Foundation Module
Cellular Injury: Causes, Mechanisms and Subcellular Responses
Connect the major mechanisms, morphological changes and cellular responses for rapid KMU-focused revision.
1. THE TOPIC IN ONE CONNECTED FLOW
Cell injury begins when a harmful stimulus exceeds the cell’s capacity to maintain homeostasis. The outcome depends on the type, severity and duration of the insult. Mild injury can remain reversible, whereas continuing damage to mitochondria and cellular membranes can push the cell beyond recovery.
Hypoxia, ischemia, chemicals, physical agents, genetic or other stress
ATP depletion, mitochondrial dysfunction, calcium imbalance, reactive oxygen species
Ion-pump failure, anaerobic glycolysis, reduced protein synthesis
Cell swelling, organelle swelling and membrane blebbing
Removal of stimulus permits recovery if critical structures remain intact
Persistent mitochondrial failure and severe membrane damage prevent recovery
2. KEY CLINICAL CONNECTIONS
Reduced blood flow → reduced oxygen and nutrient delivery + impaired waste removal → ATP depletion → ion-pump failure → cellular swelling.
This explains why ischemia generally produces more severe injury than isolated hypoxia.
Restored oxygen supply → increased reactive oxygen species → lipid peroxidation + protein and DNA damage → additional cellular injury.
Reperfusion saves viable tissue but may paradoxically injure already damaged cells.
External material → endocytosis or phagocytosis → lysosomal digestion = heterophagy.
Damaged intracellular components → sequestration → lysosomal degradation and recycling = autophagy.
Liver → bile → intestine → reabsorption → portal blood → liver.
This recycling occurs with bile acids and may prolong persistence of some drugs in the body.
3. AIM HIGH-YIELD INTEGRATION REVIEW
The cause initiates a sequence of cellular events that produces structural and functional disease changes.
Mild, brief injury can recover; severe or persistent injury can progress beyond reversibility.
Loss of ATP-dependent ion transport causes sodium and water accumulation within injured cells.
Reduced blood flow compromises oxygen, nutrients and waste removal, making injury more severe than isolated hypoxia.
Oxidative stress links free-radical injury with membrane dysfunction and cellular structural damage.
Cell swelling and membrane blebs may occur while the cell still retains the ability to recover.
Persistent failure of energy production together with severe membrane disruption marks the point beyond recovery.
Heterophagy digests external material; autophagy removes and recycles the cell’s own damaged components.
Do not confuse phagocytosis with heterophagy. Phagocytosis is the uptake of large extracellular particles; heterophagy is their subsequent lysosomal digestion.