Ch23 Endocrine Emergencies.docx

Chapter 23 Endocrine Emergencies Unit Summary The endocrine system directly or indirectly influences almost every cell, organ, and function of the body. Patients with an endocrine disorder often have a broad range of signs and symptoms, necessitating a thorough assessment and immediate treatment to avert life-threatening emergencies. The endocrine system comprises a network of glands that produce and secrete hormones. This unit will provide a thorough discussion of the endocrine system. National EMS Education Standard Competencies Medicine Integrates assessment findings with principles of epidemiology and pathophysiology to formulate a field impression and implement a comprehensive treatment/disposition plan for a patient with a medical complaint. Endocrine Disorders Awareness that • Diabetic emergencies cause altered mental status ( pp 1218, 1221, 1224) Anatomy, physiology, pathophysiology, assessment, and management of • Acute diabetic emergencies (pp 1221-1230) Anatomy, physiology, epidemiology, pathophysiology, psychosocial impact, presentations, prognosis, and management of • Acute diabetic emergencies (pp 1221-1230) • Diabetes (pp 1221-1225) • Adrenal disease (pp 1231-1233) • Pituitary and thyroid disorders (pp 1233-1236) Knowledge Objectives Describe the incidence, morbidity, and mortality of endocrine emergencies. (pp 1221-1222) Discuss the anatomy and physiology of the organs and structures of the endocrine system. (pp 1212-1217) Explain how to size up scene safety when responding to a patient with an endocrine system emergency. (p 1218) Analyze the nature of the illness for a broad range of endocrine disorders. (p 1218) Indicate the considerations that go into making a transport decision for the patient with an endocrine emergency. (p 1219) Specify how to investigate the chief complaint of a patient with an endocrine disorder, including how to take the patient’s history using the SAMPLE mnemonic. (pp 1219-1220) Describe the technique for performing a comprehensive physical examination on a patient with an endocrine emergency. (p 1220) Examine ways in which you can communicate effectively with patients who have endocrine disorders. (pp 1219-1221) Specify how to manage airway, breathing, and circulation in patients with endocrine system emergencies. (pp 1218-1219) Define and explain the terms diabetes, low blood glucose, and high blood glucose. (pp 1221, 1226-1230) Compare the pathophysiology, assessment, and management of type 1 diabetes with that of type 2 diabetes. (pp 1223-1225) Discuss the role of glucose as a major source of energy for the body, and explain the relationship of glucose to insulin. (pp 1221-1223) Compare hyperglycemic and hypoglycemic diabetic emergencies, including their pathophysiology, assessment, and management. (pp 1226-1230) Outline some age-related considerations to keep in mind when managing a pediatric patient who is experiencing a hypoglycemic crisis. (p 1228) Discuss the steps in conducting a primary and secondary assessment of a patient with a diminished level of consciousness who is suspected of having diabetes. (pp 1218-1220) Describe the interventions for providing emergency medical care during a hypoglycemic crisis to conscious and unconscious patients who have a history of diabetes. (pp 1226-1227) Provide the generic and trade names, form, dose, administration, indications, and contraindications for administering 50% dextrose to a patient with hypoglycemia. (p 1227) Explain some age-related considerations to keep in mind when managing an older adult patient who is thought to have undiagnosed diabetes. (p 1223) Define hyperosmolar nonketotic coma/hyperosmolar hyperglycemic nonketotic coma (HONK/HHNC), and name the signs characteristic of the condition. (p 1230) Define hyperglycemia and discuss its pathophysiology, assessment, and management. (pp 1227-1230) Describe the interventions for providing emergency medical care during a hyperglycemic crisis to conscious and unconscious patients who have a history of diabetes. (pp 1229-1230) List the signs and symptoms of diabetic ketoacidosis (DKA), and describe its relationship to hyperglycemia. (pp 1227-1230) Identify the special challenges children face during an episode of DKA. (p 1228) Compare primary and secondary adrenal insufficiency, including their incidence, morbidity and mortality, pathophysiology, assessment, and management. (pp 1231-1232) Define addisonian crisis, discuss what triggers this emergency, and identify its chief clinical manifestation and other signs and symptoms. (p 1232) Define Cushing syndrome, list the physical manifestations characteristic of the disorder, and discuss its pathophysiology, assessment, and management. (p 1233) Discuss the clinical presentation of a patient with an adrenal gland tumor. (p 1233) Define congenital adrenal hyperplasia . (p 1233) Compare the effects of hypothyroidism and hyperthyroidism on the cardiovascular, metabolic, neurologic, musculoskeletal, and gastrointestinal systems, and discuss the general somatic and emotional effects of each condition. (pp 1233-1236) Explain the relationship of Graves disease to hyperthyroidism, and discuss the characteristic physical signs of the disease. (p 1234) Explain the relationship of Hashimoto disease to hyperthyroidism, and compare Hashimoto disease with Graves disease. (p 1234) Outline the characteristic signs of myxedema coma, and describe its relationship to hypothyroidism. (pp 1234-1235) Discuss the incidence, morbidity, and mortality associated with myxedema coma, explain why it is considered to be an emergency, and outline appropriate treatment. (pp 1234-1235) Describe thyrotoxicosis and thyroid storm, and specify their relationship to hyperthyroidism. (p 1235) Define inborn errors of metabolism , explain how they are categorized, and give examples from each category. (p 1236) Skills Objectives 1. Demonstrate the assessment and care of a patient with hypoglycemia and a decreased level of consciousness. (pp 1226-1227) 2. Demonstrate how to administer glucose to a patient with an altered mental status. (pp 1226-1227) 3. Demonstrate how to administer 50% dextrose to a patient with hypoglycemia. (pp 1226-1227 4. Demonstrate how to administer glucagon to a patient with hypoglycemia. (p 1227) Readings and Preparation Review all instructional materials including Chapter 23 of Nancy Caroline’s Emergency Care in the Streets, Seventh Edition, and all related presentation support materials. Contact the patient education programs at your local hospital, along with the American Diabetes Association, and request to use their available educational materials. This content is usually an excellent way to prepare. Support Materials • Lecture PowerPoint presentation • Case Study PowerPoint presentation • Available charts and diagrams of the endocrine system Enhancements • Direct students to visit the companion website to Nancy Caroline’s Emergency Care in the Streets, Seventh Edition, at http://www.paramedic.emszone.com for online activities. • Invite a guest speaker who suffers from diabetes mellitus to visit the class to provide a patient’s perspective on a particular endocrine or disorder. • Direct students to view this online video of a diabetic child demonstrating how he measures carbs and sets up his pump: http://www.youtube.com/watch?v=I-xWPEzNl_o&NR=1&feature=fvwp • Direct students to view this online video of an insulin infusion pump change: http://www.youtube.com/watch?v=eSJz7vFSZ0Y&feature=related • Provide students with samples of glucometers, test strips and lancing devices from various manufacturers. • Content connections: Remind students that endocrine disorders, especially diabetes, can mimic psychiatric/behavioral emergencies. They should keep these conditions in mind when assessing the patient with a possible psychiatric disorder. • Cultural considerations: It is important to discuss negative stereotypes in relation to persons exhibiting signs and symptoms of an altered mental status. Some of the most common mistakes providers make is to assume patients are “just drunk.” While some of the patients you provide care to will be intoxicated, it is important to complete an objective assessment. Teaching Tips • Remind students that glucose is the other significant part of the equation for proper cell metabolism, and that the difference between oxygen deficits and glucose deficits can be difficult to determine, because both affect cell function. As a result, the behavior of a patient with a glucose deficiency can be as unpredictable as the hypoxic patient. • Use charts, graphs, and diagrams in order to help students understand the mechanisms of diabetes. Visuals will be very helpful when describing the balancing act between glucose and insulin. • Emphasize to students that most suspected diabetic emergencies will be treated with glucose, regardless of cause. • Remind students that it is not necessarily their job to diagnose their patients. They should not get so caught up in the patient’s specific diagnosis that they fail to recognize and treat potential complications of the disease. Unit Activities Writing activities: Assign students a component of the endrocrine system. Students should prepare a written assignment coverning current published medical research on commonly related conditions. Student presentations: Students may present their group assignment or, alternatively, present the results of their written assignment. Group activities: Divide students into groups. Have students analyze their last oral intake for carbohydrate levels using commonly accepted charts. Students could present their findings as a presentation. Visual thinking: Have students prepare a visual diagram relating an endocrine-based illness with associated anatomy/physiology. Students should pay particular attention to signs and symptoms of these illnesses and the location of origin. Pre-Lecture You are the Medic “You are the Medic” is a progressive case study that encourages