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UT Arlington NURS 5315 Exam 3 (pdf) | 2026/2027 | Advanced Pathophysiology Q&A | Pathophysiology

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This document helps you master NURS 5315 Advanced Pathophysiology Exam 3 at UT Arlington via targeted Q&A with detailed rationales. It covers comprehensive, system-specific pathophysiological concepts—including **cardiovascular** (cardiac cycle, pressures, valve function, conduction, myocardial pathologies), **respiratory** (conducting airways, respiratory zone, transpulmonary pressure), **renal** (kidney functions, metabolic waste excretion, RAAS, acid-base balance), **gastrointestinal** (Crohn's vs. ulcerative colitis, portal hypertension and esophageal varices, celiac disease), **endocrine**, **immune** (hematologic alterations), and **neurologic** disorders. It also addresses **fluid/electrolyte** imbalances, **inflammatory processes**, **cellular adaptations**, and **multisystem pathophysiology**. Engineered for retention and clinical judgment with NGN-style clinical scenarios, this test pack simplifies complex pathophysiology content, saving preparation time and ensuring you secure an A on your NURS 5315 Exam 3 assessment.

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UT Arlington NURS 5315 Exam 3 (pdf) | 2026/2027 | Advanced
Pathophysiology Q&A | Pathophysiology

1. A 22-year-old woman presents with fatigue, pallor, and heavy menstrual
bleeding. Laboratory studies show hemoglobin 8.5 g/dL, MCV 72 fL, serum
ferritin 5 ng/mL, and normal vitamin B12 and folate levels. What is the most
likely diagnosis?

A) Vitamin B12 deficiency anemia

B) Folic acid deficiency anemia

C) Iron deficiency anemia

D) Anemia of chronic disease

Correct Answer: Iron deficiency anemia

Rationale: Iron deficiency anemia is characterized by microcytic (low MCV)
and hypochromic red blood cells, low serum ferritin (indicating depleted iron
stores), and occurs in the setting of chronic blood loss (heavy menses). The
normal B12 and folate levels rule out macrocytic anemias.



2. A patient with chronic renal failure is found to have a normocytic,
normochromic anemia. This type of anemia is primarily caused by:

A) Iron deficiency

B) Vitamin B12 deficiency

C) Decreased erythropoietin production

D) Hemolysis

Correct Answer: Decreased erythropoietin production

Rationale: The kidneys produce erythropoietin (EPO), which stimulates red
blood cell production in the bone marrow. In chronic renal failure, damaged
kidneys produce insufficient EPO, leading to a normocytic, normochromic
anemia.



3. Which of the following is a key pathophysiologic feature of sickle cell
anemia?

A) Increased red blood cell production

,B) A point mutation in the beta-globin gene

C) Iron overload

D) Decreased platelet count

Correct Answer: A point mutation in the beta-globin gene

Rationale: Sickle cell anemia is caused by a single nucleotide substitution
(point mutation) in the beta-globin gene, resulting in the production of
abnormal hemoglobin S. Under low oxygen conditions, hemoglobin S
polymerizes, causing red blood cells to sickle.



4. A patient with sickle cell disease presents with acute chest pain, fever,
and hypoxia. This is most consistent with:

A) Aplastic crisis

B) Splenic sequestration

C) Acute chest syndrome

D) Vaso-occlusive crisis

Correct Answer: Acute chest syndrome

Rationale: Acute chest syndrome is a leading cause of death in sickle cell
disease, characterized by chest pain, fever, pulmonary infiltrates, and
hypoxia. It is often triggered by infection or fat embolism from bone marrow
infarction.



5. A patient with immune thrombocytopenic purpura (ITP) has a platelet
count of 15,000/µL. The underlying pathophysiologic mechanism is:

A) Decreased bone marrow production of platelets

B) Increased platelet destruction by autoantibodies

C) Sequestration of platelets in the spleen

D) Disseminated intravascular coagulation

Correct Answer: Increased platelet destruction by autoantibodies

,Rationale: ITP is an autoimmune disorder in which autoantibodies (usually
IgG) bind to platelet membrane glycoproteins, marking them for destruction
by macrophages in the spleen, leading to severe thrombocytopenia.



6. A patient with heparin-induced thrombocytopenia (HIT) develops a low
platelet count and a deep vein thrombosis. The pathophysiologic mechanism
of HIT involves:

A) Direct bone marrow suppression

B) Autoantibodies against platelet factor 4 (PF4) complexed with heparin

C) Splenic sequestration of platelets

D) Decreased platelet production

Correct Answer: Autoantibodies against platelet factor 4 (PF4) complexed
with heparin

Rationale: HIT is an immune-mediated disorder in which antibodies recognize
PF4 bound to heparin, forming immune complexes that activate platelets,
leading to both thrombocytopenia and paradoxical thrombosis.



7. A patient with chronic myeloid leukemia (CML) has the Philadelphia
chromosome. This chromosomal abnormality results in the formation of
which fusion gene?

A) PML-RARA

B) BCR-ABL

C) EWS-FLI1

D) PAX3-FOXO1

Correct Answer: BCR-ABL

Rationale: The Philadelphia chromosome is a translocation between
chromosomes 9 and 22, resulting in the BCR-ABL fusion gene. This gene
produces a constitutively active tyrosine kinase that drives uncontrolled
proliferation of leukemic cells.

, 8. A patient with Hodgkin lymphoma presents with a painless, enlarged
cervical lymph node. A biopsy reveals which pathognomonic cell type?

A) Leukemic blast

B) Reed-Sternberg cell

C) Plasma cell

D) Burkitt cell

Correct Answer: Reed-Sternberg cell

Rationale: Reed-Sternberg cells are large, multinucleated cells that are the
hallmark of Hodgkin lymphoma. Their presence in a lymph node biopsy is
diagnostic and distinguishes it from non-Hodgkin lymphomas.



9. A patient with hemophilia A has a deficiency of which clotting factor?

A) Factor II

B) Factor VIII

C) Factor IX

D) Factor XI

Correct Answer: Factor VIII

Rationale: Hemophilia A is an X-linked recessive disorder caused by a
deficiency of clotting factor VIII. Hemophilia B is caused by a deficiency of
factor IX.



10. Von Willebrand disease is characterized by a deficiency of von Willebrand
factor (vWF). What is the primary function of vWF?

A) To activate factor X

B) To stabilize factor VIII and promote platelet adhesion

C) To convert fibrinogen to fibrin

D) To activate plasminogen

Correct Answer: To stabilize factor VIII and promote platelet adhesion

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