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NUR 2063 Essentials of Pathophysiology Exam 2 Prep 2026 | 200 Practice Questions with Answers & Rationales | Rasmussen University

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NUR 2063 Essentials of Pathophysiology Exam 2 Prep 2026 | 200 Practice Questions with Answers & Rationales | Rasmussen University

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NUR 2063 / NUR2063: Essentials of Pathophysiology Exam 2 –
Practice Test Bank (200 Questions)
1. Which of the following assessment findings indicates an alteration in homeostatic control
mechanisms?

A) Bradycardia

B) Fever

C) Hypertension

D) Tachypnea

Answer: B – Fever

Explanation: Fever represents a change in the body's homeostatic set point, triggered when pyrogens
act on the hypothalamus to "reset" the thermoregulatory center to a higher temperature. While
bradycardia, hypertension, and tachypnea can be physiological responses to various conditions, they do
not inherently indicate a fundamental resetting of homeostatic mechanisms, making fever the hallmark
sign of an altered homeostatic control.



2. A patient presents with redness, warmth, swelling, and pain at the site of an injury. Which physiologic
process is most responsible for these symptoms?

A) Vasoconstriction and decreased blood flow

B) Platelet aggregation and clot formation

C) Increased vascular permeability and vasodilation caused by inflammatory mediators

D) Fibroblast proliferation and collagen deposition

Answer: C – Increased vascular permeability and vasodilation caused by inflammatory mediators

Explanation: The cardinal signs of inflammation (redness, warmth, swelling, pain) result directly from
vasodilation (causing redness and warmth) and increased vascular permeability (causing
swelling/edema). Inflammatory mediators such as histamine and prostaglandins are responsible for
these vascular changes. Vasoconstriction would cause pallor and coldness, not the signs described.



3. Which type of hypersensitivity reaction involves IgE antibodies and mast cell degranulation?

A) Type I hypersensitivity reaction

B) Type II hypersensitivity reaction

C) Type III hypersensitivity reaction

,D) Type IV hypersensitivity reaction

Answer: A – Type I hypersensitivity reaction

Explanation: Type I hypersensitivity reactions (immediate allergic reactions) are mediated by IgE
antibodies that bind to mast cells and basophils. Upon re-exposure to an allergen, cross-linking of IgE
triggers mast cell degranulation, releasing histamine and other mediators that cause the characteristic
symptoms of allergies, such as anaphylaxis.



4. In left-sided heart failure, which symptom is most likely to present first?

A) Peripheral edema

B) Pulmonary congestion leading to dyspnea and orthopnea

C) Jugular venous distension

D) Hepatomegaly

Answer: B – Pulmonary congestion leading to dyspnea and orthopnea

Explanation: Left-sided heart failure causes blood to back up into the pulmonary circulation, leading to
increased hydrostatic pressure in the pulmonary capillaries. This results in pulmonary congestion,
initially manifesting as dyspnea (shortness of breath) and orthopnea (difficulty breathing when lying
flat). Peripheral edema, JVD, and hepatomegaly are more characteristic of right-sided heart failure.



5. Which laboratory finding is most indicative of a myocardial infarction (heart attack)?

A) Elevated creatine kinase (CK)

B) Elevated troponin I or T

C) Elevated lactate dehydrogenase (LDH)

D) Elevated C-reactive protein (CRP)

Answer: B – Elevated troponin I or T

Explanation: Troponin I and T are highly specific cardiac regulatory proteins released into the
bloodstream when myocardial necrosis occurs. While CK and LDH are also released after an MI, they lack
troponin's specificity. An elevated troponin level is the gold standard biochemical marker for diagnosing
myocardial infarction.



6. A patient with chronic bronchitis will typically have which arterial blood gas (ABG) pattern?

A) Respiratory alkalosis with hypoxemia (low PaCO₂, high pH)

B) Respiratory acidosis with hypoxemia (low PaO₂, high PaCO₂, low pH)

,C) Metabolic alkalosis with hypoxemia (high HCO₃⁻, high pH)

D) Metabolic acidosis with hypoxemia (low HCO₃⁻, low pH)

Answer: B – Respiratory acidosis with hypoxemia (low PaO₂, high PaCO₂, low pH)

Explanation: In chronic bronchitis, chronic airway inflammation and mucus hypersecretion lead to
airway obstruction, causing carbon dioxide retention (hypercapnia, high PaCO₂) and decreased oxygen
levels (hypoxemia, low PaO₂). The retained CO₂ combines with water to form carbonic acid, lowering
blood pH, which is compensated by renal retention of bicarbonate over time. The classic ABG pattern is
respiratory acidosis with hypoxemia.



