Chapter 39 ENDOCRINE HEALTH
The endocrine system is comprised of a number of small glands, some of which are structurally independent, while others are found within some organs. These glands secrete hormones, which aid in maintaining homeostasis in the body. Over- or under-production of these hormones can have widespread effects on the body because of the relation between the endocrine system and other systems in the body. An understanding of the function of these hormones gives health care professionals the ability to care for individuals with an endocrine disorder.
I was dreaming that I was drinking an ice cold drink of water, it was great, so cool … then I woke up. Oh no, it’s happening again! What is going on with me? I’m just so thirsty all the time. The teachers are getting really tired of me leaving the classroom heaps of times to go to the toilet. The thing is I’m not mucking around. I really do need to go. Plus, I’m so tired now, the thought of doing physical education at school freaks me out and there is no way I want to try out for the netball team, I’m just too tired. God, I’m scared, what if I’m sick? I’m at the fridge getting a cold drink. It’s 4 am. I turn to go back to bed and there is mum … I just start crying.
I knew something was wrong with Emma, and had so many times thought it was just part of growing up — you know, hormonal changes and all that goes with an adolescent girl. I had discussed her continual thirst and tiredness with my friends and none of them seemed to have experienced the same problems with their girls. Now, this person who is a diabetes educator is trying to tell me Emma has diabetes! I don’t believe it! She is my little girl, I feel as if my world is falling apart. I know I have to be strong for Emma but I faint at the sight of blood and the nurse is talking about injections and blood tests … I just don’t understand — what have I done wrong?
As a diabetes educator I am often faced with this situation when adolescents are diagnosed with type I diabetes. The experiences often involve parents feeling they have failed the child and done something wrong, and the child often feels as if their life is now virtually over. As these individuals are going to be dealing with diabetes now for life, an extensive education including family support is paramount to their continuing holistic health. That is where I come in.
A hormone is a chemical substance secreted into the blood by an endocrine gland (Figure 39.1). The hormone is transported via the blood to areas of the body where it is needed to stimulate a specific cellular activity. Target organs are those that respond to a particular hormone. Some hormones can control other hormones by influencing their action, metabolism, synthesis and transport. A hormone can be described as a chemical regulator that integrates and coordinates cellular activities. Hormones are either steroids or proteins, and only target cells have the ability to respond to a specific hormone. After entering the blood, some hormones become bound to plasma proteins, while others are transported in an unbound state. Most hormones are continuously secreted at a rate determined by stimulation of the gland that releases them. Table 39.1 lists all the major hormones.
The pituitary gland is about the size of a grape and is positioned at the base of the brain in a depression in the sphenoid bone. It lies just beneath the hypothalamus, to which it is connected by a stalk containing blood vessels and nervous tissue. It has two functional lobes: the anterior lobe comprised of glandular tissue, and the posterior lobe comprised of nervous tissue. Each lobe performs specific functions.
Hyper-function of the anterior pituitary gland commonly results from a tumour, which creates pressure on cerebral structures and causes neurological manifestations, such as severe headaches and visual disturbances, or excessive secretion of pituitary hormones, with consequent increased stimulation of the target organs. It is a chronic progressive disorder marked by hormonal dysfunction and skeletal overgrowth, which can appear in two forms: gigantism and acromegaly.
Gigantism occurs in childhood and begins before epiphyseal closure. Children with gigantism may grow up to 15 cm a year, have slow sexual development and may have slow mental development. Gigantism is often the result of a tumour growing on the pituitary gland. Radiation therapy, surgical removal of the tumour and drug therapy may be used to decrease secretion of the growth hormone and slow down the excessive growth pattern. With this treatment, prognosis for the individual with gigantism is generally good.
Acromegaly occurs in adulthood and develops after epiphyseal closure. In acromegaly, over-secretion of growth hormone (GH) causes atrophy of skeletal muscle and formation of new bone and cartilage. The long bones are unable to grow in length, but the smaller bones of the hands, feet and face grow, giving the individual a characteristic appearance, with an enlarged lower jaw, bulging forehead and thickened ears and nose. The extremities become elongated and enlarged, resulting in large hands and feet. Thickening of the tongue may cause the voice to sound deep and hollow, associated with slurred speech. Acromegaly is a chronic disfiguring disease that often shortens life expectancy, as it may lead to respiratory, cerebrovascular and congestive heart diseases. Surgical intervention to remove the pituitary tumour often leads to hypopituitarism, and the tumours tend to recur.