critical-thinking skills. Instructor Directions Direct students to read the “You are the Medic” scenario found throughout Chapter 23. • You may wish to assign students to a partner or a group. Direct them to review the discussion questions at the end of the scenario and prepare a response to each question. Facilitate a class dialogue centered on the discussion questions and the Patient Care Report. • You may also use this as an individual activity and ask students to turn in their comments on a separate piece of paper. Lecture I. Introduction A. The endocrine system influences almost every cell, organ, and function of the body. 1. Patients with an endocrine disorder often have a broad range of signs and symptoms. a. A thorough assessment and immediate treatment are required to prevent life-threatening emergencies. II. Anatomy and Physiology A. Endocrine system 1. Network of glands that produce and secrete chemical messengers (hormones) 2. The main function is to: a. Maintain homeostasis b. Promote permanent structural change 3. To maintain homeostasis, there must be responses to changes in the body. a. Example: Low glucose or calcium levels 4. Exocrine glands (exo-: outside) a. Secrete chemicals for elimination b. Have ducts that carry secretions to surface of skin or body cavity c. Examples: Sweat glands, salivary glands, liver 5. Endocrine glands (endo-: inside) a. Secrete chemicals used inside the body b. Release hormones directly into surrounding tissue and blood c. These hormones: i. Increase or decrease rate of cellular metabolism ii. Transfer information between cells to coordinate body functions like regulation of mood, metabolism, and sexual development and function 6. Hormones of the endocrine system: a. Are released directly into the bloodstream b. Act more slowly than nerve impulses c. Travel through the bloodstream to target tissues i. Each cell has a receptor site on the cell membrane, which: (a) Recognize and bind to their particular hormones (b) Initiate an appropriate signal ii. When the hormone attaches to the receptor site it delivers “messages” to alter cell function. 7. Many cells contain multiple receptors and act as targets for several hormones or molecules. a. Agonists i. Molecules that bind to a cell’s receptor and trigger a response by that cell ii. Produce an action or biologic effect b. Antagonists i. Molecules that bind to a cell’s receptor and block agonists ii. Hormone antagonists are widely used as drugs. B. Mechanisms of hormonal regulation Hormones operate within positive or negative feedback systems to maintain an optimal operating environment in the body. Release of hormones is regulated by: a. Chemical factors b. Other hormonal factors c. Neural control 3. Endocrine regulation maintains hormone secretion through negative feedback. a. Example: Release of epinephrine from adrenal medulla in response to stress 4. Disease occurs when normal cell signaling is interrupted and positive feedback is given. a. System stops providing negative feedback to regulate function 5. The hypothalamus and pituitary gland are related through the vascular system. a. The hypothalamic–pituitary system controls the function of multiple peripheral endocrine organs. b. Hypothalamus produces its own regulatory hormones i. Regulatory hormones control the release of hormones by the pituitary gland. ii. Some hormones have physiologic effects that depend on their concentration. (a) Example: If the hypothalamus detects an increase in the body’s salt concentration, it signals the posterior pituitary to increase secretion of antidiuretic hormone (ADH). (1) Increased ADH levels stimulate the renal tubules to reabsorb sodium and water. (2) ADH also acts as a vasopressor. C. Components of the endocrine system Hypothalamus a. Small region of the brain that contains several control centers for body functions and emotions b. The primary link between the endocrine and nervous systems 2. Pineal gland a. Located in the posterior end of the third ventricle of the brain b. Synthesizes and secretes melatonin, a hormone that affects sleep/wake patterns and seasonal functions 3. Pituitary gland a. Often called “master gland” i. Secretions control activity of other endocrine glands b. Located at the base of the brain c. About the size of a grape d. Connected to the hypothalamus by a thin tissue e. Divided into two regions, or lobes: i. Anterior pituitary (a) Produces and secretes seven hormones: Growth, thyroid-stimulating, adrenocorticotropin, melatonin-stimulating, and three gonadotropic hormones ii. Posterior pituitary (a) Secretes two hormones (ADH and oxytocin) but does not produce them f. Production and secretion of pituitary hormones is influenced by factors like emotion and seasonal change. 4. Thyroid gland a. Secretes thyroxine when body’s metabolic rate decreases i. Body’s major metabolic hormone ii. Stimulates energy production in cells iii. Cannot be produced without the proper level of iodine intake (a) Lack of thyroxine diminishes physical and mental growth. iv. Production regulated by negative feedback mechanism b. Secretes calcitonin, which: i. Helps maintain calcium levels in the blood ii. Stimulates bone-building cells to absorb excess calcium iii. Stimulates kidneys to absorb and excrete excess calcium 5. Thymus gland (thymus) a. Part of the immune system b. Located anteriorly and superiorly in the chest, posterior to the sternum c. Can shrink rapidly with severe stress or chronic illness d. Helps immune system identify and destroy foreign intruders e. Lymphocytes: White blood cells that assist the lymphatic system with immunity i. T lymphocytes (T cells) evolve from stem cells in the thymus. ii. T cells directly target and destroy antigens including viruses, fungi, parasites, tumor cells, and some bacteria—a process called cell-mediated immunity. iii. Types of T cells include: (a) Killer (cytotoxic) T cells: Attack antigens directly and trigger phagocytosis, preventing its reproduction. (b) Helper T cells: Release lymphokines, which deliver messages about antigens to B cells. (c) Suppressor T cells: Contain immune response, which can otherwise cause excessive inflammation, resulting in severe tissue damage. 6. Parathyroid glands a. Assist in the regulation of calcium. b. Parathyroid hormone (PTH) i. Acts as an antagonist to calcitonin ii. Secreted when calcium blood levels are low iii. Stimulates the bone-dissolving cells to break down bone and release calcium into the bloodstream iv. Decreases the amount of calcium released in the urine 7. Adrenal glands a. Paired rectangular structures located on top of the kidneys b. Coordinate several functions, such as: i. Secreting hormones that suppress inflammation ii. Governing the body’s use of nutrients iii. Regulating how much sodium is excreted in the urine c. Consist of two parts that produce different types of hormones: i. Adrenal cortex (outer part) produces mineralocorticoids, glucocorticoids, and sex hormones, which regulate the body’s: (a) Metabolism (b) Balance of salt and water (c) Immune system (d) Sexual function ii. Adrenal medulla (inner part) produces catecholamines (epinephrine and norepinephrine) (a) Increase pulse and respiratory rates and blood pressure in response to stress d. During stress, the anterior pituitary releases adrenocorticotropic hormone (ACTH). i. ACTH targets the adrenal cortex and causes it to secrete cortisol (a glucocorticoid), which stimulates other cells to increase their energy production. e. Adrenal cortex secretes aldosterone (a mineralocorticoid) in response to a drop in blood pressure or volume, a decrease in sodium level, or an increase in potassium level. i. Stimulates the kidneys to reabsorb sodium from the urine and excrete potassium ii. Reduces the amount of salt and water lost through the sweat and salivary glands f. When stimulated by the hypothalamus, the adrenal medulla secretes small amounts of norepinephrine and large amounts of epinephrine. i. Norepinephrine raises blood pressure by causing blood vessels and skeletal muscles to constrict. ii. Epinephrine stimulates sympathetic nervous system receptors and stimulates the liver to convert glycogen to glucose for use as energy in the cells. iii. Result is increased levels of oxygen and glucose in the blood and faster circulation of blood to the brain, heart, and muscles 8. Pancreas a. Digestive gland that is considered both an endocrine gland and an exocrine gland b. Endocrine component comprises the islets of Langerhans i. Cell groups within the pancreas that act like “an organ within an organ” ii. Alpha cells secrete glucagon, and beta cells secrete insulin. (a) Responsible for regulation of blood glucose levels iii. Delta cells secrete somatostatin. (a) Inhibits insulin and glucagon secretion c. When blood glucose level falls, glucagon is secreted to raise it. i. Stimulates the liver to change glycogen into sugar and secrete it into the bloodstream d. When blood glucose level rises, insulin is secreted. i. Transports glucose to the cells ii. Stimulates the liver to take in more glucose and store it as glycogen for later use iii. Only hormone that decreases the blood glucose levels 9. Gonads a. Main source of sex hormones b. Testes in men i. Located in the scrotum ii. Produce hormones called androgens (a) The most important is testosterone. (b) Regulate changes associated with puberty (1) Growth spurts (2) Deepening of the voice (3) Growth of facial and pubic hair (4) Muscle growth and strength c. Ovaries in women i. Release eggs ii. Secrete the hormones estrogen and progesterone. (a) Estrogen signals the anterior pituitary gland to secrete luteinizing hormone (LH) when an egg is developing in an ovarian follicle. (b) Both assist in the regulation of the menstrual cycle. (c) At puberty, estrogen supports development of the secondary sex characteristics. (1) Enlargement of the breasts (2) Uterine enlargement (3) Fat deposits in the hips and thighs (4) Development of underarm and pubic hair III. Patient Assessment A. Endocrine emergencies tend to affect many organ systems. 