Art & science life sciences: 24
Endocrine system: part 1 Johnstone C et al (2014) Endocrine system: part 1. Nursing Standard. 28, 38, 42-49. Date of submission: December 19 2012; date of acceptance: April 29 2013.
Abstract This article, which forms part of the life sciences series and is the first of two articles on the endocrine system, examines the structure and function of the organs of the endocrine system. It is important that nurses understand how the endocrine system works and its role in maintaining health. The role of the endocrine system and the types, actions and control of hormones are explored. The gross structure of the pituitary and thyroid glands are described along with relevant physiology. Several disorders of the thyroid gland are outlined. The second article examines growth hormone, the pancreas and adrenal glands.
Authors Carolyn Johnstone Lecturer in nursing, School of Nursing and Midwifery, University of Dundee, Dundee, Scotland. Charles Hendry Retired, was senior lecturer, School of Nursing and Midwifery, University of Dundee. Alistair Farley Retired, was lecturer in nursing, School of Nursing and Midwifery, University of Dundee. Ella McLafferty Retired, was senior lecturer, School of Nursing and Midwifery, University of Dundee. Correspondence to: [email protected]
Keywords Endocrine system, homeostatis, hyperthyroidism, hypothalamus, hypothyroidism, pituitary gland, thyroid gland
Review All articles are subject to external double-blind peer review and checked for plagiarism using automated software.
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THE ENDOCRINE SYSTEM is composed of endocrine glands and hormone-producing tissues, hormones and hormone receptors (Scott 2010). The endocrine glands include the pineal glands, pituitary gland, thyroid gland, parathyroid glands, thymus gland and adrenal glands. Several organs and tissues that secrete hormones are also present and include, for example the hypothalamus, heart, stomach, pancreas, ovaries in females and testes in males (Sherwood 2012) (Figure 1). While the glands and tissues of the endocrine system are mostly separated from each other, they work as an integrated system.
Role of the endocrine system The endocrine glands produce hormones, or chemical messengers, that are secreted into the interstitial fluid, diffuse into blood capillaries and are carried via the circulatory system to target organs (Tortora and Derrickson 2012). The receptors of those target organs are molecules consisting of proteins that bind specifically with hormones to stimulate particular physiological changes in the target cell (Scott 2010). Importantly, the endocrine and nervous systems work collaboratively to manage and co-ordinate other body systems (Cohen 2013). Both systems are involved in maintaining a stable internal environment (homeostasis). The nervous system releases neurotransmitters at nerve synapses that act on specific muscles and glands, and are concerned with rapid changes, while the endocrine system releases hormones involved in slower and more precise adjustments (Tortora and Derrickson 2012). The functions of the endocrine system are to (Sherwood 2012): 4Maintain homeostasis through the regulation of nutrient metabolism, and water and electrolyte balance. 4Regulate growth and production of cells. 4Control the responses of the body to external stimuli, especially stress. 4Control reproduction. 4Control and integrate circulatory and digestive activities in collaboration with the autonomic nervous system.
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Most endocrine hormones circulate in the bloodstream, however some hormones are local hormones, called paracrines, that act on target cells in close proximity or on the same cells that secreted them (autocrines), without first entering the bloodstream (Tortora and Derrickson 2012). Hormones can be grouped according to their molecular structure into polypeptides, steroids, amines and eicosanoids. Polypeptides include hormones from the anterior and posterior pituitary, parathyroid glands and endocrine tissue of the pancreatic gland (Scott 2010). Steroids are derived from steroid cholesterol and include hormones from the adrenal cortex, testes and ovaries. These hormones can be recognised by the ending of ‘sterone’ (Cohen 2013). Amines are derived from amino acids and include thyroid hormones, adrenaline (epinephrine) and noradrenaline (norepinephrine) (Scott 2010). Eicosanoids are derived from arachidonic acid, a polyunsaturated fatty acid, and include prostaglandins and leucotrienes. Biologically, they have a broad range of effects and mediate the inflammatory response and the transmission of pain impulses (Scott 2010). Steroid hormones and thyroid hormones are lipid-soluble. Amine, polypeptide and eicosanoid hormones are water-soluble (Tortora and Derrickson 2012).
Regulation of hormonal secretion Several mechanisms control regulation of hormone secretion, including: 4Hypothalamic regulation through the release of tropic hormones, hormones that have other endocrine glands as their target. 4Regulation through rhythmic variations. 4Chemical regulation. 4Neural regulation. A hormone is released in response to a specific stimulus, for example low levels of thyroxine act as a stimulus to the hypothalamus to increase secretion of thyrotropin-releasing hormone (TRH) which in turn acts on the anterior pituitary causing it to release thyroid-stimulating hormone (TSH). TSH acts on the thyroid gland to increase secretion of thyroxine. The amount of hormone released is usually maintained within a particular range. The pituitary gland and hypothalamus regulate other endocrine glands and their hormones through tropic hormones (Scott 2010). Maintaining hormone secretion within a particular range is achieved through negative feedback. This process occurs when further secretion is controlled by the hormone itself or the result of its action. There is a negative effect
on the endocrine gland to decrease its output when the target organ becomes too active. An example of this mechanism is when the pituitary gland releases TSH that, in turn, stimulates secretion of hormones from the thyroid gland. When blood levels of thyroid hormones increase, negative feedback stops the release of further TSH, slowing the release of thyroid hormones and their blood levels decrease. When the levels of thyroid hormone decrease below the normal range, TSH is released, allowing the process to start again (Cohen 2013). Hormone secretion can also be regulated through rhythmic variations. For example, adrenocortical hormones follow a 24-hour cycle related to the sleep pattern of an individual, and the level of secretion is at its highest before waking, at around 6am, and at its lowest at around midnight (Sherwood 2012). Another example is the menstrual cycle, which follows a monthly cyclical pattern (Cohen 2013).
FIGURE 1 Position of the major endocrine glands in the body Hypothalamus Pineal gland Parathyroid glands (situated behind the thyroid gland)
Pituitary gland
Thyroid gland
Heart
Thymus gland
Stomach
Adrenal glands Pancreas Ovaries in females
Testes in males
PETER LAMB
Types and actions of hormones
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Art & science life sciences: 24 Chemical regulation of hormone secretion occurs when endocrine glands are controlled by chemical substances and not the pituitary gland. For example, glucagon and insulin release are controlled by changes in blood glucose level (Scott 2010). The pancreas is stimulated to release insulin and suppress glucagon when levels of blood glucose increase. Conversely, glucagon release and insulin suppression occur when levels of blood glucose fall (Scott 2010). Neural regulation of hormone secretion occurs as a result of several mechanisms. Oxytocin and antidiuretic hormone (ADH) or vasopressin are manufactured by neurosecretory cells of the hypothalamus (Figure 2). Several nervous system stimuli affect levels of ADH. Catecholamine (adrenaline and noradrenaline) secretion from the adrenal medulla is under control of the autonomic nervous system and is released in response to stress and during exercise (Tortora and Derrickson 2012). When hormones are released, they are transported to their target cells. Particular hormones bind to specific receptor cells on the cell wall membrane or within the cell walls. Polypeptides and amino acids bind to the cell wall membrane, whereas smaller, more lipid soluble steroids and thyroid hormones bind to receptors within the cells (Scott 2010). The number of receptors on a target cell ranges from 2,000-100,000 for a particular hormone (Tortora and Derrickson 2012). Activation of the target
FIGURE 2 Hypothalamus and pituitary gland Hypothalamus
Posterior pituitary
Paraventricular nucleus
Neurosecretory cell
Infundibulum Anterior pituitary
Sphenoid bone
PETER LAMB
Hypophyseal portal system
cell is affected by the amount of hormone in the blood, the number of receptors on the cell and the sensitivity of the receptor to the hormone (Clare 2011). When the hormone molecules bind to the receptors, they produce a variety of hormonal effects, depending on the hormone and target cells. These effects include (Clare 2011): 4Changes in the permeability of the cell membrane to specific substances. 4Regulation of the manufacture of proteins. 4Activation and de-activation of enzymes. 4Initiation of secretory activity. 4Stimulation of mitosis. All hormones are eventually inactivated by enzymes in the liver, kidneys, blood or target cells. They are removed from plasma through metabolic destruction or binding with tissues and excreted mainly via the urinary system (Sherwood 2012), some are excreted in faeces (Clare 2011). Endocrine function can be assessed by measuring the concentrations of hormones in urine and their breakdown products if liver and kidney function are normal (Sherwood 2012). For example, the presence of the hormone human chorionic gondadotrophin in urine has been the basis of pregnancy testing for many years.
