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UTA NURS 5315 Advanced Pathophysiology Exam 2 Practice Test | 100 Questions with Detailed Rationales

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Strengthen your understanding of immune dysfunction, hematological disorders, neoplasia, and disease mechanisms with 100 practice questions and detailed rationales. Designed for graduate nursing students studying advanced pathophysiology and clinical disease processes.

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PASSPOINT PRO | GRADUATE NURSING




NURS 5315
Advanced Pathophysiology
Exam 2 Practice Exam
Immunity, Hematology, and Neoplasia; clinical case questions emphasizing
mechanisms, distinguishing findings, diagnostic patterns, and progression.




100 A-D 100
Practice Questions Multiple Choice Explained Answers




Original study and revision material • PassPoint Pro

, NURS 5315 • Exam 2 Practice Exam




Exam 2 Practice Exam
Focus: Immunity, Hematology, and Neoplasia; clinical case questions emphasizing mechanisms, distinguishing
findings, diagnostic patterns, and progression.

Instructions: Choose the single best answer from A–D for every question. Answers and 3-sentence explanations
follow each item.




1. An older adult has bone pain, anemia, and elevated total protein. Which downstream
outcome can follow this process?
A. Pathologic fractures and kidney failure may occur
B. Untreated disease can progress to blast crisis
C. Immune cytopenias and recurrent infections may develop
D. Bulky disease can compress thoracic structures

Answer: A. Pathologic fractures and kidney failure may occur
Explanation: Progressive Multiple myeloma can lead to pathologic fractures and kidney failure may occur. The risk
is linked to clonal plasma cells produce monoclonal immunoglobulin and damage bone. Early recognition relies on
lytic lesions, renal injury, anemia, or hypercalcemia may occur.



2. A patient has splenomegaly and striking granulocytic leukocytosis. What is the most
likely causal pathway?
A. Clonal myeloid precursor proliferation crowds out normal marrow production
B. BCR-ABL1 tyrosine kinase drives uncontrolled myeloid proliferation
C. Malignant Reed-Sternberg cells stimulate a reactive inflammatory microenvironment
D. Clonal plasma cells produce monoclonal immunoglobulin and damage bone

Answer: B. BCR-ABL1 tyrosine kinase drives uncontrolled myeloid proliferation
Explanation: Chronic myeloid leukemia is driven by BCR-ABL1 tyrosine kinase drives uncontrolled myeloid
proliferation. The case is consistent with marked leukocytosis with a left-shifted granulocyte series. A supporting
objective pattern is philadelphia chromosome t(9;22) and BCR-ABL1 fusion are detectable.



3. A patient with heavy menstrual bleeding has fatigue and microcytosis. Which measured
abnormality would reinforce this interpretation?
A. Bite cells and Heinz body formation may be observed
B. Elevated methylmalonic acid and homocysteine
C. Low ferritin with increased total iron-binding capacity
D. Low serum iron with low or normal TIBC and normal or high ferritin

Answer: C. Low ferritin with increased total iron-binding capacity
Explanation: The predicted diagnostic signature is low ferritin with increased total iron-binding capacity. This
follows from insufficient iron limits hemoglobin synthesis and causes small pale erythrocytes. Correlate it with the
clinical clue: pica and koilonychia may accompany chronic iron depletion.




UTA • Advanced Pathophysiology • PassPoint Pro Page 2

, NURS 5315 • Exam 2 Practice Exam




4. A patient develops jaundice and dark urine after an oxidant medication. Which finding is
most consistent with the suspected disease process?
A. Neuropathy accompanies megaloblastic anemia
B. Pica and koilonychia may accompany chronic iron depletion
C. Iron is sequestered despite adequate or elevated body stores
D. Episodic intravascular hemolysis after oxidant stress

Answer: D. Episodic intravascular hemolysis after oxidant stress
Explanation: A characteristic feature of G6PD deficiency hemolysis is episodic intravascular hemolysis after
oxidant stress. The finding reflects inadequate NADPH protection allows oxidative injury to erythrocytes. The
associated objective pattern is bite cells and Heinz body formation may be observed.



5. A septic patient bleeds from intravenous sites and develops digital ischemia. Which
investigation result would most support the working explanation?
A. Prolonged PT and aPTT with high D-dimer and low fibrinogen
B. Abnormal von Willebrand assays with possible prolonged aPTT
C. Schistocytes and high LDH with usually normal coagulation studies
D. Prolonged aPTT with normal PT and platelet count

Answer: A. Prolonged PT and aPTT with high D-dimer and low fibrinogen
Explanation: The predicted diagnostic signature is prolonged PT and aPTT with high D-dimer and low fibrinogen.
This follows from systemic coagulation activation consumes platelets and clotting factors. Correlate it with the
clinical clue: simultaneous thrombosis and bleeding develop.



6. A young adult has painless cervical adenopathy and intermittent night sweats. Which
downstream outcome can follow this process?
A. Leukostasis or severe infectious complications may develop
B. Bulky disease can compress thoracic structures
C. Immune cytopenias and recurrent infections may develop
D. Untreated disease can progress to blast crisis

Answer: B. Bulky disease can compress thoracic structures
Explanation: Progressive Hodgkin lymphoma can lead to bulky disease can compress thoracic structures. The risk
is linked to malignant Reed-Sternberg cells stimulate a reactive inflammatory microenvironment. Early recognition
relies on contiguous nodal spread and systemic B symptoms may appear.



7. An older adult has bone pain, anemia, and elevated total protein. Which pathophysiologic
mechanism most directly accounts for this presentation?
A. Malignant Reed-Sternberg cells stimulate a reactive inflammatory microenvironment
B. Clonal myeloid precursor proliferation crowds out normal marrow production
C. Clonal plasma cells produce monoclonal immunoglobulin and damage bone
D. BCR-ABL1 tyrosine kinase drives uncontrolled myeloid proliferation

Answer: C. Clonal plasma cells produce monoclonal immunoglobulin and damage bone
Explanation: Multiple myeloma is driven by clonal plasma cells produce monoclonal immunoglobulin and damage
bone. The case is consistent with lytic lesions, renal injury, anemia, or hypercalcemia may occur. A supporting
objective pattern is monoclonal protein with clonal marrow plasma cells.




UTA • Advanced Pathophysiology • PassPoint Pro Page 3

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