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T2: F&E
Chapter 17 F& E
| Question | Answer |
|---|---|
| Cations | positively charged |
| anion | negatively charged |
| Example of cations | sodium (Na), potassium (K), calcium (Ca), and magnesium (Mg) |
| Examples of anions | bicarbonate (HCO3), chloride (Cl), and phosphate (PO4) |
| Prevalent cation in intracellular fluid (ICF). | potassium (K) |
| Prevalent anion in ICF. | phosphate (PO4) |
| Prevalent cation in extracellular fluid (ECF). | sodium (Na) |
| Prevalent anion in ECF. | chloride (Cl) |
| bicarbonate (HCO3) level | 22-26 mEq/L |
| Chloride (Cl) level | 96-106 mEq/L |
| Phosphate (PO4) level | 2.4-4.4 mg/dL |
| Potassium (K) level | 3.5-5.0 mEq/L |
| Magnesium (Mg) level | 1.5-2.5 mEq/L |
| Sodium (Na) level | 135-145 mEq/L |
| Total Calcium (Ca) level | 8.6-10.2 mg/dL |
| Ionized Ca level | 4.6-5.3 mg/dL |
| Movement of molecules from an area of high concentration to one of low concentration. | simple diffusion |
| Uses a protein carrier in the cell membrane to move molecules. | facilitated diffusion |
| Example of facilitated diffusion. | glucose transport into the cell. |
| Uses external energy to move molecules against the concentration gradient - from an area of low concentration to an area of high concentration. | active transport |
| Example of active transport. | sodium-potassium pump - ATP is used to move sodium out of the cell and potassium into the cell |
| The movement of water through a semipermeable membrane that does not allow solutes to cross. | osmosis |
| How does the water move in osmosis? | Water moves from the less concentration side (has more water) to the more concentrated side (has less water). This requires no energy. |
| When does osmosis stop? | When the concentration differences disappear or hydrostatis pressure builds sufficiently to oppose any further movement of water. |
| Amount of pressure required to stop osmotic flow of water. Determined by concentration of solutes in solution. | osmotic pressure |
| Fluids with the same osmolality, or tonicity, as the cell interior. There is no fluid movement with these fluids. | isotonic |
| Solutions in which the solutes are less concentrated than the cells are called. | hypotonic (hypoosmolar) |
| Solutions in which solutes are more concentrated than the cells are called. | hypertonic (hyperosmolar) |
| What happens to red blood cells in isotonic fluids? | there is no impact on the RBC |
| What happens to RBCs if they are surrounded by hypotonic fluid? | Water moves into the cell, causing it to swell and possibly to burst. |
| What happens to RBCs if they are surrounded by hypertonic fluid? | Water leaves the cell to dilute the ECF; the cell shrinks and eventually may die. |
| The blood pressure generated by the contraction of the heart. | hydrostatic pressure |
| What does hydrostatic pressure do at the capillary level? | Is the major force that pushes water out of the vascular system and into the interstitial space. |
| The osmotic pressure caused by plasma colloids in solution. The plasma protein molecules attract water, pulling fluid from the tissue space to the vascular space. | oncotic pressure aka colloidal osmotic pressure |
| The distribution of body water. | fluid spacing |
| The normal distribution of fluid in the ICF and ECF compartments. | first spacing |
| An abnormal accumulation of interstitial fluid (i.e. edema). | second spacing |
| When fluid accumulates in a portion of the body from which it is not easily exchanged with the rest of the ECF. The fluid is trapped and unavailable for functional use. (i.e. ascites) | third spacing |
| These in the hypothalamus sense a body fluid deficit or increase in plasma osmolality, which stimulates first and antidiuretic hormone release (ADH). | osmoreceptors |
| ADH is also called? | vasopressin |
| Where is ADH synthesized? | hypothalamus |
| Where is ADH stored? | posterior pituitary |
| What is the action of ADH? | Acts in the renal distal and collecting tubules causing water reabsorption. |
| If the plasma osmolality is decreased or there is water excess, what happens to ADH? | Secretion of ADH is suppressed, resulting in urinary excretion of water. |
| These are secreted by the adrenal cortex and help regulate both water and electrolytes. | glucocorticoids and mineralocorticoids |
