2/3/2013 9:32:00 AM Topics on blueprint: Ch.

14, 17 Hypovolemia o fluid volume deficit, can occur with abnormal loss of body fluids o assessment: I/O , monitor pt. for cardiovascular changes, monitor respiratory status, assessment of neurological functions includes evaluation of LOC, pupillary response and voluntary movement of the extremities, degree of muscle strength and reflexes. Accurate daily weights, inspect for skin turgor and temperature o Etiology: inc. insensible water loss or perspiration (high fever, stroke), diabetes insipidus, osmotic diuresis, hemorrhage, GI losses (diarrhea, vomiting, NG suction, fistula drainage), over use of diuretics, inadequate fluid intake, and third space fluid shifts (burns, intestinal obstruction) o Signs and symptoms: restlessness, drowsiness, lethargy, confusion, thist dry mucous membranes, decr. Skin turgor, decr. Capillary refill, , postural hypotension, inc. pulse, dec. CVP, dec. urine output,concentrated urine, inc. respiratory rate,weakness, dizziness, weightloss, seizures, coma o Treatments:goal of treatment is to correct the underlying cause and to replace both water and any needed electrolytes. Balanced IV solution such as Ringers solution are usually given. Isotonic (0.9%) sodium chloride is used when rapid volume replacement is indicated. Blood is administered when volume loss is due to blood loss. o Diagnosis deficit fluid volume R/T excessive ECF losses or decrease fluid intake decreased cardiac output R/T excessive ECF losses or decreased fluid intake risk of deficient fluid volume R/T ECF losses or decreased fluid intake potential complications: Hypovolemic shock

Hypervolemia o Assessment: I/O , monitor pt. for carsiovascular changes, monitor respiratory status, assessment of neurological functions includes evaluation of LOC, pupillary response and voluntary movement of the extremities, degree of muscle strength and reflexes. Accurate daily weights, inspect for skin turgor and temperature o Etiology: Fluid volume excess, excessive isotonic or hypotonic IV fluids, Heart failure, renal failure, primary polysipsia, SIADH, cushings symdrome, longeterm use of corticosteroids. o Signs and symptoms: headache, confusion, ;ethargy, peripheral edema, jugular venous distention, full and bounding pulse, inc. BP, inc. CVP, polyuria, dyspnea, crackles, luminary edema, muscle spasms, weight gain, seizures coma. o Treatments: goal of treatment is removal of fluids without producing abnormal changes in electrolyte composition or osmolality of ECF. Diuretics and fluid restriction are the primary forms of therapy. o Dietary needs: Restriction of sodium intake may also be indicated o Diagnosis Excessive fluid volume R/T increased water and/or sodium retention Risk for imbalanced fluid volume R/T increased water and/or sodium retention Impaired gas exchange R/T water retention leading to pulmonary edema Risk for impaired skin integrity R/T edema Disturbed body image R/T altered body appearance secondary to edema Potential complications: pulmonary edema, ascites

o Hyponatremia (Na < 135 mEq/L) o Etiology: Excessive sodium loss: GI losses (diarrhea, vomiting, fistulas, NG suction) Renal losses (diuretics, adrenal

insufficiency, Na+ wasting renal disease) skin losses (burns, wound drainage) Inadequate sodium intake: fasting diets Excessive water gain (dec. sodium concentration): Excessive hypotonic IV fluids, primary polydipsia Disease states: SIADH, heart failure, primary hypoaldosteronism. o Signs and symptoms: Hyponatremia with decreased ECF volume (irritability, apprehension, confusion, dizziness, personality changes, tremors , seizures, coma, dry mucous membranes, postural hypotention, dec. CVP, dec. jugular venous filing, tachycardia, thread pulse, cold and clammy skin) Hyponatremia with normal/ increased ECF volume (headache, apathy, confusion, muscle spasms, seizures, coma, nausea, vomiting, diarrhea, abdominal cramps, weight gain, ^ BP ^ CVP) o Treatments: if caused by water excess all that is needed is fluid restrictions. Drugs that block the activity of ADH (vasopressin) are used in tx of hyponatremia. Tx of hyponatremia associated with fluid loss includes fluid replacement with sodium containing solutions. Conivaptan (vaprisol) results in ^ urine output w/o loss of electrolytes (it should not be used in pts. With hypovolemic hyponatremia). Tolvaptan (Samsca) is used to treat hyponatremia associated with heart failure, liver cirrhosis, and SIADH. o Dietary needs: fluid restriction o Diagnosis Risk for injusry R/T altered sensorium and decreased LOC secondary to abnormal CNS function Risk for electrolyte imbalance R/T excessive loss of sodium and/ or excessiveintake of water Potential complication: severe neurologic changes Hypernatremia (Na > 145 mEq/L)

