Rationale: Myxedema coma is a life-threatening, end-stage expression of hypothyroidism. It is characterized by coma, hypothermia, CV collapse, hypoventilation, and severe metabolic disorders that include low sodium, low glucose and lactic acidosis. Treatment includes aggressive management of precipitating factors; supportive therapy such as management of CV status, hyponatremia, and hypoglycemia; and thyroid replacement therapy. If hypothermia is present, active rewarming is contraindicated because it may induce vasodilation and vascular collapse. Administering sedatives frequently could be harmful since the person is unable to metabolize sedatives, analgesics, and anesthetic drugs.

Rationale: Cortisol plays a central role in the normal functioning of the immune response and inflammation. Exophthalmos is associated with Graves disease and secondary sex characteristics are a function of adrenal androgens. Potassium and sodium are regulated by mineralocorticoids.

Rationale: In secondary disorders of endocrine function, the target gland is essentially normal, but defective levels of stimulating hormones or releasing factors from the pituitary system alter its function.

Rationale: Acute adrenal crisis is a life-threatening situation. Exposure to even a minor illness or stress can cause a client with Addison disease to develop nausea, vomiting, muscular weakness, hypotension, dehydration, and vascular collapse (which causes a change in LOC). Hemorrhage (low BP) can be caused by septicemia, adrenal trauma, anticoagulant therapy, adrenal vein thrombosis, or adrenal metastases. A hyperactive reflex may indicate disease of the pyramidal tract above the level of the reflex arc being tested. Generalized hyperactivity of DTRs may be caused by hyperthyroidism. Any tear or hole in the membrane that surrounds the brain and spinal cord (dura) can allow the fluid that surrounds those organs to leak. This fluid is called the cerebrospinal fluid (CSF). When it leaks out, the pressure around the brain and spinal cord drops. Causes of leakage through the dura include certain head, brain, or spinal surgeries; head injury; placement of tubes for epidural anesthesia or pain medications; or lumbar puncture. Irregular heart rates (dysrhythmias) may be caused by many different factors, including coronary artery disease, electrolyte imbalances in the blood (such as sodium or potassium), changes in the heart muscle, or injury from a heart attack.

Rationale: GH is inhibited by increased glucose levels, free fatty acid release, cortisol, and obesity. It is stimulated by hypoglycemia, fasting starvation, increased blood levels of amino acids, and stress conditions such as trauma, excitement, emotional stress, and heavy exercise.

Rationale: An increased white cell count and the presence of adventitious fluid in the lungs are not classic findings associated with hypothyroidism. Myxedema, weight gain, lethargy, and dry skin and nails are commonly associated with low levels of thyroid hormones.

Rationale: The adrenal cortex is responsible for secreting three types of hormones: the glucocorticoids, the mineralocorticoids, and the adrenal androgens. The adrenal medulla produces epinephrine and norepinephrine. There are no alternate production sites for adrenal cortical hormones. The adrenal androgens are not responsible for normal sexual function.

Rationale: The actions of insulin are threefold: (1) it promotes glucose uptake by target cells and provides for glucose storage as glycogen, (2) it prevents fat and glycogen breakdown, and (3) it inhibits gluconeogenesis and increases protein synthesis. Insulin acts to promote fat storage by increasing the transport of glucose into fat cells. It also facilitates triglyceride synthesis from glucose in fat cells and inhibits the intracellular breakdown of stored triglycerides. Insulin also inhibits protein breakdown. It does not directly influence the metabolic needs of body cells.

Rationale: ACTH mediates between the anterior pituitary gland and the adrenal cortex in the HPA system. ACTH is released by the pituitary, not the hypothalamus, and CRH acts on the pituitary, not the adrenal cortex. CRH flows from the hypothalamus to the pituitary, not vice versa.

Rationale: Nephropathies and retinopathies are common complications of poor glycemic control. Complications of diabetes are not noted to be more acute in younger individuals. Hyperglycemia is not normally associated with pain or weight gain. Conscientious diabetes control does not result in a resolution of the disease.

Rationale: GH excess is associated with tumor formation and consequent compression of cranial nerves is responsible for vision. Damage to the hypothalamus and liver are not common sequelae. While the beta cells of the pancreas can “burn out,” the primary effect of excess GH is to increase insulin secretion.

