PCCN Endocrine Exam 97 Questions with Verified Answers,100% CORRECT

PCCN Endocrine Exam 97 Questions with Verified Answers Imbalances in which of the following hormones will MOST DIRECTLY impact fluid balance: A. Aldosterone and cortisol. B. Thyroxin and ADH. C. Aldosterone and ADH. D. Cortisol and epinephrine. - CORRECT ANSWER C. Aldosterone is a mineral corticoid that regulates extracellular fluid volume by increasing reabsorption of sodium and chloride, which causes water to be retained. Aldosterone is released by the adrenal cortex through activation of the renin angiotensin aldosterone system. Antidiuretic hormone (ADH) is secreted from the posterior lobe of the pituitary gland. ADH regulates the osmotic pressure of extracellular fluid by regulating the amount of water reabsorbed in the renal tubules. ADH release is stimulated by an increase in osmotic pressure. Cortisol is the major glucocorticoid and is responsible for metabolism and utilization of carbohydrates, proteins, and fats. It also has anti-inflammatory effects. Cortisol plays an indirect role in fluid balance but is known as the stress hormone that has the primary effects of increasing circulating glucose and decreasing the immune response. Thyroxine is produced by the thyroid gland under the influence of thyroid stimulating hormone (TSH). Thyroxine stimulates metabolism in many tissues but is not related to fluid balance. The anterior pituitary releases which of these hormones: A. Aldosterone. B. Antidiuretic hormone (ADH). C. Thyroxine. D. ACTH (adrenocorticotropic hormone). - CORRECT ANSWER D. Anterior pituitary hormones include growth hormone (also called somatotropin), adrenocorticotropic hormone (ACTH), thyroid stimulating hormone (TSH), gonadotropins (follicle stimulating hormone and luteinizing hormone), and some other hormones that affect pregnancy and lactation. All of the hormones from the anterior pituitary except growth hormone affect other glands and cause them to synthesize and release specific hormones. ACTH affects the adrenal cortex to control synthesis and release of cortisol. TSH causes the thyroid gland to synthesize and release thyroid hormones. Growth hormone affects metabolism of many tissues and stimulates hormone production by the liver. The major posterior pituitary hormone of significance in critically ill patients is: A. Cortisol. B. Epinephrine. C. Aldosterone. D. Antidiuretic hormone (ADH). - CORRECT ANSWER D. ADH (also called vasopressin) is formed in the hypothalamus and stored in the posterior pituitary. ADH works on the distal convoluted tubule and collecting ducts in the kidney to make them more permeable to water, thus causing the kidney to reabsorb water. The major stimuli to ADH secretion are hyperosmolality and volume depletion. The water retention induced by ADH will both lower the plasma osmolality and raise the extracellular volume toward normal. ADH also causes vasoconstriction of arterioles to support blood pressure. Cortisol is the major glucocorticoid released by the adrenal cortex. Cortisol affects metabolism in all cells of the body and regulates utilization of carbohydrates, proteins, and fats. It also has anti-inflammatory effects. Excess cortisol production causes Cushing's syndrome; a deficiency of cortisol is adrenal insufficiency which is common in critically ill patients. Chronic adrenal insufficiency is called Addison's disease and involves a deficiency of both cortisol and aldosterone. Aldosterone is the most important mineralocorticoid produced by the adrenal cortex. It's most important function is to regulate Na+ and K+ movement through the renal tubules. Aldosterone causes the kidney to retain Na+ and excrete K+. Epinephrine (or adrenalin) is a catecholamine produced by the adrenal medulla. It works by stimulating alpha receptors in peripheral vessels to cause vasoconstriction in all vascular beds except heart, brain, and certain skeletal muscles (the "fight or flight" response) and by stimulating beta receptors in the heart to increase heart rate and contractility. Your patient was admitted following a closed head injury 2 days ago. He is awake but confused, complaining of severe thirst, and drinking as much water as he can get. His urine output has been 4 liters in the last 8 hours. Urinalysis reveals a urine osmolality of 250 mOsm/kg and specific gravity of 1.002. His serum Na+ level = 150 mEq/L, K+ = 3.6 mEq/L, glucose = 100 mg/dl. Based on his symptoms and labs, what is the most likely diagnosis: A. SIADH. B. HHNS (hyperglycemic hyperosmolar nonketotic state). C. New onset diabetes mellitus. D. Diabetes insipidus. - CORRECT ANSWER D. Diabetes insipidus (DI) is impaired renal conservation of water due to either inadequate secretion of ADH (central DI) or an insufficient renal response to ADH (nephrogenic DI). Common causes of DI are hypothalamic or pituitary tumor, closed head injury with damage to the hypothalamus, and neurosurgery. Decreased amounts of ADH cause the kidney tubules to become impermeable to water, resulting in massive diuresis of dilute urine that can lead to dehydration. If the thirst mechanism is functional, polydipsia (drinking excessive amounts of water) occurs in an effort to balance large water losses. Lab work shows increased plasma osmolality and hypernatremia, with decreased urine osmolality (normal = above 500mOsm/kg) and low urine specific gravity due to the large water content of urine. To quickly calculate plasma osmolality: double the Na+ concentration and add the glucose divided by 18. In this case, 2 X 150 = 300 plus 5.5 (glucose of 100 divided by 18) for a serum osmolality of about 305 mOsm/kg (normal is about 290 mOsm/kg). In SIADH (syndrome of inappropriate ADH) there is an overproduction of ADH which results in excessive reabsorption of water by the kidneys and water intoxication. Labs in SIADH show decreased serum osmolality and hyponatremia due to dilution of solutes by excess water, and increased urine osmolality and high urine Na+ content with high specific gravity due to overconcentration of urine. In both diabetes mellitus and HHNS, blood glucose levels are significantly elevated. Following thyroidectomy surgery, your patient develops hypocalcemia and hyperphosphatemia. In this patient these electrolyte disturbances are most likely due to: A. Hypoparathyroidism. B. Hyperparathyroidism. C. Hypothyroidism. D. Hyperthyroidism. - CORRECT ANSWER A. Hypoparathyroidism can be caused by damage or ischemia to the parathyroid glands during thyroid surgery. The four parathyroid glands are located on the posterior surface of the thyroid gland and are responsible for regulation of plasma calcium and phosphorus levels. Parathormone, the hormone produced by the parathyroid gland, increases calcium absorption from the GI tract and causes renal tubular reabsorption of calcium and magnesium and decreases renal reabsorption of phosphorus and bicarbonate. Hypoparathyroidism can cause hypocalcemia and hyperphosphatemia (calcium and phosphate have a reciprocal relationship : when one goes up the other goes down). Hyperparathyroidism is not significant in critical care. The two most important hormones produced by the thyroid gland are thyroxine (T4), and triiodothyronine (T3). Thyroxine and triiodothyronine stimulate metabolism in many tissues of the body, so hyperthyroidism speeds up metabolism and hypothyroidism slows it down. These two hormones have no direct effect on calcium or phosphorus levels. The adrenal cortex produces which of the following hormones: A.Cortisol & aldosterone. B. Epinephrine and aldosterone. C. ADH and aldosterone. D. Norepinephrine and epinephrine. - CORRECT ANSWER A. The adrenal cortex produces three major types of hormones: glucocorticoids, mineralocorticoids, and androgens. Cortisol is the major glucocorticoid and is responsible for metabolism and utilization of carbohydrates, proteins, and fats. It also has anti-inflammatory effects. Aldosterone is the most important mineralocorticoid produced by the adrenal cortex and is responsible for regulation of