NURS 5315 EXAM 5 (UTA) NEWEST 2026 ACTUAL EXAM
TEST BANK| NURS5315 ADVANCED PATHOPHYSIOLOGY
EXAM 5 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. Lab results show
hemoglobin 8.2 g/dL, MCV 78 fL, reticulocyte count 1.2%, serum ferritin 450 ng/mL, transferrin saturation
18%, and serum creatinine 3.5 mg/dL. Which pathophysiologic mechanism is most likely contributing to the
anemia?
A) Iron deficiency due to gastrointestinal losses
B) Diminished erythropoietin production with functional iron deficiency
C) Vitamin B12 deficiency due to impaired absorption
D) Hemolysis from uremic toxins
Answer: B
Rationale: In CKD, erythropoietin production is reduced, and inflammation induces hepcidin, causing functional
iron deficiency despite adequate ferritin. Low transferrin saturation (18%) with normal/high ferritin indicates iron
is sequestered. Microcytosis (MCV 78) is consistent with iron-restricted erythropoiesis. Option A is unlikely
without bleeding history; ferritin is not low. B12 deficiency causes macrocytosis, not microcytosis. Hemolysis
would increase reticulocytes, which is low here.
2 A patient with severe sepsis develops thrombocytopenia (platelets 45,000/¼L) and prolonged PT/PTT. D-dimer
is markedly elevated, fibrinogen is 110 mg/dL. Which of the following best describes the underlying
pathophysiology?
A) Immune-mediated destruction of platelets and consumption of clotting factors
B) Excessive activation of coagulation with depletion of clotting factors and secondary fibrinolysis
C) Impaired synthesis of clotting factors due to liver dysfunction
D) Vitamin K deficiency leading to decreased factors II, VII, IX, X
Answer: B
Rationale: The scenario is classic for disseminated intravascular coagulation (DIC). Sepsis triggers widespread
activation of coagulation, consuming platelets and clotting factors, leading to prolonged PT/PTT and
thrombocytopenia. Elevated D-dimer and low fibrinogen indicate secondary fibrinolysis. Option A describes
immune thrombocytopenia, which does not typically affect PT/PTT or D-dimer. Option C would not explain
elevated D-dimer. Vitamin K deficiency does not cause thrombocytopenia or elevated D-dimer.
3 A patient with known glucose-6-phosphate dehydrogenase (G6PD) deficiency develops acute hemolytic anemia
after receiving an antibiotic. Which laboratory finding would be most consistent with this condition?
A) Positive direct antiglobulin test (Coombs test)
B) Elevated unconjugated bilirubin and decreased haptoglobin
C) Schistocytes on peripheral smear
D) Low serum iron and increased total iron-binding capacity
,Answer: B
Rationale: G6PD deficiency leads to oxidative hemolysis, resulting in extravascular hemolysis with elevated
unconjugated bilirubin and decreased haptoglobin. The direct antiglobulin test (A) is typically negative because
hemolysis is not immune-mediated. Schistocytes (C) are seen in microangiopathic hemolytic anemia, not G6PD.
Low serum iron with increased TIBC (D) suggests iron deficiency, not acute hemolysis.
4 A patient with polycythemia vera (PV) is being evaluated for thrombotic risk. Which of the following laboratory
abnormalities is most directly associated with increased blood viscosity and thrombotic complications in PV?
A) Elevated platelet count with abnormal aggregation
B) Increased red cell mass with normal plasma volume
C) Leukocytosis with left shift
D) Decreased erythropoietin level
Answer: B
Rationale: In PV, increased red cell mass (hematocrit >55%) elevates blood viscosity, predisposing to thrombosis.
While thrombocytosis and platelet dysfunction (A) contribute, the primary driver is increased red cell mass.
Leukocytosis (C) is common but not directly viscosity-related. Low erythropoietin (D) is a diagnostic feature but
not directly thrombogenic.
5 A patient with sickle cell disease (HbSS) presents with acute chest syndrome. Which of the following
mechanisms best explains the development of pulmonary complications in this condition?