Hypofunction of the anterior pituitary gland can also result from a tumour in the gland, or it can be secondary to trauma of the hypothalamus. Other causes of hypofunction include disorders such as sarcoidosis, and infections such as tuberculosis or brucellosis. Hypopituitarism results in an absence or deficiency of growth hormone and gonadotrophin and is marked by growth retardation, which in children causes dwarfism and delay of puberty. It can present in three forms:
Damage to the posterior lobe of the pituitary gland can result in decreased or increased secretion of ADH. Diabetes insipidus is a rare condition caused by posterior lobe damage, and results from a deficiency of ADH. This results in the kidney tubules failing to reabsorb water. Without antidiuretic hormone, the individual has polyuria, passing vast quantities of dilute, colourless urine, up to 30 L in 24 hours. To compensate for the dehydration from the excessive fluid loss the individual experiences polydipsia (excessive thirst) and drinks large amounts of fluid. Treatment for people with diabetes insipidus involves medication such as vasopressin, which has a good prognosis. During the acute stage of this condition, clients need supportive care in relation to their polyuria and increased need for fluids.
Pituitary function may be assessed by estimating the level of trophic hormones and by measuring the response to stimulation or suppression tests. The most common tests for evaluating anterior pituitary function are the serum growth hormone test and the insulin intolerance test. The insulin intolerance test, also called the growth hormone stimulation test, provides information about the secretion of growth hormone and ACTH. Investigations may also include X-ray or computerised tomography (CT) scan of the skull.
Testing posterior pituitary function includes the water-deprivation test, which is performed when the client’s symptoms indicate diabetes insipidus. This test is based on the principle that withholding fluid for several hours stimulates secretion of ADH. In a person suspected of having diabetes insipidus, the urine may be tested to determine specific gravity. A low specific gravity is suggestive of diabetes insipidus.
The thyroid gland lies in the neck just below the larynx. It consists of two lateral lobes positioned either side of the trachea. The lobes are joined together by a central mass called the isthmus, which lies anteriorly across the trachea. The thyroid gland is covered by a connective tissue capsule that forms trabeculae, which then pass inwards and divide the gland into lobes. The thyroid gland produces:
Hyperthyroidism (also referred to as thyrotoxicosis) is hyper-functioning of the thyroid gland and may be caused by many factors, such as thyroiditis or an overproduction of thyroid stimulating hormone (TSH). An increase in the secretion of thyroid hormones affects the basal metabolic rate, as well as the functions of other body systems. The manifestations of hyper-functioning are generally related to increased metabolic processes. The condition can be caused by genetic or immunological factors, thyroid gland nodules or chronic inflammation of the thyroid gland.
An autoimmune disorder, Graves’ disease is a common hyperthyroid disease. Antibodies stimulate the thyroid gland, leading to glandular hypertrophy. Graves’ disease more commonly affects young women. Symptoms include all the characteristics of hyperthyroidism — tachycardia, nervousness, hyperactivity and excitability. The individual will have a voracious appetite but loses weight and can be quite underweight. Diarrhoea is common, as peristaltic rate increases. Excessive sweating and extreme thirst are also common, because of the increased metabolic rate. One outstanding characteristic of Graves’ disease is that of exophthalmos, or protrusion of the eyeballs, which is due to oedema in the tissues behind the eye, and does not resolve even when the hyperthyroidism is corrected. A serious complication of Graves’ disease is thyroid storm (or crisis), which is discussed in Clinical Interest Box 39.1.
CLINICAL INTEREST BOX 39.1 Thyroid storm, or thyroid crisis
This situation occurs in a person with advanced hyperthyroid disease. A thyroid crisis can be instigated by emotional stress, infection, trauma, cardiovascular disease or after thyroid surgery, and results from a sudden release of thyroid hormone into the bloodstream. This causes a sudden increase of the symptoms of hyperthyroidism and is considered a medical emergency, as the severe tachycardia, tachypnoea and increase in body temperature can be life-threatening.
The thyroid gland can become enlarged, hyperactive or hypoactive as a result of pathophysiological changes. An enlarged thyroid gland may be the result of a simple goitre, thyroiditis or neoplasia. Goitre refers to any thyroid enlargement and may be associated with either over-secretion or under-secretion of thyroid hormones. Goitre can cause local problems by exerting pressure on the trachea, which may produce dysphagia or respiratory distress. Simple goitre (non-toxic goitre) is due to an iodine deficiency that causes a compensatory enlargement of the thyroid gland in an attempt to maintain thyroid hormone production. Endemic goitre occurs in regions away from coastal areas, where there is little iodine in the soil and water. The introduction of iodised salt has reduced the incidence in most Western countries. Exopthalmic goitre occurs in hyperthyroidism.
