Art & science life sciences: 25

Endocrine system: part 2 Hendry C et al (2014) Endocrine system: part 2. Nursing Standard. 28, 39, 43-48. Date of submission: April 15 2013; date of acceptance: June 17 2013.

Abstract This article, the last in the life sciences series, is the second of two articles on the endocrine system. It discusses human growth hormone, the pancreas and adrenal glands. The relationships between hormones and their unique functions are also explored. It is important that nurses understand how the endocrine system works and its role in maintaining health to provide effective care to patients. Several disorders caused by human growth hormone or that affect the pancreas and adrenal glands are examined.

Authors Charles Hendry Retired, was senior lecturer, School of Nursing and Midwifery, University of Dundee, Dundee, Scotland. Alistair Farley Retired, was lecturer in nursing, School of Nursing and Midwifery, University of Dundee, Dundee. Ella McLafferty Retired, was senior lecturer, School of Nursing and Midwifery, University of Dundee, Dundee. Carolyn Johnstone Lecturer in nursing, School of Nursing and Midwifery, University of Dundee, Dundee. Correspondence to: [email protected]

Keywords Acromegaly, adrenal glands, diabetes, endocrine system, human growth hormone, pancreas

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THE ENDOCRINE SYSTEM is composed of endocrine glands and hormone-producing tissues, hormones and receptors (Scott 2011). Hormones work as individual units and also work together in certain circumstances. The interdependence of these hormones is identified in this article. Growth hormone, as its name suggests, is responsible for growth in the human body, but it also has an important role in blood glucose control. Hormones released from the pancreas and adrenal glands are responsible for the metabolism of nutrients and for glucose control in certain circumstances.

Human growth hormone Human growth hormone is the most plentiful hormone produced by the anterior pituitary gland in humans (Sherwood 2013). Somatotrophs are cells in the anterior pituitary that secrete human growth hormone for short periods every few hours. This occurs mainly during sleep. Two hypothalamic hormones are responsible for controlling secretion of human growth hormone. The first is growth hormone-releasing hormone (GHRH) and the second is growth hormone-inhibiting hormone (GHIH) or somatostatin (Sherwood 2013). Human growth hormone acts on most tissues in the body, promoting the synthesis of protein, which is vital for growth to occur (Cohen 2013). The hormone promotes the formation and secretion of small protein hormones called insulinlike growth factors (IGFs) (Tortora and Derrickson 2012). The growth-promoting activities of human growth hormone are directly mediated by IGFs. The presence of human growth hormone results in the secretion of IGFs from the liver, skeletal muscles, cartilage, bone and other tissues (Tortora and Derrickson 2012). IGFs also stimulate the uptake of amino acids by cells and protein synthesis (Tortora and Derrickson 2012). IGFs stimulate cells to grow and multiply. During childhood and the teenage years, the effects of IGFs and human growth hormone increase the rate of growth in the skeleton and skeletal muscle (Cohen 2013). In adults, IGFs and human growth hormone maintain muscle and bone mass, and support tissue repair (Tortora and Derrickson 2012). IGFs increase levels of fatty acids in cells by enhancing the breakdown of fat (lipolysis) stored may 28 :: vol 28 no 39 :: 2014 43

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Art & science life sciences: 25 in adipose tissue. Fatty acids can be used as fuel by body cells, preserving glucose for areas of the body unable to store glycogen such as the brain, which must have a continuous supply of glucose (Sherwood 2013). Human growth hormone and IGFs slow the uptake of glucose by most body cells during carbohydrate metabolism and may stimulate glucose release by liver cells. Blood glucose level is a major regulator of GHRH and GHIH secretions. When blood glucose levels are low, the hypothalamus is stimulated to release GHRH, which is circulated to the anterior pituitary by the portal system. GHRH stimulates somatotrophs in the anterior pituitary to release growth hormone. Human growth hormone then stimulates the secretion of IGFs, which increase the breakdown of glycogen in the liver to glucose, resulting in an increase in blood glucose levels. The increase in blood glucose levels above normal inhibits the release of GHRH and stimulates the release of GHIH from the hypothalamus. When GHIH reaches the anterior pituitary, it inhibits the secretion of human growth hormone. Therefore, a decreasing amount of human growth hormone and IGFs slows the breakdown of glycogen in the liver and slows the release of glucose into the bloodstream. Blood glucose, therefore, returns to normal levels. When blood glucose levels fall below normal, the release of GHIH is inhibited and the cycle commences again; this is an example of negative feedback control (Tortora and Derrickson 2012).