Hypothalamus and pituitary gland The hypothalamus is a small area situated below the thalamus in the brain, and is connected directly to the pituitary gland by a stalk called the infundibulum (Figure 2) (Clare 2011). The hypothalamus connects the nervous and endocrine systems (Tortora and Derrickson 2012). The pituitary gland is situated in a shallow depression of the sphenoid bone, known as the sella turcica, behind the area where the optic nerves cross (Cohen 2013). It is approximately the size and shape of a pea (Waugh and Grant 2010) and is divided into anterior and posterior lobes (Figure 2). The anterior pituitary, also known as the adenohypophysis, comprises approximately 75% of the total weight (0.5g) of the gland. The posterior pituitary is known as the neurohypophysis (Tortora and Derrickson 2012). The anterior pituitary is composed of epithelial tissue whereas the posterior pituitary is composed of neural tissue. The lobes have different functions and are controlled differently by the hypothalamus. The hormonal response in the posterior pituitary is triggered by an action potential originating in the cell body in the hypothalamus and moving down the axon of the neurone to the axon terminal in the posterior pituitary, thereby following a
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nerve pathway (Sherwood 2012). The anterior pituitary connects to the hypothalamus by a portal system, which ensures that hormones are circulated directly to the anterior pituitary without travelling through the general circulation first. Therefore, blood from the capillaries in the hypothalamus flows into portal veins that carry blood to capillaries in the anterior pituitary (Tortora and Derrickson 2012). The hypothalamus secretes nine hormones, seven of which stimulate hormones in the anterior pituitary (Sherwood 2012) (Table 1). These hypothalamic hormones are called inhibiting or releasing hormones (Scott 2010). Dopamine or prolactin-inhibiting hormone is the same as the neurotransmitter found in the basal nuclei, thus highlighting the close relationship between the endocrine and nervous systems (Sherwood 2012). The hormones from the anterior pituitary are released into a second capillary network, which drains into the general circulation where they travel to target tissues and bind to receptors where they take effect. Release of hormones from the anterior pituitary depends on two mechanisms. The first mechanism is the release of stimulatory or inhibitory hormones from the hypothalamus, which have a regulatory effect on the release of hormones from the anterior pituitary. The second mechanism involves negative feedback (Tortora and Derrickson 2013). Two hormones, oxytocin and ADH, synthesised in the hypothalamus are stored in the posterior pituitary until they are required (Cohen 2013). The posterior pituitary does not synthesise hormones. More than 10,000 hypothalamic secretory neurones have their axons and axon terminals in the posterior pituitary (Jenkins and Tortora 2013). When the hormones are produced in the neurosecretory cells of the hypothalamus, they are stored in secretory granules and moved to the axon terminals in the posterior pituitary ready for release by exocytosis (Figure 2), which is triggered by nerve impulses (Tortora and Derrickson 2012). Oxytocin has an effect on two target tissues: the uterus and breasts of a mother during and after childbirth. Oxytocin is released in response to the cervix of the uterus stretching during delivery of the baby. It acts on smooth muscle in the uterus wall causing it to contract (Tortora and Derrickson 2012). It also stimulates the release of milk from the mammary glands when an infant suckles (Sherwood 2012). ADH conserves water during formation of urine in the kidneys (Sherwood 2012). Urine output will increase substantially if ADH is not
present and to the detriment of health. ADH also reduces the amount of water lost through sweating, and it causes arterioles to constrict which in turn increases blood pressure (BP) (Tortora and Derrickson 2012). The role of ADH is important when there is a decrease in blood volume caused by dehydration, haemorrhage, diarrhoea or excessive sweating. When osmoreceptors in the hypothalamus identify a rise in the osmotic pressure of the blood and a decrease in blood volume (Sherwood 2012), they activate the neurosecretory cells in the hypothalamus, which in turn causes the release of ADH from the posterior pituitary (Simmons 2010). ADH is transported via the blood to the kidneys, sweat glands and smooth muscle in the blood vessel walls. Water loss is slowed by the actions of ADH on the kidneys and sweat glands. Smooth muscle in blood vessel walls contract, narrowing the lumen of the vessels and increasing BP. Osmoreceptors are inhibited when the osmotic pressure is low and the blood volume is raised, causing a reduction in the secretion of ADH (Tortora and Derrickson 2012). Typically, diabetes insipidus is caused by a failure of ADH secretion (neurogenic diabetes insipidus), and nephrogenic diabetes insipidus can also occur if the renal tubules become resistant to ADH (Alexander et al 2006). If there is a reduction in the amount of ADH produced by the hypothalamus, excess amounts of dilute urine are produced, leading to diabetes insipidus (Ball 2009).
TABLE 1 Hypothalamic hormones and their actions on anterior pituitary hormones Hypothalamic hormone
Action
Thyrotropin-releasing hormone
Stimulates the release of thyrotropin (thyroid-stimulating hormone (TSH)) and prolactin
Corticotropin-releasing hormone
Stimulates the release of corticotropin
Gonadotropin-releasing hormone
Stimulates the release of folliclestimulating hormone and luteinising hormone (gonadotropins)
Growth hormone-releasing hormone
Stimulates the release of growth hormone
Somatostatin (growth hormone-inhibiting hormone)
Inhibits the release of growth hormone and TSH
Prolactin-releasing hormone
Stimulates the release of prolactin
Dopamine (prolactin-inhibiting hormone)
Inhibits the release of prolactin
(Sherwood 2012)
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Art & science life sciences: 24 The common signs and symptoms of this condition are polydipsia, polyuria and dehydration. When other causes of these symptoms are ruled out, treatment aims to maintain fluid and electrolyte balance. Drug treatment is dependent on the underlying cause of diabetes insipidus.
