NURS 5315 Advanced Pathophysiology
Final ACTUAL EXAM 2026/2027: 100%
Verified Questions & Correct Answers
Question 1: A 68-year-old male with type 2 diabetes, hypertension, and chronic kidney disease
(eGFR 35) presents with acute decompensated heart failure. His medications include metformin,
lisinopril, and furosemide. Laboratory studies show potassium 5.8 mEq/L, bicarbonate 18 mEq/L,
and an elevated anion gap. Which interconnected pathophysiological mechanism best explains his
acid-base disturbance?
A. Lactic acidosis from metformin accumulation causing primary metabolic acidosis with inadequate
respiratory compensation
B. Type 4 renal tubular acidosis from aldosterone resistance due to diabetes and ACE inhibitor,
compounded by hyperkalemic-induced ammonia genesis impairment
C. Diabetic ketoacidosis from insulin deficiency with secondary hyperaldosteronism
D. Respiratory acidosis from pulmonary edema causing carbon dioxide retention
Correct Answer: B
Rationale: This patient demonstrates type 4 RTA (hyperkalemic distal RTA) from multifactorial
aldosterone resistance: diabetes causes hyporeninemic hypoaldosteronism, and ACE inhibitors
further reduce angiotensin II/aldosterone. Hyperkalemia impairs renal ammonia genesis (NH3 + H⁺
→ NH₄⁺), reducing net acid excretion. The CKD limits bicarbonate regeneration. This creates a
high anion gap metabolic acidosis with inappropriate hyperkalemia, distinct from other causes.
,Question 2: A patient with cirrhosis develops hepatorenal syndrome following a variceal bleed.
Which pathophysiological cascade best explains this syndrome?
A. Primary renal parenchymal damage from bilirubin toxicity
B. Splanchnic arterial vasodilation from portal hypertension → effective arterial blood volume
depletion → renal vasoconstriction via RAAS and sympathetic activation
C. Direct hepatocyte necrosis causing tubular obstruction
D. Autoimmune attack on renal tubules
Correct Answer: B
Rationale: Hepatorenal syndrome (HRS) is functional renal failure without structural kidney
damage. Portal hypertension causes splanchnic arterial vasodilation (NO, prostacyclin), reducing
effective arterial blood volume. This triggers baroreceptor-mediated RAAS activation, sympathetic
nervous system stimulation, and ADH release—causing intense renal cortical vasoconstriction
(despite overall vasodilation) and progressive oliguric renal failure. This represents extreme
activation of compensatory mechanisms in decompensated cirrhosis.
Question 3: In sepsis-induced acute respiratory distress syndrome (ARDS), which cellular
mechanism links the systemic inflammatory response to alveolar-capillary membrane damage?
A. Direct bacterial invasion of type II pneumocytes
B. Neutrophil sequestration and activation in pulmonary capillaries releasing proteases, oxidants,
and inflammatory mediators causing diffuse alveolar damage
C. Viral replication in endothelial cells
D. Autoantibody-mediated basement membrane destruction
Correct Answer: B
,Rationale: Sepsis causes systemic complement activation and cytokine release (TNF-α, IL-1, IL-8),
upregulating endothelial adhesion molecules. Neutrophils marginate, adhere, and migrate into
alveoli, releasing: (1) proteases (elastase, collagenase) degrading basement membrane, (2)
reactive oxygen species causing oxidative injury, and (3) additional cytokines amplifying
inflammation. This causes increased permeability edema, surfactant dysfunction by type II cell
damage, and hyaline membrane formation—creating the characteristic V/Q mismatch and
refractory hypoxemia.
Question 4: A patient with long-standing rheumatoid arthritis develops amyloidosis with nephrotic
syndrome. Which pathophysiological mechanism explains this complication?
A. Autoimmune destruction of renal podocytes
B. Chronic inflammation with sustained acute phase response → hepatic synthesis of serum
amyloid A (SAA) → formation of amyloid fibrils deposited in glomeruli causing proteinuria
C. Crystal deposition from uric acid
D. Direct invasion of kidney by synovial tissue
Correct Answer: B
Rationale: Secondary (AA) amyloidosis complicates chronic inflammatory diseases (RA, familial
Mediterranean fever, chronic infections). Sustained IL-1, IL-6, and TNF-α drive hepatic SAA
synthesis. SAA cleavage products form β-pleated sheet fibrils resistant to proteolysis, depositing in
kidneys (glomeruli causing nephrotic syndrome), liver, and spleen. This represents a systemic
consequence of uncontrolled inflammation with extracellular protein misfolding and tissue
deposition.
