4 3 case study endocrine and neural drug treatment

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Open Resources for Nursing (Open RN); Ernstmeyer K, Christman E, editors. Nursing Pharmacology [Internet]. 2nd edition. Eau Claire (WI): Chippewa Valley Technical College; 2023.

Nursing Pharmacology [Internet]. 2nd edition.

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Chapter 9 Endocrine System

9.1. endocrine introduction, learning objectives.

• Identify the classifications and actions of endocrine system drugs

• Give examples of when, how, and to whom endocrine system drugs may be administered

• Identify the side effects and special considerations associated with endocrine system drug therapy

• Identify the considerations and implications of using endocrine system medications across the life span

• Apply evidence-based concepts when using the nursing process

• Identify indications, side effects, and potential drug interactions associated with the use of herbal supplements

• Identify and interpret related laboratory tests

• Identify nursing responsibilities related to health teaching and health promotion

Have you ever wondered how your body controls functions such as digestion, metabolism, and the stress response? The endocrine system is always working behind the scenes, regulating various organs by releasing hormones and using feedback loops. This chapter will discuss medications that affect three of the major endocrine glands: the adrenal glands, the pancreas, and the thyroid.

9.2. BASIC CONCEPTS OF THE ENDOCRINE SYSTEM

Before we discuss endocrine medications, let’s review endocrine system anatomy and hormones to better understand the mechanism of action of endocrine medications.

Review of Anatomy and Physiology of the Endocrine System

You may never have thought of it this way, but when you send a text message to two friends to meet you at a restaurant at six, you’re sending digital signals that you hope will affect their behavior—even though they are some distance away. Similarly, certain cells send chemical signals to other cells in the body that influence their behavior. This long-distance intercellular communication, coordination, and control are critical for homeostasis, and it is the fundamental function of the endocrine system.

Whereas the nervous system uses neurotransmitters to communicate, the endocrine system uses  hormones  for chemical signaling. These hormone signals are sent by the endocrine organs. Hormones are transported primarily via the bloodstream throughout the body, where they bind to receptors on target cells, inducing a characteristic response. Some of the glands in the endocrine system include the pituitary, thyroid, parathyroid, adrenal, and pineal glands. See Figure 9.1 for an illustration of the endocrine system.[ 1 ] Some of these glands have both endocrine and nonendocrine functions. For example, the pancreas contains cells that function in digestion, as well as cells that secrete the hormones insulin and glucagon, which regulate blood glucose levels.[ 2 ]

Overview of the Endocrine System

This chapter will discuss medications that affect three major endocrine glands and their hormones: the adrenal glands, the pancreas, and the thyroid. See Table 9.2  for a list of hormones associated with each of these glands and their effects.[ 3 ]

Hormones Associated With Adrenal Glands, Pancreas, and Thyroid and Their Effects

View in own window

Regulation of Hormone Secretion

To prevent abnormal hormone levels and a potential disease state, hormone levels must be tightly controlled. Feedback loops govern the initiation and maintenance of hormone secretion in response to various stimuli.

The most common method of hormone regulation is the  negative feedback loop.  Negative feedback is characterized by the inhibition of further secretion of a hormone in response to adequate levels of that hormone. This allows blood levels of the hormone to be regulated within a narrow range. An example of a negative feedback loop is the release of glucocorticoid hormones from the adrenal glands, as directed by the hypothalamus and pituitary gland. As glucocorticoid concentrations in the blood rise, the hypothalamus and pituitary gland reduce their signaling to the adrenal glands to prevent additional glucocorticoid secretion.[ 4 ] See Figure 9.2 for an illustration of a negative feedback loop.[ 5 ]

Negative Feedback Loop

Endocrine Gland Stimuli

Endocrine glands can be stimulated by humoral stimuli, by stimulation of another hormone, or by neural stimuli.  Humoral stimuli  are changes in blood levels of nonhormone chemicals that cause the release or inhibition of a hormone to maintain homeostasis. For example, osmoreceptors in the hypothalamus detect changes in  blood osmolarity  (the concentration of solutes in the blood plasma). If blood osmolarity is too high, meaning that the blood is not dilute enough, osmoreceptors signal the hypothalamus to release ADH (antidiuretic hormone). ADH causes the kidneys to reabsorb more water and reduce the volume of urine produced. This reabsorption causes a reduction of the osmolarity of the blood by diluting the blood to the appropriate level. Another example of humoral stimuli is the regulation of blood glucose. High blood glucose levels cause the release of insulin from the pancreas, which increases glucose uptake by cells and liver storage of glucose as glycogen.

An endocrine gland may also secrete a hormone in response to the presence of another hormone produced by a different endocrine gland. For example, the thyroid gland secretes T4 into the bloodstream when triggered by thyroid-stimulating hormone (TSH) that is released from the anterior pituitary gland.

In addition to these chemical signals, hormones can also be released in response to  neural stimuli . An example of neural stimuli is the activation of the fight-or-flight response by the sympathetic nervous system. When an individual perceives danger, sympathetic neurons signal the adrenal glands to secrete norepinephrine and epinephrine. The two hormones dilate blood vessels, increase the heart and respiratory rate, and suppress the digestive and immune systems. These responses boost the body’s transport of oxygen to the brain and muscles, thereby improving the body’s ability to fight or flee.[ 6 ]

Hypothalamus–Pituitary Complex

The  hypothalamus–pituitary complex  can be thought of as the “command center” of the endocrine system. This complex secretes several hormones that directly produce responses in target tissues, as well as hormones that regulate the synthesis and secretion of hormones of other glands. In addition, the hypothalamus–pituitary complex coordinates the messages of the endocrine and nervous systems. In many cases, a stimulus received by the nervous system must pass through the hypothalamus–pituitary complex to be translated into hormones that can initiate a response. See Figure 9.3 for an illustration of the hypothalamus–pituitary complex.[ 7 ] The hypothalamus connects to the pituitary gland by the stalk-like infundibulum. The pituitary gland consists of an anterior and posterior lobe, with each lobe secreting different hormones in response to signals from the hypothalamus.

Illustration of the Hypothalamus–Pituitary Complex

Posterior Pituitary

The posterior pituitary gland does not produce hormones, but stores and secretes two hormones produced by the hypothalamus: oxytocin and antidiuretic hormone (ADH).

ANTIDIURETIC HORMONE (ADH)

Blood osmolarity, the concentration of sodium ions and other solutes, is constantly monitored by  osmoreceptors  in the hypothalamus. Blood osmolarity may change in response to the consumption of certain foods and fluids, as well as in response to disease, injury, medications, or other factors. In response to high blood osmolarity, which can occur during dehydration or following a very salty meal, the osmoreceptors signal the posterior pituitary to release antidiuretic hormone (ADH). Its effect is to cause increased water reabsorption by the kidneys. As more water is reabsorbed by the kidneys, a greater amount of water is returned to the blood, thus causing a decrease in blood osmolarity. The release of ADH is controlled by a negative feedback loop. As blood osmolarity decreases, the hypothalamic osmoreceptors sense the change and prompt a corresponding decrease in the secretion of ADH. As a result, less water is reabsorbed by the kidneys.

Drugs can also affect the secretion of ADH or imitate its effects. For example, alcohol consumption inhibits the release of ADH, resulting in increased urine production that can eventually lead to dehydration and a hangover. Vasopressin is a synthetic ADH medication used to treat very low blood pressure. It is called vasopressin because in very high concentrations it also causes constriction of blood vessels, in addition to the retention of water. Vasopressin is also used to treat a disease called  diabetes insipidus (DI)  that causes dehydration due to an underproduction of ADH.[ 8 ]

Anterior Pituitary

In contrast to the posterior pituitary, the anterior pituitary does manufacture hormones. However, the secretion of hormones from the anterior pituitary is regulated by two classes of hormones secreted by the hypothalamus called releasing hormones. Releasing hormones then stimulate the secretion of hormones from the anterior pituitary (see Figure 9.4 [ 9 ]). The anterior pituitary produces seven hormones. These are the growth hormone (GH), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), beta endorphin, and prolactin. Of the hormones of the anterior pituitary, TSH, ACTH, FSH, and LH are collectively referred to as  tropic hormones  (trope- = “turning”) because they turn on or off the function of other endocrine glands. This module will focus on the effects of TSH and ACTH.

Hypothalamus Releases Hormones to Regulate Release of Hormones From Anterior Pituitary

THYROID-STIMULATING HORMONE (TSH)

The activity of the thyroid gland is regulated by the thyroid-stimulating hormone (TSH). TSH is released from the anterior pituitary in response to the thyrotropin-releasing hormone (TRH) from the hypothalamus and triggers the secretion of thyroid hormones by the thyroid gland. In a classic negative feedback loop, elevated levels of thyroid hormones in the bloodstream then trigger a drop in production of TRH and subsequently, the production of TSH. TSH is further discussed in the “ Thyroid Medications ” section of this chapter.

ADRENOCORTICOTROPIC HORMONE (ACTH)

The adrenocorticotropic hormone (ACTH) is released from the anterior pituitary in response to the corticotropin-releasing hormone (CRH) from the hypothalamus. ACTH then stimulates the adrenal cortex to secrete corticosteroid hormones such as cortisol. A variety of stressors can also influence the release of ACTH, and the role of ACTH in the stress response is discussed under the “ Corticosteroids ” section of this chapter.[ 10 ]

“Endocrine gland match-up” by E. Christman for   Open RN   is licensed under   CC BY 4.0

9.3. CORTICOSTERIODS

This section will review the anatomy and physiology of the adrenal gland, outline common disorders affecting the adrenal gland, apply the nursing process to administering corticosteroids, and then discuss the medication classes of corticosteroids.

Review Anatomy and Physiology of the Adrenal Glands

The adrenal gland consists of the adrenal cortex that is composed of glandular tissue and the adrenal medulla that is composed of nervous tissue. Each region secretes its own set of hormones.

The adrenal cortex is a component of the  hypothalamic-pituitary-adrenal (HPA) axis . The hypothalamus stimulates the release of ACTH from the pituitary, which then stimulates the adrenal cortex to produce steroid hormones that are important for the regulation of the stress response, blood pressure and blood volume, nutrient uptake and storage, fluid and electrolyte balance, and inflammation.

The  adrenal medulla  is neuroendocrine tissue composed of postganglionic sympathetic nervous system (SNS) neurons that secrete the hormones epinephrine and norepinephrine. It is an extension of the autonomic nervous system, which regulates homeostasis in the body. See Figure 9.5 [ 1 ] for an illustration of the adrenal gland and associated hormones.

Adrenal Gland and Associated Hormones

One of the major functions of the adrenal gland is to respond to stress. The body responds in different ways to short-term stress and long-term stress following a pattern known as the  general adaptation syndrome (GAS) . Stage one of GAS is called the alarm reaction. This is short-term stress, also called the fight-or-flight response, and is mediated by the hormones epinephrine and norepinephrine from the adrenal medulla. Their function is to prepare the body for extreme physical exertion. If the stress is not soon relieved, the body adapts to the stress in the second stage called the stage of resistance. If a person is starving for example, the body may send signals to the gastrointestinal tract to maximize the absorption of nutrients from food. If the stress continues for a longer term however, the body responds with symptoms such as depression, suppressed immune response, or severe fatigue. These symptoms are mediated by the hormones of the adrenal cortex, especially cortisol.

Adrenal hormones also have several nonstress-related functions, including the increase of blood sodium and glucose levels, which will be described in further detail below.

Mineralocorticoids: Aldosterone

The most superficial region of the adrenal cortex is the zona glomerulosa, which produces a group of hormones collectively referred to as  mineralocorticoids  because of their effect on body minerals, especially sodium and potassium. These hormones are essential for fluid and electrolyte balance.  Aldosterone  is the major mineralocorticoid that is important in the regulation of the concentration of sodium and potassium ions in the body. The secretion of aldosterone by the adrenal cortex is prompted by the HPA axis when the hypothalamus triggers ACTH release from the anterior pituitary. It is released in response to elevated blood levels of potassium (K+), low blood levels of sodium (Na+), low blood pressure, or low blood volume. Aldosterone targets the kidneys and increases the excretion of K+ and the retention of Na+, which, in turn, causes the retention of water, thus increasing blood volume and blood pressure.

