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EXAMS
ACTUAL &As|ALREADY GRADED A+ | Questions & Answers (Verified
Answers) With Rationales ( Update)
This Document Contains:
2026 NIGHTINGALE PATHOPHYSIOLOGY FINAL EXAM Exam
Questions & Answers (Verified Answers) With Rationales
100% Guaranteed Pass
Complete A+ Guide
2026 NIGHTINGALE PATHOPHYSIOLOGY FINAL EXAM
ACTUAL &As|ALREADY GRADED A+ - 2026/2027 Update
Page 1
,Question 1
A researcher discovers a mutation in the gene encoding the regulatory subunit of protein kinase A
(PKA) that renders the holoenzyme complex insensitive to cAMP. In a cell line homozygous for this
mutation, which of the following downstream effects is most likely to be observed upon stimulation
of a Gs-coupled receptor?
A) Increased phosphorylation of CREB and enhanced transcription of cAMP-responsive genes
B) No change in PKA activity, but sustained activation of adenylyl cyclase
C) Failure to dissociate the catalytic and regulatory subunits of PKA, leading to absent kinase activity
D) Constitutive activation of PKA independent of receptor stimulation
Answer: C) Failure to dissociate the catalytic and regulatory subunits of PKA, leading to absent
kinase activity
Explanation: cAMP binding to regulatory subunits normally causes dissociation and activation of
catalytic subunits. A mutation preventing cAMP binding or dissociation keeps the
holoenzyme intact and inactive. Options A and D describe gain-of-function effects,
opposite to the mutation. Option B is incorrect because adenylyl cyclase activation
occurs upstream and is unaffected by PKA mutation.
Question 2
In a patient with chronic hypoxemia due to pulmonary fibrosis, which of the following
compensatory mechanisms is most likely to be maladaptive and contribute to further tissue
damage?
A) Increased erythropoietin production leading to polycythemia
B) Hypoxic pulmonary vasoconstriction causing right ventricular hypertrophy
C) Enhanced 2,3-BPG synthesis in erythrocytes shifting the oxygen dissociation curve rightward
D) Upregulation of hypoxia-inducible factor (HIF)-1± target genes promoting angiogenesis
Answer: B) Hypoxic pulmonary vasoconstriction causing right ventricular hypertrophy
Explanation: Hypoxic pulmonary vasoconstriction increases pulmonary artery pressure, leading to
right ventricular hypertrophy and potential cor pulmonale, which is maladaptive.
Polycythemia (A) and rightward shift (C) are compensatory but not directly damaging.
Angiogenesis (D) is adaptive. The question asks for maladaptive contribution to tissue
damage, and right heart failure causes systemic congestion and hypoxia.
Page 2
,Question 3
A 45-year-old individual presents with recurrent thromboembolic episodes. Laboratory evaluation
reveals prolonged activated partial thromboplastin time (aPTT) that does not correct with mixing
studies. Which of the following pathophysiological mechanisms is most likely responsible?
A) Deficiency of protein C or protein S
B) Presence of lupus anticoagulant (antiphospholipid antibody)
C) Mutation in factor V Leiden causing resistance to activated protein C
D) Antithrombin III deficiency
Answer: B) Presence of lupus anticoagulant (antiphospholipid antibody)
Explanation: Lupus anticoagulant prolongs aPTT that does not correct with mixing due to an
inhibitor, and it is associated with thrombosis, not bleeding. Protein C/S deficiency and
factor V Leiden cause thrombosis but do not prolong aPTT. Antithrombin III deficiency
also causes thrombosis but does not prolong aPTT. The non-correcting aPTT is key.
Question 4
Which of the following best explains why individuals with a loss-of-function mutation in the CFTR
gene develop recurrent respiratory infections?
A) Impaired chloride secretion leads to dehydrated mucus that impairs mucociliary clearance
B) Increased sodium absorption causes airway edema and narrowing
C) Defective bicarbonate transport reduces airway pH, inhibiting bacterial killing
D) Accumulation of intracellular chloride triggers apoptosis of epithelial cells
Answer: A) Impaired chloride secretion leads to dehydrated mucus that impairs mucociliary
clearance
Explanation: CFTR mutation impairs chloride secretion, reducing water content in mucus, making it
thick and sticky, which impedes mucociliary clearance and fosters infection. Option B
describes increased sodium absorption (ENaC upregulation) which also contributes but
the primary mechanism is dehydrated mucus. Option C is a secondary effect; option D
is incorrect. The question asks for the best explanation.