o Etiology: excessive sodium intake:IV fluids: (hypertonic NaCl, excessive isotonic NaCl, IV sodium bicarbonate) hypertonic tube feedings without water supplements, near-drowning in salt water. Inadequate water intake: unconscious or cognitively inpaired individuals. Excessive water loss (^ sodium concentration): ^ insensible water loss (high fever, heatstroke, prolonged hyperventilation), osmotic diuretic therapy, diarrhea Disease states: diabetes insipidus, primary hyperaldosteronism, cushings syndrome, uncontrolled diabetes mellitus. o Signs and symptoms: Hypernatremia with dec. ECF Volume: restlessness, agitation, twitching, seizures, coma, intense thirst, dry, swollen tongue, sticky mucous membranes, postural hypotention, dec. CVP, weightloss lethargy. Hypernatremia with normal/ increased ECF Volume: restlessness, agitation, twitching, seizures, coma, intense thirst, flushed skin, weight gain, peripheral and pulmonary edema, ^ BP, ^ CVP o Treatments: goal of treatment is to dilute the sodium concentration with sodium free IV fluids, such as 5% dextrose in water, and to promote excretion of the excess sodium by administering diuretics o Dietary needs: sodium restrictions o Diagnosis: Risk for injury R/T altered sensorium and seizures secondary to abnormal CNS function Risk for electrolyte imbalance R/T intake of sodium and/ or loss of water Potential complication: seizures and coma leading to irreversible brain damage

Hypokalemia (K+ <3.5 mEq/L)

o Can result from abnormal losses of K from a shift from ECF to ICF, or rarely from deficient dietary K intake. o Most common causes of hypokalemia are abnormal losses, via either the kidneys or the GI tract. o Abnormal losses occur when the patient is diuresing, particularly in a pt. with an elevated aldosterone level. o Hypokalemia is pften associated with the treatment of diabetic ketoacidosis because of a combination of factors, including an ^ in urinary potassium loss and a shift of potassium into cells woth the administration of insulin and correction of metabolic acidosis o Etiology: Potassium loss: GI losses (diarrhea, vomiting, fistulas, NG suction) Renal losses (diuretics, hyperaldosteronism (aldosterone is released when the circulating blood volume is low; it causes sodium retention in kidneys, but loss of potassium in the urine), magnesium depletion(low magnesium stimulates renin release and subsequently increased aldosterone levels, which results in k excretion)) skin losses (diaphoresis) dialysis. Shift of Potassium into cell: increased insulin (i.g., IV dextrose load) , alkalosis (can cause a shift of K into cells in exchange for hydrogen, thus lowering the K in the ECF and causing systematic hypokalemia), tissue repair, ^ epinephrine (e.g. stress) Lack of Potassium intake: starvation diet low in potassium, failure to include potassium in parenteral

fluids in NPO. o Signs and symptoms: Fatigue, muscle weakness, leg cramps, nausea vomiting paralytic ileus , soft, flabby muscles, parethesias, decreased reflexes, weak, irregular pulse, polyuria, hyperglycemia Electrocardiogram changes: ST segmented depression, flattened T wave, presence of U wave, ventricular

dysrhythmias (e.g., PVC), bradycardia, enhanced digitalis effect Treatments: increasing dietary intake of potassium and potassium chloride supplements (KCL). KCL can be given orally or IV. Except in severe deficiencies, KCL is never given unless there is urine output of at least 0.5mL/ kg of body weight per hour. The preferred maximum concentration is 40 mEq/L (in severe cases up to 80 mEq/L). the rate of adm. Should not exceed 10 to 20 mEq per hour and should be administered by

infusion pump to ensure correct administration rate. (assess iv sites at least hourly for phlebitis and infiltration) KCL given IV must always be diluted. Never give in IV push. IV bags must be inverted several times. Never add a KCL to a hanging IV bag to prevent giving a bolus dose. o Dietary needs: potassium rich foods o Diagnosis Risk for electrolyte imbalance R/T excessive loss of potassium Risk for injury R/T muscle weakness and hyporeflexia Potential complication dysrhythmias