Aldosterone is also a key component of the renin-angiotensin-aldosterone system (RAAS) in which specialized cells of the kidneys secrete renin in response to low blood volume or low blood pressure. Renin then catalyzes the conversion of the blood protein angiotensinogen, which is produced by the liver, to the hormone Angiotensin I. Angiotensin I is converted in the lungs to Angiotensin II by the angiotensin-converting enzyme (ACE). Angiotensin II has three major functions: initiating vasoconstriction of the arterioles, thus decreasing blood flow; stimulating kidney tubules to reabsorb sodium and water, thus increasing blood volume; and signaling the adrenal cortex to secrete aldosterone, which further increases blood volume and blood pressure. It is important to understand these effects because many cardiac medications target the effects of aldosterone and the RAAS system. For example, drugs that block the production of Angiotensin II are known as ACE inhibitors. ACE inhibitors are used to help lower blood pressure in clients with hypertension by blocking the ACE enzyme from converting Angiotensin I to Angiotensin II, which, in turn, causes vasodilation of the arterioles. Another medication called spironolactone is used as a diuretic because it blocks the effects of aldosterone and, thus, causes the kidneys to eliminate water and sodium to decrease blood volume and blood pressure.

Glucocorticoids: Cortisol

The intermediate region of the adrenal cortex produces hormones called glucocorticoids because of their role in glucose metabolism. In response to long-term stressors, the HPA axis triggers the release of glucocorticoids. Their overall effect is to inhibit tissue building while stimulating the breakdown of stored nutrients to maintain adequate fuel supplies. In conditions of long-term stress, cortisol promotes the catabolism of glycogen to glucose, stored triglycerides into fatty acids and glycerol, and muscle proteins into amino acids. These raw materials can then be used to synthesize additional glucose and ketones for use as body fuels. However, the negative effects of catabolism for energy can result in muscle breakdown and weakness, poor wound healing, and the suppression of the immune system.

Many medications contain glucocorticoids to treat various conditions, such as cortisone injections for inflamed joints; prednisone tablets, IV medications, and steroid-based inhalers to manage inflammation that occurs in asthma; and hydrocortisone creams that are applied to relieve itchy skin rashes.

The deepest region of the adrenal cortex produces small amounts of a class of steroid sex hormones called androgens. During puberty and most of adulthood, androgens are produced in the gonads. The androgens produced in the adrenal cortex supplement the gonadal androgens.

Adrenal Medulla: Epinephrine and Norepinephrine

As noted earlier, the adrenal cortex releases glucocorticoids in response to long-term stress such as severe illness. In contrast, the adrenal medulla releases its hormones in response to acute, short-term stress mediated by the sympathetic nervous system (SNS). The medullary tissue is composed of unique postganglionic SNS neurons called chromaffin cells that produce the neurotransmitters epinephrine (also called adrenaline) and norepinephrine (also called noradrenaline), which are chemically classified as catecholamines. Epinephrine is produced in greater quantities and is the more powerful hormone.

The secretion of medullary epinephrine and norepinephrine is controlled by a neural pathway that originates from the hypothalamus in response to danger or stress. Both epinephrine and norepinephrine increase the heart rate, pulse, and blood pressure to prepare the body to fight the perceived threat or flee from it. In addition, the pathway dilates the airways, raising blood oxygen levels. It also prompts vasodilation, further increasing the oxygenation of important organs such as the lungs, brain, heart, and skeletal muscle while also prompting vasoconstriction to blood vessels serving less-essential organs such as the gastrointestinal tract, kidneys, and skin. It also downregulates some components of the immune system. Other effects include a dry mouth, loss of appetite, pupil dilation, and a loss of peripheral vision.

Disorders Involving the Adrenal Glands

Several disorders are caused by the dysregulation of the hormones produced by the adrenal glands. For example, Cushing’s disease is a disorder characterized by high blood glucose levels, the development of a moon-shaped face, a buffalo hump on the back of the neck, rapid weight gain, and hair loss. It is caused by hypersecretion of cortisol as the result of an ACTH-producing pituitary tumor. Cushing’s syndrome can also be caused by long-term use of corticosteroid medications.

In contrast, the hyposecretion of corticosteroids can result in Addison’s disease, a disorder that causes low blood glucose levels and low blood sodium levels. Addisonian crisis is a life-threatening condition due to severely low blood pressure resulting from a lack of corticosteroid levels.[ 2 ],[ 3 ],[ 4 ],[ 5 ]

View a supplementary YouTube video about ACTH and the adrenal gland:

ACTH and the Adrenal Gland[ 6 ]

Applying the Nursing Process to Corticosteroids

Before initiating long-term systemic corticosteroid therapy, a thorough history and physical examination should be performed to assess for risk factors or preexisting conditions that may potentially be exacerbated by glucocorticoid therapy, such as diabetes, dyslipidemia, cerebrovascular disease (CVD), GI disorders, affective disorders, or osteoporosis. At a minimum, baseline measures of body weight, height, bone mineral density, and blood pressure should be obtained, along with laboratory assessments that include a complete blood count (CBC), blood glucose values, and lipid profile. In children, nutritional and pubertal status should also be examined. Symptoms of and/or exposure to serious infections should also be assessed as corticosteroids are contraindicated in clients with untreated systemic infections. Concomitant use of other medications should also be assessed before initiating therapy as significant drug interactions have been noted between glucocorticoids and several drug classes. Females of childbearing age should also be questioned about the possibility of pregnancy because use in pregnancy may increase the risk of cleft palate in offspring.[ 7 ]

Implementation

Long-term corticosteroid therapy should never be stopped abruptly due to the risk of Addisonian crisis. Instead, the dose should be tapered to allow the body to resume natural production of adrenal hormone levels. Addisonian crisis is a potentially life-threatening condition resulting from an acute insufficiency of adrenal hormones that can occur if chronic corticosteroid therapy is suddenly stopped.

Clients on long-term corticosteroid therapy who are also at high risk for fractures are recommended to receive concurrent pharmacological treatment for osteoporosis. Alendronate, a bisphosphonates class of medication, is often used, in addition to other osteoporosis preventative measures such as weight-bearing exercise and calcium/vitamin D supplementation.[ 8 ]

The lowest effective dose should be used for treatment of the underlying condition, and the dose should be reevaluated regularly to determine if further reductions can be instituted.

The parameters described under “Assessment” should be monitored regularly. Health care professionals should monitor for adrenal suppression in clients who have been treated with corticosteroids for greater than two weeks or in multiple short courses of high-dose therapy. Symptoms of adrenal insufficiency include weakness/fatigue, malaise, nausea, vomiting, diarrhea, abdominal pain, headache (usually in the morning), poor weight gain and/or growth in children, myalgia, arthralgia, psychiatric symptoms, hypotension, and hypoglycemia. If these symptoms occur, further lab work, such as an early morning cortisol test, should be performed.[ 9 ]

Corticosteroids

Mechanism of Action:  Glucocorticoids cause profound and varied metabolic effects as described earlier in this section. In addition, they modify the body’s immune responses.[ 10 ]

Indications:  Corticosteroids are used as replacement therapy in adrenal insufficiency, as well as for the management of various dermatologic, ophthalmologic, rheumatologic, pulmonary, hematologic, and gastrointestinal (GI) disorders. In respiratory conditions, systemic corticosteroids are used for the treatment of acute exacerbations of chronic obstructive pulmonary disease (COPD) and severe asthma. Mineralocorticoids are primarily involved in the regulation of electrolyte and water balance. Glucocorticoids are predominantly involved in carbohydrate, fat, and protein metabolism and also have anti-inflammatory, immunosuppressive, anti-proliferative, and vasoconstrictive effects. Prednisone is perhaps the most widely used of the systemic corticosteroids. It is generally used as an anti-inflammatory and immunosuppressive agent. Hydrocortisone is a commonly used topical cream for itching, and its oral formulation is used to treat Addison’s disease.[ 11 ] Methylprednisolone is a commonly used injectable corticosteroid. Fludrocortisone has much greater mineralocorticoid potency and, therefore, is commonly used to replace aldosterone in Addison’s disease.[ 12 ] See Figure 9.6 [ 13 ],[ 14 ],[ 15 ] for images of various formulations of corticosteroids.

Examples of Corticosteroid Medications (fluticasone inhaler, intravenous methylprednisolone, and prednisone tablets)

Corticosteroids are used for a variety of disorders such as the following:

• Endocrine disorders such as adrenocortical insufficiency
• Rheumatic disorders such as rheumatoid arthritis
• Collagen diseases such as systemic lupus erythematosus
• Dermatologic diseases such as severe psoriasis
• Allergic states such as contact dermatitis or drug hypersensitivity reactions
• Ophthalmic diseases such as optic neuritis
• Respiratory diseases such as asthma or COPD
• Neoplastic diseases such as leukemia
• Gastrointestinal diseases such as ulcerative colitis
• Nervous system diseases such as multiple sclerosis[ 16 ]

Nursing Considerations:  Despite their beneficial effects, long-term systemic use of corticosteroids is associated with well-known adverse events, including osteoporosis and fractures, adrenal suppression, hyperglycemia and diabetes, cardiovascular disease and dyslipidemia, dermatological and GI events, psychiatric disturbances, and immunosuppression. One side effect that is unique to children is growth suppression.[ 17 ] Therefore, the lowest possible dose of corticosteroid should be used to control the condition under treatment to avoid the development of these adverse effects. When reduction in dosage is possible, the reduction should be gradual and should not be stopped abruptly because of the associated HPA suppression that occurs with long-term administration. This hypothalamus-pituitary-adrenal (HPA) suppression can cause an impaired stress response, which may persist for months after discontinuation of therapy; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted. Alternate day therapy is a corticosteroid dosing regimen in which twice the usual daily dose of corticoid is administered every other morning. The purpose of this mode of therapy is to minimize undesirable effects that can occur during long-term administration.

Dosages are variable and tailored to the disease process and the individual.

Side Effects/Adverse Effects:  Adverse/side effects of corticosteroids include fluid and electrolyte imbalances; muscle weakness; peptic ulcers; thin, fragile skin that bruises easily; poor wound healing; and the development of Cushing’s syndrome. Corticosteroids may mask some signs of infection, and new infections may appear during their use. Psychic derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, and personality changes to severe depression.

Health Teaching & Health Promotion:  Teach clients taking long-term prednisone therapy to never abruptly stop taking the medication and to report any adverse/side effects or new signs of infection.[ 18 ] Glucocorticoid medication can cause immunosuppression, which makes it more difficult to detect signs of infection. Clients should seek advice from health care providers regarding vaccination administration while on glucocorticoids. Clients should report unusual swelling, weight gain, fatigue, bone pain, bruising, nonhealing sores, and visual and behavioral disturbances to the provider.

Use of glucocorticoid therapy may cause an increase in blood glucose levels. Clients should be advised to consume diets that are high in protein, calcium, and potassium.

Now let’s take a closer look at the medication grid comparing different formulations of corticosteroids in Table 9.3 .[ 19 ],[ 20 ],[ 21 ],[ 22 ],[ 23 ] Medication grids are intended to assist students to learn key points about each medication. Because information about medication is constantly changing, nurses should always consult evidence-based resources to review current recommendations before administering specific medication. Basic information related to each class of medication is outlined below. Detailed information on a specific medication can be found for free at  DailyMed . On the home page, enter the drug name in the search bar to read more about the medication. Prototype/generic medications listed in the grids below are also linked to a DailyMed page.

Prednisone, Methylprednisolone, Hydrocortisone, and Fludrocortisone Medication Grid

Critical Thinking Activity 9.3

A client in a long-term care facility who has COPD receives prednisone 10 mg daily to help manage her respiratory status. Upon reviewing the client’s chart, the nurse notices that the client was diagnosed with osteoporosis in the past but is not currently receiving medications indicated for osteoporosis. The nurse is concerned because the client requires assistance and is a fall risk, so the nurse plans to call the provider.