A) Chronic hemolysis leading to pulmonary hypertension
B) Vaso-occlusion by sickled red cells causing pulmonary infarction and infection
C) Autoimmune-mediated inflammation of pulmonary vasculature
D) Iron overload from transfusions causing pulmonary fibrosis
Answer: B
Rationale: Acute chest syndrome in sickle cell disease results from vaso-occlusion of pulmonary microvasculature
by sickled red cells, leading to infarction, and often compounded by infection. While chronic hemolysis contributes
to pulmonary hypertension (A) over time, the acute event is vaso-occlusive. Option C is not typical. Iron overload
(D) causes cardiomyopathy, not acute chest syndrome.
6 A patient with immune thrombocytopenic purpura (ITP) has a platelet count of 12,000/¼L. Which of the
following findings would most likely be present on bone marrow examination?
A) Decreased megakaryocytes with increased iron stores
B) Increased megakaryocytes with normal erythroid and myeloid precursors
C) Myelofibrosis with decreased cellularity
D) Lymphocytic infiltration with atypical cells
Answer: B
Rationale: ITP is characterized by immune-mediated destruction of platelets, leading to a compensatory increase in
megakaryocytes in the bone marrow. Other cell lines are typically normal. Option A would suggest impaired
production. Myelofibrosis (C) is not typical. Lymphocytic infiltration (D) suggests lymphoma or leukemia.
7 A patient with chronic lymphocytic leukemia (CLL) develops autoimmune hemolytic anemia (AIHA). Which
laboratory finding is most consistent with this complication?
A) Elevated lactate dehydrogenase (LDH) and indirect bilirubin with spherocytes on smear
B) Low haptoglobin and elevated direct bilirubin
C) Schistocytes and thrombocytopenia
D) Hemoglobinuria and hemosiderinuria
,Answer: A
Rationale: AIHA in CLL is typically warm antibody type, causing extravascular hemolysis with elevated LDH,
indirect (unconjugated) bilirubin, and spherocytes. Haptoglobin is low, but direct bilirubin (B) is not elevated;
indirect is. Schistocytes (C) indicate microangiopathic hemolysis. Hemoglobinuria (D) occurs in intravascular
hemolysis, which is less common in warm AIHA.
8 A patient is found to have prolonged PT and PTT that correct with mixing studies (normal plasma). Which of
the following is the most likely cause?
A) Factor VIII inhibitor
B) Vitamin K deficiency
C) Lupus anticoagulant
D) Disseminated intravascular coagulation
Answer: B
Rationale: Correction with mixing indicates a deficiency of clotting factors, not an inhibitor. Vitamin K deficiency
leads to decreased factors II, VII, IX, X, causing prolonged PT and PTT. Factor VIII inhibitor (A) would not correct
with mixing. Lupus anticoagulant (C) is an inhibitor that typically causes prolonged PTT that does not correct. DIC
(D) may not correct fully due to consumption.
9 A patient with multiple myeloma presents with anemia and rouleaux formation on peripheral smear. Which of
the following best explains the anemia?
A) Iron deficiency from gastrointestinal bleeding
B) Suppression of erythropoiesis by tumor necrosis factor and interleukin-6
C) Autoimmune hemolysis
D) Microangiopathic hemolytic anemia
Answer: B
Rationale: In multiple myeloma, cytokines such as IL-6 and TNF suppress erythropoiesis, leading to anemia of
chronic disease. Rouleaux is due to paraproteins, not iron deficiency (A). Hemolysis (C) is not typical.
Microangiopathic hemolysis (D) is not associated with myeloma.
10 A patient with hereditary hemorrhagic telangiectasia (HHT) presents with iron deficiency anemia. Which of the
following is the most likely etiology?
