Ch 03

Question 1

A 55-year-old patient with chronic heart failure presents with bilateral lower extremity edema. Which pathophysiological mechanism is primarily responsible for this edema formation?

A. Decreased capillary hydrostatic pressure due to vasodilation
B. Increased capillary hydrostatic pressure from venous congestion
C. Increased plasma oncotic pressure from hyperalbuminemia
D. Decreased interstitial hydrostatic pressure from lymphatic drainage

Answer 1

Correct Answer: B. Increased capillary hydrostatic pressure from venous congestion

Rationale: In heart failure, impaired cardiac output leads to venous congestion, elevating capillary hydrostatic pressure, which opposes reabsorption and favors filtration per Starling’s forces. This is a graduate-level concept emphasizing how backward failure in the right ventricle contributes to peripheral edema, distinguishing it from forward failure symptoms like fatigue.

Question 2

In a patient with liver cirrhosis, edema develops primarily due to:

A. Increased hydrostatic pressure in the portal vein
B. Decreased plasma oncotic pressure from hypoalbuminemia
C. Enhanced lymphatic clearance of interstitial fluid
D. Reduced osmotic gradient favoring fluid reabsorption

Answer 2

Correct Answer: B. Decreased plasma oncotic pressure from hypoalbuminemia

Rationale: Liver cirrhosis impairs albumin synthesis, reducing plasma oncotic pressure, which normally draws fluid back into capillaries. This imbalance shifts Starling forces toward filtration, leading to ascites and peripheral edema. Advanced practice nurses must recognize this to guide diuretic therapy and albumin infusions while monitoring for complications like hepatorenal syndrome.

Question 3

A patient with deep vein thrombosis develops unilateral leg edema due to venous obstruction. This is best explained by:

A. Decreased osmotic pressure in the interstitial space
B. Increased hydrostatic pressure in the capillary bed
C. Enhanced permeability of the lymphatic vessels
D. Reduced oncotic pressure in the plasma compartment

Answer 3

Correct Answer: B. Increased hydrostatic pressure in the capillary bed

Rationale: Venous obstruction elevates upstream hydrostatic pressure, disrupting Starling’s equilibrium and promoting fluid leakage into the interstitium. APRNs should integrate this with Doppler ultrasound findings to differentiate from other causes like cellulitis, ensuring timely anticoagulation to prevent pulmonary embolism.

Question 4

In lymphatic obstruction, such as in filariasis, interstitial edema occurs primarily because:

A. Hydrostatic pressure decreases in the capillaries
B. Oncotic pressure increases in the interstitial fluid
C. Fluid accumulation exceeds lymphatic drainage capacity
D. Osmotic gradients favor rapid reabsorption into veins

Answer 4

Correct Answer: C. Fluid accumulation exceeds lymphatic drainage capacity

Rationale: Lymphatic dysfunction impairs protein and fluid clearance from the interstitium, leading to high-protein edema (lymphedema). This contrasts with low-protein edema in hypoalbuminemia, guiding APRNs toward compression therapy and surgical options while assessing for secondary infections in chronic cases.

Question 5

Infants are more prone to dehydration because:

A. Their TBW percentage is lower due to higher body fat
B. They have a higher TBW percentage and greater fluid turnover
C. Muscle mass increases TBW stability with age
D. Renal concentrating ability is mature at birth

Answer 5

Correct Answer: B. They have a higher TBW percentage and greater fluid turnover

Rationale: Infants have ~75-80% TBW (versus 60% in adults), with immature renal function amplifying fluid losses from diarrhea or fever. APRNs must calculate maintenance fluids using Holliday-Segar formula, adjusting for insensible losses to prevent hyponatremic seizures in graduate-level pediatric care.

Question 6

An elderly patient with reduced muscle mass is at risk for overhydration because:

A. TBW increases with age due to fat accumulation
B. Decreased TBW percentage leads to concentrated electrolytes
C. Higher body fat reduces fluid distribution volume
D. Increased renal excretion prevents fluid retention

Answer 6

Correct Answer: C. Higher body fat reduces fluid distribution volume

Rationale: Aging decreases muscle (high water content) and increases fat (low water), reducing TBW and predisposing to dilutional hyponatremia with excess fluids. This informs APRN fluid prescribing in geriatrics, emphasizing osmolality monitoring to avoid cerebral edema.