1. What cues in the client’s medical history cause the nurse to be concerned about the risk for a fracture?

2. What medication(s) may be prescribed concurrently with prednisone to reduce the risk for a fracture?

3. What other client teaching can the nurse provide to help reduce the client’s risk for a fracture?

4. Bedside glucose testing with sliding scale insulin is ordered for this client, although she has no history of diabetes mellitus. What is the rationale for these orders?

5. What cues would cause the nurse to contact the provider with the hypothesis that adrenal suppression is occurring?

Note: Answers to the Critical Thinking activities can be found in the “ Answer Key ” section at the end of the book.

9.4. ANTIDIABETICS

This section will review the anatomy and physiology of the pancreas, discuss diabetes mellitus and insulin treatment, apply the nursing process to administering antidiabetics, and then discuss antihyperglycemic medications.

Review of Anatomy and Physiology of the Pancreas

The pancreas is a long, slender organ located near the stomach (see Figure 9.7 ).[ 1 ] Although it is primarily an  exocrine gland , secreting a variety of digestive enzymes, the pancreas also has an endocrine function. Pancreatic islets, clusters of cells formerly known as the islets of Langerhans, secrete glucagon and insulin. Glucagon plays an important role in blood glucose regulation because low blood glucose levels stimulate its release. On the other hand, elevated blood glucose levels stimulate the release of insulin.

Regulation of Blood Glucose Levels by Insulin and Glucagon

Glucose is the preferred fuel for all body cells. The body derives glucose from the breakdown of the carbohydrate-containing foods and drinks we consume. Glucose not immediately taken up by cells for fuel can be stored by the liver and muscles as glycogen or converted to triglycerides and stored in the adipose tissue. Hormones regulate both the storage and the utilization of glucose as required. Receptors located in the pancreas sense blood glucose levels, and subsequently, the pancreatic cells secrete glucagon or insulin to maintain normal levels.

Receptors in the pancreas can sense the decline in blood glucose levels, such as during periods of fasting or during prolonged labor or exercise. In response, the alpha cells of the pancreas secrete the hormone glucagon, which has these effects:

• It stimulates the liver to convert stores of glycogen back into glucose. This response is known as glycogenolysis. The glucose is then released into the circulation for use by body cells.
• It stimulates the liver to take up amino acids from the blood and convert them into glucose. This response is known as gluconeogenesis.
• It stimulates lipolysis, the breakdown of stored triglycerides into free fatty acids and glycerol. Some of the free glycerol released into the bloodstream travels to the liver, which converts it into glucose. This is also a form of gluconeogenesis.

Taken together, these actions increase blood glucose levels. The activity of glucagon is regulated through a negative feedback mechanism; rising blood glucose levels inhibit further glucagon production and secretion. See Figure 9.8 [ 2 ] for an illustration of homeostatic regulation of blood glucose levels.

Homeostatic Regulation of Blood Glucose Levels. Blood glucose concentration is tightly maintained between 70 mg/dL and 110 mg/dL. If blood glucose concentration rises above this range, insulin is released, which stimulates body cells to remove glucose (more...)

Insulin  facilitates the uptake of glucose into skeletal and adipose body cells. The presence of food in the intestine triggers the release of gastrointestinal tract hormones. This, in turn, triggers insulin production and secretion by the beta cells of the pancreas. Once nutrient absorption occurs, the resulting surge in blood glucose levels further stimulates insulin secretion.

Insulin triggers the rapid movement of glucose transporter vesicles to the cell membrane, where they are exposed to the extracellular fluid. The transporters then move glucose by facilitated diffusion into the cell interior.

Insulin also reduces blood glucose levels by stimulating  glycolysis , the metabolism of glucose for generation of ATP. It further stimulates the liver to convert excess glucose into glycogen for storage, and it inhibits enzymes involved in glycogenolysis and gluconeogenesis. Finally, insulin promotes triglyceride and protein synthesis. The secretion of insulin is regulated through a negative feedback mechanism. As blood glucose levels decrease, further insulin release is inhibited.

Common Disorder of the Pancreas: Diabetes Mellitus

Dysfunction of insulin production and secretion, as well as the target cells’ responsiveness to insulin, can lead to a condition called diabetes mellitus, a common disease that affects the ability of the body to produce and/or utilize insulin. There are two main forms of diabetes mellitus.  Type 1 diabetes  is an autoimmune disease affecting the beta cells of the pancreas. The beta cells of people with type 1 diabetes do not produce insulin; thus, synthetic insulin must be administered by injection or infusion.  Type 2 diabetes  accounts for approximately 95 percent of all cases. It is acquired, and lifestyle factors such as poor diet and inactivity greatly increase a person’s risk. In type 2 diabetes, the body’s cells become resistant to the effects of insulin. In response, the pancreas increases its insulin secretion, but over time, the beta cells become exhausted. In many cases, type 2 diabetes can be reversed by moderate weight loss, regular physical activity, and consumption of a healthy diet. However, if blood glucose levels cannot be controlled, oral diabetic medication is implemented, and eventually the type 2 diabetic may require insulin.

Diabetes is diagnosed when lab tests reveal that blood glucose levels are higher than normal, a condition called  hyperglycemia .[ 3 ] According to the American Diabetes Association (ADA), normal fasting blood glucose levels for non-diabetic clients are 80-130 mg/dL. Glycosylated hemoglobin, also called A1C, is used to assess long-term blood glucose levels over three months. The ADA states that A1C target levels vary according to age and health, but the generalized A1C target is less than 7%, which equates to an average blood glucose level of 154.[ 4 ]

Insulin Treatment

Because the hallmark of type 1 diabetes is absent or near-absent β-cell function, insulin treatment is essential for individuals with type 1 diabetes. Current evidence-based recommendations regarding pharmacological treatment of type 1 diabetes from the American Diabetes Association (ADA) include the following:

• Most people with type 1 diabetes should be treated with multiple daily injections of prandial and basal insulin or continuous subcutaneous insulin infusion.
• Most individuals with type 1 diabetes should use rapid-acting insulin analogs to reduce hypoglycemia risk.
• Individuals with type 1 diabetes on prandial insulin doses should be educated on carbohydrate intake, premeal blood glucose levels, and anticipated physical activity.
• Individuals with type 1 diabetes who have been successfully using continuous subcutaneous insulin infusion should have continued access to this therapy after they turn 65 years of age.

Basal insulin  can be long-acting (insulin glargine or insulin detemir) or intermediate-acting (insulin isophane suspension [NPH]).  Prandial insulins  are used with meals and may be rapid-acting (insulin lispro, insulin aspart, or insulin glulisine) or short- acting (regular insulin).

According to the ADA, insulin requirements can be estimated based on weight, with typical doses ranging from 0.4 to 1.0 units/kg/day. Higher amounts are required during puberty, pregnancy, and medical illness. Physiologic insulin secretion varies with glycemia, meal size, and tissue demands for glucose. To approach this variability in people using insulin treatment, most individuals with type 1 diabetes are treated with multiple daily injections of basal and mealtime insulin or continuous subcutaneous insulin infusion. Thus, health teaching for individuals with type 1 diabetes should include how to match mealtime insulin doses to carbohydrate intake, fat and protein content, as well as their anticipated physical activity. Ensuring that clients and/or caregivers understand correct insulin injection technique is also important to optimize glucose control and insulin use safety.[ 5 ]

Clients on insulin therapy are at risk for  hypoglycemia . It is essential for the nurse to monitor for signs of hypoglycemia and to intervene appropriately. See Table 9.4a for symptoms of hypoglycemia. Hypoglycemia is defined as a blood glucose level below 70 mg/dL; severe hypoglycemia refers to a blood glucose level below 40 mg/dL.

Hypoglycemia Symptoms

If a client with diabetes shows a sudden change in mood or mental status or other symptoms of hypoglycemia, the nurse should immediately check the blood glucose level. Health care agencies use hypoglycemia protocols so that the nurse can react quickly to episodes of hypoglycemia before they become severe. Hypoglycemia protocols contain orders for immediate treatment by the nurse. For instance, in clients who can tolerate oral intake, 15 grams of rapidly digested carbohydrates (such as 4 ounces of fruit juice) are recommended. In clients who are NPO or can’t take oral treatment, dextrose 50% IV or glucagon IM or subcutaneously is administered. Clients who have had a hypoglycemic episode should be monitored closely for the following 24 hours because they are at increased risk for another episode. The provider and the oncoming nurse should be notified of hypoglycemia episodes to discuss the possible cause of the hypoglycemic event and make insulin adjustments, if needed, to avoid additional hypoglycemia. Tracking hypoglycemia episodes and analyzing causes are important performance improvement activities.[ 6 ]

The arrival of continuous glucose monitors to clinical practice has been proven to reduce nocturnal hypoglycemia in people using insulin pumps with glucose sensors due to automatic suspension of insulin delivery at a preset glucose level. The U.S. Food and Drug Administration has approved two hybrid closed-loop pump systems.[ 7 ] A hybrid closed-loop pump system automatically adjusts basal insulin delivery every five minutes based on sensor glucose to maintain blood glucose levels as close to a specific target as possible.[ 8 ]

According to the ADA, lifestyle modifications that improve health should be emphasized, along with any pharmacologic therapy. Lifestyle modifications include healthy food choices to stabilize blood glucose levels, as well as daily exercise.

HYPOKALEMIA

All insulin products cause a shift in potassium from the extracellular to intracellular space, which can possibly lead to hypokalemia. Untreated hypokalemia may cause respiratory paralysis, ventricular arrhythmia, and death. Monitor potassium levels in clients at risk for hypokalemia due to other medications such as diuretics.

INSULIN PENS

Insulin pens are often used in inpatient settings, as well as for self-administration, to facilitate safe and accurate self-administration of insulin. See Figure 9.9 [ 9 ] for an image of an insulin pen.

Insulin Pen

According to the ISMP, insulin pens offer several advantages over vials beyond dosing accuracy, convenience, and ease of use:

• Each pen is already labeled by the manufacturer with the product name and product barcode (whereas syringes of insulin prepared on the care unit from vials run the risk of being unlabeled).
• Each pen can be individually labeled with the client’s name (and ideally with a client-specific barcode).
• The pen provides the client’s insulin in a form ready for administration.
• The pen lessens nursing time needed to prepare and administer insulin.
• Insulin pens reduce medication waste that can occur when dispensing 10 mL-sized insulin vials for each client.

However, improper sharing of insulin pens among multiple clients has exposed clients to blood-borne pathogens. Insulin pens should never be reused for multiple clients; even if the needle is changed between clients, there can still be body fluid exposure.[ 10 ]

HIGH-ALERT MEDICATION AND PREVENTION OF ERRORS

Insulin is a high-alert medication that can be associated with significant client harm when used in error. A variety of error types have been associated with insulin therapy, including administration of the wrong insulin product, improper dosing (underdosing and overdosing), dose omissions, incorrect use of insulin delivery devices, wrong route (intramuscular versus subcutaneous), and improper client monitoring. Many errors result in serious hypoglycemia or hyperglycemia. Hypoglycemia is often caused by a failure to adjust insulin therapy in response to a reduction in nutritional intake or an excessive insulin dose stemming from a prescribing or dose measurement error. Other factors that contribute to serious hypoglycemia include inappropriate timing of insulin doses with food intake, creatinine clearance, body weight, changes in medications that affect blood glucose levels, poor communication during client transfer to different care teams, and poor coordination of blood glucose testing with insulin administration at mealtime.

In an inpatient setting, manifestations of poor glycemic control, including severe hypoglycemia and hyperglycemia, are deemed hospital-acquired conditions by the Centers for Medicare and Medicaid Services (CMS). CMS notes that poor glycemic control can be reasonably prevented with implementation of evidence-based guidelines; thus, the CMS denies payment for diabetic ketoacidosis, hypoglycemic coma, and other serious conditions related to poor glycemic control. Agency policies and procedures should be closely followed to avoid these errors and manifestations of poor glycemic control.