Hyperkalemia (K+ > 5.0 mEq/L) o Most common cause is renal failure. o Potassium sparing drugs and ACE inhibitors are types of drugs that reduce the kkidneys ability to excrete potassium. o Must be monitored electrocardiographically to detect dysrhythmias and to monitor the effects of therapy o Etiology: Excess potassium intake: excessive or rapid parenteral administration. Potassium-cotaining drugs (e.g. potassium-penicillin) potassium-containing salt substitute.

Shift of potassium out of cells: acidosis, tissue catabolism (e.g., fever, sepsis, burns) crush injury, tumor lysis syndrome. Failure to eliminate potassium: renal disease, potassium-sparing diuretics, adrenal insufficiency, ACE inhibitors. o Signs and symptoms: Irritability, anxiety, abdominal cramping, diarrhea, weakness of lower extremeties, paresthesias, irregular impulse, cardiac arrest if hyperkalemia sudden or severe. Electrocardiogram changes: tall, peaked T wave, prolonged PR interval, ST segment depression, loss of P wave, widening QRS, ventricular fibrillation, ventricular standstill o Treatments: administer fluids and possibly diuretics, Kayexalate(administered via the GI tract binds potassium in exchange for sodium, and the resin is excreted in feces) o Pts. With moderate hyperkalemia should additionally receive one of the treatments to force K into cells, usually IV insulin and glucose. The pt. experiencing dangerous cardiac dysrhythmias should receive IV calcium gluconate immediately while the potassium is being eliminated and forced into cells. Hemodialysis is an effective means of removing potassium from the body in the patients with renal failure. Dietary needs: withhold potassium from diet Diagnosis Risk for electrolyte imbalance R/T excessive retention or cellular release of potassium Risk for injury R/T lower extremity muscle weakness and seizures Potential complication: dysrhythmias

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Hypocalcemia Ca2+ <8.6 mg/dL

o About two thirds of hypercalcemia cases are cause by hyperparathyroidism and one third are caused by malignancy, especially from breast cancer, lung cancer, and multiple myeloma. o Malignancies lead to hypercalcemia trough bone destruction from tumor invasion or through tumor secretion of a parathyroid-related protein, which stimulates calcium release from bones o It rarely occurs from increase calcium intake. o Excessive calcium leads to reduced excitability of both muscles and nerve o Any pt who has had thyroid or neck surgery must be closely observed in the immediate post-op period for manifestations of hypocalcemia because of the proximity of the surgery to the parathyroid glands. o Etiology: Decreased total calcium: Chronic kidney disease, elevated phosphorus, primary hypoparathyroidism, Vit D deficiency, mag. Deficiency, acute pancreatitis, loop diuretics (furosemide) chronic alcoholism, diarrhea, dec. serum albumin (pt is usually asymptomatic due to normal ionized calcium level) Decreased Ionized Calcium: alkalosis, excess administration of citrated blood o Signs and symptoms: Easy fatigability, depression, anxiety, confusion, numbness and tingling in extremities and region around mouth, hyperreflexia, muscle cramps, chvosteks sign, trousseaus sign, laryngeal spasm, tetany, seizures Electrolycardiogram changes: elongation of ST segment, prolonged QT interval, ventricular tachycardia o Treatment: oral or IV calcium supplements. (not given IM because it can cause severe local reactions like burns, necrosis, and tissue sloughing) pain and anxiety must be adequately treated.

o Diet: a diet in calcium-rich foods is usually ordered along with vitamin D supplements o Diagnosis: risk of electrolyte imbalance related to decreased production of PTH. Risk for injury related to tetany and seizures potential complications: fracture, respiratory arrest Hypercalcemia Ca2+ >10.2 mg/dL o Etiology: Increased total calcium: multiple myeloma, malignancies with bone metastasis, prolonged immobilization, hyperparathyroidism, Vit D overdose, thiazide diuretics, Milk-alkali syndrome Increased ionized calcium: acidosis o Signs and symptoms: Lethargy, weakness, depressed reflexes, decreased memory, confusion, personality changes, psychosis, anorexia, nausea, vomiting, bone pain, fractures, polyuria, dehydration, nephrolithiasis, stupor, coma Electrocardiogram changes: shortened ST segment, shortened QT interval, Ventricular dysrhythmias, increased digitalis effect. Treatments: promotion of excretion of calcium in urine by administration of calcium in urine by administration of a loop diuretic, and hydration of the patient with isotonic saline infusions. o The patient must drink 3000 to 4000 mL of fluid daily to promote the renal excretion of calcium and to decrease the possibility of kidney stone formation. o Mobilization with weight bearing activity is encouraged to

