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Questions and Answers
What is necrosis characterized by?
What is necrosis characterized by?
Apoptosis is a type of cell death that occurs normally in physiologic conditions.
Apoptosis is a type of cell death that occurs normally in physiologic conditions.
True
What is hypoxia?
What is hypoxia?
Inadequate oxygenation of the blood
Which of the following are causes of cell injury? (Select all that apply)
Which of the following are causes of cell injury? (Select all that apply)
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What happens during reversible cell injury?
What happens during reversible cell injury?
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What is the primary effect of hypoxia on cells?
What is the primary effect of hypoxia on cells?
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Cellular aging can be caused by oxidative stress and free radicals.
Cellular aging can be caused by oxidative stress and free radicals.
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What is apoptosis?
What is apoptosis?
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Which type of necrosis is characterized by the preservation of the structural outlines of coagulated cells?
Which type of necrosis is characterized by the preservation of the structural outlines of coagulated cells?
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Match the following types of necrosis with their descriptions:
Match the following types of necrosis with their descriptions:
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The process of _____ involves the activation of intracellular proteases leading to the fragmentation of apoptotic bodies.
The process of _____ involves the activation of intracellular proteases leading to the fragmentation of apoptotic bodies.
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What is the cause of fatty change in cells?
What is the cause of fatty change in cells?
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What are free radicals?
What are free radicals?
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Study Notes
Cell Injury
- Cell injury occurs when the cell's ability to adapt to stress or stimuli is exceeded.
- Two principal patterns of cell death:
- Necrosis: Cell death due to noxious conditions characterized by swelling, protein denaturation, and organellar breakdown.
- Apoptosis: Programmed cell death occurring in normal or physiologic conditions.
Causes of Cell Injury
- Hypoxia: Insufficient oxygen supply to the blood.
- Physical agents: Trauma, extreme temperatures, radiation, electric shock, and sudden changes in atmospheric pressure.
- Chemicals and drugs: Alter membrane permeability, osmotic homeostasis, or enzyme cofactor integrity.
- Microbiologic agents: Viruses, bacteria, fungi, and parasites.
- Immunologic reactions: Immune system responses causing cell injury, such as anaphylactic reactions.
- Genetic defects: e.g. Down's syndrome and sickle cell anemia.
- Nutritional imbalances: Protein-calorie insufficiency, vitamin deficiencies, and diets rich in animal fat.
- Aging: The natural process of aging contributes to cellular changes and vulnerability to injury.
Mechanisms of Cell Injury
- Four intracellular systems are vulnerable to injury:
- Cell membrane integrity
- Aerobic respiration
- Protein synthesis
- Genetic apparatus
- Calcium influx: Ischemia or toxins cause an influx of calcium from the extracellular space and release of mitochondrial calcium, activating enzymes that damage cells.
- Free radical generation: Important mediators of cell death.
Ischemic and Hypoxic Injury
-
Reversible Injury:
- Reduced ATP
- Influx of extracellular calcium
- Reduced plasma membrane sodium pump
- Accumulation of intracellular sodium
- Diffusion of potassium out of the cell
- Cellular swelling
- Decreased intracellular pH
-
Irreversible Injury:
- Severe vacuolization and calcium accumulation in mitochondria
- Extensive damage to the plasma membrane
- Swelling of lysosomes
- Continued loss of essential cellular components
- Activation of lysosomal enzymes
Mechanisms of Irreversible Injury
- Progressive loss of membrane phospholipids
- Cytoskeletal abnormalities
- Toxic oxygen radicals
- Lipid breakdown products
Free Radical Mediation of Cell Injury
-
Free radicals are chemically unstable species involved in various processes:
- Chemical injury
- Radiation injury
- Oxygen toxicity
- Cellular aging
- Microbial killing
- Inflammatory damage
- Tumor killing
-
Generation of free radicals:
- Absorption of radiant energy
- Redox reactions
- Enzymatic catabolism
Chemical Injury
-
Mechanisms:
- Combining with critical molecular components or cellular organelles
- Conversion to reactive toxic metabolites
-
Example: Carbon tetrachloride (CCl4): Converted to a toxic free radical that causes membrane peroxidation and liver damage.
