NURS 5315 EXAM 3 (UTA) NEWEST 2026
ACTUAL, EXAM TEST BANK | NURS5315
ADVANCED PATHOPHYSIOLOGY EXAM 3
REVIEW WITH COMPLETE REAL EXAM
QUESTIONS AND CORRECT VERIFIED
ANSWERS/ALREADY GRADED A+ (MOST
RECENT!!) — 300 Questions
Section 1: Alterations in Hematologic Function (Questions 1–30)
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
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, 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.
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
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.
3. 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
Answer: B
Rationale: Acute chest syndrome in sickle cell disease is triggered by
vaso-occlusion in the pulmonary microvasculature. Intravascular
hemolysis releases free hemoglobin, which scavenges nitric oxide,
leading to endothelial dysfunction, vasoconstriction, and increased
adhesion molecule expression. This exacerbates sickling and vascular
occlusion. Option A is incorrect because nitric oxide is decreased, not
increased. Option C is a less common mechanism. Option D is not a
primary factor.
4. A patient with chronic lymphocytic leukemia (CLL) develops
autoimmune hemolytic anemia (AIHA). Which of the following
laboratory findings would most likely be present?
A) Elevated haptoglobin and normal LDH
B) Positive direct antiglobulin test (DAT) with anti-IgG and anti-C3d
C) Low reticulocyte count and elevated bilirubin
D) Schistocytes on peripheral smear and thrombocytopenia
Answer: B
Rationale: AIHA in CLL is typically warm autoimmune hemolytic
anemia due to IgG antibodies. The direct antiglobulin test (DAT) is
positive for IgG and often complement (C3d). Haptoglobin is low (A),
, not elevated; reticulocyte count is high due to compensatory
erythropoiesis (C); schistocytes (D) are seen in microangiopathic
hemolytic anemias, not AIHA.
5. A patient with polycythemia vera (PV) is at increased risk for
thrombotic events despite a normal platelet count. Which of the
following best explains this thrombophilic state?
A) Increased platelet aggregation due to JAK2 V617F mutation-
mediated signaling
B) Decreased levels of protein C and protein S from hepatic congestion
C) Hyperviscosity from elevated white blood cell count
D) Enhanced fibrinolysis leading to consumption of clotting factors
Answer: A
Rationale: In PV, the JAK2 V617F mutation leads to constitutive
activation of the JAK-STAT pathway in myeloid cells, including
platelets. This results in increased platelet activation and aggregation,
promoting thrombosis even with normal platelet counts. Hyperviscosity
(C) from elevated hematocrit also contributes but is not the primary
mechanism; option B is not typical; option D is incorrect because
fibrinolysis is not enhanced.
6. A patient with immune thrombocytopenia (ITP) has a platelet count of
15,000/mcL and experiences epistaxis. Which of the following
treatments would be most appropriate to rapidly increase platelet count?
A) Intravenous immunoglobulin (IVIG) 1 g/kg daily for 2 days
ACTUAL, EXAM TEST BANK | NURS5315
ADVANCED PATHOPHYSIOLOGY EXAM 3
REVIEW WITH COMPLETE REAL EXAM
QUESTIONS AND CORRECT VERIFIED
ANSWERS/ALREADY GRADED A+ (MOST
RECENT!!) — 300 Questions
Section 1: Alterations in Hematologic Function (Questions 1–30)
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
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, 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.
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
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.
3. 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
Answer: B
Rationale: Acute chest syndrome in sickle cell disease is triggered by
vaso-occlusion in the pulmonary microvasculature. Intravascular
hemolysis releases free hemoglobin, which scavenges nitric oxide,
leading to endothelial dysfunction, vasoconstriction, and increased
adhesion molecule expression. This exacerbates sickling and vascular
occlusion. Option A is incorrect because nitric oxide is decreased, not
increased. Option C is a less common mechanism. Option D is not a
primary factor.
4. A patient with chronic lymphocytic leukemia (CLL) develops
autoimmune hemolytic anemia (AIHA). Which of the following
laboratory findings would most likely be present?
A) Elevated haptoglobin and normal LDH
B) Positive direct antiglobulin test (DAT) with anti-IgG and anti-C3d
C) Low reticulocyte count and elevated bilirubin
D) Schistocytes on peripheral smear and thrombocytopenia
Answer: B
Rationale: AIHA in CLL is typically warm autoimmune hemolytic
anemia due to IgG antibodies. The direct antiglobulin test (DAT) is
positive for IgG and often complement (C3d). Haptoglobin is low (A),
, not elevated; reticulocyte count is high due to compensatory
erythropoiesis (C); schistocytes (D) are seen in microangiopathic
hemolytic anemias, not AIHA.
5. A patient with polycythemia vera (PV) is at increased risk for
thrombotic events despite a normal platelet count. Which of the
following best explains this thrombophilic state?
A) Increased platelet aggregation due to JAK2 V617F mutation-
mediated signaling
B) Decreased levels of protein C and protein S from hepatic congestion
C) Hyperviscosity from elevated white blood cell count
D) Enhanced fibrinolysis leading to consumption of clotting factors
Answer: A
Rationale: In PV, the JAK2 V617F mutation leads to constitutive
activation of the JAK-STAT pathway in myeloid cells, including
platelets. This results in increased platelet activation and aggregation,
promoting thrombosis even with normal platelet counts. Hyperviscosity
(C) from elevated hematocrit also contributes but is not the primary
mechanism; option B is not typical; option D is incorrect because
fibrinolysis is not enhanced.
6. A patient with immune thrombocytopenia (ITP) has a platelet count of
15,000/mcL and experiences epistaxis. Which of the following
treatments would be most appropriate to rapidly increase platelet count?
A) Intravenous immunoglobulin (IVIG) 1 g/kg daily for 2 days
