyroid gland. It can also present in patients taking the drugs interferon and amiodarone, a drug used in the treatment of some cardiac arrhythmias. Thyroiditis causes either a slow and chronic cell destruction, causing hypothyroidism, or conversely rapid cell destruction. If rapid cell destruction occurs, it produces symptoms of hyperthyroidism.

Toxic multinodular goitre

This type of goitre is characterized by an enlarged gland with distinct nodules. It tends to occur in an older age group outwith childbearing age.

Toxic adenoma (single nodule)

Toxic adenoma of the thyroid is an autonomously functioning thyroid nodule that produces excessive amounts of thyroid hormone leading to increased serum levels of T₃ and/or T₄ and suppression of serum TSH. The normal thyroid tissue that surrounds the nodule is often suppressed.

Pathophysiology

Excessive thyroid hormones produce signs and symptoms caused by an increase in the metabolic rate resulting in a variety of symptoms (Table 10.2).

Table 10.2 Symptoms of hyperthyroidism

• Heat intolerance, excessive sweating • Irritability and restlessness • Weight loss, despite increased appetite • Diarrhoea • Tachycardia, palpitations • Atrial fibrillation, angina • Dyspnoea • Fatigue but difficulty in sleeping • Weak muscles, difficulty in getting up from a squatting position • Fine tremor of hands • Amenorrhoea and infertility

Diagnosis

Clinical examination is confirmed by laboratory measurements of thyroid hormones. Both T₄ (thyroxine) and T₃ (tri-iodothyronine) levels are elevated but TSH (thyroid stimulating hormone) is almost undetectable. Ultrasound scanning is also used in the diagnosis of this condition.

Management

There are three approaches to treatment of this condition.

Antithyroid drug therapy

These drugs are prescribed to inhibit the synthesis of thyroid hormones. Carbimazole is the most commonly used drug, in dosages of 30–40 mg/day. If patients are sensitive to carbimazole, another drug which may be prescribed is propylthiouracil, 300–600 mg daily. The patient continues this therapy until a euthyroid state is achieved, then a maintenance dose is prescribed for approximately 1 year. Monitoring of the patient by her GP continues as required.

Rare but major possible side-effects of carbimazole are agranulocytosis (a partial or complete absence of neutrophils), or pancytopenia (deficiency in all blood cells) due to suppression of bone marrow function; and patients must be advised that if they develop a sore throat or unexplained fever, they must immediately seek medical advice.

Surgery

Partial thyroidectomy is only performed after the patient has achieved a euthyroid state and is useful if there is a large or unsightly goitre. Oral potassium iodide may occasionally be prescribed 1–2 weeks prior to surgery to reduce thyroid size and vascularity and inhibit thyroid hormone release, thereby reducing the risk of postoperative haemorrhage (Watkinson 2003).

Radioactive iodine therapy

Radioactive iodine, iodine 131, may be used to treat hyperthyroidism. It is given orally in a single dose at an outpatient clinic. It acts by destroying follicular cells or inhibiting the cells’ ability to replicate. Patients are advised that eating should be avoided for at least 4 h after administration of the isotope. This is to allow the drug to be absorbed adequately. Following this, the patient should drink at least 2 L of fluid over 24 h in order to excrete the free radioactive iodine as quickly as possible. This treatment is not usually offered to women of childbearing age (Dibbs 2001).

Whichever treatment is prescribed for the treatment of hyperthyroidism the patient will be anxious, due not only to her condition, but also due to the risks of each treatment. Careful explanation of the method of administration of drugs, and their risks must be given.

If operative treatment is prescribed, the patient is usually admitted prior to surgery for demonstration of postoperative physiotherapy. Information regarding the procedure should be provided to ensure they have understood medical explanations.

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