enhance bone mineralization Nursing diagnosis: risk for electrolyte imbalance r/t excessive bone destruction.. risk for injury related to neuromuscular and sensorium changes..potential complications: dysrhythmias . Phosphate imbalances Phosphate is a primary anion in the ICF and is essential to the function of muscle, RCBs, and the nervous system. A reciprocal

relationship exist between phosphorus and calcium in that a high serum phosphate level tends to cause a low calcium concentration in the serum. Hypophosphatemia o Seen in the patient who is malnourished or has malreabsorption syndrome o Mild to moderate hypophosphatemia is usually asymptomatic. o Severe hypophosphatemia may be fatal because of decreased cellular function. o Etiology: malabsorption syndrome, nutritional recovery syndrome (reversal or treatment of starvation) glucose administration, total parenteral nutrition, alcohol withdrawal, phosphate bounding antiacids, recovery from diabetic ketoacidosis, respiratory alkalosis o Signs and symptoms: Central nervous system dysfunction (confusion, coma) muscle weakness, including respiratory muscle weakness and difficulty weaning, renal tubular wasting of magnesium, calcium, HCO3,cardiac problems (dysrhythmias, dec. stroke volume) osteomalasia, rhabdomyolysis. o Treatments: management of mild deficiency may involve oral supplements and ingestion of foods high in phosphorous. Severe deficiency can be serious and may require IV administration of sodium phosphate or potassium phosphate. Frequent monitoring levels is necessary to guide IV therapy. o Dietary needs: Hyperphosphatemia o Major condition that can lead to Hyperphosphatemia o Is acute or chronic renal failure that results in an altered ability of the kidney to excrete phosphate. o Etiology: Renal failure, chemotherapeutic agents, enemas containing phosphorus (e.g., fleet enema) excessive

ingestion (e.g., milk, phosphate containing laxatives) large Vit D intake, hypoparathyroidism o Signs and symptoms: Hypocalcemia, muscle problems; tetany, deposition of calcium-phosphate precipitates in skin, soft tissue, cornea, vicera, blood vessels. o Treatments: aimed at identifying and treating the underlying cause. Adequate hydration and correction of hypo calcemic conditions can enhace the renal excretion of phosphate through the action of PTH o Dietary needs: restriction of foods and fluids high in phosphorus Osmolality: measures the osmotic force of solute per unit of weight of solute. Used to describe fluids inside the body. o Assessment: normal plasma osmolality is between 275 and 295 mOsm/kg a value greater than 295 indicates that the concentrationof particle is too great or the water content is too little (water deficit). A value less than 275 indicates too little solute for the amount of water or too much water for the amount of solute (water excess). Because the major determinants of the plasma osmolality are sodium and glucose, one can calculate the effective plasma osmolality based on the concentration of those substances. o Isotonic: fluids with the same osmolality as the cell interior o Hypotonic: solutes are less concentrated than the cells. o Hypertonic: solutes more concentrated than cell. Spacing a term used to describe the disruption of body water. o First spacing describes the normal distribution of fluid in the ICF and ECF o Second spacing refers to an abnormal accumulation of interstitial fluid (edema) o Third spacingoccurs when fluid accumulates in a portion of the body from which it is not easily exchanged with the rest of the ECF. It is trapped and unavailable for functional use

