Chapter 17 F& E
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| Cations | positively charged
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| anion | negatively charged
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| Example of cations | sodium (Na), potassium (K), calcium (Ca), and magnesium (Mg)
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| Examples of anions | bicarbonate (HCO3), chloride (Cl), and phosphate (PO4)
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| Prevalent cation in intracellular fluid (ICF). | potassium (K)
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| Prevalent anion in ICF. | phosphate (PO4)
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| Prevalent cation in extracellular fluid (ECF). | sodium (Na)
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| Prevalent anion in ECF. | chloride (Cl)
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| bicarbonate (HCO3) level | 22-26 mEq/L
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| Chloride (Cl) level | 96-106 mEq/L
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| Phosphate (PO4) level | 2.4-4.4 mg/dL
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| Potassium (K) level | 3.5-5.0 mEq/L
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| Magnesium (Mg) level | 1.5-2.5 mEq/L
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| Sodium (Na) level | 135-145 mEq/L
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| Total Calcium (Ca) level | 8.6-10.2 mg/dL
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| Ionized Ca level | 4.6-5.3 mg/dL
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| Movement of molecules from an area of high concentration to one of low concentration. | simple diffusion
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| Uses a protein carrier in the cell membrane to move molecules. | facilitated diffusion
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| Example of facilitated diffusion. | glucose transport into the cell.
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| Uses external energy to move molecules against the concentration gradient - from an area of low concentration to an area of high concentration. | active transport
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| Example of active transport. | sodium-potassium pump - ATP is used to move sodium out of the cell and potassium into the cell
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| The movement of water through a semipermeable membrane that does not allow solutes to cross. | osmosis
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| 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.
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| When does osmosis stop? | When the concentration differences disappear or hydrostatis pressure builds sufficiently to oppose any further movement of water.
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| Amount of pressure required to stop osmotic flow of water. Determined by concentration of solutes in solution. | osmotic pressure
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| Fluids with the same osmolality, or tonicity, as the cell interior. There is no fluid movement with these fluids. | isotonic
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| Solutions in which the solutes are less concentrated than the cells are called. | hypotonic (hypoosmolar)
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| Solutions in which solutes are more concentrated than the cells are called. | hypertonic (hyperosmolar)
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| What happens to red blood cells in isotonic fluids? | there is no impact on the RBC
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| What happens to RBCs if they are surrounded by hypotonic fluid? | Water moves into the cell, causing it to swell and possibly to burst.
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| 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.
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| The blood pressure generated by the contraction of the heart. | hydrostatic pressure
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| 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.
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| 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
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| The distribution of body water. | fluid spacing
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| The normal distribution of fluid in the ICF and ECF compartments. | first spacing
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| An abnormal accumulation of interstitial fluid (i.e. edema). | second spacing
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| 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
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| These in the hypothalamus sense a body fluid deficit or increase in plasma osmolality, which stimulates first and antidiuretic hormone release (ADH). | osmoreceptors
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| ADH is also called? | vasopressin
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| Where is ADH synthesized? | hypothalamus
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| Where is ADH stored? | posterior pituitary
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| What is the action of ADH? | Acts in the renal distal and collecting tubules causing water reabsorption.
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| 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.
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| These are secreted by the adrenal cortex and help regulate both water and electrolytes. | glucocorticoids and mineralocorticoids
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| What is the primary effect of glucocorticoids (e.g. cortisol)? | Have an anti-inflammatory effect and increase serum glucose levels.
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| Example of mineralocorticoids. | aldosterone
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| What is the function of mineralocorticoids (aldosterone)? | Causes sodium retention and potassium excretion. Water is retained with sodium.
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| Decreased renal perfusion or decreased sodium delivery to the distal portion of the renal tubule activates what? | the renin-angiotensin-aldosterone system (RAAS)
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| What results due to the activation of the RAAS? | aldersterone is secreted
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| 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.
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| These are hormones produced by cardiomyocytes. | natriuretic peptides - ANP and BNP
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| Natriuretic peptides are natural antagonists to the RAAS and are produced in response to what? | Increased atrial pressure and high serum sodium levels.
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| What is the function of natriuretic peptides? | They suppress secretion of aldosterone, renin, and ADH, and the action of angiotensin II.
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| 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.
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| The invisible vaporization from the lungs and skin that helps regulate body temperature. | insensible water loss
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| How much insensible water is lost in a day? | normally about 600-900 mL/day
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| 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.
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| What are some hormonal changes that can occur in older adults? | A decrease in renin and aldosterone, and an increase in ADH and ANP.
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| What are some electrolytes that can be lost or become imbalanced due to NG suction? | Na, K, H, and Cl
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| Abnormal loss of normal body fluids, inadequate intake, or plasma-to-interstitial fluid shift. | ECF volume deficit (hypovolemia)
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| 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
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| 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
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| 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.
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| 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
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| This solution is usually given to replace both water and any needed electrolytes. | Lactated Ringer's
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| This solution is used when rapid volume replacement is indicated. | isotonic (0.9%) sodium chloride
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| What is administered when volume loss is a result of blood loss? | blood
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| What is the treatment for hypovolemia? | replace water and electrolytes with balanced IV solutions (LR & NS)
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| 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.
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| If fluid excess leads to ascites or pleural effusions what may need to be done? | an abdominal paracentesis or thoracentesis
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| 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
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| Urine specific gravity | 1.010-1.025
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| A urine specific gravity that is greater than 1.025 indicates what? | concentrated urine
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| A urine specific gravity that is less than 1.010 indicates what? | dilute urine
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| 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.
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| 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.