One strategy for look-alike medications such as Humalog and Humalin is tall man lettering on the label. Tall man lettering describes a method for differentiating the unique letter characters of similar drug names known to be confused with one another, such as HumaLOG and HumaLIN.

ISMP recommends the following safe practice guidelines for the administration of insulin by the nurse[ 11 ]:

• Client-specific insulin pens are stored on clinical units in a manner that prevents their inadvertent use on more than one client.
• A coordinated process is developed to ensure timely blood glucose checks and administration of prandial insulin in conjunction with meal delivery.
• Verbal communication of point-of-care blood glucose value results are avoided as much as possible and are NEVER routinely used as the only source of information when determining insulin doses.
• Appropriately label all clinician-prepared syringes of subcutaneous insulin, unless the medication is prepared at the client’s bedside and is immediately administered to the client without any break in the process.
• Confirms that there is an appropriate indication
• Assesses the client’s most current blood glucose value
• Assesses the client for symptoms of hypoglycemia
• Informs the client of their most current blood glucose level
• Informs the client of their dose, the full name of the product, and the insulin’s intended action
• An individual insulin pen is never used for more than one client.
• Barcode scanning is used to verify that a client-specific pen is used to administer the correct insulin to the correct client.
• Prior to transitions of care, a process is in place to ensure that clients will have the necessary prescriptions, supplies, a follow-up care plan, and printed instructions for all prescribed insulin and blood glucose monitoring.
• Demonstration of proper dose measurement and self-administration using the same administration device that will be used at home (e.g., vial and syringe, pen, pump)
• Correct monitoring of blood glucose values
• The signs and symptoms of hyper- and hypoglycemia and how to respond if these symptoms occur
• Common types of errors possible with their insulin therapy and how to prevent or detect these errors
• The importance of regular follow-up with their primary care provider/specialist, including the date of their next appointment
• Clients who self-administer concentrated U-500 insulin using a vial and syringe are taught to use only a U-500 syringe and communicate their doses in terms of the name and concentration of the insulin and the actual dose in units using only the U-500 syringe

LIFE SPAN CONSIDERATIONS

Older adults are at higher risk for hypoglycemia episodes. The ADA has established the following evidence-based recommendations from well-conducted studies for older adult clients with diabetes[ 12 ]:

• Consider the assessment of medical, psychological, functional (self-management abilities), and social domains in older adults to provide a framework to determine targets and therapeutic approaches for diabetes management.
• Screen for geriatric syndromes (i.e., polypharmacy, cognitive impairment, depression, urinary incontinence, falls, persistent pain, and frailty) in older adults, as they may affect diabetes self-management and diminish quality of life.
• Screening for early detection of mild cognitive impairment or dementia should be performed for adults 65 years of age or older at the initial visit, annually, and as appropriate.
• Because older adults with diabetes have a greater risk of hypoglycemia than younger adults, episodes of hypoglycemia should be ascertained and addressed at routine visits.
• For older adults with type 1 diabetes, continuous glucose monitoring should be considered to reduce hypoglycemia.
• Optimal nutrition and protein intake is recommended for older adults; regular exercise, including aerobic activity, weight-bearing exercise, and/or resistance training, should be encouraged in all older adults who can safely engage in such activities.
• For older adults with type 2 diabetes, overweight/obesity, and capacity to safely exercise, an intensive lifestyle intervention focused on dietary changes, physical activity, and modest weight loss (e.g., 5–7%) should be considered for its benefits on quality of life, mobility and physical functioning, and cardiometabolic risk factor control.
• In older adults with type 2 diabetes at increased risk of hypoglycemia, medication classes with low risk of hypoglycemia are preferred.
• Overtreatment of diabetes is common in older adults and should be avoided.
• Deintensification (or simplification) of complex regimens is recommended to reduce the risk of hypoglycemia and polypharmacy, if it can be achieved within the individualized A1C target.
• Consider costs of care and insurance coverage rules when developing treatment plans in order to reduce risk of cost-related nonadherence.

Children and Adolescents

Type 1 diabetes is the most common form of diabetes in youth. Unique aspects of care and management of children and adolescents with type 1 diabetes must be considered, such as changes in insulin sensitivity related to physical growth and sexual maturation, ability to provide self-care, supervision in the childcare and school environment, neurological vulnerability to hypoglycemia and hyperglycemia in young children, as well as possible adverse neurocognitive effects of diabetic ketoacidosis (DKA). The ADA has established several evidence-based recommendations from well-conducted studies for children and adolescents with diabetes, including, but not limited to, the following[ 13 ]:

• Youth with type 1 diabetes and their parents/caregivers (for clients aged <18 years) should receive culturally sensitive, developmentally appropriate, and individualized health teaching regarding diabetes self-management and support according to national standards at initial diagnosis and routinely thereafter.
• Individualized medical nutrition therapy is recommended for children and adolescents with type 1 diabetes as an essential component of the overall treatment plan.
• Monitoring carbohydrate intake, whether by carbohydrate counting or experience-based estimation, is a key component to optimizing glycemic management.
• Encourage developmentally appropriate family involvement in diabetes management tasks for children and adolescents, recognizing that premature transfer of diabetes care responsibility to the youth can result in diabetes burnout, suboptimal diabetes management, and deterioration in glycemic control.
• Providers should consider asking youth and their parents/caregivers about social adjustment (peer relationships) and school performance to determine whether further intervention is needed.
• Assess youth with diabetes for psychosocial and diabetes-related distress, generally starting at 7–8 years of age.
• Starting at puberty, preconception counseling should be incorporated into routine diabetes care for all girls of childbearing potential.
• Begin screening youth with type 1 diabetes for disordered eating between 10 and 12 years of age. The Diabetes Eating Problems Survey-Revised (DEPS-R) is a reliable, valid, and brief screening tool for identifying disturbed eating behavior.
• All children and adolescents with type 1 diabetes should monitor glucose levels multiple times daily (up to 6–10 times/day by blood glucose meter or continuous glucose monitoring), including prior to meals and snacks, at bedtime, and as needed for safety in specific situations such as exercise, driving, or the presence of symptoms of hypoglycemia.
• Real-time continuous glucose monitoring should be offered for diabetes management in youth with diabetes on multiple daily injections or insulin pump therapy who are capable of using the device safely (either by themselves or with caregivers). The choice of device should be made based on client circumstances, desires, and needs.
• Automated insulin delivery systems or insulin pump therapy should be offered for diabetes management to youth with type 1 diabetes who are capable of using the device safely (either by themselves or with caregivers). The choice of device should be made based on client circumstances, desires, and needs.
• A1C goals must be individualized and reassessed over time. An A1C of <7% is appropriate for many children. Less stringent A1C goals (such as <7.5% or 8%) may be appropriate for clients who cannot articulate symptoms of hypoglycemia; have hypoglycemia unawareness; lack access to analog insulins, advanced insulin delivery technology, and/or continuous glucose monitoring; cannot check blood glucose regularly; or have nonglycemic factors that increase A1C (e.g., high glycators).
• Blood pressure should be measured at every routine visit. In youth with high blood pressure (blood pressure ≥90th percentile for age, sex, and height or, in adolescents aged ≥13 years, blood pressure ≥120/80 mmHg) on three separate measurements, ambulatory blood pressure monitoring should be strongly considered.
• In addition to lifestyle modification, ACE inhibitors or angiotensin receptor blockers should be started for treatment of confirmed hypertension (defined as blood pressure consistently ≥95th percentile for age, sex, and height or, in adolescents aged ≥13 years, ≥130/80 mmHg). Due to the potential teratogenic effects, females should receive reproductive counseling, and ACE inhibitors and angiotensin receptor blockers should be avoided in females of childbearing age who are not using reliable contraception.
• Elicit a smoking history at initial and follow-up diabetes visits; discourage smoking in youth who do not smoke and encourage smoking cessation in those who do smoke.
• All youth with type 2 diabetes and their families should receive comprehensive diabetes self-management teaching and support that is specific to youth with type 2 diabetes and is culturally appropriate.
• Nutrition for youth with prediabetes and type 2 diabetes, like for all children and adolescents, should focus on healthy eating patterns that emphasize consumption of nutrient-dense, high-quality foods and decreased consumption of calorie-dense, nutrient-poor foods, particularly sugar-added beverages.

Applying the Nursing Process to Administering Antidiabetics

Clients with diabetes should be continuously monitored for signs of hypoglycemia and hyperglycemia. When a client with diabetes is experiencing stress or an infection, the nurse should plan to assess the blood glucose levels more frequently.

The nurse should follow agency policy and ISMP guidelines for safe insulin administration. See the “ Preventing Medication Errors ” section in the “Legal/Ethical” chapter for more information about ISMP guidelines regarding insulin as a “High-Alert Medication.” Onset and peak times of insulin and sulfonylureas, in association with anticipated mealtimes, should always be considered to avoid hypoglycemia episodes. If a hypoglycemia episode occurs, the nurse should intervene quickly using the agency’s established hypoglycemia protocol, and the event should be reported to the provider and in the shift-to-shift report. Symptomatic hyperglycemia should be immediately reported to the provider. Health teaching should be provided to clients and their family members and/or caregivers according to ADA and ISMP guidelines.

The nurse should evaluate A1C levels to determine effectiveness (and compliance with) the treatment regimen.

Antihyperglycemic Medication: Insulins

There are several different types of insulins that vary in terms of onset, peak, and duration. It is critical for the nurse to be knowledgeable of these differences to help prevent episodes of hypoglycemia due to mismatched administration of insulin with food intake.

Rapid-Acting Insulin

Rapid-acting insulins include insulin lispro (Humalog) and insulin aspart (Novolog) and are also available via inhalation (Afrezza). See Figure 9.10 [ 14 ] for an image of Novolog insulin.

Figure 9.10

Novolog Insulin

Mechanism of Action:  Insulins lower blood glucose by stimulating peripheral glucose uptake by skeletal muscle and fat and by inhibiting hepatic glucose production.

Indications:  Rapid-acting insulins are also called prandial insulins because they are administered with meals to mimic the effects of endogenous insulin release when food is eaten. Dosages of rapid-acting insulin are individualized based on carbohydrate intake, premeal glucose levels, and anticipated activity.

Nursing Considerations:  Humalog-100 (100 units per mL) and Humalog-200 (200 units per mL) are administered subcutaneously. Humalog-100 insulin can be administered intravenously under close supervision of blood glucose and potassium levels. Humalog-100 can be mixed with NPH insulin, but Humalog-200 should not be mixed with another insulin. Inspect insulin visually before use. It should appear clear and colorless; do not use if particulate matter or coloration is seen. Humalog-100 is available in vials, KwikPens, and cartridges; Humalog-200 is only available in KwikPens. Administer subcutaneously into the outer lateral aspect of the upper arm, the abdomen (from below the costal margin to the iliac crest and more than two inches from the umbilicus), the anterior upper thighs, or the buttocks. Rotate injection sites within the same region from one injection to the next to reduce the risk of lipodystrophy. Lipodystrophy can be a lump or small dent in the skin that forms when a person performs injections repeatedly in the same spot.

Because of the rapid onset of insulin lispro and insulin aspart and the potential for hypoglycemia, these insulins should be administered within 15 minutes before or right after eating a meal. Peak serum levels are seen 30 to 90 minutes after dosing. Inhaled insulin enters the bloodstream within 1 minute and peaks in 30-60 minutes. Inhaled insulin is contraindicated in clients with chronic lung disease such as asthma or COPD.

Side Effects/Adverse Effects:  Adverse effects of all insulins include hypoglycemia and hypokalemia. Inhaled insulin has a Boxed Warning for potentially causing acute bronchoconstriction.

Health Teaching & Health Promotion:  See ISMP guidelines for client teaching in the previous “High-Alert Medication and Prevention of Errors” subsection.