1. Do not take these emergencies lightly. B. Scene size-up 1. Address hazards, and follow standard precautions. 2. Check the following for medications that may give you clues: a. Bureau tops b. Bedside tables c. Medicine cabinets d. Refrigerator 3. Bring any medication bottles to the hospital C. Primary assessment 1. Identify and manage life threats immediately. a. Check for a medical identification bracelet or necklace in patients with altered mental status. 2. Form a general impression. a. Observe the following: i. Patient’s overall appearance ii. Skin color and appearance iii. Does the patient make eye contact? iv. Answer questions appropriately and without difficulty speaking? b. Signs and symptoms depend on hormone production or secretion that is affected. c. Patient’s position may offer clues as to the severity of the condition. i. An unresponsive patient may be experiencing an endocrine crisis, such as: (a) Hypoglycemia (b) Hyperglycemia (c) A myxedema coma with severe thyroid deficiency d. Diaphoresis is a sign of severe distress. i. Present in thyrotoxicosis, along with pulmonary edema e. Signs and symptoms of specific conditions include: i. “Buffalo hump,” “moon face,” and acne are signs of Cushing disease. ii. Mottled skin is associated with pancreatitis. iii. Enlarged or abnormal body parts may occur with: (a) Edema with syndrome of inappropriate antidiuretic hormone (SIADH) (b) Anasarca with myxedema coma iv. Underweight or overweight may indicate an endocrine dysfunction such as: (a) Hypothyroidism (b) Hyperthyroidism (c) Diabetes v. Exophthalmos is present in Graves’ disease. vi. Abnormal development may be present in children with panhypopituitarism. 3. Airway and breathing a. Ensure the airway is patent. b. Investigate any abnormal breathing sounds for obstruction. c. Maintain airway as needed through: i. Patient positioning ii. Suctioning iii. Basic airways d. Assess breathing effort. i. Administer oxygen if: (a) The rate is greater than 24 breaths/min. (b) The rate is less than 8 breaths/min. e. Supplemental oxygen is recommended in all cases of suspected respiratory involvement. i. Even with a normal pulse oximetry reading 4. Circulation a. Assess skin color, moisture, and temperature. b. Obtain blood pressure. c. Pale, cool, moist skin may be a sign of: i. Shock ii. Hypoglycemia d. Hot, dry skin may be a sign of: i. Fever ii. Hyperglycemia e. IV administration or blood replenishment may be necessary. 5. Transport decision a. Many patients with endocrine disorders should be transported to a facility that specializes in these conditions. b. Transport the patient rapidly to the closest facility if the patient’s condition is unstable. D. History taking 1. Especially useful in diabetic emergencies (genetic disease) 2. Consider the patient’s signs and symptoms and any pertinent negatives. 3. If a patient is unresponsive: a. Obtain a blood glucose level. b. Manage any abnormalities appropriately. 4. Use SAMPLE to gather information. 5. Signs and symptoms of endocrine disorders in patients with undiagnosed or poorly managed diabetes include: a. Polyphagia b. Polyuria c. Polydipsia 6. The following may occur with hyperthyroidism and thyrotoxicosis: a. Tachycardias b. PVCS c. PACs d. Atrial dysrhythmias 7. Ascertain any allergies prior to administering medication. 8. Document the following: a. All medications the patient is currently taking b. Whether the patient has been compliant with the regimen i. Medications are often a clue to already diagnosed conditions. 9. Ask females of childbearing age about their last menstrual period (LMP). E. Secondary assessment 1. Begin the physical exam with observation. a. General appearance b. The position in which the patient is found i. An awkward position often indicates brainstem damage. ii. Decorticate or decerebrate posturing are both signs of serious illness. 2. Identify as many atypical findings as possible. 3. A focused assessment is usually not necessary unless trauma is present. a. Full-body scan is more appropriate b. Always manage life threats first. 4. Finer abnormalities will help determine treatment. a. Condition of skin i. Cold and clammy skin may indicate: (a) Shock (b) Severe hypoglycemia. ii. Cold and dry skin may indicate: (a) Overdose of sedative drugs (b) Alcohol intoxication iii. Hot and dry skin suggests: (a) Hyperglycemia (b) Fever (c) Possibly heat stroke 5. Two goals with comatose patients a. Determine the patient’s level of consciousness. i. Will be used later to determine whether the condition is improving or deteriorating b. Look for signs that might be clues to the source of coma. 6. Vital signs a. Look for a combination of hypertension and bradycardia. i. Suggests increased intracranial pressure b. Be alert for abnormal respiratory patterns, such as: i. Cheyne-Stokes breathing (a) Usually points to a nonneurologic source of coma ii. Kussmaul respirations (a) Often present in patients experiencing a diabetic ketoacidosis (DKA) event iii. More worrisome abnormal breathing patterns, including: (a) Central neurogenic ventilation (b) Huffing and puffing that do not seem to move much air c. Look for pararespiratory motions. i. Sneezing and yawning require an intact brainstem. ii. Hiccupping and coughing may indicate brainstem damage. F. Reassessment 1. Once you have initiated your treatment plan, continually reassess the patient for changes. a. Reassess critical patients at least every 5 minutes. b. Noncritical patients may be reassessed every 15 minutes. c. Document your findings. 2. A patient whose gag reflex is absent cannot protect his or her own airway from aspiration. a. Be prepared to suction the airway. b. Consider intubation if the patient does not regain consciousness with treatment. 3. If breathing is abnormally slow or shallow, assist with bag-mask ventilation. 4. Give supplemental oxygen whether the patient is breathing spontaneously or being ventilated. 5. Obtain blood specimens early in patients with diabetes. a. Administration of prehospital dextrose or other medications will significantly change the chemical makeup of subsequent blood samples. 6. If altered mental status: a. Establish either: i. An IV with 0.9% NS ii. A saline lock. b. Immediately determine the blood glucose level. i. Initiate treatment of 12.5 g to 25 g of D50 if the reading is less than 60 mg/dL. c. Consider administering naloxone (Narcan) if: i. The patient’s condition does not improve after a dose of D50 ii. And you have a reason to suspect a narcotics overdose 7. Address the patient’s emotional needs. 8. Monitor the cardiac rhythm of every comatose patient. 9. During neurologic assessment, the most important consideration is the trend shown by several measurements. a. Recheck vital signs, pupils, and level of consciousness. i. Every 5 minutes in unstable patients ii. Every 15 minutes in stable patients b. Record your findings immediately. i. Every patient you transport should have at least two sets of vital signs documented. ii. Your record is a legal document and a permanent part of the patient’s medical record. IV. Emergency Medical Care A. Transport for comatose patients 1. If the patient is intubated, transport supine with a cervical collar in place. a. Decreases the risk of unintentional extubation 2. If the patient is not intubated, you may transport the patient in the stable side position (unless precluded by injuries). 3. If there are indications of increasing intracranial pressure, transport with: a. The head elevated to 30° to 45° and midline 4. Always keep the mouth and pharynx suctioned free of secretions, vomitus, and blood. V. Pathophysiology, Assessment, and Management of Glucose Metabolic Derangements A. Endocrine disorders are caused by either hypersecretion or insufficient secretion of a gland. 1. Hypersecretion presents as overactivity of the organ regulated by the gland. 2. Insufficient secretion of a gland presents as underactivity of the organ controlled by the gland. 3. Glucose metabolic derangements (disorders) are caused by dysfunction of the pancreas. a. Impairs the body’s ability to metabolize glucose 4. The effects of a disturbance of endocrine gland function are determined by: a. The degree of dysfunction of the gland b. The age and sex of the patient 5. Most significant endocrine emergencies result in: a. Compromise of the ABCs b. Improper fluid balance c. Deteriorating mental status d. Abnormal vital signs and blood glucose levels B. Diabetes mellitus 1. A metabolic disorder in which the body’s ability to metabolize simple carbohydrates (glucose) is impaired a. Characterized by: i. Polyphagia: An increased appetite caused by the inability of glucose to be transported across the cell membrane ii. Polydipsia: A significant thirst caused by dehydration brought about by an increase in diuresis iii. Polyuria: The passage of large quantities of urine containing glucose b. Glucose (dextrose) i. One of the basic sugars in the body ii. Along with oxygen, it is the primary fuel for cellular metabolism. c. Insulin i. Hormone produced by the islets of Langerhans in the pancreas ii. Assists in: (a) Metabolism of carbohydrates (b) Transport of glucose into the cells d. In people with this disease, either: i. Pancreas does not produce enough insulin or ii. The body’s cells do not respond to the effects of the insulin that is produced. e. In either case: i. There is an elevated level of glucose in the blood and glucose in the urine. (a) Glucose builds up and flows out of the body. f. In 2010 an estimated 25.8 million people had diabetes. i. 8.3% of the population ii. Of those, 7 million are undiagnosed. iii. In 2007, diabetes was the seventh leading cause of death in the United States. 