Question 7

Net filtration in capillaries is increased by:

A. Elevated oncotic pressure in plasma
B. Reduced hydrostatic pressure gradients
C. Forces favoring filtration exceeding opposing forces
D. Pharmacological enhancement of lymphatic flow

Answer 7

Correct Answer: C. Forces favoring filtration exceeding opposing forces

Rationale: Starling’s equation (net filtration = Kf[(Pc - Pi) - (πp - πi)]) shows imbalance when hydrostatic push (Pc) > oncotic pull (πp), as in hypertension. APRNs apply this in differential diagnosis of pitting versus non-pitting edema.

Question 8

In treating edema with loop diuretics like furosemide, the primary effect on Starling forces is:

A. Increasing plasma oncotic pressure
B. Decreasing capillary hydrostatic pressure via volume reduction
C. Enhancing capillary permeability
D. Promoting osmotic diuresis without affecting filtration

Answer 8

Correct Answer: B. Decreasing capillary hydrostatic pressure via volume reduction

Rationale: Diuretics reduce intravascular volume, lowering Pc and shifting balance toward reabsorption. Graduate-level rationale includes monitoring for hypokalemia and acute kidney injury, integrating with RAAS inhibitors for synergistic effects in heart failure management.

Question 9

A patient with nephrotic syndrome develops edema due to:

A. Venous obstruction increasing hydrostatic pressure
B. Plasma protein losses reducing oncotic pressure
C. Lymphatic obstruction from infection
D. Increased vascular volume from hyperaldosteronism

Answer 9

Correct Answer: B. Plasma protein losses reducing oncotic pressure

Rationale: Nephrotic syndrome involves glomerular damage, proteinuria (>3.5g/day), and hypoalbuminemia, diminishing πp. APRNs target with ACE inhibitors to reduce proteinuria, monitoring lipid profiles for cardiovascular risks.

Question 10

Increased capillary membrane permeability leading to edema is exemplified by:

A. Burns causing protein leakage
B. Heart failure with venous congestion
C. Liver failure with hypoalbuminemia
D. Renal failure with fluid overload

Answer 10

Correct Answer: A. Burns causing protein leakage

Rationale: Inflammation increases permeability, allowing proteins into interstitium and equalizing oncotic gradients. This high-protein edema requires APRN-led fluid resuscitation with colloids, preventing hypovolemic shock while addressing infection risks.

Question 11

In response to hypovolemia, sodium reabsorption is primarily promoted by:

A. Atrial natriuretic hormone (ANH) secretion
B. Aldosterone via the renin-angiotensin system
C. Decreased renin release from juxtaglomerular cells
D. Enhanced urinary excretion of sodium

Answer 11

Correct Answer: B. Aldosterone via the renin-angiotensin system

Question 12

ANH regulates sodium by:

A. Promoting renal tubular reabsorption
B. Inhibiting aldosterone and promoting natriuresis
C. Increasing angiotensin II production
D. Decreasing glomerular filtration rate

Answer 12

Correct Answer: B. Inhibiting aldosterone and promoting natriuresis

Rationale: ANH, released from atria in hypervolemia, counters RAAS by natriuresis and vasodilation. Graduate rationale involves its role in heart failure, where nesiritide (ANH analog) may be considered for decongestion.

Question 13

SIADH is characterized by:

A. Hypertonic hyponatremia with euvolemia
B. Hypotonic hyponatremia with hypervolemia
C. Isotonic hyponatremia with pseudohyponatremia
D. Hypertonic hypernatremia with dehydration

Answer 13

Correct Answer: A. Hypertonic hyponatremia with euvolemia

Rationale: Inappropriate ADH causes water retention, diluting serum Na+ without volume expansion signs. APRNs differentiate via urine osmolality (>100 mOsm/kg), treating with fluid restriction or vaptans.

Question 14

Diabetes insipidus typically presents with:

A. Hypotonic hyponatremia from water retention
B. Hypertonic hypernatremia from water loss
C. Isotonic fluid balance with normal sodium
D. Hypotonic state from solute diuresis

Answer 14

Correct Answer: B. Hypertonic hypernatremia from water loss

Rationale: Deficient ADH or renal response leads to dilute urine and hyperosmolality. Central versus nephrogenic distinction guides desmopressin use, with APRNs calculating free water deficit for correction.

