"The Body's Broken Code: A 100-Q&A
Intensive Drill for NR 283
Pathophysiology Exam 1 (With Clinical
Rationales)’’
### Section 1: Cellular Biology & Adaptation (Questions 1-25)
**1. Q: What is the definition of atrophy?**
**A:** Decrease in the size of cells, leading to a reduced organ/tissue
mass.
**Rationale:** This occurs due to disuse, denervation, ischemia, or
malnutrition. It is a reversible adaptation aimed at decreasing oxygen
demand.
**2. Q: What is hypertrophy?**
**A:** Increase in the size of individual cells, resulting in an enlarged
organ.
**Rationale:** Caused by increased workload (e.g., muscle building)
or hormonal stimulation. In cardiac issues, it is a compensatory
mechanism.
**3. Q: What is hyperplasia?**
**A:** Increase in the *number* of cells in a tissue.
,**Rationale:** Occurs only in tissues capable of mitotic division (e.g.,
skin, liver). Hormonal or compensatory (e.g., liver regeneration).
**4. Q: What is metaplasia?**
**A:** Reversible replacement of one mature cell type with another
(less specialized) cell type.
**Rationale:** Often a response to chronic irritation (e.g., smoker's
lungs: columnar to squamous) to withstand stress.
**5. Q: What is dysplasia?**
**A:** Abnormal changes in cell size, shape, and organization.
**Rationale:** Not true cancer, but is considered a pre-cancerous
(neoplastic) lesion if severe.
**6. Q: What is the primary cause of cellular injury via hypoxia?**
**A:** Lack of oxygen to the cell.
**Rationale:** Hypoxia impairs oxidative phosphorylation in
mitochondria, stopping ATP production, which leads to sodium-
potassium pump failure and cellular swelling.
**7. Q: What type of necrosis is associated with tuberculosis?**
**A:** Caseous necrosis.
**Rationale:** Characterized by a "cheesy" appearance due to the
combination of coagulative and liquefactive necrosis, often walled off
by granulomas.
, **8. Q: What is liquefactive necrosis?**
**A:** Necrosis where cells are completely digested by hydrolytic
enzymes, turning the tissue into a liquid viscous mass.
**Rationale:** Occurs in the brain and in abscesses due to bacterial
infections.
**9. Q: What is coagulative necrosis?**
**A:** Necrosis where cell outlines remain intact but cellular
proteins are denatured.
**Rationale:** Occurs in most solid organs (heart, kidney, liver)
following ischemia (infarction).
**10. Q: What is the "point of no return" in cell injury?**
**A:** Severe mitochondrial damage and loss of membrane
integrity.
**Rationale:** Once ATP production ceases permanently and
lysosomal enzymes leak, the cell cannot recover.
**11. Q: What is apoptosis?**
**A:** Programmed, controlled cell death.
**Rationale:** Physiologic (eliminating worn-out cells) and
pathologic (eliminating DNA-damaged cells to prevent cancer). Does
NOT cause inflammation.
**12. Q: What is the hallmark of reversible cell injury?**
**A:** Cellular swelling (hydropic change) and fatty change.
Intensive Drill for NR 283
Pathophysiology Exam 1 (With Clinical
Rationales)’’
### Section 1: Cellular Biology & Adaptation (Questions 1-25)
**1. Q: What is the definition of atrophy?**
**A:** Decrease in the size of cells, leading to a reduced organ/tissue
mass.
**Rationale:** This occurs due to disuse, denervation, ischemia, or
malnutrition. It is a reversible adaptation aimed at decreasing oxygen
demand.
**2. Q: What is hypertrophy?**
**A:** Increase in the size of individual cells, resulting in an enlarged
organ.
**Rationale:** Caused by increased workload (e.g., muscle building)
or hormonal stimulation. In cardiac issues, it is a compensatory
mechanism.
**3. Q: What is hyperplasia?**
**A:** Increase in the *number* of cells in a tissue.
,**Rationale:** Occurs only in tissues capable of mitotic division (e.g.,
skin, liver). Hormonal or compensatory (e.g., liver regeneration).
**4. Q: What is metaplasia?**
**A:** Reversible replacement of one mature cell type with another
(less specialized) cell type.
**Rationale:** Often a response to chronic irritation (e.g., smoker's
lungs: columnar to squamous) to withstand stress.
**5. Q: What is dysplasia?**
**A:** Abnormal changes in cell size, shape, and organization.
**Rationale:** Not true cancer, but is considered a pre-cancerous
(neoplastic) lesion if severe.
**6. Q: What is the primary cause of cellular injury via hypoxia?**
**A:** Lack of oxygen to the cell.
**Rationale:** Hypoxia impairs oxidative phosphorylation in
mitochondria, stopping ATP production, which leads to sodium-
potassium pump failure and cellular swelling.
**7. Q: What type of necrosis is associated with tuberculosis?**
**A:** Caseous necrosis.
**Rationale:** Characterized by a "cheesy" appearance due to the
combination of coagulative and liquefactive necrosis, often walled off
by granulomas.
, **8. Q: What is liquefactive necrosis?**
**A:** Necrosis where cells are completely digested by hydrolytic
enzymes, turning the tissue into a liquid viscous mass.
**Rationale:** Occurs in the brain and in abscesses due to bacterial
infections.
**9. Q: What is coagulative necrosis?**
**A:** Necrosis where cell outlines remain intact but cellular
proteins are denatured.
**Rationale:** Occurs in most solid organs (heart, kidney, liver)
following ischemia (infarction).
**10. Q: What is the "point of no return" in cell injury?**
**A:** Severe mitochondrial damage and loss of membrane
integrity.
**Rationale:** Once ATP production ceases permanently and
lysosomal enzymes leak, the cell cannot recover.
**11. Q: What is apoptosis?**
**A:** Programmed, controlled cell death.
**Rationale:** Physiologic (eliminating worn-out cells) and
pathologic (eliminating DNA-damaged cells to prevent cancer). Does
NOT cause inflammation.
**12. Q: What is the hallmark of reversible cell injury?**
**A:** Cellular swelling (hydropic change) and fatty change.
