Chapter 47 NURSING ASSESSMENT: endocrine system

Written by JoAnne Konick-McMahan

Adapted by Valerie Cheetham

LEARNING OBJECTIVES

KEY TERMS

aldosterone

antidiuretic hormone (ADH)

calcitonin

catecholamines

corticosteroid

cortisol

glucagon

growth hormone (GH)

hormone

insulin

islets of Langerhans

negative feedback

oxytocin

parathyroid hormone (PTH)

target tissue

thyroxine

triiodothyronine

trophic hormones

The endocrine system and the nervous system are two of the primary communicating and coordinating systems in the body. The nervous system communicates through nerve impulses; the endocrine system communicates through chemical substances known as hormones, and it plays a role in reproduction, growth and development, and regulation of energy. The endocrine system is composed of glands or glandular tissues that produce, store and secrete hormones, which travel through the blood to specific target cells throughout the body.

The endocrine glands include the hypothalamus, pituitary, thyroid, parathyroids, adrenals, pancreas, ovaries, testes, pineal and thymus (see Fig 47-1). The thymus gland is important in the function of the immune system and is discussed in Chapter 13. The pineal gland, which secretes melatonin, is involved in stimulating gonadal function.1 In addition to the endocrine glands, other body organs secrete hormones. For example, the kidneys secrete erythropoietin, the heart secretes atrial natriuretic peptide and the gastrointestinal tract secretes numerous peptide hormones (e.g. gastrin). These hormones are discussed in their respective assessment chapters.

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Figure 47-1 Location of the major endocrine glands. The parathyroid glands actually lie on the posterior surface of the thyroid.

Structures and functions of the endocrine system

HORMONES

Classifications and functions

A hormone is a chemical substance synthesised and secreted by a specific organ or tissue. Most hormones have common characteristics, including: (1) secretion in small amounts at variable but predictable rates; (2) circulation through the blood; and (3) binding to specific cellular receptors either in the cell membrane or within the cell.

Hormones are classified by their chemical structure as either lipid-soluble hormones or water-soluble (protein-based) hormones. Lipid-soluble hormones include steroid hormones (all hormones produced by the adrenal cortex and sex glands) and thyroid hormones. All other hormones are water soluble.2 The differences in solubility become important in understanding how hormones interact with target cells.

Hormones control a number of physiological activities. Important hormonal functions are related to reproduction, response to stress and injury, electrolyte balance, energy metabolism, growth, maturation and ageing. Hormones also play a role in nervous system function. Some hormones have a regulatory effect on nervous tissue. For example, catecholamines are hormones when they are secreted by the adrenal medulla, but act as neurotransmitters when they are secreted by nerve cells in the brain and peripheral nervous system. When adrenaline travels through the blood, it is a hormone and affects target tissues. When it travels across synaptic junctions, it acts as a neurotransmitter.

Hormones can also influence behaviour.3 For example, excess growth hormone, cortisol and parathyroid hormone can cause mood swings. Depression has been associated with adrenal insufficiency and hypothyroidism. Table 47-1 summarises the major hormones, the glands or tissues from which they are synthesised, target organs or tissues, and functions.

Targets and receptors

Hormones exert their effects on target tissue. The hormone recognises the target tissue through receptors (the site that interacts with the hormone) on, or within, cells of the target tissue. The specificity of hormone–target cell interaction is determined by receptors in a ‘lock-and-key’ type of mechanism. Thus, a hormone will act only on cells that have a receptor specific for that hormone (see Fig 47-2). It is important to note that there are two types of receptors: those within the cell (e.g. steroid and thyroid hormone receptors) and those on the cell membrane (e.g. protein hormone receptors). The location of the receptor sites affects the mechanism of action for the hormone.

Regulation of hormonal secretion

The regulation of endocrine activity is controlled by specific mechanisms of varying levels of complexity. These mechanisms stimulate or inhibit hormone synthesis and secretion and include simple feedback, complex feedback, nervous system control and physiological rhythms.

