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NR507/ NR 507 Midterm Exam (Latest Version) Advanced Pathophysiology | 100 Questions and 100% Verified Correct Answers| 100% Correct |Grade A – Chamberlain

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NR507/ NR 507 Midterm Exam (Latest Version) Advanced Pathophysiology | 100 Questions and 100% Verified Correct Answers| 100% Correct |Grade A – Chamberlain Question1. Which physiologic change is expected during starvation? A. Increased insulin secretion B. Increased gluconeogenesis C. Enhanced glycogen storage D. Reduced fatty acid utilization Correct Answer: B. Increased gluconeogenesis Rationale: During starvation, the body increases gluconeogenesis to maintain blood glucose levels for essential organs (brain, RBCs), since dietary glucose is unavailable. Insulin levels fall while glucagon rises, promoting hepatic gluconeogenesis from amino acids, glycerol, and lactate. Question2. A patient with chronic kidney disease develops anemia primarily due to: A. Increased hemolysis B. Reduced erythropoietin production C. Iron deficiency from blood loss D. Bone marrow suppression Correct Answer: B. Reduced erythropoietin production Rationale: Chronic kidney disease leads to decreased production of erythropoietin (EPO) by the peritubular fibroblasts in the damaged kidneys, resulting in reduced stimulation of red blood cell production in the bone marrow and normocytic, normochromic anemia. Question3. Which mechanism best explains hyponatremia in heart failure? A. Excessive sodium loss in urine B. Increased aldosterone secretion alone C. Dilutional effect from water retention D. Decreased antidiuretic hormone secretion Correct Answer: C. Dilutional effect from water retention

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NR507/ NR 507 Midterm Exam (Latest
Version) Advanced Pathophysiology | 100
Questions and 100% Verified Correct
Answers| 100% Correct |Grade A –
Chamberlain


Question1. Which physiologic change is expected during starvation?

A. Increased insulin secretion
B. Increased gluconeogenesis
C. Enhanced glycogen storage
D. Reduced fatty acid utilization
✅ Correct Answer: B. Increased gluconeogenesis

Rationale: During starvation, the body increases gluconeogenesis to maintain blood glucose levels for
essential organs (brain, RBCs), since dietary glucose is unavailable. Insulin levels fall while glucagon
rises, promoting hepatic gluconeogenesis from amino acids, glycerol, and lactate.

Question2. A patient with chronic kidney disease develops anemia primarily due to:

A. Increased hemolysis
B. Reduced erythropoietin production
C. Iron deficiency from blood loss
D. Bone marrow suppression
✅ Correct Answer: B. Reduced erythropoietin production

Rationale: Chronic kidney disease leads to decreased production of erythropoietin (EPO) by the
peritubular fibroblasts in the damaged kidneys, resulting in reduced stimulation of red blood cell
production in the bone marrow and normocytic, normochromic anemia.

Question3. Which mechanism best explains hyponatremia in heart failure?

A. Excessive sodium loss in urine

,B. Increased aldosterone secretion alone
C. Dilutional effect from water retention
D. Decreased antidiuretic hormone secretion
✅ Correct Answer: C. Dilutional effect from water retention

Rationale: In heart failure, decreased cardiac output leads to nonosmotic release of ADH (arginine
vasopressin), causing water retention that exceeds sodium retention. This dilutional effect reduces
serum sodium concentration, resulting in dilutional hyponatremia.

Question4. A patient with chronic obstructive pulmonary disease develops respiratory acidosis.
Which compensatory response is expected?

A. Decreased bicarbonate reabsorption
B. Increased renal bicarbonate retention
C. Reduced hydrogen ion excretion
D. Increased respiratory rate
✅ Correct Answer: B. Increased renal bicarbonate retention

Rationale: Respiratory acidosis (increased CO₂/carbonic acid) is compensated by the kidneys retaining
bicarbonate (HCO₃⁻) and excreting more hydrogen ions (H⁺) to buffer the excess acid and raise pH
toward normal. This metabolic compensation takes 3–5 days to fully develop.

Question5. Which type of cell death involves cellular swelling, membrane rupture, and an
inflammatory response?

A. Apoptosis
B. Autophagy
C. Necrosis
D. Pyroptosis
✅ Correct Answer: C. Necrosis

Rationale: Necrosis is pathological cell death characterized by cellular swelling (oncosis), organelle
degeneration, plasma membrane rupture, and release of cellular contents triggering inflammation.
Apoptosis is programmed, orderly cell death without inflammation. The distinction is critical to
understanding pathological vs. physiological cell death.

