NSG 3113 Pathophysiology Final Exam
2026/2027 | Complete Practice Questions,
Correct Answers & Detailed Rationales
Question 1
What is the primary pathophysiological mechanism responsible for the
development of pulmonary congestion in left-sided heart failure?
A. Decreased systemic vascular resistance
B. Inability of the left ventricle to adequately pump blood into the
systemic circulation leading to increased hydrostatic pressure in the
pulmonary capillaries
C. Right ventricular hypertrophy blocking venous return
D. Primary constriction of the bronchial smooth muscle
Correct Answer: B. Inability of the left ventricle to adequately pump
blood into the systemic circulation leading to increased hydrostatic
pressure in the pulmonary capillaries
Detailed Rationale: Left-sided heart failure impairs the heart's ability to
clear blood from the pulmonary circuit. As blood backs up behind the
failing left ventricle, pulmonary capillary hydrostatic pressure rises,
forcing fluid out of the capillaries and into the interstitial and alveolar
spaces, causing pulmonary congestion and edema.
Question 2
,A client develops acute tubular necrosis (ATN) following severe
hypovolemic shock. Which category of acute kidney injury does this
represent?
A. Prerenal AKI
B. Intrarenal (intrinsic) AKI
C. Postrenal AKI
D. Chronic kidney disease stage 5
Correct Answer: B. Intrarenal (intrinsic) AKI
Detailed Rationale: While severe hypovolemic shock initially causes
prerenal AKI due to decreased renal perfusion, prolonged ischemia
results in direct structural damage to the renal tubular epithelial cells,
classifying the resulting acute tubular necrosis as an intrarenal
(intrinsic) form of AKI.
Question 3
Which pathophysiological change is characteristic of chronic bronchitis,
a component of Chronic Obstructive Pulmonary Disease (COPD)?
A. Destruction of alveolar walls and loss of elastic recoil
B. Hyperplasia of goblet cells and mucous hypersecretion in the large
airways
C. Primary pulmonary hypertension without airway involvement
D. Reversible bronchospasm triggered by specific allergens
Correct Answer: B. Hyperplasia of goblet cells and mucous
hypersecretion in the large airways
,Detailed Rationale: Chronic bronchitis is defined clinically by a chronic
productive cough and pathologically by inflammation, hypertrophy of
bronchial mucous glands, and goblet cell hyperplasia, leading to excess
mucus production and airway obstruction. (Alveolar destruction
describes emphysema).
Question 4
What is the primary biochemical mechanism leading to metabolic
acidosis in Diabetic Ketoacidosis (DKA)?
A. Excessive accumulation of lactic acid due to peripheral tissue hypoxia
B. Lipolysis of adipose tissue releasing free fatty acids that are
converted by the liver into ketone bodies (acetoacetate and beta-
hydroxybutyrate)
C. Renal retention of hydrogen ions due to acute tubular necrosis
D. Inability of the kidneys to reabsorb filtered bicarbonate
Correct Answer: B. Lipolysis of adipose tissue releasing free fatty acids
that are converted by the liver into ketone bodies (acetoacetate and
beta-hydroxybutyrate)
Detailed Rationale: Absolute insulin deficiency triggers unrestrained
lipolysis. The resulting excess free fatty acids are transported to the
liver, where beta-oxidation converts them into acidic ketone bodies,
which consume plasma bicarbonate buffers and cause a high anion-gap
metabolic acidosis.
Question 5
, A client experiences an ischemic stroke due to a thrombotic occlusion of
the middle cerebral artery. What is the fundamental cellular event that
occurs in the ischemic penumbra?
A. Immediate irreversible necrosis of all brain tissue within minutes
B. Potentially salvageable tissue experiencing cellular energy failure and
excitotoxicity due to excessive glutamate release
C. Proliferation of glial scar tissue without neuronal involvement
D. Massive hemorrhage into the subarachnoid space
Correct Answer: B. Potentially salvageable tissue experiencing cellular
energy failure and excitotoxicity due to excessive glutamate release
Detailed Rationale: The ischemic penumbra is the region surrounding
the core infarct. Although cells here experience metabolic dysfunction
and are at risk for glutamate-driven excitotoxicity and apoptosis, they
retain collateral blood flow and are potentially salvageable if prompt
reperfusion is achieved.
Question 6
Laboratory results for a client show microcytic, hypochromic
erythrocytes, low serum ferritin, and elevated total iron-binding
capacity (TIBC). Which type of anemia is indicated?
