NR 507 Advanced Pathophysiology
Expanded Original Q&A; Midterm Study Guide • 2025/2026 Preparation
Use: This guide expands the publicly visible preview of the linked Stuvia listing into original study material. It does not
reproduce paid/locked content or claim to contain actual confidential examination questions.
Preview scope: The listing is 16 pages, written for 2025/2026, and publicly previews a Cellular Injury section. The listing
description also identifies inflammation, genetics, endocrine and cardiovascular disorders, neurological pathology, and immune
dysfunction as major areas.
NR 507 Advanced Pathophysiology • Original Midterm Study Guide 1
, 1. Cellular Injury & Adaptation
Q: A patient has reversible ischemic cell injury. Why does the cell swell?
Answer & rationale: Reduced oxidative phosphorylation lowers ATP. The Na+/K+-ATPase cannot maintain ion gradients,
intracellular sodium rises, and water follows. If the insult is removed early, function can recover.
Q: Which adaptation is an increase in cell size rather than cell number?
Answer & rationale: Hypertrophy. Hyperplasia increases cell number. Atrophy decreases cell size and/or tissue mass.
Metaplasia is a reversible change from one mature cell type to another.
Q: What makes an injury irreversible?
Answer & rationale: Major clues include inability to reverse mitochondrial dysfunction, profound ATP failure, severe
membrane damage, and nuclear breakdown. In practice, the point of no return reflects loss of essential membrane and
mitochondrial function.
Q: Why does ischemia-reperfusion injury generate oxidative stress?
Answer & rationale: Restoration of oxygen can produce reactive oxygen species (ROS). ROS can oxidize membrane lipids,
proteins, and nucleic acids, amplifying injury even after blood flow returns.
NR 507 Advanced Pathophysiology • Original Midterm Study Guide 2
, 2. Necrosis, Apoptosis & Cell Death
Q: Contrast apoptosis and necrosis.
Answer & rationale: Apoptosis is regulated, energy-dependent cell death with cell shrinkage and fragmentation, usually
without major inflammation. Necrosis follows severe injury and involves membrane disruption, leakage of intracellular contents,
and inflammation.
Q: What nuclear changes are associated with necrosis?
Answer & rationale: Pyknosis is nuclear shrinkage and condensation; karyorrhexis is nuclear fragmentation; karyolysis is
nuclear fading/dissolution. The sequence is commonly remembered as P-K-K: pyknosis, karyorrhexis, karyolysis.
Q: What is coagulative necrosis classically associated with?
Answer & rationale: Ischemic injury in solid organs such as the heart and kidney, with preservation of tissue architecture for a
period despite cell death. Brain infarction is the major exception, where liquefactive necrosis occurs.
NR 507 Advanced Pathophysiology • Original Midterm Study Guide 3
Expanded Original Q&A; Midterm Study Guide • 2025/2026 Preparation
Use: This guide expands the publicly visible preview of the linked Stuvia listing into original study material. It does not
reproduce paid/locked content or claim to contain actual confidential examination questions.
Preview scope: The listing is 16 pages, written for 2025/2026, and publicly previews a Cellular Injury section. The listing
description also identifies inflammation, genetics, endocrine and cardiovascular disorders, neurological pathology, and immune
dysfunction as major areas.
NR 507 Advanced Pathophysiology • Original Midterm Study Guide 1
, 1. Cellular Injury & Adaptation
Q: A patient has reversible ischemic cell injury. Why does the cell swell?
Answer & rationale: Reduced oxidative phosphorylation lowers ATP. The Na+/K+-ATPase cannot maintain ion gradients,
intracellular sodium rises, and water follows. If the insult is removed early, function can recover.
Q: Which adaptation is an increase in cell size rather than cell number?
Answer & rationale: Hypertrophy. Hyperplasia increases cell number. Atrophy decreases cell size and/or tissue mass.
Metaplasia is a reversible change from one mature cell type to another.
Q: What makes an injury irreversible?
Answer & rationale: Major clues include inability to reverse mitochondrial dysfunction, profound ATP failure, severe
membrane damage, and nuclear breakdown. In practice, the point of no return reflects loss of essential membrane and
mitochondrial function.
Q: Why does ischemia-reperfusion injury generate oxidative stress?
Answer & rationale: Restoration of oxygen can produce reactive oxygen species (ROS). ROS can oxidize membrane lipids,
proteins, and nucleic acids, amplifying injury even after blood flow returns.
NR 507 Advanced Pathophysiology • Original Midterm Study Guide 2
, 2. Necrosis, Apoptosis & Cell Death
Q: Contrast apoptosis and necrosis.
Answer & rationale: Apoptosis is regulated, energy-dependent cell death with cell shrinkage and fragmentation, usually
without major inflammation. Necrosis follows severe injury and involves membrane disruption, leakage of intracellular contents,
and inflammation.
Q: What nuclear changes are associated with necrosis?
Answer & rationale: Pyknosis is nuclear shrinkage and condensation; karyorrhexis is nuclear fragmentation; karyolysis is
nuclear fading/dissolution. The sequence is commonly remembered as P-K-K: pyknosis, karyorrhexis, karyolysis.
Q: What is coagulative necrosis classically associated with?
Answer & rationale: Ischemic injury in solid organs such as the heart and kidney, with preservation of tissue architecture for a
period despite cell death. Brain infarction is the major exception, where liquefactive necrosis occurs.
NR 507 Advanced Pathophysiology • Original Midterm Study Guide 3