Patterns of Acute Cell Injury
-
Reversible Injury:
- Light microscopic changes: Cell swelling, cytoplasmic eosinophilia, and fatty change.
- Ultrastructural changes: Plasma membrane blebbing, mitochondrial swelling, dilatation of endoplasmic reticulum, nuclear alterations.
-
Necrosis:
- Morphologic changes resulting from enzymatic digestion and protein denaturation.
- Cytoplasmic changes: Eosinophilia, glassy appearance, vacuolation, and calcification.
- Nuclear changes: Karyolysis, pyknosis, and karyorrhexis.
Types of Necrosis
- Coagulative necrosis: Preservation of structural outlines of the coagulated cell or tissue.
- Liquefactive necrosis: Caused by bacterial or fungal infections, resulting in the accumulation of white blood cells.
- Gangrenous necrosis: Ischemic coagulative necrosis with superimposed infection and liquefactive necrosis.
- Caseous necrosis: Characteristic of tuberculous infection, characterized by a cheese-like appearance.
- Fat necrosis: Focal areas of fat destruction following acute pancreatitis.
Apoptosis
- Programmed cell death occurring in various physiologic and pathologic conditions.
- Morphologic features:
- Nuclear chromatin condensation,
- Karyorrhexis
- Formation of apoptotic bodies
- Apoptosis does not elicit an inflammatory response.
-
Initiation of apoptosis:
- Withdrawal of growth factors or hormones
- Engagement of specific receptors
- Injury by radiation, toxins, and free radicals
- Intrinsic protease activation
Intracellular Accumulations
- Abnormal substances accumulate in cells either transiently or permanently.
-
Categories of accumulations:
- Normal endogenous substance produced at an increased rate
- Normal or abnormal endogenous substance that can't be metabolized
- Abnormal exogenous substance deposited due to inability to transport it to other sites.
Fatty Change (Steatosis)
- Abnormal accumulation of triglycerides within parenchymal cells.
- Most often seen in the liver, but can occur in other organs.
- Causes: Toxins, diabetes mellitus, protein malnutrition, obesity, and anoxia.
Cholesterol and Cholesterol Esters
- Accumulation in macrophages, smooth muscle cells leading to foam cells and atheromas.
- Xanthomas: Accumulation of fat within macrophages of subcutaneous connective tissues.
Proteins
- Accumulation can occur in various conditions, such as glomerular diseases with proteinuria.
Glycogen
- Accumulation can happen due to abnormal metabolism of glucose or glycogen.
Pigments
- Colored substances, either exogenous or endogenous.
- Melanin: Accumulates in the epidermis.
- Hemosiderin: Accumulates in tissues due to local or systemic iron overload.
Pathologic Calcification
- Abnormal accumulation of calcium salts, with smaller amounts of other minerals.
- Dystrophic calcification: Deposits in dead or dying tissues.
- Metastatic calcification: Deposits in normal tissues due to hypercalcemia.
Causes of Hypercalcemia
- Primary endocrine dysfunction
- Tumors associated with increased bone catabolism
- Ingested exogenous substances
- Sarcoidosis
- Advanced renal failure
Cellular Adaptations of Growth And Differentiation
- Cells adapt to changing conditions, often responding to stress or stimuli.
- Atrophy: Shrinkage in cell size due to loss of cell substance.
- Hypertrophy: Increase in cell size due to increased synthesis of structural proteins and organelles.
- Hyperplasia: Increase in the number of cells in an organ or tissue.
- Metaplasia: Reversible change in which one adult cell type is replaced by another.
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Description
Test your knowledge on the mechanisms of cell injury and its various causes. This quiz covers the differences between necrosis and apoptosis, and explores the multiple factors that can lead to cell damage. Understand the implications of physical agents, chemicals, and genetic factors in cellular health.