2. Life-altering complications from diabetes include: a. Kidney failure i. Diabetes is the principal cause of kidney failure. ii. The glomeruli of the kidney become sclerotic, causing: (a) Necrosis of the papillary tissue (b) Nephropathy (c) Renal failure iii. High levels of blood glucose may result in decreased kidney function over time. b. Heart disease or stroke i. Adults with diabetes are two to four times more likely to die of heart disease or to have a stroke. ii. When diabetes is not properly controlled, lipolysis raises the level of fat in the blood (dyslipidemia). (a) Increases risk of atherosclerosis and coronary artery disease iii. The microscopic deterioration of the vessel walls (microangiopathy) is a condition in which swelling of membrane cells restricts the flow of blood to organs and tissues. (a) Ischemia causes necrosis. (b) Central nerve damage can cause cardiac dysrhythmias. c. Cerebrovascular disease, stroke, and hypertension i. Microangiopathy is characterized by cerebrovascular disease and associated with an increased incidence of stroke. ii. Peripheral artery disease impairs circulation to the lower extremities. iii. Hypertension is present in two out of three persons with diabetes. d. Eyes i. In adults, diabetes is the primary cause of new cases of blindness. (a) High blood glucose levels damage the vessels of the eye. (b) Scar tissue may pull the retina from the eye or retinal detachment. (c) Cataracts form when fructose and sorbitol are deposited in the lens. e. Neuropathy (nerve damage that results in loss of sensation and function) i. When associated with diabetes often affects peripheral nerves, causing diminished sensation and function in the extremities. (a) Paresthesia and dysesthesia can blunt pain perception, causing ulcers to go unnoticed until they become seriously infected. (b) Gangrene may develop in adjacent tissues due to poor circulation. (c) Infection may spread to the bone, which can result in amputation. 3. Many conditions associated with diabetes can be delayed/prevented with lifestyle changes and continued management. a. Blood glucose levels are more difficult to control during stress/physical activity. b. Economic costs of diabetes were about $174 billion in 2007 and continue to rise. i. Disability, lost productivity, premature mortality, cost of health care c. Chronic and acute complications are associated with diabetes mellitus. i. More severe in people who require insulin ii. Left untreated, diabetes leads to: (a) Organ system dysfunction (b) Wasting of body tissues (c) Death iii. The severity of complications correlates with: (a) Average blood glucose level (b) Age of onset iv. No cure (a) Treatment focuses on maintaining blood glucose levels within the normal range. 4. Type 1 diabetes mellitus a. Pathophysiology i. Referred to as insulin-dependent diabetes mellitus, IDDM, or juvenile diabetes because it generally affects children ii. Although a hereditary predisposition exists, environmental factors may be part of the cause. iii. Beta cells in the islets of Langerhans have been destroyed and no longer produce insulin. (a) Supplementary, synthetic insulin must be administered daily by injection or pump. (b) Strict dietary control must be observed (c) Increased activity and alcohol consumption can lead to low blood glucose levels. b. Assessment i. Determine whether the patient is compliant with disease management. ii. With altered mental status, suspect a low blood glucose level. iii. Additional chronic conditions may include: (a) Renal failure (b) Congestive heart failure (c) CAD (d) Hypertension (e) Vision and hearing impairment iv. Assess for signs of sores or infections. v. Ask about: (a) Tingling, numbness, or swelling of the extremities (b) Vision changes (c) Headaches (d) Dizziness (e) Bleeding (f) Sores in the mouth (g) Recent change in bowel or eating habits c. Management i. Some patients use insulin pumps to treat their disease. (a) Consists of an infusion set, a reservoir for insulin, and the pump itself (b) Alternative to multiple daily injections (c) Provides improved control of blood glucose levels (d) Also called continuous subcutaneous insulin infusion therapy ii. Several types of insulin available in the United States: Rapid-acting, regular or short-acting, intermediate-acting, and long-acting. (a) Differs in onset of action, duration, and peak time 5. Type 2 diabetes mellitus a. Pathophysiology i. Condition in which blood glucose levels are elevated. ii. Accounts for about 90% of diabetes in the United States. iii. Typically develops later in life, but is becoming more common in younger people. iv. May be related to metabolic syndrome. (a) Risk factors: Excess weight, lack of physical activity, genetic factors v. In many patients, the pancreas produces enough insulin but the body cannot effectively use it (insulin resistance). vi. Can also be caused by a deficiency in insulin production b. Assessment i. Symptoms may include: (a) Fatigue (b) Nausea (c) Frequent urination (d) Thirst (e) Unexplained weight loss (f) Blurred vision (g) Frequent infections and slow healing of wounds (h) Being cranky, confused, or shaky (i) Unresponsiveness (j) Seizure ii. Symptoms tend to develop gradually and become noticeable in middle age. iii. A small percentage of persons do not display any symptoms. c. Management i. Weight loss, exercise, and a nutritious diet help to control type 2 diabetes. ii. Food intake must be spread throughout the day in coordination with daily medications/insulin injections. iii. Oral medications may be used alone or in combination. (a) Consult a physician or pharmacist prior to the addition of any medication due to the risk of interaction. C. Gestational diabetes 1. Pathophysiology a. Form of glucose intolerance that occurs during pregnancy b. Occurs more often in women who: i. Are African American, Hispanic/Latino, and Native American ii. Are obese iii. Have a family history of diabetes c. Increases risk of type 2 diabetes d. Resolves before delivery for most women e. Usually diagnosed in the third trimester i. Hormones produced by the placenta may impede the function of insulin. ii. Often results in macrosomia, or a large baby 2. Assessment a. Blood glucose crosses the placental barrier. b. When a pregnant woman is hyperglycemic, high levels of glucose enter the fetus, causing increased production of insulin by the fetus to normalize levels. c. Extra glucose is converted into fat. i. Babies are often large and require cesarean sections. 3. Management a. Stabilize blood glucose levels as soon as possible. b. Includes diet modification, exercise, and blood glucose testing c. Insulin injections may be required. D. Hypoglycemia 1. Pathophysiology a. In persons with insulin-dependent diabetes, often results from too much insulin, too little food, or both b. Central nervous system tissue depends on glucose for energy. i. If the level of blood glucose drops dramatically, the brain is literally starved. 2. Assessment a. Patient will tremble, have a rapid pulse rate, sweat, and feel hungry. b. If condition persists, cerebral dysfunction will progress to permanent brain damage. c. Additional signs and symptoms include: i. Headache ii. Mental confusion iii. Memory loss iv. Incoordination v. Slurred speech vi. Irritability vii. Dilated pupils viii. Seizures and coma in severe cases d. Normal blood glucose levels range from approximately 70 to 120 mg/dL. i. Hypoglycemia occurs when blood glucose levels drop to 45 mg/dL or less. e. Hypoglycemia develops rapidly and should be suspected in any patient with diabetes who presents with: i. Bizarre behavior ii. Neurologic signs iii. Coma f. Hypoglycemic episodes may also be due to: i. Alcoholism ii. Poisons or overdose of certain drugs (notably aspirin) iii. Certain cancers iv. Liver disease v. Kidney disease vi. Some other conditions g. Persons with diabetes may also experience: i. Head injury ii. Stroke iii. Seizures iv. Meningitis v. Other traumatic injuries or conditions 3. Management a. Treat suspected hypoglycemia immediately or permanent brain damage may ensue. b. Measure the patient’s blood glucose level. i. Administration of concentrated glucose with a suspected stroke may exacerbate cerebral damage. c. When a comatose patient is 55+ years or the family gives a history of recent transient ischemic attacks, rule out hypoglycemia with a field glucose test. i. Clean the site to be punctured with alcohol. ii. Allow the patient’s arm to hang briefly to allow blood to flow to the fingertips. iii. Grasp the finger near the area to be pricked and squeeze for 3 seconds. iv. Use the lancet device and apply adequate pressure to puncture the skin. v. Keep the hand down, prick the side of the fingertip, and squeeze gently until you obtain a drop of blood. vi. Apply the blood to the test strips. d. Administer sugar by mouth if the patient is: i. Alert ii. Able to swallow iii. Has an intact gag reflex e. With a comatose patient, pay attention to the airway and supplemental oxygen. f. Do not use an advanced airway until you have given the patient D50 (50% dextrose). i. Start an IV with a small-bore catheter in a big vein. ii. Begin a 0.9% normal saline (NS) infusion. iii. Confirm that the IV is patent iv. Inject a test bolus of 10 to 20 mL of NS infusion fluid. v. Recheck its status by lowering the IV bag and looking for backflow of blood. (a) D50 is hypertonic and acidic and can cause serious damage to surrounding tissue. vi. If reliable, administer 12.5 to 25 g of D50 slowly, over at least 3 minutes. (a) If the cause of coma is hypoglycemia, the patient will often awaken rapidly. (1) With severe hypoglycemia, another 25 g of D50 may be required. g. Administer glucagon IM if the patient is unresponsive and hypoglycemic and you cannot obtain IV access. i. Glucagon increases blood glucose levels and relaxes the smooth muscle of the gastrointestinal tract if administered parenterally. h. Patients with type 1 diabetes require immediate access to oral carbohydrates or additional glucose administration. E. Hyperglycemia and diabetic ketoacidosis 1. Pathophysiology a. Hyperglycemia (high blood glucose level) is a classic symptom of diabetes. i. Early signs include frequent and excessive thirst and urination. ii. Occurs when blood glucose levels exceed 120 mg/dL. (a) In patients with diabetes, physicians try to maintain glucose levels at less than 160 mg/dL. iii. Can be caused by: (a) Excessive food intake (b) Insufficient insulin dosages (c) Infection or illness (d) Injury (e) Surgery (f) Emotional stress iv. Onset may be rapid (minutes) or gradual (hours to days) b. Untreated hyperglycemia will progress to diabetic ketoacidosis (DKA) i. Associated predominately with type 1 diabetes ii. Life-threatening condition iii. Occurs when certain acids accumulate in the body because insulin is not available iv. Common causes include: (a) Infection (b) Injury (c) Alcohol use (d) Emotional discord (e) Illness (stroke or myocardial infarction) v. Patients tend to be teenagers and young adults. c. Rising blood glucose leads to massive osmotic diuresis (passing large amounts of urine). i. Osmotic diuresis and vomiting cause dehydration and even shock. 