Question 15

Hypovolemic hypernatremia (Na+ >145 mEq/L) is treated by:

A. Rapid infusion of hypertonic saline
B. Volume replacement with isotonic fluids followed by hypotonic correction
C. Immediate use of loop diuretics
D. Restriction of free water intake

Answer 15

Correct Answer: B. Volume replacement with isotonic fluids followed by hypotonic correction

Rationale: Restore volume first to prevent shock, then correct Na+ slowly (≤10 mEq/L/day) to avoid demyelination. APRNs integrate with osmolality checks.

Question 16

Risks of rapid correction in euvolemic hypernatremia include:

A. Cerebral edema from osmotic shifts
B. Dehydration from excessive diuresis
C. Hyperkalemia from cell shifts
D. Hypotension from volume depletion

Answer 16

Correct Answer: A. Cerebral edema from osmotic shifts

Rationale: Rapid hypotonic fluid lowers serum osmolality, drawing water into brain cells. Graduate-level care emphasizes correction rates ≤0.5 mEq/L/hr in chronic cases.

Question 17

In dilutional hyponatremia (<135 mEq/L), cerebral edema occurs due to:

A. Hyperosmotic extracellular fluid drawing water out of cells
B. Hypoosmotic plasma causing water influx into brain cells
C. Increased sodium excretion overwhelming reabsorption
D. Decreased ADH suppressing water retention

Answer 17

B. Hypoosmotic plasma causing water influx into brain cells

Rationale: Low serum osmolality creates a gradient, leading to cell swelling and seizures. APRNs assess symptom severity for 3% saline use.

Question 18

To prevent osmotic demyelination in hyponatremia correction, guidelines recommend:

A. Rapid elevation of Na+ by 18-20 mEq/L in 24 hours
B. Limiting Na+ rise to 6-8 mEq/L in 24 hours
C. Exclusive use of hypertonic saline without monitoring
D. Ignoring urine output during correction

Answer 18

B. Limiting Na+ rise to 6-8 mEq/L in 24 hours

Rationale: Overcorrection risks pontine myelinolysis; monitor hourly Na+ and use DDAVP if overcorrecting, per expert consensus.

Question 19

In metabolic alkalosis, chloride levels typically:

A. Increase proportionally with sodium retention
B. Decrease due to bicarbonate-chloride exchange
C. Remain stable independent of pH changes
D. Rise from enhanced renal reabsorption

Answer 19

B. Decrease due to bicarbonate-chloride exchange

Rationale: Renal compensation in alkalosis involves Cl- loss for HCO3- retention. APRNs recognize in vomiting, prescribing saline.

Question 20

Implications of chloride dysregulation in acid-base homeostasis include:

A. Compensatory respiratory acidosis in hypochloremia
B. Worsened metabolic alkalosis in chloride depletion
C. No effect on bicarbonate buffering
D. Direct causation of respiratory alkalosis

Answer 20

B. Worsened metabolic alkalosis in chloride depletion

Rationale: Low Cl- impairs HCO3- excretion, perpetuating alkalosis. Graduate care involves acetazolamide to promote bicarbonaturia.

Question 21

Insulin regulates potassium by:

A. Promoting renal excretion in the distal tubule
B. Facilitating cellular uptake into skeletal muscle and liver
C. Inhibiting aldosterone-mediated shifts
D. Enhancing gastrointestinal absorption

Answer 21

B. Facilitating cellular uptake into skeletal muscle and liver

Rationale: Insulin activates Na+/K+-ATPase, shifting K+ intracellularly. APRNs use in hyperkalemia, monitoring glucose.

Question 22

Aldosterone’s role in potassium balance is to:

A. Increase K+ reabsorption in the proximal tubule
B. Promote K+ secretion in the distal tubule
C. Decrease K+ uptake in ICF compartments
D. Stabilize membrane potentials without excretion

Answer 22

B. Promote K+ secretion in the distal tubule

Rationale: Aldosterone enhances ENaC and ROMK channels for K+ secretion. In hypoaldosteronism, hyperkalemia ensues, treated with fludrocortisone.