Simple feedback

The regulation of hormone levels in the blood depends on a highly specialised mechanism called feedback. Feedback is based on the blood level of a particular substance. This substance may be a hormone or other chemical compound regulated by, or responsive to, a hormone. With negative feedback, the most common type of feedback system, the gland responds by increasing or decreasing the secretion of a hormone based on feedback from various factors. Negative feedback is similar to the functioning of a thermostat in which cold air in a room activates the thermostat to release heat, and hot air turns off the thermostat to prevent more warm air from entering the room.

The pattern of insulin secretion is a physiological example of negative feedback between glucose and insulin. Elevated blood glucose levels stimulate the secretion of insulin from the pancreas. As blood glucose levels decrease, the stimulus for insulin secretion also decreases (see Fig 47-4). This homeostatic mechanism is considered negative feedback as it reverses the change in blood glucose level. Another example of negative feedback is the relationship between calcium and parathyroid hormone (PTH). Low blood levels of calcium stimulate the parathyroid gland to release PTH, which acts on bone, the intestines and the kidneys to increase blood calcium levels. The increased blood calcium levels then inhibit further PTH release (see Fig 47-5).

Positive feedback is a second method of regulation of hormone secretion. The positive feedback mechanism increases the target organ action beyond normal. The action of oxytocin in childbirth is an example. The hormone oxytocin from the posterior pituitary stimulates and increases uterine contractions. Oxytocin release is stimulated by pressure receptors in the vagina. As the fetus enters the vagina during childbirth, the pressure receptors sense increased pressure and signal the brain to release more oxytocin. Oxytocin release leads to stronger uterine contractions. With birth, the stimulus to the pressure receptors in the vagina ends, thus leading to decreased oxytocin secretion.

Rhythms

Another regulatory mechanism affecting many hormonal secretions involves the rhythms of secretions. These rhythms originate in brain structures. A common physiological rhythm is the circadian rhythm, in which a hormone level fluctuates predictably during a 24-hour period.5 These rhythms may be related to sleep–wake or dark–light cycles. For example, cortisol rises early in the day, declines towards evening and rises again towards the end of sleep to peak by morning (see Fig 47-7). Growth hormone (GH) and prolactin secretion peak during sleep. TSH secretion is also maximal during sleep and ebbs 3 hours after a person awakens in the morning. The menstrual cycle is an example of a body rhythm that is longer than 24 hours (ultradian). These rhythms must be considered when interpreting hormone levels on laboratory results. (See diagnostic studies section in this chapter and Ch 50.)

HYPOTHALAMUS

The relationship between the hypothalamus and the pituitary gland is one of the most important aspects of the endocrine system. Although the pituitary gland has been referred to as the ‘master gland’, most of its functions rely on an interrelationship with the hypothalamus. The hypothalamus and the pituitary gland integrate communication between the nervous and endocrine systems.

The hypothalamus is located in the most central part of the diencephalon area of the brain (see Fig 47-1). Although it is really part of the brain, the hypothalamus secretes many hormones. Two important groups of hormones from the hypothalamus are releasing hormones and inhibiting hormones.6 The function of these hormones is to either stimulate (release) or inhibit the secretion of hormones from the anterior pituitary gland (see Box 47-1).

The hypothalamus also contains neurons, which receive input from the brainstem and limbic system. These neurons influence the limbic system, brainstem and spinal cord. This creates a circuit to facilitate the coordination of the endocrine system, autonomic nervous system (ANS) and expression of complex behavioural responses, such as anger and feelings of fear and pleasure.

PITUITARY

The pituitary gland (also called the hypophysis) is very small—about the size of a pea. It is located in the sella turcica under the hypothalamus at the base of the brain above the sphenoid bone (see Fig 47-1). The pituitary is connected to the hypothalamus by the infundibular (hypophyseal) stalk. This stalk serves as a communication mechanism between the hypothalamus and the pituitary. The pituitary consists of two parts: the anterior (adenohypophysis) lobe and the posterior (neurohypophysis) lobe. Hormones secreted from each of these pituitary lobes serve very different functions.

