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N212 Pathophysiology Exam 2 - Practice Questions Eastwick College Update Complete Test Bank | Comprehensive Nursing Board Review

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N212 Pathophysiology Exam 2 - Practice Questions Eastwick College Update Complete Test Bank | Comprehensive Nursing Board Review

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2026-2027 N212 Pathophysiology Exam 2 - Practice
Questions Eastwick College Update Complete Test
Bank 3 Versions

Master complex disease mechanisms and pass your second milestone assessment with
this complete 2026 N212 Pathophysiology practice exam bank tailored for Eastwick
College students. This comprehensive preparation guide features realistic test
questions with verified correct answers and detailed clinical rationales covering
advanced cellular alterations, immunological responses, and systemic homeostatic
disruptions. It is an indispensable study tool for nursing students looking to streamline
their study routines, build diagnostic confidence, and secure an A+ grade.

Question 1: A patient with chronic bronchitis has developed cor
pulmonale. Which pathophysiological mechanism explains this
complication?

A) Left ventricular hypertrophy due to systemic hypertension
B) Right ventricular hypertrophy due to pulmonary hypertension
C) Left ventricular dilation due to volume overload
D) Right ventricular atrophy due to decreased pulmonary blood flow

Answer: B) Right ventricular hypertrophy due to pulmonary
hypertension

Rationale: Cor pulmonale is right ventricular hypertrophy and dilation caused
by pulmonary hypertension. Chronic bronchitis causes hypoxia and
pulmonary vasoconstriction, leading to increased pulmonary vascular
resistance and right ventricular workload. Over time, this results in right-
sided heart failure .




Question 2: A patient with polycythemia vera has a hematocrit of 65%.
Which complication is this patient at highest risk for?

,A) Bleeding
B) Thrombosis
C) Anemia
D) Infection

Answer: B) Thrombosis

Rationale: Polycythemia vera causes increased red blood cell mass and blood
viscosity, significantly increasing the risk of thrombosis (venous and arterial).
This can lead to stroke, myocardial infarction, and deep vein thrombosis.
Phlebotomy is used to reduce hematocrit to < 45% to lower this risk .




Question 3: A patient with chronic kidney disease develops uremic
pericarditis. Which mechanism is responsible for this complication?

A) Immune complex deposition
B) Viral infection
C) Uremic toxins causing inflammation
D) Bacterial infection

Answer: C) Uremic toxins causing inflammation

Rationale: Uremic pericarditis results from inflammation of the pericardium
due to accumulation of uremic toxins in end-stage renal disease. Symptoms
include chest pain and pericardial friction rub. It can progress to cardiac
tamponade. Treatment includes dialysis and anti-inflammatory agents .




Question 4: A patient with hereditary spherocytosis presents with
jaundice and splenomegaly. Which mechanism causes these
manifestations?

,A) Decreased red blood cell production
B) Increased red blood cell destruction in the spleen
C) Increased bilirubin production from hemolysis
D) Both B and C

Answer: D) Both B and C

Rationale: Hereditary spherocytosis causes defective red blood cell
membranes, leading to increased destruction in the spleen (extravascular
hemolysis). This increases bilirubin production, causing jaundice.
Splenomegaly results from increased workload on the spleen. Treatment may
include splenectomy .




Question 5: A patient with chronic renal failure has a serum creatinine
of 6 mg/dL and BUN of 80 mg/dL. Which acid-base disturbance is
expected?

A) Respiratory acidosis
B) Metabolic acidosis with elevated anion gap
C) Metabolic alkalosis
D) Respiratory alkalosis

Answer: B) Metabolic acidosis with elevated anion gap

Rationale: Chronic renal failure causes accumulation of acids (sulfates,
phosphates, organic acids) due to impaired excretion, leading to metabolic
acidosis with elevated anion gap. Respiratory acidosis would show elevated
PaCO₂. The kidneys also fail to regenerate bicarbonate, worsening the
acidosis .

, Question 6: A patient with liver disease has a prolonged prothrombin
time (PT). Which mechanism explains this finding?

A) Increased vitamin K absorption
B) Decreased synthesis of clotting factors (II, VII, IX, X)
C) Increased platelet production
D) Decreased fibrinolysis

Answer: B) Decreased synthesis of clotting factors (II, VII, IX, X)

Rationale: The liver synthesizes clotting factors II, VII, IX, and X, which are
vitamin K-dependent. Liver disease impairs synthesis, leading to prolonged
PT and bleeding risk. Vitamin K deficiency can also cause prolonged PT, but
in liver disease, the primary mechanism is impaired synthesis .




Question 7: A patient with heart failure develops cardiogenic
pulmonary edema. Which mechanism is primarily responsible?

A) Decreased capillary oncotic pressure
B) Increased pulmonary capillary hydrostatic pressure
C) Increased capillary permeability
D) Lymphatic obstruction

Answer: B) Increased pulmonary capillary hydrostatic pressure

Rationale: Cardiogenic pulmonary edema results from left-sided heart failure,
which increases pulmonary venous pressure and capillary hydrostatic
pressure. Fluid shifts from the capillaries into the alveoli, causing edema. This
leads to dyspnea, orthopnea, and crackles on auscultation .




Question 8: A patient with emphysema presents with a barrel chest.
Which pathophysiological change causes this finding?

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