Question 23

Hypokalemia (<3.5 mEq/L) affects cardiac function by:

A. Shortening the QT interval
B. Predisposing to U waves and arrhythmias
C. Stabilizing membrane potentials
D. Causing peaked T waves

Answer 23

B. Predisposing to U waves and arrhythmias

Rationale: Low K+ prolongs repolarization, risking torsades. APRNs correlate with digoxin toxicity.

Question 24

Hyperkalemia (>5.0 mEq/L) impacts neuromuscular function through:

A. Hyperpolarization leading to muscle spasms
B. Depolarization causing weakness or paralysis
C. No effect on action potentials
D. Enhanced acetylcholine release

Answer 24

B. Depolarization causing weakness or paralysis

Rationale: High K+ reduces resting potential gradient, inactivating Na+ channels. Emergency calcium stabilizes membranes.

Question 25

Decreased potassium intake leading to hypokalemia is exacerbated by: A. High aldosterone suppressing shifts B. Diuretics increasing renal losses C. Acidosis promoting cellular uptake D. Insulin deficiency

Answer 25

B. Diuretics increasing renal losses Rationale: Loop/thiazides block reabsorption; APRNs replace K+ orally/IV, monitoring ECG.

Question 26

Diagnostic algorithms for hypokalemia differentiation include: A. Ignoring urine K+ levels B. Measuring urine K+ to distinguish renal vs. extrarenal losses C. Sole reliance on serum aldosterone D. Excluding transcellular shifts

Answer 26

B. Measuring urine K+ to distinguish renal vs. extrarenal losses Rationale: Urine K+ >20 mEq/L suggests renal loss (e.g., hyperaldosteronism). TTKG refines diagnosis.

Question 27

In acute kidney injury, hyperkalemia occurs due to: A. Increased renal excretion B. Decreased glomerular filtration reducing K+ clearance C. Enhanced aldosterone secretion D. Cellular uptake shifts

Answer 27

B. Decreased glomerular filtration reducing K+ clearance Rationale: Oliguria impairs excretion; APRNs initiate kayexalate or dialysis.

Question 28

Electrocardiographic manifestations of hyperkalemia include: A. Flat T waves and short PR interval B. Peaked T waves and widened QRS C. U waves and prolonged QT D. Normal sinus rhythm without changes

Answer 28

B. Peaked T waves and widened QRS Rationale: Progressive changes risk asystole; calcium gluconate is first-line stabilization.

Question 29

Parathyroid hormone (PTH) maintains calcium by: A. Decreasing bone resorption B. Increasing renal calcium excretion C. Promoting bone resorption and renal reabsorption D. Inhibiting vitamin D activation

Answer 29

C. Promoting bone resorption and renal reabsorption Rationale: PTH activates osteoclasts and distal tubule reabsorption; APRNs assess in hyperparathyroidism.

Question 30

Calcitonin counters hypercalcemia by: A. Enhancing intestinal calcium absorption B. Inhibiting osteoclast activity C. Promoting renal calcium loss D. Stimulating PTH release

Answer 30

B. Inhibiting osteoclast activity Rationale: Reduces bone release; used in hypercalcemia management with bisphosphonates.

Question 31

Hypocalcemia (<9.0 mg/dL total) from inadequate intestinal absorption is seen in: A. Vitamin D excess B. Malabsorption syndromes like celiac disease C. Hyperparathyroidism D. Bone metastases

Answer 31

B. Malabsorption syndromes like celiac disease Rationale: Fat malabsorption impairs vitamin D; treat with ergocalciferol.

Question 32

Association of hypocalcemia with hypothyroidism involves: A. Increased PTH secretion B. Reduced calcitonin C. Impaired vitamin D metabolism D. Enhanced phosphate excretion

Answer 32

Impaired vitamin D metabolism Rationale: Thyroid hormone deficiency affects hydroxylation; monitor TSH and calcium.