| What is the primary effect of glucocorticoids (e.g. cortisol)? | Have an anti-inflammatory effect and increase serum glucose levels. |
| Example of mineralocorticoids. | aldosterone |
| What is the function of mineralocorticoids (aldosterone)? | Causes sodium retention and potassium excretion. Water is retained with sodium. |
| Decreased renal perfusion or decreased sodium delivery to the distal portion of the renal tubule activates what? | the renin-angiotensin-aldosterone system (RAAS) |
| What results due to the activation of the RAAS? | aldersterone is secreted |
| What else can stimulate the release of aldosterone? | Increased serum potassium, decreased serum sodium, and release of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland. |
| These are hormones produced by cardiomyocytes. | natriuretic peptides - ANP and BNP |
| Natriuretic peptides are natural antagonists to the RAAS and are produced in response to what? | Increased atrial pressure and high serum sodium levels. |
| What is the function of natriuretic peptides? | They suppress secretion of aldosterone, renin, and ADH, and the action of angiotensin II. |
| What is the function of natriuretic peptides in the renal tubules? | They promote excretion of sodium and water, resulting in a decrease blood volume and pressure. |
| The invisible vaporization from the lungs and skin that helps regulate body temperature. | insensible water loss |
| How much insensible water is lost in a day? | normally about 600-900 mL/day |
| In older adults structural changes to the kidney and a decrease in the renal blood flow lead to what? | A decrease in GFR, decrease in creatinine clearance, and the loss of ability to concentrate urine and conserve water. |
| What are some hormonal changes that can occur in older adults? | A decrease in renin and aldosterone, and an increase in ADH and ANP. |
| What are some electrolytes that can be lost or become imbalanced due to NG suction? | Na, K, H, and Cl |
| Abnormal loss of normal body fluids, inadequate intake, or plasma-to-interstitial fluid shift. | ECF volume deficit (hypovolemia) |
| Causes of fluid volume deficit. | Inc. insensible water loss or perspiration (high fever, heatstroke); DI; osmotic diuresis; hemorrhage; GI losses: vomiting, NG suction, diarrhea, fistula drainage; overuse of diuretics; inadequate fluid intake; 3rd space shifts: burns, intestinal obstruct |
| Clinical manifestations of hypovolemia. | Restless, drowsy, lethargy, confusion, thirst, dry mucous membranes, decreased skin turgor, dec cap refill, postural hypotension, inc pulse, dec CVP, dec UO, inc RR, weak, dizzy, weight loss, seizures, coma |
| Causes of ECF volume excess (hypervolemia). | Excess isotonic or hypotonic IV fluids, HF, renal failure, primary polydipsia, SIADH, Cushing syndrome, long term use of corticosteroids. |
| Clinical manifestations of hypervolemia. | Headache, confusion, lethargy, per. edema, JVD, bounding pulse, inc BP, inc CVP, polyuria (w/normal renal function), dyspnea, crackles, pulm. edema, muscle spasms, weight gain, seizures, coma |
| This solution is usually given to replace both water and any needed electrolytes. | Lactated Ringer's |
| This solution is used when rapid volume replacement is indicated. | isotonic (0.9%) sodium chloride |
| What is administered when volume loss is a result of blood loss? | blood |
| What is the treatment for hypovolemia? | replace water and electrolytes with balanced IV solutions (LR & NS) |
| What is the treatment for hypervolemia? | Remove fluid w/o changing electrolyte composition or osmolality of ECF. Diuretics & fluid restriction are primary forms of therapy, sodium intake restriction. |
| If fluid excess leads to ascites or pleural effusions what may need to be done? | an abdominal paracentesis or thoracentesis |
| What are some nursing interventions to monitor fluid deficiency or excess? | Monitor I&Os, monitor cardiovascular changes; assess resp. status; neurologic changes; daily weights; skin assessment |
| Urine specific gravity | 1.010-1.025 |
| A urine specific gravity that is greater than 1.025 indicates what? | concentrated urine |
| A urine specific gravity that is less than 1.010 indicates what? | dilute urine |
| What are some cardiovascular s/s to watch for with fluid volume excess/deficit? | Changes in BP, pulse force, and JVD. Orthostatic hypotension may be evident in patients w/fluid volume deficit. |
