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NURS 5315 EXAM 3 - ADVANCED PATHOPHYSIOLOGY 80 CASE-BASED QUESTIONS WITH RATIONALES80 Questions with Correct Answers and Rationales| GAURANTEED PASS WITH 70+ TEST BANK QUESTIONS 2026 CARRICULUM VERRIFIED TEST INSTANT PDF DOWNLOAD

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NURS 5315 EXAM 3 - ADVANCED PATHOPHYSIOLOGY 80 CASE-BASED QUESTIONS WITH RATIONALES80 Questions with Correct Answers and Rationales| GAURANTEED PASS WITH 70+ TEST BANK QUESTIONS 2026 CARRICULUM VERRIFIED TEST INSTANT PDF DOWNLOAD

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NURS 5315 EXAM 3 - ADVANCED PATHOPHYSIOLOGY

80 CASE-BASED QUESTIONS WITH RATIONALES80

Questions with Correct Answers and Rationales|

GAURANTEED PASS WITH 70+ TEST BANK QUESTIONS 2026

CARRICULUM VERRIFIED TEST INSTANT PDF DOWNLOAD



Question 1:

A patient with chronic kidney disease (CKD) stage 4 presents with
fatigue and pallor. Laboratory findings: hemoglobin 8.2 g/dL, MCV 78
fL, serum iron 30 mcg/dL, TIBC 400 mcg/dL, ferritin 150 ng/mL, and
erythropoietin level inappropriately normal. Which pathophysiologic
mechanism best explains the anemia in this patient?

A) Iron deficiency due to decreased gastrointestinal absorption

B) Impaired erythropoietin production leading to inadequate
erythroid precursor stimulation

C) Chronic inflammation causing hepcidin-mediated iron
sequestration

D) Folate deficiency from dietary restrictions

Correct Answer: C

Rationale: In CKD, anemia often results from a combination of
erythropoietin deficiency and chronic inflammation. The normal
erythropoietin level is inappropriate for the degree of anemia,

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suggesting relative deficiency. However, the low MCV with normal
ferritin and elevated TIBC indicates iron-restricted erythropoiesis
due to hepcidin upregulation from inflammation, which sequesters
iron in macrophages. Option A is less likely because GI absorption is
not the primary issue; option B is incorrect because erythropoietin is
not low; option D is not supported by MCV or history.

Question 2:

A patient with a history of recurrent deep vein thrombosis (DVT) and
pulmonary embolism (PE) is found to have a prolonged activated
partial thromboplastin time (aPTT) that does not correct with mixing
studies. Which of the following is the most likely underlying cause?

A) Factor V Leiden mutation

B) Antiphospholipid syndrome (APS)

C) Protein C deficiency

D) Antithrombin III deficiency

Correct Answer: B

Rationale: A prolonged aPTT that does not correct with mixing
studies suggests the presence of an inhibitor, such as lupus
anticoagulant in antiphospholipid syndrome. Despite the prolonged
aPTT, APS is prothrombotic. Factor V Leiden (A) and protein C
deficiency (C) are associated with normal aPTT; antithrombin III
deficiency (D) also typically does not prolong aPTT. The lack of
correction points to an inhibitor rather than a factor deficiency.

Question 3:

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A patient with sickle cell disease (HbSS) develops acute chest
syndrome after a vaso-occlusive crisis. Which of the following
pathophysiologic mechanisms contributes most directly to the
development of acute chest syndrome?

A) Increased nitric oxide production leading to vasodilation and
pulmonary congestion

B) Intravascular hemolysis causing free hemoglobin scavenging of
nitric oxide and endothelial dysfunction

C) Bone marrow embolism from necrotic bone marrow

D) Pulmonary vasospasm due to cold exposure

Correct Answer: B

Rationale: Acute chest syndrome in sickle cell disease is strongly
associated with intravascular hemolysis, which releases free
hemoglobin that scavenges nitric oxide, leading to pulmonary
vasoconstriction, endothelial dysfunction, and inflammation. This
creates a cycle of hypoxia and sickling. While bone marrow
embolism (C) can occur, it is less common. Option A is incorrect
because nitric oxide is decreased, not increased. Option D describes
a trigger but not the primary mechanism.

Question 4:

A 65-year-old male presents with progressive fatigue, glossitis, and
paresthesias in his lower extremities. Laboratory studies reveal:
hemoglobin 9.1 g/dL, MCV 112 fL, serum B12 180 pg/mL (low), and

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positive intrinsic factor antibodies. Which pathophysiologic process
is responsible for this patient's condition?

A) Autoimmune destruction of gastric parietal cells

B) Dietary deficiency of cobalamin

C) Malabsorption due to ileal resection

D) Transcobalamin deficiency

Correct Answer: A

Rationale: This patient has pernicious anemia, characterized by
autoimmune destruction of gastric parietal cells, leading to
decreased intrinsic factor production and subsequent B12
malabsorption. The positive intrinsic factor antibodies confirm this
diagnosis. The neurologic symptoms (paresthesias) are
characteristic of B12 deficiency. Option B is unlikely given the
antibody findings; option C would not cause positive antibodies;
option D is rare and presents differently.

Question 5:

A patient with acute myeloid leukemia (AML) presents with bleeding
gums, petechiae, and a platelet count of 15,000/μL. Which
mechanism best explains the thrombocytopenia in this patient?

A) Immune-mediated platelet destruction

B) Bone marrow infiltration by leukemic blasts

C) Disseminated intravascular coagulation (DIC)

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Institución
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WGU D648 Leveraging AI and Technology in Strategic

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Subido en
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