Short-Acting Insulin

Short-acting insulins include regular insulin with a brand name of Humulin R or Novolin R. A concentrated formulation of Humulin R u-500 is also available. See Figure 9.11 [ 15 ] for an image of Humulin R insulin.

Figure 9.11

Humulin R Insulin

Mechanism of Action:  The primary activity of insulin is the regulation of glucose metabolism. Insulin lowers blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production.

Indications:  Short-acting insulins are given with meals to mimic the effects of endogenous insulin release when food is eaten. Dosages of short-acting insulin are individualized based on carbohydrate intake, premeal glucose levels, and anticipated activity levels.

Nursing Considerations:  Regular insulin is generally administered subcutaneously. Regular insulin can be administered intravenously under close supervision of blood glucose and potassium levels. It is available in vials and insulin pens. Inspect insulin visually before use. It should appear clear and colorless; do not use if particulate matter or coloration is seen. Administer subcutaneously into the outer lateral aspect of the upper arm, the abdomen (from below the costal margin to the iliac crest and more than two inches from the umbilicus), the anterior upper thighs, or the buttocks. Rotate injection sites within the same region from one injection to the next to reduce the risk of lipodystrophy. Subcutaneous doses should be administered approximately 30 minutes before meals because this is the typical onset of action. Peak effects occur in 3 hours with a duration of 8 hours. Do not mix with insulin preparations other than NPH.

Humulin R u-500 should only be administered in u-500 insulin syringes to avoid dosage calculation errors.

Side Effects/Adverse Effects:  Adverse effects of insulin include hypoglycemia and hypokalemia.

Health Teaching & Health Promotion:  See IMSP guidelines for client teaching in the previous “High-Alert Medication and Prevention of Errors” subsection.

Intermediate-Acting Insulin

NPH insulin, also known as isophane insulin, is an intermediate–acting insulin. Brand names include Humulin-N or Novolin-N. Mixtures of short- and intermediate-acting insulin include Humulin 70/30 or Novolin 70/30.

Indications:  Intermediate insulins are administered once or twice daily to mimic endogenous basal insulin levels.

Nursing Considerations:  NPH insulin is a white and cloudy suspension. Gently roll or invert vial/pen several times to resuspend the insulin before administration. It should only be administered subcutaneously. It may be mixed with rapid-acting or short-acting insulins, but those insulins should be drawn into the syringe before the NPH is added. Administer subcutaneously into the outer lateral aspect of the upper arm, the abdomen (from below the costal margin to the iliac crest and more than two inches from the umbilicus), the anterior upper thighs, or the buttocks. Rotate injection sites within the same region from one injection to the next to reduce the risk of lipodystrophy. The onset of action and peak is affected by the site of injection, physical activity level, and other variables, but the median peak level occurs in four hours. See Figure 9.12 [ 16 ] for an image of Novolin-N (a cloudy insulin) that can be mixed with Novolin R (a clear insulin).

Figure 9.12

Comparison of Novolin-N (a cloudy insulin) That Can Be Mixed With Novolin-R (a clear insulin)

Mixed medications such as Humulin 70/30 should be administered subcutaneously approximately 30 minutes before a meal. They are typically dosed twice daily (with each dose intended to cover two meals or a meal and a snack).

Unopened vials should be stored in the refrigerator until the expiration date. Opened vials should be labelled with the open date and stored in the refrigerator for up to 28-42 days (depending on the formulation/insulin type) and then discarded. Unopened pens should be stored in the refrigerator until the expiration date. Used pens should be stored at room temperature, but kept away from heat and light, for up to 10-28 days (depending on the formulation/insulin type) and then discarded.

Long-Acting Insulin

Insulin glargine (Lantus) and insulin detemir (Levemir) are long-acting insulins given once or twice daily. See Figure 9.13 [ 17 ] for an image of a Levemir insulin pen.

Figure 9.13

Vial Used for Levemir Insulin Pen

Indications:  Long-acting insulins are given once or twice daily. In type 1 diabetics, long-acting insulin should be used concomitantly with rapid- or short-acting insulin at mealtimes.

Nursing Considerations:  Long-acting insulin has a relatively constant concentration/time profile over 24 hours with no pronounced peak in comparison to NPH insulin. It should only be administered subcutaneously and is available in vials and insulin pens. Inspect insulin visually before use. It should appear clear and colorless; do not use if particulate matter or coloration is seen. Administer subcutaneously into the outer lateral aspect of the upper arm, the abdomen (from below the costal margin to the iliac crest and more than two inches from the umbilicus), the anterior upper thighs, or the buttocks. Rotate injection sites within the same region from one injection to the next to reduce the risk of lipodystrophy.

Mechanism of Action:  Glucagon increases blood glucose concentration during an episode of hypoglycemia. See Figure 9.14 [ 18 ] for an image of an emergency glucagon kit.

Figure 9.14

Emergency Glucagon Kit

Indications:  Glucagon is indicated as a treatment for severe hypoglycemia (low blood sugar), which may occur in clients with diabetes mellitus. Glucagon injection is used for clients who are unable to safely swallow carbohydrates to treat hypoglycemia due to the effects of hypoglycemia or other medical conditions.

Nursing Considerations:  Glucagon may be administered subcutaneously, intramuscularly (IM), or intravenously. Peak glucose levels occur within 13-20 minutes of subcutaneous or IM injection.

Side Effects/Adverse Effects:  A side effect of glucagon is hyperglycemia.

Health Teaching & Health Promotion:  Clients with type 1 diabetes may have less of an increase in blood glucose levels compared with clients with stable type 2 diabetes, so a supplementary carbohydrate should be given as soon as possible, especially to a pediatric client.[ 19 ]

Now let’s take a closer look at the medication grid comparing insulins in Table 9.4b .[ 20 ]

Insulins and Glucagon Medication Grid

General administration considerations:

• Review orders closely because they may include a standard meal dose, a “sliding scale” dose, and a carb-related dose
• Always read drug labelling closely as there are several types of dosages and formulations
• See agency policies and ISMP guidelines for safe administration of insulin
• When administering with an insulin pen, after inserting the pen, count to five before removing the needle

General therapeutic effects:

• Maintain serum blood glucose in normal range and achieve individualized target level of A1C (often 7%)

General side effects:

• Hypoglycemia and hypokalemia

Antihyperglycemic Medication: Oral Antihyperglycemics

There are several different classes of oral antihyperglycemic medications used in conjunction with a healthy diet and exercise for the management of type 2 diabetes. According to the American Diabetes Association, metformin is the preferred initial pharmacologic agent for the treatment of type 2 diabetes.[ 21 ] Other commonly used antihyperglycemic medications are glipizide and sitagliptin. The mechanism of action and administration considerations for these prototypes are described below.

Mechanism of Action:  Glipizide is in the sulfonylurea class of antihyperglycemic medication. The mechanism of action is the stimulation of insulin secretion from the beta cells of pancreatic islet tissue and is thus dependent on functioning beta cells in the pancreatic islets. Peak plasma concentrations occur 1 to 3 hours after a single oral dose.

Indications:  Glipizide is used to improve glycemic control in individuals with type 2 diabetes.

Nursing Considerations:  All sulfonylurea drugs are capable of producing severe hypoglycemia. Hypoglycemia may be difficult to recognize in the elderly and in people who are taking beta-adrenergic blocking drugs. Sulfonylurea medications should be given 30 minutes before a meal due to hypoglycemic effects.

Glipizide is contraindicated in type 1 diabetics or for use of diabetic ketoacidosis; insulin should be used to treat this condition. Treatment of clients with glucose 6-phosphate dehydrogenase (G6PD) deficiency with sulfonylurea agents can lead to hemolytic anemia.

Side Effects/Adverse Effects:  The hypoglycemic action of sulfonylureas may be potentiated by certain drugs such as nonsteroidal anti-inflammatory agents and other drugs that are highly protein bound.

Health Teaching & Health Promotion:  Clients should take the medication at the same time each day. It is important that clients understand that the medication helps control episodes of hyperglycemia but does not cure diabetes. Clients should be instructed regarding the signs of hyperglycemia and hypoglycemia. The use of sulfonylureas and alcohol may cause a disulfiram-like reaction.

Mechanism of Action:  Metformin is in the biguanide class of antihyperglycemics. It decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization. Unlike sulfonylureas, metformin does not produce hypoglycemia. See Figure 9.15 [ 22 ] for an image of a metformin tablet.

Figure 9.15

Indications:  Metformin is an adjunct to diet and exercise to improve glycemic control in individuals with type 2 diabetes.

Nursing Considerations:  Metformin hydrochloride should be given in divided doses with meals. The therapeutic goal should be to decrease both fasting plasma glucose and glycosylated hemoglobin levels to near normal by using the lowest effective dose of metformin, either when used as monotherapy or in combination with sulfonylurea or insulin.

Metformin is contraindicated in clients with kidney disease (e.g., serum creatinine levels ≥1.5 mg/dL [males] or ≥1.4 mg/dL [females]) and should be temporarily discontinued in clients undergoing radiologic studies involving intravascular administration of iodinated contrast materials because use of such products may result in acute alteration of renal function. It is also contraindicated in clients with metabolic acidosis.

Lactic acidosis is a rare, but serious, metabolic complication that can occur due to metformin accumulation during treatment with metformin; when it occurs, it is fatal in approximately 50% of cases. The risk of lactic acidosis increases with the degree of renal dysfunction and the client’s age. Metformin should be promptly withheld in the presence of any condition associated with hypoxemia, dehydration, or sepsis. Because impaired hepatic function may significantly limit the ability to clear lactate, metformin should be avoided in clients with hepatic disease. The onset of lactic acidosis often is subtle and accompanied only by nonspecific symptoms such as malaise, myalgias, respiratory distress, increasing somnolence, and nonspecific abdominal distress.

Side Effects/Adverse Effects:  Common adverse effects include diarrhea, nausea/vomiting, weakness, flatulence, indigestion, abdominal discomfort, and headache.

Health Teaching & Health Promotion:  Clients should take the medication at the same time each day. It is important that clients understand that the medication helps control episodes of hyperglycemia but does not cure diabetes. Clients should be instructed regarding the signs of hyperglycemia and hypoglycemia. The client may be at risk for lactic acidosis and should report chills, low blood pressure, muscle pain, or dyspnea immediately to the health care provider. The use of medications like metformin can cause a metallic taste in the mouth.

Sitagliptin

Mechanism of Action:  Sitagliptin is an orally active inhibitor of dipeptidyl peptidase-4 (DPP-4) enzyme that slows the inactivation of incretin hormones involved in the regulation of glucose homeostasis and, thus, increases insulin release and decreases glucagon levels in the circulation. See Figure 9.16 [ 23 ] for an image of sitagliptin.

Figure 9.16

Indications:  It is used as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes.

Nursing Considerations:  Sitagliptin is taken once daily and can be taken with or without food. It can cause hypoglycemia. Dose adjustment should occur for clients with kidney disease depending on their glomerular filtration rate. Report hypersensitivity reactions, blisters/erosions, headache, or symptoms of pancreatitis, heart failure, severe arthralgia, and upper respiratory infection.

Side Effects/Adverse Effects:  Common side effects include hypoglycemia. Individuals may also experience hypersensitivity reactions, blisters/erosions, headache, or symptoms of pancreatitis, heart failure, severe arthralgia, or upper respiratory infection.

Health Teaching & Health Promotion:  Clients should take the medication at the same time each day. It is important that clients understand that the medication helps control episodes of hyperglycemia but does not cure diabetes. Clients should be instructed regarding the signs of hyperglycemia and hypoglycemia. Clients should stop taking the medication if symptoms of hypersensitivity occur and follow up immediately with their provider to determine the next course of treatment.