Na+ and K+ movement through the renal tubules. Its major effect is to cause renal reabsorption of Na+ and excretion of K+ and H+ ions. Epinephrine and norepinephrine are produced by the adrenal medulla. Both are catecholamines that stimulate alpha receptors in peripheral blood vessels to cause vasoconstriction (norepinephrine has more alpha effect than epinephrine), and beta receptors in the heart to increase heart rate and contractility (epinephrine has more beta effect than norepinephrine). Both also affect many other body functions as well. Diabetes insipidus is the result of an altered level of or abnormal response to which hormone: A. Nitric oxide. B. Renin. C. Aldosterone. D. ADH . - CORRECT ANSWER D. Diabetes insipidus is a disorder involving a deficit of antidiuretic hormone (central diabetes insipidus) or the failure of the kidneys to respond to antidiuretic hormone (nephrogenic diabetes insipidus). Central diabetes insipidus is much more common than nephrogenic diabetes insipid. Central diabetes insipidus is what nurses are more likely to see in the critical care environment. Aldosterone is released by the adrenal cortex and is responsible for sodium balance: it causes renal tubules to retain Na+ and excrete K+. Renin is an enzyme that is released by juxtaglomerular cells in the kidney in response to decreased blood flow and pressure in renal arterioles. Renin results in conversion of angiotensin I to angiotensin II, which stimulates aldosterone secretion. Nitric oxide is produced by endothelial cells lining blood vessels and causes vessel dilation. The major physiological problem responsible for symptoms and requiring treatment in SIADH is: A. Hyponatremia. B. Hypertension. C. Hyperkalemia. D. Severe hyperglycemia. - CORRECT ANSWER A. SIADH is overproduction of antidiuretic hormone (also called vasopressin) which causes water reabsorption in the renal tubules and leads to water intoxication. Signs and symptoms of hyponatremia include decreased urine output with concentrated urine, headache, confusion/personality changes, weight gain, weakness, lethargy, muscle cramps, nausea/vomiting, anorexia, decreased tendon reflexes. Seizures, coma and death can occur if serum sodium falls below 115 mEq/L. Laboratory values indicative of SIADH include hyponatremia (Na < 130 mEq/L), plasma hypoosmolality (< 280 mOsm/kg), urine hyperosmolality (> 500 mOsm/Kg), and increased urine sodium concentration (> 20mEq/L). Management of SIADH depends on its duration and severity. Aggressive management of hyponatremia is indicated in patients with severe symptoms such as seizures or mental status changes and those with extremely low levels of sodium (less than 110 mEq/L). Administration of 3% hypertonic saline can be used in these emergent circumstances. It is recommended that the total serum sodium be corrected at a rate of 0.5-2 mEq/L/h. Furosemide (Lasix) increases excretion of free water and can be used along with isotonic or hypertonic saline in severe cases. In patients with chronic hyponatremia, fluid restriction of 800 ml/day is the mainstay of treatment, with the goal of achieving a negative water balance and a slow increase in serum sodium. Important nursing interventions for a patient with SIADH include all of the following EXCEPT: A. Restrict oral fluids to < 1000ml/day. B. Use D5W for all IV drips. C. Accurate I&O and daily weights. D. Irrigate NG tubes with NS. E. Assess for signs of heart failure and neuro status changes. - CORRECT ANSWER B. The main problem is water intoxication resulting in hyponatremia, so free water needs to be restricted and measures to increase the serum sodium should be instituted. IV drips should be in a saline base and oral fluids should be those with high sodium content. If an NG tube is present it should be irrigated with normal saline instead of water. Additional nursing care involves accurate intake & output and daily weights to help monitor fluid status. The patient should be assessed for signs of heart failure as sodium administration can result in hypervolemia. Neuro status is monitored closely for signs of decreasing level of consciousness, and seizure precautions may be necessary. Laboratory values reflecting Na+, K+, and urine and serum osmolality are followed closely. The major physiological problems responsible for symptoms and requiring treatment in diabetes insipidus are: A. Hypervolemia and hyponatremia. B. Severe hypotension and hyperkalemia. C. Severe hypokalemia and hypertension. D. Fluid volume deficit and hypernatremia. - CORRECT ANSWER D. Diabetes insipidus is due to a deficiency of antidiuretic hormone (ADH) or an inability of the kidney to respond to ADH. This deficiency causes a massive diuresis of dilute urine (polyuria) resulting in dehydration (fluid volume deficit). If the fluid volume deficit is severe enough and the patient is unable to respond to thirst by increasing water intake, hypovolemic shock can occur. Serum osmolality is increased (> 295 mOsm/kg), urine osmolality is decreased, and urine specific gravity is decreased (reflecting the dilute urine concentration). Serum sodium levels rise as osmolality increases (> 145 mEq/L). Hypernatremia can cause movement of intracellular water out of cerebral cells, resulting in confusion, irritability, lethargy, seizures, and coma. Cushing's syndrome is due to which of the following: A. Underproduction of insulin. B. Overproduction of thyroxine. C. Overproduction of cortisol. D. Underproduction of cortisol. - CORRECT ANSWER C. Cushing's syndrome is hypercortisolism, or overproduction of cortisol by the adrenal cortex. It can be caused by an adrenal tumor that secretes excess cortisol, a pituitary tumor that secretes excess ACTH which then results in excess cortisol secretion by the adrenal cortex (this is Cushing's disease), or secondary to cortisol therapy for some other condition. Underproduction of cortisol (chronic adrenal insufficiency) is Addison's disease. Underproduction of insulin causes Type I diabetes mellitus. Overproduction of thyroxine causes Graves disease. Graves disease is due to which of the following: A. Hypothyroidism. B. Hypoadrenalism. C. Hyperadrenalism. D. Hyperthyroidism. - CORRECT ANSWER D. Graves disease is an autoimmune disease in which the body produces antibodies to thyroid tissue that bind to TSH receptors on thyroid cells and cause them to produce excess thyroxine. Hyperthyroidism results in increased metabolism and increased sympathetic nervous system activity. Symptoms include tachycardia, excess heat production and heat intolerance, weight loss, anxiety & irritability, insomnia, enlarged thyroid gland (goiter), and bulging of the eyeballs (exophthalmos). Cardiac complications include atrial fibrillation and heart failure. Thyroid storm (also called thyroid crisis) is a life-threatening hypermetabolic condition due to hyperthyroidism and is a metabolic emergency requiring immediate treatment. Symptoms are similar to those of hyperthyroidism but are exaggerated, with fevers as high as 106 degrees, heart failure, and exhaustion. If untreated it can result in coma and death. Hyperadrenalism results in increased cortisol production and causes Cushing's syndrome. Hypoadrenalism results in adrenal insufficiency and causes Addison's disease. Hypothyroidism causes myxedema. An autoimmune disease in which antibodies destroy pancreatic beta cells resulting in insulin deficiency is: A. Type II diabetes mellitus. B. Type I diabetes mellitus. C. Pancreatitis. D. Pancreatic cancer. - CORRECT ANSWER B. Type I diabetes is usually an autoimmune disease in which the body forms antibodies against pancreatic beta cells and destroys them. Since beta cells are responsible for insulin formation, type I diabetes results in insulin deficiency and requires the administration of exogenous insulin for treatment. Type I diabetes used to be called 'juvenile' diabetes because many patients develop the disease in childhood. It is less common but more severe than type II diabetes. Pancreatic cancer usually begins in the pancreatic ducts