Question 5: In diabetic nephropathy progression from microalbuminuria to overt proteinuria, which
structural change is most characteristic?
, A. Tubular atrophy and interstitial fibrosis only
B. Mesangial expansion with accumulation of extracellular matrix, thickening of glomerular
basement membrane, and nodular glomerulosclerosis (Kimmelstiel-Wilson lesions)
C. Minimal change disease with foot process effacement
D. Rapidly progressive crescentic glomerulonephritis
Correct Answer: B
Rationale: Diabetic nephropathy pathophysiology involves: (1) hyperglycemia-induced mesangial
cell expansion and ECM accumulation (collagen IV, fibronectin) from TGF-β activation and AGE
formation, (2) GBM thickening from increased matrix synthesis, and (3) characteristic nodular
glomerulosclerosis (Kimmelstiel-Wilson nodules)—mesangial areas of acellular, hyaline material.
These changes increase permeability (albuminuria) and reduce filtration surface (progressive GFR
decline). Tubulointerstitial fibrosis develops secondarily.
Question 6: A patient with chronic obstructive pulmonary disease (COPD) and right heart failure
(cor pulmonale) develops peripheral edema. Which hemodynamic mechanism is primary?
A. Left ventricular systolic dysfunction causing backward failure
B. Pulmonary hypertension from hypoxic vasoconstriction and vascular remodeling → increased
right ventricular afterload → RV dilation and failure → systemic venous congestion
C. Nephrotic syndrome from smoking-related glomerular disease
D. Liver cirrhosis from alpha-1 antitrypsin deficiency
Correct Answer: B
Rationale: Cor pulmonale is right heart failure secondary to pulmonary disease. COPD causes: (1)
chronic hypoxia → hypoxic pulmonary vasoconstriction, (2) destruction of pulmonary capillary bed
(emphysema), and (3) chronic respiratory acidosis → H⁺-mediated vasoconstriction. These cause
pulmonary hypertension, increasing RV afterload. The thin-walled RV cannot compensate, leading
Final ACTUAL EXAM 2026/2027: 100%
Verified Questions & Correct Answers
Question 1: A 68-year-old male with type 2 diabetes, hypertension, and chronic kidney disease
(eGFR 35) presents with acute decompensated heart failure. His medications include metformin,
lisinopril, and furosemide. Laboratory studies show potassium 5.8 mEq/L, bicarbonate 18 mEq/L,
and an elevated anion gap. Which interconnected pathophysiological mechanism best explains his
acid-base disturbance?
A. Lactic acidosis from metformin accumulation causing primary metabolic acidosis with inadequate
respiratory compensation
B. Type 4 renal tubular acidosis from aldosterone resistance due to diabetes and ACE inhibitor,
compounded by hyperkalemic-induced ammonia genesis impairment
C. Diabetic ketoacidosis from insulin deficiency with secondary hyperaldosteronism
D. Respiratory acidosis from pulmonary edema causing carbon dioxide retention
Correct Answer: B
Rationale: This patient demonstrates type 4 RTA (hyperkalemic distal RTA) from multifactorial
aldosterone resistance: diabetes causes hyporeninemic hypoaldosteronism, and ACE inhibitors
further reduce angiotensin II/aldosterone. Hyperkalemia impairs renal ammonia genesis (NH3 + H⁺
→ NH₄⁺), reducing net acid excretion. The CKD limits bicarbonate regeneration. This creates a
high anion gap metabolic acidosis with inappropriate hyperkalemia, distinct from other causes.
,Question 2: A patient with cirrhosis develops hepatorenal syndrome following a variceal bleed.
Which pathophysiological cascade best explains this syndrome?
A. Primary renal parenchymal damage from bilirubin toxicity
B. Splanchnic arterial vasodilation from portal hypertension → effective arterial blood volume
depletion → renal vasoconstriction via RAAS and sympathetic activation
C. Direct hepatocyte necrosis causing tubular obstruction
D. Autoimmune attack on renal tubules
Correct Answer: B
Rationale: Hepatorenal syndrome (HRS) is functional renal failure without structural kidney
damage. Portal hypertension causes splanchnic arterial vasodilation (NO, prostacyclin), reducing
effective arterial blood volume. This triggers baroreceptor-mediated RAAS activation, sympathetic
nervous system stimulation, and ADH release—causing intense renal cortical vasoconstriction
(despite overall vasodilation) and progressive oliguric renal failure. This represents extreme
activation of compensatory mechanisms in decompensated cirrhosis.