Anterior pituitary

The anterior lobe accounts for 80% of the gland by weight. As mentioned previously, the anterior pituitary is regulated by the hypothalamus through releasing and inhibiting hormones. These hypothalamic hormones reach the anterior pituitary through a network of capillaries known as the hypothalamus–hypophyseal portal system. The releasing and inhibiting hormones in turn affect the secretion of six hormones from the anterior pituitary (see Fig 47-8 and Box 47-1).

Posterior pituitary

The posterior pituitary is composed of nerve tissue and is essentially an extension of the hypothalamus. The communication between the hypothalamus and the posterior pituitary occurs through nerve tracts known as the median eminence. The hormones secreted by the posterior pituitary, antidiuretic hormone (ADH) and oxytocin, are actually produced in the hypothalamus. These hormones travel down the nerve tracts from the hypothalamus to the posterior pituitary and are stored until their release is triggered by the appropriate stimuli (see Fig 47-8).

Antidiuretic hormone

The major physiological role of ADH is regulation of fluid volume by stimulation of reabsorption of water in the renal tubules. ADH, also called vasopressin, is a potent vasoconstrictor.

The most important stimulus to ADH secretion is plasma osmolality (a measure of the solute concentration of circulating blood; see Fig 47-9). Plasma osmolality will increase when there is a decrease in extracellular fluid or an increase in solute concentration (see Ch 16). The increased plasma osmolality activates osmoreceptors, which are extremely sensitive, specialised neurons in the hypothalamus. These activated osmoreceptors stimulate ADH release.8 Table 47-2 presents factors that affect ADH release. When ADH is released, the renal tubules reabsorb water, creating a more concentrated urine. When ADH release is inhibited, renal tubules do not reabsorb water, thus creating more dilute urine.

THYROID GLAND

The thyroid gland is located in the anterior portion of the neck in front of the trachea. It consists of two encapsulated lateral lobes connected by a narrow isthmus (see Fig 47-10). The thyroid is a highly vascular organ and is regulated by TSH from the anterior pituitary. The three hormones produced and secreted by the thyroid gland are thyroxine, triiodothyronine and calcitonin.

ADRENAL GLANDS

The adrenal glands are small, paired, highly vascularised glands located on the upper portion of each kidney. Each gland consists of two parts: the medulla and the cortex (see Fig 47-11). Each part has distinct functions, and the glands act independently of one another.

Adrenal cortex

The adrenal cortex is the outer part of the adrenal gland. It secretes more than 50 steroid hormones, which are classified as glucocorticoids, mineralocorticoids and androgens. Cholesterol is the precursor for steroid hormone synthesis. Glucocorticoids (e.g. cortisol) are named for their effects on glucose metabolism. Mineralocorticoids (e.g. aldosterone) are essential for the maintenance of fluid and electrolyte balance. Adrenal androgens are produced and secreted in small but significant amounts. The term corticosteroid refers to any of the hormones synthesised by the adrenal cortex (excluding androgens).

Cortisol

Cortisol, the most abundant and potent glucocorticoid, is necessary to maintain life. One major function of cortisol is the regulation of blood glucose concentration. Cortisol increases blood glucose levels through stimulation of hepatic gluconeogenesis (conversion of amino acids to glucose) and inhibiting protein synthesis. Cortisol also decreases peripheral glucose use in the fasting state. Additionally, glucocorticoids stimulate lipolysis in adipose tissue, thereby mobilising glycerol and free fatty acids.