and affects the ability of the pancreas to produce digestive enzymes. It is due to proliferation of cancerous cells and is not an autoimmune disease. Pancreatitis is inflammation of the pancreas. Normally the pancreas produces enzymes that travel through the pancreatic ducts to the small intestine where they become activated to aid in digestion. In pancreatitis, the enzymes become activated while still in the pancreas and begin irritating and digesting the pancreas itself. Type II diabetes is due to insulin resistance rather than a deficiency of insulin. The body is unable to utilize insulin appropriately in the metabolism of glucose. Type II diabetes used to be called 'adult-onset' diabetes. Type II diabetes can sometimes be managed by healthy eating and exercise, but oral antidiabetic medications or even insulin may be necessary. You are caring for a 20 year old woman admitted to the ICU with lethargy, confusion, abdominal pain, and vomiting. Her mother says she has 'juvenile' diabetes and takes insulin. She is getting married in 2 weeks and has been under a lot of stress with wedding plans and such. Her mom doesn't know if she has been checking her glucose or taking her insulin regularly, but she has been complaining of being thirsty for the last 2 days and had a recent urinary tract infection treated with antibiotics. Vital signs are: BP 96/54 mmHg, sinus tach at 116, respirations are deep and rapid at 32 and her breath has a 'fruity' odor. ABGs show: pH = 7.15, PaCO2 = 25, PaO2 = 80 mmHg, HCO3 = 12 mEq/L. Labs: Na+ = 132 mEq/L, K+ = 4.2 mEq/L, Cl = 96 mEq/L, glucose = 520 mg/dL, creatinine = 1.2 mg/dL, serum osmolality = 300 mOsm/kg, anion gap = 24 mEq/L. Urine ketones = 2+, urine glucose 2+. What is the most likely diagnosis: A. DKA (di - CORRECT ANSWER A. The hallmarks of DKA are hyperglycemia (her blood glucose is 520 mg/dL), ketonemia (fruity breath is evidence of ketonemia), and metabolic acidosis with a large anion gap (her pH is 7.15 and the anion gap is 24 mEq/L [normal is 8-12]). She also has ketones and glucose in her urine. DKA most often occurs in younger people with Type I diabetes and is often precipitated by infection, missed insulin treatments, stress, or conditions such as MI, stroke, trauma, and pancreatitis. In DKA, because there is no insulin produced, the body metabolizes fats and proteins instead of glucose as a source of energy, resulting in ketones as a byproduct of this metabolism. SIADH (syndrome of inappropriate antidiuretic hormone) is over production of ADH and causes water intoxication, not acidosis or hyperglycemia. HHNS (hyperosmolar hyperglycemic nonketotic state) used to be called hyperglycemic hyperosmolar nonketotic coma. It is a form of hyperglycemic crisis that occurs in older people with Type II diabetes. In HHNS, because there is some insulin present, the body does not have to resort to fat or protein metabolism, therefore there is no ketosis present. However, the hyperglycemia and volume deficit are more severe than with DKA, and the mortality rate is higher. Diabetes insipidus is due to a lack of ADH. Although some of the symptoms such as polyuria and polydipsia are the same as those seen in DKA, diabetes insipidus does not cause hyperglycemia or metabolic acidosis. You are caring for a 20 year old woman admitted to the ICU with DKA. Her lab work shows: ABGs: pH = 7.15, PaCO2 = 25, PaO2 = 80 mmHg, HCO3 = 12 mEq/L. Labs: Na+ = 132 mEq/L, K+ = 4.2 mEq/L, Cl = 96 mEq/L, glucose = 520 mg/dL, creatinine = 1.2 mg/dL, serum osmolality = 300 mOsm/kg, anion gap = 24 mEq/L. Urine ketones = 2+, urine glucose 2+. Treatment of her DKA would include all of the following EXCEPT: A. Lasix to promote potassium loss in urine, as serum potassium concentration will elevate as acidosis is corrected. B. IV potassium replacement to correct hypokalemia. C. Rapid fluid administration with normal saline to replace intravascular and intracellular volume deficit. D. Regular insulin IV bolus followed by regular insulin infusion. - CORRECT ANSWER A. In DKA, metabolic acidosis is due to ketones that are produced by fat and protein metabolism that occurs when glucose cannot be utilized by cells because of insulin deficiency. The excess hydrogen ions in acidosis enter the cell and cause potassium to leave the cell, thus raising the serum potassium level. Potassium is then excreted in the urine because of the glucose osmotic diuresis that occurs in DKA, resulting in a total body potassium deficit. As acidosis is corrected, potassium ions move back in to the cell and can cause significant hypokalemia if potassium is not replaced. For every 0.1 decrease in pH, there is a 0.6 increase in serum K+: so in this patient with a pH of 7.15 the K+ should be 6.3 mEq/L. Thus, her K+ of 4.2 mEq/L represents a significant potassium deficit. Fluid repletion is usually initiated with isotonic saline (0.9 % sodium chloride). NS will replace the fluid deficit, correct the extracellular volume depletion more rapidly than 0.45% normal saline, lower the plasma osmolality (since it is still hypoosmotic compared to serum), and reduce the serum glucose concentration by dilution and by increasing urinary losses as renal perfusion is increased. In the absence of heart failure, NS is usually infused at a rate of about 1000 mL/h (10 to 15 mL/kg lean body weight per hour). NS should be infused as quickly as possible in patients who are in shock. Insulin therapy lowers the serum glucose concentration and decreases ketone production by reducing both lipolysis and glucagon secretion. The only indication for delaying insulin therapy is a serum potassium below 3.3 mEq/L, since insulin will worsen the hypokalemia by driving potassium into the cells. DKA can be treated either with an IV bolus (0.1 U/kg body weight), followed by a continuous infusion of regular insulin at a dose of 0.1 U/kg per h or Your patient is a 74 year old man admitted after his son found him confused and obtunded at home after he failed to answer the phone for several hours. He had been complaining of a cough and feeling alternatingly hot and chilled for two days. He has a history of diabetes, heart failure, and an MI 3 years ago. On admission he is barely arousable and unable to communicate, BP is 80/46, sinus tachycardia at 120, respirations 14 and shallow, skin and mucus membranes are dry. Lab work shows: ABGs: pH = 7.33, PaCO2 = 48 mmHg, PaO2 = 64 mmHg, HCO3 = 22 mEq/L. Labs: Na+ = 148 mEq/L, K+ = 4.0 mEq/L, Cl = 118 mEq/L, glucose = 1150 mg/dL, creatinine = 2.2 mg/dL, serum osmolality = 378 mOsm/kg, anion gap = 8 mEq/L. Urine ketones = negative, urine glucose 2+. Based on presentation and labs, what is the most likely diagnosis: A. DKA (diabetic ketoacidosis). B. HHNS (Hyperosmolar hyperglycemic nonketotic state). C. SIADH. D. Diabet - CORRECT ANSWER B. HHNS is a form of hyperglycemic crisis that occurs more commonly in older people with Type II diabetes and is often precipitated by some type of stress such as infection or acute illness. DKA and HHNS are both serious complications of diabetes but they differ clinically according to the presence of ketoacidosis and the degree of hyperglycemia. In DKA, because there is a deficiency of insulin, the body resorts to fat and protein metabolism which results in ketoacidosis with arterial pH < 7.3 in mild cases and < 7.0 in severe cases. HHS occurs in Type II diabetes which is due to insulin resistance rather than insulin deficiency. In HHNS, because there is some insulin present, the body does not have to resort to fat or protein metabolism, therefore there is no ketoacidosis and the arterial pH is often normal or only slightly acidotic. Serum glucose level in DKA is usually between 500-800 mg/dL while in HHNS it often exceeds 1000 mg/dL. Diabetes insipidus is due to a lack of ADH. Although some of the symptoms such as polyuria and polydipsia are the same as those seen in DKA or HHNS, diabetes insipidus does not cause hyperglycemia or metabolic acidosis. In SIADH (syndrome of inappropriate ADH) there is an overproduction of ADH which