Now let’s take a closer look at the medication grid comparing oral antihyperglycemics in Table 9.4c .[ 24 ]

Oral Antihyperglycemics Medication Grid

Critical Thinking Activity 9.4

A client with diabetes mellitus type 2 is admitted to the hospital for hip replacement surgery. The nurse reviews the following orders:

Diabetic diet with carb counting

Bedside blood glucose testing before meals and at bedtime with sliding scale Humalog insulin

Sliding scale Humalog insulin based on preprandial glucose level:

• 0-150: No coverage

• 151-175: 2 units

• 176-200: 4 units

• 201-225: 6 units

• 226-250: 8 units

• Over 250: call the provider

Insulin coverage per carbohydrate intake at meals: Humalog 2 units/carb

Metformin 1000 mg twice daily

Humulin-N 20 units at breakfast and at bedtime

Hypoglycemia protocol

1. Explain the difference between type 1 and type 2 diabetes.

2. The client states that he usually does not take insulin at home. What is the likely rationale for insulin therapy while hospitalized?

3. The client’s blood sugar before breakfast is 223 and he eats three carbs at breakfast. What types and amounts of insulin will the nurse administer?

4. The nurse reviews the client’s morning lab results and finds a creatinine of 1.8. She plans to call the provider to discuss the impact of the results on the medications ordered. Which medication may require a dosage adjustment based on these results?

5. When the nurse enters the room around 4 p.m., she discovers that the client has become irritable and is shaky. The nurse performs a bedside blood glucose and obtains a value of 60. What is the nurse’s best response?

6. What is the likely cause of the client’s condition? Explain using the onset and peak actions of the insulin orders.

7. On admission, the client’s A1C level was 10%. What does this lab value indicate?

8. The provider states the discharge plan is to initiate Lantus (insulin glargine) therapy at home, based on the admitting A1C level. What patient teaching should the nurse plan to provide before discharge?

9.5. THYROID MEDICATIONS

This section will review the anatomy and physiology of the thyroid, outline common thyroid disorders, review the anatomy and physiology of the parathyroid gland, outline common parathyroid disorders, apply the nursing process to administering thyroid medications, and then discuss thyroid and osteoporosis medications.

Review of Anatomy and Physiology of the Thyroid

The thyroid is a butterfly-shaped organ located anterior to the trachea, just inferior to the larynx (see Figure 9.17 ).[ 1 ] Each of the thyroid lobes is embedded with parathyroid glands.

Figure 9.17

Thyroid Gland

Synthesis and Release of Thyroid Hormones

Thyroid hormone production is dependent on the hormone’s essential component: iodine. T3 and T4 hormones are produced when iodine attaches to a glycoprotein called thyroglobulin. The following steps outline the hormone’s assembly: binding of TSH to thyroid receptors causes the cells to actively transport iodide ions across their cell membrane from the bloodstream. As a result, the concentration of iodide ions “trapped” in the thyroid cells is many times higher than the concentration in the bloodstream. The iodide ions undergo oxidation (i.e., their negatively charged electrons are removed), and enzymes link the iodine to tyrosine to produce triiodothyronine (T3), a thyroid hormone with three iodines, or thyroxine (T4), a thyroid hormone with four iodines. These hormones remain in the thyroid follicles until TSH stimulates the release of free T3 and T4 into the bloodstream. In the bloodstream, less than one percent of the circulating T3 and T4 remains unbound. This free T3 and T4 can cross the lipid bilayer of cell membranes and be taken up by cells. The remaining 99 percent of circulating T3 and T4 is bound to specialized transport proteins called thyroxine-binding globulins (TBGs), to albumin, or to other plasma proteins. This “packaging” prevents their free diffusion into body cells. When blood levels of T3 and T4 begin to decline, bound T3 and T4 are released from these plasma proteins and readily cross the membrane of target cells. T3 is more potent than T4, and many cells convert T4 to T3 through the removal of an iodine atom.

Regulation of Thyroid Hormone Synthesis

A negative feedback loop controls the regulation of thyroid hormone levels. As shown in Figure 9.18 ,[ 2 ] low blood levels of T3 and T4 stimulate the release of thyrotropin-releasing hormone (TRH) from the hypothalamus, which triggers secretion of TSH from the anterior pituitary. In turn, TSH stimulates the thyroid gland to secrete T3 and T4. The levels of TRH, TSH, T3, and T4 are regulated by a negative feedback system in which increasing levels of T3 and T4 decrease the production and secretion of TSH.

Figure 9.18

Negative Feedback Loop: Controls Regulation of Thyroid Hormone Levels

Functions of Thyroid Hormones

The thyroid hormones T3 and T4 are often referred to as metabolic hormones because their levels influence the body’s basal metabolic rate, which is the amount of energy used by the body at rest. When T3 and T4 bind to intracellular receptors located on the mitochondria, they cause an increase in nutrient breakdown and the use of oxygen to produce ATP. In addition, T3 and T4 initiate the transcription of genes involved in glucose oxidation. Although these mechanisms prompt cells to produce more ATP, the process is inefficient, and an abnormally increased level of heat is released as a byproduct of these reactions. This calorigenic effect ( calor – = “heat”) raises body temperature.

Adequate levels of thyroid hormones are also required for protein synthesis and for fetal and childhood tissue development and growth. They are especially critical for normal development of the nervous system both in utero and in early childhood, and they continue to support neurological function in adults. Thyroid hormones also have a complex interrelationship with reproductive hormones, and deficiencies can influence libido, fertility, and other aspects of reproductive function. Finally, thyroid hormones increase the body’s sensitivity to catecholamines (epinephrine and norepinephrine) from the adrenal medulla by upregulation of receptors in the blood vessels. When levels of T3 and T4 hormones are excessive, this effect accelerates the heart rate, strengthens the heartbeat, and increases blood pressure. Because thyroid hormones regulate metabolism, heat production, protein synthesis, and many other body functions, thyroid disorders can have severe and widespread consequences.

The thyroid gland also secretes another hormone called calcitonin. Calcitonin is released in response to elevated blood calcium levels. It decreases blood calcium concentrations in these ways:

• Inhibiting the activity of osteoclasts (bone cells that breakdown bone matrix and release calcium into the circulation)
• Decreasing calcium absorption in the intestines
• Increasing calcium loss in the urine

Pharmaceutical preparations of calcitonin are prescribed to reduce osteoclast activity in people with osteoporosis. Osteoporosis is a disease that can be caused by glucocorticoids.

Calcium is critical for many other biological processes. It is a second messenger in many signaling pathways and is essential for muscle contraction, nerve impulse transmission, and blood clotting. Given these roles, it is not surprising that blood calcium levels are tightly regulated by the endocrine system. The parathyroid glands are primarily involved in calcium regulation.

Disorders of the Thyroid Gland

As discussed above, dietary iodine is required for the synthesis of T3 and T4. For much of the world’s population, foods do not provide adequate levels of iodine because the amount varies according to the level in the soil in which the food was grown, as well as the irrigation and fertilizers used. Marine fish and shrimp tend to have high levels because they concentrate iodine from seawater, but many people in landlocked regions lack access to seafood. Thus, the primary source of dietary iodine in many countries is iodized salt. Fortification of salt with iodine began in the United States in 1924, and international efforts to iodize salt in the world’s poorest nations continue today.

Dietary iodine deficiency can result in the impaired ability to synthesize T3 and T4, leading to a variety of severe disorders. When T3 and T4 cannot be produced, TSH is secreted in increasing amounts. As a result of this hyperstimulation, thyroglobulin and colloid accumulate in the thyroid gland and increase the overall size of the thyroid gland, a condition called a  goiter  (see Figure 9.19 [ 3 ]). A goiter is only a visible indication of the deficiency. Other disorders related to iodine deficiency include impaired growth and development, decreased fertility, and prenatal and infant death. Moreover, iodine deficiency is the primary cause of preventable mental retardation worldwide. Neonatal hypothyroidism (cretinism) is characterized by cognitive deficits, short stature, and sometimes deafness and muteness in children and adults born to mothers who were iodine-deficient during pregnancy.

Figure 9.19

In areas of the world with access to iodized salt, dietary deficiency is rare. Instead, inflammation of the thyroid gland is a common cause of  hypothyroidism , or low blood levels of thyroid hormones. Hypothyroidism is a disorder characterized by a low metabolic rate, weight gain, cold extremities, constipation, reduced libido, menstrual irregularities, and reduced mental activity, and requires long-term thyroid hormone replacement therapy. In contrast,  hyperthyroidism —an abnormally elevated blood level of thyroid hormones—is often caused by a pituitary or thyroid tumor. In Graves’ disease, the hyperthyroid state results from an autoimmune reaction in which antibodies overstimulate the follicle cells of the thyroid gland. Hyperthyroidism can lead to an increased metabolic rate, excessive body heat and sweating, diarrhea, weight loss, tremors, and increased heart rate. The person’s eyes may bulge (called exophthalmos) as antibodies produce inflammation in the soft tissues of the orbits. The person may also develop a goiter. Hyperthyroidism is often treated by thyroid surgery or with radioactive iodine (RAI) therapy. Clients are asked to follow radiation precautions after RAI treatment to limit radiation exposure to others, especially pregnant women and young children, such as sleeping in a separate bed and flushing the toilet 2-3 times after use. The RAI treatment may take up to several months to have its effect. The end result of thyroid surgery or RAI treatment is often hypothyroidism, which is treated by thyroid hormone replacement therapy.[ 4 ]

Review of Anatomy and Physiology of the Parathyroid Glands

The parathyroid glands are four tiny, round structures usually embedded in the posterior surface of the thyroid gland (see Figure 9.20 ).[ 5 ] The primary function of the parathyroid glands is to regulate blood calcium levels by producing and secreting  parathyroid hormone (PTH)  in response to low blood calcium levels.

Figure 9.20

Parathyroid Glands

PTH secretion causes the release of calcium from the bones by stimulating osteoclasts that degrade bone and then release calcium into the bloodstream. PTH also inhibits osteoblasts, the cells involved in bone deposition, thereby keeping calcium in the blood. PTH also causes increased reabsorption of calcium (and magnesium) in the kidney and initiates the production of the steroid hormone calcitriol, which is the active form of vitamin D3. Calcitriol then stimulates increased absorption of dietary calcium by the intestines. A negative feedback loop regulates the levels of PTH, with rising blood calcium levels inhibiting further release of PTH. (See Figure 9.21 for an illustration of the role of parathyroid hormone in maintaining blood calcium homeostasis.)[ 6 ]

Figure 9.21

Parathyroid Hormone in Maintaining Blood Calcium Homeostasis

Disorders of the Parathyroid Glands

Abnormally high activity of the parathyroid gland can cause  hyperparathyroidism , a disorder caused by an overproduction of PTH that results in excessive degradation of bone and elevated blood levels of calcium, also called hypercalcemia. Hyperparathyroidism can thus significantly decrease bone density, which can lead to spontaneous fractures or deformities. As blood calcium levels rise, cell membrane permeability to sodium is also decreased, and thus the responsiveness of the nervous system is reduced. At the same time, calcium deposits may collect in the body’s tissues and organs, impairing their functioning.

In contrast, abnormally low blood calcium levels may be caused by parathyroid hormone deficiency, called  hypoparathyroidism , which may develop following injury or surgery involving the thyroid gland. Low blood calcium increases membrane permeability to sodium, thus increasing the responsiveness of the nervous system, resulting in muscle twitching, cramping, spasms, or convulsions. Severe deficits can paralyze muscles, including those involved in breathing, and can be fatal.

Applying the Nursing Process to Administering Thyroid Medications

When administering thyroid replacement medications, the nurse should plan to monitor TSH levels before and during therapy for effectiveness. Drug interactions may occur with several other medications, so review drug labeling information carefully before administering.

Levothyroxine should be administered consistently every morning 30-60 minutes before a meal. For clients who are NPO, levothyroxine can also be given intravenously (IV).

Elevated levels of thyroid hormone can cause cardiac dysrhythmias; immediately report any symptoms of tachycardia, chest pain, or palpitations to the provider.

Thyroid and Osteoporosis Medication Classes

Thyroid replacement medication.