Question 33

Hypercalcemia (>10.5 mg/dL) symptoms like renal calculi result from: A. Decreased urinary calcium excretion B. Increased bone resorption and hypercalciuria C. Reduced intestinal absorption D. PTH suppression

Answer 33

B. Increased bone resorption and hypercalciuria Rationale: Excess Ca2+ overwhelms reabsorption; hydrate to dilute.

Question 34

Bisphosphonates treat hypercalcemia by: A. Enhancing osteoclast activity B. Inhibiting bone resorption C. Promoting vitamin D synthesis D. Increasing renal excretion

Answer 34

B. Inhibiting bone resorption Rationale: Bind hydroxyapatite, apoptosis of osteoclasts; APRNs monitor jaw necrosis.

Question 35

Hypophosphatemia (<2.0 mg/dL) causes in critical care include: A. Reduced renal losses B. Refeeding syndrome with cellular uptake C. Decreased intestinal absorption D. Hyperparathyroidism suppressing shifts

Answer 35

Correct Answer: B. Refeeding syndrome with cellular uptake Rationale: Insulin drives phosphate intracellularly; supplement IV.

Question 36

Clinical implications of hypophosphatemia involve: A. Enhanced muscle strength B. Respiratory failure from diaphragm weakness C. No effect on ATP production D. Stabilized cell membranes

Answer 36

Correct Answer: B. Respiratory failure from diaphragm weakness Rationale: Low ATP impairs contractility; APRNs replete before weaning ventilation.

Question 37

Hyperphosphatemia (>4.5 mg/dL) in chronic kidney disease leads to: A. Primary hypoparathyroidism B. Secondary hyperparathyroidism from PTH stimulation C. Decreased vascular calcification D. Enhanced bone density

Answer 37

Correct Answer: B. Secondary hyperparathyroidism from PTH stimulation Rationale: High phosphate lowers Ca2+, stimulating PTH; use binders like sevelamer.

Question 38

Mechanisms in renal failure include: A. Increased glomerular filtration B. Reduced phosphate excretion C. Suppressed PTH D. Vitamin D activation

Answer 38

Correct Answer: B. Reduced phosphate excretion Rationale: Low GFR accumulates phosphate; dialysis indications include refractory levels.

Question 39

Hypomagnesemia (<1.5 mEq/L) causes include: A. Enhanced renal reabsorption B. Malabsorption syndromes like Crohn's C. Decreased enzymatic reactions D. Hypercalcemia suppression

Answer 39

Correct Answer: B. Malabsorption syndromes like Crohn's Rationale: GI losses deplete Mg2+; repletes with oral/IV, monitoring arrhythmias.

Question 40

Hypermagnesemia (>3.0 mEq/L) effects on systems: A. Enhanced neuromuscular excitability B. Hypotension and bradycardia from smooth muscle relaxation C. No cardiovascular impact D. Increased deep tendon reflexes

Answer 40

Correct Answer: B. Hypotension and bradycardia from smooth muscle relaxation Rationale: Blocks Ca2+ channels; treat with calcium in overdose.

Question 41

pH is defined as: A. Positive logarithm of H+ concentration B. Negative logarithm of H+ concentration C. Direct measure of H+ ions D. Independent of buffering

Answer 41

Correct Answer: B. Negative logarithm of H+ concentration Rationale: pH = -log[H+]; small changes reflect large H+ shifts, guiding ABG interpretation.

Question 42

Body buffers acute pH changes via: A. Exclusive renal excretion B. Bicarbonate, protein, and phosphate systems C. Lungs alone D. No immediate mechanisms

Answer 42

Correct Answer: B. Bicarbonate, protein, and phosphate systems Rationale: Immediate buffering; APRNs use Henderson-Hasselbalch for prediction.

Question 43

Bicarbonate buffer compensates by: A. Releasing H+ in acidosis B. Binding H+ in acidosis to form carbonic acid C. No role in pH maintenance D. Exclusive metabolic function

Answer 43

Correct Answer: B. Binding H+ in acidosis to form carbonic acid Rationale: H+ + HCO3- ⇌ H2CO3 ⇌ CO2 + H2O; lungs exhale CO2.

Question 44

Kidneys compensate respiratory acidosis by: A. Decreasing HCO3- reabsorption B. Increasing HCO3- generation and H+ excretion C. Promoting CO2 retention D. Reducing glutamine metabolism

Answer 44

Correct Answer: B. Increasing HCO3- generation and H+ excretion Rationale: Takes days; APRNs monitor in COPD exacerbations.