Another major effect of glucocorticoids is their anti-inflammatory action and supportive actions in response to stress. A marked increase in the rate of cortisol secretion by the adrenal cortex aids the body in coping more effectively with stressful situations. Cortisol decreases the inflammatory response by stabilising the membranes of cellular lysosomes and preventing increased capillary permeability. The lysosomal stabilisation reduces the release of proteolytic enzymes and thereby their destructive effects on surrounding tissue. Cortisol can also inhibit production of prostaglandins, thromboxanes and leukotrienes and alter the cell-mediated immune response. Cortisol helps maintain vascular integrity and fluid volume. It has a mineralocorticoid effect because it can bind to mineralocorticoid receptors.

Cortisol is secreted in a diurnal pattern (see Fig 47-7). The major control of cortisol is by means of a negative feedback mechanism that involves the secretion of corticotrophin-releasing hormone (CRH) from the hypothalamus. CRH stimulates the secretion of ACTH by the anterior pituitary. Cortisol levels are also increased by surgical stress, burns, infection, fever, acute anxiety and hypoglycaemia.

PANCREAS

The pancreas is a long, tapered, lobular, soft gland located behind the stomach and anterior to the first and second lumbar vertebrae. The pancreas has both exocrine and endocrine functions. The hormone-secreting portion of the pancreas is referred to as the islets of Langerhans. The islets account for less than 2% of the gland and consist of four types of hormone-secreting cells: alpha, beta, delta and F cells. Alpha cells produce and secrete the hormone glucagon; beta cells produce and secrete insulin; delta cells produce and secrete somatostatin; and F (or PP) cells secrete pancreatic polypeptide.

Glucagon

Glucagon is synthesised and released from pancreatic alpha cells in response to low levels of blood glucose, protein ingestion and exercise. Glucagon increases blood glucose levels by stimulating glycogenolysis, gluconeogenesis and ketogenesis. Usually, glucagon and insulin function in a reciprocal manner to maintain normal blood glucose levels. The exception is after ingestion of a high-protein, carbohydrate-free diet, in which case both hormones are secreted. In this instance, glucagon counteracts the inhibitory effect of insulin on gluconeogenesis, and normal blood glucose levels are maintained.

Insulin

Insulin is the principal regulator of the metabolism and storage of ingested carbohydrates, fats and proteins. Insulin facilitates glucose transport across cell membranes in most tissues. However, the brain, nerves, lens of the eye, hepatocytes, erythrocytes and cells in the intestinal mucosa and kidney tubules are not dependent on insulin for glucose uptake. An increased blood glucose level is the major stimulus for insulin synthesis and secretion. Other stimuli to insulin secretion are increased amino acid levels and vagal stimulation. Insulin secretion is usually inhibited by low blood glucose levels, glucagon, somatostatin, hypokalaemia and catecholamines (see Table 47-3).

A major effect of insulin on glucose metabolism occurs in the liver, where the hormone enhances glucose incorporation into glycogen and triglycerides by altering enzymatic activity and inhibiting gluconeogenesis. Another major effect occurs in peripheral tissues, where insulin facilitates glucose transport into cells, transport of amino acids across muscle membranes and their synthesis into protein, and transport of triglycerides into adipose tissue. Thus, insulin is a storage, or anabolic, hormone.

The endocrine system is concerned with the regulation of body processes and the maintenance of internal homeostasis despite vastly changing substrates, as is seen in glucose homeostasis after food ingestion. After a meal, insulin is responsible for the storage of nutrients (anabolism). In the fasting state (during which ingested glucose is not readily available), hormones such as catecholamines, cortisol and glucagon break down stored complex fuels (catabolism) to provide simple glucose as fuel for energy.

Assessment of the endocrine system

Hormones affect every body tissue and system, causing great diversity in the signs and symptoms of endocrine dysfunction. Therefore, assessment of the endocrine system is often difficult and requires keen clinical skills to detect manifestations of disorders. Endocrine dysfunction may result from deficient or excessive hormone secretion, transport abnormalities, an inability of the target tissue to respond to a hormone or inappropriate stimulation of the target-tissue receptor.