2. Assessment a. Signs and symptoms of hypoglycemia and hyperglycemia can be similar. b. Hyperglycemia usually progresses slowly (12 to 48 hours), with the patient’s level of consciousness deteriorating gradually. c. Patients in DKA are seldom deeply comatose. d. Increase in blood glucose level and degree of ketoacidosis are not predictably correlated, so rely on clinical presentation rather than on test results. e. Signs and symptoms of DKA include: i. Polyuria (excessive urine output) ii. Polydipsia (excessive thirst) iii. Polyphagia (excessive eating) iv. Nausea and vomiting v. Tachycardia vi. Deep, rapid respirations (Kussmaul respirations) vii. Warm, dry skin and dry mucous membranes viii. Fruity odor of ketones on the breath ix. Abdominal pain, hypotension, and sometimes fever 3. Management a. Physician will probably order treatment for DKA if: i. Patient history and physical exam are consistent with DKA and ii. Glucose level is more than 300 mg/dL. b. In most instances, insulin therapy should be delivered at the hospital. c. Follow the procedure for any comatose patient with regard to airway maintenance and oxygen. i. Be alert for vomiting, and have suction ready. ii. Start an IV and infuse up to 1 L of NS during the first half hour or as suggested by protocol or online medical control. d. Monitor cardiac rhythm. i. Sharply peaked T waves may indicate dangerously high levels of potassium, (a) Administration of sodium bicarbonate may be necessary. ii. As potassium levels rise, the QRS complex will widen and may blend with the T wave, developing into a sine wave and becoming bradycardic. (a) Management with calcium chloride or gluconate may be indicated. e. Complications of DKA are frequently associated with its management. i. The infusion of insulin may lead to hypoglycemia. ii. Hypokalemia may result when insulin shifts potassium back into the cells. iii. Cerebral edema may occur if blood glucose levels shift too rapidly (more prevalent in pediatric patients). F. Hyperosmolar nonketotic coma (HONK) 1. Pathophysiology a. Also called hyperosmolar hyperglycemic nonketotic coma (HHNC) b. Metabolic derangement that occurs principally in patients with type 2 diabetes c. Characterized by: i. Hyperglycemia ii. Hyperosmolarity iii. Absence of significant ketosis d. Fewer than 10% of patients present in a comatose state. e. Most have severe dehydration and focal or global neurologic deficits. f. Clinical features of HONK/HHNC and DKA tend to overlap. g. Often develops in patients with diabetes who have a secondary illness that leads to reduced fluid intake 2. Assessment a. Patients do not experience ketoacidosis. b. Approximately 30% do not have a prior diagnosis of diabetes. c. Stress response tends to increase hormones that favor elevated glucose levels and that often counter the effects of insulin, including: i. Cortisol ii. Catecholamines (epinephrine and norepinephrine) iii. Glucagon iv. Many others d. Neurologic changes may be found, including: i. Drowsiness and lethargy ii. Delirium and coma iii. Focal or generalized seizures iv. Visual disturbances v. Hemiparesis vi. Sensory deficits 3. Management a. Prehospital treatment follows the pathway for dehydration and altered mental status. i. Airway management is the top priority. ii. Endotracheal intubation may be indicated for comatose patients. iii. Cervical spine immobilization should be used for all unresponsive patients found lying down. iv. Large-bore IV access should be gained as soon as possible but should not delay transfer. v. Obtain a blood glucose level as soon as possible. b. A bolus of 500 mL 0.9% NS is appropriate for nearly all adults who are clinically dehydrated. i. In patients with a history of congestive heart failure and/or renal insufficiency, a 250-mL bolus may be more appropriate. ii. Patients may receive 1 to 2 L within the first hour. c. Administer 12.5 to 25 g of D50 if the glucose level is less than 60 to 80 mg/dL (depending on local protocols). VI. Pathophysiology, Assessment, and Management of Other Disorders of the Pancreas A. Pancreatitis 1. Pathophysiology a. Inflammation of the pancreas b. Acute pancreatitis is a medical emergency. i. Can lead to dehydration and hypotension ii. 60% to 80% of cases are caused by: (a) Gallstones (b) Chronic alcohol abuse iii. Other potential causes include: (a) Certain medications (b) Trauma (c) Pancreatic cancer (d) Genetic predisposition c. Chronic pancreatitis is a progressive disease. i. Eventually leads to the loss of all endocrine and exocrine functions ii. Often causes chronic pain iii. Often diagnosed by computed tomography (CT) 2. Assessment a. Acute pancreatitis may present with: i. Flank and/or epigastric pain that worsens if the patient is supine ii. Tachycardia iii. Fever iv. Jaundice b. Typically an attack is a result of a large, heavy meal or excessive drinking. c. Patients may also experience: i. Nausea and vomiting ii. Abdominal distention or muscle spasms d. Necrosis and organ failure may develop. e. Laboratory diagnostics include determinations of serum amylase, lipase, and trypsin. 3. Management a. Most patients are managed with supportive care. b. Patients should not eat until nausea has subsided. c. Patients should be transported. d. Pain management is not always effective but can be considered. e. Endoscopic retrograde cholangiopancreatography (ERCP) is used for patients with cholelithiases. f. For patients with chronic pancreatitis: i. Lifestyle changes are critical, including: (a) Changes in diet (b) Termination of alcohol and tobacco use ii. Analgesics are used to control pain. iii. Pancreatic enzymes assist with steatorrhea and malabsorption. iv. Surgical intervention may be considered. g. Patients should be monitored for pancreatic cancer. VII. Pathophysiology, Assessment, and Management of Adrenal Insufficiency A. Adrenal insufficiency 1. Characterized by decreased function of the adrenal cortex and consequent underproduction of cortisol and aldosterone 2. Results in: a. Weakness b. Dehydration c. Inability to maintain adequate blood pressure 3. Cortisol’s primary role is to assist with the response to stress, but it also: a. Helps to maintain blood pressure and cardiovascular function b. Regulates the metabolism of carbohydrates, proteins, and fats c. Modulates glucose levels by balancing the effects of insulin d. Slows the inflammatory response 4. Abnormal adrenal cortical function produces: a. Abnormalities in the metabolism of carbohydrates and protein b. Disturbances in salt and water metabolism 5. Usually well tolerated but may be complicated by factors such as infection or stress 6. Affects about 4 persons per 100,000 in the United States B. Primary adrenal insufficiency (Addison disease) 1. Pathophysiology a. Caused by atrophy or destruction of both adrenal glands b. Leads to deficiency of all the steroid hormones these glands produce c. Rare disease (about 1/100,000 persons in the United States) d. Usually the result of idiopathic atrophy i. Immune system creates antibodies that attack and destroy the adrenal cortex e. Occurs when at least 90% of the adrenal cortex has been destroyed f. Less commonly caused by: i. Tuberculosis ii. Bacterial, viral, or fungal infection iii. Adrenal hemorrhage iv. Cancer of the adrenal glands 2. Assessment a. Signs of chronic adrenal insufficiency include: i. Unexplained weight loss ii. Fatigue iii. Vomiting iv. Diarrhea v. Anorexia vi. Salt craving vii. Muscle and joint pain viii. Abdominal pain ix. Postural dizziness x. Increased pigmentation in the extensor surfaces, palmar creases, and oral mucosa b. Body improperly regulates sodium, potassium, and water in body fluids. i. Blood volume and pressure fall. ii. Sodium concentration of the blood falls. iii. Blood potassium rises. 3. Management a. Assess and manage ABCs. b. If needed, use the coma protocol of glucose, thiamine, and naloxone (Narcan). c. Initiate aggressive fluid replacement using 5% dextrose in normal saline. d. Hydrocortisone, 100 mg IV, is indicated in the acute management of a crisis. C. Secondary adrenal insufficiency 1. Pathophysiology a. Relatively common b. Characterized by a lack of adrenocorticotropic hormone (ACTH) secretion from the pituitary gland i. ACTH stimulates the adrenal cortex to manufacture and secrete cortisol. c. May also occur in patients who abruptly stop taking corticosteroids i. Corticosteroid treatments suppress natural cortical production. 