Question 45

Respiratory acidosis in COPD is due to: A. Hyperventilation increasing CO2 elimination B. Hypoventilation causing CO2 retention C. Metabolic compensation alone D. Reduced bicarbonate levels

Answer 45

Correct Answer: B. Hypoventilation causing CO2 retention Rationale: pCO2 >45 mmHg lowers pH; BiPAP supports ventilation.

Question 46

Renal compensation involves: A. Decreased H+ secretion B. Increased bicarbonate reabsorption C. Promotion of alkalosis D. No change in pH

Answer 46

Correct Answer: B. Increased bicarbonate reabsorption Rationale: Raises HCO3- to normalize pH; chronic in COPD.

Question 47

In diabetic ketoacidosis, metabolic acidosis occurs from: A. Bicarbonate gain B. Accumulation of ketoacids C. CO2 retention D. Hydrogen loss

Answer 47

Correct Answer: B. Accumulation of ketoacids Rationale: Beta-hydroxybutyrate consumes HCO3-; insulin resolves.

Question 48

Anion gap calculation aids in: A. Ignoring unmeasured anions B. Differentiating causes like lactic acidosis (high gap) vs. diarrhea (normal gap) C. Excluding renal failure D. Direct bicarbonate therapy indication

Answer 48

Correct Answer: B. Differentiating causes like lactic acidosis (high gap) vs. diarrhea (normal gap) Rationale: AG = Na+ - (Cl- + HCO3-); >12 suggests organic acids.

Question 49

Respiratory alkalosis from anxiety is caused by: A. CO2 retention B. Hyperventilation decreasing pCO2 C. Bicarbonate loss D. Hydrogen gain

Answer 49

Correct Answer: B. Hyperventilation decreasing pCO2 Rationale: pCO2 <35 mmHg raises pH; rebreathing calms.

Question 50

Metabolic alkalosis differs by: A. Primary respiratory compensation B. Bicarbonate increase or H+ loss, e.g., vomiting C. No renal involvement D. Immediate resolution

Answer 50

Correct Answer: B. Bicarbonate increase or H+ loss, e.g., vomiting Rationale: Gastric H+ loss; saline-responsive if volume-depleted.

Question 51

In severe diarrhea, the stepwise management includes: A. Immediate potassium replacement without fluids B. Fluid resuscitation, then electrolyte correction, with monitoring C. Ignoring acid-base status D. Diuretics to enhance losses

Answer 51

Correct Answer: B. Fluid resuscitation, then electrolyte correction, with monitoring Rationale: Isotonic saline restores volume; K+ after urine output, ABG guides.

Question 52

Hypokalemia in this scenario worsens: A. Metabolic alkalosis B. Metabolic acidosis from bicarbonate loss C. Respiratory compensation D. No acid-base impact

Answer 52

Correct Answer: B. Metabolic acidosis from bicarbonate loss Rationale: Diarrhea loses HCO3-, low K+ shifts H+ extracellularly worsening acidosis.

Question 53

In SIADH, ADH dysregulation causes: A. Water excretion leading to dehydration B. Water retention diluting sodium C. Hypernatremia from solute gain D. No osmotic changes

Answer 53

Correct Answer: B. Water retention diluting sodium Rationale: Inappropriate ADH concentrates urine; restrict fluids.

Question 54

Risks of Na overcorrection include: A. Cerebral dehydration B. Central pontine myelinolysis from rapid osmotic shifts C. Improved neurological status D. Hyponatremic seizures

Answer 54

B. Central pontine myelinolysis from rapid osmotic shifts Rationale: Brain cells lose osmolytes; slow correction prevents.

Question 55

ECG changes in hyperkalemia prompt: A. Ignoring until symptoms B. Immediate calcium for membrane stabilization C. Beta-blockers D. Potassium supplementation

Answer 55

B. Immediate calcium for membrane stabilization Rationale: Antagonizes depolarization; temporary until K+ lowered.

Question 56

In end-stage renal disease, dialysis is indicated for: A. Mild peaked T waves B. Refractory hyperkalemia >6.5 mEq/L or ECG changes C. Normal potassium D. Hypokalemia

Answer 56

B. Refractory hyperkalemia >6.5 mEq/L or ECG changes Rationale: Removes K+; bridge with insulin/glucose.

Question 57

Bone resorption in malignancy involves: A. PTH suppression B. PTH-related protein mimicking PTH C. Decreased osteoclast activity D. Vitamin D deficiency

Answer 57

B. PTH-related protein mimicking PTH Rationale: Humoral hypercalcemia; denosumab inhibits RANKL.

Question 58

Differential from primary hyperparathyroidism: A. Low PTH in malignancy vs. high in primary B. No difference in calcium levels C. Identical treatments D. Malignancy has lower phosphate

Answer 58

A. Low PTH in malignancy vs. high in primary Rationale: PTH assay differentiates; surgery for primary, chemo for malignancy.