Endocrine disorders may have specific or non-specific (vague) clinical manifestations. Specific signs and symptoms, such as the classic ‘polys’ (polyuria, polydipsia and polyphagia) in diabetes mellitus, make the assessment easier. Non-specific signs and symptoms, such as tachycardia, palpitations, fatigue or altered mood, are more problematic. Non-specific changes should alert the healthcare provider to the possibility of an endocrine disorder. The most common non-specific symptoms, fatigue and depression, are often accompanied by other manifestations, such as changes in energy level, alertness, sleep patterns, mood, affect, weight, skin, hair, personal appearance and sexual function.

SUBJECTIVE DATA

The lack of clear-cut manifestations of endocrine problems requires a conscientious and detailed health history. A careful health history will yield data to help sort out possible causes and the effect of the problem on the person’s life (see Table 47-5).

TABLE 47-5

Endocrine system

HEALTH HISTORY

Health perception–health management pattern
Nutritional–metabolic pattern
Elimination pattern
Activity–exercise pattern
Sleep–rest pattern
Cognitive–perceptual patternaan
Self-perception–self-concept pattern
Role–relationship pattern
Sexuality–reproductive pattern
Women
Men
Coping–stress tolerance pattern
Value–belief pattern

*If yes, describe.

Important health information

Functional health patterns

Nutritional–metabolic pattern

A major function of the endocrine system is regulating metabolism and maintaining homeostasis, so the patient with endocrine dysfunction will often experience alterations in nutritional metabolic patterns. Reported changes in appetite and weight can indicate endocrine dysfunction. Weight loss with increased appetite may indicate hyperthyroidism or diabetes mellitus, particularly type 1. Weight loss with decreased appetite may indicate hypopituitarism, hypocortisolism or gastroparesis (decreased gastric motility and emptying due to autonomic neuropathy) from diabetes mellitus. Weight gain may indicate hypothyroidism and, if the weight gain is concentrated in the truncal area, hypercortisolism. In addition, weight gain in a genetically susceptible patient may increase the risk of type 2 diabetes mellitus.

Difficulty swallowing or a change in neck size may indicate a thyroid disorder or inflammation. Questions related to increased SNS activity (e.g. nervousness, palpitations, sweating, tremors) may assist in identifying a thyroid disorder or phaeochromocytoma. Heat or cold intolerance may indicate hyperthyroidism or hypothyroidism, respectively.

The patient should also be asked about changes to the skin or hair, since hair distribution and skin and hair colour and texture can all indicate endocrine dysfunction. Hair loss can indicate hypopituitarism, hypothyroidism, hypoparathyroidism or increased testosterone and other androgens. Increased body hair may indicate hypercortisolism. Decreased skin pigmentation can occur in hypopituitarism, hypothyroidism and hypoparathyroidism, whereas increased skin pigmentation, particularly in sun-exposed areas, can indicate hypocortisolism. A patient with hypothyroidism or excess growth hormone may complain of coarse, leathery skin. A patient with hyperthyroidism may comment about fine, silky hair.

OBJECTIVE DATA

Most endocrine glands are inaccessible to direct examination. With the exception of the thyroid and male gonads, the glands are deeply encased in the body, protected against injury and trauma. However, assessment can be accomplished using a variety of objective data. It is imperative to understand the actions of hormones so that the function of a gland can be assessed by monitoring the target tissue.

Physical examination

It is important to keep in mind that the endocrine system affects every body system. Clinical manifestations of endocrine function vary significantly depending on the gland involved. Specific clinical findings for the various endocrine problems are discussed in Chapters 48 and 49. Regardless of the type of endocrine dysfunction, the following general examination procedure should be followed.

Integument

The colour and texture of the skin, hair and nails should be noted. The overall skin colour should also be noted, as well as pigmentation and possible ecchymosis. Hyperpigmentation of the skin (particularly on the knuckles, elbows, knees, genitalia and palmar creases) is a classic finding in Addison’s disease, but is also seen with ACTH-producing tumours and acromegaly.12 The skin should be palpated for its texture and the presence of moisture. The hair distribution should be examined not only on the head, but also on the face, trunk and extremities. The appearance and texture of the hair should be examined. Dull, brittle hair, excessive hair growth or hair loss may indicate endocrine dysfunction.

