NURS 6320 COMPLETE Questions and Answers
| chapter 2-32 | Verified Answers
A patient's blood gases reveal the following findings: pH, 7.3; bicarbonate (HCO3) 27
mEq/L; carbon dioxide (CO2), 58 mm Hg. What is the interpretation of these gases?
a. Respiratory alkalosis
b. Metabolic acidosis
c. Respiratory acidosis
d. Metabolic alkalosis - ANSW ANS: C
The values provided in this question characterize only acute uncompensated respiratory
acidosis.
What causes the clinical manifestations of confusion, convulsions, cerebral
hemorrhage, and coma in hypernatremia?
a. High sodium in the blood vessels pulls water out of the brain cells into the blood
vessels, causing brain cells to shrink.
b. High sodium in the brain cells pulls water out of the blood vessels into the brain cells,
causing them to swell.
c. High sodium in the blood vessels pulls potassium out of the brain cells, which slows
the synapses in the brain.
d. High sodium in th - ANSW ANS: A
Hypertonic (hyperosmolar) imbalances result in an extracellular fluid concentration
greater than 0.9% salt solution (e.g., water loss or solute gain); cells shrink in a
hypertonic fluid (see Table 3-7). This shrinking of cells results in the symptoms
described in the question. The other options do not accurately describe the cause of
these symptoms as they relate to hypernatremia
Vomiting-induced metabolic alkalosis, resulting in the loss of chloride, causes:
a. Retained sodium to bind with the chloride
b. Hydrogen to move into the cell and exchange with potassium to maintain cation
balance
,c. Retention of bicarbonate to maintain the anion balance
d. Hypoventilation to compensate for the metabolic alkalosis - ANSW ANS: C
When vomiting with the depletion of ECF and chloride (hypochloremic metabolic
alkalosis) causes acid loss, renal compensation is not effective; the volume depletion
and loss of electrolytes (sodium [Na+], potassium [K+], hydrogen [H+], chlorine [Cl-])
stimulate a paradoxic response by the kidneys. The kidneys increase sodium and
bicarbonate reabsorption with the excretion of hydrogen. Bicarbonate is reabsorbed to
maintain an anionic balance because the ECF chloride concentration is decreased. The
other options do not accurately describe the mechanism that results from vomiting-
induced metabolic alkalosis.
Insulin is used to treat hyperkalemia because it:
a. Stimulates sodium to be removed from the cell in exchange for potassium.
b. Binds to potassium to remove it through the kidneys.
c. Transports potassium from the blood to the cell along with glucose.
d. Breaks down the chemical components of potassium, causing it to be no longer
effective. - ANSW ANS: C
Insulin contributes to the regulation of plasma potassium levels by stimulating the Na+,
potassium-adenosine triphosphatase (K+-ATPase) pump, thereby promoting the
movement of potassium simultaneously into the liver and muscle cells with glucose
transport after eating. The intracellular movement of potassium prevents an acute
hyperkalemia related to food intake. The other options do not accurately describe how
insulin is used to treat hyperkalemia
During acidosis, the body compensates for the increase in serum hydrogen ions by
shifting hydrogen ions into the cell in exchange for which electrolyte?
a. Oxygen
b. Sodium
c. Potassium
d. Magnesium - ANSW ANS: C
In states of acidosis, hydrogen ions shift into the cells in exchange for intracellular fluid
potassium; hyperkalemia and acidosis therefore often occur together. This is not true of
the other options.
,Causes of hyperkalemia include:
a. Hyperparathyroidism and malnutrition
b. Vomiting and diarrhea
c. Renal failure and Addison disease
d. Hyperaldosteronism and Cushing disease - ANSW ANS: C
Hyperkalemia should be investigated when a history of renal disease, massive trauma,
insulin deficiency, Addison disease, use of potassium salt substitutes, or metabolic
acidosis exists. The other options are not known to be causes of hyperkalemia
In hyperkalemia, what change occurs to the cells' resting membrane potential?
a. Hypopolarization
b. Hyperexcitability
c. Depolarization
d. Repolarization - ANSW ANS: A
If extracellular potassium concentration increases without a significant change in
intracellular potassium, then the resting membrane potential becomes more positive
(i.e., changes from -90 to -80 mV) and the cell membrane is hypopolarized (i.e., the
inside of the cell becomes less negative or partially depolarized [increase excitability]).
