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Basic Pathology: Cell injury, adaptation & death – page 2

93 Basic Pathology MCQs on Cell injury, adaptation & death with answers and explanations.

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Q21EasyCell injury, adaptation & death

A patient with hyperparathyroidism has calcium deposits in normal lung and kidney tissue. This process is:

Answer: B. Metastatic calcification

Metastatic calcification occurs in otherwise normal tissue when serum calcium is raised. Dystrophic calcification occurs in damaged tissue with normal calcium.

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Q22EasyCell injury, adaptation & death

In acute pancreatitis, the digestive enzymes that escape and digest surrounding fat come from which cells?

Answer: A. Pancreatic acinar cells

Acinar cells secrete lipase, amylase and proteases. Their leakage causes enzymatic fat necrosis.

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Q23EasyCell injury, adaptation & death

A diabetic's lower limb loses its blood supply; the dead tissue involves several layers and appears black and dry. This is described clinically as:

Answer: B. Gangrenous necrosis

Gangrenous necrosis is a clinical term for ischemic coagulative necrosis of a limb involving multiple tissue layers; superimposed infection makes it 'wet'.

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Q24EasyCell injury, adaptation & death

Focal bacterial infections, and occasionally fungal infections, typically produce which pattern of necrosis?

Answer: C. Liquefactive

Microbes attract neutrophils whose enzymes liquefy tissue, forming pus in an abscess.

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Q25EasyCell injury, adaptation & death

Reduction in cell size due to loss of cell substance, as in a limb kept in a cast, is termed:

Answer: D. Atrophy

Atrophy is shrinkage of cells through loss of cellular substance; when enough cells shrink, the organ becomes smaller.

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Q26EasyCell injury, adaptation & death

In an atrophic organ, the individual cells are best described as:

Answer: B. Smaller but still viable

Atrophic cells are shrunken with fewer organelles yet remain alive and functional at a lower level. Replacement by another cell type is metaplasia.

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Q27EasyCell injury, adaptation & death

A bodybuilder's muscle mass increases through training. This change is:

Answer: D. Physiological hypertrophy

Skeletal muscle fibers cannot divide; increased workload enlarges fibers, a normal (physiological) hypertrophy.

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Q28EasyCell injury, adaptation & death

A diabetic patient's foot shows swollen, foul-smelling, infected necrotic tissue. This is best described as:

Answer: B. Wet gangrene

Wet gangrene is ischemic necrosis complicated by bacterial infection, adding liquefaction. Dry gangrene is coagulative necrosis without significant infection.

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Q29EasyCell injury, adaptation & death

In which type of necrosis does enzymatic digestion of dead cells predominate over protein denaturation?

Answer: D. Liquefactive

Liquefactive necrosis results from digestion by hydrolytic enzymes, often from neutrophils, turning tissue into fluid.

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Q30EasyCell injury, adaptation & death

An elderly patient bedridden for three months has thin, weak thigh muscles. The most likely cause of this atrophy is:

Answer: C. Disuse from prolonged immobilization

Decreased workload causes disuse atrophy of skeletal muscle, with loss of fiber size and protein content.

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Q31EasyCell injury, adaptation & death

Which form of cell death is characterized by a reduction in cell size?

Answer: C. Apoptosis

Apoptotic cells shrink, with dense cytoplasm. Necrosis (oncosis) is associated with swelling of the cell and its organelles.

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Q32EasyCell injury, adaptation & death

A pathologist sees dead hepatocytes surrounded by neutrophils in a liver biopsy. This inflammatory response suggests the cells died by:

Answer: A. Necrosis

Necrotic cells rupture and release contents that trigger inflammation. Apoptotic bodies are removed quickly without an inflammatory response.

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Q33EasyCell injury, adaptation & death

Accumulation of triglyceride-filled vacuoles within hepatocytes is termed:

Answer: B. Steatosis (fatty change)

Steatosis is abnormal intracellular triglyceride accumulation, commonly in liver due to alcohol, obesity or diabetes. It is reversible, unlike cirrhosis.

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Q34EasyCell injury, adaptation & death

The wear-and-tear pigment lipofuscin appears in H&E-stained tissue as:

Answer: D. Fine yellow-brown granules

Lipofuscin, a complex of lipids and proteins from membrane peroxidation, appears as finely granular yellow-brown pigment, often near the nucleus.

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Q35EasyCell injury, adaptation & death

Which form of cell death also occurs in normal, healthy tissue to remove unwanted cells?

Answer: D. Apoptosis

Apoptosis is a regulated program used in embryogenesis, hormone-dependent involution and cell turnover. Necrosis is always pathological.

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Q36EasyCell injury, adaptation & death

A cell dies while its plasma membrane stays intact and no inflammatory reaction follows. This is:

Answer: B. Apoptosis

In apoptosis the membrane remains intact and fragments are cleared quietly by phagocytes. Necrosis and necroptosis rupture the membrane and provoke inflammation.

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Q37EasyCell injury, adaptation & death

Reversibly injured cells show small clear cytoplasmic vacuoles from distended ER segments. This change is called:

Answer: B. Hydropic (vacuolar) change

Failure of ion pumps lets water enter, producing hydropic or vacuolar degeneration. Fatty change shows lipid vacuoles, mainly in liver.

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Q38EasyCell injury, adaptation & death

Which morphological feature favours necrosis over apoptosis?

Answer: B. Cell swelling

Necrotic cells swell; apoptotic cells shrink, condense chromatin, form apoptotic bodies and are removed without inflammation.

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Q39EasyCell injury, adaptation & death

A section shows deeply eosinophilic cytoplasm, shrunken, fragmented or fading nuclei and enzymatic breakdown of cell contents with nearby inflammation. The process is:

Answer: B. Necrosis

Increased eosinophilia with pyknosis, karyorrhexis, karyolysis and enzymatic digestion describes necrosis. Apoptosis lacks enzymatic digestion and inflammation.

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Q40EasyCell injury, adaptation & death

A gradual loss of replicative capacity and lifespan of cells, associated with telomere shortening, is termed:

Answer: D. Cellular ageing (replicative senescence)

Replicative senescence reflects telomere shortening, DNA damage and reduced proliferation. Apoptosis is a discrete death program, not a progressive decline.

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