Advanced Pathophysiology: Fluid & Electrolyte Imbalances 2026
|Maryville
1. Which physiological mechanism explains why a patient with chronic liver
failure develops systemic edema?
A. Increased plasma oncotic pressure due to excessive albumin synthesis
B. Decreased capillary hydrostatic pressure due to portal hypertension
C. Decreased capillary permeability in the peripheral vasculature
D. Decreased plasma oncotic pressure secondary to hypoalbuminemia
Answer: D
Rationale: Liver failure results in impaired albumin synthesis. Since albumin is the
primary determinant of plasma oncotic pressure, its decrease allows fluid to shift from the
intravascular space to the interstitial space.
2. In the Renin-Angiotensin-Aldosterone System (RAAS), what is the specific role
of Angiotensin II on the adrenal cortex?
A. To stimulate the release of Antidiuretic Hormone (ADH)
B. To inhibit the conversion of Angiotensinogen to Angiotensin I
C. To trigger the secretion of Aldosterone
D. To promote the excretion of sodium in the distal tubule
Answer: C
Rationale: Angiotensin II acts on the adrenal cortex to stimulate the synthesis and
secretion of aldosterone, which then promotes sodium and water reabsorption in the
kidneys.
,3. A patient presents with a serum sodium of 120 mEq/L and high urine
osmolality. Which condition is most consistent with these findings?
A. Diabetes Insipidus
B. Psychogenic Polydipsia
C. Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
D. Hypovolemic Dehydration
Answer: C
Rationale: SIADH involves excessive ADH release, leading to water retention (dilutional
hyponatremia) and concentrated urine (high urine osmolality).
4. What is the primary mechanism by which Hyperkalemia alters cardiac
conduction?
A. It decreases the resting membrane potential, moving it closer to the threshold
B. It increases the resting membrane potential, making cells less excitable
C. It increases the duration of the action potential plateau phase
D. It causes rapid hyperpolarization of the myocardial cells
Answer: A
Rationale: Hyperkalemia raises the resting membrane potential (making it less negative),
bringing it closer to the threshold potential, which initially increases excitability but
eventually impairs repolarization.
5. Which electrolyte imbalance is a patient most at risk for when receiving a
rapid infusion of insulin and glucose?
A. Hyperkalemia
B. Hypokalemia
C. Hypocalcemia
D. Hypermagnesemia
Answer: B
, Rationale: Insulin facilitates the entry of glucose into cells and simultaneously stimulates
the Na+/K+-ATPase pump, shifting potassium from the ECF into the ICF, potentially
causing hypokalemia.
6. Which clinical sign is associated with hypocalcemia and is elicited by tapping
the facial nerve?
A. Chvostek sign
B. Babinski sign
C. Trousseau sign
D. Homans sign
Answer: A
Rationale: The Chvostek sign is a twitching of the facial muscles in response to tapping
over the facial nerve, indicating increased neuromuscular excitability due to hypocalcemia.
7. A patient with a pH of 7.25, PaCO2 of 55 mmHg, and HCO3 of 24 mEq/L is
experiencing which acid-base disturbance?
A. Metabolic Acidosis
B. Respiratory Alkalosis
C. Metabolic Alkalosis
D. Respiratory Acidosis
Answer: D
Rationale: The low pH (<7.35) indicates acidosis, and the elevated PaCO2 (>45 mmHg)
with a normal bicarbonate indicates the primary cause is respiratory retention of CO2.
8. How does the body compensate for metabolic acidosis?
A. Kidneys retain H+ ions
B. Lungs increase the rate and depth of respirations (Kussmaul breathing)
C. Lungs decrease the rate and depth of respirations
D. Kidneys excrete bicarbonate ions
Answer: B
|Maryville
1. Which physiological mechanism explains why a patient with chronic liver
failure develops systemic edema?
A. Increased plasma oncotic pressure due to excessive albumin synthesis
B. Decreased capillary hydrostatic pressure due to portal hypertension
C. Decreased capillary permeability in the peripheral vasculature
D. Decreased plasma oncotic pressure secondary to hypoalbuminemia
Answer: D
Rationale: Liver failure results in impaired albumin synthesis. Since albumin is the
primary determinant of plasma oncotic pressure, its decrease allows fluid to shift from the
intravascular space to the interstitial space.
2. In the Renin-Angiotensin-Aldosterone System (RAAS), what is the specific role
of Angiotensin II on the adrenal cortex?
A. To stimulate the release of Antidiuretic Hormone (ADH)
B. To inhibit the conversion of Angiotensinogen to Angiotensin I
C. To trigger the secretion of Aldosterone
D. To promote the excretion of sodium in the distal tubule
Answer: C
Rationale: Angiotensin II acts on the adrenal cortex to stimulate the synthesis and
secretion of aldosterone, which then promotes sodium and water reabsorption in the
kidneys.
,3. A patient presents with a serum sodium of 120 mEq/L and high urine
osmolality. Which condition is most consistent with these findings?
A. Diabetes Insipidus
B. Psychogenic Polydipsia
C. Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
D. Hypovolemic Dehydration
Answer: C
Rationale: SIADH involves excessive ADH release, leading to water retention (dilutional
hyponatremia) and concentrated urine (high urine osmolality).
4. What is the primary mechanism by which Hyperkalemia alters cardiac
conduction?
A. It decreases the resting membrane potential, moving it closer to the threshold
B. It increases the resting membrane potential, making cells less excitable
C. It increases the duration of the action potential plateau phase
D. It causes rapid hyperpolarization of the myocardial cells
Answer: A
Rationale: Hyperkalemia raises the resting membrane potential (making it less negative),
bringing it closer to the threshold potential, which initially increases excitability but
eventually impairs repolarization.
5. Which electrolyte imbalance is a patient most at risk for when receiving a
rapid infusion of insulin and glucose?
A. Hyperkalemia
B. Hypokalemia
C. Hypocalcemia
D. Hypermagnesemia
Answer: B
, Rationale: Insulin facilitates the entry of glucose into cells and simultaneously stimulates
the Na+/K+-ATPase pump, shifting potassium from the ECF into the ICF, potentially
causing hypokalemia.
6. Which clinical sign is associated with hypocalcemia and is elicited by tapping
the facial nerve?
A. Chvostek sign
B. Babinski sign
C. Trousseau sign
D. Homans sign
Answer: A
Rationale: The Chvostek sign is a twitching of the facial muscles in response to tapping
over the facial nerve, indicating increased neuromuscular excitability due to hypocalcemia.
7. A patient with a pH of 7.25, PaCO2 of 55 mmHg, and HCO3 of 24 mEq/L is
experiencing which acid-base disturbance?
A. Metabolic Acidosis
B. Respiratory Alkalosis
C. Metabolic Alkalosis
D. Respiratory Acidosis
Answer: D
Rationale: The low pH (<7.35) indicates acidosis, and the elevated PaCO2 (>45 mmHg)
with a normal bicarbonate indicates the primary cause is respiratory retention of CO2.
8. How does the body compensate for metabolic acidosis?
A. Kidneys retain H+ ions
B. Lungs increase the rate and depth of respirations (Kussmaul breathing)
C. Lungs decrease the rate and depth of respirations
D. Kidneys excrete bicarbonate ions
Answer: B