Rationale: Type 1A, or immune-mediated, diabetes involves the autoimmune destruction of pancreatic beta cells and a consequent absolute lack of insulin. Exogenous insulin is required as dietary control alone is insufficient. The central problem is an absolute lack of insulin production rather than deranged release.

Rationale: Inadequate levels of hypothalamic GHRH will result in adequate production but inadequate release of GH by the pituitary. Genetic short stature is less likely given the disparity between his height and his twin’s, and a shortage of IGF receptors is not a noted pathology. While poorly controlled diabetes can contribute to short stature, excess insulin production is not a likely factor.

Rationale: Thyroid hormone is essential for normal growth and brain development, almost half of which occurs during the first 6 months of life. If untreated, congenital hypothyroidism causes intellectual disability and impairs physical growth. Down syndrome is a congenital birth defect and not caused by hypothyroidism.

Rationale: The hyperthyroidism that constitutes Graves disease can often be mitigated by the administration of beta-adrenergic blocking medications. Levothyroxine would be used to address hypothyroidism. Calcium channel blockers are not an identified treatment modality for Graves disease. Somatostatin analogs are used to treat GH excess.

Rationale: Hyperfunction is usually associated with excessive hormone production. This can result from excessive stimulation and hyperplasia of the endocrine gland or from a hormone-producing tumor. A clinical example of this phenomenon is evidenced by the case of a woman with vaginal small cell carcinoma who also presented with Cushing syndrome. After testing, it was determined that the tumor was secreting ACTH. In this situation, the cause was not related to a pituitary problem. There is a connection between Cushing syndrome and the carcinoma. The thyroid gland is not responsible for Cushing syndrome.

Rationale: Acromegaly is associated with adult onset, and is nearly always involves an adenoma. Increased GH as a child and liver dysfunction are not noted contributors to acromegaly. High levels of GH can cause overproduction of insulin and eventual diabetes, but diabetes does not itself lead to acromegaly.

Rationale: Hyperosmolar hyperglycemic state is characterized by high blood glucose (>600 mg/dL [33.3 mmol/L]), dehydration (dry lips), depression of sensorium, hemiparesis, seizures, and coma. The client may also experience weakness, polyuria, and excessive thirst. HHS may occur in various conditions, including type 2 diabetes, acute pancreatitis, severe infection, MI, and treatment with oral or parenteral nutrition solutions.

Rationale: Type 2 diabetes in obese people is thought to link to the actions of free fatty acids, which include beta cell dysfunction (lipotoxicity), insulin resistance, glucose underutilization, and the accumulation of FFAs and triglycerides to reduce hepatic insulin sensitivity.

Rationale: An insulin reaction necessitates intervention in addition to careful observation. The ideal response to an insulin reaction in a still conscious client is the administration of 15 to 20 g of glucose in a concentrated carbohydrate source. Glucagon or D50 would be indicated if the client is unconscious or unable to swallow.

Rationale: The suppression of the HPA system that accompanies steroid therapy requires time for a return to normal function. Dependency on the drug itself is not the rationale for tapering, and HPA function is suppressed, not heightened, during therapy. Abrupt cessation can contribute to an Addison-like response, not Cushing syndrome.

Rationale: A number of disease conditions and pharmacologic agents can decrease the amount of binding protein in the plasma or influence the binding of hormone. Glucocorticoid medications and systemic disease conditions such as protein malnutrition, nephritic syndrome, and cirrhosis decrease TBG concentrations.

Rationale: Suboptimal response to infection in a person with diabetes is caused by the presence of chronic complications, such as vascular disease and neuropathies, and by the presence of hyperglycemia and altered neutrophil function. Certain types of infections occur with increased frequency in people with diabetes: soft tissue infections of the extremities, osteomyelitis, UTIs and pyelonephritis, Candida infections of the skin/mucous surfaces, dental caries, and periodontal disease.

Rationale: Glucose entry into red blood cells is not insulin dependent, and the rate at which glucose becomes attached to the hemoglobin molecule depends on blood glucose levels. A1C levels thus indirectly indicate glucose levels. Hemoglobin synthesis, the metabolic needs of hemoglobin, and an agonist role of insulin do not underlie the A1C test.

Rationale: Approximately two-thirds of the glucose that is ingested with a meal is removed from the blood and stored in the liver as glycogen. Between meals, the liver releases glucose as a means of maintaining blood glucose within its normal range. Normal glucose metabolism does not involve large variations in blood glucose levels in response to food intake, and excess glucose does not normally remain in circulation. Glucose levels are not primarily maintained by the kidneys.