| What are some respiratory changes that may occur w/fluid volume excess? | Can result in pulmonary congestion & pulmonary edema as inc hydrostatic pressure forces fluid into the alveoli. The patient will experience SOB & moist crackles on auscultation. |
| What respiratory changes may occur with fluid volume deficit? | Increased respiratory rate as a result of decreased tissue perfusion and resultant hypoxia. |
| Changes in neurologic function may occur with fluid volume excess/deficit due to what? | cerebral edema or reduced cerebral tissue perfusion |
| When monitoring a patient for any neurologic changes due to fluid volume excess/deficit, what should be assessed? | the patient's LOC, pupillary response, and voluntary movement of extremities |
| Why is it important to monitor the patient's weight with hypervolemia? | Should be weighed the same time every day, wearing the same garments, & on the same scale. An increase of 1 kg (2.2 lb) is equal to 1000 mL (1L) of fluid retention (provided the pt has maintained a usual dietary intake or has been NPO) |
| hypernatremia | elevated serum sodium, may occur with water loss or sodium gain |
| What are some of the causes of hypernatremia? | Excess sodium intake, inadequate water loss, disease states |
| Excessive sodium intake with hypernatremia. | IV fluids: hypertonic NaCl, excessive isotonic NaCl, IV sodium bicarb; hypertonic tube feedings w/o water supplements; near drowning in salt water |
| Inadequate water intake with hypernatremia. | Can occur if the patient is unconscious or cognitively impaired . |
| Excessive water loss with hypernatremia (increased sodium concentration). | Increased insensible water loss (high fever, heatstroke, prolonged hyperventilation); osmotic diuretic therapy; diarrhea |
| What are some disease states that can cause hypernatremia? | Diabetes Insipidus (DI), primary hyperaldosteronism, Cushing syndrome, uncontrolled diabetes mellitus |
| What are some clinical manifestations of hypernatremia with decreased ECF volume? | restlessness, agitation, twitching, seizures, coma, intense thirst: dry, swollen tongue, sticky mucous membranes, postural hypotension, dec CVP, weight loss, inc pulse, weakness, lethargy |
| What are some clinical manifestations of hypernatremia with increased ECF volume? | restlessness, agitation, twitching, seizures, coma, intense thirst, flushed skin, weight gain, peripheral & pulmonary edema, inc BP, inc CVP |
| What is the treatment of hypernatremia? | Treat the underlying cause. In primary water deficit, fluid replacement orally or IV w/isotonic or hypotonic fluids (D5W, or 0.45% NaCl); if sodium excess dilute the NA conc. w/ D5W & excrete Na w/diuretics, monitor levels & pts response to therapy. |
| What is the greatest risk for patients who have developed hypernatremia over several days or longer? | Quickly reducing serum sodium levels can cause a rapid shift of water back into the cells, resulting in cerebral edema and neurologic complications. |
| Results from loss of sodium containing fluids and/or from water excess. | hyponatremia |
| What are some common causes of hyponatremia? | excessive sodium loss, inadequate sodium intake, excessive water gain (decreased sodium concentration), disease states |
| Causes for excessive sodium loss. | GI losses: diarrhea, vomiting, fistulas, NG suction; Renal losses: diuretics, adrenal insufficiency, Na wasting renal disease; skin losses: burns, wound drainage |
| Cause for inadequate sodium intake. | fasting diets |
| Cause excessive water gain (decrease sodium concentration) | excessive hypotonic IV fluids; primary polydipsia |
| What are some disease states that can cause hyponatremia? | SIADH, heart failure, primary hypoaldosteronism |
| What are the clinical manifestations of hyponatremia with decreased ECF volume? | irritability, apprehension, confusion, dizziness, personality changes, tremors, seizures, coma, dry mucous membranes, postural hypotension, dec CVP, dec jugular venous filling, inc pulse, thready pulse, cold & clammy skin |
| What are the clinical manifestations of hyponatremia with normal or increased ECF volume? | headache, apathy, confusion, muscle spasms, seizures, coma, N/V/D, abdominal cramps, weight gain, inc BP, inc CVP |
