QCM : Cell Injury and Death Mechanisms — 24 questions

Explication

Adaptation is a reversible response that allows survival under stress. Irreversible injury and necrosis occur when damage exceeds the cell’s ability to recover.

Explication

If the injurious stimulus stops early enough, the cell can recover and return toward its original state. Morphologic changes can lag behind biochemical injury, so early damage may still be reversible.

Explication

Hypoxia, especially from ischemia, lowers oxygen availability and impairs aerobic respiration. The other choices are different causes of injury, not oxygen deprivation itself.

Explication

Some toxins are bioactivated into reactive metabolites that cause free radical damage and lipid peroxidation. The other options describe unrelated mechanisms of injury.

Explication

Hydropic change is a reversible injury characterized by water-driven swelling and vacuolization from ER distention. Necrosis and apoptosis are distinct forms of cell death.

Explication

Irreversibility is linked to failure to recover mitochondrial dysfunction and severe lysosomal damage. Early swelling and blebbing are typical of reversible injury.

Explication

Coagulative necrosis preserves cellular outlines because protein denaturation blocks proteolysis for a time. Liquefactive necrosis instead digests tissue into a liquid mass.

Explication

Necrotic cells become more eosinophilic because RNA is lost and denatured proteins bind eosin more strongly. Apoptotic bodies are a feature of apoptosis, not necrosis.

Explication

Apoptosis is defined by cell shrinkage, chromatin condensation, and later apoptotic body formation. Cell swelling and inflammation are more typical of necrosis.

Explication

The intrinsic pathway begins with mitochondrial outer membrane permeabilization mediated by BAX and BAK, leading to cytochrome c release and caspase activation. Fas/FADD belongs to the extrinsic pathway.

Explication

Autophagy helps cells survive stress by sequestering cytoplasmic cargo and degrading it in lysosomes. Necroptosis is a form of programmed necrosis, not a survival pathway.

Explication

Necroptosis depends on RIPK1 and RIPK3 activation, which drives MLKL phosphorylation and membrane disruption. The caspase-8 pathway belongs to apoptosis, not necroptosis.

Explication

Oxidative stress is the buildup of damaging free radicals when ROS production exceeds scavenging capacity. This can injure membranes, proteins, and DNA.

Explication

Lipid peroxidation occurs when free radicals attack unsaturated fatty-acid double bonds in membrane phospholipids. This produces unstable intermediates that propagate further injury.

Explication

Ischemia is hypoxia due to reduced blood flow, which also limits delivery of substrates needed for energy production. Hypoxia can occur with blood flow maintained.

Explication

Reperfusion injury involves reactive oxygen species, calcium overload, neutrophil recruitment, and sometimes complement activation. These processes can damage tissue that might otherwise have recovered.

Explication

Toxic metabolite conversion refers to bioactivation of a compound into a reactive metabolite, often through cytochrome P-450 enzymes. This reactive product can injure cells, often through free radical formation.

Explication

Some IgM antibodies deposit in ischemic tissues, and when blood flow returns, complement can bind and activate locally to worsen injury. This is an immune-mediated component of reperfusion damage.

Explication

Hypertrophy is an increase in cell and organ size, usually driven by increased workload and growth-factor signaling. Hyperplasia increases cell number instead.

Explication

Metaplasia is a reversible switch in differentiated cell type, often from columnar to squamous epithelium under chronic irritation. The new lining may be more stress-tolerant but can lose specialized functions.

Explication

Steatosis is the abnormal accumulation of triglycerides in parenchymal cells, classically in the liver. The other options describe calcification, hemosiderin, or glycogen storage rather than fatty change.

Explication

Lipofuscin is the wear-and-tear pigment formed from lipid-phospholipid polymers plus protein and is a marker of oxidative injury. Hemosiderin stores iron, carbon pigment causes anthracosis, and bilirubin is not the described intracellular aging pigment.

Explication

Dystrophic calcification occurs in damaged or necrotic tissues even when serum calcium levels are normal. The distractor describing normal tissue with hypercalcemia refers to metastatic calcification.

Explication

Replicative senescence is a permanent growth arrest reached after a finite number of divisions. It is different from cell swelling, hypertrophy, or calcification.