NU 518 Exam 2 EXAM with Questions and
Answers/Plus a Rationale Updated 2026
A+/Instant Download PDF
Table of Contents
Advanced Pathophysiology of Cardiovascular and Renal Systems
Pharmacotherapeutics for Acute and Chronic Alterations
Diagnostic Reasoning and Clinical Management
Genetics, Epigenetics, and Cellular Regulation in Disease
A 64-year-old male with a history of chronic kidney disease (CKD) Stage 3b and heart failure with
reduced ejection fraction (HFrEF) presents with worsening peripheral edema and dyspnea. Laboratory
analysis reveals a serum potassium of 5.4 mEq/L and an estimated glomerular filtration rate (eGFR) of
32 mL/min/1.73m
2
. Which of the following alterations in renal handling of electrolytes is most responsible for maintaining
his current potassium level despite his decreased GFR?
A. Downregulation of Na+/K+ ATPase pumps in the principal cells of the collecting duct.
B. Compensatory upregulation of aldosterone-independent potassium secretion in the distal nephron
and increased fecal excretion.
C. Increased reabsorption of sodium in the proximal convoluted tubule via NHE3 cotransporters.
D. Decreased expression of ROMK (Renal Outer Medullary Potassium) channels in response to apical
sodium delivery.
Answer: B
,Rationale: In advanced CKD, the remaining nephrons undergo hypertrophy and upregulate potassium
secretion per nephron, driven partly by aldosterone-independent mechanisms and increased expression
of apical potassium channels, alongside a significant compensatory increase in gastrointestinal (fecal)
potassium excretion. Option A is incorrect because downregulation of Na+/K+ ATPase would decrease
potassium secretion, worsening hyperkalemia. Option C is incorrect because proximal sodium
reabsorption does not directly drive distal potassium secretion in this manner. Option D is incorrect
because ROMK channels are upregulated, not decreased, to facilitate potassium excretion when
potassium levels are elevated.
CORRECT ANSWER : B
A 45-year-old female patient undergoes genetic testing after a family history of sudden cardiac death.
The report indicates a loss-of-function mutation in the KCNQ1 gene, which encodes the pore-forming
subunit of the slow delayed rectifier potassium current (I
Ks
) in cardiac myocytes. During which phase of the cardiac action potential will this mutation cause the
most profound physiological delay?
A. Phase 0
B. Phase 1
C. Phase 2
D. Phase 3
Answer: D
Rationale: The KCNQ1 gene mediates the slow delayed rectifier potassium current (I
Ks
), which is critical for Phase 3 repolarization of the cardiac action potential, returning the membrane
potential to its resting state; impairment leads to Long QT Syndrome Type 1. Phases 0 (depolarization), 1
(transient outward current), and 2 (plateau phase dominated by calcium influx) are not primarily
dependent on I
Ks
, for their baseline morphology. Therefore, options A, B, and C are incorrect as they reflect different ion
channel dynamics.
CORRECT ANSWER : D
A 58-year-old female presents to the emergency department with acute decompensated heart failure.
She is tachycardic, tachypneic, and has a brain natriuretic peptide (BNP) level of 1,400 pg/mL.
Physiologically, BNP exerts its beneficial compensatory effects in this state by binding to natriuretic
peptide receptor-A (NPR-A) and stimulating the synthesis of which intracellular secondary messenger?
A. Cyclic adenosine monophosphate (cAMP)
B. Inositol trisphosphate (IP
3
)
C. Cyclic guanosine monophosphate (cGMP)
D. Diacylglycerol (DAG)
Answer: C
Rationale: BNP binds to NPR-A, a membrane-bound guanylyl cyclase receptor, which converts GTP to
cyclic guanosine monophosphate (cGMP), leading to vasodilation, natriuresis, and inhibition of the
renin-angiotensin-aldosterone system. Options A, B, and C are incorrect because cAMP, IP
3
, and DAG are secondary messengers utilized by different neurohormonal pathways (e.g., beta-
adrenergic and G-protein coupled receptors) rather than the particulate guanylyl cyclase system
activated by natriuretic peptides.