The calcium and phosphate balance is influenced by which three substances?
a. Parathyroid hormone, vasopressin, and vitamin D
b. Parathyroid hormone, calcitonin, and vitamin D
c. Thyroid hormone, vasopressin, and vitamin A
d. Thyroid hormone, calcitonin, and vitamin A - ANSW ANS: B
Three hormones regulate calcium and phosphate balance: parathyroid hormone (PTH),
vitamin D, and calcitonin. Vasopressin, thyroid hormone, and vitamin A do not influence
calcium and phosphate balance
It is true that Kussmaul respirations indicate:
, a. Anxiety is a cause of respiratory acidosis.
b. A compensatory measure is needed to correct metabolic acidosis.
c. Diabetic ketoacidosis is the cause of the metabolic acidosis.
d. More oxygen is necessary to compensate for respiratory acidosis - ANSW ANS: B
Deep, rapid respirations (Kussmaul respirations) are indicative of respiratory
compensation for metabolic acidosis. The other options are not true.
Chvostek and Trousseau signs indicate which electrolyte imbalance?
a. Hypokalemia
b. Hyperkalemia
c. Hypocalcemia
d. Hypercalcemia - ANSW ANS: C
Two clinical signs of hypocalcemia are the Chvostek sign and Trousseau sign. These
clinical signs are not indicative of any of the other options.
An excessive use of magnesium-containing antacids and aluminum-containing antacids
can result in:
a. Hypomagnesemia
b. Hypophosphatemia
c. Hyponatremia
d. Hypokalemia - ANSW ANS: B
The most common causes of hypophosphatemia are intestinal malabsorption and
increased renal excretion of phosphate. Inadequate absorption is associated with
vitamin D deficiency, the use of magnesium and aluminum-containing antacids (which
bind with phosphorus), long-term alcohol abuse, and malabsorption syndromes. The
excessive use of such antacids will not result in the other options.
The most common cause of hypermagnesemia is:
a. Hepatitis
c. Trauma to the hypothalamus
| chapter 2-32 | Verified Answers
A patient's blood gases reveal the following findings: pH, 7.3; bicarbonate (HCO3) 27
mEq/L; carbon dioxide (CO2), 58 mm Hg. What is the interpretation of these gases?
a. Respiratory alkalosis
b. Metabolic acidosis
c. Respiratory acidosis
d. Metabolic alkalosis - ANSW ANS: C
The values provided in this question characterize only acute uncompensated respiratory
acidosis.
What causes the clinical manifestations of confusion, convulsions, cerebral
hemorrhage, and coma in hypernatremia?
a. High sodium in the blood vessels pulls water out of the brain cells into the blood
vessels, causing brain cells to shrink.
b. High sodium in the brain cells pulls water out of the blood vessels into the brain cells,
causing them to swell.
c. High sodium in the blood vessels pulls potassium out of the brain cells, which slows
the synapses in the brain.
d. High sodium in th - ANSW ANS: A
Hypertonic (hyperosmolar) imbalances result in an extracellular fluid concentration
greater than 0.9% salt solution (e.g., water loss or solute gain); cells shrink in a
hypertonic fluid (see Table 3-7). This shrinking of cells results in the symptoms
described in the question. The other options do not accurately describe the cause of
these symptoms as they relate to hypernatremia
Vomiting-induced metabolic alkalosis, resulting in the loss of chloride, causes:
a. Retained sodium to bind with the chloride
b. Hydrogen to move into the cell and exchange with potassium to maintain cation
balance
,c. Retention of bicarbonate to maintain the anion balance
d. Hypoventilation to compensate for the metabolic alkalosis - ANSW ANS: C
When vomiting with the depletion of ECF and chloride (hypochloremic metabolic
alkalosis) causes acid loss, renal compensation is not effective; the volume depletion
and loss of electrolytes (sodium [Na+], potassium [K+], hydrogen [H+], chlorine [Cl-])
stimulate a paradoxic response by the kidneys. The kidneys increase sodium and
bicarbonate reabsorption with the excretion of hydrogen. Bicarbonate is reabsorbed to
maintain an anionic balance because the ECF chloride concentration is decreased. The
other options do not accurately describe the mechanism that results from vomiting-
induced metabolic alkalosis.
