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 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
B) Oral prednisone 1 mg/kg daily
C) Rituximab 375 mg/m2 weekly for 4 weeks
D) Platelet transfusion of 6 units
Answer: A
Rationale: IVIG provides a rapid increase in platelet count within 24-48 hours by blocking Fc receptors on
macrophages, reducing platelet destruction. It is preferred for severe bleeding or urgent need. Corticosteroids (B)
take days to weeks; rituximab (C) takes weeks; platelet transfusion (D) is generally ineffective in ITP due to rapid
destruction.
7 A patient with hemophilia A (factor VIII deficiency) develops an inhibitor to factor VIII after replacement
therapy. Which of the following laboratory findings is most consistent with this complication?
A) Prolonged prothrombin time (PT) that corrects with mixing
B) Prolonged activated partial thromboplastin time (aPTT) that does not correct with mixing
,C) Normal aPTT and prolonged bleeding time
D) Decreased factor VIII activity and decreased von Willebrand factor antigen
Answer: B
Rationale: An inhibitor (antibody) to factor VIII causes a prolonged aPTT that does not correct upon mixing with
normal plasma, indicating an inhibitor rather than a factor deficiency. PT (A) is normal in hemophilia A; bleeding
time (C) is normal; von Willebrand factor (D) is normal in hemophilia A.
8 A patient with myelodysplastic syndrome (MDS) has a bone marrow biopsy showing increased blasts (12%)
and ring sideroblasts. Which of the following genetic mutations is most commonly associated with this
phenotype?
A) JAK2 V617F
B) BCR-ABL1
C) SF3B1
D) FLT3-ITD
Answer: C
Rationale: Ring sideroblasts are characteristic of MDS with ring sideroblasts (MDS-RS), and SF3B1 mutations are
found in over 80% of these cases. SF3B1 is a splicing factor gene. JAK2 (A) is associated with myeloproliferative
neoplasms; BCR-ABL1 (B) with CML; FLT3-ITD (D) with AML.
9 A patient with disseminated intravascular coagulation (DIC) secondary to sepsis has a platelet count of
30,000/mcL, prolonged PT and aPTT, elevated D-dimer, and low fibrinogen. Which of the following is the most
appropriate initial management?
A) Administer fresh frozen plasma (FFP) and cryoprecipitate
B) Administer heparin infusion to inhibit thrombin generation
C) Administer tranexamic acid to inhibit fibrinolysis
D) Administer vitamin K to correct coagulopathy
Answer: A
Rationale: In DIC with active bleeding and low fibrinogen, replacement of clotting factors with FFP and
cryoprecipitate (which contains fibrinogen) is indicated. Heparin (B) is controversial and may worsen bleeding;
tranexamic acid (C) is contraindicated as it can promote thrombosis; vitamin K (D) is not effective in acute DIC.
10 A patient with hereditary spherocytosis presents with a hemolytic crisis after a viral infection. Laboratory
findings show hemoglobin 7.0 g/dL, reticulocyte count 12%, and elevated indirect bilirubin. Which of the
following findings on peripheral smear would be most consistent with this diagnosis?
A) Schistocytes and helmet cells
B) Spherocytes with absent central pallor
C) Target cells and basophilic stippling
D) Sickle cells and Howell-Jolly bodies
Answer: B
Rationale: Hereditary spherocytosis is characterized by spherocytes on peripheral smear—small, dense red cells
with loss of central pallor due to membrane protein defects. Schistocytes (A) are seen in microangiopathic
hemolytic anemia; target cells (C) in liver disease or thalassemia; sickle cells (D) in sickle cell disease.
, 11 A 45-year-old man with a history of chronic kidney disease (stage 4) presents with fatigue and pallor.
Laboratory findings show hemoglobin 9.1 g/dL, MCV 78 fL, MCH 26 pg, reticulocyte count 0.5%, and serum
erythropoietin level inappropriately low for the degree of anemia. The peripheral smear shows normocytic,
normochromic red cells with occasional burr cells. Which of the following is the most likely pathophysiologic
mechanism underlying this patient's anemia?
A) Decreased heme synthesis due to iron deficiency
B) Impaired erythropoietin production leading to reduced erythroid progenitor stimulation
C) Increased destruction of erythrocytes due to microangiopathic hemolysis
D) Megaloblastic maturation arrest due to folate deficiency
Answer: B
Rationale: Chronic kidney disease leads to decreased production of erythropoietin by the kidneys, resulting in
normocytic, normochromic anemia with low reticulocyte count and inappropriately low EPO. Iron deficiency (A)
would typically show microcytic hypochromic cells; microangiopathic hemolysis (C) would show schistocytes and
elevated reticulocytes; folate deficiency (D) would cause macrocytic anemia.