A) Chronic blood loss from gastrointestinal telangiectasias
B) Impaired iron absorption due to hepcidin dysregulation
C) Hemolysis from abnormal red cell morphology
D) Bone marrow infiltration by arteriovenous malformations
Answer: A
Rationale: HHT is characterized by telangiectasias and arteriovenous malformations that can bleed, especially in the
GI tract, leading to chronic blood loss and iron deficiency anemia. Hepcidin dysregulation (B) is not a feature.
Hemolysis (C) is not typical. Marrow infiltration (D) does not occur.
11 A 45-year-old male with a history of chronic alcoholism presents with fatigue and pallor. Laboratory findings
show macrocytic anemia, elevated homocysteine, and normal methylmalonic acid. Which of the following is
the most likely cause of his anemia?
A) Vitamin B12 deficiency due to pernicious anemia
B) Folate deficiency due to dietary insufficiency
C) Iron deficiency due to chronic blood loss
D) Anemia of chronic disease
, Answer: B
Rationale: Macrocytic anemia with elevated homocysteine but normal methylmalonic acid is characteristic of folate
deficiency, not B12 deficiency. Chronic alcoholism often leads to folate deficiency due to poor diet and impaired
absorption. Pernicious anemia would show elevated methylmalonic acid. Iron deficiency causes microcytic anemia,
and anemia of chronic disease is typically normocytic.
12 In a patient with advanced chronic kidney disease (CKD) not yet on dialysis, which pathophysiologic
mechanism is primarily responsible for the development of anemia?
A) Increased destruction of erythrocytes due to uremic toxins
B) Decreased production of erythropoietin by peritubular interstitial cells
C) Iron sequestration in reticuloendothelial macrophages
D) Folate deficiency due to dietary restrictions
Answer: B
Rationale: In CKD, the primary cause of anemia is insufficient erythropoietin (EPO) production by the kidneys,
specifically from peritubular interstitial cells. While uremic toxins can shorten red cell survival and iron
sequestration occurs in anemia of chronic disease, the hallmark of CKD anemia is EPO deficiency. Folate
deficiency is not a primary mechanism.
13 A patient with a history of recurrent thromboembolism is found to have a mutation in the prothrombin gene
(G20210A). Which of the following best describes the pathophysiologic consequence of this mutation?
A) Increased synthesis of a dysfunctional prothrombin that resists inactivation by activated protein C
B) Elevated plasma prothrombin levels due to increased mRNA stability and translation
C) Decreased activity of antithrombin III due to impaired binding to prothrombin
D) Enhanced cleavage of factor V by prothrombin, leading to a hypercoagulable state
Answer: B
Rationale: The prothrombin G20210A mutation is a gain-of-function polymorphism in the 3'-untranslated region of
the prothrombin gene, leading to increased prothrombin mRNA stability and higher plasma prothrombin levels.
This results in a hypercoagulable state. Option A describes factor V Leiden, not prothrombin mutation.
Antithrombin III activity is not directly affected, and prothrombin does not cleave factor V.
14 A patient with sickle cell disease experiences an acute vaso-occlusive crisis. Which of the following molecular
events is the primary trigger for the sickling of erythrocytes in the microvasculature?
A) Decreased pH and increased 2,3-BPG leading to hemoglobin S polymerization
B) Oxidative damage to the red cell membrane from free heme release
C) Increased adhesion of sickled cells to endothelium via integrin activation
D) Formation of irreversibly sickled cells due to calcium influx
Answer: A
Rationale: The primary trigger for sickling in vaso-occlusive crisis is hemoglobin S polymerization under conditions
of low oxygen tension, acidosis, and increased 2,3-BPG, which reduce hemoglobin's oxygen affinity and promote
deoxygenation. While adhesion and membrane damage contribute to the crisis, polymerization is the initiating
event. Calcium influx occurs later.
15 A 50-year-old female with no significant medical history presents with easy bruising and petechiae. Laboratory
results show: platelet count 15,000/¼L, normal PT and aPTT, and normal hemoglobin and WBC. Which of the
following is the most likely diagnosis?