Thyroid gland The butterfly-shaped thyroid gland has two lobes, one on each side of the trachea below the level of the larynx. The lobes are connected by a narrow piece of tissue called the isthmus (Scott 2010). The gland is encased in a capsule consisting of connective tissue (Cohen 2013), weighs approximately 30g and is the only endocrine gland to store large quantities of its secretory products, a supply lasting approximately 100 days (Tortora and Derrickson 2012). The thyroid gland moves during swallowing because of fascia that bind it to the larynx (Raisbeck 2009). Both lobes function as one unit, and produce tetra-iodothyronine or thyroxine (T4), tri-iodothyronine (T3) and calcitonin. T3 contains three iodine molecules while T4 contains four iodine molecules (Cohen 2013). The thyroid gland is made up of numerous microscopic spherical follicles surrounded by capillaries (Clare 2011) and this gives the gland its high vascularity (Carson 2009). The follicles are composed of single layers of epithelial cells containing a lumen filled with colloid. Thyroglobulin with attached iodine molecules is a precursor to the thyroid hormones and is the main constituent of the colloid containing the thyroid hormones in varying stages of synthesis (Sherwood 2012). Between the follicles are parafollicular cells that produce calcitonin (Tortora and Derrickson 2012). Tyrosine is an amino acid that is necessary for the formation of the thyroid hormones. Adequate tyrosine is manufactured in the body, therefore it is not required in the diet, however iodine is required for the formation of thyroid hormones and is required in the diet in the form of iodide. Iodide can be found in table salt, seafood, milk and vegetables grown in iodine-rich soil (Carson 2009). Iodide is converted in the follicle cells to iodine and then linked to tyrosine molecules to create T3 and T4 (Clare 2011). The thyroid hormones are lipid soluble and are able to diffuse through the plasma membrane into the interstitial fluid and bloodstream. T3 is normally secreted in lower quantities than T4, however when T4 enters a body cell it is converted to T3. Most of the hormones are transported in the bloodstream combined with a transport protein called thyroxine-binding globulin (Tortora and
Derrickson 2012). When blood levels of T3 and T4 are low or the metabolic rate is slowed, the hypothalamus is stimulated to produce TRH. TRH enters the portal system and reaches the anterior pituitary where it stimulates the production of TSH. TSH in turn stimulates the thyroid follicles in the thyroid gland to release T3 and T4 into the bloodstream until the metabolic rate returns to normal. A raised level of T3 inhibits the release of TRH and TSH (Tortora and Derrickson 2012). Thyroid hormones do not have any discrete target organs, but they affect almost all tissues of the body because they are the body’s major metabolic hormones (Sherwood 2012). However, they do not have an effect on the adult brain, spleen, testes, uterus or thyroid gland (Clare 2011). Thyroid hormones are necessary for many functions, including (Jenkins and Tortora 2013): 4Regulation of metabolism and heat production. During metabolism, thyroid hormones stimulate protein synthesis and increase the use of glucose and fatty acids for the production of heat. They increase lipolysis and enhance cholesterol secretion, in turn reducing cholesterol levels. 4Regulation of the rate of oxygen consumption and energy expenditure. 4Enhancement of some actions of catecholamines adrenaline and noradrenaline. By increasing the heart’s responsiveness to a catecholamine, the hormones increase the heart rate and force of its contractions. 4Normal development of the nervous and musculoskeletal systems together with human growth hormone and insulin. The actions of thyroid hormones are slow. The response to an increase in thyroid hormone is detectable after a delay of several hours and the maximal response is not evident for several days. The duration of the response is also long (Sherwood 2012), with the half-life of T4 being approximately seven days and the half-life of T3 being one day (Irizarry et al 2014). Thyroid hormones are broken down in the liver and skeletal muscle, and most of the iodine is recycled although some is lost in urine and faeces. There is some debate about the function of calcitonin. According to Cohen (2013), there is no evidence that it is important in humans nor does a deficiency of calcitonin lead to disease. However, Scott (2010) and Tortora and Derrickson (2012) stated that it is useful in the maintenance of blood calcium levels. The synthetic form of calcitonin can be used in the management of osteoporosis (British National Formulary (BNF) 2012).
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Parathyroid glands There are four parathyroid glands, usually situated at each corner of the thyroid gland, and they are the smallest known endocrine glands in the body (Scott 2010). The parathyroid glands function as a single unit producing parathyroid hormone (PTH), with the target cells of PTH being in the bones and kidneys (Clare 2011). The functions of PTH are to regulate the amount of calcium, magnesium and phosphate in the blood (Tortora and Derrickson 2012). PTH raises blood calcium and magnesium by slowing loss through the kidneys. At this time, PTH increases the loss of phosphates in the urine, therefore decreasing phosphate levels and increasing calcium and magnesium levels in the blood. PTH also promotes calcium release from bone tissue, increasing the amount of circulating calcium in the blood (Tortora and Derrickson 2012). Control of PTH levels is via negative feedback based on the amount of calcium circulating in the blood. Low circulating calcium increases the secretion of PTH. Calcitriol is released from the kidneys in response to a reduction of calcium in the blood (Clare 2011). It is the active form of vitamin D and is modified in the liver and then the kidneys (Cohen 2013). Calcitriol stimulates the absorption of calcium from the digestive tract to raise blood calcium levels. Therefore, PTH and calcitriol work together to regulate the amount of calcium in the blood (Cohen 2013). It also inhibits the release of calcitonin from the thyroid gland (Clare 2011). However, when calcitriol levels are high enough, it inhibits the release of PTH, preventing an uncontrolled increase of calcium in the blood. Calcium is important in the maintenance of healthy bones and teeth, and it is also important in the transmission of nerve impulses and muscle contraction (Clare 2011). If there is a lack of PTH production resulting in inadequate levels of calcium ions in the blood, muscular spasms involving particularly the hands and face can occur – this is called tetany. If too much PTH is produced, calcium is released from bone tissue. Calcium loss from bone tissue will lead to bones that are weaker and more likely to fracture. In addition, there will be excess calcium in the kidneys leading to an increased risk of kidney stone formation (Jones and Huether 2006).
Disorders of the thyroid The two most common disorders associated with the thyroid gland are hypothyroidism and hyperthyroidism. Thyroid disease is ten times more common in women than men
(Warren 2006). The signs and symptoms of hypothyroidism and hyperthyroidism relate to the effects of the thyroid hormones on the different tissues in the body.
Hypothyroidism
Hypothyroidism can occur in both infants and adults. Congenital hypothyroidism occurs when the thyroid gland does not form sufficiently during fetal development, resulting in significant deficiency or absence of thyroid hormones. In the absence of treatment, infants will experience impaired growth and mental development (Cohen 2013). Neonatal screening for hypothyroidism occurs in most developed countries. A sample of blood is taken from the infant between five and seven days after birth and tested for T4 levels and TSH. If the infant is found to have a deficiency, he or she will be treated with thyroid hormone replacement therapy to reduce the risk of permanent cognitive deficits. In adults, hypothyroidism is commonly caused by the progressive autoimmune disorder Hashimoto’s disease. It is characterised by the production of antibodies in response to thyroid antigens, resulting in the destruction of thyroid tissue. Other causes of hypothyroidism include the destruction of thyroid tissue as a result of (Carson 2009, Sherwood 2012, Cohen 2013): 4Surgery for hyperthyroidism. 4Surgery or radiation treatment for cancer. 4Deficiency of TSH and/or TRH. 4Inadequate dietary intake of iodine. 4Some drugs, including lithium carbonate to treat bipolar disorders or amiodarone to treat arrhythmias. The signs and symptoms of hypothyroidism can be vague (Box 1) and the disorder is not always identified at an early stage. Diagnosis is made following a blood test for thyroid function, which will usually indicate a
BOX 1 Signs and symptoms of hypothyroidism 4Constipation. 4Depression. 4Dry skin and hair. 4Fatigue. 4Heavy or irregular menstrual periods. 4Myxoedema of the face, hands and feet. 4Poor tolerance to cold. 4Slow mental responsiveness. 4Slow reflexes. 4Slow, weak pulse. 4Weight gain. (Howlett and Levy 2009)
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Art & science life sciences: 24 raised TSH and low T4 levels. Hypothyroidism is treated with levothyroxine, a synthetic form of thyroxine. It should be taken once daily before breakfast for life (BNF 2012). Symptoms should improve after two to three weeks of treatment and thyroid function needs to be monitored regularly (initially every three to four weeks) to ensure the dose of levothyroxine is adequate.