12 A 60-year-old woman with no prior hematologic disease undergoes a routine complete blood count. Results:
Hb 12.8 g/dL, WBC 8,500/µL, platelets 450,000/µL. The automated analyzer flags the platelet count as 'high'
and the blood smear shows large, pale blue-staining fragments that are indistinguishable from platelets. Which
of the following is the most appropriate next step to confirm the presence of true thrombocytosis?
A) Repeat the complete blood count in 6 months
B) Perform a platelet aggregation study
C) Obtain a manual platelet count from a citrated blood sample
D) Measure the serum thrombopoietin level
Answer: C
Rationale: The presence of large platelet fragments (likely from a patient with a condition like myelofibrosis or with
EDTA-induced platelet clumping) can be falsely counted as platelets by automated analyzers. A manual platelet
count using a citrated sample reduces clumping and provides an accurate count. Repeating the CBC (A) would not
resolve the artifact; platelet aggregation (B) assesses function, not count; thrombopoietin (D) is not diagnostic for
artifact.
13 A 35-year-old woman presents with easy bruising and heavy menstrual bleeding. Laboratory data: platelet
count 30,000/µL, PT 12 seconds, aPTT 32 seconds, bleeding time >15 minutes. A bone marrow biopsy shows
increased megakaryocytes. Which of the following laboratory findings would most likely distinguish immune
thrombocytopenic purpura (ITP) from other causes of thrombocytopenia?
A) Elevated levels of platelet-associated IgG
B) Decreased levels of von Willebrand factor multimers
C) Presence of schistocytes on peripheral smear
D) Prolonged thrombin time
Answer: A
Rationale: ITP is characterized by autoantibodies against platelet glycoproteins, leading to increased platelet
destruction. Elevated platelet-associated IgG is a hallmark. Decreased von Willebrand factor multimers (B) are
seen in von Willebrand disease; schistocytes (C) indicate microangiopathic hemolytic anemia; prolonged thrombin
time (D) suggests heparin contamination or dysfibrinogenemia.
14 A 50-year-old man with a history of recurrent deep vein thrombosis is found to have a prolonged aPTT that
does not correct with mixing studies (immediate and 2-hour incubation). His PT is normal, and he has no
bleeding history. Which of the following is the most likely diagnosis?
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 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
B) Oral prednisone 1 mg/kg daily
C) Rituximab 375 mg/m2 weekly for 4 weeks
D) Platelet transfusion of 6 units
Answer: A
Rationale: IVIG provides a rapid increase in platelet count within 24-48 hours by blocking Fc receptors on
macrophages, reducing platelet destruction. It is preferred for severe bleeding or urgent need. Corticosteroids (B)
take days to weeks; rituximab (C) takes weeks; platelet transfusion (D) is generally ineffective in ITP due to rapid
destruction.
7 A patient with hemophilia A (factor VIII deficiency) develops an inhibitor to factor VIII after replacement
therapy. Which of the following laboratory findings is most consistent with this complication?
A) Prolonged prothrombin time (PT) that corrects with mixing
B) Prolonged activated partial thromboplastin time (aPTT) that does not correct with mixing
,C) Normal aPTT and prolonged bleeding time
D) Decreased factor VIII activity and decreased von Willebrand factor antigen
Answer: B
Rationale: An inhibitor (antibody) to factor VIII causes a prolonged aPTT that does not correct upon mixing with
normal plasma, indicating an inhibitor rather than a factor deficiency. PT (A) is normal in hemophilia A; bleeding
time (C) is normal; von Willebrand factor (D) is normal in hemophilia A.
8 A patient with myelodysplastic syndrome (MDS) has a bone marrow biopsy showing increased blasts (12%)
and ring sideroblasts. Which of the following genetic mutations is most commonly associated with this
phenotype?
A) JAK2 V617F
B) BCR-ABL1
C) SF3B1
D) FLT3-ITD
Answer: C
Rationale: Ring sideroblasts are characteristic of MDS with ring sideroblasts (MDS-RS), and SF3B1 mutations are
found in over 80% of these cases. SF3B1 is a splicing factor gene. JAK2 (A) is associated with myeloproliferative
neoplasms; BCR-ABL1 (B) with CML; FLT3-ITD (D) with AML.
9 A patient with disseminated intravascular coagulation (DIC) secondary to sepsis has a platelet count of
30,000/mcL, prolonged PT and aPTT, elevated D-dimer, and low fibrinogen. Which of the following is the most
appropriate initial management?