Question 3: In sepsis-induced acute respiratory distress syndrome (ARDS), which cellular
mechanism links the systemic inflammatory response to alveolar-capillary membrane damage?
A. Direct bacterial invasion of type II pneumocytes
B. Neutrophil sequestration and activation in pulmonary capillaries releasing proteases, oxidants,
and inflammatory mediators causing diffuse alveolar damage
C. Viral replication in endothelial cells
D. Autoantibody-mediated basement membrane destruction
Correct Answer: B
,Rationale: Sepsis causes systemic complement activation and cytokine release (TNF-α, IL-1, IL-8),
upregulating endothelial adhesion molecules. Neutrophils marginate, adhere, and migrate into
alveoli, releasing: (1) proteases (elastase, collagenase) degrading basement membrane, (2)
reactive oxygen species causing oxidative injury, and (3) additional cytokines amplifying
inflammation. This causes increased permeability edema, surfactant dysfunction by type II cell
damage, and hyaline membrane formation—creating the characteristic V/Q mismatch and
refractory hypoxemia.
Question 4: A patient with long-standing rheumatoid arthritis develops amyloidosis with nephrotic
syndrome. Which pathophysiological mechanism explains this complication?
A. Autoimmune destruction of renal podocytes
B. Chronic inflammation with sustained acute phase response → hepatic synthesis of serum
amyloid A (SAA) → formation of amyloid fibrils deposited in glomeruli causing proteinuria
C. Crystal deposition from uric acid
D. Direct invasion of kidney by synovial tissue
Correct Answer: B
Rationale: Secondary (AA) amyloidosis complicates chronic inflammatory diseases (RA, familial
Mediterranean fever, chronic infections). Sustained IL-1, IL-6, and TNF-α drive hepatic SAA
synthesis. SAA cleavage products form β-pleated sheet fibrils resistant to proteolysis, depositing in
kidneys (glomeruli causing nephrotic syndrome), liver, and spleen. This represents a systemic
consequence of uncontrolled inflammation with extracellular protein misfolding and tissue
deposition.
Question 5: In diabetic nephropathy progression from microalbuminuria to overt proteinuria, which
structural change is most characteristic?
, A. Tubular atrophy and interstitial fibrosis only
B. Mesangial expansion with accumulation of extracellular matrix, thickening of glomerular
basement membrane, and nodular glomerulosclerosis (Kimmelstiel-Wilson lesions)
C. Minimal change disease with foot process effacement
D. Rapidly progressive crescentic glomerulonephritis
Correct Answer: B
Rationale: Diabetic nephropathy pathophysiology involves: (1) hyperglycemia-induced mesangial
cell expansion and ECM accumulation (collagen IV, fibronectin) from TGF-β activation and AGE
formation, (2) GBM thickening from increased matrix synthesis, and (3) characteristic nodular
glomerulosclerosis (Kimmelstiel-Wilson nodules)—mesangial areas of acellular, hyaline material.
These changes increase permeability (albuminuria) and reduce filtration surface (progressive GFR
decline). Tubulointerstitial fibrosis develops secondarily.
Question 6: A patient with chronic obstructive pulmonary disease (COPD) and right heart failure
(cor pulmonale) develops peripheral edema. Which hemodynamic mechanism is primary?
A. Left ventricular systolic dysfunction causing backward failure
B. Pulmonary hypertension from hypoxic vasoconstriction and vascular remodeling → increased
right ventricular afterload → RV dilation and failure → systemic venous congestion
C. Nephrotic syndrome from smoking-related glomerular disease
D. Liver cirrhosis from alpha-1 antitrypsin deficiency
Correct Answer: B
Rationale: Cor pulmonale is right heart failure secondary to pulmonary disease. COPD causes: (1)
chronic hypoxia → hypoxic pulmonary vasoconstriction, (2) destruction of pulmonary capillary bed
(emphysema), and (3) chronic respiratory acidosis → H⁺-mediated vasoconstriction. These cause
pulmonary hypertension, increasing RV afterload. The thin-walled RV cannot compensate, leading