Acromegaly Acromegaly is a rare condition affecting approximately six people per 100,000 of the population (NHS Choices 2012). It occurs when there is excess secretion of human growth hormone after adolescence when the epiphyseal plates have closed and further growth in height cannot occur, but the bones of the hands, feet, cheeks and jaws thicken and other tissues enlarge such as the eyelids, lips, tongue and nose (Sherwood 2013). Acromegaly is usually caused by a pituitary adenoma, usually a benign tumour of glandular epithelium, and the signs and symptoms develop slowly over several years (Vance 2010). The signs and symptoms depend on several factors, including age, levels of human growth hormone and IGF, tumour size and delay in diagnosis (Lugo et al 2012), and include: Soft tissue overgrowth. Coarse facial features, such as prominent supraorbital ridge, broad nose and hirsutism. Thickened skin and skin tags. Hyperhidrosis. 44 may 28 :: vol 28 no 39 :: 2014

Cystic acne. Joint pain. Diabetes mellitus. Heart failure. Respiratory failure. Diagnosis is made by measuring human growth hormone and insulin-like growth factor-1 (IGF-1) levels in the blood. People with acromegaly are unable to suppress human growth hormone levels in the presence of a glucose tolerance test, therefore a glucose tolerance test that shows elevated growth hormone and raised IGF-1 levels confirms the diagnosis of acromegaly. A magnetic resonance imaging (MRI) scan may also be used to identify an adenoma in the pituitary gland, which may be the cause of acromegaly (NHS Choices 2012). Options for treatment include (Aghi and Blevins 2009): Pituitary surgery to remove the adenoma. Radiotherapy. Drugs, including somatostatin analogues such as lanreotide or octreotide.

Pancreas The pancreas lies behind the stomach in the C-shaped area of the duodenum. It is approximately 12.5-15.0cm in length and has an excellent supply of capillaries that allow for rapid release of hormones into the bloodstream and target tissues (Clare 2011). The pancreas is both an exocrine and endocrine gland. It acts as an exocrine gland because it produces enzymes that are secreted via a duct into the gastrointestinal tract where they catabolise foodstuffs. It is also an endocrine gland because it secretes hormones that enter the bloodstream directly. The endocrine cells of the pancreas are called pancreatic islets or Islets of Langerhans, and there are one to two million pancreatic islets found in clusters scattered among the acinar cells (Tortora and Derrickson 2012). The pancreatic islets contain alpha, beta, delta and F cells that produce different hormones. Alpha cells produce glucagon, beta cells produce insulin, delta cells produce somatostatin and F cells produce pancreatic polypeptide. Pancreatic polypeptide may be involved in inhibiting the secretion of somatostatin, causing the gallbladder to contract and secreting digestive enzymes from the pancreas (Tortora and Derrickson 2012). Beta cells account for approximately 60% of the pancreatic islets (Sherwood 2013). Insulin secretion from beta cells increases in response to hyperglycaemia. Insulin promotes the transport of glucose across cell membranes, ensuring the cell can metabolise glucose for energy, thereby lowering blood glucose levels (Cohen 2013).

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It also acts on several nutrients, for example, it speeds up synthesis of fatty acids and increases uptake of amino acids, to achieve stable blood glucose levels. It does this by stimulating the production of glycogen from glucose and inhibiting the breakdown of glycogen to glucose. As well as lowering blood glucose levels, insulin lowers levels of fatty acids and amino acids and promotes storage (Sherwood 2013). It does this by promoting their uptake by the cells where they are converted to glycogen, triglycerides and proteins (Sherwood 2013). Glucagon is released from the alpha cells of the pancreatic islets when blood glucose levels are low. Glucagon primarily opposes the actions of insulin. It affects similar metabolic processes as insulin, but in most cases, the actions of glucagon are the opposite of those of insulin. Glucagon promotes the breakdown of glycogen to glucose (glycogenolysis), and it generates glucose from molecules other than carbohydrates, such as amino acids from protein and glycerol from triglycerides in a process known as gluconeogenesis, thereby increasing blood glucose levels (Seeley et al 2008). It promotes lipolysis and inhibits triglyceride synthesis. Glucagon also promotes the conversion of fatty acids to ketone bodies, which may be used as an energy source. It inhibits protein synthesis in the liver and promotes the breakdown of liver protein (Sherwood 2013). Therefore, insulin tends to put nutrients into storage when blood levels of these nutrients are high, especially after a meal, while glucagon promotes catabolism of nutrient stores to keep blood nutrient levels high, particularly blood glucose. Therefore, glucagon increases the blood glucose level while insulin lowers it. When the blood glucose level falls below normal (hypoglycaemia), glucagon acts to increase it. When the blood glucose level is higher than normal (hyperglycaemia), insulin acts to lower it. These actions are achieved through negative feedback. Pancreatic somatostatin produced by delta cells acts on neighbouring cells, where it inhibits the release of insulin from beta cells and glucagon from alpha cells (Tortora and Derrickson 2012). It also acts to inhibit the digestion of nutrients and slows the absorption of nutrients from the gastrointestinal tract (Sherwood 2013). In the anterior pituitary, the effects of somatostatin inhibit the release of human growth hormone (Tortora and Derrickson 2013).