7. Which electrolyte imbalance is most commonly associated with chronic kidney disease (CKD)?

A) Hypokalemia (low potassium)

B) Hyperkalemia (high potassium)

C) Hyponatremia (low sodium)

D) Hypocalcemia (low calcium)

Answer: B – Hyperkalemia (high potassium)

Explanation: As kidney function declines in CKD, the kidneys lose their ability to effectively excrete
potassium. This leads to the progressive accumulation of potassium in the blood, a condition known as
hyperkalemia. Hyperkalemia is a dangerous and common electrolyte disturbance in CKD and can lead to
life-threatening cardiac arrhythmias.



8. Why does nephrotic syndrome lead to generalized edema (swelling)?

A) Increased hydrostatic pressure due to sodium and water retention

B) Loss of plasma proteins (especially albumin) in the urine, reducing plasma oncotic pressure

C) Blockage of lymphatic drainage

D) Increased capillary permeability from inflammation

Answer: B – Loss of plasma proteins (especially albumin) in the urine, reducing plasma oncotic pressure

Explanation: In nephrotic syndrome, damage to the glomerular filtration barrier allows large amounts of
protein, primarily albumin, to leak into the urine (proteinuria). The resulting hypoalbuminemia
decreases the plasma oncotic (colloid osmotic) pressure. This reduces the force that normally holds fluid
within the vascular space, causing fluid to shift into the interstitial tissues, leading to generalized edema.



9. What is the primary difference between stable angina and unstable angina?

, A) Stable angina is caused by plaque rupture; unstable angina is not

B) Stable angina occurs predictably with exertion and is relieved by rest/nitroglycerin; unstable angina is
unpredictable, may occur at rest, and is a sign of impending MI

C) Stable angina causes ST-segment elevation; unstable angina does not

D) Stable angina requires immediate hospitalization; unstable angina does not

Answer: B – Stable angina is predictable with exertion and relieved by rest/nitroglycerin; unstable
angina is unpredictable, may occur at rest, and signals an impending MI

Explanation: Stable angina is predictable, triggered by increased myocardial oxygen demand, and
resolves with rest or nitroglycerin. Unstable angina is unpredictable, may occur at rest, is more severe,
and is considered an acute coronary syndrome requiring immediate intervention as it indicates an
impending myocardial infarction.



10. Which pathophysiologic mechanism underlies the development of a deep vein thrombosis (DVT)?

A) Platelet destruction and thrombocytopenia

B) Endothelial proliferation and angiogenesis

C) Virchow's triad: venous stasis, endothelial injury, and hypercoagulability

D) Arterial vasospasm and platelet aggregation

Answer: C – Virchow's triad: venous stasis, endothelial injury, and hypercoagulability

Explanation: The formation of a DVT is explained by the three components of Virchow's triad: (1) venous
stasis (slowed blood flow), (2) endothelial injury (damage to the vessel wall), and (3) hypercoagulability
(an increased tendency for the blood to clot). These factors often coexist and create a prothrombotic
state, leading to the development of a venous thrombus.



11. Why does emphysema cause a "barrel chest" appearance?

A) Chronic coughing causes hypertrophy of the chest wall muscles

B) Air trapping and hyperinflation of the lungs increase the anteroposterior diameter of the chest

C) Kyphoscoliosis causes a permanent deformity of the thoracic spine

D) Pleural effusion accumulates and expands the thoracic cavity

Answer: B – Air trapping and hyperinflation of the lungs increase the anteroposterior diameter of the
chest

Explanation: In emphysema, destruction of alveolar walls leads to loss of elastic recoil and airway
collapse during exhalation, resulting in air trapping and hyperinflation. The lungs become overdistended,

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