PCCN Endocrine Exam with Questions and Answers, Exams of Medicine

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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. ANSWERY ¥ 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). ANSWERY ¥ 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. ACTII 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 (ADIT). ANSWERY ¥ D. ADI (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 ADII 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+. In both diabetes mellitus and HIINS, blood glucose levels are significantly elevated. lollowing 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. ANSWERV V 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. ANSWERV V 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 Nat 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. ANSWERV VY 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. 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. ANSWERV ¥ D. Diabetes insipidus is due to a deficiency of antidiuretic hormone (ADH) or an inability of the kidney to respond to ADH. This deficicney 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. ANSWERV ¥ 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 ACTII 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. ANSWERV V 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. Ilypothyroidism causes myxedema. An autoimmune disease in which antibodies destroy pancreatic beta cells resulting in insulin deficiency is: A. Type II diabetes mellitus. What is the most likely diagnosis: A. DKA (di ANSWERV V 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. IILINS (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 protcin 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, scrum 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. TV 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. ANSWERV V 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 pII 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 scrum 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. Ie 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: Nat = 148 mEq/L, K+ = 4.0 mEq/L, Cl= 118 mEq/L, 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. ANSWERV V 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 IIIINS, the pI 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 hypoyolemia-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, resulling 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 (13). C. Elevated TSH (thyroid stimulating hormone) level. D. Reduced serum iodine levels. ANSWERV V 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. [lypothyroidism 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. ‘SH 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. ANSWERV V 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 ce /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. 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. ANSWER¥ Vv 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. ANSWERV ¥ 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 Ilypertonic Ilyperosmolar Non-Ketotic Syndrome (IIIINS) 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. ANSWERV ¥ 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 inerease. 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. 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. ANSWERV ¥ 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 oceurs. 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. ANSWERV ¥ 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 Antidiurctic Hormone) EXCEPT: A. Traumatic brain injury B. Bronchogenic cancer C. Pancreatitis D. Pneumonia ANSWERY V¥ 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 SLADH. 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. ANS WERV V 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.