Arthur C. Guyton, the great professor of physiology, always began his lectures with, “The essence of physiology is regulation and control.” That statement is true for the endocrine system, which is regarded as one of the two physiologic regulating and control systems—the other being the nervous system. Many interrelationships exist between the endocrine and the nervous systems. Dysfunction of the endocrine system is associated with overproduction or underproduction of a single hormone or multiple hormones. This dysfunction may be the primary reason for surgery or it may coexist in patients who need surgery on other organ systems. To ensure appropriate nursing interventions for the patient with endocrine dysfunction in the postanesthesia care unit (PACU), the perianesthesia nurse must understand the physiology and pathophysiology of the endocrine system.
Arthur C. Guyton, the great professor of physiology, always began his lectures with, “The essence of physiology is regulation and control.”1 That statement is true for the endocrine system, which is regarded as one of the two physiologic regulating and control systems—the other being the nervous system. Many interrelationships exist between the endocrine and the nervous systems. Dysfunction of the endocrine system is associated with overproduction or underproduction of a single hormone or multiple hormones. This dysfunction may be the primary reason for surgery or it may coexist in patients who need surgery on other organ systems. To ensure appropriate nursing interventions for the patient with endocrine dysfunction in the postanesthesia care unit (PACU), the perianesthesia nurse must understand the physiology and pathophysiology of the endocrine system.2,3
Endocrine GlandA group of hormone-secreting and hormone-excreting cells.
GluconeogenesisThe conversion of amino acids into glucose.
GlycogenesisThe deposition of glycogen in the liver.
HormoneA biochemical substance secreted by a specific endocrine gland transported in the blood to distant points in the body for regulation of rates of physiologic processes.
LipolysisThe mobilization of deposited fat.
Releasing FactorA hormone of unknown chemical structure secreted by the hypothalamus.
Releasing HormoneA hormone secreted from the hypothalamus.
StressA chemical or physical disturbance in the cells or tissues produced by a change either in the external environment or within the body that necessitates a response to counteract the disturbance.
Target OrganA gland whose activities are regulated by tropic hormones.
Tropic HormoneA hormone that regulates the blood level of a specific hormone secreted from another endocrine gland.
This intricate system is responsible for the regulation of many body processes through the secretion of certain hormones. The primary organs associated with this system are the hypothalamus, pineal body, pituitary glands (anterior and posterior), thyroid, parathyroids, thymus, adrenal gland, pancreas, and reproductive glands (ovaries and testes).
The hypothalamus coordinates communication between the endocrine system and nervous system by way of the pituitary gland. The pituitary gland consists of an anterior lobe and a posterior lobe. The anterior lobe is responsible for specific physiologic processes including stress response and growth, whereas the posterior lobe responds to the hypothalamus and regulates functions associated with lactation and blood pressure. The pineal body produces melatonin to regulate sleep patterns, the thyroid regulates metabolism, and the parathyroid regulates the level of calcium in the blood and bone. In addition, the thymus gland is a primary immune system organ that supports lymphocyte activity. The adrenal gland produces steroid hormones including mineralocorticoids, glucocorticoids, and androgens. These hormones regulate functions associated with metabolism and response to stress. The pancreas is responsible for secretion of various hormones including insulin and is also considered a gastrointestinal (GI) organ as it secretes pancreatic juice into the GI tract to aid in the breakdown of nutrients. Finally, the reproductive organs regulate sexual reproduction through the release of hormones including estrogen, progesterone, and testosterone by the ovaries and production of sperm and mainly testosterone by the testes.