| What are the main s/s of hypernatremia? | thirst, lethargy, agitation, seizures, and coma, impaired LOC, symptoms of fluid volume deficit (dec skin turgor, weakness, hypotension) |
| What are the main s/s of hyponatremia? | confusion, irritability, headache, seizures, and coma |
| What is the treatment for hyponatremia caused by water excess? | fluid restriction |
| If severe symptoms (seizures) occurred in hyponatremia caused by water excess, how would you treat it? | Small amoutns of IV hypertonic saline solution (3% NaCl) can restore the serum sodium level while the body is returning to a normal water balance. |
| How would you treat hyponatremia associated with abnormal fluid loss? | fluid replacement with sodium containing solutions |
| This drug is used in hyponatremia to increase urine output w/o loss of electrolytes such as sodium & potassium. This should not be used in patients w/hyponatremia from excess water loss. | conivaptan (Vaprisol) |
| This drug is used in hyponatremia associated with heart failure, liver cirrhosis, and SIADH. | tolvaptan (Samsca) |
| Drug therapy for hyponatremia involves agents that block the activity of what? | ADH (vasopressin) |
| What is the major ICF cation? | potassium |
| What is potassium used for? | Transmission and conduction of nerve and muscle impulses, cellular growth, maintenance of cardiac rhythms, acid-base balance |
| This maintains the concentration difference by moving potassium into the cell and sodium out. | sodium-potassium pump |
| What functions are commonly affected by potassium imbalances? | neuromuscular and cardiac |
| Potassium is required for this to be deposited in muscle and liver cells. | glycogen |
| What are some good sources of potassium? | diet: mainly from fruits, dried fruits, & veggies; salt substitutes, parenteral sources: IV fluids, transfusion of stored, hemolyzed blood, and medications (e.g. potassium penicillin). |
| What is the primary route for potassium loss? | kidneys; eliminate 90% of daily K intake |
| What type of relationship does sodium and potassium have? | inverse |
| Factors that cause sodium retention (e.g. low blood volume, increased aldosterone level) causes what to happen with potassium? | causes potassium loss in the urine |
| Large urine volumes can be associated with excess loss of this in the urine. | potassium |
| If kidney function is significantly impaired what can happen to the potassium? | retained potassium can lead to toxic levels |
| What is the most common cause of hyperkalemia? | renal failure |
| What are some other causes of hyperkalemia? | Adrenal insufficiency: acidosis, massive cell destruction, and exercise can lead to shift of K from ICF to ECF, increasing K levels; digoxin like drugs & beta-adrenergic drugs; potassium sparing diuretics, ARBs, & ACEI |
| How does adrenal insufficiency lead to retention of K? | there is a subsequent aldosterone deficiency |
| Examples of massive cell destruction that can cause potassium retention. | burn or crush injury, tumor lysis, severe infections |
| In metabolic acidosis, potassium ions shift from the ICF to the ECF in exchange for these moving into the cell. | hydrogen ions |
| How do digoxin like drugs and beta-adrenergic blocking drugs result in a higher ECF potassium concentration? | they impair entry of potassium into cells |
| These drugs may inhibit the development of hyperkalemia by reducing the kidney's ability to excrete potassium. | K sparing diuretics (amiloride - Midamor, spironolactone - Aldactone), ARBs, and ACEI (enalapril - Vasotec, lisinopril (Prinivil) |
| What are some clinical manifestations of hyperkalemia? | irritability, anxiety, abdominal cramping, diarrhea, weakness of lower extremities, paresthesias, irregular pulse, cardiac arrest if hyperkalemia is sudden or severe |
| What are some ECG changes associated with hyperkalemia? | tall, peaked T wave; prolonged PRI; ST segment depression; loss of P wave; widening QRS; Vfib; ventricular standstill |
| What is the treatment of mild hyperkalemia with functioning kidneys? | It may be sufficient to withhold potassium from the diet and IV sources and increase renal elimination by administering fluids and possibly diuretics. |
| This drug is administered orally or rectally and binds to potassium in exchange for sodium and the resin is excreted in feces. | kayexelate |