2. Assessment a. Signs and symptoms may appear suddenly (addisonian crisis). i. May be triggered by an acute exacerbation of chronic insufficiency ii. Most common cause is corticosteroid withdrawal b. About 25% of patients first experience symptoms during an addisonian crisis. c. Chief clinical manifestation is shock. d. Symptoms may also include: i. Weakness ii. Lethargy iii. Confusion or loss of consciousness iv. Low blood pressure v. Elevated temperature vi. Severe pain in the lower back, legs, or abdomen vii. Severe vomiting and diarrhea 3. Management a. Unrecognized, untreated episode may be fatal. b. Maintain ABCs. i. Follow the procedure for altered mental status or coma. ii. Be alert for vomiting; have suction ready. c. Begin rehydrating the patient, and correct electrolyte and acid-base abnormalities. i. Start an IV, and infuse up to 1 L of 0.9% NS. ii. If the patient is hypotensive, administer an NS bolus at 20 mL/kg. d. Check the patient’s glucose level. i. Administer 25 to 50 g of D50 to correct the hypoglycemia. ii. D5NS is the preferred IV fluid. e. Monitor cardiac rhythm. i. Changes in serum electrolytes can lead to marked myocardial instability. VIII. Pathophysiology, Assessment, and Management of Other Adrenal Emergencies A. Cushing syndrome 1. Pathophysiology a. Caused by: i. Excess cortisol production by the adrenal glands (a) Example: Tumors of the pituitary gland or adrenal cortex ii. Excessive use of cortisol or other similar corticosteroid hormones (a) Example: For the treatment of life-threatening illnesses b. Causes characteristic changes: i. Metabolism of carbohydrate, protein, and fat is disturbed. (a) Blood glucose level rises. ii. Protein synthesis is impaired. (a) Body proteins are broken down. (b) Leads to loss of muscle fibers and muscle weakness iii. Bones become weaker and more susceptible to fracture. 2. Assessment a. Other common signs and symptoms include: i. Weakness and fatigue ii. Depression and mood swings iii. Increased thirst and urination iv. Low blood glucose level v. Weight gain (a) Abdomen (b) Face (“moon face”) (c) Neck (d) Upper back (“buffalo hump”) vi. Thinning of the skin (a) Easy bruising (b) Pink or purple stretch marks (striae) vii. Increased acne, facial hair growth, and scalp hair loss in women, and cessation of menstrual periods viii. Darkening of skin (acanthosis) on the neck ix. Obesity and poor growth in height in children 3. Management a. Assess and manage ABCs. b. Manage life threats immediately. c. Prehospital treatment is generally supportive. d. Obtain a blood glucose level and administer D50 if indicated. B. Adrenal gland tumor 1. Pheochromocytoma: Tumor of the adrenal gland a. Usually in the medulla b. Causes excessive release of the hormones epinephrine and norepinephrine c. Less than 10% are malignant 2. Most common in young adult to mid-adult life 3. Combination of symptoms that are frequent but sporadic is common a. May increase in frequency, duration, and severity C. Congenital adrenal hyperplasia (CAH) 1. Inadequate production of cortisol and aldosterone a. Some states require testing of infants at birth. b. Susceptible to infection and stress c. May result in an acute adrenal crisis 2. Children may present with undefined signs and symptoms. 3. Signs associated with CAH include: a. Female infants with enlarged parts of the vagina, possibly resembling a penis b. Male infants exhibiting signs of puberty as a toddler, including: i. Increased musculature ii. Penis growth iii. Pubic hair iv. Lowering of the voice c. Child with excessive facial and/or body hair and initial rapid growth. d. Numerous respiratory infections and illnesses and high blood pressure e. Salt wasting caused by insufficient aldosterone levels may lead to: i. Dehydration ii. Low blood pressure iii. Low sodium levels iv. High potassium levels in the blood f. Short stature and severe acne 4. Usually requires lifetime treatment with cortisol and/or aldosterone replacement therapy. 5. Surgery can correct genital deformities. 6. Dexamethasone may be prescribed to a pregnant woman if the condition is diagnosed in the first trimester. IX. Pathophysiology, Assessment, and Management of Thyroid, Parathyroid, and Pituitary Gland Disorders A. Hypothyroidism and hyperthyroidism 1. Anterior pituitary gland secretes thyroid-stimulating hormone (TSH) in response to the hypothalamus’s secretion of thyrotropin-releasing hormone (TRH). a. Approximately 20 million Americans have a thyroid disorder. i. Many are unaware of their condition. b. Likely to require supplemental oxygen. i. Hyperthyroid metabolic activity increases oxygen demand. ii. Hypothyroid conditions may lead to diminished respiratory effort. (a) May require positive-pressure ventilation. B. Graves disease 1. Most severe and common cause of hyperthyroidism 2. More common in women 3. Overall incidence of 1.4 cases per 1,000 persons 4. Tends to follow a chronic course of remission and relapse a. May be fatal if not treated 5. Autoimmune disorder in which the thyroid gland hypertrophies (enlarges) as its activity increases. a. Produces a visible mass (goiter) in the anterior part of the neck. b. Overactive gland secretes an excessive amount of thyroxine c. Other signs and symptoms may include: i. Increased appetite with marked weight loss (a) May progress to cachexia ii. Polydipsia iii. Exophthalmos (protruding eyeballs) iv. Pretibial myxedema (an “orange peel” appearance and nonpitting edema of the skin on the anterior part of the leg below the knee) d. Increased stress on the heart may lead to heart failure. C. Hashimoto disease 1. Another cause of hyperthyroidism a. More common in women b. Result of the infiltration of T lymphocytes and plasma cells 2. An autoimmune disorder that affects the TSH (thyroid-stimulating hormone) receptors 3. Hypothyroidism follows after antibodies destroy the follicles. D. Myxedema coma 1. If the supply of thyroid hormones becomes inadequate: a. Organ tissues do not grow or mature. b. Energy production declines. c. Actions of other hormones are affected. 2. Adult hypothyroidism is sometimes called myxedema. a. Patients often have localized accumulations of mucinous material in the skin. b. Manifested by a slowing of metabolic processes i. Due to the reduction or absence of thyroid hormone c. Symptoms i. May be exhibited by all organ systems ii. Severity is consistent with the degree of hormone deficiency iii. Include: (a) Fatigue (b) Feeling cold (c) Weight gain (d) Dry skin (e) Sleepiness iv. Often subtle and can be mistaken for other conditions 3. Continued decrease of hormone levels may lead to myxedema coma. a. Accompanied by physiologic decompensation that leads to peripheral vasoconstriction b. Often precipitated by triggers, including: i. Infection (especially pulmonary and urinary tract) ii. Exposure to cold iii. Trauma iv. Surgery v. Certain medications c. Hallmark is deterioration of mental status d. Most cases occur during the winter in women older than 60 years. e. Consistent finding is hypothermia i. Absence of fever in the presence of infection is common 4. Hypothyroidism decreases intestinal motility. a. Associated with decreased metabolic rate i. Can lead to drug toxicity, especially in the elderly ii. Causes levels of medications to rise to toxic levels in the blood (a) Especially those that affect the central nervous system (b) Can precipitate myxedema coma 5. If not diagnosed and treated immediately, the mortality rates are approximately 50%. a. Administer supplemental oxygen therapy to correct hypoxia. b. Intubation and ventilation may be indicated c. Monitor the patient’s cardiac status. i. Hypotension may respond to crystalloid therapy. ii. Vasopressive agents may be necessary. (a) Administer 25 to 50 g of D50 if glucose levels are less than 60 mg/dL. d. Treat hypothermia with passive rewarming methods. i. Aggressive rewarming may lead to vasodilation and hypotension. ii. Active rewarming is necessary for hemodynamically unstable patients with profound hypothermia e. Avoid sedatives, narcotics, and anesthetics. E. Thyrotoxicosis 1. Toxic condition caused by excessive levels of circulating thyroid hormone. 2. May be caused by: a. Hyperthyroidism b. Goiters c. Autoimmune disorders d. Thyroid cancer 3. Thyroid storm: Rare, life-threatening condition a. Usually triggered by : i. A stressful event ii. Increased volume of thyroid hormones in the circulation b. May present with the normal signs and symptoms of hyperthyroidism, as well as: i. Fever ii. Severe tachycardia iii. Nausea iv. Vomiting v. Altered mental status vi. Heart failure F. Hyperparathyroidism 1. Marked by increased parathyroid hormone level, which results in: a. Increased levels of blood calcium b. Hypercalcemia c. Decreased phosphate blood levels 2. Primary causes result from the gland itself. 3. Secondary causes occur elsewhere in the body. 4. The most common cause is a benign neoplasia on the gland (adenoma). 5. Signs and symptoms can be vague and may include: a. Fatigue b. Weakness c. Nausea d. Vomiting e. Confusion f. Pathologic fractures secondary to thinning bones or kidney stones 6. Surgery to remove the enlarged gland is definitive management. 7. Patients with mild forms require monitoring of calcium blood levels. 8. Manage ABCs, and provide supportive care. G. Panhypopituitarism 1. Inadequate production or absence of the pituitary hormones, including: a. Adrenocorticotropic hormone (ACTH) b. Cortisol c. Thyroxine (T4) d. Luteinizing hormone (LH) e. Follicle-stimulating hormone (FSH) f. Growth hormone g. Antidiuretic hormone (ADH) 2. Clinical presentation varies depending on the hormone(s) that are lacking. 3. Often a result of the hypothalamus functioning abnormally. a. Hormone replacement therapy needs to be monitored throughout the patient’s life. H. Diabetes insipidus (DI) 1. The body is unable to regulate fluid caused by: a. The lack of ADH (central diabetes insipidus) or b. The kidneys are unable to respond appropriately (nephrogenic diabetes insipidus). 2. One difference in DI and DM is the amount of glucose present in the urine: a. DI: Very diluted glucose b. DM: Excess glucose 3. Dehydration and electrolyte imbalances may occur. 4. Risk of water intoxication and hyponatremia is also possible. 