results in excessive reabsorption of water by the kidneys and water intoxication The hallmarks of SIADH are hyponatremia, hypoosmolality of plasma, and high osmolality and specific gravity of urine due to excess water reabsorption by the kidney. SIADH does not cause hyperglycemia or acidosis. You are caring for a 74 year old man with HHNS. His labs are: ABGs: pH = 7.33, PaCO2 = 48 mmHg, PaO2 = 64 mmHg, HCO3 = 22 mEq/L. Labs: Na+ = 148 mEq/L, K+ = 4.0 mEq/L, Cl = 118 mEq/L, glucose = 1150 mg/dL, creatinine = 2.2 mg/dL, serum osmolality = 378 mOsm/kg, anion gap = 8 mEq/L. Appropriate treatment would include all of the following EXCEPT: A. Sodium bicarbonate to correct metabolic acidosis. B. Rapid fluid administration with normal saline to replace intravascular and intracellular volume. deficit C. IV potassium replacement to correct or prevent hypokalemia. D. Regular insulin IV bolus followed by regular insulin infusion. - CORRECT ANSWER A. Treatment of HHNS and DKA are similar in terms of fluid replacement to correct both hypovolemia and hyperosmolality, and insulin administration to correct hyperglycemia. Because no ketones are produced in HHNS, the pH is usually normal or only slightly acidotic, so administering sodium bicarbonate would not be indicated. A total body potassium deficit is usually present in both DKA and HHNS because of increased renal potassium excretion due to glucose osmotic diuresis and to hypovolemia-induced hyperaldosteronism. Despite this deficit, the serum potassium concentration is usually normal or may even be elevated due to insulin deficiency and hyperosmolality, both of which result in potassium movement out of the cells and in to the serum. Insulin administration causes potassium to move into the cells, resulting in a fall in the serum potassium concentration. To prevent hypokalemia, potassium chloride (20 to 30 mEq/L) is generally added to the replacement fluid once the serum potassium concentration falls below 5.3 mEq/L. In a patient with acute decompensated heart failure an evaluation of thyroid function may provide an indication of hypothyroidism which contributes to the decompensation. Which lab values would provide the strongest evidence of hypothyroidism: A. Reduced TSH (thyroid stimulating hormone) level. B. Elevated Triiodothyronine levels (T3). C. Elevated TSH (thyroid stimulating hormone) level. D. Reduced serum iodine levels. - CORRECT ANSWER C. When hypothyroidism is present the pituitary will release TSH into the system to produce more thyroid (T3, T4) resulting in increased levels of TSH in the serum. T3 levels are often maintained as T4 converts to T3 when hypothyroidism is present. T4 levels will subsequently drop. Hypothyroidism can result from lack of iodine in the system. Iodine is needed to create thyroxin. Iodine must be consumed and is not produced in the body. The routine evaluation of thyroid function with iodine levels is not recommended as iodine deficiency is rarely present with the advent of iodized salt and foods that contain iodine. TSH remains the gold standard for evaluation. When comparing your patients ordered medications with the home medication list you note that the patient was on prednisone 2mg daily and is not ordered any prednisone now. An appropriate response to this information is: A. Do nothing since the dose of prednisone is a small dose and this change should not have any negative impact on the patient. B. Notify the provider of the discrepancy as you know a sudden cessation in steroids can result in the development of Cushing's disease. C. Carefully monitor the patient for signs and symptoms of steroid withdrawal then notify the provider if these symptoms appear. D. Notify the provider of the discrepancy as you know a sudden cessation in steroids can result in an adrenal crisis. - CORRECT ANSWER D. The sudden cessation of steroids can result in adrenal crisis (Addison's Disease) as the body's natural process for producing cortisol has been inactive while the patient has been on steroids. Even low doses for prolonged periods of time decrease the effectiveness of the natural feedback loop. Steroids should be tapered over time to allow the body to begin producing cortisol releasing factor and adrenocorticotropin (ACTH). Cushing's Disease results from an overproduction or too much cortisol. Notification of a provider of the medication discrepancy is a better choice and allows for the opportunity to avert the development of an adrenal crisis. You know that diabetes insipidus is a complication that occurs in some patients post traumatic brain injury. One of the early hallmark signs of the development of diabetes insipidus includes: A. An unexplained decrease in urine output to less than 100 cc /24 hours. B. Sudden unexplained increase of blood glucose levels to greater than 600 mg/dl. C. Rapid increase in sodium level by 10-15 mEq/L over 2 hours. D. Unexplained increase in urine output of 200ml/hour x 2 hours. - CORRECT ANSWER D. A sudden unexplained increase in urine output raises concerns for diabetes insipidus in the patient with traumatic brain injury as hypothalamus is not producing antidiuretic hormone (ADH) or the posterior pituitary is not releasing ADH. This results in a loss of regulatory control of the body's water balance and an over production of urine. Serum sodium levels will increase as the patient continues to diurese, however, this is not an early sign. Diabetes insipidus is a disease involving the hypothalamus and the posterior pituitary and the production / release of antidiuretic hormone. This will not directly impact the blood glucose level. In the patient with diabetes insipidus expected laboratory values include: A. Elevated serum sodium, elevated serum osmolality, decreased urine specific gravity. B. Elevated serum sodium, elevated urine osmolality, decreased urine specific gravity. C. Decreased serum sodium, decreased serum osmolality, increased urine specific gravity, D. Decreased serum sodium, decreased serum osmolality, increased urine specific gravity. - CORRECT ANSWER A. Diabetes insipidus results in overdiuresis of large volumes of dilute urine leaving the body dehydrated. This will result in elevated serum osmolality with significant hypernatremia. Conversely urine concentration is low with reduced urine osmolality and low specific gravity. The patient with diabetes insipidus often experiences significant hypovolemia and will need fluid resuscitation. The type of fluid most often used is: A. Hypotonic solutions. B. Colloidal solutions. C. Hypertonic solutions. D. Isotonic solutions. - CORRECT ANSWER A. Patients with diabetes insipidus are hypovolemic and experience cellular dehydration. The goal of fluid resuscitation is to restore osmotic balance by returning volume to the cell. Hypotonic solutions, such as 0.45% Saline and D5W, have a lower concentration of solvent to solution than the blood cells. This will result in the hypotonic solution moving from an area of lower concentration (the vessel) to an area of higher concentration (the blood cells) restoring the osmotic relationship of particles to solution in the cells. Hypertonic solutions (10% Dextrose in Water, 3% Saline, 5% Dextrose in 0.45% Saline, and 5% Dextrose in 0.9% Saline) have a higher concentration of solvents to solution than the blood cells. This will result in the hypertonic solution drawing fluid out of the cell into the vascular bed. Isotonic solutions essentially have the same solvent to solution ratio as the blood cell. This results in isotonic solutions (0.9% normal saline, ringers lactate) remaining in the vascular bed. During fluid resuscitation with a hypotonic solution the nurse needs to carefully monitor the patient with diabetes insipidus for the development of: A. Ventricular tachycardia. B. Acute kidney injury. C. Cerebral edema. D. Thromboembolism. - CORRECT ANSWER C. During the process of fluid resuscitation with a hypotonic solution the sodium level will decrease. The decrease is not due to loss of sodium but to an increase in plasma volume as fluid is pulled into the cell from the hypotonic solution in the vascular bed, equalizing the concentration of particles to solution. The brain has a higher osmolality than the rest of the body and therefore is more likely to draw fluid into the cerebral compartment resulting in cerebral edema. Primary assessment findings consistent with the development of diabetes insipidus (DI) include: A. Polyuria, polydipsia, rapid shallow respirations, ketone free urine. B. Polyuria, polydipsia, Kussmaul's Breathing, ketones in urine. C. Unexplained increase in urine output of 200ml/hour x 2 hours, urine specific gravity <1.005, hypernatremia. D. Urine output less than 500 ml/24 hours, urine specific gravity >1.010, hyponatremia. - CORRECT ANSWER C. Diabetes insipidus (DI) is characterized by a decrease or absence of antidiuretic hormone. One early sign is an unexplained increase in urine output of > 200 ml/hr over 2 hours. As excessive urine production continues the urine becomes more dilute and the urine specific gravity deceases. Hypernatremia occurs secondary to the dehydration. Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized by an excess of antidiuretic hormone or an enhanced response. This results in a volume overload state as the urine output drops considerably and fluid retention occurs. As urine output decreases, the urine becomes more concentrated and urine specific gravity will increase. Additionally, as the patient becomes volume overloaded the sodium levels will decrease secondary to the hypervolemia. Diabetic Ketoacidosis (DKA) and Hypertonic Hyperosmolar Non-Ketotic Syndrome (HHNS) both present with polyuria and polydipsia. DKA presentation includes Kussmaul's respiratory pattern secondary to metabolic acidosis and there are ketones present in the urine. The respiratory pattern with HHNS is rapid and shallow and there are no ketones present in the urine. Primary manifestations of syndrome of inappropriate antidiuretic hormone (SIADH): A. Unexplained increase in urine output of >200ml/hour x 2 hours, urine specific gravity <1.005, hypernatremia. B. Polyuria, polydipsia, rapid shallow respirations, ketone free urine. C. Urine output less than 500 ml/24 hours, urine specific gravity >1.010, hyponatremia. D. Polyuria, polydipsia, Kussmaul's Breathing, ketones in urine. - CORRECT ANSWER C. Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized by an excess of antidiuretic hormone or an enhanced response. This results in a volume overload state as the urine output drops considerably and fluid retention occurs. As urine output decreases, the urine becomes more concentrated and urine specific gravity will increase. Additionally, as the patient becomes volume overloaded the sodium levels will decrease secondary to the hypervolemia. Diabetes insipidus (DI) is characterized as a decreased level or absence of antidiuretic hormone. One early sign is an unexplained increase in urine output of > 200 ml/hr over 2 hours. As excessive urine production continues the urine becomes more dilute and the urine specific gravity deceases. Hypernatremia occurs secondary to the dehydration. Diabetic Ketoacidosis (DKA) and Hypertonic Hyperosmolar Non-Ketotic Syndrome (HHNS) both present with polyuria and polydipsia. DKA presentation includes Kussmaul's respiratory pattern secondary to metabolic acidosis and there are ketones present in the urine. The respiratory pattern for HHNS is rapid and shallow and there are no ketones present in the urine. Signs and symptoms indicative of diabetic ketoacidosis (DKA) include: A. Unexplained increase in urine output of >200ml/hour x 2 hours, urine specific gravity <1.005, hypernatremia. B. Polyuria, polydipsia, Kussmaul's breathing, ketones in urine. C. Polyuria, polydipsia, rapid shallow respirations, ketone free urine. D. Urine output less than 500 ml/24 hours, urine specific gravity >1.010, hyponatremia. - CORRECT ANSWER B. Diabetic Ketoacidosis (DKA) and Hypertonic Hyperosmolar Non-Ketotic Syndrome (HHNS) both present with polyuria and polydipsia. DKA presentation includes Kussmaul's respiratory pattern (deep gasping air hunger) secondary to metabolic acidosis and there are ketones present in the urine. The respiratory pattern with HHNS is rapid and shallow and there are no ketones present in the urine. Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized by an excess of antidiuretic hormone or an enhanced response. This results in a volume overload state as the urine output drops considerably and fluid retention occurs. As urine output decreases, the urine becomes more concentrated and urine specific gravity will increase. Additionally, as the patient becomes volume overloaded the sodium levels will decrease secondary to the hypervolemia. Diabetes insipidus (DI) is characterized by a decrease or absence of antidiuretic hormone. One early sign is an unexplained increase in urine output of > 200 ml/hr over 2 hours. As excessive urine production continues the urine becomes more dilute and the urine specific gravity deceases. Hypernatremia occurs secondary to the dehydration. Signs and symptoms indicative of hyperglycemic hypoosmolar nonketotic syndrome (HHNS): A. Unexplained increase in urine output of 200ml/hour x 2 hours, urine specific gravity <1.005, hypernatremia. B. Polyuria, polydipsia, Kussmaul's breathing, ketones in urine. C. Urine output less than 500 ml/24 hours, urine specific gravity >1.010, hyponatremia. D. Polyuria, polydipsia, rapid shallow respirations, ketone free urine. - CORRECT ANSWER D. Diabetic Ketoacidosis (DKA) and Hypertonic Hyperosmolar Non-Ketotic Syndrome (HHNS) both present with polyuria and polydipsia. DKA presentation includes Kussmaul's respiratory pattern (deep gasping air hunger) secondary to metabolic acidosis and ketones are present in the urine. The respiratory pattern with HHNS is rapid and shallow and there are no ketones present in the urine. Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized an excess of antidiuretic hormone or an enhanced response. This results in a volume overload state as the urine output drops considerably and fluid retention occurs. As urine output decreases, the urine becomes more concentrated and urine specific gravity will increase. Additionally, as the patient becomes volume overloaded the sodium levels will decrease secondary to the hypervolemia. Diabetes insipidus (DI) is characterized as a decreased (absence) of antidiuretic hormone. One early sign is an unexplained increase in urine output of > 200 ml/hr over 2 hours. As excessive urine production continues the urine becomes more dilute and the urine specific gravity deceases. Hypernatremia occurs secondary to the dehydration. When treating the patient with diabetic ketoacidosis the nurse knows that the administration of insulin will have what effect on the potassium A. Insulin will shift potassium out of the cell which can result in a rise in potassium level. B. Insulin will shift potassium into the cell which can result in an increase in the serum potassium level. C. There is no impact on the potassium with insulin administration. D. Insulin will shift potassium into the cell which can result in a decrease in serum potassium level. - CORRECT ANSWER D. As metabolic acidosis develops hydrogen ions move from the serum into the cells in exchange for potassium. The administration of insulin results in a movement of potassium back in to the cell. Movement of potassium back into the cell results in a decrease in serum potassium levels. All of the following conditions can predispose the patient to the development of SIADH (Syndrome of Inappropriate Antidiuretic Hormone) EXCEPT: A. Traumatic brain injury B. Bronchogenic cancer C. Pancreatitis D. Pneumonia - CORRECT ANSWER C. Pancreatitis is a gastrointestinal disorder that does not impact the production or release of antidiuretic hormone. Causes of SIADH are divided into several subcategories: neurologic disorders, tumors, pulmonary diseases, and drugs. Traumatic brain injury and lung cancers are sited frequently as primary causes of SIADH. Your