Rationale: Some chemicals, such as epinephrine, can function as both a hormone and be closely integrated with the central and peripheral nervous systems as well as the immune systems, leading to current terminology such as “neuroendocrine.” Hormones modulate, but do not initiate, changes in the body. One hormone may exert multiple effects on multiple body systems. Hormones are produced by a variety of body tissues, not solely by endocrine glands.

Rationale: A characteristic of hormones is that a single hormone can exert various effects in different tissues. For example, erythropoietin, a traditional circulating hormone, is made in the kidney and stimulates erythropoiesis in the bone marrow.

Rationale: The half-life of a hormone—the time it takes for the body to reduce the concentration of the hormone by one half—is positively correlated with its percentage of protein binding. Thyroxine, which is more than 99% protein bound, has a half-life of 6 days whereas aldosterone, 15% bound, has a half-life of only 25 minutes.

Rationale: PET/CT are done because the CT component allows for examination of tissue structure while PET scans provide information about tissue function. They are not done for reasons related to primary vs. metastatic tumor identification nor for reasons related to differing sizes of tumors. The radiation associated with CT scanning is not therapeutic.

Rationale: Thyroid ultrasound is recommended for managing thyroid nodules and can aid in visualization of the nodule for biopsy (fine-needle aspiration [FNA]), which is necessary to help distinguish benign from malignant etiology. Magnetic resonance imaging is the preferred choice for pituitary and hypothalamic imaging. Isotopic imaging includes radioactive scanning of the thyroid (e.g., using radioiodine), parathyroids (e.g., using sestamibi), and adrenals (e.g., using metaiodobenzylguanidine [MIBG] to detect pheochromocytoma).

Rationale: Steroids such as estrogen are produced in the smooth endoplasmic reticulum. Synthesis and release are not separate processes, as in the case of peptide hormones. Prohormones are associated with peptides, polypeptides, and protein hormones.

Rationale: Because estrogen is a steroid hormone, its receptors in target cells are located inside the cell membrane, and their blockage does not affect the movement of the hormone into and out of the cell. Receptors are specific for each hormone, so no hormones other than estrogen will be blocked. Up-regulation occurs when hormone levels are decreased, and in this case the estrogen level will increase. Second messengers, such as cAMP, are only activated by peptide hormones and catecholamines.

Rationale: Steroid hormones are bound to protein carriers for transport and are inactive in the bound state. Their activity depends on the availability of transport carriers.

Rationale: Growth hormone is a very large and complex protein which has approximately 200 amino acids.

Rationale: Acetylsalicylic acid (aspirin) competes with thyroid hormone for binding to transport proteins. When aspirin is administered to people with excessive levels of circulating thyroid hormone, such as during thyroid crisis, serious effects may occur because of the increased dissociation of free hormone from the binding proteins. The other medications do not have this effect.

Rationale: Second messengers interact with hormones that cannot cross the cell membrane and they mediate the ultimate effect on the cell. They are not produced by the hormone-producing cell and they are necessary to bring about hormonal effects, not simply for increasing the intensity of the effect. They are not an alternative mechanism of effect but rather a prerequisite for certain hormonal effects on body cells.

Rationale: In positive feedback control, rising levels of a hormone cause another gland to release a hormone that is stimulating to the first. Increased estradiol production during the follicular stage of the menstrual cycle causes increased FSH production by the anterior pituitary gland. This stimulates further increases in estradiol levels until the demise of the follicle.

Rationale: When a GH-secreting tumor is suspected, the GH response to a glucose load is measured as part of the diagnostic workup. Normally, a glucose load would suppress GH levels. However, in adults with GH-secreting tumors (a condition known as acromegaly), GH levels are not suppressed.

Rationale: Diagnosis of Hashimoto thyroiditis is usually made by detecting elevated levels of anti-thyroid peroxidase antibodies (TPOAb) in the serum. Gigantism is diagnosed as an excessive secretion of growth hormone. There may be high levels of insulin-like growth factor 1 (IGF-1), which also stimulates excessive skeletal growth. States of hyperparathyroidism are associated with increased levels of 1,25-(OH)2D3. Parathyroid hormone (PTH) is an important regulator of calcium and phosphate levels in the blood. Diabetes is diagnosed following fasting plasma glucose test level of 126 mg/dL (6.99 mmol/L) or greater. Glycated hemoglobin testing (Hemoglobin A1C) is a test that measures the quantity of a subtype of hemoglobin that has been glucated, meaning glucose molecules have become bound to the hemoglobin molecule. In conditions of hyperglycemia, the A1C level is increased.