Page 3
, Question 5
A researcher is studying a tumor that overexpresses Bcl-2. Which of the following is the most likely
consequence of this overexpression in terms of tumor progression?
A) Increased sensitivity to chemotherapy-induced apoptosis
B) Enhanced angiogenesis through upregulation of VEGF
C) Resistance to apoptosis, allowing survival of cells with DNA damage
D) Increased cell proliferation via activation of cyclin-dependent kinases
Answer: C) Resistance to apoptosis, allowing survival of cells with DNA damage
Explanation: Bcl-2 is an anti-apoptotic protein; overexpression inhibits apoptosis, promoting
survival of genetically damaged cells and resistance to therapy. Option A is opposite.
Option B is not a direct effect of Bcl-2. Option D is incorrect; Bcl-2 does not directly
stimulate proliferation.
Question 6
A patient with a history of chronic alcoholism presents with jaundice, ascites, and esophageal
varices. Laboratory findings show elevated serum bilirubin (direct and indirect), decreased
albumin, and prolonged prothrombin time. Which of the following is the most likely cause of the
prolonged prothrombin time?
A) Vitamin K deficiency due to fat malabsorption
B) Decreased synthesis of clotting factors by the liver
C) Consumption of clotting factors due to disseminated intravascular coagulation
D) Increased fibrinolysis secondary to portal hypertension
Answer: B) Decreased synthesis of clotting factors by the liver
Explanation: Chronic liver disease impairs synthesis of clotting factors (except factor VIII), leading
to prolonged PT. Vitamin K deficiency (A) can occur but is less common in alcoholism
without cholestasis. DIC (C) would also show thrombocytopenia and elevated D-dimer.
Increased fibrinolysis (D) is not typical. The clinical picture of cirrhosis points to
synthetic dysfunction.
Page 4
Download Download
EXAMS
ACTUAL &As|ALREADY GRADED A+ | Questions & Answers (Verified
Answers) With Rationales ( Update)
This Document Contains:
2026 NIGHTINGALE PATHOPHYSIOLOGY FINAL EXAM Exam
Questions & Answers (Verified Answers) With Rationales
100% Guaranteed Pass
Complete A+ Guide
2026 NIGHTINGALE PATHOPHYSIOLOGY FINAL EXAM
ACTUAL &As|ALREADY GRADED A+ - 2026/2027 Update
Page 1
,Question 1
A researcher discovers a mutation in the gene encoding the regulatory subunit of protein kinase A
(PKA) that renders the holoenzyme complex insensitive to cAMP. In a cell line homozygous for this
mutation, which of the following downstream effects is most likely to be observed upon stimulation
of a Gs-coupled receptor?
A) Increased phosphorylation of CREB and enhanced transcription of cAMP-responsive genes
B) No change in PKA activity, but sustained activation of adenylyl cyclase
C) Failure to dissociate the catalytic and regulatory subunits of PKA, leading to absent kinase activity
D) Constitutive activation of PKA independent of receptor stimulation
Answer: C) Failure to dissociate the catalytic and regulatory subunits of PKA, leading to absent
kinase activity
Explanation: cAMP binding to regulatory subunits normally causes dissociation and activation of
catalytic subunits. A mutation preventing cAMP binding or dissociation keeps the
holoenzyme intact and inactive. Options A and D describe gain-of-function effects,
opposite to the mutation. Option B is incorrect because adenylyl cyclase activation
occurs upstream and is unaffected by PKA mutation.
Question 2
In a patient with chronic hypoxemia due to pulmonary fibrosis, which of the following
compensatory mechanisms is most likely to be maladaptive and contribute to further tissue
damage?
