15 The endocrine system
Endocrine Gland: A group of hormone-secreting and hormone-excreting cells.
Gluconeogenesis: The conversion of amino acids into glucose.
Glycogenesis: The deposition of glycogen in the liver.
Hormone: A biochemical substance secreted by a specific endocrine gland and transported in the blood to distant points in the body for regulation of rates of physiologic processes.
Lipolysis: The mobilization of deposited fat.
Releasing Factor: A hormone of unknown chemical structure secreted by the hypothalamus.
Releasing Hormone: A hormone secreted from the hypothalamus.
Stress: A 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 Organ: A gland whose activities are regulated by tropic hormones.
Tropic Hormone: A hormone that regulates the blood level of a specific hormone secreted from another endocrine gland.
Arthur C. Guyton, the great professor of physiology, always began his lecture 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
Mediators of the endocrine system: the hormones
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
Physiology of the endocrine glands
Pituitary gland
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 stimulates the production and release of adrenocorticotropin (ACTH). The increased concentration of ACTH causes the hypothalamus to decrease its production of corticotropin-releasing hormone, 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 corticotropin-releasing hormone.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 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
Hormones of the adenohypophysis
Growth hormone, or somatotropin
The growth hormone is unique because it stimulates no target gland but 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. Giantism 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
Thyroid-stimulating hormone, or thyrotropin
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
Adrenocorticotropin
Adrenocorticotropin 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, corticotropin-releasing hormone (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
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