A) Administer fresh frozen plasma (FFP) and cryoprecipitate
B) Administer heparin infusion to inhibit thrombin generation
C) Administer tranexamic acid to inhibit fibrinolysis
D) Administer vitamin K to correct coagulopathy
Answer: A
Rationale: In DIC with active bleeding and low fibrinogen, replacement of clotting factors with FFP and
cryoprecipitate (which contains fibrinogen) is indicated. Heparin (B) is controversial and may worsen bleeding;
tranexamic acid (C) is contraindicated as it can promote thrombosis; vitamin K (D) is not effective in acute DIC.
10 A patient with hereditary spherocytosis presents with a hemolytic crisis after a viral infection. Laboratory
findings show hemoglobin 7.0 g/dL, reticulocyte count 12%, and elevated indirect bilirubin. Which of the
following findings on peripheral smear would be most consistent with this diagnosis?
A) Schistocytes and helmet cells
B) Spherocytes with absent central pallor
C) Target cells and basophilic stippling
D) Sickle cells and Howell-Jolly bodies
Answer: B
Rationale: Hereditary spherocytosis is characterized by spherocytes on peripheral smear—small, dense red cells
with loss of central pallor due to membrane protein defects. Schistocytes (A) are seen in microangiopathic
hemolytic anemia; target cells (C) in liver disease or thalassemia; sickle cells (D) in sickle cell disease.
, 11 A 45-year-old man with a history of chronic kidney disease (stage 4) presents with fatigue and pallor.
Laboratory findings show hemoglobin 9.1 g/dL, MCV 78 fL, MCH 26 pg, reticulocyte count 0.5%, and serum
erythropoietin level inappropriately low for the degree of anemia. The peripheral smear shows normocytic,
normochromic red cells with occasional burr cells. Which of the following is the most likely pathophysiologic
mechanism underlying this patient's anemia?
A) Decreased heme synthesis due to iron deficiency
B) Impaired erythropoietin production leading to reduced erythroid progenitor stimulation
C) Increased destruction of erythrocytes due to microangiopathic hemolysis
D) Megaloblastic maturation arrest due to folate deficiency
Answer: B
Rationale: Chronic kidney disease leads to decreased production of erythropoietin by the kidneys, resulting in
normocytic, normochromic anemia with low reticulocyte count and inappropriately low EPO. Iron deficiency (A)
would typically show microcytic hypochromic cells; microangiopathic hemolysis (C) would show schistocytes and
elevated reticulocytes; folate deficiency (D) would cause macrocytic anemia.
12 A 60-year-old woman with no prior hematologic disease undergoes a routine complete blood count. Results:
Hb 12.8 g/dL, WBC 8,500/µL, platelets 450,000/µL. The automated analyzer flags the platelet count as 'high'
and the blood smear shows large, pale blue-staining fragments that are indistinguishable from platelets. Which
of the following is the most appropriate next step to confirm the presence of true thrombocytosis?
A) Repeat the complete blood count in 6 months
B) Perform a platelet aggregation study
C) Obtain a manual platelet count from a citrated blood sample
D) Measure the serum thrombopoietin level
Answer: C
Rationale: The presence of large platelet fragments (likely from a patient with a condition like myelofibrosis or with
EDTA-induced platelet clumping) can be falsely counted as platelets by automated analyzers. A manual platelet
count using a citrated sample reduces clumping and provides an accurate count. Repeating the CBC (A) would not
resolve the artifact; platelet aggregation (B) assesses function, not count; thrombopoietin (D) is not diagnostic for
artifact.
13 A 35-year-old woman presents with easy bruising and heavy menstrual bleeding. Laboratory data: platelet
count 30,000/µL, PT 12 seconds, aPTT 32 seconds, bleeding time >15 minutes. A bone marrow biopsy shows
increased megakaryocytes. Which of the following laboratory findings would most likely distinguish immune
thrombocytopenic purpura (ITP) from other causes of thrombocytopenia?
A) Elevated levels of platelet-associated IgG
B) Decreased levels of von Willebrand factor multimers
C) Presence of schistocytes on peripheral smear
D) Prolonged thrombin time
Answer: A
Rationale: ITP is characterized by autoantibodies against platelet glycoproteins, leading to increased platelet
destruction. Elevated platelet-associated IgG is a hallmark. Decreased von Willebrand factor multimers (B) are
seen in von Willebrand disease; schistocytes (C) indicate microangiopathic hemolytic anemia; prolonged thrombin
time (D) suggests heparin contamination or dysfibrinogenemia.
14 A 50-year-old man with a history of recurrent deep vein thrombosis is found to have a prolonged aPTT that
does not correct with mixing studies (immediate and 2-hour incubation). His PT is normal, and he has no
bleeding history. Which of the following is the most likely diagnosis?