Insulin is used to treat hyperkalemia because it:
a. Stimulates sodium to be removed from the cell in exchange for potassium.
b. Binds to potassium to remove it through the kidneys.
c. Transports potassium from the blood to the cell along with glucose.
d. Breaks down the chemical components of potassium, causing it to be no longer
effective. - ANSW ANS: C
Insulin contributes to the regulation of plasma potassium levels by stimulating the Na+,
potassium-adenosine triphosphatase (K+-ATPase) pump, thereby promoting the
movement of potassium simultaneously into the liver and muscle cells with glucose
transport after eating. The intracellular movement of potassium prevents an acute
hyperkalemia related to food intake. The other options do not accurately describe how
insulin is used to treat hyperkalemia
During acidosis, the body compensates for the increase in serum hydrogen ions by
shifting hydrogen ions into the cell in exchange for which electrolyte?
a. Oxygen
b. Sodium
c. Potassium
d. Magnesium - ANSW ANS: C
In states of acidosis, hydrogen ions shift into the cells in exchange for intracellular fluid
potassium; hyperkalemia and acidosis therefore often occur together. This is not true of
the other options.
,Causes of hyperkalemia include:
a. Hyperparathyroidism and malnutrition
b. Vomiting and diarrhea
c. Renal failure and Addison disease
d. Hyperaldosteronism and Cushing disease - ANSW ANS: C
Hyperkalemia should be investigated when a history of renal disease, massive trauma,
insulin deficiency, Addison disease, use of potassium salt substitutes, or metabolic
acidosis exists. The other options are not known to be causes of hyperkalemia
In hyperkalemia, what change occurs to the cells' resting membrane potential?
a. Hypopolarization
b. Hyperexcitability
c. Depolarization
d. Repolarization - ANSW ANS: A
If extracellular potassium concentration increases without a significant change in
intracellular potassium, then the resting membrane potential becomes more positive
(i.e., changes from -90 to -80 mV) and the cell membrane is hypopolarized (i.e., the
inside of the cell becomes less negative or partially depolarized [increase excitability]).
The calcium and phosphate balance is influenced by which three substances?
a. Parathyroid hormone, vasopressin, and vitamin D
b. Parathyroid hormone, calcitonin, and vitamin D
c. Thyroid hormone, vasopressin, and vitamin A
d. Thyroid hormone, calcitonin, and vitamin A - ANSW ANS: B
Three hormones regulate calcium and phosphate balance: parathyroid hormone (PTH),
vitamin D, and calcitonin. Vasopressin, thyroid hormone, and vitamin A do not influence
calcium and phosphate balance
It is true that Kussmaul respirations indicate:
, a. Anxiety is a cause of respiratory acidosis.
b. A compensatory measure is needed to correct metabolic acidosis.
c. Diabetic ketoacidosis is the cause of the metabolic acidosis.
d. More oxygen is necessary to compensate for respiratory acidosis - ANSW ANS: B
Deep, rapid respirations (Kussmaul respirations) are indicative of respiratory
compensation for metabolic acidosis. The other options are not true.
Chvostek and Trousseau signs indicate which electrolyte imbalance?
a. Hypokalemia
b. Hyperkalemia
c. Hypocalcemia
d. Hypercalcemia - ANSW ANS: C
Two clinical signs of hypocalcemia are the Chvostek sign and Trousseau sign. These
clinical signs are not indicative of any of the other options.
An excessive use of magnesium-containing antacids and aluminum-containing antacids
can result in:
a. Hypomagnesemia
b. Hypophosphatemia
c. Hyponatremia
d. Hypokalemia - ANSW ANS: B
The most common causes of hypophosphatemia are intestinal malabsorption and
increased renal excretion of phosphate. Inadequate absorption is associated with
vitamin D deficiency, the use of magnesium and aluminum-containing antacids (which
bind with phosphorus), long-term alcohol abuse, and malabsorption syndromes. The
excessive use of such antacids will not result in the other options.
The most common cause of hypermagnesemia is:
a. Hepatitis
c. Trauma to the hypothalamus