patient was admitted with a new diagnosis of lung cancer. You note his urine output is low and report this to the physician. Lab test were ordered and the results are as follow: Serum Na 120 mEq/L, serum potassium 3.6 mEq/L, BUN 10mEq/L, Creatinine 1.2 mg/dL, serum osmolality 250 mOsm/L, urine osmolality 468 mOsm/L. Based on these lab findings one of your first nursing priorities is to: A. Place the patient on seizure precautions. B. Monitor I and O. C. Assess for the development hypovolemic shock. D. Monitor for arrhythmias. - CORRECT ANSWER A. The lab values represent signs of Syndrome of Inappropriate Antidiuretic Hormone (SIADH). As the sodium level drops the risk of seizures increases. At levels of <120 mEq/L the nurse should carefully monitor the patient for the development of this complication. Intake and output is important in this population but does not take precedence over protecting the patient from harm. Patients develop hypervolemia with SIADH as they retain volume. Monitoring for fluid overload and signs of such complications as heart failure in a cardiac patient with SIADH would be appropriate. In the patient with SIADH and a sodium level of 126 mEq/L all of the following are ways to increase the sodium levels EXCEPT: A. Place the patient on a fluid restriction. B. Administer a loop diuretic. C. Administer hypertonic (3%) saline IV. D. Liberalize sodium intake. - CORRECT ANSWER C. Hypertonic saline infusions are recommended in patients with a serum sodium level of < 115 mEq/L. Administration of 3% saline is dangerous and should be reserved for those with significant hyponatremia. In SIADH the hyponatremia is the result of volume overload not necessarily sodium loss. Fluid restriction and loop diuretic will help reduce the volume and allow the sodium levels to rise. Carefully liberalizing the sodium intake may also be beneficial. Your patient has been diagnosed with Syndrome of Inappropriate Antidiuretic Hormone (SIADH). His sodium level is 113mEq/L and an infusion of 3% normal saline has been ordered. While this hypertonic saline solution is infusing which of the following assessment findings might indicate the infusion is too rapidly correcting the hyponatremia: A.Development of seizures. B. Development of hypotension. C. Development of pulmonary edema. D. Change in mental status. - CORRECT ANSWER D. Hypertonic (3%) saline is used when severe hyponatremia is present and/or if symptoms of hyponatremia exist such as seizures. Hypertonic saline draws fluid from the cell into the intravascular space. As volume is drawn into the vascular bed the serum sodium will become more dilute and the serum sodium level will decrease. A too rapid reduction of serum sodium (>12mEq/L per 24 hours) can result in the development of central pontine myelinosis or cerebral osmotic demyelination syndrome. This will be manifested first with changes in neurologic function, including altered mental status, emotional lability, spastic quadriplegia, dysarthria, dysphagia, ophthalmoplegia, ataxia, and nystagmus. Hypotension is not a direct effect of sodium correction and unlikely as the patient will develop a hypervolemic state which should support the blood pressure. The likelihood of seizures should decrease as the sodium is corrected. Pulmonary edema may occur due to the fluid being drawn into the intravascular space. It is important to monitor volume status with infusion of 3% saline, especially in cardiac and renal patients. The hypervolemic state that causes fluid overload is from the hypertonic saline, not the too rapid correction of sodium. Your patient has been admitted with glucose of 755 mg/dl, pH of 7.30, elevated serum osmolality and decreased urine specific gravity. It will be important to carefully monitor this patient for signs of: A. Complete heart block due to AV node ischemia. B. Acute pulmonary edema. C. Hypokalemia secondary to intra to extracullar shifting. D. Hypovolemic shock. - CORRECT ANSWER D. This patient has the signs and symptoms of diabetic ketoacidosis (DKA). With large glucose molecules circulating in the vascular bed a hypertonic state develops. This causes fluid to be drawn into the intravascular space and an osmotic diuresis occurs. Polyuria results and hypovolemia occurs. The high serum osmolality indicates signs of dehydration. Nurses need to monitor for the development of hypovolemic shock. Pulmonary edema is not an early complication with DKA but could occur after fluid resuscitation is initiated. Potassium will shift from intracellular to extracellular space during DKA but this should increase the serum potassium level. DKA has no direct impact on the cardiac conduction system. You patient with diabetic ketoacidosis was admitted 4 hours ago and is being treated with IV fluids and IV insulin. His initial lab work demonstrated a blood glucose level of 585 mg/dl, pH of 7.30, potassium of 3.6 mEq/L. His repeat lab work is as follows: glucose 302 mg/dl, pH of 7.35, potassium of 3.6 mEq/L. Based on these findings you would anticipate the following changes: A. Change from IV insulin to SQ insulin. B. Administer bicarbonate to continue to correct the acidosis. C. Change the IV fluid from 0.9% normal saline to D5.45%normal. D. Administer potassium. - CORRECT ANSWER D. As insulin administration continues, extracellular potassium will be driven into the cell and the serum potassium level will continue to drop putting the patient at risk for hypokalemia. The pH is back to low normal. There is no support for the administration of bicarbonate unless the patient is severely acidotic - pH < 7.0. When the patient's blood sugar nears 250mg/dl it is important to add dextrose to the IV fluids to prevent the development of cerebral edema. The insulin will move glucose into the cells. As more glucose moves in to the cells the serum osmolality decreases. If serum osmolality is lower than intracellular osmolality, water moves into the cells. In the brain, cerebral edema will occur. The infusion of some glucose into the intravascular space will decrease this effect. IV insulin should converted to SQ insulin after the glucose level is < 250 mg/dl. You are monitoring the glucose levels hourly on your patient with diabetic ketoacidosis and note that she was admitted with a glucose level of 532. Her hourly levels have been as follows: 1 hour 486 mg/dL 2 hour 415 mg/dL 3 hour 302 mg/dL In reviewing these values you know: A. A reduction in blood sugar greater than 100 mg/dL is dangerous and can result in the rapid development of cerebral edema and hypokalemia. B. The blood glucose level remains too high putting the patient at risk for continued hypovolemia and will need more aggressive treatment of the blood sugar. C. The reduction in blood sugar is appropriate and the infusion of normal saline should have glucose added to it to prevent the development of cerebral edema. D. This gradual decline in blood glucose levels is appropriate and you should continue current therapy. - CORRECT ANSWER A. Blood sugar levels should not be reduced any faster than 100mg/dL. A rapid reduction in blood sugar levels can result in the development of cerebral edema as glucose quickly moves from outside the cell into the cell. This transfer of the large glucose molecules will then draw volume into the cell. If this is done too quickly cerebral edema can occur. As similar effect occurs with potassium. As insulin moves glucose into the cell potassium follows and moves from extracellular to intracellular. This will drop the serum potassium level and hypokalemia can result if this occurs too quickly. Dextrose is added to normal saline solutions only after the blood sugar has dropped to < 250 mg/dL. The patient presenting with Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS) will present with the following findings:. A. Hypotension, tachycardia, pH normal, ketonuria. B. Hypotension, tachycardia, deep gasping air breaths, pH elevated, ketonuria. C. Hypotension, tachycardia, rapid shallow respirations, pH normal, no ketonuria. D. Hypertension, bradycardia, pH