BIOD 331 PATHOPHYSIOLOGY EXAM 6 || 2026–2027||quESTIOnS AnD
AnSwErS wITH rATIOnALES/GrADED A+/2026 uPDATE/100%
cOrrEcT /InSTAnT DOwnLOAD
SECTION 1: HEMATOLOGIC DISORDERS (QUESTIONS 1-25)
Question 1
A patient with iron deficiency anemia has which peripheral blood smear finding?
A) Macrocytic ovalocytes (B12/folate deficiency)
B) Microcytic, hypochromic red blood cells
C) Schistocytes (helmet cells)
D) Spherocytes
Answer: B) Microcytic, hypochromic red blood cells
Rationale: Iron deficiency anemia causes microcytic (small MCV) and hypochromic (low MCHC) RBCs
due to insufficient iron for heme synthesis. Macrocytic ovalocytes (A) occur in B12/folate deficiency.
Schistocytes (C) indicate microangiopathic hemolytic anemia (TTP, DIC, HUS). Spherocytes (D) occur in
hereditary spherocytosis or autoimmune hemolytic anemia. Common causes of iron deficiency include
chronic blood loss (GI bleeding, menorrhagia), inadequate dietary intake, and malabsorption (celiac
disease, gastric bypass).
Question 2
A patient with vitamin B12 deficiency (pernicious anemia) has a mean corpuscular volume (MCV) of
110 fL (normal 80-100). This type of anemia is classified as:
A) Microcytic anemia
B) Normocytic anemia
,C) Macrocytic anemia
D) Hypochromic anemia
Answer: C) Macrocytic anemia
Rationale: Macrocytic anemia (MCV >100 fL) is caused by impaired DNA synthesis, leading to
megaloblastic erythroblasts. Causes include vitamin B12 deficiency (pernicious anemia, dietary
deficiency, malabsorption) and folate deficiency. Pernicious anemia is caused by autoimmune
destruction of gastric parietal cells, leading to intrinsic factor deficiency and B12 malabsorption.
Treatment is lifelong vitamin B12 injections (1000 mcg IM monthly). Neurologic symptoms (subacute
combined degeneration of the spinal cord) are also seen in B12 deficiency (not in folate deficiency).
Question 3
A patient with sickle cell disease develops acute chest syndrome. The underlying pathophysiology is:
A) Massive iron overload from transfusions
B) Vaso-occlusion in pulmonary microvasculature leading to infarction and inflammation
C) Autoimmune destruction of RBCs
D) Vitamin B12 deficiency
Answer: B) Vaso-occlusion in pulmonary microvasculature leading to infarction and inflammation
Rationale: Acute chest syndrome in sickle cell disease results from vaso-occlusion of sickled RBCs in
pulmonary microvasculature, causing pulmonary infarction, inflammation, and hypoxemia. It presents
with fever, chest pain, cough, and new pulmonary infiltrate on chest X-ray. It is a leading cause of
death in sickle cell disease and requires urgent treatment (exchange transfusion, oxygen, antibiotics,
pain management). Other complications of sickle cell disease include vaso-occlusive pain crises,
stroke, priapism, avascular necrosis of femoral head, and splenic sequestration.
Question 4
A patient with heparin-induced thrombocytopenia (HIT) develops arterial thrombosis. The mechanism
is:
,A) Direct platelet activation by heparin
B) Immune complexes (IgG-heparin-PF4) activating platelets via Fc receptors
C) Decreased antithrombin III activity
D) Bone marrow suppression
Answer: B) Immune complexes (IgG-heparin-PF4) activating platelets via Fc receptors
Rationale: HIT is an immune-mediated reaction where antibodies form against heparin-platelet factor
4 (PF4) complexes. These immune complexes bind to platelet Fc receptors, activating platelets and
causing paradoxical thrombosis (not bleeding despite thrombocytopenia). This can cause life-
threatening arterial and venous thrombosis (DVT, PE, stroke, MI). Treatment requires stopping heparin
and using non-heparin anticoagulants (argatroban, fondaparinux, bivalirudin). Platelet transfusion is
contraindicated (may worsen thrombosis). HIT typically occurs 5-10 days after heparin exposure.