Management of hyperthyroidism involves assisting the individual and their family to manage the symptoms associated with hyperthyroidism until it is controlled with medication, or surgery if indicated. Surgical intervention may involve a subtotal thyroidectomy, which removes part of the thyroid gland, leaving enough gland to produce adequate thyroid hormone, or a total thyroidectomy may be performed if the gland is cancerous. A person who has had a total thyroidectomy requires long-term hormone replacement. The critical pathway in Table 39.2 outlines the nursing care of a client undergoing thyroidectomy surgery.
Hypothyroidism is characterised by a decreased secretion of thyroid hormones. Hypothyroidism may be congenital or it may develop later in life. Cretinism is the congenital form of hypothyroidism and results from absence or underdevelopment of the thyroid gland or it may occur from severe maternal iodine deficiency during pregnancy. The manifestations of cretinism are related to a marked depression of metabolic processes and progressive mental impairment. Typically the infant is overweight, lethargic, has dry thick skin, coarse features, a broad flat nose and protruding tongue and abdomen. If the disease goes unchecked, sexual organs fail to develop and muscle growth is retarded. Treatment is started as soon as diagnosis is made and involves lifelong thyroid hormone replacement therapy (HRT).
Myxoedema is acquired hypothyroidism and develops when the thyroid gland stops functioning effectively. Hypo-thyroidism can also result from surgical intervention used to correct hyperthyroidism. The most common natural cause of hypothyroidism is an autoimmune disorder, Hashimoto’s disease. Symptoms of hypothyroidism are the opposite of those of hyperthyroidism. The individual is fatigued, drowsy, sensitive to cold temperatures, gains excessive weight, has thin nails and brittle hair, decreased pulse and respiratory rates and irregular menstruation. Hypothyroidism responds well to HRT and symptoms may disappear after a few months of treatment.
A combination of tests is generally performed to evaluate thyroid function, including direct tests of thyroid function, tests that measure concentration and binding of the thyroid hormones and tests involving the use of scanning or imaging techniques. Blood tests are performed to measure serum hormone levels, which assist in the diagnosis of hyperthyroidism and hypothyroidism. Radioactive iodine tests, such as the radioactive iodine uptake test, evaluate thyroid function by measuring the amount of orally ingested iodine that accumulates in the thyroid gland after 2, 6 and 24 hours. Thyroid scanning is visualisation of the thyroid gland after administration of a radioisotope. Thyroid ultrasonography helps evaluate thyroid structure and differentiation between a cyst and a tumour on the thyroid gland.
The parathyroids are four small glands embedded in the posterior surface of each lobe of the thyroid gland. The parathyroid glands produce parathyroid hormone (PTH), also referred to as parathormone, which is primarily responsible for the regulation of blood calcium and phosphate levels. Parathormone promotes the reabsorption of calcium into the blood after destruction of bone cells (osteoclasts) and inhibits the reabsorption of phosphate in the renal tubules.
Hyperparathyroidism involves hyper-functioning of the parathyroid glands resulting in an overproduction of PTH. This condition can be caused by hereditary factors, tumours or enlargement of the glands. Secondary hyper-functioning can be caused by renal disease, osteomalacia or rickets. Excessive parathormone production causes hypercalcaemia (excessive calcium in the blood). As the calcium is pulled from the bones, individuals with this condition display manifestations that are widespread and include symptoms such as backache, bone curvature and pathological fractures from bone weakness. Renal stones may develop because of the high calcium output in the urine. The digestive system increases absorption of calcium, causing abdominal pain, vomiting and constipation. Hypercalcaemia leads to hyperactivity of muscles, causing impaired neuromuscular coordination and cardiac arrhythmias.
Treatment of hyperparathyroidism is directed at the cause and often results in good prognosis for the client. Surgical removal of tumours or removal of the parathyroid glands may be necessary, leaving half of one parathyroid gland, which is all that is required to maintain normal parathormone levels. Other treatments include diuretic therapy to force increased excretion of calcium by the kidneys, and decreasing calcium intake in the diet.