5. Management may include synthetic ADH. I. Inborn errors of metabolism (IEM) 1. Hereditary diseases that result in the body being unable to transform food to energy 2. Identification may be difficult because of vague signs, such as: a. Failure to thrive b. Poor feeding in infants 3. A neonate with sepsis or who is critically ill should be assessed for IEM. 4. Two categories: a. Disorders that result in toxic accumulations i. Maple syrup urine disease—A genetic disorder that causes a buildup of the amino acids leucine, isoleucine, and valine ii. Phenylketonuria—The body’s inability to break down the amino acid phenylalanine b. Disorders of energy production or utilization i. Hereditary fructose intolerance—A lack of aldolase B, the enzyme responsible for breaking down fructose ii. Galactosemia—The inability to break down the simple sugar galactose X. Summary A. The endocrine system influences almost every cell, organ, and function of the body. B. Patients with an endocrine disorder often have a range of signs and symptoms. A thorough assessment and immediate treatment are needed to avert life threats. C. The endocrine system comprises a network of glands that produce and secrete hormones. The main function is to maintain homeostasis and promote permanent structural changes. D. Hormones travel through the bloodstream to target tissues. E. The major components of the endocrine system are the hypothalamus, pineal gland, pituitary, thyroid, thymus, parathyroid, adrenals, pancreas, and reproductive organs (gonads). The pancreas has a role in hormone production and digestion. F. The hypothalamus links the endocrine and nervous systems. G. The pineal gland synthesizes and secretes melatonin, a hormone that helps regulate sleep/wake patterns. H. The pituitary gland is often referred to as the “master gland” because its secretions regulate other endocrine glands. I. The thyroid secretes thyroxine, the body’s major metabolic hormone, in order to stimulate energy production in cells, increasing the rate at which cells consume oxygen and use carbohydrates, fats, and proteins. It also secretes calcitonin, which helps maintain blood calcium levels. J. The thymus gland helps the immune system identify and destroy pathogens, disease-causing pathogens, and various pathogenic processes, such as cancer. K. Three types of T cells evolve from stem cells in the thymus: killer T cells, helper T cells, and suppressor T cells. These specialized white blood cells help the lymphatic system defend against pathogens. L. The parathyroid gland helps regulate blood calcium levels by secreting parathyroid hormone, which directs specialized cells to dissolve bone, thereby releasing calcium. M. The adrenal glands, located atop the kidneys, consist of the cortex and the medulla. They produce hormones that help regulate metabolism, the balance of salt and water, the immune system, and sexual function. Adrenal hormones also help the body cope with stress by increasing pulse, respiratory rate, and blood pressure. N. The pancreas secretes digestive enzymes and the hormones glucagon and insulin, which regulate blood glucose levels. O. The gonads—the testes in men and the ovaries in women— are the main source of sex hormones. P. The testes are in the scrotum and produce hormones called androgens. Testosterone, the most important androgen in men, regulates sexual development during puberty, including growth spurts, deepening of the voice, growth of facial and pubic hair, and muscle growth and strength. Q. The ovaries release ova (eggs) and secrete the hormones estrogen and progesterone, which regulate sexual development and help regulate the menstrual cycle and pregnancy. R. Diabetes is a metabolic disorder in which the body’s ability to metabolize glucose is impaired. It is characterized by the passage of large quantities of urine containing glucose, significant thirst, and deterioration of body function. S. Endocrine emergencies can be difficult to assess because they affect many organ systems. Do not take these calls lightly because poor outcomes can result quickly. T. In type 1 diabetes, most patients do not produce insulin. They require daily insulin injections throughout their lives to control blood glucose levels. U. When checking vital signs, be alert for signs of increased intracranial pressure, unusual breathing patterns, and pararespiratory motions. V. Management of an endocrine emergency may require intubation, administration of supplemental oxygen, infusion of dextrose, or other measures. All findings must be thoroughly documented. W. In type 1 diabetes, the beta cells in the islets of Langerhans have been destroyed and no longer produce insulin. Blood glucose must be monitored closely and insulin administered at least daily by injection or pump. X. The most common form of diabetes is type 2 diabetes (formerly called “adult-onset diabetes”), in which the blood glucose level is elevated. Y. Hypoglycemia in a person with insulin-dependent diabetes is often the result of having taken too much insulin, eaten too little food, or both. The patient will tremble, have a rapid pulse rate, sweat, and feel hungry. Z. Hyperglycemia is a classic symptom of diabetes mellitus. Common early signs include frequent and excessive thirst and urination. AA. Untreated hyperglycemia will progress to diabetic ketoacidosis (DKA), which is life-threatening. DKA occurs when acids accumulate because insulin is not available. BB. Hyperosmolar nonketotic coma/hyperosmolar hyperglycemic nonketotic coma (HONK/HHNC) is a metabolic derangement that occurs principally in patients with type 2 diabetes. It is characterized by hyperglycemia, hyperosmolarity, and an absence of significant ketosis. CC. Gestational diabetes is a form of glucose intolerance that usually manifests itself late in pregnancy. DD. Adrenal insufficiency is characterized by underproduction of cortisol and aldosterone, which leads to weakness, dehydration, and the inability to maintain adequate blood pressure or to properly respond to stress. Primary adrenal insufficiency (Addison disease) is caused by atrophy or destruction of both adrenal glands, leading to deficiency of the steroid hormones produced by these glands. EE. Secondary adrenal insufficiency is a lack of adrenocorticotropic hormone (ACTH) secretion from the pituitary gland. FF. Acute adrenal insufficiency is called an addisonian crisis and may result from an acute exacerbation of chronic insufficiency, usually brought on by stress, trauma, surgery, or infection. GG. Cushing syndrome is caused by excess cortisol production by the adrenal glands or by excessive use of corticosteroid hormones. HH. Pheochromocytoma is generally a nonmalignant adrenal gland tumor that causes excessive release of epinephrine and norepinephrine. II. Congenital adrenal hyperplasia (CAH) is a condition of the adrenal gland in which insufficient cortisol and aldosterone are produced. JJ. Thyroid hormones are critical for cell metabolism and organ function. If their supply is inadequate, the metabolic rate decreases, organ tissues do not grow or mature, energy production declines, and the actions of other hormones are affected. KK. Graves disease is the most severe and common cause of hyperthyroidism. The disease can produce goiter, exophthalmos, and pretibial myxedema. LL. Hashimoto disease, another cause of hyperthyroidism, is an autoimmune disease in which the thyroid gland is enlarged as a result of the infiltration of T lymphocytes and plasma cells. MM. Symptoms of hypothyroidism include fatigue, feeling cold, weight gain, dry skin, and sleepiness. Continued decrease of thyroid hormone levels may lead to myxedema coma. NN. In a myxedema coma, reduced or absent thyroid hormone slows the body’s metabolic processes. OO. Thyrotoxicosis is a toxic condition caused by excessive levels of circulating thyroid hormone. A thyroid storm is a rare, life-threatening condition that may occur in patients with thyrotoxicosis. PP. In hyperparathyroidism, blood calcium levels increase, resulting in hypercalcemia and decreased phosphate blood levels. Post-Lecture This section contains various student-centered end-of-chapter activities designed as enhancements to the instructor’s presentation. As time permits, these activities may be presented in class. They are also designed to be used as homework activities. Assessment in Action This activity is designed to assist the student in gaining a further understanding of issues surrounding the provision of prehospital care. The activity incorporates both critical thinking and application of paramedic knowledge. Instructor Directions 1. Direct students to read the “Assessment in Action” scenario located in the Prep Kit at the end of Chapter 23. 2. Direct students to read and individually answer the quiz questions at the end of the scenario. Allow approximately 10 minutes for this part of the activity. Facilitate a class review and dialogue of the answers, allowing students to correct responses as may be needed. Use the quiz question answers noted below to assist in building this review. Allow approximately 10 minutes for this part of the activity. 3. You may wish to ask students to complete the activity on their own and turn in their answers on a separate piece of paper. Answers to Assessment in Action Questions 1. Answer: A. Decreased level of consciousness Rationale: Although all of her signs and symptoms give cause for concern, her decreased level of consciousness, with the presence of vomiting, make maintaining a patent airway of paramount concern. 2. Answer: C. Beta blockers Rationale: This patient has a decreased level of consciousness and signs and symptoms of a thyroid storm. This condition is life threatening and, if left untreated, could result in coma or death. This patient needs immediate care that includes IV fluids, possibly beta blockers to control her heart rate, and transport to an appropriate medical facility. 3. Answer: B. Stressful event Rationale: A thyroid storm is often precipitated by a stressful event. In this case, the patient and her family were recently evicted from their home. 4. Answer: D. All of the above Rationale: This patient has an overstimulated sympathetic nervous system. There are many conditions that could mimic these signs and symptoms, including thyroid storm, malignant hyperthermia, and cocaine overdose. 