Hyperthyroidism
Hyperthyroidism occurs when the thyroid gland produces excess thyroid hormones. It is also known as Graves’ disease. It may be accompanied by a goitre (Figure 3), which is uniform overgrowth of the thyroid gland with a smooth surface (Cohen 2013). Hyperthyroidism
FIGURE 3
SCIENCE PHOTO LIBRARY
A patient with a goitre
BOX 2 Signs and symptoms of hyperthyroidism 4Exophthalmos. 4Fatigue. 4Increased bowel frequency or diarrhoea. 4Insomnia. 4Irritability, tenseness and anxiety. 4Lack of concentration. 4Muscle weakness. 4Poor tolerance to heat and increased perspiration. 4Reduced menstrual flow. 4Tachycardia and/or palpitations. 4Tremor. 4Weight loss with or without increased appetite. (Howlett and Levy 2009)
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is also an autoimmune disorder in which thyroid stimulating immunoglobulin (TSI) is produced and targets TSH receptors on the thyroid cells. TSI stimulates secretion and growth of TSH, but there is no negative feedback control of TSI. Signs and symptoms of hyperthyroidism are listed in Box 2. For individuals with hyperthyroidism, thyroid blood function tests, usually demonstrate low TSH and increased T4 levels. There are three treatment options for hyperthyroidism that are used singly or in combination depending on the severity of the disorder. The first option is to administer antithyroid medication, which inhibits the synthesis of thyroid hormones. The drug most commonly used is carbimazole, with propylthiouracil being reserved for patients who are intolerant of carbimazole, or who are pregnant or breastfeeding. Therapy is usually administered for approximately 12-18 months (BNF 2012). The second option involves administration of radioactive iodine in the form of a single dose of iodine 131 to severely restrict or destroy some thyroid tissue, thereby reducing the amount of T4 produced. If unsuccessful, it may be administered again. It may be necessary to administer antithyroid drugs before and after treatment with iodine 131. Because the thyroid gland stores up to 100 days’ supply of thyroid hormones, some of the hormones can be released, causing what is termed a thyroid storm (crisis). Hormone replacement therapy may be necessary if treatment using radioactive iodine results in the person developing hypothyroidism (Howlett and Levy 2009). The third option for treatment is surgery, where all or part of the thyroid gland is removed. However, patients require close monitoring post-surgery because complications may include (Furtado 2011): 4Bleeding. 4Nerve injury. 4Lymphatic structure injury. 4Secondary hypoparathyroidism – underactive parathyroid function as a result of the removal of the parathyroid glands during surgery to remove the thyroid gland. 4Thyroid storm. Nursing management is aimed at detecting and minimising these complications. Following surgery, the patient should be nursed in an upright position with support for the neck to reduce strain on the incision and enhance comfort. The patient’s temperature, pulse, BP, respiration rate and pulse oximetry should be monitored frequently. A fall in BP with a rise in pulse rate may be indicative of haemorrhage. Should bleeding compress the airways, immediate
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removal of the clips holding the wound edges together may be necessary. Dressings and drains should be checked for any signs of bleeding. Inspiratory stridor or tachypnoea may be indicative of damage to the laryngeal nerve (Alexander et al 2006).
deficits in endocrine function. While some patients with such deficits may be cared for in specialist units, others will be cared for in general medical and surgical wards. Similarly, community nursing staff are increasingly caring for patients with long-term endocrine deficits such as diabetes mellitus NS
Conclusion
GLOSSARY
In this first of two articles on the endocrine system, the focus has been on providing an overview of the system before considering the hypothalamus and the pituitary gland and the thyroid and parathyroid glands. Understanding the structure and function of the endocrine system will enable the nurse to care more effectively for patients who may be experiencing
Exocytosis A process in which membrane-enclosed secretory vesicles form inside the cell, fuse with the plasma membrane and release their contents into the interstitial fluid. Leucotrienes Compounds that produce allergic and inflammatory reactions similar to histamine. Osmoreceptors Specialised neurones in the hypothalamus that are stimulated by a rise in osmolality of the extracellular fluid especially when the sodium concentration has risen promoting the release of antidiuretic hormone.
POINTS FOR PRACTICE 4Using a source of your choice, review your knowledge and understanding of what is meant by the term negative feedback mechanism. 4Design a care plan for a patient who is returning from surgery following a partial thyroidectomy. 4Devise a diagram or aide-memoire to assist a student in your practice area to learn about the hormones released from the pituitary gland (anterior and posterior). Reference should also be made to their target tissues and actions.
Prostaglandins Hormone-like substances that participate in a wide range of body functions, including contraction and relaxation of smooth muscle, dilation and constriction of blood vessels, and modulation of inflammation. Thyroid storm (crisis) High levels of thyroid hormone in the bloodstream resulting in worsening signs and symptoms of hyperthyroidism. Body temperature can rise to 41°C.
References Alexander MF, Fawcett JN, Runciman PJ (2006) Nursing Practice: Hospital and Home. The Adult. Third edition. Churchill Livingstone Elsevier, Edinburgh. Ball S (2009) Diabetes insipidus. Medicine. 37, 8, 414-415. British National Formulary (2012) British National Formulary No. 63. BMJ Group and the Royal Pharmaceutical Society of Great Britain, London. Carson M (2009) Assessment and management of patients with hypothyroidism. Nursing Standard. 23, 18, 48-56. Clare C (2011) The endocrine system. In Peate I, Nair M (Eds) Fundamentals of Anatomy and Physiology for Student Nurses.
Wiley-Blackwell, Chichester, 192-223. Cohen BJ (2013) Memmler’s The Human Body in Health and Disease. 12th edition. Lippincott Williams and Wilkins, Philadelphia PA. Furtado L (2011) Thyroidectomy: post-operative care and common complications. Nursing Standard. 25, 34, 43-52. Howlett TA, Levy MJ (2009) Endocrine disease. In Kumar P, Clark M (Eds) Kumar And Clark’s Clinical Medicine. Seventh edition. Saunders Elsevier, Edinburgh, 963-1027. Irizarry L, Youssef NA, Wray AA (2014) Thyroid Hormone Toxicity. emedicine.medscape.com/ article/819692-overview (Last accessed: May 2 2014).
Jenkins GW, Tortora GJ (2013) Anatomy and Physiology. From Science to Life. Third edition. John Wiley and Sons, Hoboken NJ. Jones RE, Huether SE (2006) Alterations of hormonal regulation. In McCance KL and Huether SE Pathophysiology. The Biologic Basis for Disease in Adults and Children. Fifth edition. Elsevier Mosby, St Louis MO. Raisbeck E (2009) Understanding thyroid disease. Practice Nurse. 37, 1, 34-36. Scott WN (2010) Anatomy & Physiology Made Incredibly Easy. Lippincott Williams & Wilkins, London. Sherwood L (2012) Introduction to Human Physiology. Eighth edition. Thomson Brooks/Cole, Australia.
Simmons S (2010) Flushing out the truth about diabetes insipidus. Nursing. 40, 1, 55-59. Tortora GJ, Derrickson BH (2012) Principles of Anatomy and Physiology. 13th edition. John Wiley and Sons, Hoboken NJ. Tortora GJ, Derrickson BH (2013) Essentials of Anatomy and Physiology. International Student Version. Ninth edition. John Wiley and Sons, Hoboken NJ. Warren E (2006) Thyroid disease in primary care. Practice Nurse. 31, 1, 18, 20, 23, 25. Waugh A, Grant A (2010) Ross and Wilson Anatomy and Physiology in Health and Illness. 11th edition. Churchill Livingstone Elsevier, Edinburgh.