A hormone is a biochemical substance synthesized in an endocrine gland and secreted into body fluids for regulation or control of physiologic processes in other cells of the body. Biochemically, hormones are either proteins (or derivatives of proteins or amino acids) or steroids.1–3
Protein hormones, such as the releasing hormones, catecholamines, and parathormone, fit the fixed-receptor model of hormone action. In this model, the stimulating hormone, called the first messenger, combines with a specific receptor for that hormone on the surface of the target cell. This hormone-receptor combination activates the enzyme adenylate cyclase in the membrane. The portion of the adenylate cyclase that is exposed to the cytoplasm causes the immediate conversion of cytoplasmic adenosine triphosphate into cyclic adenosine monophosphate (AMP). The cyclic AMP then acts as a second messenger and initiates any number of cellular functions.1–3
In the mobile receptor model, a steroid hormone—because of its lipid solubility—passes through the cell membrane into the cytoplasm where it binds with a specific receptor protein. The combined receptor protein-hormone either diffuses or is transported through the nuclear membrane and transfers the steroid hormone to a smaller protein. In the nucleus, the hormone activates specific genes to form the messenger ribonucleic acid (RNA). The messenger RNA then passes out of the nucleus into the cytoplasm where it promotes the translation process in the ribosomes to form new proteins. Hormones that fit the fixed-receptor model produce an almost instantaneous response on the part of the target organ. In contrast, because of their action on the genes to cause protein synthesis when the steroid hormones are secreted, a characteristic delay in the initiation of hormone response varies from minutes to days.1–3
The pituitary gland rests in the sella turcica of the sphenoid bone at the base of the brain. This gland is divided into anterior and posterior lobes. Because of its glandular nature, the anterior lobe is called the adenohypophysis; the posterior lobe is an outgrowth of a part of the nervous system, the hypothalamus, and is called the neurohypophysis. The pituitary gland receives its arterial blood supply from two paired systems of vessels: (1) the right and left superior hypophyseal arteries from above and (2) the right and left inferior hypophyseal arteries from below. The anterior lobe receives no arterial blood supply. Instead, its entire blood supply is derived from the hypophyseal portal veins. This rich capillary system facilitates the rapid discharge of releasing hormones that have target cells in the anterior hypophysis.1–3
Although the pituitary gland is called the master gland, it is actually regulated by other endocrine glands and by the nervous system. The secretion of the hormones of the anterior hypophysis is primarily influenced and controlled by the higher centers in the hypothalamus. Releasing hormones are secreted by the hypothalamic nuclei through the infundibular tract to the portal venous system of the pituitary gland to their respective target cells of the adenohypophysis. Consequently, the hypothalamus brings about fine regulation of the action of the anterior pituitary, and still higher nervous centers apparently further modulate the production of the releasing factors. As a result, the many influences that enter the brain and central nervous system impinge on the anterior pituitary gland either to enhance or to dampen its activity.1–3
Hormonal control of the pituitary involves certain feedback systems. For example, corticotropin-releasing hormone (CRH) stimulates the production and release of adrenocorticotropin (ACTH). The increased concentration of ACTH causes the hypothalamus to decrease its production of CRH, which in turn reduces ACTH production and ultimately reduces the blood level of ACTH. Therefore, when exogenous corticoids are administered chronically, ACTH secretion decreases and the adrenal cortex atrophies. However, the removal of endogenous corticoids with a bilateral adrenalectomy can result in a tumor of the pituitary gland because of the absence of the feedback depression of the CRH.1–3
The posterior lobe of the pituitary gland has an abundant nerve supply. Nerve cell bodies in the posterior lobe produce two neurosecretions (antidiuretic hormone [ADH] and oxytocin), which are stored as granules at the site of the nerve cell bodies. When the hypothalamus detects a need for either neurohypophyseal hormone, nerve impulses are sent to the posterior lobe, and the hormone is released by granules into the neighboring capillaries. Consequently, the hormonal function of the posterior lobe is under direct nervous system regulation.1–3
The growth hormone is unique because it stimulates no target gland but instead acts on all tissues of the body. Its primary functions are maintaining blood glucose levels and regulating skeletal growth. Growth hormone conserves blood glucose by increasing fat metabolism for energy. It enhances the active transport of amino acids into cells, increases the rate of protein synthesis, and promotes cell division. In addition, growth hormone enhances the formation of somatomedin, which acts directly on cartilage and bone to promote growth. The active secretion of growth hormone is regulated in the hypothalamus via growth hormone–releasing hormone. Stimuli such as hypoglycemia, exercise, and trauma cause the hypothalamus to secrete growth hormone–releasing hormone, which is transported to the anterior lobe of the pituitary gland and released into the blood. Secretion of growth hormone can be inhibited by somatostatin, also called growth hormone–inhibiting hormone, which is secreted by the hypothalamus and the delta cells of the pancreas.1–3
Hyposecretion of the growth hormone before puberty leads to dwarfism or failure to grow. After puberty, growth hormone hypofunction can result in the condition known as Simmonds disease. This disease is characterized by premature senility, weakness, emaciation, mental lethargy, and wrinkled dry skin. Gigantism is the result of growth hormone hyperfunction before puberty. After puberty, when the epiphyses of the long bones have closed, growth hormone hyperfunction leads to acromegaly. In this disease, the face, hands, and feet become enlarged. Patients with acromegaly are prone to airway obstruction caused by protruding lower jaws and enlarged tongues. Therefore, constant vigilance to the respiratory status of these patients is essential in the PACU.1–3