A. Pernicious anemia
B. Iron deficiency anemia
C. Anemia of chronic disease
D. Hemolytic anemia
Correct Answer: B. Iron deficiency anemia
2026/2027 | Complete Practice Questions,
Correct Answers & Detailed Rationales
Question 1
What is the primary pathophysiological mechanism responsible for the
development of pulmonary congestion in left-sided heart failure?
A. Decreased systemic vascular resistance
B. Inability of the left ventricle to adequately pump blood into the
systemic circulation leading to increased hydrostatic pressure in the
pulmonary capillaries
C. Right ventricular hypertrophy blocking venous return
D. Primary constriction of the bronchial smooth muscle
Correct Answer: B. Inability of the left ventricle to adequately pump
blood into the systemic circulation leading to increased hydrostatic
pressure in the pulmonary capillaries
Detailed Rationale: Left-sided heart failure impairs the heart's ability to
clear blood from the pulmonary circuit. As blood backs up behind the
failing left ventricle, pulmonary capillary hydrostatic pressure rises,
forcing fluid out of the capillaries and into the interstitial and alveolar
spaces, causing pulmonary congestion and edema.
Question 2
,A client develops acute tubular necrosis (ATN) following severe
hypovolemic shock. Which category of acute kidney injury does this
represent?
A. Prerenal AKI
B. Intrarenal (intrinsic) AKI
C. Postrenal AKI
D. Chronic kidney disease stage 5
Correct Answer: B. Intrarenal (intrinsic) AKI
Detailed Rationale: While severe hypovolemic shock initially causes
prerenal AKI due to decreased renal perfusion, prolonged ischemia
results in direct structural damage to the renal tubular epithelial cells,
classifying the resulting acute tubular necrosis as an intrarenal
(intrinsic) form of AKI.
Question 3
Which pathophysiological change is characteristic of chronic bronchitis,
a component of Chronic Obstructive Pulmonary Disease (COPD)?
A. Destruction of alveolar walls and loss of elastic recoil
B. Hyperplasia of goblet cells and mucous hypersecretion in the large
airways
C. Primary pulmonary hypertension without airway involvement
D. Reversible bronchospasm triggered by specific allergens
Correct Answer: B. Hyperplasia of goblet cells and mucous
hypersecretion in the large airways
,Detailed Rationale: Chronic bronchitis is defined clinically by a chronic
productive cough and pathologically by inflammation, hypertrophy of
bronchial mucous glands, and goblet cell hyperplasia, leading to excess
mucus production and airway obstruction. (Alveolar destruction
describes emphysema).
Question 4
What is the primary biochemical mechanism leading to metabolic
acidosis in Diabetic Ketoacidosis (DKA)?
A. Excessive accumulation of lactic acid due to peripheral tissue hypoxia
B. Lipolysis of adipose tissue releasing free fatty acids that are
converted by the liver into ketone bodies (acetoacetate and beta-
hydroxybutyrate)
C. Renal retention of hydrogen ions due to acute tubular necrosis
D. Inability of the kidneys to reabsorb filtered bicarbonate
Correct Answer: B. Lipolysis of adipose tissue releasing free fatty acids
that are converted by the liver into ketone bodies (acetoacetate and
beta-hydroxybutyrate)
Detailed Rationale: Absolute insulin deficiency triggers unrestrained
lipolysis. The resulting excess free fatty acids are transported to the
liver, where beta-oxidation converts them into acidic ketone bodies,
which consume plasma bicarbonate buffers and cause a high anion-gap
metabolic acidosis.
Question 5
, A client experiences an ischemic stroke due to a thrombotic occlusion of
the middle cerebral artery. What is the fundamental cellular event that
occurs in the ischemic penumbra?
A. Immediate irreversible necrosis of all brain tissue within minutes
B. Potentially salvageable tissue experiencing cellular energy failure and
excitotoxicity due to excessive glutamate release
C. Proliferation of glial scar tissue without neuronal involvement
D. Massive hemorrhage into the subarachnoid space
Correct Answer: B. Potentially salvageable tissue experiencing cellular
energy failure and excitotoxicity due to excessive glutamate release
Detailed Rationale: The ischemic penumbra is the region surrounding
the core infarct. Although cells here experience metabolic dysfunction
and are at risk for glutamate-driven excitotoxicity and apoptosis, they
retain collateral blood flow and are potentially salvageable if prompt
reperfusion is achieved.
Question 6
Laboratory results for a client show microcytic, hypochromic
erythrocytes, low serum ferritin, and elevated total iron-binding
capacity (TIBC). Which type of anemia is indicated?
A. Pernicious anemia
B. Iron deficiency anemia
C. Anemia of chronic disease
D. Hemolytic anemia
Correct Answer: B. Iron deficiency anemia