A) Hemolytic uremic syndrome (HUS)
B) Immune thrombocytopenic purpura (ITP)
TEST BANK| NURS5315 ADVANCED PATHOPHYSIOLOGY
EXAM 5 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. Lab results show
hemoglobin 8.2 g/dL, MCV 78 fL, reticulocyte count 1.2%, serum ferritin 450 ng/mL, transferrin saturation
18%, and serum creatinine 3.5 mg/dL. Which pathophysiologic mechanism is most likely contributing to the
anemia?
A) Iron deficiency due to gastrointestinal losses
B) Diminished erythropoietin production with functional iron deficiency
C) Vitamin B12 deficiency due to impaired absorption
D) Hemolysis from uremic toxins
Answer: B
Rationale: In CKD, erythropoietin production is reduced, and inflammation induces hepcidin, causing functional
iron deficiency despite adequate ferritin. Low transferrin saturation (18%) with normal/high ferritin indicates iron
is sequestered. Microcytosis (MCV 78) is consistent with iron-restricted erythropoiesis. Option A is unlikely
without bleeding history; ferritin is not low. B12 deficiency causes macrocytosis, not microcytosis. Hemolysis
would increase reticulocytes, which is low here.
2 A patient with severe sepsis develops thrombocytopenia (platelets 45,000/¼L) and prolonged PT/PTT. D-dimer
is markedly elevated, fibrinogen is 110 mg/dL. Which of the following best describes the underlying
pathophysiology?
A) Immune-mediated destruction of platelets and consumption of clotting factors
B) Excessive activation of coagulation with depletion of clotting factors and secondary fibrinolysis
C) Impaired synthesis of clotting factors due to liver dysfunction
D) Vitamin K deficiency leading to decreased factors II, VII, IX, X
Answer: B
Rationale: The scenario is classic for disseminated intravascular coagulation (DIC). Sepsis triggers widespread
activation of coagulation, consuming platelets and clotting factors, leading to prolonged PT/PTT and
thrombocytopenia. Elevated D-dimer and low fibrinogen indicate secondary fibrinolysis. Option A describes
immune thrombocytopenia, which does not typically affect PT/PTT or D-dimer. Option C would not explain
elevated D-dimer. Vitamin K deficiency does not cause thrombocytopenia or elevated D-dimer.
3 A patient with known glucose-6-phosphate dehydrogenase (G6PD) deficiency develops acute hemolytic anemia
after receiving an antibiotic. Which laboratory finding would be most consistent with this condition?
A) Positive direct antiglobulin test (Coombs test)
B) Elevated unconjugated bilirubin and decreased haptoglobin
C) Schistocytes on peripheral smear
D) Low serum iron and increased total iron-binding capacity
,Answer: B
Rationale: G6PD deficiency leads to oxidative hemolysis, resulting in extravascular hemolysis with elevated
unconjugated bilirubin and decreased haptoglobin. The direct antiglobulin test (A) is typically negative because
hemolysis is not immune-mediated. Schistocytes (C) are seen in microangiopathic hemolytic anemia, not G6PD.
Low serum iron with increased TIBC (D) suggests iron deficiency, not acute hemolysis.
4 A patient with polycythemia vera (PV) is being evaluated for thrombotic risk. Which of the following laboratory
abnormalities is most directly associated with increased blood viscosity and thrombotic complications in PV?
A) Elevated platelet count with abnormal aggregation
B) Increased red cell mass with normal plasma volume
C) Leukocytosis with left shift
D) Decreased erythropoietin level
Answer: B
Rationale: In PV, increased red cell mass (hematocrit >55%) elevates blood viscosity, predisposing to thrombosis.
While thrombocytosis and platelet dysfunction (A) contribute, the primary driver is increased red cell mass.
Leukocytosis (C) is common but not directly viscosity-related. Low erythropoietin (D) is a diagnostic feature but
not directly thrombogenic.
5 A patient with sickle cell disease (HbSS) presents with acute chest syndrome. Which of the following
mechanisms best explains the development of pulmonary complications in this condition?