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Endocrine system: part 1 Johnstone C et al (2014) Endocrine system: part 1. Nursing Standard. 28, 38, 42-49. Date of submission: December 19 2012; date of acceptance: April 29 2013.
Abstract This article, which forms part of the life sciences series and is the first of two articles on the endocrine system, examines the structure and function of the organs of the endocrine system. It is important that nurses understand how the endocrine system works and its role in maintaining health. The role of the endocrine system and the types, actions and control of hormones are explored. The gross structure of the pituitary and thyroid glands are described along with relevant physiology. Several disorders of the thyroid gland are outlined. The second article examines growth hormone, the pancreas and adrenal glands.
Authors Carolyn Johnstone Lecturer in nursing, School of Nursing and Midwifery, University of Dundee, Dundee, Scotland. Charles Hendry Retired, was senior lecturer, School of Nursing and Midwifery, University of Dundee. Alistair Farley Retired, was lecturer in nursing, School of Nursing and Midwifery, University of Dundee. Ella McLafferty Retired, was senior lecturer, School of Nursing and Midwifery, University of Dundee. Correspondence to: [email protected]
Keywords Endocrine system, homeostatis, hyperthyroidism, hypothalamus, hypothyroidism, pituitary gland, thyroid gland
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THE ENDOCRINE SYSTEM is composed of endocrine glands and hormone-producing tissues, hormones and hormone receptors (Scott 2010). The endocrine glands include the pineal glands, pituitary gland, thyroid gland, parathyroid glands, thymus gland and adrenal glands. Several organs and tissues that secrete hormones are also present and include, for example the hypothalamus, heart, stomach, pancreas, ovaries in females and testes in males (Sherwood 2012) (Figure 1). While the glands and tissues of the endocrine system are mostly separated from each other, they work as an integrated system.
Role of the endocrine system The endocrine glands produce hormones, or chemical messengers, that are secreted into the interstitial fluid, diffuse into blood capillaries and are carried via the circulatory system to target organs (Tortora and Derrickson 2012). The receptors of those target organs are molecules consisting of proteins that bind specifically with hormones to stimulate particular physiological changes in the target cell (Scott 2010). Importantly, the endocrine and nervous systems work collaboratively to manage and co-ordinate other body systems (Cohen 2013). Both systems are involved in maintaining a stable internal environment (homeostasis). The nervous system releases neurotransmitters at nerve synapses that act on specific muscles and glands, and are concerned with rapid changes, while the endocrine system releases hormones involved in slower and more precise adjustments (Tortora and Derrickson 2012). The functions of the endocrine system are to (Sherwood 2012): 4Maintain homeostasis through the regulation of nutrient metabolism, and water and electrolyte balance. 4Regulate growth and production of cells. 4Control the responses of the body to external stimuli, especially stress. 4Control reproduction. 4Control and integrate circulatory and digestive activities in collaboration with the autonomic nervous system.
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Most endocrine hormones circulate in the bloodstream, however some hormones are local hormones, called paracrines, that act on target cells in close proximity or on the same cells that secreted them (autocrines), without first entering the bloodstream (Tortora and Derrickson 2012). Hormones can be grouped according to their molecular structure into polypeptides, steroids, amines and eicosanoids. Polypeptides include hormones from the anterior and posterior pituitary, parathyroid glands and endocrine tissue of the pancreatic gland (Scott 2010). Steroids are derived from steroid cholesterol and include hormones from the adrenal cortex, testes and ovaries. These hormones can be recognised by the ending of ‘sterone’ (Cohen 2013). Amines are derived from amino acids and include thyroid hormones, adrenaline (epinephrine) and noradrenaline (norepinephrine) (Scott 2010). Eicosanoids are derived from arachidonic acid, a polyunsaturated fatty acid, and include prostaglandins and leucotrienes. Biologically, they have a broad range of effects and mediate the inflammatory response and the transmission of pain impulses (Scott 2010). Steroid hormones and thyroid hormones are lipid-soluble. Amine, polypeptide and eicosanoid hormones are water-soluble (Tortora and Derrickson 2012).
Regulation of hormonal secretion Several mechanisms control regulation of hormone secretion, including: 4Hypothalamic regulation through the release of tropic hormones, hormones that have other endocrine glands as their target. 4Regulation through rhythmic variations. 4Chemical regulation. 4Neural regulation. A hormone is released in response to a specific stimulus, for example low levels of thyroxine act as a stimulus to the hypothalamus to increase secretion of thyrotropin-releasing hormone (TRH) which in turn acts on the anterior pituitary causing it to release thyroid-stimulating hormone (TSH). TSH acts on the thyroid gland to increase secretion of thyroxine. The amount of hormone released is usually maintained within a particular range. The pituitary gland and hypothalamus regulate other endocrine glands and their hormones through tropic hormones (Scott 2010). Maintaining hormone secretion within a particular range is achieved through negative feedback. This process occurs when further secretion is controlled by the hormone itself or the result of its action. There is a negative effect
on the endocrine gland to decrease its output when the target organ becomes too active. An example of this mechanism is when the pituitary gland releases TSH that, in turn, stimulates secretion of hormones from the thyroid gland. When blood levels of thyroid hormones increase, negative feedback stops the release of further TSH, slowing the release of thyroid hormones and their blood levels decrease. When the levels of thyroid hormone decrease below the normal range, TSH is released, allowing the process to start again (Cohen 2013). Hormone secretion can also be regulated through rhythmic variations. For example, adrenocortical hormones follow a 24-hour cycle related to the sleep pattern of an individual, and the level of secretion is at its highest before waking, at around 6am, and at its lowest at around midnight (Sherwood 2012). Another example is the menstrual cycle, which follows a monthly cyclical pattern (Cohen 2013).
FIGURE 1 Position of the major endocrine glands in the body Hypothalamus Pineal gland Parathyroid glands (situated behind the thyroid gland)
Pituitary gland
Thyroid gland
Heart
Thymus gland
Stomach
Adrenal glands Pancreas Ovaries in females
Testes in males
PETER LAMB
Types and actions of hormones
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Art & science life sciences: 24 Chemical regulation of hormone secretion occurs when endocrine glands are controlled by chemical substances and not the pituitary gland. For example, glucagon and insulin release are controlled by changes in blood glucose level (Scott 2010). The pancreas is stimulated to release insulin and suppress glucagon when levels of blood glucose increase. Conversely, glucagon release and insulin suppression occur when levels of blood glucose fall (Scott 2010). Neural regulation of hormone secretion occurs as a result of several mechanisms. Oxytocin and antidiuretic hormone (ADH) or vasopressin are manufactured by neurosecretory cells of the hypothalamus (Figure 2). Several nervous system stimuli affect levels of ADH. Catecholamine (adrenaline and noradrenaline) secretion from the adrenal medulla is under control of the autonomic nervous system and is released in response to stress and during exercise (Tortora and Derrickson 2012). When hormones are released, they are transported to their target cells. Particular hormones bind to specific receptor cells on the cell wall membrane or within the cell walls. Polypeptides and amino acids bind to the cell wall membrane, whereas smaller, more lipid soluble steroids and thyroid hormones bind to receptors within the cells (Scott 2010). The number of receptors on a target cell ranges from 2,000-100,000 for a particular hormone (Tortora and Derrickson 2012). Activation of the target
FIGURE 2 Hypothalamus and pituitary gland Hypothalamus
Posterior pituitary
Paraventricular nucleus
Neurosecretory cell
Infundibulum Anterior pituitary
Sphenoid bone
PETER LAMB
Hypophyseal portal system
cell is affected by the amount of hormone in the blood, the number of receptors on the cell and the sensitivity of the receptor to the hormone (Clare 2011). When the hormone molecules bind to the receptors, they produce a variety of hormonal effects, depending on the hormone and target cells. These effects include (Clare 2011): 4Changes in the permeability of the cell membrane to specific substances. 4Regulation of the manufacture of proteins. 4Activation and de-activation of enzymes. 4Initiation of secretory activity. 4Stimulation of mitosis. All hormones are eventually inactivated by enzymes in the liver, kidneys, blood or target cells. They are removed from plasma through metabolic destruction or binding with tissues and excreted mainly via the urinary system (Sherwood 2012), some are excreted in faeces (Clare 2011). Endocrine function can be assessed by measuring the concentrations of hormones in urine and their breakdown products if liver and kidney function are normal (Sherwood 2012). For example, the presence of the hormone human chorionic gondadotrophin in urine has been the basis of pregnancy testing for many years.