Question 59

Third-spacing in ascites is due to: A. Fluid shift into vascular space B. Accumulation in non-functional compartments like peritoneum C. Enhanced lymphatic return D. Decreased interstitial pressure

Answer 59

B. Accumulation in non-functional compartments like peritoneum Rationale: Reduces effective circulating volume; paracentesis relieves.

Question 60

Implications for volume assessment in critically ill: A. Overestimation of intravascular volume B. Underestimation due to hidden fluid losses C. No impact on hemodynamics D. Simplified by weight alone

Answer 60

B. Underestimation due to hidden fluid losses Rationale: Use CVP or ultrasound; APRNs adjust fluids accordingly.

Question 61

When considering water balance, which statement demonstrates the correct balance? Isotonic fluids cause increased cellular swelling. Hypertonic fluid causes increased cellular swelling. Hypotonic fluid causes cellular swelling. Hypernatremia causes cellular swelling.

Answer 61

Hypotonic fluid causes cellular swelling. Hypotonic extracellular fluid (ECF) causes intracellular water gain and swelling. When the ECF is hypotonic, water moves from the intravascular space to the interstitial space, across the cell membrane, and into the cell. This action causes the cell to swell. An isotonic solution is equal to the plasma in concentration of solute molecules. Therefore no net water will move because equilibrium exists. The cell size is unchanged. A hypertonic fluid has excessive solute; therefore water will leave the cell and move into the vascular space to help balance this excess. Water leaving the cell results in cell shrinkage. Hypernatremia can occur with an acute gain in sodium or a loss of water, but generally it does not cause cellular swelling.

Question 62

Which statement is true regarding hyperchloremia? Occurs with a deficit of sodium Occurs with an excess of bicarbonate Has specific symptoms such as thirst Requires treatment of the underlying disorder

Answer 62

Requires treatment of the underlying disorder Hyperchloremia (too much chloride) is usually related to an underlying disorder, and therefore treatment is centered on the underlying disorder. Because chloride usually follows sodium, this condition usually occurs with an increase in sodium and a deficit of bicarbonate. Normally, neither specific symptoms are observed nor treatments are available for chloride excess.

Question 63

Which statement is true regarding hyponatremia? Is commonly caused by inadequate sodium intake Can occur with a decrease in total body water (TBW) Never occurs with burns, vomiting, or diarrhea Occurs when sodium drops below 135 mEq/L

Answer 63

Occurs when sodium drops below 135 mEq/L Hyponatremia occurs when the serum sodium drops below 135 mEq/L. It is the most common electrolyte disorder in individuals who are hospitalized. Although inadequate sodium intake can cause hyponatremia, it is uncommon. It can also occur with an increase in TBW or as a result of burns, vomiting, diarrhea, or gastrointestinal suctioning.

Question 64

Which statement is true regarding potassium balance? Potassium is the major extracellular electrolyte. During acidosis, potassium shifts into the cell. Aldosterone is secreted when potassium is decreased. Insulin causes the movement of potassium into the cell.

Answer 64

Insulin causes the movement of potassium into the cell. Insulin causes movement of potassium into the cell and is one of the treatments for hyperkalemia. Potassium balance is especially significant in the treatment of conditions requiring insulin administration, such as insulin-dependent diabetes mellitus (type 1). Potassium is the major intracellular electrolyte and maintains the osmotic balance of the intracellular fluid (ICF) space. During acidosis, potassium is shifted out of the cell in exchange for hydrogen ions. Aldosterone is secreted when potassium is elevated, resulting in the excretion of potassium by the kidneys.