Diabetes mellitus Diabetes mellitus is defined as a metabolic disorder with multiple aetiology. Chronic hyperglycaemia

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is present and the metabolism of carbohydrate, protein and fat are affected as a result of problems with insulin secretion, insulin action or a combination of both (Scottish Intercollegiate Guidelines Network (SIGN) 2010). In the UK, diabetes mellitus affects more than two million people and accounts for approximately 10% of the NHS budget (Doherty et al 2012). There are two main types of diabetes mellitus: type 1 and type 2. Type 2 diabetes accounts for 85-90% of cases and is strongly, although not exclusively, linked to obesity (Hall 2011). The prevalence of diabetes is rising, and many people may be unaware they have the condition because symptoms can sometimes be vague and may be attributed to advancing age (O’Shea 2010). Type 1 diabetes is thought to be caused by autoimmune destruction of beta cells in the pancreas, therefore little or no insulin is produced (Moser et al 2012). Type 2 diabetes can occur when high levels of insulin are circulating in the blood, but insulin is unable to act on its target tissues (insulin resistance) causing blood glucose levels to rise. This results in more insulin being produced to inhibit the rise in blood glucose levels, but the insulin is still unable to act on the target cells. The output of insulin will eventually decrease when the pancreatic islet cells are unable to cope with the amount of insulin required and cease to function (Hall 2011). Diagnosis of diabetes mellitus is confirmed if the fasting venous plasma glucose is equal to or more than 7.0mmol/L and if the venous plasma glucose is 11.1mmol/L at two hours after a 75g oral glucose load in an oral glucose tolerance test (NHS Choices 2013a). Other causes of raised blood glucose relating to pregnancy or cardiovascular disease must be ruled out (SIGN 2010). Glycated haemoglobin (HbA1c) can be used as a diagnostic test for diabetes mellitus where strict quality assurance measures, such as ensuring consistent procedures and test materials thereby leading to greater confidence in the test result, can be used. An HbA1c of 6.5% or 48 mmol/mol is recommended as the cut-off point for diagnosis (NHS Choices 2013a). Signs and symptoms of diabetes mellitus are similar in patients with type 1 and type 2 diabetes. They typically include polydipsia, polyuria and polyphagia. Other features may include nocturia, weight loss, tiredness or lethargy, visual disturbances, irritability, glycosuria and specifically in type 2 diabetes, thrush infections and other recurrent infections such as boils (Gale and Anderson 2009). may 28 :: vol 28 no 39 :: 2014 45

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Art & science life sciences: 25 Management of type 1 diabetes

The usual management of patients with type 1 diabetes is self-measurement of blood glucose levels and regular administration of exogenous insulin. There are several ways of making the administration of insulin easier and less risky for patients. For example, insulin pens that enable an accurate dose of insulin to be administered can be used. Continuous subcutaneous insulin infusion can also be used (Moser et al 2012), and these pumps are useful in treating patients with poor glycaemic control (SIGN 2010).

Management of type 2 diabetes

The usual management of patients with type 2 diabetes is a combination of lifestyle changes and/ or drug administration. Lifestyle changes should include (Gale and Anderson 2009): Measures to achieve weight loss if body mass index is more than 25. Increased exercise levels. Smoking cessation. Blood pressure (BP) monitoring. Reduction in alcohol consumption and salt intake, and improved diet. There are several drugs available to treat type 2 diabetes, including (NHS Choices 2013b): Sulfonylureas such as glibenclamide, which stimulate beta cells to secrete more insulin. Metformin, which suppresses gluconeogenesis, and increases the peripheral use of glucose. Alpha glycosidase inhibitor acarbose blocks enzymes, which digest complex carbohydrates, slowing glucose absorption. Thiazolidinediones, such as pioglitazone, which increase the receptiveness of muscle and fat cells to insulin. Dipeptidylpeptidase-4 (DPP-4) inhibitors or gliptins, such as saxagliptin, which increase insulin secretion and lower glucagon secretion. If the beta cells in the pancreas have degraded to such a state that no insulin is being produced, patients may be commenced on insulin therapy with or without oral medication.