Question6. A cell under hypoxic conditions will first attempt to maintain ATP production through:

A. Oxidative phosphorylation in the mitochondria
B. Anaerobic glycolysis producing lactate
C. Beta-oxidation of fatty acids

,D. Ketone body utilization
✅ Correct Answer: B. Anaerobic glycolysis producing lactate

Rationale: When oxygen is unavailable, cells shift from aerobic oxidative phosphorylation (36
ATP/glucose) to anaerobic glycolysis (2 ATP/glucose), producing lactate as a byproduct. This leads to
lactic acidosis. Sustained hypoxia eventually leads to cell injury and death if ATP demands cannot be
met.

Question7. Which of the following correctly describes the pathophysiology of cellular injury from
free radicals?

A. Free radicals donate electrons to stabilize membrane lipids
B. Free radicals cause lipid peroxidation of cell membranes, protein denaturation, and DNA strand
breaks
C. Free radicals stimulate mitochondrial function and increase ATP production
D. Free radicals activate anti-apoptotic Bcl-2 proteins
✅ Correct Answer: B. Free radicals cause lipid peroxidation of cell membranes, protein
denaturation, and DNA strand breaks

Rationale: Reactive oxygen species (ROS/free radicals) are highly unstable molecules with unpaired
electrons that react with cellular components causing: lipid peroxidation (membrane damage), protein
cross-linking/denaturation (enzyme dysfunction), and DNA strand breaks (mutagenesis). Antioxidants
(SOD, catalase, glutathione, vitamins C/E) neutralize free radicals.

Question8. A patient with liver failure develops coagulopathy. The primary pathophysiological
mechanism is:

A. Thrombocytopenia from bone marrow suppression
B. Impaired synthesis of clotting factors II, VII, IX, and X (vitamin K-dependent)
C. Excessive fibrinolysis from plasmin overactivation
D. Increased von Willebrand factor production
✅ Correct Answer: B. Impaired synthesis of clotting factors II, VII, IX, and X (vitamin K-
dependent)

Rationale: The liver synthesizes virtually all coagulation factors (I, II, V, VII, VIII, IX, X, XI, XII,
XIII) and anticoagulant proteins (protein C, S, antithrombin). Hepatic failure impairs this synthesis.
Factors II, VII, IX, X (vitamin K-dependent) are most affected. PT/INR is the most sensitive test for
hepatic synthetic function.

Question9. Which of the following best describes the pathophysiology of ischemia-reperfusion
injury?

, A. Reperfusion of ischemic tissue reduces cell death by restoring oxygen and nutrients
B. Restoration of blood flow after ischemia paradoxically worsens injury through massive ROS
generation, calcium overload, and inflammation
C. Ischemia-reperfusion injury primarily affects the liver and spleen only
D. Reperfusion injury is prevented by maintaining high oxygen delivery
✅ Correct Answer: B. Restoration of blood flow after ischemia paradoxically worsens injury
through massive ROS generation, calcium overload, and inflammation

Rationale: Ischemia-reperfusion injury: during ischemia, xanthine oxidase accumulates; upon
reperfusion, oxygen reintroduction generates massive ROS burst. Additionally, calcium influx,
neutrophil activation, complement activation, and mitochondrial permeability transition pore opening
amplify injury. This is the basis of myocardial stunning post-MI and cerebral injury post-stroke.

Question10. A patient develops metabolic alkalosis after prolonged vomiting. Which laboratory
finding is expected?

A. pH < 7.35, HCO₃⁻ < 22 mEq/L, PaCO₂ < 35 mmHg
B. pH > 7.45, HCO₃⁻ > 26 mEq/L, PaCO₂ > 45 mmHg (compensatory hypoventilation)
C. pH > 7.45, HCO₃⁻ < 22 mEq/L, PaCO₂ < 35 mmHg
D. pH < 7.35, HCO₃⁻ > 26 mEq/L, PaCO₂ > 45 mmHg
✅ Correct Answer: B. pH > 7.45, HCO₃⁻ > 26 mEq/L, PaCO₂ > 45 mmHg (compensatory
hypoventilation)

Rationale: Prolonged vomiting causes loss of HCl from gastric secretions, elevating plasma HCO₃⁻
(metabolic alkalosis). The respiratory compensation is hypoventilation (retaining CO₂) to lower pH
back toward normal. ABG: pH >7.45, HCO₃⁻ >26 mEq/L, PaCO₂ elevated (compensatory). Also
expect hypokalemia and hypochloremia from vomiting.

Question11. Which cytokine is primarily responsible for the fever response during acute
inflammation?

A. Interleukin-10 (IL-10)
B. Transforming growth factor-beta (TGF-β)
C. Interleukin-1 (IL-1) and Tumor Necrosis Factor-alpha (TNF-α)
D. Interleukin-4 (IL-4)
✅ Correct Answer: C. Interleukin-1 (IL-1) and Tumor Necrosis Factor-alpha (TNF-α)

Rationale: Endogenous pyrogens IL-1β, TNF-α, and IL-6 are released by macrophages during
inflammation and act on the hypothalamic thermoregulatory center via prostaglandin E₂ (PGE₂) to

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