| Patients with moderate hyperkalemia should be treated with this to force potassium into the cells. | IV insulin and glucose; sodium bicarb if the patient is acidotic |
| For patients that have significant hyperkalemia, what should they be monitored for? | Should be monitored for dysrhythmias and should receive IV calcium gluconate immediately. Monitor BP b/c rapid administration of calcium can cause hypotension. |
| What are the causes of hypokalemia? | Increased loss of K via the kidneys or GI tract (most common); increased shift of K from ECF to ICF; dietary K deficiency (rare); magnesium deficiency; metabolic alkalosis, skin loss: diaphoresis; dialysis |
| GI tract losses of potassium are associated with? | diarrhea, laxative abuse, vomiting, and ileostomy drainage |
| Renal loss of potassium occur when? | the patient has a low magnesium level or is diuresing, particularly in the patient with an elevated aldosterone level (hyperaldosteronism) |
| This is released when the circulating blood volume is low, causing sodium retention in the kidneys w/a loss of potassium in the urine. | aldosterone |
| Low plasma magnesium stimulates this, which results in potassium excretion. | stimulates renin release and subsequent increased aldosterone levels |
| What are some factors that cause potassium to move from the ECF to the ICF? | insulin therapy (esp in conjunction with diabetic ketoacidosis) & beta-adrenergic stimulation (catecholamine release in stress, coronary ischemia delirium tremens, admin of B-agonists) |
| This can cause a shift of K into cells in exchange for hydrogen, thus lowering the K in the ECF and causing symptomatic hypokalemia. | alkalosis |
| Lack of K intake for hypokalemia include: | starvation; diet low in K; failure to include K in parenteral fluids if NPO |
| Shift of K into cells for hypokalemia include: | increased insulin (e.g. IV dextrose load); alkalosis; tissue repair; increase epinephrine (e.g. stress) |
| What are some clinical manifestations of hypokalemia? | fatigue; muscle weakness, leg cramps; N/V, paralytic ileus; soft, flabby muscles; paresthesias, decreased reflexes; weak, irregular pulse; polyuria; hyperglycemia |
| Hypokalemia alters this, resulting in hyperpolarization (an increased negative charge w/i the cell) and impaired muscle contraction. CM involves changes in cardiac (most important) and muscle function. | the resting membrane potential |
| Skeletal muscle weakness and paralysis may occur with hypokalemia; initially affects what muscles? | leg muscles |
| Severe hypokalemia can cause weakness or paralysis of respiratory muscles which can lead to? | shallow respirations and respiratory arrest |
| How can hyperglycemia occur in hypokalemia? | Can impair function in nonmuscle tissue by impairing insulin secretion. |
| What ECG changes are associated with hypokalemia? | ST segment depression; flattened T wave; presence of U wave; prolonged QRS; ventricular dysrhythmias (e.g. PVCs); bradycardia |
| Treatment of hypokalemia consists of what? | Oral or IV KCl supplements and increased dietary intake of K. |
| Except in severe deficiencies, KCl is not given unless? | There is urine output of at least 0.5 mL/kg of body weight per hour |
| IV KCl must always be _____ and never given in ____ amounts. | diluted; concentrated |
| The rate of IV administration of KCl should not exceed what? | 10-20 mEq/hour and must be administered by infusion pump to ensure correct administration rate |
| Because KCl is irritating to the vein what should be assessed hourly? | assess IV sites for phlebitis and infiltration |
| Infiltration can cause what to the surrounding tissue? | necrosis & sloughing |
| What should be used when rapid correction of hypokalemia is necessary? | a central IV line |
| This is the major cation in the structure of bones and teeth. | Calcium (Ca) |
| What is the function of Ca? | formation of teeth and bone; blood clotting; transmission of nerve impulses; myocardial contractions; & muscle contractions |
| Calcium absorption requires the active form of what? | Vitamin D |
| What is the main source of calcium? | dietary intake |
| What are the sources of Vitamin D? | either ingested in the diet or formed in the skin in the presence of sunlight |
| What are the 3 forms of calcium? | free or ionized; bound to protein (primarily albumin); and complexed with phophate, citrate or carbonate |
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