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| What respiratory changes may occur with fluid volume deficit? | Increased respiratory rate as a result of decreased tissue perfusion and resultant hypoxia.
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| Changes in neurologic function may occur with fluid volume excess/deficit due to what? | cerebral edema or reduced cerebral tissue perfusion
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| 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
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| 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)
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| hypernatremia | elevated serum sodium, may occur with water loss or sodium gain
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| What are some of the causes of hypernatremia? | Excess sodium intake, inadequate water loss, disease states
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| 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
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| Inadequate water intake with hypernatremia. | Can occur if the patient is unconscious or cognitively impaired .
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| Excessive water loss with hypernatremia (increased sodium concentration). | Increased insensible water loss (high fever, heatstroke, prolonged hyperventilation); osmotic diuretic therapy; diarrhea
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| What are some disease states that can cause hypernatremia? | Diabetes Insipidus (DI), primary hyperaldosteronism, Cushing syndrome, uncontrolled diabetes mellitus
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| 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
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| 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
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| 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.
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| 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.
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| Results from loss of sodium containing fluids and/or from water excess. | hyponatremia
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| What are some common causes of hyponatremia? | excessive sodium loss, inadequate sodium intake, excessive water gain (decreased sodium concentration), disease states
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| 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
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| Cause for inadequate sodium intake. | fasting diets
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| Cause excessive water gain (decrease sodium concentration) | excessive hypotonic IV fluids; primary polydipsia
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| What are some disease states that can cause hyponatremia? | SIADH, heart failure, primary hypoaldosteronism
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| 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
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| 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
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| 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)
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| What are the main s/s of hyponatremia? | confusion, irritability, headache, seizures, and coma
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| What is the treatment for hyponatremia caused by water excess? | fluid restriction
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| 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.
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| How would you treat hyponatremia associated with abnormal fluid loss? | fluid replacement with sodium containing solutions
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| 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)
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| This drug is used in hyponatremia associated with heart failure, liver cirrhosis, and SIADH. | tolvaptan (Samsca)
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| Drug therapy for hyponatremia involves agents that block the activity of what? | ADH (vasopressin)
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| What is the major ICF cation? | potassium
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| What is potassium used for? | Transmission and conduction of nerve and muscle impulses, cellular growth, maintenance of cardiac rhythms, acid-base balance
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| This maintains the concentration difference by moving potassium into the cell and sodium out. | sodium-potassium pump
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| What functions are commonly affected by potassium imbalances? | neuromuscular and cardiac
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| Potassium is required for this to be deposited in muscle and liver cells. | glycogen
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| 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).
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| What is the primary route for potassium loss? | kidneys; eliminate 90% of daily K intake
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| What type of relationship does sodium and potassium have? | inverse
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| 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
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| Large urine volumes can be associated with excess loss of this in the urine. | potassium
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| If kidney function is significantly impaired what can happen to the potassium? | retained potassium can lead to toxic levels
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| What is the most common cause of hyperkalemia? | renal failure
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| 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
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| How does adrenal insufficiency lead to retention of K? | there is a subsequent aldosterone deficiency
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| Examples of massive cell destruction that can cause potassium retention. | burn or crush injury, tumor lysis, severe infections
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| In metabolic acidosis, potassium ions shift from the ICF to the ECF in exchange for these moving into the cell. | hydrogen ions
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| How do digoxin like drugs and beta-adrenergic blocking drugs result in a higher ECF potassium concentration? | they impair entry of potassium into cells
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| 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)
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| 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
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| 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
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| 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.
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| This drug is administered orally or rectally and binds to potassium in exchange for sodium and the resin is excreted in feces. | kayexelate
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| 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
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| 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.
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| 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
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| GI tract losses of potassium are associated with? | diarrhea, laxative abuse, vomiting, and ileostomy drainage
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| 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)
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| 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
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| Low plasma magnesium stimulates this, which results in potassium excretion. | stimulates renin release and subsequent increased aldosterone levels
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| 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)
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| 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
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| Lack of K intake for hypokalemia include: | starvation; diet low in K; failure to include K in parenteral fluids if NPO
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| Shift of K into cells for hypokalemia include: | increased insulin (e.g. IV dextrose load); alkalosis; tissue repair; increase epinephrine (e.g. stress)
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| 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
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| 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
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| Skeletal muscle weakness and paralysis may occur with hypokalemia; initially affects what muscles? | leg muscles
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| Severe hypokalemia can cause weakness or paralysis of respiratory muscles which can lead to? | shallow respirations and respiratory arrest
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| How can hyperglycemia occur in hypokalemia? | Can impair function in nonmuscle tissue by impairing insulin secretion.
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| 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
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| Treatment of hypokalemia consists of what? | Oral or IV KCl supplements and increased dietary intake of K.
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| 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
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| IV KCl must always be _____ and never given in ____ amounts. | diluted; concentrated
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| 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
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| Because KCl is irritating to the vein what should be assessed hourly? | assess IV sites for phlebitis and infiltration
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| Infiltration can cause what to the surrounding tissue? | necrosis & sloughing
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| What should be used when rapid correction of hypokalemia is necessary? | a central IV line
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| This is the major cation in the structure of bones and teeth. | Calcium (Ca)
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| What is the function of Ca? | formation of teeth and bone; blood clotting; transmission of nerve impulses; myocardial contractions; & muscle contractions
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| Calcium absorption requires the active form of what? | Vitamin D
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| What is the main source of calcium? | dietary intake
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| What are the sources of Vitamin D? | either ingested in the diet or formed in the skin in the presence of sunlight
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| 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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