Questions: Cellular Adaptation: Hypertrophy and Hyperplasia

Question 1

A patient with long-standing hypertension develops a thickened left ventricular wall. Which adaptation occurs, and why does it take this form rather than another?

• A. Hyperplasia, because the heart needs more cells to handle increased workload
• B. Hypertrophy, because mature cardiomyocytes cannot divide and instead enlarge
• C. Hyperplasia, because cardiac tissue is highly regenerative
• D. Hypertrophy, because the heart compensates by forming more contractile proteins in new cells

Answer: (B)

Mature cardiomyocytes have permanently exited the cell cycle and cannot undergo hyperplasia. When demand increases (as with hypertension), individual cardiomyocytes enlarge — synthesizing more contractile proteins and expanding their organelles. This is hypertrophy. Option A reflects the misconception that more work always leads to more cells. Option D mixes up mechanisms: new contractile proteins are synthesized within existing cells, not in new cells.

Question 2

After surgical removal of 70% of the liver, the remaining tissue regrows to near-normal size within weeks. Which adaptation best explains this?

• A. Hypertrophy — the remaining cells grow larger to compensate
• B. Hyperplasia — hepatocytes retain the ability to divide and proliferate
• C. Metaplasia — liver cells transform into a more resilient cell type
• D. Both hypertrophy and hyperplasia in equal proportions

Answer: (B)

Hepatocytes retain proliferative capacity throughout life. After partial hepatectomy, growth signals (HGF, TGF-α) drive existing hepatocytes to re-enter the cell cycle and divide — hyperplasia. This is fundamentally different from cardiac adaptation, where proliferative capacity is absent. Some early hypertrophy does occur, but the dominant mechanism restoring liver mass is hyperplasia.

Question 3

Hypertrophy and hyperplasia are interchangeable terms for cellular growth — the distinction is mainly semantic.

• T. True
• F. False

Answer: False

They are mechanistically distinct. Hypertrophy increases cell size through more protein synthesis without cell division; hyperplasia increases cell number through mitosis. The distinction matters clinically and biologically: which adaptation occurs depends on whether the cell type retains proliferative capacity. The heart cannot undergo hyperplasia; the liver can. Conflating them leads to errors in predicting organ responses to injury and stress.

Question 4

Pathologic hypertrophy, such as that seen in the heart under chronic pressure overload, is reversible if the underlying stimulus is removed.

• T. True
• F. False

Answer: True

Reversibility is a defining feature of adaptive (as opposed to neoplastic) changes. A hypertrophied left ventricle can regress with effective blood pressure control. This distinguishes hypertrophy from neoplasia, which is irreversible and autonomous. The clinical implication is that treating the underlying cause — not just symptoms — can reverse the structural change. Recognizing this reversibility window is a key insight in managing conditions like hypertensive heart disease.

Question 5

A skeletal muscle fiber grows larger with resistance training, but a cut in the skin heals by producing new cells. Why do these two tissues respond differently to demand?

Model answer: Skeletal muscle fibers are post-mitotic — they cannot divide. Under training stress, they adapt by hypertrophy: synthesizing more actin, myosin, and mitochondria within existing fibers. Skin (keratinocytes and fibroblasts) retains proliferative capacity, so wound healing proceeds by hyperplasia — cell division restores tissue mass. The type of adaptation is determined by whether the cell type can still undergo mitosis.

Proliferative capacity is the gating factor: tissues that cannot divide adapt by growing larger cells; tissues that can divide respond by producing more cells. Many tissues can do both simultaneously (e.g., the pregnant uterus), but understanding the mechanism requires knowing which cells are post-mitotic.