NSG 527 FINAL EXAM MASTER KEY (WILKES
2026/2027)
Advanced Pathophysiology (NSG 527)
Graduate-Level Cellular Mechanisms, Hemodynamics, & Systemic Alterations
PART I: CELLULAR BIOLOGY, ADAPTATION, & INJURY
**1. A patient presents with a myocardial infarction. The cardiologist states the goal is
to restore perfusion within 20 minutes to prevent "reperfusion injury." What is the
precise pathophysiologic mechanism of reperfusion injury?**
A. The sudden influx of calcium causes immediate cell division, leading to aneurysm
formation.
B. Restoration of oxygen generates massive amounts of reactive oxygen species (ROS)
via the xanthine oxidase pathway, causing lipid peroxidation and mitochondrial
permeability transition pore (MPTP) opening.
C. Reperfusion causes an immediate shift to anaerobic metabolism, producing lethal
levels of lactic acid.
D. The sudden return of blood washes away all protective antioxidants from the tissue.
Answer: B**
*Rationale:* During ischemia, ATP breaks down to hypoxanthine, and xanthine
dehydrogenase is converted to xanthine oxidase. When oxygen is suddenly restored
(reperfusion), xanthine oxidase uses this new oxygen to convert hypoxanthine to uric
, acid, unleashing a massive burst of superoxide free radicals (ROS). These ROS attack
cell membranes (lipid peroxidation) and mitochondria. The MPTP opens, collapsing the
mitochondrial membrane potential, stopping ATP production, and causing
apoptotic/necrotic cell death. The tissue was ischemic, but the *act of re-oxygenating*
it delivers the fatal blow.
**2. Differentiate the cellular mechanisms of Apoptosis versus Necrosis.**
* **Apoptosis (Programmed Cell Death):**
* *Mechanism:* Requires ATP. Activated by intrinsic (mitochondrial/cytochrome c
release) or extrinsic (Fas ligand/death receptor) pathways. Activates *caspases*
(executioner enzymes).
* *Morphology:* Cell shrinks, chromatin condenses (pyknosis), nuclear
fragmentation (karyorrhexis), cell blebs into apoptotic bodies.
* *Inflammation:* **None.** Membranes remain intact; no cellular contents leak
out. Macrophages phagocytose the bodies before they can cause inflammation.
* **Necrosis (Accidental Cell Death):**
* *Mechanism:* Caused by severe, irreversible injury (ischemia, toxins, trauma).
Loss of ATP $\rightarrow$ failure of Na+/K+ pump $\rightarrow$ cellular swelling
(oncosis) $\rightarrow$ calcium influx activating destructive phospholipases,
proteases, and endonucleases.
* *Morphology:* Cell swells, organelles dissolve, plasma membrane ruptures.
* *Inflammation:* **Severe.** Ruptured membrane dumps cellular debris and
intracellular enzymes into the extracellular space, triggering a robust acute
inflammatory response.
**3. A biopsy of a patient's esophagus shows columnar epithelium replacing the normal
stratified squamous epithelium. The pathologist notes this is a reversible cellular
adaptation. What is this process, and what is the driving mechanism?**
A. Metaplasia; driven by chronic irritation (acid reflux) causing stem cells to
differentiate into a more resistant cell type.
B. Dysplasia; driven by genetic mutations leading to uncontrolled proliferation.
2026/2027)
Advanced Pathophysiology (NSG 527)
Graduate-Level Cellular Mechanisms, Hemodynamics, & Systemic Alterations
PART I: CELLULAR BIOLOGY, ADAPTATION, & INJURY
**1. A patient presents with a myocardial infarction. The cardiologist states the goal is
to restore perfusion within 20 minutes to prevent "reperfusion injury." What is the
precise pathophysiologic mechanism of reperfusion injury?**
A. The sudden influx of calcium causes immediate cell division, leading to aneurysm
formation.
B. Restoration of oxygen generates massive amounts of reactive oxygen species (ROS)
via the xanthine oxidase pathway, causing lipid peroxidation and mitochondrial
permeability transition pore (MPTP) opening.
C. Reperfusion causes an immediate shift to anaerobic metabolism, producing lethal
levels of lactic acid.
D. The sudden return of blood washes away all protective antioxidants from the tissue.
Answer: B**
*Rationale:* During ischemia, ATP breaks down to hypoxanthine, and xanthine
dehydrogenase is converted to xanthine oxidase. When oxygen is suddenly restored
(reperfusion), xanthine oxidase uses this new oxygen to convert hypoxanthine to uric
, acid, unleashing a massive burst of superoxide free radicals (ROS). These ROS attack
cell membranes (lipid peroxidation) and mitochondria. The MPTP opens, collapsing the
mitochondrial membrane potential, stopping ATP production, and causing
apoptotic/necrotic cell death. The tissue was ischemic, but the *act of re-oxygenating*
it delivers the fatal blow.
**2. Differentiate the cellular mechanisms of Apoptosis versus Necrosis.**
* **Apoptosis (Programmed Cell Death):**
* *Mechanism:* Requires ATP. Activated by intrinsic (mitochondrial/cytochrome c
release) or extrinsic (Fas ligand/death receptor) pathways. Activates *caspases*
(executioner enzymes).
* *Morphology:* Cell shrinks, chromatin condenses (pyknosis), nuclear
fragmentation (karyorrhexis), cell blebs into apoptotic bodies.
* *Inflammation:* **None.** Membranes remain intact; no cellular contents leak
out. Macrophages phagocytose the bodies before they can cause inflammation.
* **Necrosis (Accidental Cell Death):**
* *Mechanism:* Caused by severe, irreversible injury (ischemia, toxins, trauma).
Loss of ATP $\rightarrow$ failure of Na+/K+ pump $\rightarrow$ cellular swelling
(oncosis) $\rightarrow$ calcium influx activating destructive phospholipases,
proteases, and endonucleases.
* *Morphology:* Cell swells, organelles dissolve, plasma membrane ruptures.
* *Inflammation:* **Severe.** Ruptured membrane dumps cellular debris and
intracellular enzymes into the extracellular space, triggering a robust acute
inflammatory response.
**3. A biopsy of a patient's esophagus shows columnar epithelium replacing the normal
stratified squamous epithelium. The pathologist notes this is a reversible cellular
adaptation. What is this process, and what is the driving mechanism?**
A. Metaplasia; driven by chronic irritation (acid reflux) causing stem cells to
differentiate into a more resistant cell type.
B. Dysplasia; driven by genetic mutations leading to uncontrolled proliferation.