Adrenal glands There are two adrenal glands, one situated on top of each kidney. As a result of their position, they can also be called suprarenal glands (Cohen 2013). They each weigh between 3.5g and 5g, are covered by a connective tissue capsule and have an excellent blood supply (Tortora and Derrickson 2012). The adrenal glands are made up of two separate structures that function as endocrine glands independently: a peripheral 46 may 28 :: vol 28 no 39 :: 2014

area termed the adrenal cortex and a central area termed the adrenal medulla (Scott 2011).

Cortex

The adrenal cortex contains three main areas (Seeley et al 2008): The zona glomerulosa is the outermost zone where cells are closely packed and organised in spherical clusters. This zone produces mineralocorticoids, principally aldosterone. The zona fasciculata is the middle layer where cells are arranged in long straight columns. This layer is the largest of the layers and produces the glucocorticoids cortisol, cortisone and corticosterone. It also produces small quantities of the sex hormones androgen and oestrogen. The zona reticularis is the innermost layer made up of cells that are organised in branching cords. It produces some sex hormones, for example androgens. Mineralocorticoids The main mineralocorticoid produced in the zona glomerulosa is aldosterone, which is important in the maintenance of fluid balance. This is achieved through regulation of the amount of sodium that is reabsorbed from the kidneys accompanied by water reabsorption and secretion of potassium (Scott 2011). Aldosterone is an essential hormone in the body, and without it a person will die quickly from circulatory shock as a result of loss of plasma volume (Sherwood 2013). The main control mechanism for regulating the release of aldosterone is the renin-angiotensinaldosterone pathway. This pathway is triggered by a fall in BP in the kidneys or a reduction in the delivery of sodium to the distal tubules of the kidney. Increased levels of potassium and decreased levels of sodium in the blood stimulate the release of mineralocorticoids (Clare 2011). Regulation of aldosterone is not under anterior pituitary control (Sherwood 2013). A reduction in blood volume causes a decrease in BP. This, in turn, stimulates the juxtaglomerular cells in the kidneys to secrete the enzyme renin. The level of renin in the blood increases and renin then converts the plasma protein angiotensinogen, which is produced in the liver, to angiotensin I. Angiotensin I then circulates in the blood and travels to the lungs where it is converted to angiotensin II by angiotensinconverting enzyme. The increased blood level of angiotensin II stimulates the adrenal cortex to secrete aldosterone. Rising levels of aldosterone in the blood circulates to the kidneys where aldosterone increases re-absorption of sodium, which in turn increases re-absorption of water from the kidneys, decreasing the amount of water lost in urine and resulting in

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an increased blood volume. Angiotensin II also stimulates the contraction of smooth muscle in the walls of the arterioles, increasing BP through vasoconstriction of the arterioles (Tortora and Derrickson 2012). Glucocorticoids Cortisol accounts for approximately 95% of glucocorticoid activity (Tortora and Derrickson 2012). Glucocorticoids have several important functions in the regulation of metabolism and are involved in the stress response (Scott 2011). They respond to stressful situations by increasing the concentration of blood glucose at the expense of storing proteins and fats (Sherwood 2013). They do this by speeding up the breakdown of proteins mainly in muscle tissue, freeing amino acids to enter the bloodstream (Tortora and Derrickson 2012). These amino acids can be converted to glucose or they may be needed to repair damaged tissue or for synthesis of new cellular structures (Cohen 2013, Sherwood 2013). This mechanism is useful during periods of fasting or between meals when the stores of glycogen in the liver are used up, meaning that glucose stores can be replenished to provide adequate levels of glucose to the brain. Glucocorticoids also delay the uptake of glucose for use by many cells to ensure the brain receives an adequate supply of glucose. Glucocorticoids stimulate the breakdown of triglycerides to release fatty acids from fat stores in adipose tissue (Tortora and Derrickson 2012), ensuring that fatty acids are available as an alternative source of energy instead of glucose (Sherwood 2013). The production of glucocorticoids is regulated by a negative feedback system. When there are low levels of glucocorticoids in the blood, the hypothalamus secretes corticotropin-releasing hormone, which triggers the anterior pituitary to release adrenocortiocotropic hormone (ACTH). ACTH is transported in the blood to the adrenal cortex, where it acts to stimulate the secretion of glucocorticoids.

