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This premium study resource features a comprehensive bank of 180 highly rigorous, multi-choice practice exam questions explicitly tailored to the advanced nursing curriculum.

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This premium study resource features a comprehensive bank of 180 highly rigorous, multi-choice practice exam questions explicitly tailored to the advanced nursing curriculum.

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NSG 3850 Exam 2 Pathophysiology II
Comprehensive Test Bank High-Yield Prep
Questions, Verified Answers & Clinical
Rationales (A+ Graded Guide)




Question 1

A patient with chronic kidney disease presents with a hemoglobin level of 8.2
g/dL. The nurse understands that this anemia is primarily caused by a deficiency
in which hormone?

 A) Renin
 B) Angiotensin
 C) Erythropoietin
 D) Aldosterone
 VERIFIED ANSWER: C
 EXPLANATION: Erythropoietin is synthesized and secreted by the kidneys in
response to cellular hypoxia. It travels to the bone marrow to stimulate the
production of red blood cells. In chronic kidney disease, functional renal
tissue is lost, leading to deficient erythropoietin production and subsequent
chronic anemia.

, Question 2

During a blood transfusion, a patient experiences acute hemolytic transfusion
reaction symptoms including lower back pain and hematuria. Which
hypersensitivity mechanism mediates this life-threatening response?

 A) Type I (IgE-mediated)
 B) Type II (Tissue-specific/Cytotoxic)
 C) Type III (Immune complex-mediated)
 D) Type IV (Cell-mediated/Delayed)
 VERIFIED ANSWER: B
 EXPLANATION: An acute hemolytic transfusion reaction is a classic Type II
hypersensitivity reaction. Pre-existing antibodies (IgG or IgM) in the
recipient's plasma bind to foreign antigens on the donor's red blood cells,
activating the complement cascade and causing immediate intravascular
hemolysis.
Question 3

A patient is diagnosed with Pernicious Anemia. The nurse notes that the
patient's peripheral blood smear demonstrates macrocytic, normochromic red
blood cells. What is the fundamental cause of this disorder?

 A) Chronic dietary iron deficiency
 B) Autoimmune destruction of gastric parietal cells
 C) Acute blood loss from the gastrointestinal tract
 D) Defective synthesis of the alpha polypeptide chain
 VERIFIED ANSWER: B
 EXPLANATION: Pernicious anemia is an autoimmune gastritis condition
where the immune system destroys gastric parietal cells. These cells are
responsible for secreting intrinsic factor, which is required for Vitamin B12

, absorption in the ileum. Vitamin B12 deficiency alters DNA synthesis,
resulting in macrocytic (megaloblastic) RBC development.
Question 4

A nurse is evaluating the lab results of a patient suspected of having
Disseminated Intravascular Coagulation (DIC). Which unique laboratory
finding strongly confirms the widespread degradation of fibrin clots?

 A) Elevated D-dimer levels
 B) Prolonged Prothrombin Time (PT)
 C) Decreased platelet count
 D) Depleted fibrinogen levels
 VERIFIED ANSWER: A
 EXPLANATION: While prolonged PT, low platelets, and low fibrinogen
occur in DIC, they can also occur in other clotting or hepatic disorders. An
elevated D-dimer specifically measures fibrin degradation products resulting
from the breakdown of cross-linked fibrin clots, confirming simultaneous
systemic clotting and fibrinolysis.
Question 5

A patient with a history of deep vein thrombosis (DVT) is diagnosed with a
pulmonary embolism. The nurse recognizes that this represents a failure in
which phase of the V/Q (Ventilation/Perfusion) relationship?

 A) Decreased ventilation with normal perfusion
 B) Alveolar dead space where ventilation occurs without perfusion
 C) Intrapulmonary shunting where perfusion occurs without ventilation
 D) Diffuse airway collapse blocking both ventilation and perfusion
 VERIFIED ANSWER: B
 EXPLANATION: A pulmonary embolism physically obstructs blood flow
through the pulmonary vasculature, resulting in an area of the lung that is

, ventilated (receives air) but not perfused (does not receive blood). This
mismatch is termed alveolar dead space.
Question 6

Which physiological process describes the compensation mechanism for a
patient in acute respiratory acidosis due to hypoventilation?

 A) Hyperventilation to blow off excess carbon dioxide
 B) Renal retention of bicarbonate ions and excretion of hydrogen ions
 C) Cellular shifting of potassium ions out of the cell into plasma
 D) Increased hepatic synthesis of plasma albumin proteins
 VERIFIED ANSWER: B
 EXPLANATION: In respiratory acidosis, the primary defect is high arterial
CO2. Since the lungs cannot adequately clear it due to hypoventilation, the
kidneys compensate over a period of 24 to 72 hours by
conserving/reabsorbing bicarbonate (HCO3-) ions and excreting metabolic
hydrogen (H+) ions to normalize pH.
Question 7

A client with advanced emphysema exhibits a barrel chest.
Pathophysiologically, what causes this structural change in the thoracic cavity?

 A) Chronic hypertrophy of the intercostal muscles
 B) Hyperinflation of the alveoli and air trapping due to loss of elastic recoil
 C) Accumulation of purulent fluid within the pleural space
 D) Fibrotic thickening and shortening of the alveolar septa
 VERIFIED ANSWER: B
 EXPLANATION: Emphysema involves the destruction of alveolar walls and
a loss of lung elastic recoil. Air becomes trapped in the distal airways during
expiration, causing chronic pulmonary hyperinflation. Over time, the chest

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