(ascites, sequestration of fluid in the abdominal cavity with peritonitis, and edema associated with burns, traumas, or sepsis) Arterial blood gases and interpretation o pH: 7.35- 7.45 o PaCO2: 35- 45 mm Hg o Bicarbonate: 22-26 mEq/L o Pao2: 80-100 mm Hg o SaO2: >95% Antidiuretic hormone (actions/effects) o Water balance is maintained via the finely tuned balance of water intake and excretion. A body fluid deficit or increase in plasma osmolality is sensed by the osmoreceptors in the hypothalamus, which in turn stimulate thirst and antidiuretic hormone release (ADH). Thirst causes the patient to drink water. ADH ,which is synthesized in the hypothalamus and stored in the posterior pituitary, acts in the renal distal and collecting tubules causing water reabsorption. Together these factors result in increased free water in the body and decreased plasma osmolality. If the plasma osmolality decreased or there is water excess, secretion of ADH is suppressed , resulting in urinary excretion of water o Under the hypothalamic control, the posterior pituitary releases ADH, which regulates water retention by the kidneys. The distal tubules and collecting ducts in the kidney respond to ADH by becoming more permeable to water so that water is reabsorbed from the tubular filtrate into the blood and not excreted in urine. Other factors that stimulate ADH release include stress, nausea, nicotine, and morphine. These factors usually result in shifts of osmolality within the range of normal values. It is common for the postoperative patient to have low serum osmolality after surgery, possibly because of the stress and opioid analgesia. SIADH:

o Etiology: a pathologic condition Syndrome of inappropriate antidiuretic hormone secretion are cause by abnormal ADH production in CNS disorders (brain tumors, brain injury) and certain malignancies (small cell lung cancer) o The inappropriate ADH causes water retention, which produces a decrease in plasma osmolality below the normal value and a relative increase in urine osmolality with a decrease in urine volume . o Signs and symptoms: o Treatments RAAS and its relationship of potassium/ sodium o Aldosterone is a mineralocorticoid with potent sodium retaining and potassium excreting capabilities. Secretions of aldosterone may be simulated by the decreased renal perfusion or decreased sodium delivery to the distal portion of the renal tubule. The kidneys respond by secreting renin into the plasma. Angiotensinogen, produced in the liver and normally found in the blood is acted on by the renin to form angiotensin I which is converted to angiotensin II. It then stimulates the adrenal cortex to secrete aldosterone. Acid-Base Balance o Metabolic acidosis o Occurs when an acid other than carbonic acid accumulates in the body or when bicarbonate is lost from body fluids, In bith cases a bicarbonate deficit results. Ketoacid accumulate in diabetic ketoacidosis and lactic acid accumulation with shock are examples of accumulation of acids. Severe diarrhea results in loss of bicarbonate and secrete hydrogen ions. o Gain of fixed acid, inability to excrete acid or loss of base. S/S: neurologic (drowsiness, confusion, headache, coma), Cardiovascular (dec. bp, dysrhythmias[re;ated to hyperkalemia from compensation], warm flush skin [r/t peripheral vasodilation] ) GI (nausea, vomiting,

diarrhea, abdominal pain) Respiratory (deep, rapid respirations [compensatory action by the lungs]) Etiology: diabetic ketoacidosis, lactic acidosis, starvation, severe diarrhea, renal tubular acidosis, renal failure, GI fistulas, shock Blood gas interpretations: plasma pH: dec., PaCO2 normal, HCO3 dec.

o Metabolic alkalosis o Occurs when a loss of acid or a gain in bicarbonate occurs. o Loss of strong acid or gain of base S/S: neurologic ( dizziness, irritability, nervousness, confusion) cardiovascular (tachycardia, dysrhythmias r/t hypokalemia from compensation) GI (nausea, vomiting, anorexia) neuromuscular (tetany, tremors, tingling of fingers and toes, muscle cramps, hypertonic muscles and seizures) Etiology: severe vomiting, excessive gastric suctioning, diuretic therapy, potassium deficit, excessive NaHCO3 intake, excessive mineralo-corticoids Blood gas interpretations: plasma pH: ^, PaCO2 normal, HCO3: ^

o Respiratory acidosis o Occurs when there is hypoventilation. Hypoventilation results in a buildup of carbon dioxide; subsequently, carbon acid accumulates in the blood. Carbonic acid dissociates, liberating hydrogen ios, and there is a decrease in pH. If carbon dioxide is not eliminated from the blood, acidosis results from accumulation of carbonic acid. o Patho: CO2 retention from hypoventilation S/S: neuro (drowsiness, disorientation, dizziness, headache, coma) Cardiovascular ( dec. bp, ventricular fibrillation [related to hyperkalemia from compensation] warm flush skin r/e peripheral vasodilation) neuromuscular (seizures) Repiratory (hypoventilation