A) Increased erythropoietin production leading to polycythemia
B) Hypoxic pulmonary vasoconstriction causing right ventricular hypertrophy
C) Enhanced 2,3-BPG synthesis in erythrocytes shifting the oxygen dissociation curve rightward
D) Upregulation of hypoxia-inducible factor (HIF)-1± target genes promoting angiogenesis
Answer: B) Hypoxic pulmonary vasoconstriction causing right ventricular hypertrophy
Explanation: Hypoxic pulmonary vasoconstriction increases pulmonary artery pressure, leading to
right ventricular hypertrophy and potential cor pulmonale, which is maladaptive.
Polycythemia (A) and rightward shift (C) are compensatory but not directly damaging.
Angiogenesis (D) is adaptive. The question asks for maladaptive contribution to tissue
damage, and right heart failure causes systemic congestion and hypoxia.
Page 2
,Question 3
A 45-year-old individual presents with recurrent thromboembolic episodes. Laboratory evaluation
reveals prolonged activated partial thromboplastin time (aPTT) that does not correct with mixing
studies. Which of the following pathophysiological mechanisms is most likely responsible?
A) Deficiency of protein C or protein S
B) Presence of lupus anticoagulant (antiphospholipid antibody)
C) Mutation in factor V Leiden causing resistance to activated protein C
D) Antithrombin III deficiency
Answer: B) Presence of lupus anticoagulant (antiphospholipid antibody)
Explanation: Lupus anticoagulant prolongs aPTT that does not correct with mixing due to an
inhibitor, and it is associated with thrombosis, not bleeding. Protein C/S deficiency and
factor V Leiden cause thrombosis but do not prolong aPTT. Antithrombin III deficiency
also causes thrombosis but does not prolong aPTT. The non-correcting aPTT is key.
Question 4
Which of the following best explains why individuals with a loss-of-function mutation in the CFTR
gene develop recurrent respiratory infections?
A) Impaired chloride secretion leads to dehydrated mucus that impairs mucociliary clearance
B) Increased sodium absorption causes airway edema and narrowing
C) Defective bicarbonate transport reduces airway pH, inhibiting bacterial killing
D) Accumulation of intracellular chloride triggers apoptosis of epithelial cells
Answer: A) Impaired chloride secretion leads to dehydrated mucus that impairs mucociliary
clearance
Explanation: CFTR mutation impairs chloride secretion, reducing water content in mucus, making it
thick and sticky, which impedes mucociliary clearance and fosters infection. Option B
describes increased sodium absorption (ENaC upregulation) which also contributes but
the primary mechanism is dehydrated mucus. Option C is a secondary effect; option D
is incorrect. The question asks for the best explanation.
Page 3
, Question 5
A researcher is studying a tumor that overexpresses Bcl-2. Which of the following is the most likely
consequence of this overexpression in terms of tumor progression?
A) Increased sensitivity to chemotherapy-induced apoptosis
B) Enhanced angiogenesis through upregulation of VEGF
C) Resistance to apoptosis, allowing survival of cells with DNA damage
D) Increased cell proliferation via activation of cyclin-dependent kinases
Answer: C) Resistance to apoptosis, allowing survival of cells with DNA damage
Explanation: Bcl-2 is an anti-apoptotic protein; overexpression inhibits apoptosis, promoting
survival of genetically damaged cells and resistance to therapy. Option A is opposite.
Option B is not a direct effect of Bcl-2. Option D is incorrect; Bcl-2 does not directly
stimulate proliferation.
Question 6
A patient with a history of chronic alcoholism presents with jaundice, ascites, and esophageal
varices. Laboratory findings show elevated serum bilirubin (direct and indirect), decreased
albumin, and prolonged prothrombin time. Which of the following is the most likely cause of the
prolonged prothrombin time?
A) Vitamin K deficiency due to fat malabsorption
B) Decreased synthesis of clotting factors by the liver
C) Consumption of clotting factors due to disseminated intravascular coagulation
D) Increased fibrinolysis secondary to portal hypertension
Answer: B) Decreased synthesis of clotting factors by the liver
Explanation: Chronic liver disease impairs synthesis of clotting factors (except factor VIII), leading
to prolonged PT. Vitamin K deficiency (A) can occur but is less common in alcoholism
without cholestasis. DIC (C) would also show thrombocytopenia and elevated D-dimer.
Increased fibrinolysis (D) is not typical. The clinical picture of cirrhosis points to
synthetic dysfunction.
Page 4