elevated, no ketonuria. - CORRECT ANSWER C. Patients with HHNS are generally hypovolemic and will exhibit sings of volume deficit with tachycardia and hypotension. The respiratory pattern will be rapid and shallow in response to decreased perfusion to the lungs. Deep gasping breaths are specific to the Kussmaul's respiratory pattern seen with acidosis. pH levels are normal with HHNS and reduced with diabetic ketoacidosis. Ketonuria is a finding with diabetic ketoacidosis and not HHNS. Patients with HHNS are generally type II diabetics and do not have an absence of insulin so ketosis is not present. While treating your patient with diabetic ketoacidosis it is important to monitor for complications related to the treatment with IV fluids and insulin replacement. Monitoring for the following is a top priority: A. Decrease in mental status. B. Tachycardia. C. Hyperkalemia. D. Bradycardia. - CORRECT ANSWER A. Assessment for the development of cerebral edema is a high priority in the nurse caring for a patient in the early stages of diabetic ketoacidosis. The administration of insulin allows glucose to move from the vascular bed in to the cell. This movement results in volume following the large glucose molecules to maintain osmolality. If this process occurs too quickly cerebral edema occurs. Patients with DKA are usually tachycardic on presentation due to the hypovolemia. Neither tachycardia nor bradycardia are a direct result of the treatment. Most often hypokalemia will develop in the course of treating DKA as insulin moves potassium into the cell and serum potassium will decrease. Your ICU patient who has been a noninsulin dependent diabetic has blood sugars as high as 450 and is very upset that she is requiring insulin with every blood sugar check. In your attempt to alleviate her concerns you review her treatment plan and recognize the following that is the most likely cause of her elevated blood sugar: A. Regular diet. B. Tube feedings. C. IV cortisol started on admission. D. The home dose of metformin not started on admission. - CORRECT ANSWER C. Steroids have been found to block the action of insulin resulting in insulin resistance. Additionally, steroids stimulate glucose secretion by the liver increasing available glucose. Steroid also reduces glucose movement into adipose tissue and muscles. All of these changes result in an elevation of blood glucose levels that can be significant while on steroids. Which of the following indicates resolution of the metabolic acidosis in diabetic ketoacidosis: A. No ketones in the urine. B. Normalization of the anion gap. C. Normalization of urine output to 1cc/kg/hour. D. Normalization of the serum glucose. - CORRECT ANSWER B. Correction of diabetic ketoacidosis occurs when the acidosis corrects. An anion gap that narrows demonstrates resolution of the acidosis. Which of the following hormones secreted by adrenal cortex is responsible for sodium and water retention when released: A. Epinephrine. B. Cortisol. C. Aldosterone. D. Antidiuretic hormone. - CORRECT ANSWER C. Aldosterone is one of the mineralocorticoids secreted by the adrenal cortex that is responsible for the retention of sodium and water. Cortisol and catecholamines (epinephrine and norepinephrine) are medullary hormones secreted by the adrenal medulla. Antidiuretic hormone is responsible for the regulation of water but is secreted by the posterior pituitary in response to changes in osmolality. During the treatment of diabetic ketoacidosis the patient may experience a drop in potassium as potassium moves back into the cell. Which of the following treatment strategies is responsible for the movement of potassium from the extracellular fluid to the cell: A. Dextrose. B. Bicarbonate infusion. C. Insulin. D. Potassium administration. - CORRECT ANSWER C. Insulin will result in the movement of potassium from the extracellular fluid back into the cell. As DKA and metabolic acidosis develops hydrogen ions move from extracellular fluid into the cell. In an attempt to maintain electrolyte balance potassium moves from the cell to the extracellular fluid. The administration of insulin will move hydrogen ions back to the extracellular fluid and allow potassium to reenter the cell. The osmolar state of the serum in a patient with Syndrome of Inappropriate Antidiuretic Hormone (SIADH) will be: A. It will remain normal. B. Hypoosmolar. C. Greater than the urine osmolality. D. Hyperosmolar. - CORRECT ANSWER B. With SIADH there is an absence of the natural feedback mechanism related to the release of ADH resulting in 'water intoxication' as the body thinks it should conserve water. This results in a hypoosmolar state with low serum osmolality and high urine osmolality as there is little urine output. Your patient is admitted with a blood glucose level of 500 mg/dl. Which of the following findings would help you identify this situation as diabetic ketoacidosis (DKA) and not Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS): A. Decreased urine specific gravity. B. Presence of glucose in the urine. C. Elevated serum osmolality. D. Presence of ketones in the urine. - CORRECT ANSWER D. DKA by definition includes the production of ketones resulting in ketosis and ketonuria. HHNS usually occurs in type II diabetics with a relative insulin deficiency. When a deficiency of insulin exists (HHNS) instead of an absence of insulin (DKA) ketonuria does not occur. Mild serum ketones may be present in HHNS but often times the serum ketone level is normal. Ketonuria is one finding that differentiates DKA from HHNS. Both DKA and HHNS can result in glucosuria, elevated serum osmolality and decreased urine specific gravity. You have admitted an elderly female patient with suspected myxedema coma. Which of the following lab tests is the most sensitive indicator of myxedema coma: A. TSH (thyroid stimulating hormone). B. Liver enzymes. C. CBC. D. Basic metabolic panel. - CORRECT ANSWER A.Myxedema coma results from profound hypothyroidism. Evaluation of thyroid function is necessary for diagnosis. The TSH is the most sensitive indicator of thyroid function. The other lab test will provide information regarding changes that have occurred as a result of the thyroid dysfunction but will not provide a diagnosis for myxedema coma. When caring for the patient with myxedema coma the nurse recognizes that nursing care will include: A. Holding all IV steroids. B. Holding all thyroid replacement medications. C. Monitoring for seizures secondary to the hypernatremia. D. Warming the body temperature to normal. - CORRECT ANSWER D. Patients presenting with myxedema coma usually are hypothermic and treatment goals include warming the body to normothermia. Other treatment strategies would include the administration of IV thyroid and in some instances steroid administration when adrenal insufficiency also exists. Patients with myxedema coma experience hyponatremia not hypernatremia. Seizures are most common with hyponatremia and the patients should be placed on seizure precautions when the serum sodium level is <110 mg/dl. Critically ill patients are at increased risk for this disorder secondary to the stress of critical illness: A. Thyroid storm. B. Diabetes insipidus. C. Adrenal insufficiency. D. Syndrome of inappropriate antidiuretic hormone. - CORRECT ANSWER C. The incidence of adrenal insufficiency secondary to the stress of critical illness has been reported to be as high 30% in critically ill patients and may be higher in those with septic shock. The other disorders may occur in critical illness but are not related to stress. Which of the following is a specific finding associated with adrenal insufficiency: A. Hypernatremia with fluid overload. B. Hyperglycemia in the non-diabetic patient. C. Unexplained persistent hypotension unresponsive to vasopressor therapy. D. Hypokalemia with abnormally elevated creatinine. - CORRECT ANSWER C. Hemodynamic instability despite adequate fluid and vasopressor therapy is the most common feature of adrenal insufficiency. In addition to