Question 5
A patient with immune thrombocytopenic purpura (ITP) has a low platelet count. The mechanism is:
A) Decreased platelet production in bone marrow
B) Autoantibodies (IgG) against platelet glycoproteins leading to splenic destruction
C) Disseminated intravascular coagulation (DIC)
D) Splenic sequestration without destruction
Answer: B) Autoantibodies (IgG) against platelet glycoproteins leading to splenic destruction
Rationale: ITP is an autoimmune disorder where IgG autoantibodies target platelet glycoproteins
(e.g., GPIIb/IIIa). Antibody-coated platelets are destroyed by splenic macrophages, causing isolated
thrombocytopenia. Bone marrow production is normal or increased (megakaryocytes are increased).
DIC (C) causes consumption of clotting factors with bleeding and thrombosis. Treatment includes
corticosteroids (prednisone), IVIG, anti-D (for Rh-positive patients), rituximab, and splenectomy (for
refractory cases). Avoid antiplatelet agents (aspirin, clopidogrel) and anticoagulants.
, Question 6
A patient with polycythemia vera has an elevated hematocrit. The most serious complication of this
condition is:
A) Iron deficiency
B) Thrombotic events (stroke, MI, DVT)
C) Hemolytic anemia
D) Bone marrow failure
Answer: B) Thrombotic events (stroke, MI, DVT)
Rationale: Polycythemia vera (PV) is a myeloproliferative neoplasm with increased RBC mass, leading
to hyperviscosity. The resulting sluggish blood flow increases the risk of thrombosis—arterial (stroke,
MI, transient ischemic attack) and venous (DVT, PE, hepatic vein thrombosis/Budd-Chiari syndrome,
splanchnic vein thrombosis). Treatment includes phlebotomy to keep hematocrit <45 percent, low-
dose aspirin, and hydroxyurea (for high-risk patients). Iron deficiency (A) may develop from
phlebotomy but is not the most serious complication.
Question 7
A patient with disseminated intravascular coagulation (DIC) has both bleeding and thrombosis. The
underlying pathophysiology is:
A) Isolated platelet deficiency
B) Widespread activation of coagulation leading to consumption of clotting factors and platelets, with
fibrinolysis
C) Vitamin K deficiency
D) Autoimmune destruction of clotting factors
Answer: B) Widespread activation of coagulation leading to consumption of clotting factors and
platelets, with fibrinolysis
AnSwErS wITH rATIOnALES/GrADED A+/2026 uPDATE/100%
cOrrEcT /InSTAnT DOwnLOAD
SECTION 1: HEMATOLOGIC DISORDERS (QUESTIONS 1-25)
Question 1
A patient with iron deficiency anemia has which peripheral blood smear finding?
A) Macrocytic ovalocytes (B12/folate deficiency)
B) Microcytic, hypochromic red blood cells
C) Schistocytes (helmet cells)
D) Spherocytes
Answer: B) Microcytic, hypochromic red blood cells
Rationale: Iron deficiency anemia causes microcytic (small MCV) and hypochromic (low MCHC) RBCs
due to insufficient iron for heme synthesis. Macrocytic ovalocytes (A) occur in B12/folate deficiency.
Schistocytes (C) indicate microangiopathic hemolytic anemia (TTP, DIC, HUS). Spherocytes (D) occur in
hereditary spherocytosis or autoimmune hemolytic anemia. Common causes of iron deficiency include
chronic blood loss (GI bleeding, menorrhagia), inadequate dietary intake, and malabsorption (celiac
disease, gastric bypass).
Question 2
A patient with vitamin B12 deficiency (pernicious anemia) has a mean corpuscular volume (MCV) of
110 fL (normal 80-100). This type of anemia is classified as:
A) Microcytic anemia
B) Normocytic anemia
,C) Macrocytic anemia
D) Hypochromic anemia
Answer: C) Macrocytic anemia
Rationale: Macrocytic anemia (MCV >100 fL) is caused by impaired DNA synthesis, leading to
megaloblastic erythroblasts. Causes include vitamin B12 deficiency (pernicious anemia, dietary
deficiency, malabsorption) and folate deficiency. Pernicious anemia is caused by autoimmune
destruction of gastric parietal cells, leading to intrinsic factor deficiency and B12 malabsorption.
Treatment is lifelong vitamin B12 injections (1000 mcg IM monthly). Neurologic symptoms (subacute
combined degeneration of the spinal cord) are also seen in B12 deficiency (not in folate deficiency).