CORRECT ANSWER : C
A 72-year-old patient with type 2 diabetes and hypertension is initiated on an SGLT2 inhibitor
(empagliflozin) for cardiorenal protection. Mechanistically, how does inhibiting glucose and sodium
Answers/Plus a Rationale Updated 2026
A+/Instant Download PDF
Table of Contents
Advanced Pathophysiology of Cardiovascular and Renal Systems
Pharmacotherapeutics for Acute and Chronic Alterations
Diagnostic Reasoning and Clinical Management
Genetics, Epigenetics, and Cellular Regulation in Disease
A 64-year-old male with a history of chronic kidney disease (CKD) Stage 3b and heart failure with
reduced ejection fraction (HFrEF) presents with worsening peripheral edema and dyspnea. Laboratory
analysis reveals a serum potassium of 5.4 mEq/L and an estimated glomerular filtration rate (eGFR) of
32 mL/min/1.73m
2
. Which of the following alterations in renal handling of electrolytes is most responsible for maintaining
his current potassium level despite his decreased GFR?
A. Downregulation of Na+/K+ ATPase pumps in the principal cells of the collecting duct.
B. Compensatory upregulation of aldosterone-independent potassium secretion in the distal nephron
and increased fecal excretion.
C. Increased reabsorption of sodium in the proximal convoluted tubule via NHE3 cotransporters.
D. Decreased expression of ROMK (Renal Outer Medullary Potassium) channels in response to apical
sodium delivery.
Answer: B
,Rationale: In advanced CKD, the remaining nephrons undergo hypertrophy and upregulate potassium
secretion per nephron, driven partly by aldosterone-independent mechanisms and increased expression
of apical potassium channels, alongside a significant compensatory increase in gastrointestinal (fecal)
potassium excretion. Option A is incorrect because downregulation of Na+/K+ ATPase would decrease
potassium secretion, worsening hyperkalemia. Option C is incorrect because proximal sodium
reabsorption does not directly drive distal potassium secretion in this manner. Option D is incorrect
because ROMK channels are upregulated, not decreased, to facilitate potassium excretion when
potassium levels are elevated.
CORRECT ANSWER : B
A 45-year-old female patient undergoes genetic testing after a family history of sudden cardiac death.
The report indicates a loss-of-function mutation in the KCNQ1 gene, which encodes the pore-forming
subunit of the slow delayed rectifier potassium current (I
Ks
) in cardiac myocytes. During which phase of the cardiac action potential will this mutation cause the
most profound physiological delay?
A. Phase 0
B. Phase 1
C. Phase 2
D. Phase 3
Answer: D
Rationale: The KCNQ1 gene mediates the slow delayed rectifier potassium current (I
Ks
), which is critical for Phase 3 repolarization of the cardiac action potential, returning the membrane
potential to its resting state; impairment leads to Long QT Syndrome Type 1. Phases 0 (depolarization), 1
(transient outward current), and 2 (plateau phase dominated by calcium influx) are not primarily
dependent on I
Ks
, for their baseline morphology. Therefore, options A, B, and C are incorrect as they reflect different ion
channel dynamics.
CORRECT ANSWER : D
A 58-year-old female presents to the emergency department with acute decompensated heart failure.
She is tachycardic, tachypneic, and has a brain natriuretic peptide (BNP) level of 1,400 pg/mL.
Physiologically, BNP exerts its beneficial compensatory effects in this state by binding to natriuretic
peptide receptor-A (NPR-A) and stimulating the synthesis of which intracellular secondary messenger?
A. Cyclic adenosine monophosphate (cAMP)
B. Inositol trisphosphate (IP
3
)
C. Cyclic guanosine monophosphate (cGMP)
D. Diacylglycerol (DAG)
Answer: C
Rationale: BNP binds to NPR-A, a membrane-bound guanylyl cyclase receptor, which converts GTP to
cyclic guanosine monophosphate (cGMP), leading to vasodilation, natriuresis, and inhibition of the
renin-angiotensin-aldosterone system. Options A, B, and C are incorrect because cAMP, IP
3
, and DAG are secondary messengers utilized by different neurohormonal pathways (e.g., beta-
adrenergic and G-protein coupled receptors) rather than the particulate guanylyl cyclase system
activated by natriuretic peptides.
CORRECT ANSWER : C
A 72-year-old patient with type 2 diabetes and hypertension is initiated on an SGLT2 inhibitor
(empagliflozin) for cardiorenal protection. Mechanistically, how does inhibiting glucose and sodium