A) Chronic hemolysis leading to pulmonary hypertension
B) Vaso-occlusion by sickled red cells causing pulmonary infarction and infection
C) Autoimmune-mediated inflammation of pulmonary vasculature
D) Iron overload from transfusions causing pulmonary fibrosis
Answer: B
Rationale: Acute chest syndrome in sickle cell disease results from vaso-occlusion of pulmonary microvasculature
by sickled red cells, leading to infarction, and often compounded by infection. While chronic hemolysis contributes
to pulmonary hypertension (A) over time, the acute event is vaso-occlusive. Option C is not typical. Iron overload
(D) causes cardiomyopathy, not acute chest syndrome.
6 A patient with immune thrombocytopenic purpura (ITP) has a platelet count of 12,000/¼L. Which of the
following findings would most likely be present on bone marrow examination?
A) Decreased megakaryocytes with increased iron stores
B) Increased megakaryocytes with normal erythroid and myeloid precursors
C) Myelofibrosis with decreased cellularity
D) Lymphocytic infiltration with atypical cells
Answer: B
Rationale: ITP is characterized by immune-mediated destruction of platelets, leading to a compensatory increase in
megakaryocytes in the bone marrow. Other cell lines are typically normal. Option A would suggest impaired
production. Myelofibrosis (C) is not typical. Lymphocytic infiltration (D) suggests lymphoma or leukemia.
7 A patient with chronic lymphocytic leukemia (CLL) develops autoimmune hemolytic anemia (AIHA). Which
laboratory finding is most consistent with this complication?
A) Elevated lactate dehydrogenase (LDH) and indirect bilirubin with spherocytes on smear
B) Low haptoglobin and elevated direct bilirubin
C) Schistocytes and thrombocytopenia
D) Hemoglobinuria and hemosiderinuria
,Answer: A
Rationale: AIHA in CLL is typically warm antibody type, causing extravascular hemolysis with elevated LDH,
indirect (unconjugated) bilirubin, and spherocytes. Haptoglobin is low, but direct bilirubin (B) is not elevated;
indirect is. Schistocytes (C) indicate microangiopathic hemolysis. Hemoglobinuria (D) occurs in intravascular
hemolysis, which is less common in warm AIHA.
8 A patient is found to have prolonged PT and PTT that correct with mixing studies (normal plasma). Which of
the following is the most likely cause?
A) Factor VIII inhibitor
B) Vitamin K deficiency
C) Lupus anticoagulant
D) Disseminated intravascular coagulation
Answer: B
Rationale: Correction with mixing indicates a deficiency of clotting factors, not an inhibitor. Vitamin K deficiency
leads to decreased factors II, VII, IX, X, causing prolonged PT and PTT. Factor VIII inhibitor (A) would not correct
with mixing. Lupus anticoagulant (C) is an inhibitor that typically causes prolonged PTT that does not correct. DIC
(D) may not correct fully due to consumption.
9 A patient with multiple myeloma presents with anemia and rouleaux formation on peripheral smear. Which of
the following best explains the anemia?
A) Iron deficiency from gastrointestinal bleeding
B) Suppression of erythropoiesis by tumor necrosis factor and interleukin-6
C) Autoimmune hemolysis
D) Microangiopathic hemolytic anemia
Answer: B
Rationale: In multiple myeloma, cytokines such as IL-6 and TNF suppress erythropoiesis, leading to anemia of
chronic disease. Rouleaux is due to paraproteins, not iron deficiency (A). Hemolysis (C) is not typical.
Microangiopathic hemolysis (D) is not associated with myeloma.
10 A patient with hereditary hemorrhagic telangiectasia (HHT) presents with iron deficiency anemia. Which of the
following is the most likely etiology?