Adrenal medulla

The adrenal medulla is the central part of the adrenal gland and functions as part of the sympathetic nervous system. It comprises modified post-ganglionic sympathetic neurones called chromaffin cells that secrete two major hormones, 80% of which is adrenaline (epinephrine) and 20% of which is noradrenaline (norepinephrine) (Tortora and Derrickson 2012). Secretion of these hormones is regulated by the sympathetic nervous system in response to stress, and these hormones augment the flight or fight response (Jenkins and Tortora 2013).

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Disorders associated with the adrenal glands Phaeochromocytoma is a rare disorder of the adrenal medulla, where an adrenal medulla tumour causes excessive amounts of adrenaline and noradrenaline to be secreted (Carson 2006). It is a rare cause of hypertension. There are two main disorders associated with the adrenal cortex: Addison’s disease and Cushing’s disease. They are both relatively rare, but can cause serious illness if they are not treated appropriately.

Addison’s disease

Addison’s disease is caused by a primary failure of the adrenal cortex resulting from autoimmune destruction of the layers of the adrenal cortex (Chakera and Vaidya 2010). Other causes of adrenal cortex insufficiency include tuberculosis, cancer, infections and toxins (Crawford and Harris 2012). Secondary deficiency of the adrenal cortex can be caused by the sudden cessation of long-term high dose glucocorticoid therapy, which is why it is important to reduce glucocorticoid therapy slowly to minimise the likelihood of this happening (British National Formulary 2014). Addison’s disease affects most systems in the body as a result of the functions of adrenal cortex hormones, and therefore the signs and symptoms are many and varied. They include muscle weakness and atrophy, changes in skin pigmentation where the skin can take on a bronzed appearance or vitiligo. The patient may complain of weight loss and anorexia. There may be evidence of hypotension and neurological changes, including headaches, lethargy and mood swings (Chakera and Vaidya 2010). Diagnosis is made by an ACTH stimulation test, where intravenous ACTH is administered to the patient and plasma cortisol levels are assessed at 30 minutes and one hour. Patients with Addison’s disease will show little or no response to ACTH (Carson 2006). Management of Addison’s disease involves daily replacement of deficient glucocorticoids and mineralocorticoids usually by taking hydrocortisone (NHS Choices 2013c). In the event of acute stress, additional cortisol must be administered to approximate that which would usually be released under such conditions in a healthy individual. If the disease is not treated, the patient may experience an adrenal (addisonian) crisis, which is a medical emergency and requires immediate replacement of sodium and glucose, and the administration of steroids (Crawford and Harris 2012).

Cushing’s disease

Cushing’s disease occurs as a result of excessive secretion of cortisol by the adrenal cortex, caused by a tumour of the adrenal gland secreting cortisol may 28 :: vol 28 no 39 :: 2014 47

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Art & science life sciences: 25 or from an ACTH-secreting adenoma in the pituitary gland that stimulates excessive secretion of cortisol (Longmore et al 2014). All body systems are affected by the disease. The symptoms commonly associated with Cushing’s disease include obesity with a round moon face, thin skin that bruises easily, muscle weakness, bone loss and raised blood glucose levels (Cohen 2013). Diagnosis is made by an overnight dexamethasone suppression test, where dexamethasone is administered at 23.00 or 24.00 hours and a blood sample is taken at 08.00 hours to measure cortisol levels. Management involves surgery to remove the adenoma or radiotherapy (Crawford and Harris 2012).

Conclusion Understanding the structure and function of the endocrine system will enable nurses to provide better care for patients who may be experiencing endocrine disorders. While many patients with such disorders are cared for in specialised units, others will be admitted to general medical or surgical wards. Community nursing staff are increasingly caring for patients with long-term

endocrine disorders and thyroid dysfunction. This article is the last in the life sciences series NS

POINTS FOR PRACTICE  What advice would you give to a patient newly diagnosed with type 2 diabetes mellitus in respect of lifestyle changes?  Patients with Addison’s disease are required to take hydrocortisone for life. Identify the potential long-term effects of hydrocortisone use.  How would you respond to a patient in your care with a blood glucose of 2.9mmol/L?

GLOSSARY Glycated haemoglobin A form of haemoglobin that can be measured to identify the average plasma glucose concentration over prolonged periods. Hyperhidrosis Excessive sweating, which can be focal or generalised. Vitiligo Presence of pale white patches on the skin, usually as a result of a lack of melanin.

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Endocrine system: part 2.

This article, the last in the life sciences series, is the second of two articles on the endocrine system. It discusses human growth hormone, the panc...
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