5. Answer: A. Palpitations Rationale: As the condition progresses, some additional signs and symptoms include: tremors, weakness, fatigue, agitation, sleeping disturbances, chest pain, racing heart or palpitations, hair loss, weight loss, and changes to menstrual cycles and bowel movements. 6. Answer: D. All of the above Rationale: Possible causes of thyrotoxicosis are Graves’ disease, thyroid cancer, and goiters. However, it is likely she has Graves’ disease because of the presence of exophthalmos, or bulging of the eyes. In this case, the patient could have no previous diagnosis because she was not likely receiving medical care. 7. Answer: D. Blood testing Rationale: Blood tests will be required. Graves’ disease presents with low levels of thyroid-stimulating hormone and high levels of thyroxine. Additional Questions 8. Rationale: By actively training your brain to be on the lookout for these components you will become aware of subtleties other providers may miss. All of these observations will assist you in determining the cause of your patient’s condition. 9. Rationale: Again, some signs may be subtle or not obvious without observing and palpating the body. For example, pretibial myxedema may be a sign that is missed if the paramedic fails to obtain pedal pulses. Assignments A. Review all materials from this lesson and be prepared for a lesson quiz to be administered (date to be determined by instructor). B. Read Chapter 24, Hematologic Emergencies, for the next class session. Unit Assessment Keyed for Instructors 1. Compare and contrast the function of endocrine and exocrine glands. Answer: Exocrine glands ( exo- means “outside”) secrete chemicals for elimination. These glands have ducts that carry their secretions to the surface of the skin or into a body cavity. Sweat glands, salivary glands, and the liver are examples of exocrine glands. Endocrine glands ( endo means “inside”) secrete or release chemicals that are used inside the body. These glands lack ducts, so they release hormones directly into the surrounding tissue and blood. Hormones act on the body’s cells by increasing or decreasing the rate of cellular metabolism. They transfer information from one set of cells to another to coordinate body functions, such as the regulation of mood, growth and development, metabolism, tissue function, and sexual development and function. (p 1212) 2. What are the eight hormones secreted by the pituitary gland? Answer: The pituitary is divided into the following two regions, or lobes: The anterior pituitary, which produces and secretes seven hormones (growth hormone, thyroid-stimulating hormone, adrenocorticotropin hormone, melatoninstimulating hormone, and three gonadotropic hormones). The posterior pituitary secretes two hormones (ADH and oxytocin) but does not produce them. ADH and oxytocin are synthesized in hypothalamic neurons but are stored in the posterior pituitary gland until the hypothalamus sends nerve signals to the pituitary to release them. (pp 1213-1216) 3. What gland secretes epinephrine and norepinephrine? Answer: Following stimulation from the hypothalamus, the adrenal medulla secretes small amounts of norepinephrine and large amounts of epinephrine. Norepinephrine raises blood pressure by causing blood vessels and skeletal muscles to constrict. Epinephrine stimulates sympathetic nervous system receptors throughout the body. In addition, it stimulates the liver to convert glycogen to glucose for use as energy in the cells. The action of both hormones results in increased levels of oxygen and glucose in the blood and faster circulation of blood to the brain, heart, and muscles, which in turn enables the body to respond to the short-term emergency situation. (p 1216) 4. Where are the islets of Langerhans located, and what function do they perform? Answer: The pancreas is a digestive gland that is considered both an endocrine gland and an exocrine gland. It secretes digestive enzymes into the duodenum through the pancreatic duct. The exocrine component is responsible for the secretion of the digestive enzymes. The endocrine component comprises the islets of Langerhans. These cell groups within the pancreas act like “an organ within an organ.” The main hormones they secrete are glucagon, secreted by the alpha cells, and insulin, secreted by the beta cells. Glucagon and insulin are responsible for the regulation of blood glucose levels. Somatostatin, secreted by delta cells, is responsible for the inhibition of insulin and glucagon secretion in cellular metabolism. (p 1216) 5. What are the three Ps that indicate the body’s ability to metabolize simple carbohydrates (glucose) is impaired? Answer: Polyphagia is an increased appetite caused by the inability of glucose to be transported across the cell membrane. Polydipsia is a significant thirst caused by dehydration brought about by an increase in diuresis. Polyuria is the passage of large quantities of urine containing glucose. Excess glucose is excreted and attracts water, resulting in excessive diuresis. (p 1221) 6. Why is kidney failure a priniciple result of diabetes? Answer: Diabetes is the principal cause of kidney failure, accounting for 44% of new cases in 2008. The glomeruli of the kidney become sclerotic, causing necrosis of the papillary tissue and leading to nephropathy (end-stage renal disease) and renal failure. High levels of glucose in the blood cause the kidneys to work harder than normal and may result in decreased kidney function over a period of time. (p 1222) 7. What is diabetic neuropathy, and where does it commonly occur? Answer: Neuropathy is nerve damage that results in a loss of sensation and function in the area innervated by the affected nerves. The damage can cause sexual impotence, neurogenic bladder, constipation, or diarrhea. Neuropathy associated with diabetes often affects peripheral nerves, causing diminished sensation and function in the extremities. Persons with peripheral neuropathy often have paresthesia, a pinprick sensation in the hands, feet, arms, or legs. Paresthesia and dysesthesia—the absence of sensation—can blunt pain perception, making it possible for foot ulcers to go unnoticed until they become seriously infected. Because many of these persons also have poor circulation in the extremities, gangrene may develop in adjacent tissues and infection may spread to the bone. In fact, more than 60% of nontraumatic lower limb amputations can be attributed to diabetes. (p 1222) 8. Compare and contrast type 1 and type 2 diabetes. Answer: In type 1 diabetes, the endocrine system of most patients does not produce any insulin. These patients require daily injections of supplementary, synthetic insulin throughout their lives to control their levels of blood glucose. In addition to daily insulin injections, strict dietary control must be observed. The most common form of diabetes is type 2 diabetes (formerly called adult-onset diabetes), a condition in which blood glucose levels are elevated. About 90% of all people with diabetes in the United States have type 2 diabetes, which typically develops later in life, usually when the patient is middle-aged, although the disease is becoming more common in younger people. In many people with type 2 diabetes, the pancreas actually produces enough insulin; however, for reasons not fully understood, the body cannot effectively use it. This condition is known as insulin resistance. (pp 1223-1224) 9. What is gestational diabetes? Answer: Gestational diabetes is usually diagnosed at 28 weeks of gestation or later in the third trimester of pregnancy. It is thought that hormones produced by the placenta during pregnancy impede the function of insulin. Because this condition does not occur until later in pregnancy, it does not produce birth defects but it often results in macrosomia, or a large baby. Blood glucose crosses the placental barrier.When a pregnant woman is hyperglycemic, high levels of glucose enter the fetus, causing an increased production of insulin by the fetus to normalize blood glucose levels. The extra glucose is converted into fat, and women experiencing gestational diabetes often deliver large babies and may encounter difficult deliveries. Often cesarean sections are required. (p 1225) 10. Discuss blood glucose levels in hypoglycemia and hyperglycemia. Answer: Normal blood glucose levels range from approximately 70 to 120 mg/dL; hypoglycemia occurs when blood glucose levels drop to 45 mg/dL or less. Hypoglycemia develops very rapidly, from minutes to a few hours and should be suspected in any patient with diabetes who presents with bizarre behavior, neurologic signs, or coma. Often the hypoglycemic patient appears intoxicated because of slurred speech and lack of coordination and may be paranoid, hostile, and aggressive. Hyperglycemia usually progresses slowly, over a period of 12 to 48 hours, with the patient’s level of consciousness deteriorating only gradually. Patients in DKA are seldom deeply comatose, so if the patient is totally unresponsive, look for another source of the coma, such as head injury, stroke, or drug overdose. Hyperglycemia occurs when levels of glucose in the blood exceed the normal range (80 to 120 mg/dL). In patients with diabetes, physicians try to maintain glucose levels at less than 160 mg/dL. (pp 1226-1228) Unit Assessment 1. Compare and contrast the function of endocrine and exocrine glands. 2. What are the eight hormones secreted by the pituitary gland? 3. What gland secretes epinephrine and norepinephrine? 4. Where are the islets of Langerhans located, and what function do they perform? 5. What are the three Ps that indicate the body’s ability to metabolize simple carbohydrates (glucose) is impaired? 6. Why is kidney failure a priniciple result of diabetes? 7. What is diabetic neuropathy, and where does it commonly occur? 8. Compare and contrast type 1 and type 2 diabetes. 9. What is gestational diabetes? 10. Discuss blood glucose levels in hypoglycemia and hyperglycemia.