Question 65

Which statement is true regarding hypokalemia? Hypokalemia occurs when the serum level is below 45 mEq/L. One cause of hypokalemia is diabetic ketoacidosis. Dietary causes of hypokalemia are common. Diuretics do not cause hypokalemia.

Answer 65

One cause of hypokalemia is diabetic ketoacidosis. Hypokalemia is low potassium. Therefore hypokalemia is defined as a serum level less than 3.5 mEq/L. It is often caused by diuretics. Diabetic ketoacidosis does cause hypokalemia. Potassium is shifted out of the cell in exchange for hydrogen and then excreted. The serum level may remain within a normal range, but then when insulin is administered, potassium is shifted back into the cells and a deficit occurs. Potassium balance is especially significant in the treatment of conditions requiring insulin administration, such as insulin-dependent diabetes mellitus (type 1). Dietary causes are uncommon.

Question 66

Hypernatremia is defined as levels above 145 mEq/L. 5.0 mEq/L. 105 mEq/L. 9.0 mg/dL.

Answer 66

145 mEq/L. Hypernatremia is defined as serum levels above 145 mEq/L. Hyperkalemia is defined as serum levels above 5.0 mEq/L, and hyperchloremia is defined as serum levels above 105 mEq/L. Hypocalcemia occurs when serum calcium concentrations are less than 9.0 mg/dL.

Question 67

Which statement is true regarding magnesium? Hypomagnesemia occurs with a concentration greater than 2.5 mEq/L. Magnesium is a major extracellular cation. Thirty percent is stored in the muscle and bone. Symptoms of hypomagnesemia include weakness and depression.

Answer 67

Symptoms of hypomagnesemia include weakness and depression. Symptoms of low magnesium include weakness, tetany, increased reflexes, depression, ataxia, convulsions, and irritability. Magnesium level is normal when between 1.5 and 3.0 mEq/L and is a major intracellular cation. Thirty percent is stored in the cells, with 40% to 60% stored in the bones and muscle.

Question 68

Which statement describes acidemia? State in which the pH of arterial blood is greater than 7.45 State in which the pH of arterial blood is less than 7.35 Systemic decrease in hydrogen ion concentration Systemic excess of base

Answer 68

State in which the pH of arterial blood is less than 7.35 Acidemia is a state in which the pH of arterial blood is less than 7.35. Alkalemia is a state in which the pH of arterial blood is greater than 7.45. A systemic increase in hydrogen ion concentration or loss of base is termed acidosis. A systemic decrease in hydrogen ion concentration or an excess of base is termed alkalosis.

Question 69

Common causes of edema formation (increased filtration of fluid from capillaries and lymph into surrounding tissues) include which of the following? (Select all that apply.) Decreased capillary hydrostatic pressure Decreased capillary oncotic pressure Increased capillary membrane permeability Lymphatic obstruction Sodium retention

Answer 69

Decreased capillary oncotic pressure Increased capillary membrane permeability Lymphatic obstruction Sodium retention

Question 70

Which are clinical manifestations of hypokalemia? (Select all that apply.) Decreased insulin secretion Impaired renal function Decreased neuromuscular excitability Increased contractility of skeletal muscle

Answer 70

Decreased insulin secretion Impaired renal function Decreased neuromuscular excitability Carbohydrate metabolism is affected by depressing insulin secretion and alters hepatic and skeletal muscle glycogen synthesis. Renal function may be impaired with a decreased ability to concentrate urine, and renal tubular atrophy and fibrosis may occur. Neuromuscular excitability is decreased causing skeletal muscle weakness, smooth muscle atony, and cardiac dysrhythmias. Hypokalemia causes the skeletal muscle to be weak.

Question 71

Which treatments are appropriate for hyperkalemia? (Select all that apply.) Calcium gluconate Treating the contributing cause Glucagon Buffered solutions

Answer 71

Calcium gluconate Treating the contributing cause Buffered solutions Calcium gluconate, treating the contributing cause, and buffered solutions are all appropriate treatments. Calcium gluconate can be administered to restore normal neuromuscular irritability when serum potassium levels are dangerously high. Glucose, which readily stimulates insulin secretion, or the administration of glucose and insulin for those with diabetes, facilitates cellular entry of potassium. Buffered solutions correct metabolic acidosis and lower serum potassium. Glucagon is administered to treat beta-blocker overdose or hypoglycemia.