Neck

When inspecting the thyroid gland, observation should be made first with the patient in the normal position (preferably with side lighting), then in slight extension and then as the patient swallows some water. The trachea should be midline and the neck should appear symmetrical. Any unusual bulging over the thyroid area should be noted. If there is no noticeable enlargement of the thyroid gland, palpation can be done. (Because palpation can trigger the release of thyroid hormones, palpation should be deferred in the patient with a visibly enlarged thyroid gland.) When an enlarged thyroid is noted, the lateral lobes should be auscultated with the stethoscope bell to determine the presence of a bruit.

The thyroid gland is difficult to palpate. Thyroid palpation requires considerable practice, as well as validation by a more experienced examiner. Water should always be available for the patient to swallow as part of this examination. There are two acceptable approaches to thyroid palpation: anterior or posterior. For anterior palpation the nurse stands in front of the patient, with the patient’s neck flexed. The nurse places the thumb horizontally with the upper edge along the lower border of the cricoid cartilage. The thumb is moved over the isthmus as the patient swallows water. The fingers are then placed laterally to the anterior border of the sternocleidomastoid muscle, and each lateral lobe is palpated before and while the patient swallows water.

For posterior palpation the nurse stands behind the patient. With the thumbs of both hands resting on the nape of the patient’s neck, the nurse uses the index and middle fingers of both hands to feel for the thyroid isthmus and for the anterior surfaces of the lateral lobes. To facilitate the examination of each lobe and to relax the neck muscles, the nurse asks the patient to flex the neck slightly forwards and to the right. The thyroid cartilage is displaced to the right by the left hand and fingers. The nurse palpates with the right hand after placing the thumb deep and behind the sternocleidomastoid muscle with the index and middle fingers in front of it; the area is palpated with the right hand (see Fig 47-12). While this is done, the patient is asked to swallow water. This procedure is then repeated on the left side. The thyroid is palpated for its size, shape, symmetry and tenderness, and for any nodules.

In a normal person the thyroid is often not palpable. If palpable, it usually feels smooth, with a firm consistency, and is not tender with gentle pressure. Nodules, enlargement, asymmetry or hardness is abnormal, and the patient should be referred for further evaluation.

Diagnostic studies of the endocrine system

Accurately performed laboratory tests and radiological examinations contribute to the diagnosis of an endocrine problem. Laboratory tests usually involve blood and urine testing. Ultrasound may be used as a screening tool to localise endocrine growths, such as thyroid nodules. Radiological tests include regular X-ray, computed tomography (CT) and magnetic resonance imaging (MRI). With all diagnostic testing, the nurse is responsible for explaining the procedure to the patient and family. Diagnostic studies common to the endocrine system are presented in Table 47-7.

LABORATORY STUDIES

Laboratory studies used to diagnose endocrine problems may include direct measurement of the hormone level, or they may provide an indirect indication of gland function by evaluating blood or urine components affected by the hormone (e.g. electrolytes).

Hormones with fairly constant basal levels (e.g. T4) require only a single measurement. Notation of sample time on the laboratory slip and sample is important for hormones with circadian or sleep-related secretion (e.g. cortisol). Evaluation of other hormones may require multiple blood sampling, such as in suppression (e.g. dexamethasone) and stimulation (e.g. glucose tolerance) tests. In these situations, it is often necessary to obtain intravenous access to administer medications and fluids and to take multiple blood samples.

Thyroid studies

A number of tests are available to evaluate thyroid function. The most sensitive and accurate laboratory test is measurement of TSH; thus, it is often recommended as a first diagnostic test for evaluation of thyroid function.13 Common additional tests ordered in the presence of abnormal TSH include total T4, free T4 and total T3. Free T4 is the unbound thyroxine and is a more accurate reflection of thyroid function than total T4. Less common tests that are used to help in the differentiation of various types of thyroid disease include T3, free T3 resin uptake, thyroid autoantibodies, thyroid scanning, ultrasound and biopsy.