Question 3
A patient with sickle cell disease develops acute chest syndrome. The underlying pathophysiology is:
A) Massive iron overload from transfusions
B) Vaso-occlusion in pulmonary microvasculature leading to infarction and inflammation
C) Autoimmune destruction of RBCs
D) Vitamin B12 deficiency
Answer: B) Vaso-occlusion in pulmonary microvasculature leading to infarction and inflammation
Rationale: Acute chest syndrome in sickle cell disease results from vaso-occlusion of sickled RBCs in
pulmonary microvasculature, causing pulmonary infarction, inflammation, and hypoxemia. It presents
with fever, chest pain, cough, and new pulmonary infiltrate on chest X-ray. It is a leading cause of
death in sickle cell disease and requires urgent treatment (exchange transfusion, oxygen, antibiotics,
pain management). Other complications of sickle cell disease include vaso-occlusive pain crises,
stroke, priapism, avascular necrosis of femoral head, and splenic sequestration.
Question 4
A patient with heparin-induced thrombocytopenia (HIT) develops arterial thrombosis. The mechanism
is:
,A) Direct platelet activation by heparin
B) Immune complexes (IgG-heparin-PF4) activating platelets via Fc receptors
C) Decreased antithrombin III activity
D) Bone marrow suppression
Answer: B) Immune complexes (IgG-heparin-PF4) activating platelets via Fc receptors
Rationale: HIT is an immune-mediated reaction where antibodies form against heparin-platelet factor
4 (PF4) complexes. These immune complexes bind to platelet Fc receptors, activating platelets and
causing paradoxical thrombosis (not bleeding despite thrombocytopenia). This can cause life-
threatening arterial and venous thrombosis (DVT, PE, stroke, MI). Treatment requires stopping heparin
and using non-heparin anticoagulants (argatroban, fondaparinux, bivalirudin). Platelet transfusion is
contraindicated (may worsen thrombosis). HIT typically occurs 5-10 days after heparin exposure.
Question 5
A patient with immune thrombocytopenic purpura (ITP) has a low platelet count. The mechanism is:
A) Decreased platelet production in bone marrow
B) Autoantibodies (IgG) against platelet glycoproteins leading to splenic destruction
C) Disseminated intravascular coagulation (DIC)
D) Splenic sequestration without destruction
Answer: B) Autoantibodies (IgG) against platelet glycoproteins leading to splenic destruction
Rationale: ITP is an autoimmune disorder where IgG autoantibodies target platelet glycoproteins
(e.g., GPIIb/IIIa). Antibody-coated platelets are destroyed by splenic macrophages, causing isolated
thrombocytopenia. Bone marrow production is normal or increased (megakaryocytes are increased).
DIC (C) causes consumption of clotting factors with bleeding and thrombosis. Treatment includes
corticosteroids (prednisone), IVIG, anti-D (for Rh-positive patients), rituximab, and splenectomy (for
refractory cases). Avoid antiplatelet agents (aspirin, clopidogrel) and anticoagulants.
, Question 6
A patient with polycythemia vera has an elevated hematocrit. The most serious complication of this
condition is:
A) Iron deficiency
B) Thrombotic events (stroke, MI, DVT)
C) Hemolytic anemia
D) Bone marrow failure
Answer: B) Thrombotic events (stroke, MI, DVT)
Rationale: Polycythemia vera (PV) is a myeloproliferative neoplasm with increased RBC mass, leading
to hyperviscosity. The resulting sluggish blood flow increases the risk of thrombosis—arterial (stroke,
MI, transient ischemic attack) and venous (DVT, PE, hepatic vein thrombosis/Budd-Chiari syndrome,
splanchnic vein thrombosis). Treatment includes phlebotomy to keep hematocrit <45 percent, low-
dose aspirin, and hydroxyurea (for high-risk patients). Iron deficiency (A) may develop from
phlebotomy but is not the most serious complication.
Question 7
A patient with disseminated intravascular coagulation (DIC) has both bleeding and thrombosis. The
underlying pathophysiology is:
A) Isolated platelet deficiency
B) Widespread activation of coagulation leading to consumption of clotting factors and platelets, with
fibrinolysis
C) Vitamin K deficiency
D) Autoimmune destruction of clotting factors
Answer: B) Widespread activation of coagulation leading to consumption of clotting factors and
platelets, with fibrinolysis