with hypoxia (lungs are unable to compensate when there is a resp. problem)) Etiology:causes: chronic obstructive pulmonary disease, barbiturate or sedative overdose, chest wall abnormality (obesity), severe pneumonia, atelectasis, respiratory muscle weakness, mechanical hypoventilation Blood gas interpretations: plasma pH dec., PaCO 2 ^, HCO3 normal (uncompensated)

o Respiratory alkalosis o Occurs with hyperventilation. The primary cause of respiratory alkalosis is hypoxemia from acute pulmonary disorders. Anxiety, CNS disorders, and the mechanical overventilation also increase the ventilation rate and decrease the partial pressure of arterial carbonic acid and alkalosis. o Increased CO2 excretion from hyperventilation o Patho: increased CO2 excretion from hyperventilation S/S: neurologic (lethargy, light-headedness, confusion ) cardiovascular (tachycardia, dysrhythmias r/t hypokalemia from compensation) GI (Nausea, vomiting, epigastric pain) Neuromuscular (tetany, numbness, tingling of extremities, hyperreflexia, seizures) respiratory (hyperventilation [lungs are unable to compensate when there is a respiratory problem]) Etiology: causes: hyperventilation (caused by hypoxia pulmonary emboli, anxiety, fear, pain, exercise, fever) stimulated respiratory caused by septicemia, encephalitis, brain injury, salicylate poisoning, mechanical hyperventilation Blood gas interpretations:plasma pH ^, PaCO2 dec, HCO3 normal (uncompensated)

Fluid volume status??? (I dont know what she I s looking for in this I cant find anything in the nook that says this specifically. If you guys can find it let me know ) o Components

o Indicators o Monitoring Genetics o Study of inheritance; study of genes o Autosomal recessive: are caused by mutations of two gene pairs on a chromosome. A person who inherits one copy of the recessive allele does not develop the disease because the normal allele predominates however this person is a carrier. Males and females are affected equally heterozygotes are carriers and usually asymptomatic. Affected individuals will have unaffected parents. 25% chance offspring of 2 heterozygous parents will be affected. 50% they will be carriers. Frequently there is a negative family history for disease. Examples: cystic fibrosis, tay-sachs disease, sickle cell disease. o Autosomal dominant: are caused by a mutation of a single gene pair on a chromosome. Males and females are equally affected. More common than recessive disorders and usually less severe. Affected individuals show variable expression. Incomplete penetrance in some conditions affected individuals may have an affected parent. Children of a heterozygous (affected parent) will have a 50% chance of being affected. Examples: Huntingtons disease, Breast and ovarian cancer related to BRCA genes o X-linked recessive: are caused by a mutation on the x chromosome. Usually only males are effected by this disorder because women who carry the mutated gene on one x chromosome have another x chromosome to compensate for the mutation. Women who carry the gene can transmit the mutation to their offspring Examples: Hemophilia, wiskott-aldrich syndrome o X-linked dominant: are very rare. (nothing in book or slides)

o Stem cells: cells in the body that have that ability to divide and remain a stem cell or differentiate into specialized cells such as brain cell o muscle cell. Perhaps the most important potential application of human stem cells is the generation of tissues that could be used for cell-based therapies. Embryonic stem cells have the ability to become any one of the hundreds of types of cells in the human body. They are derived from human embryo cells that are 4-5 days old. They are pluripotent and can differentiate into any cell type that they are stimulated to become Adult stem cells are undifferentiated cells that are found in small numbers in many adult organs and tissues including the brain, bone marrow, peripheral blood, blood vessels, skeletal muscles, skin, teeth, heart, gut, liver, ovarian epithelium, and testis. Their primary role is to maintain and repair tissue in which they are found. They are usually thought of as multipotent cells, giving rise to a closely related family of cells within the tissue.

o GINA The genetic information nondiscrimination act prohibits discrimination in health care coverage and employment based on genetic information. It prevents health insurers from denying coverage, adjusting premiums , and discriminating against a person solely based on his or her genetic or family history information. Prevents insurers from requesting that a person have a genetic test. Prohibits employers from using genetic information for hiring, firing, or promoting decisions regarding terms of employment. GINAs health coverage nondiscriminatory protection does not extend to life insurance, disability insurance, and long-term care insurance.

2/3/2013 9:32:00 AM Med-surg study guide Chapter 14, 17

2/3/2013 9:32:00 AM