Mechanism of Action:  Oral levothyroxine sodium is a synthetic T4 hormone that exerts the same physiologic effect as endogenous T4, thereby maintaining normal T4 levels when a deficiency is present.

Indications:  Levothyroxine is a thyroid replacement drug used to treat hypothyroidism. See Figure 9.22 [ 7 ] for an image of levothyroxine.

Figure 9.22

Levothyroxine

Nursing Considerations:  Levothyroxine tablets should be taken with a full glass of water as the tablet may rapidly disintegrate. It should be administered as a single daily dose, on an empty stomach, one-half to one hour before breakfast, and at least four hours before or after drugs known to interfere with levothyroxine absorption. For clients who are NPO, levothyroxine can also be given intravenously (IV).

Levothyroxine is contraindicated for clients with hyperthyroidism and adrenal insufficiency until the condition is corrected. Many clients who undergo treatment for hyperthyroidism may develop hypothyroidism. Overtreatment with levothyroxine may cause symptoms of hyperthyroidism with increased heart rate, cardiac wall thickness, and cardiac contractility that may precipitate angina or arrhythmias, particularly in clients with cardiovascular disease and in older adults. Levothyroxine therapy in this population should be initiated at lower doses. If cardiac symptoms develop or worsen, the nurse should withhold the medication, contact the health care provider, and anticipate a lower dose prescribed or the medication to be withheld for one week and then restarted at a lower dose.

Addition of levothyroxine therapy in clients with diabetes mellitus may worsen glycemic control and result in the need for higher dosages of antidiabetic medication. Carefully monitor glycemic control, especially when thyroid therapy is started, changed, or discontinued.

Levothyroxine increases the response to oral anticoagulant therapy. Therefore, a decrease in the dose of anticoagulant may be warranted with correction of the hypothyroid state or when the levothyroxine dose is increased. Closely monitor INR results and anticipate dosage adjustments.

Levothyroxine can affect, or be affected by, several other medications, so carefully read drug label information when therapy is initiated.

Side Effects/Adverse Effects:  There are risks to the mother and fetus associated with untreated hypothyroidism in pregnancy. Because TSH levels may increase during pregnancy, TSH should be monitored, and levothyroxine dosage may require adjustment during pregnancy.[ 8 ]

Health Teaching & Health Promotion:  Clients should take thyroid replacement medications at the same time each day. Clients should be aware that thyroid replacement medications do not cure hypothyroidism and therapy is lifelong. Clients should notify their health care provider if they experience signs of headache, diarrhea, sweating, or heat intolerance. Medications should be spaced four hours apart from medications like antacid, iron, or calcium supplements. Clients will be followed closely by their health care provider regarding their response to medication therapy and serum thyroid levels will be taken.[ 9 ]

Antithyroid Medication

Mechanism of Action:  Propylthiouracil inhibits the synthesis of thyroid hormones.

Indications:  Propylthiouracil (PTU) is an antithyroid medication used to treat hyperthyroidism or to ameliorate symptoms of hyperthyroidism in preparation for thyroidectomy or radioactive iodine therapy.

Nursing Considerations:  Propylthiouracil is administered orally. The total daily dosage is usually given in three equal doses at approximately 8-hour intervals. Propylthiouracil can cause hypothyroidism necessitating routine monitoring of TSH and free T4 levels, with adjustments in dosing to maintain a euthyroid state.

Side Effects/Adverse Effects:  Liver injury resulting in liver failure, liver transplantation, or death has been reported. Clients should be instructed to report any symptoms of hepatic dysfunction (anorexia, pruritus, and right upper quadrant pain), particularly in the first six months of therapy.

Agranulocytosis is a potentially life-threatening side effect of propylthiouracil therapy. Agranulocytosis typically occurs within the first three months of therapy. Clients should be instructed to immediately report any symptoms suggestive of agranulocytosis, such as fever or sore throat.

Cases of vasculitis resulting in severe complications and death have been reported in clients receiving propylthiouracil therapy. If vasculitis is suspected, discontinue therapy and initiate appropriate intervention.

Propylthiouracil crosses the placenta and can cause fetal liver failure, a goiter, and cretinism if administered to a pregnant woman.

Health Teaching & Health Promotion:  Clients should take the medication as directed at regular dosing intervals. They should monitor their weight 2-3 times per week. Additionally, clients should be advised that medications may cause drowsiness, and they should report any signs of sore throat, fever, headache, jaundice, bleeding, or bruising.

Osteoporosis Medication: Calcitonin

Mechanism of Action:  Calcitonin is a calcitonin receptor agonist. Calcitonin is released by the thyroid gland. It acts primarily on bone and also has effects on the kidneys and the gastrointestinal tract.

Indications:  Calcitonin is used to treat osteoporosis.

Nursing Considerations:  Calcitonin is administered via nasal spray with one spray in one side of the nose daily. See Figure 9.23 [ 10 ] for an image of calcitonin nasal spray. The nasal spray pump should be primed before the first administration. Unopened calcitonin can be stored in the refrigerator until opened but should not be refrigerated between doses. Opened bottles stored at room temperature should be discarded after 30 days of initial dose.

Figure 9.23

Administration of Calcitonin

Side Effects/Adverse Effects:  Adverse effects include serious hypersensitivity reactions (bronchospasm, swelling of the tongue or throat, anaphylaxis and anaphylactic shock), hypocalcemia, nasal mucosa adverse events, and malignancy.

Calcitonin should not be used during pregnancy.

Health Teaching & Health Promotion:  Clients should be advised to take medications as directed. They should report any signs of hypercalcemia or an allergic response. Clients should receive instruction on the process of self-injection. They should also be advised that they may experience flushing and warmth following injection. Post-menopausal women should adhere to a diet high in calcium and vitamin D and should be educated regarding the importance of exercise for reversing bone loss.[ 11 ]

Osteoporosis Medication: Alendronate

Mechanism of Action:  Alendronate is a bisphosphonate that inhibits osteoclast-mediated bone resorption. By preventing the breakdown of bone and enhancing the formation of new bone, alendronate assists in reversing bone loss and decreases the risk of fractures.

Indications:  Alendronate is used for the prevention and treatment of osteoporosis in postmenopausal women, to increase bone mass in men with osteoporosis, and for glucocorticoid-induced osteoporosis.

Nursing Considerations:  Check dosages carefully because some formulations are administered daily, whereas others are administered weekly. Alendronate should be taken after arising for the day but should be administered at least one-half hour before the first food, beverage, or medication of the day with plain water only. Other beverages (including mineral water), food, and some medications are likely to reduce the absorption of alendronate. Clients should not lie down for at least 30 minutes and until after their first food of the day. Clients may also require calcium and vitamin D supplementation, especially if concurrently taking glucocorticoids.

Alendronate is contraindicated in the following conditions: pregnancy, hypocalcemia, the inability to sit or stand for 30 minutes after swallowing, esophageal abnormalities that delay emptying, and clients at risk for aspiration. Alendronate is not recommended for clients with kidney disease with creatinine clearance less than 35 mL/min.

Discontinue alendronate if severe musculoskeletal pain occurs. A bone mineral density measurement should be made at the initiation of therapy and repeated after 6 to 12 months of combined alendronate and glucocorticoid treatment.

Side Effects/Adverse Effects:  Side effects include upper GI disturbances, severe musculoskeletal pain, and risk of osteonecrosis of the jaw.

Health Teaching & Health Promotion:  Clients should take medication as directed at the same time each day, first thing in the morning. Clients should remain upright after they take medication for 30 minutes to minimize stomach and esophageal irritation. Clients should eat a balanced diet and may seek advice from the health care provider regarding supplementation with calcium and vitamin D. Clients should participate in regular exercise to help increase bone strength.[ 12 ]

Osteoporosis: Calcium + Vitamin D

Mechanism of Action:  Calcium and vitamin D are essential nutrients that play a vital role in bone health. Calcium is necessary for the formation and maintenance of healthy bones, while vitamin D helps the body absorb and use calcium.

Indications:  Calcium and vitamin D supplements are often prescribed to prevent and treat osteoporosis, as they help maintain bone density and strength.

Nursing Considerations:  The therapeutic effects of calcium and vitamin D supplements may vary depending on the individual’s health status and the presence of any underlying medical conditions.

Side Effects/Adverse Effects:  Side effects include hypercalcemia, kidney stones, and gastrointestinal problems such as constipation, bloating, and abdominal discomfort.

Health Teaching & Health Promotion:  Clients should take with food to enhance absorption and monitor for signs of hypercalcemia such as kidney stones and gastrointestinal upset.

Now let’s take a closer look at the medication grid comparing thyroid and osteoporosis medications in Table 9.5 .[ 13 ] Medication grids are intended to assist students to learn key points about each medication. Because information about medication is constantly changing, nurses should always consult evidence-based resources to review current recommendations before administering specific medication. Basic information related to each class of medication is outlined below. Detailed information on a specific medication can be found for free at  DailyMed . On the home page, enter the drug name in the search bar to read more about the medication. Prototype/generic medications listed in the grids below are also linked to a DailyMed page.

Thyroid and Osteoporosis Medications Grid

Critical Thinking Activity 9.5

A client has been diagnosed with hypothyroidism and receives a prescription for levothyroxine.

What health teaching should the nurse provide regarding this medication?

9.6. HORMONAL CONTRACEPTIVES

This section will introduce classes of common hormonal contraceptives. Hormonal methods of contraception use hormones to prevent pregnancy. These methods work by preventing ovulation, thickening cervical mucus, and altering the lining of the uterus. Hormonal methods of birth control include combined and progestin only medication options. Contraceptive medications are available in various forms, including pills, patches, rings inserted into the vagina, injections, intrauterine devices, and implants inserted under the skin.

Combined Hormonal Contraceptives

Combined hormonal contraceptives (CHCs) are a type of birth control that contain estrogen and progestin hormones. These hormonal contraceptives are widely available in various forms such as pills, patches, vaginal rings, and injections. Ortho Tri-Cyclen is a popular prototype contraceptive.

Mechanism of Action:  CHCs, such as Ortho Tri-Cyclen, prevent ovulation while thickening mucus to prevent the sperm from reaching the egg and thicken the lining of the uterus to prevent implantation of the fertilized egg.

Indications:  These medications are used to prevent pregnancy.

Nursing Considerations:  Clients should be monitored for adverse effects such as hypertension, thromboembolic events, and abnormal vaginal bleeding.

Side Effects/Adverse Effects:  Common side effects of Ortho Tri-Cyclen include nausea, breast tenderness, and mood changes. Adverse effects include thromboembolic events, especially in clients who smoke.

Health Teaching & Health Promotion:  Clients should take the medication at the same time every day. They must adhere to dosing schedule in order to ensure optimal contraceptive efficacy. Clients should be educated that although CHCs prevent pregnancy, they do not prevent sexually transmitted diseases. Many medications also decrease effectiveness of CHCs, and clients should be instructed to use back-up contraception when on certain medications such as antibiotics.[ 1 ]

Progestin-Only Contraceptive

Progestin-only contraceptives only contain progestin rather than combined estrogen and progestin. An example of a progestin only contraceptive is norethindrone, also known as a mini-pill.

Mechanism of Action:  The mini-pill works by thickening the cervical mucus, which makes it difficult for sperm to enter the uterus, and by thinning the lining of the uterus, which makes it less receptive to implantation of a fertilized egg.

Indications:  This medication prevents pregnancy.

Nursing Considerations:  The mini-pill is commonly prescribed for women who cannot tolerate estrogen or those who are breast feeding. It does not impact milk production.

Side Effects/Adverse Effects:  Common side effects include irregular menstrual bleeding or spotting, headache, breast tenderness, nausea, weight gain, and mood changes. Adverse effects of the mini-pill include potential ectopic pregnancy, thrombosis, and liver problems.

