"Cellular Adaptations: 10 MCQs (Hypertrophy, Hyperplasia, Atrophy)"
Cellular Adaptations: 10 MCQs
Test yourself on hypertrophy, hyperplasia and atrophy. Try each question first, then tap Show answer to check the answer and explanation.
Answer: B. Pressure overload from hypertension causes pathologic hypertrophy. Cardiac myocytes have very limited ability to divide, so they adapt by making more protein and more myofilaments, which makes each cell larger and stronger. The number of myocytes does not increase.
Q2. Which tissue increases its mass almost entirely by hypertrophy rather than hyperplasia?
A. Liver
B. Endometrium
C. Cardiac muscle
D. Bone marrow
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Answer: C. Hyperplasia needs cells that can divide. Cardiac muscle cells are essentially non-dividing, so the heart can grow only by hypertrophy. The liver, endometrium and bone marrow all contain dividing cells and readily undergo hyperplasia.
Q3. The enlargement of the uterus during pregnancy is mainly due to:
A. Hypertrophy of smooth muscle cells, stimulated by oestrogen through oestrogen receptors
B. Metaplasia of smooth muscle into skeletal muscle
C. Oedema of the myometrium
D. Atrophy of the endometrium
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Answer: A. The pregnant uterus is a classic example of physiologic, hormone-induced hypertrophy. Oestrogen acts through oestrogen receptors to increase smooth muscle protein synthesis, and the individual smooth muscle cells become much larger.
Q4. Which signalling pathway is considered most important in physiologic hypertrophy, such as that caused by exercise?
A. PI3K/AKT pathway
B. G-protein-coupled receptor pathway
C. Ubiquitin–proteasome pathway
D. Caspase pathway
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Answer: A. The PI3K/AKT pathway is most important in physiologic hypertrophy. G-protein-coupled receptor pathways, activated by growth factors and vasoactive agents such as angiotensin II and endothelin-1, are more important in pathologic hypertrophy. The ubiquitin–proteasome pathway degrades proteins in atrophy, and caspases drive apoptosis.
Q5. In cardiac hypertrophy, the heart re-expresses fetal forms of some proteins. What change occurs in myosin heavy chain?
A. β isoform is replaced by α isoform, giving faster contraction
B. α isoform is replaced by β isoform, giving slower but more energy-economical contraction
C. Myosin heavy chain synthesis stops completely
D. Myosin is replaced by actin
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Answer: B. Hypertrophied myocardium switches from the adult α isoform to the fetal β isoform of myosin heavy chain. The β isoform contracts more slowly but uses energy more economically. The same "fetal gene programme" also increases atrial natriuretic factor (ANF), which promotes salt excretion and reduces the load on the heart.
Q6. A healthy 35-year-old man donates the right lobe of his liver to his brother. Within a few weeks, his remaining liver has returned almost to its original size. This is an example of:
A. Physiologic hypertrophy
B. Pathologic hyperplasia
C. Metaplasia
D. Compensatory hyperplasia
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Answer: D. After partial hepatectomy, growth factors bind receptors on the surviving hepatocytes and drive them to divide, so the liver regrows. This is compensatory (physiologic) hyperplasia. If hepatocytes cannot divide, for example in some forms of hepatitis, the liver can regenerate from intrahepatic stem cells instead.
Q7. A 48-year-old woman has had irregular, heavy menstrual bleeding for six months. An endometrial biopsy shows crowded, proliferating glands without atypia. What is the most likely cause, and what is the long-term concern?
A. Excess progesterone; no increased cancer risk
B. Unopposed oestrogen; increased risk of endometrial carcinoma
C. Excess androgen; increased risk of prostate cancer
D. Papillomavirus infection; increased risk of skin warts
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Answer: B. Normally, rising progesterone stops oestrogen-driven endometrial proliferation. If the balance tips towards oestrogen, endometrial hyperplasia develops and is a common cause of abnormal uterine bleeding. Hyperplasia itself is not cancer, but repeated cell division raises the chance of genetic errors, so it is "fertile soil" for endometrial carcinoma.
Q8. A young man's leg was in a plaster cast for six weeks after a fracture. When the cast is removed, his calf muscles are visibly smaller. Which statement is correct?
A. This is denervation atrophy and is irreversible
B. This is ischaemic atrophy caused by the cast compressing the arteries
C. This is hypoplasia, because the muscle never developed fully
D. This is disuse atrophy, and the early decrease in cell size reverses when activity resumes
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Answer: D. Reduced workload causes disuse atrophy. Early on, the fibres simply shrink, and this reverses once the patient becomes active again. With much longer disuse, fibre number also falls (by apoptosis), and increased bone resorption can cause disuse osteoporosis.
Q9. Which pathway is mainly responsible for the increased breakdown of cellular proteins in atrophy?
A. Ubiquitin–proteasome pathway
B. Caspase cascade
C. Mitochondrial permeability transition
D. Complement pathway
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Answer: A. Atrophy results from less protein synthesis and more protein degradation. Nutrient deficiency and disuse activate ubiquitin ligases, which tag proteins with ubiquitin and send them to proteasomes to be broken down. The same pathway is thought to drive the rapid muscle loss of cancer cachexia. Autophagy is often increased as well.
Q10. At autopsy, an 82-year-old man's heart is small and dark brown. Microscopy shows golden-brown granules around the nuclei of the myocytes. What is this pigment?
A. Haemosiderin
B. Melanin
C. Lipofuscin
D. Bilirubin
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Answer: C. This is brown atrophy. In atrophic cells, some debris inside autophagic vacuoles resists digestion and remains as membrane-bound residual bodies containing lipofuscin, the "wear-and-tear" pigment. In large amounts it gives the tissue a brown colour.
Answer key
| Q | 1 | 2 | 3 | 4 | 5 | 6 | 7 | 8 | 9 | 10 |
|---|---|---|---|---|---|---|---|---|---|---|
| Answer | B | C | A | A | B | D | B | D | A | C |
How did you score? 8–10: excellent. 5–7: revise the mechanisms. Below 5: go back to the notes and try again.