The follicular cells of the thyroid are the target for thyroid-stimulating hormone (TSH). This hormone promotes the growth and secretory activity of the thyroid gland. Production of TSH is regulated in a reciprocal fashion by the blood levels of thyroid hormone and the formation of thyrotropin-releasing hormone in the hypothalamus.3,4
ACTH promotes glucocorticoid, mineralocorticoid, and androgenic steroid production and secretion by the adrenal cortex. This hormone is released in response to stimuli such as pain, hypoglycemia, hypoxia, bacterial toxins, hyperthermia, hypothermia, and physiologic stress. More specifically, the hypothalamus monitors for these various stressors and, on excitation, CRH is secreted, which stimulates ACTH secretion from the adenohypophysis. Levels of adrenocortical hormones in the blood regulate secretion of ACTH with a hypothalamic feedback mechanism.3,4
Gonadotropic hormones regulate the growth, development, and function of the ovaries and testes. The gonadotropic hormones are the follicle-stimulating hormone and the luteinizing hormone. Secretion of the gonadotropic hormones is stimulated by gonadotropin-releasing hormone; the hormones are secreted by the hypothalamus.4
During normal activities of daily living, ADH is secreted in small amounts into the bloodstream for promotion of reabsorption of water by the renal tubules, which leads to a decreased excretion of water by the kidneys. When ADH is secreted in large quantities, vasoconstriction of the smooth muscles occurs and ultimately elevates the blood pressure. The pressor effects of ADH are produced only with large doses that are not in the usual physiologic range. The secretion of ADH is regulated by several feedback loops, one of which involves plasma osmolality. Within the hypothalamus are osmoreceptors, whose function is secretion of ADH when plasma osmolarity is increased. Alternatively, dilution of plasma inhibits ADH secretion. The second feedback loop or major stimulus of ADH secretion is the volume or stretch receptors located in the left atrium. These receptors are activated when the extracellular fluid volume is increased; with this activation, ADH secretion is inhibited. The baroreceptors, which are located in the carotid sinus and aortic arch, are the receptors for the third feedback loop. A decrease in the arterial blood pressure stimulates the baroreceptors, which in turn stimulate a release of ADH. Both the stretch receptors and the baroreceptors transmit neuronal input to the brain via the vagus nerve.4,5
Oxytocin produces contraction of uterine muscle at the end of gestation and has a role in milk excretion—that is, in stimulation of the contraction of the surrounding myoepithelial cells of the mammary glands.4,5
Hyperfunction rarely involves more than one endocrine gland. Alternatively, hypofunction usually involves more than one endocrine gland, although instances of isolated deficiencies have been reported. A common cause of pituitary hypofunction is compression of glandular cells by the expansion of a functional or nonfunctional tumor. In this situation, an excess of one hormone may coexist with a deficiency of another.4,5
The pineal gland is situated in the diencephalon just above the roof of the midbrain. This gland is considered an intricate and highly sensitive biologic clock because the secretory activity of the pineal gland is greatest at night. The pineal gland secretes melatonin, which affects the size and secretory activity of the ovaries and other organs. The production and release of melatonin are regulated by the sympathetic nervous system. In fact, the pineal gland is considered a neuroendocrine transducer because it converts nervous system input into a hormonal output.4,5
The thyroid gland is located in the anterior middle portion of the neck immediately below the larynx. The gland consists of two lobes attached by a strip of tissue called the isthmus. Structurally, this gland is composed of tiny sacs called follicles. Each follicle is formed by a single layer of epithelial cells that surround a cavity that contains a secretory product known as colloid. This colloid fluid consists mainly of a glycoprotein-iodine complex called thyroglobulin.4,5
On stimulation with TSH, thyroid hormones are produced in the following steps: (1) iodide trapping; (2) oxidation and iodination; (3) storage of the hormones in the colloid as part of the thyroglobulin molecules; and (4) proteolysis, which can be inhibited by iodide, and release of the hormones. The two hormones released from the thyroid gland are triiodothyronine (T3) and thyroxine (T4). T4 represents more than 95% of the circulating thyroid hormone and is considered to be relatively inactive physiologically in comparison with T3. Consequently, although T3 has a relatively low concentration, it passes out of the bloodstream faster than T4, has a more rapid action, and is probably the major biologically active thyroid hormone. After these hormones are secreted by the thyroid gland, they are transported to all parts of the body by means of plasma proteins in the form of protein-bound iodinated compounds. As a result, the laboratory test for protein-bound iodine is useful for determining of the amount of circulating thyroid hormone in the blood.4,5
T3 and T4 regulate the metabolic activities of the body. More specifically, they regulate the rate of cellular oxidation. In addition, they are essential for the normal growth and development of the body. Other metabolic activities that are influenced by T3 and T4 are the promotion of protein synthesis and breakdown, increase of glucose absorption and utilization, facilitation of gluconeogenesis, and maintenance of fluid and electrolyte balance. The thyroid hormones are also involved in a feedback mechanism. The concentration of T3 and T4 in the blood regulates the secretion of TSH by the anterior pituitary gland. TSH regulates the growth and secretory activity of the thyroid gland.4,5 See Fig. 15.1.