Health Teaching & Health Promotion:  It must be taken at the same time each day, without interruption. It may not be as effective as combined hormonal contraceptives due to the challenges many clients have with taking the medication at the same time every day.[ 2 ]

Now let’s take a closer look at the contraceptive medication grid in Table 9.6 .[ 3 ]

Contraceptive Medication Grid

9.7. LEARNING ACTIVITIES

Case Study 1

Ms. J.S. is a 45-year-old woman who was admitted to the hospital with a diagnosis of severe asthma exacerbation. She has a history of asthma and has been using her inhaler more frequently in the past week due to worsening symptoms. Upon admission, she was started on prednisone therapy.

1. What is prednisone, and how does it work?

2. What are the potential side effects of prednisone therapy?

3. How should prednisone therapy be administered?

4. What monitoring should be done during prednisone therapy?

5. What health teaching should be provided regarding prednisone therapy?

Case Study 2

Mr. D.K. is a 65-year-old male who has a long-standing history of type 2 diabetes mellitus. He is currently being managed with both metformin and insulin therapy. He presents to the clinic for a routine follow-up appointment.

1. What is the role of metformin in diabetes management?

2. What is the role of insulin in diabetes management?

3. What are the potential side effects of metformin and insulin therapy?

4. How should Mr. D.K. be monitored while taking both metformin and insulin therapy?

5. What health teaching should be provided regarding these medications?

Note: Answers to the Case Studies can be found in the “ Answer Key ” sections at the end of the book.

“Endocrine Quiz” by E. Christman for   Open RN   is licensed under   CC BY 4.0

“Endocrine Flashcards” by E. Christman for   Open RN   is licensed under   CC BY 4.0

Test your clinical judgment with this NCLEX Next Generation-style bowtie question:  Endocrine Assignment 1 .[ 1 ]

Test your clinical judgment with this NCLEX Next Generation-style bowtie question:  Endocrine Assignment 2 .[ 2 ]

• IX. GLOSSARY

A lab test used to assess long-term blood glucose levels over three months. The general A1C target level is less than 7%.

A component of the hypothalamic-pituitary-adrenal (HPA) axis that produces the steroid hormones important for the regulation of the stress response, blood pressure and blood volume, nutrient uptake and storage, fluid and electrolyte balance, and inflammation.

Neuroendocrine tissue composed of postganglionic sympathetic nervous system (SNS) neurons that are stimulated by the autonomic nervous system to secrete hormones epinephrine and norepinephrine.

A mineralocorticoid released by the adrenal cortex that controls fluid and electrolyte balance through the regulation of sodium and potassium.

ADH is released by the posterior pituitary in response to stimuli from osmoreceptors indicating high blood osmolarity. Its effect is to cause increased water reabsorption by the kidneys. As more water is reabsorbed by the kidneys, the greater the amount of water that is returned to the blood, thus causing a decrease in blood osmolarity. ADH is also known as vasopressin because, in very high concentrations, it causes constriction of blood vessels, which increases blood pressure by increasing peripheral resistance.

Long-acting (insulin glargine or insulin detemir) or intermediate-acting (NPH) insulin.

The amount of energy used by the body at rest.

The concentration of solutes (such as sodium and glucose) in the blood.

A disease characterized by underproduction of ADH that causes chronic dehydration.

Gland that secretes hormones that target other organs.

Gland that secretes digestive enzymes.

The pattern in which the body responds in different ways to stress: the alarm reaction (otherwise known as the fight-or-flight response), the stage of resistance, and the stage of exhaustion.

Stimulated by insulin, the metabolism of glucose for generation of ATP.

A visible enlargement of the thyroid gland when there is hyperstimulation of TSH due to deficient levels of T3 and T4 hormones in the bloodstream or an autoimmune reaction in which antibodies overstimulate the follicle cells of the thyroid gland, causing hyperthyroidism.

Chemical signals sent by the endocrine organs and transported via the bloodstream throughout the body where they bind to receptors on target cells and induce a characteristic response.

Changes in blood levels of nonhormone chemicals that cause an endocrine gland to release or inhibit a hormone to maintain homeostasis. For example, high blood sugar causes the pancreas to release insulin.

Elevated blood glucose levels.

A disorder caused by an overproduction of PTH that results in excessive calcium resorption from bone, causing significantly decreased bone density and spontaneous fractures, decreased responsiveness of the nervous system, and calcium deposits in the body’s tissues and organs, impairing their functioning.

Abnormally elevated blood level of thyroid hormones T3 and T4, often caused by a pituitary tumor, thyroid tumor, or autoimmune reaction in which antibodies overstimulate the follicle cells of the thyroid gland.

A blood glucose level below 70 mg/dL; severe hypoglycemia refers to a blood glucose level below 40.

Abnormally low blood calcium levels caused by parathyroid hormone deficiency, which may develop following thyroid surgery. Low blood calcium can cause muscle twitching, cramping, spasms, or convulsions; severe deficits can paralyze muscles, including those involved in breathing, and can be fatal.

The hypothalamus stimulates the release of ACTH from the pituitary, which then stimulates the adrenal cortex to produce the hormone cortisol and steroid hormones important for the regulation of the stress response, blood pressure and blood volume, nutrient uptake and storage, fluid and electrolyte balance, and inflammation.

The “command center” of the endocrine system that secretes several hormones that directly produce responses in target tissues, as well as hormones that regulate the synthesis and secretion of hormones of other glands. In addition, the hypothalamus–pituitary complex coordinates the messages of the endocrine and nervous systems.

Abnormally low blood levels of thyroid hormones T3 and T4 in the bloodstream.

A hormone that facilitates the uptake of glucose into skeletal and adipose body cells.

Hormones released by the adrenal cortex that regulate body minerals, especially sodium and potassium, that are essential for fluid and electrolyte balance. Aldosterone is the major mineralocorticoid.

Characterized by the inhibition of further secretion of a hormone in response to adequate levels of that hormone.

Released in response to stimuli from the nervous system. For example, the activation of the release of epinephrine and norepinephrine in the fight-or-flight response is stimulated by the sympathetic nervous system.

Specialized cells within the hypothalamus that are sensitive to the concentration of sodium ions and other solutes in the bloodstream.

The hormone released by parathyroid glands and is involved in the regulation of blood calcium levels.

During or relating to the eating of food.

Hormones that turn on or off the function of other endocrine glands, including ACTH, FSH, LH, and TSH.

An autoimmune disease that affects the beta cells of the pancreas so they do not produce insulin; thus, synthetic insulin must be administered by injection or infusion.

A condition where the body’s cells become resistant to the effects of insulin. Over time, the beta cells become exhausted and if blood glucose levels cannot be controlled through a healthy diet and exercise, then oral diabetic medication must be implemented and eventually insulin administration may be required.

Licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/ .

• Cite this Page Open Resources for Nursing (Open RN); Ernstmeyer K, Christman E, editors. Nursing Pharmacology [Internet]. 2nd edition. Eau Claire (WI): Chippewa Valley Technical College; 2023. Chapter 9 Endocrine System.
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• ENDOCRINE INTRODUCTION
• BASIC CONCEPTS OF THE ENDOCRINE SYSTEM
• CORTICOSTERIODS
• ANTIDIABETICS
• THYROID MEDICATIONS
• HORMONAL CONTRACEPTIVES
• LEARNING ACTIVITIES

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• Camilo Jimenez

Harvey Cushing's attempt at the first human pituitary transplantation

Advances in organ and tissue transplantation continue to improve the care of patients with multiple diseases. The authors present the case of a patient with hypopituitarism secondary to a suprasellar mass, in whom the first documented pituitary gland transplantation was performed. This case study illustrates Harvey Cushing's pioneering work in pituitary transplantation in the early 20th century and the essential relationship between laboratory research and clinical practice.

• Courtney Pendleton
• Hasan A. Zaidi
• Alfredo Quiñones-Hinojosa

Diagnosis of insulinoma in a patient with hypoglycemia without obvious hyperinsulinemia

Initial diagnosis of insulinoma requires demonstration of inappropriately elevated insulin levels and concurrent hypoglycemia in the absence of administration of exogenous insulin or sulphonylureas. This article presents the case of a patient with insulinoma, who presented with hypoglycemia without coinciding evident hyperinsulinemia according to current guidelines. The article details current diagnostic criteria and highlights the role of clinical judgment in the investigation and management of cases, which do not conform to an expected pattern.

• Catarina Coelho
• Maralyn R. Druce
• Ashley B. Grossman

A case of diabetic Charcot arthropathy of the foot and ankle

Charcot arthropathy of the neuropathic foot and ankle is characterized by bone and joint destruction and deformities that may lead to ulcer, soft tissue infection, osteomyelitis and amputation. This article reviews the evaluation and treatment of this condition, highlighted by a clinical case of a man with type 2 diabetes mellitus who had Charcot collapse of the longitudinal arch, rocker bottom deformity and plantar ulcer.

• John M. Embil
• Elly Trepman

A woman with polycystic ovary syndrome treated for infertility by in vitro fertilization

This case illustrates some of the difficulties in treating anovulatory women with polycystic ovary syndrome, which is the most common cause of anovulatory infertility. Insulin resistance is a contributing factor to the pathogenesis of the syndrome. Assisted conception therapy is an effective treatment for women with polycystic ovary syndrome who are refractory to standard ovulation induction therapies or who have co-existing infertility factors. However, women with polycystic ovaries are particularly sensitive to stimulation with gonadotropins and have an increased risk of developing ovarian hyperstimulation syndrome.

• Thomas Tang
• Adam H. Balen

Pseudohypoparathyroidism type 1a and insulin resistance in a child

This article presents the case of a child with pseudohypoparathyroidism type 1a and associated endocrinopathies, namely, growth hormone deficiency, hypothyroidism, parathyroid hormone resistance and insulin resistance. The article details the natural history and management of these endocrinopathies, including the controversy over growth-hormone therapy, and potential mechanisms for insulin resistance in pseudohypoparathyroidism type 1a.

• Benjamin U. Nwosu
• Mary M. Lee

A case of severe, refractory diabetic gastroparesis managed by prolonged use of aprepitant

Gastroparesis is a complication of diabetes mellitus that is associated with prolonged periods of suboptimal glycemic control. This article describes a patient who had diabetic gastroparesis that was unresponsive to conventional treatments. Her severe vomiting was successfully controlled by use of the antiemetic drug aprepitant for 4 months before a gastric electrical stimulation device was fitted.

• Kiang Chong
• Ketan Dhatariya

Evaluation of a child for secondary causes of obesity and comorbidities

Childhood obesity is a serious public health concern. This Case Study discusses the evaluation and treatment of a child with obesity. The article details how careful assessment can exclude genetic causes of obesity in most children and outlines how children without genetic causes of the condition can benefit from individualized lifestyle modification programs.

• Robert E. Kramer
• Stephen R. Daniels

Generalized arterial calcification of infancy: treatment with bisphosphonates

Generalized arterial calcification of infancy is a rare and often fatal genetic disorder, for which no formalized treatment approach exists. This article describes a case where treatment with nitrogen-containing bisphosphonates resulted in normalization of the arterial structure.

• Kim A Ramjan
• Tony Roscioli
• Craig FJ Munns

Cyclic Cushing syndrome due to an ectopic pituitary adenoma

Cyclic Cushing syndrome is a rare disorder characterized by periodic fluctuations in adrenal cortisol secretion, with phases of hypercortisolism alternating with periods of normal or low cortisol production. This Case Study discusses diagnostic challenges and treatment options in a patient with cyclic Cushing syndrome due to an ectopic pituitary adenoma.

• Rahfa K Zerikly
• Amir H Hamrahian

A patient with stress-related onset and exacerbations of Graves disease

Emotional stress might affect thyroid function by causing immunological perturbations and also via neural pathways. This article demonstrates a case in which both the onset of Graves disease and later exacerbations of hyperthyroidism were triggered by stressful events, and discusses management strategies for patients with stress-related Graves disease.

• Roberto Vita
• Daniela Lapa
• Salvatore Benvenga

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Endocrine and Neural Disorders and Drug Treatment

• School Southern New Hampshire University - Manchester, NH
• Course Title IHP 310 - Pathophysiology and Pharmacology Concepts
• Uploaded By changu608

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