Hypothalamus and pituitary gland The hypothalamus is a small area situated below the thalamus in the brain, and is connected directly to the pituitary gland by a stalk called the infundibulum (Figure 2) (Clare 2011). The hypothalamus connects the nervous and endocrine systems (Tortora and Derrickson 2012). The pituitary gland is situated in a shallow depression of the sphenoid bone, known as the sella turcica, behind the area where the optic nerves cross (Cohen 2013). It is approximately the size and shape of a pea (Waugh and Grant 2010) and is divided into anterior and posterior lobes (Figure 2). The anterior pituitary, also known as the adenohypophysis, comprises approximately 75% of the total weight (0.5g) of the gland. The posterior pituitary is known as the neurohypophysis (Tortora and Derrickson 2012). The anterior pituitary is composed of epithelial tissue whereas the posterior pituitary is composed of neural tissue. The lobes have different functions and are controlled differently by the hypothalamus. The hormonal response in the posterior pituitary is triggered by an action potential originating in the cell body in the hypothalamus and moving down the axon of the neurone to the axon terminal in the posterior pituitary, thereby following a
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nerve pathway (Sherwood 2012). The anterior pituitary connects to the hypothalamus by a portal system, which ensures that hormones are circulated directly to the anterior pituitary without travelling through the general circulation first. Therefore, blood from the capillaries in the hypothalamus flows into portal veins that carry blood to capillaries in the anterior pituitary (Tortora and Derrickson 2012). The hypothalamus secretes nine hormones, seven of which stimulate hormones in the anterior pituitary (Sherwood 2012) (Table 1). These hypothalamic hormones are called inhibiting or releasing hormones (Scott 2010). Dopamine or prolactin-inhibiting hormone is the same as the neurotransmitter found in the basal nuclei, thus highlighting the close relationship between the endocrine and nervous systems (Sherwood 2012). The hormones from the anterior pituitary are released into a second capillary network, which drains into the general circulation where they travel to target tissues and bind to receptors where they take effect. Release of hormones from the anterior pituitary depends on two mechanisms. The first mechanism is the release of stimulatory or inhibitory hormones from the hypothalamus, which have a regulatory effect on the release of hormones from the anterior pituitary. The second mechanism involves negative feedback (Tortora and Derrickson 2013). Two hormones, oxytocin and ADH, synthesised in the hypothalamus are stored in the posterior pituitary until they are required (Cohen 2013). The posterior pituitary does not synthesise hormones. More than 10,000 hypothalamic secretory neurones have their axons and axon terminals in the posterior pituitary (Jenkins and Tortora 2013). When the hormones are produced in the neurosecretory cells of the hypothalamus, they are stored in secretory granules and moved to the axon terminals in the posterior pituitary ready for release by exocytosis (Figure 2), which is triggered by nerve impulses (Tortora and Derrickson 2012). Oxytocin has an effect on two target tissues: the uterus and breasts of a mother during and after childbirth. Oxytocin is released in response to the cervix of the uterus stretching during delivery of the baby. It acts on smooth muscle in the uterus wall causing it to contract (Tortora and Derrickson 2012). It also stimulates the release of milk from the mammary glands when an infant suckles (Sherwood 2012). ADH conserves water during formation of urine in the kidneys (Sherwood 2012). Urine output will increase substantially if ADH is not
present and to the detriment of health. ADH also reduces the amount of water lost through sweating, and it causes arterioles to constrict which in turn increases blood pressure (BP) (Tortora and Derrickson 2012). The role of ADH is important when there is a decrease in blood volume caused by dehydration, haemorrhage, diarrhoea or excessive sweating. When osmoreceptors in the hypothalamus identify a rise in the osmotic pressure of the blood and a decrease in blood volume (Sherwood 2012), they activate the neurosecretory cells in the hypothalamus, which in turn causes the release of ADH from the posterior pituitary (Simmons 2010). ADH is transported via the blood to the kidneys, sweat glands and smooth muscle in the blood vessel walls. Water loss is slowed by the actions of ADH on the kidneys and sweat glands. Smooth muscle in blood vessel walls contract, narrowing the lumen of the vessels and increasing BP. Osmoreceptors are inhibited when the osmotic pressure is low and the blood volume is raised, causing a reduction in the secretion of ADH (Tortora and Derrickson 2012). Typically, diabetes insipidus is caused by a failure of ADH secretion (neurogenic diabetes insipidus), and nephrogenic diabetes insipidus can also occur if the renal tubules become resistant to ADH (Alexander et al 2006). If there is a reduction in the amount of ADH produced by the hypothalamus, excess amounts of dilute urine are produced, leading to diabetes insipidus (Ball 2009).
TABLE 1 Hypothalamic hormones and their actions on anterior pituitary hormones Hypothalamic hormone
Action
Thyrotropin-releasing hormone
Stimulates the release of thyrotropin (thyroid-stimulating hormone (TSH)) and prolactin
Corticotropin-releasing hormone
Stimulates the release of corticotropin
Gonadotropin-releasing hormone
Stimulates the release of folliclestimulating hormone and luteinising hormone (gonadotropins)
Growth hormone-releasing hormone
Stimulates the release of growth hormone
Somatostatin (growth hormone-inhibiting hormone)
Inhibits the release of growth hormone and TSH
Prolactin-releasing hormone
Stimulates the release of prolactin
Dopamine (prolactin-inhibiting hormone)
Inhibits the release of prolactin
(Sherwood 2012)
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Art & science life sciences: 24 The common signs and symptoms of this condition are polydipsia, polyuria and dehydration. When other causes of these symptoms are ruled out, treatment aims to maintain fluid and electrolyte balance. Drug treatment is dependent on the underlying cause of diabetes insipidus.
