Nursing School Pathophysiology Question Bank

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Sample questions from Nursing School Pathophysiology Question Bank

This material has 90 questions with answers and rationales. Here are the first 5.

1. 1.A patient with left-sided heart failure develops crackles, dyspnea, and pink frothy sputum. Which pathophysiologic change most directly causes these findings?

   • A.Increased left ventricular filling pressure raises pulmonary capillary hydrostatic pressure
   • B.Reduced plasma oncotic pressure causes fluid to leave pulmonary capillaries
   • C.Pulmonary arterial obstruction increases right ventricular afterload
   • D.Bronchial smooth muscle constriction traps air in the alveoli

   Rationale: Left ventricular dysfunction raises pressure behind the ventricle, increasing pulmonary venous and capillary hydrostatic pressure and driving fluid into alveoli. Reduced oncotic pressure can cause edema but is not the primary mechanism in left-sided heart failure. Pulmonary arterial obstruction mainly strains the right ventricle, while bronchoconstriction causes airflow limitation rather than cardiogenic pulmonary edema. The exam takeaway is to connect left-sided pump failure with pulmonary congestion.

2. 2.A patient with septic shock has warm skin, hypotension, and a bounding pulse early in the course. Which mechanism best explains this presentation?

   • A.Widespread vasodilation lowers systemic vascular resistance
   • B.Severe vasoconstriction increases systemic vascular resistance
   • C.Acute blood loss reduces circulating volume
   • D.Left ventricular outflow obstruction reduces stroke volume

   Rationale: Inflammatory mediators in early septic shock cause widespread vasodilation and capillary leak, lowering systemic vascular resistance and often producing warm skin. Vasoconstriction is more characteristic of compensatory responses or other shock states and does not explain the bounding pulse. Blood loss causes hypovolemic shock, while outflow obstruction causes obstructive shock; neither is the defining mechanism here. Remember that early distributive shock can present with warm extremities despite hypotension.

3. 3.A patient with long-standing hypertension develops left ventricular hypertrophy. What is the primary stimulus for this structural change?

   • A.Chronic pressure overload increases ventricular workload
   • B.Chronic volume overload stretches the ventricle
   • C.Reduced coronary perfusion causes myocardial thinning
   • D.Increased preload causes the ventricular wall to weaken

   Rationale: Hypertension increases afterload, so the left ventricle adapts by adding sarcomeres in parallel and thickening its wall. Chronic volume overload more often produces chamber dilation and eccentric hypertrophy. Reduced coronary perfusion can impair function but does not directly explain compensatory wall thickening, and increased preload alone does not cause wall weakening. The key distinction is pressure overload and concentric hypertrophy.

4. 4.A patient with an acute myocardial infarction develops severe chest pain and elevated troponin. What does the troponin elevation indicate?

   • A.Myocardial cell injury with release of intracellular proteins
   • B.Increased cardiac workload without cell damage
   • C.Reduced oxygen demand by the myocardium
   • D.A specific measurement of coronary artery obstruction

   Answer and rationale are in the full material.

5. 5.A patient with chronic obstructive pulmonary disease has a prolonged expiratory phase and air trapping. Which pathophysiologic change most directly causes this pattern?

   • A.Loss of elastic recoil and airway narrowing impair expiration
   • B.Increased surfactant production stiffens the alveoli
   • C.Pulmonary fibrosis increases lung compliance
   • D.Pleural fluid prevents inspiration but improves expiration

   Answer and rationale are in the full material.