A) Chronic blood loss from gastrointestinal telangiectasias
B) Impaired iron absorption due to hepcidin dysregulation
C) Hemolysis from abnormal red cell morphology
D) Bone marrow infiltration by arteriovenous malformations
Answer: A
Rationale: HHT is characterized by telangiectasias and arteriovenous malformations that can bleed, especially in the
GI tract, leading to chronic blood loss and iron deficiency anemia. Hepcidin dysregulation (B) is not a feature.
Hemolysis (C) is not typical. Marrow infiltration (D) does not occur.
11 A 45-year-old male with a history of chronic alcoholism presents with fatigue and pallor. Laboratory findings
show macrocytic anemia, elevated homocysteine, and normal methylmalonic acid. Which of the following is
the most likely cause of his anemia?
A) Vitamin B12 deficiency due to pernicious anemia
B) Folate deficiency due to dietary insufficiency
C) Iron deficiency due to chronic blood loss
D) Anemia of chronic disease
, Answer: B
Rationale: Macrocytic anemia with elevated homocysteine but normal methylmalonic acid is characteristic of folate
deficiency, not B12 deficiency. Chronic alcoholism often leads to folate deficiency due to poor diet and impaired
absorption. Pernicious anemia would show elevated methylmalonic acid. Iron deficiency causes microcytic anemia,
and anemia of chronic disease is typically normocytic.
12 In a patient with advanced chronic kidney disease (CKD) not yet on dialysis, which pathophysiologic
mechanism is primarily responsible for the development of anemia?
A) Increased destruction of erythrocytes due to uremic toxins
B) Decreased production of erythropoietin by peritubular interstitial cells
C) Iron sequestration in reticuloendothelial macrophages
D) Folate deficiency due to dietary restrictions
Answer: B
Rationale: In CKD, the primary cause of anemia is insufficient erythropoietin (EPO) production by the kidneys,
specifically from peritubular interstitial cells. While uremic toxins can shorten red cell survival and iron
sequestration occurs in anemia of chronic disease, the hallmark of CKD anemia is EPO deficiency. Folate
deficiency is not a primary mechanism.
13 A patient with a history of recurrent thromboembolism is found to have a mutation in the prothrombin gene
(G20210A). Which of the following best describes the pathophysiologic consequence of this mutation?
A) Increased synthesis of a dysfunctional prothrombin that resists inactivation by activated protein C
B) Elevated plasma prothrombin levels due to increased mRNA stability and translation
C) Decreased activity of antithrombin III due to impaired binding to prothrombin
D) Enhanced cleavage of factor V by prothrombin, leading to a hypercoagulable state
Answer: B
Rationale: The prothrombin G20210A mutation is a gain-of-function polymorphism in the 3'-untranslated region of
the prothrombin gene, leading to increased prothrombin mRNA stability and higher plasma prothrombin levels.
This results in a hypercoagulable state. Option A describes factor V Leiden, not prothrombin mutation.
Antithrombin III activity is not directly affected, and prothrombin does not cleave factor V.
14 A patient with sickle cell disease experiences an acute vaso-occlusive crisis. Which of the following molecular
events is the primary trigger for the sickling of erythrocytes in the microvasculature?
A) Decreased pH and increased 2,3-BPG leading to hemoglobin S polymerization
B) Oxidative damage to the red cell membrane from free heme release
C) Increased adhesion of sickled cells to endothelium via integrin activation
D) Formation of irreversibly sickled cells due to calcium influx
Answer: A
Rationale: The primary trigger for sickling in vaso-occlusive crisis is hemoglobin S polymerization under conditions
of low oxygen tension, acidosis, and increased 2,3-BPG, which reduce hemoglobin's oxygen affinity and promote
deoxygenation. While adhesion and membrane damage contribute to the crisis, polymerization is the initiating
event. Calcium influx occurs later.
15 A 50-year-old female with no significant medical history presents with easy bruising and petechiae. Laboratory
results show: platelet count 15,000/¼L, normal PT and aPTT, and normal hemoglobin and WBC. Which of the
following is the most likely diagnosis?
A) Hemolytic uremic syndrome (HUS)
B) Immune thrombocytopenic purpura (ITP)