Thyroid gland The butterfly-shaped thyroid gland has two lobes, one on each side of the trachea below the level of the larynx. The lobes are connected by a narrow piece of tissue called the isthmus (Scott 2010). The gland is encased in a capsule consisting of connective tissue (Cohen 2013), weighs approximately 30g and is the only endocrine gland to store large quantities of its secretory products, a supply lasting approximately 100 days (Tortora and Derrickson 2012). The thyroid gland moves during swallowing because of fascia that bind it to the larynx (Raisbeck 2009). Both lobes function as one unit, and produce tetra-iodothyronine or thyroxine (T4), tri-iodothyronine (T3) and calcitonin. T3 contains three iodine molecules while T4 contains four iodine molecules (Cohen 2013). The thyroid gland is made up of numerous microscopic spherical follicles surrounded by capillaries (Clare 2011) and this gives the gland its high vascularity (Carson 2009). The follicles are composed of single layers of epithelial cells containing a lumen filled with colloid. Thyroglobulin with attached iodine molecules is a precursor to the thyroid hormones and is the main constituent of the colloid containing the thyroid hormones in varying stages of synthesis (Sherwood 2012). Between the follicles are parafollicular cells that produce calcitonin (Tortora and Derrickson 2012). Tyrosine is an amino acid that is necessary for the formation of the thyroid hormones. Adequate tyrosine is manufactured in the body, therefore it is not required in the diet, however iodine is required for the formation of thyroid hormones and is required in the diet in the form of iodide. Iodide can be found in table salt, seafood, milk and vegetables grown in iodine-rich soil (Carson 2009). Iodide is converted in the follicle cells to iodine and then linked to tyrosine molecules to create T3 and T4 (Clare 2011). The thyroid hormones are lipid soluble and are able to diffuse through the plasma membrane into the interstitial fluid and bloodstream. T3 is normally secreted in lower quantities than T4, however when T4 enters a body cell it is converted to T3. Most of the hormones are transported in the bloodstream combined with a transport protein called thyroxine-binding globulin (Tortora and
Derrickson 2012). When blood levels of T3 and T4 are low or the metabolic rate is slowed, the hypothalamus is stimulated to produce TRH. TRH enters the portal system and reaches the anterior pituitary where it stimulates the production of TSH. TSH in turn stimulates the thyroid follicles in the thyroid gland to release T3 and T4 into the bloodstream until the metabolic rate returns to normal. A raised level of T3 inhibits the release of TRH and TSH (Tortora and Derrickson 2012). Thyroid hormones do not have any discrete target organs, but they affect almost all tissues of the body because they are the body’s major metabolic hormones (Sherwood 2012). However, they do not have an effect on the adult brain, spleen, testes, uterus or thyroid gland (Clare 2011). Thyroid hormones are necessary for many functions, including (Jenkins and Tortora 2013): 4Regulation of metabolism and heat production. During metabolism, thyroid hormones stimulate protein synthesis and increase the use of glucose and fatty acids for the production of heat. They increase lipolysis and enhance cholesterol secretion, in turn reducing cholesterol levels. 4Regulation of the rate of oxygen consumption and energy expenditure. 4Enhancement of some actions of catecholamines adrenaline and noradrenaline. By increasing the heart’s responsiveness to a catecholamine, the hormones increase the heart rate and force of its contractions. 4Normal development of the nervous and musculoskeletal systems together with human growth hormone and insulin. The actions of thyroid hormones are slow. The response to an increase in thyroid hormone is detectable after a delay of several hours and the maximal response is not evident for several days. The duration of the response is also long (Sherwood 2012), with the half-life of T4 being approximately seven days and the half-life of T3 being one day (Irizarry et al 2014). Thyroid hormones are broken down in the liver and skeletal muscle, and most of the iodine is recycled although some is lost in urine and faeces. There is some debate about the function of calcitonin. According to Cohen (2013), there is no evidence that it is important in humans nor does a deficiency of calcitonin lead to disease. However, Scott (2010) and Tortora and Derrickson (2012) stated that it is useful in the maintenance of blood calcium levels. The synthetic form of calcitonin can be used in the management of osteoporosis (British National Formulary (BNF) 2012).
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Parathyroid glands There are four parathyroid glands, usually situated at each corner of the thyroid gland, and they are the smallest known endocrine glands in the body (Scott 2010). The parathyroid glands function as a single unit producing parathyroid hormone (PTH), with the target cells of PTH being in the bones and kidneys (Clare 2011). The functions of PTH are to regulate the amount of calcium, magnesium and phosphate in the blood (Tortora and Derrickson 2012). PTH raises blood calcium and magnesium by slowing loss through the kidneys. At this time, PTH increases the loss of phosphates in the urine, therefore decreasing phosphate levels and increasing calcium and magnesium levels in the blood. PTH also promotes calcium release from bone tissue, increasing the amount of circulating calcium in the blood (Tortora and Derrickson 2012). Control of PTH levels is via negative feedback based on the amount of calcium circulating in the blood. Low circulating calcium increases the secretion of PTH. Calcitriol is released from the kidneys in response to a reduction of calcium in the blood (Clare 2011). It is the active form of vitamin D and is modified in the liver and then the kidneys (Cohen 2013). Calcitriol stimulates the absorption of calcium from the digestive tract to raise blood calcium levels. Therefore, PTH and calcitriol work together to regulate the amount of calcium in the blood (Cohen 2013). It also inhibits the release of calcitonin from the thyroid gland (Clare 2011). However, when calcitriol levels are high enough, it inhibits the release of PTH, preventing an uncontrolled increase of calcium in the blood. Calcium is important in the maintenance of healthy bones and teeth, and it is also important in the transmission of nerve impulses and muscle contraction (Clare 2011). If there is a lack of PTH production resulting in inadequate levels of calcium ions in the blood, muscular spasms involving particularly the hands and face can occur – this is called tetany. If too much PTH is produced, calcium is released from bone tissue. Calcium loss from bone tissue will lead to bones that are weaker and more likely to fracture. In addition, there will be excess calcium in the kidneys leading to an increased risk of kidney stone formation (Jones and Huether 2006).
Disorders of the thyroid The two most common disorders associated with the thyroid gland are hypothyroidism and hyperthyroidism. Thyroid disease is ten times more common in women than men
(Warren 2006). The signs and symptoms of hypothyroidism and hyperthyroidism relate to the effects of the thyroid hormones on the different tissues in the body.
Hypothyroidism
Hypothyroidism can occur in both infants and adults. Congenital hypothyroidism occurs when the thyroid gland does not form sufficiently during fetal development, resulting in significant deficiency or absence of thyroid hormones. In the absence of treatment, infants will experience impaired growth and mental development (Cohen 2013). Neonatal screening for hypothyroidism occurs in most developed countries. A sample of blood is taken from the infant between five and seven days after birth and tested for T4 levels and TSH. If the infant is found to have a deficiency, he or she will be treated with thyroid hormone replacement therapy to reduce the risk of permanent cognitive deficits. In adults, hypothyroidism is commonly caused by the progressive autoimmune disorder Hashimoto’s disease. It is characterised by the production of antibodies in response to thyroid antigens, resulting in the destruction of thyroid tissue. Other causes of hypothyroidism include the destruction of thyroid tissue as a result of (Carson 2009, Sherwood 2012, Cohen 2013): 4Surgery for hyperthyroidism. 4Surgery or radiation treatment for cancer. 4Deficiency of TSH and/or TRH. 4Inadequate dietary intake of iodine. 4Some drugs, including lithium carbonate to treat bipolar disorders or amiodarone to treat arrhythmias. The signs and symptoms of hypothyroidism can be vague (Box 1) and the disorder is not always identified at an early stage. Diagnosis is made following a blood test for thyroid function, which will usually indicate a
BOX 1 Signs and symptoms of hypothyroidism 4Constipation. 4Depression. 4Dry skin and hair. 4Fatigue. 4Heavy or irregular menstrual periods. 4Myxoedema of the face, hands and feet. 4Poor tolerance to cold. 4Slow mental responsiveness. 4Slow reflexes. 4Slow, weak pulse. 4Weight gain. (Howlett and Levy 2009)
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Art & science life sciences: 24 raised TSH and low T4 levels. Hypothyroidism is treated with levothyroxine, a synthetic form of thyroxine. It should be taken once daily before breakfast for life (BNF 2012). Symptoms should improve after two to three weeks of treatment and thyroid function needs to be monitored regularly (initially every three to four weeks) to ensure the dose of levothyroxine is adequate.