Pancreatic studies

The tests given in Table 47-7 are used to evaluate the metabolism of glucose. They are important in the diagnosis and management of diabetes. (Diagnostic studies for diabetes are also discussed in Ch 48.)

Review questions

1. A characteristic common to all hormones is that they:

2. A patient is receiving radiation therapy for cancer of the kidney. The nurse monitors the patient for signs and symptoms of damage to the:

3. A patient has a serum sodium level of 152 mmol/L. The normal hormonal response to this situation is:

4. All cells in the body are believed to have intracellular receptors for:

5. When obtaining subjective data from a patient during assessment of the endocrine system, the nurse asks specifically about:

6. An appropriate technique to use during physical assessment of the thyroid gland is:

7. Endocrine disorders often go unrecognised in the older adult because:

8. An abnormal finding by the nurse during an endocrine assessment would be:

9. A patient has a total serum calcium level of 1.75 mmol/L. If this finding reflects hypoparathyroidism, the nurse would expect further diagnostic testing to reveal:

References

1 Low MJ. Neuroendocrinology. In: Kronenberg HM, Melmed S, Polonsky KS, et al, eds. Williams textbook of endocrinology. Philadelphia: Saunders, 2008.

2 Eliopoulos C. Gerontological nursing, 7th edn. Philadelphia: Lippincott Williams & Wilkins, 2010.

3 Goodman HM. Basic medical endocrinology, 4th edn. Philadelphia: Saunders, 2009.

4 Greenspan FS. The thyroid gland. In Greenspan FS, Gardner DG, eds.: Basic and clinical endocrinology, 8th edn., New York: McGraw-Hill, 2007.

5 Kronenberg HM, Melmed S, Polonsky KS, et al. Principles of endocrinology. In: Kronenberg HM, Melmed S, Polonsky KS, et al, eds. Williams textbook of endocrinology. Philadelphia: Saunders, 2008.

6 Guillemin R. Hypothalamic hormones a.k.a. hypothalamic releasing factors. J Endocrinol. 2005;184(1):11–28.

7 Styne D. Growth. In Greenspan FS, Gardner DG, eds.: Basic and clinical endocrinology, 8th edn., New York: McGraw-Hill, 2007.

8 Gordon C, Craft J. Shock. In: Craft J, Gordon C, Tiziani A, eds. Understanding pathophysiology. Sydney: Elsevier, 2011.

9 DeGroot LJ. Diagnosis and treatment of Graves’ disease. Thyroid Disease Manager. Available at www.thyroidmanager.org/Chapter11/11-frame.htm, Updated 1 April 2010. accessed 3 January 2011.

10 Shoback D, Marcus R, Bihle D. Metabolic bone disease. In Greenspan FS, Gardner DG, eds.: Basic and clinical endocrinology, 8th edn., New York: McGraw-Hill, 2007.

11 Wilson SF, Giddens JF. Health assessment for nursing practice. St Louis: Mosby, 2009.

12 Jarvis C. Physical examination and health assessment, 6th edn. St Louis: Saunders, 2008.

13 American Association of Clinical Endocrinologists (AACE). AACE Thyroid Task Force medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Amended. Available at http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf, 2006. accessed 20 December 2010.

14 Pagana KD, Pagana TJ. Diagnostic and laboratory test reference, 9th edn. St Louis: Mosby, 2009.

15 Pacak K, Eisenhofer G, et al. Pheochromocytoma: recommendations for clinical practice from the First International Symposium, October 2005. Nat Clin Pract Endocrinol Metab. 2007;3(2):92–102.

Resources

 

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See the Evolve site for more great resources at http://evolve.elsevier.com/AU/Brown/medsurg/