Rationale: Neuroendocrine actions are when a hormone produced within a neuron then travels through circulation to exert effects on target cells. Vasopressin (antidiuretic hormone) and epinephrine are examples of hormonal substances with neuroendocrine effects. Sex steroids is a paracrine action. Paracrine action or signaling is a form of cell-to-cell communication in which a cell produces a signal to induce changes in nearby cells, altering the behavior of those cells. Insulin is an autocrine hormone. Autocrine action is a mode of hormone action to which hormones bind to receptors on the cell and affects the cell that produces it, like when growth factors that stimulate cell division. Paracrine describes hormone action where hormones are released from cells and bind to receptor on nearby cells and affects their function. The anterior pituitary gland secretes LH which stimulates secretion of testosterone development of interstitial tissue of testes. There is no neuroendocrine action involved in the secretion of testosterone.

Rationale: The adrenal cortex is responsible for mineralocorticosteroids, mainly aldosterone which increases sodium absorption and potassium loss by the kidney. Glucocorticoids, mainly cortisol affects regulation of blood glucose levels. Adrenal medulla hormone epinephrine serves as neurotransmitters for the sympathetic nervous system. Growth hormone which stimulates growth of bone and muscle is secreted by anterior pituitary. The thyroid (follicular cells) increases metabolic rate by releasing T3 and T4.

Rationale: Most hormone levels are controlled by way of a negative feedback cycle, in which low levels stimulate production and/or release. A positive feedback cycle would not achieve this effect. While some hormones are released on a diurnal schedule, the dominant form of hormone regulation in the body is that of negative feedback. Hormone release is not predetermined by the pituitary gland.

Rationale: A stimulation test involves the introduction of an element that stimulates the production of another factor or hormone followed by measurement of that hormone. This is not the case in a suppression test, RIA test, or metabolite excretion test.

Rationale: The hypothalamus can be viewed as a bridge by which signals from multiple systems are relayed to the pituitary gland. The hypothalamus collects data from sources throughout the body rather than directly measuring levels. Communication normally flows from the hypothalamus to the pituitary.

Rationale: The nurse needs to know if the client may have been exposed to a nonradioactive iodine contrast material (such as those used in CT scans), as these will interfere with the use of radioiodine imaging studies of the thyroid for approximately 4 weeks. Claustrophobia and lying still is relevant to a CT or MRI but not a radioactive iodine test. The reason to administer this test is usually abnormal thyroid levels, so this question is not a priority. Fasting is not required but iodine-containing foods should be avoided.

Rationale: Up-regulation is a response to low hormone levels in which the number of receptors increases. As such, it would not likely result in signs and symptoms of deficiency but is rather a compensatory mechanism that counters a deficiency. Insufficient numbers of receptors, low affinity, and down-regulation could all contribute to signs and symptoms of a hormone deficiency.

Rationale: A single hormone can exert various effects in different tissues or, conversely, a single function can be regulated by several different hormones. Hormones act both distant from their source and more locally, as in the case of autocrine and paracrine actions. Hormones are normally present at all times.

Rationale: Steroids such as aldosterone and testosterone are a classification of hormones that are derived from cholesterol. Epinephrine and norepinephrine are both amino acids. Insulin and glucagon and classified among peptides, polypeptides, proteins, and glycoproteins. Eicosanoids and retinoids consist of fatty acid compounds.

Rationale: Glucocorticoids affect metabolism of all nutrients and have anti-inflammatory effects, which can assist with airway inflammation.

Rationale: This client is not at risk for hypoglycemia simply because of fasting. The negative feedback loop between blood glucose (BG) level and insulin levels will cause insulin levels to drop as the client’s BG drops. Then, glucagon will be released and bind to surface receptors on liver cells to send a second intracellular message for glycogen breakdown, increasing BG and preventing hypoglycemia. The client is not taking the scheduled antihypertensives so the nurse should measure blood pressure and heart rate based on degree of risk for this client. Being off these medications means there is less risk for dizziness or orthostatic hypotension. When fasting, a client is permitted to consume water to prevent dehydration.