Hyperthyroidism
Hyperthyroidism occurs when the thyroid gland produces excess thyroid hormones. It is also known as Graves’ disease. It may be accompanied by a goitre (Figure 3), which is uniform overgrowth of the thyroid gland with a smooth surface (Cohen 2013). Hyperthyroidism
FIGURE 3
SCIENCE PHOTO LIBRARY
A patient with a goitre
BOX 2 Signs and symptoms of hyperthyroidism 4Exophthalmos. 4Fatigue. 4Increased bowel frequency or diarrhoea. 4Insomnia. 4Irritability, tenseness and anxiety. 4Lack of concentration. 4Muscle weakness. 4Poor tolerance to heat and increased perspiration. 4Reduced menstrual flow. 4Tachycardia and/or palpitations. 4Tremor. 4Weight loss with or without increased appetite. (Howlett and Levy 2009)
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is also an autoimmune disorder in which thyroid stimulating immunoglobulin (TSI) is produced and targets TSH receptors on the thyroid cells. TSI stimulates secretion and growth of TSH, but there is no negative feedback control of TSI. Signs and symptoms of hyperthyroidism are listed in Box 2. For individuals with hyperthyroidism, thyroid blood function tests, usually demonstrate low TSH and increased T4 levels. There are three treatment options for hyperthyroidism that are used singly or in combination depending on the severity of the disorder. The first option is to administer antithyroid medication, which inhibits the synthesis of thyroid hormones. The drug most commonly used is carbimazole, with propylthiouracil being reserved for patients who are intolerant of carbimazole, or who are pregnant or breastfeeding. Therapy is usually administered for approximately 12-18 months (BNF 2012). The second option involves administration of radioactive iodine in the form of a single dose of iodine 131 to severely restrict or destroy some thyroid tissue, thereby reducing the amount of T4 produced. If unsuccessful, it may be administered again. It may be necessary to administer antithyroid drugs before and after treatment with iodine 131. Because the thyroid gland stores up to 100 days’ supply of thyroid hormones, some of the hormones can be released, causing what is termed a thyroid storm (crisis). Hormone replacement therapy may be necessary if treatment using radioactive iodine results in the person developing hypothyroidism (Howlett and Levy 2009). The third option for treatment is surgery, where all or part of the thyroid gland is removed. However, patients require close monitoring post-surgery because complications may include (Furtado 2011): 4Bleeding. 4Nerve injury. 4Lymphatic structure injury. 4Secondary hypoparathyroidism – underactive parathyroid function as a result of the removal of the parathyroid glands during surgery to remove the thyroid gland. 4Thyroid storm. Nursing management is aimed at detecting and minimising these complications. Following surgery, the patient should be nursed in an upright position with support for the neck to reduce strain on the incision and enhance comfort. The patient’s temperature, pulse, BP, respiration rate and pulse oximetry should be monitored frequently. A fall in BP with a rise in pulse rate may be indicative of haemorrhage. Should bleeding compress the airways, immediate
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removal of the clips holding the wound edges together may be necessary. Dressings and drains should be checked for any signs of bleeding. Inspiratory stridor or tachypnoea may be indicative of damage to the laryngeal nerve (Alexander et al 2006).
deficits in endocrine function. While some patients with such deficits may be cared for in specialist units, others will be cared for in general medical and surgical wards. Similarly, community nursing staff are increasingly caring for patients with long-term endocrine deficits such as diabetes mellitus NS
Conclusion
GLOSSARY
In this first of two articles on the endocrine system, the focus has been on providing an overview of the system before considering the hypothalamus and the pituitary gland and the thyroid and parathyroid glands. Understanding the structure and function of the endocrine system will enable the nurse to care more effectively for patients who may be experiencing
Exocytosis A process in which membrane-enclosed secretory vesicles form inside the cell, fuse with the plasma membrane and release their contents into the interstitial fluid. Leucotrienes Compounds that produce allergic and inflammatory reactions similar to histamine. Osmoreceptors Specialised neurones in the hypothalamus that are stimulated by a rise in osmolality of the extracellular fluid especially when the sodium concentration has risen promoting the release of antidiuretic hormone.
POINTS FOR PRACTICE 4Using a source of your choice, review your knowledge and understanding of what is meant by the term negative feedback mechanism. 4Design a care plan for a patient who is returning from surgery following a partial thyroidectomy. 4Devise a diagram or aide-memoire to assist a student in your practice area to learn about the hormones released from the pituitary gland (anterior and posterior). Reference should also be made to their target tissues and actions.
Prostaglandins Hormone-like substances that participate in a wide range of body functions, including contraction and relaxation of smooth muscle, dilation and constriction of blood vessels, and modulation of inflammation. Thyroid storm (crisis) High levels of thyroid hormone in the bloodstream resulting in worsening signs and symptoms of hyperthyroidism. Body temperature can rise to 41°C.
References Alexander MF, Fawcett JN, Runciman PJ (2006) Nursing Practice: Hospital and Home. The Adult. Third edition. Churchill Livingstone Elsevier, Edinburgh. Ball S (2009) Diabetes insipidus. Medicine. 37, 8, 414-415. British National Formulary (2012) British National Formulary No. 63. BMJ Group and the Royal Pharmaceutical Society of Great Britain, London. Carson M (2009) Assessment and management of patients with hypothyroidism. Nursing Standard. 23, 18, 48-56. Clare C (2011) The endocrine system. In Peate I, Nair M (Eds) Fundamentals of Anatomy and Physiology for Student Nurses.
Wiley-Blackwell, Chichester, 192-223. Cohen BJ (2013) Memmler’s The Human Body in Health and Disease. 12th edition. Lippincott Williams and Wilkins, Philadelphia PA. Furtado L (2011) Thyroidectomy: post-operative care and common complications. Nursing Standard. 25, 34, 43-52. Howlett TA, Levy MJ (2009) Endocrine disease. In Kumar P, Clark M (Eds) Kumar And Clark’s Clinical Medicine. Seventh edition. Saunders Elsevier, Edinburgh, 963-1027. Irizarry L, Youssef NA, Wray AA (2014) Thyroid Hormone Toxicity. emedicine.medscape.com/ article/819692-overview (Last accessed: May 2 2014).
Jenkins GW, Tortora GJ (2013) Anatomy and Physiology. From Science to Life. Third edition. John Wiley and Sons, Hoboken NJ. Jones RE, Huether SE (2006) Alterations of hormonal regulation. In McCance KL and Huether SE Pathophysiology. The Biologic Basis for Disease in Adults and Children. Fifth edition. Elsevier Mosby, St Louis MO. Raisbeck E (2009) Understanding thyroid disease. Practice Nurse. 37, 1, 34-36. Scott WN (2010) Anatomy & Physiology Made Incredibly Easy. Lippincott Williams & Wilkins, London. Sherwood L (2012) Introduction to Human Physiology. Eighth edition. Thomson Brooks/Cole, Australia.
Simmons S (2010) Flushing out the truth about diabetes insipidus. Nursing. 40, 1, 55-59. Tortora GJ, Derrickson BH (2012) Principles of Anatomy and Physiology. 13th edition. John Wiley and Sons, Hoboken NJ. Tortora GJ, Derrickson BH (2013) Essentials of Anatomy and Physiology. International Student Version. Ninth edition. John Wiley and Sons, Hoboken NJ. Warren E (2006) Thyroid disease in primary care. Practice Nurse. 31, 1, 18, 20, 23, 25. Waugh A, Grant A (2010) Ross and Wilson Anatomy and Physiology in Health and Illness. 11th edition. Churchill Livingstone Elsevier, Edinburgh.
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