MLT GlobeBasic Pathology: Cell injury, adaptation & death – page 4
93 Basic Pathology MCQs on Cell injury, adaptation & death with answers and explanations.
Restoring blood flow to ischemic myocardium can paradoxically worsen damage. Which of the following does NOT contribute to reperfusion injury?
Reperfusion injury arises from new ROS generation, inflammation with neutrophil influx, and complement activation. Antioxidants would reduce, not cause, this damage.
Binding of Fas ligand to its death receptor recruits an adaptor that activates which initiator caspase?
The extrinsic (death receptor) pathway activates caspase-8 (and 10). Caspases 3, 6 and 7 are executioner caspases.
Which enzyme converts superoxide anion into hydrogen peroxide, a key step in free radical removal?
Superoxide dismutase converts O2- to H2O2. Catalase and glutathione peroxidase then break down H2O2; myeloperoxidase makes hypochlorite from H2O2 in neutrophils.
Cultured human fibroblasts stop dividing after a limited number of doublings. Which mechanism chiefly explains this replicative senescence?
Each division shortens telomeres because telomerase is lacking in most somatic cells; critically short telomeres trigger permanent cell-cycle arrest. Increased telomerase would prevent this.
At the molecular level, atrophy results from which balance of protein metabolism?
Atrophic cells synthesize less protein while the ubiquitin-proteasome pathway degrades more, so cell mass falls.
In a necrotic cell, fragmentation of the pyknotic nucleus into many pieces is termed:
Nuclear changes of necrosis: pyknosis (shrinkage and condensation), karyorrhexis (fragmentation) and karyolysis (fading by DNase).
Why does the cytoplasm of a necrotic cell stain more intensely pink with eosin?
Necrotic cells lose cytoplasmic RNA, which normally binds hematoxylin, and accumulate denatured proteins that bind eosin, so they appear hypereosinophilic.
After complete coronary occlusion, how quickly do myocytes lose contractility?
ATP depletion begins within seconds and contractility is lost within about 60 seconds to 2 minutes. Irreversible injury begins after about 20-30 minutes.
What is the earliest and most frequent liver lesion in heavy alcohol drinkers?
Over 90% of heavy drinkers develop fatty liver, which is reversible. Alcoholic hepatitis and cirrhosis develop in a smaller proportion.
In immune-complex vasculitis, arterial walls show bright pink, smudgy deposits of fibrin and immune complexes. This pattern of necrosis is:
Fibrinoid necrosis is a vascular lesion where immune complexes and leaked fibrin form eosinophilic deposits in vessel walls, typical of immune-mediated vasculitis.
A genetically regulated form of cell death that depends on RIPK1/RIPK3 and MLKL but looks like necrosis microscopically is called:
Necroptosis is programmed like apoptosis but ends with membrane rupture like necrosis, mediated by RIPK3-MLKL. Pyroptosis is caspase-1/gasdermin-driven.
Karyolysis, a fading of nuclear basophilia due to DNase activity, is a marker of:
Karyolysis occurs in necrosis as DNA is enzymatically digested. Apoptosis shows chromatin condensation and fragmentation into apoptotic bodies.
Which statement about dystrophic calcification is correct?
Dystrophic calcification forms in damaged tissue with normal serum calcium and can cause dysfunction. Myeloma causes hypercalcaemia and metastatic calcification.
Which is an example of physiological, hormone-driven hypertrophy?
Oestrogen enlarges uterine smooth muscle cells in pregnancy. Liver regrowth and pubertal breast growth are hyperplasia; hypertensive LVH is pathological.
Which change shows that a cell has passed into irreversible injury?
Lysosomal rupture releases enzymes that digest the cell and marks irreversibility. Swelling, ribosome detachment and blebbing occur in reversible injury.
The mineral in dystrophic calcification consists mainly of:
Deposits are calcium phosphate in hydroxyapatite form. Dystrophic calcification also affects damaged heart valves and any type of necrosis.
Which structure typically increases in number in atrophic cells?
Atrophy reduces organelles but increases autophagy; undigested debris may persist as lipofuscin-containing residual bodies.
The earliest light-microscopic change of cell injury, generalised cellular swelling, mainly results from:
ATP depletion stops the sodium pump, so sodium and water enter the cell. Caspases and DNA fragmentation belong to apoptosis.
Which condition would NOT be expected to cause hypercalcaemia with metastatic calcification?
Metastatic calcification follows hypercalcaemia from raised PTH, bone destruction, vitamin D excess or renal failure. Hypoparathyroidism lowers serum calcium.
How does ischaemia differ from hypoxia caused by carbon monoxide poisoning?
Ischaemia cuts off blood flow entirely, so anaerobic glycolysis also fails. Hypoxia (low oxygen) still allows substrate delivery and waste removal.