the persistent hypotension other findings include hyperkalemia, hyponatremia and hypoglycemia. Patients with adrenal insufficiency who continue to have hypotension despite fluid resuscitation and norepinephrine administration may have a deficit of circulating antidiuretic hormone (ADH). In addition to fluids and norepinephrine, which of the following IV medications that can increase circulating ADH would be helpful in treating the persistent hypotension in adrenal insufficiency: A. Epinephrine. B. Vasopressin. C. Dopamine. D. Dobutamine. - CORRECT ANSWER B. Arginine vasopressin is antidiuretic hormone. The administration of vasopressin will produce the same effect as the release of antidiuretic hormone in the body. IV vasopressin will increase fluid reabsorption in the kidneys and act as a potent vasopressor resulting in vasoconstriction. While the other medications can impact the blood pressure only vasopressin mimics the effect of endogenous ADH. Patients with severely elevated triglycerides (i.e. triglyceride levels > 1,000 mg/dL) are treated with fibrates to reduce the risk for the development of: A. Thyroid storm. B. Diabetes insipidus. C. Pancreatitis. D. Syndrome of inappropriate antidiuretic hormone. - CORRECT ANSWER C. Patients with severe and very severe hypertriglyceridemia require a reduction of dietary fat and simple carbohydrate intake in additional to pharmacological therapy in order to reduce the risk of pancreatitis. A fibrate is recommended as the first line drug to treat patients at risk for triglyceride induced pancreatitis. What is true regarding glycemic control in critically ill patients: A. For most critically ill patients the therapeutic target should be 140 to 180 mg/dL. B. Insulin via intravenous infusion is the preferred method for achieving glycemic control. C. Hyperglycemia should be treated with an intravenous insulin protocol. D. Treatment should begin at a level of no greater than 180 mg/dL. E. All of the above. - CORRECT ANSWER E. Critically ill hospitalized patients with persistent hyperglycemia should be treated with an intravenous insulin protocol. Insulin via intravenous infusion is the preferred method for achieving glycemic control in the critically ill patient. Treatment should begin at a level of no greater than 180 mg/dL. For most critically ill patients the therapeutic target should be 140 to 180 mg/dL. Stricter glycemic control (110 mg/dL to 140 mg/dL) can be the target in select patients if this goal can be achieved without inducing hypoglycemia. Patients receiving intravenous insulin require blood glucose checks a minimum of every 2 hours. The best method for treating non critically ill hospitalized patients with diabetes mellitus is by a sliding scale regime rather than by scheduled insulin injections: A. True. B. False. - CORRECT ANSWER B. Hospitalized patients who are not critically ill may be treated when glucose levels are > 140 mg/dL. Scheduled subcutaneous insulin is used for glycemic control in these patients. Hospitalized patients should not be treated solely with sliding scale insulin. Sliding scale insulin alone not only fails to adequately prevent hyperglycemia, it also increases the risk for hypoglycemia. Insulin therapy should include scheduled basal, nutritional, and supplemental components The nurse knows what regarding hypoglycemia in patients with diabetes mellitus: A. Hypoglycemia is defined as a blood glucose level of < 50 mg/dL. B. Cognitive impairment typically occurs at a glucose < 50 mg/dL. C. Severe hypoglycemia in hospitalized patients has been defined as a glucose level of < 20 mg/dL. D. Hypoglycemia has been associated with prolonged length of stay but not with increased mortality. - CORRECT ANSWER B. Hypoglycemia is defined as a blood glucose level of < 70 mg/dL. Glucose is the preferred treatment for conscious patients with hypoglycemia. If glucose 15 to 20 grams is not available then any food containing glucose can be used. Glucagon is prescribed for patients at risk for severe hypoglycemia and family members are instructed on the administration. Severe hypoglycemia has been associated with an increase in mortality in several clinical trials. Although there is an association between severe hypoglycemia and increased mortality it is not clear whether there is direct causation or whether severe hypoglycemia is a marker for a more ill patient. Severe hypoglycemia in hospitalized patients has been defined as a glucose level of < 40 mg/dL. Cognitive impairment typically occurs at a glucose < 50 mg/dL. Clinical conditions associated with hypoglycemia in the hospitalized patient include altered nutrition, emesis, infection, malignancy, heart failure, renal or hepatic dysfunction, changes in corticosteroid medication regimes, and improper timing or dosing of insulin therapy. Hyperparathyroidism and malignancy are the most common causes of: A. Hyperkalemia. B. Hypokalemia. C. Hypomagnesemia. D. Hypercalcemia. - CORRECT ANSWER D. Hypercalcemia occurs when the entry of calcium into the circulation exceeds the excretion of calcium into the urine or calcium deposition in bone. Parathyroid hormone activates osteoclasts and leads to increased bone resorption (bone loss). Many types of cancer cause increased bone resorption via a variety of mechanisms. Hyperkalemia is usually due to increased potassium release from cells (as in metabolic acidosis, increased tissue breakdown, insulin deficiency, etc.) or reduced urinary potassium excretion (as in renal failure, hypoaldosteronism). Hypokalemia and hypomagnesemia are usually due to excessive gastrointestinal or urinary losses. HHS Treatment Insulin management - CORRECT ANSWER May require less insulin than in DKA May start with insulin bolus Regular insulin 0.1 U/kg/hr (or algorithm) Goal: decrease glucose slowly, not more than 50-100 mg/dL per hour Maintain insulin drip for 1-2 hours while starting SQ to prevent DKA relapse DKA Treatment Fluid Resuscitation - CORRECT ANSWER Calculate fluid deficit (50-100 mL/kg) ~ 5-6 L Administer front loaded (1-3 L in hr 1) with taper to maintenance NS or LR (iso), add Dextrose when CBG 250 (lower risk for hypoglycemia), then 1/2NS or PO water for cellular resuscitation Serum Osmolality Serum Osmo calculations - CORRECT ANSWER 275 - 295 Calculation (^ Glucose): 2Na + Glucose/18 + BUN/2.8 Calculation (Glucose WNL): ~ 2Na Isotonic IVFs Role in fluid dynamics - CORRECT ANSWER NS LR Plasmalyte Stays in vasculature Hypotonic IVFs Role in fluid dynamics - CORRECT ANSWER 0.45 NS (154 osmo) D5W (252 osmo) Pushes fluid from vasculature into cells (cellular re-hydration) Hypertonic IVFs Role in fluid dynamics - CORRECT ANSWER Hypertonic saline (2%, - 23.4%) D5 0.2 NS (321 osmo) D5 0.5 NS (406 osmo) D5 LR (525 osmo) 10% dextrose (505 osmo) Pull fluid from cell to vasculature Acute Hypoglycemia Definition/criteria/BB - CORRECT ANSWER Serum glucose < 70 More insulin relative to glucose ID cause to treat Note: increase monitoring with beta blockers, blunts SNS And masks signs of hypoglycemia Hypoglycemia Causes - CORRECT ANSWER Too much insulin Vomiting (loss of cals) Stress/exercise (high metabolism) Excess ETOH Adrenal insufficiency (low cortisol) Severe liver dz Pregnancy (parasite metabolism) Hypoglycemia Cardiac Symptoms - CORRECT ANSWER Think increased SNS, "wet, white, weak" Palpitations Tachycardia Diaphoresis Pallor/cool skin Piloerection Irritability Hypoglycemia Neuro Symptoms - CORRECT ANSWER Think insufficient fuel for neuro function Blurred vision Slurred speech Weakness HA Difficulty concentrating/confusion Fatigue Diplopia Anxiety Tremors Hypoglycemia Treatment (alert, unconscious IV, unconscious no IV) - CORRECT ANSWER Conscious: 4 oz juice/15g carb/0.5-1 amp D50 Unconscious with IV: 0.5-1 amp D50/consider D5-10W IVF Unconscious without IV: Glucagon 0.5-1 mg IM Metabolic Syndrome Definition (deadly quartet) - CORRECT ANSWER High risk for CV dz and CVA, 25 % US pop (40% by age 60) Any two of following: > HLD (Dislipidemia) triglyceride > 150, low HDL < 40m/50f > HTN SBP/DBP > 130/85 > DM (Hy