Cell Injury and Reversible Cell Injury
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Questions and Answers

What is the first effect of hypoxia on cellular function?

  • Increased ATP production
  • Impairment of aerobic respiration (correct)
  • Disruption of cellular membrane integrity
  • Activation of anaerobic glycolysis

    • Which enzyme is primarily stimulated due to decreased ATP and AMP levels?

  • Cylic AMP phosphodiesterase
  • Lactate dehydrogenase
  • ATP synthase
  • Phosphofructokinase (correct)

    • What characterizes irreversible injury in cells following ischaemia?

  • Enhanced protein synthesis
  • Mitochondrial swelling and calcium accumulation (correct)
  • Restoration of normal cellular function
  • Increased aerobic respiration

    • What physiological change is associated with acute cellular swelling during reversible injury?

    <p>Accumulation of sodium within the cell</p> Signup and view all the answers

    What triggers the generation of toxic oxygen radicals when oxygen is restored to an ischaemic area?

    <p>Activation of neutrophils</p> Signup and view all the answers

    What is a consequence of ribosome detachment from the rough endoplasmic reticulum?

    <p>Decreased protein synthesis</p> Signup and view all the answers

    What happens to extracellular calcium levels during hypoxic conditions?

    <p>They increase due to influx</p> Signup and view all the answers

    Which of the following contributes to the degradation of cytoplasmic components in irreversible injury?

    <p>Leakage of lysosomal enzymes</p> Signup and view all the answers

    What is the primary cause of cytoplasmic eosinophilia?

    <p>Cytoplasmic acidosis and loss of ribosomes</p> Signup and view all the answers

    Which type of necrosis is characterized by the preservation of structural outlines for days?

    <p>Coagulative necrosis</p> Signup and view all the answers

    Which of the following changes is NOT associated with mitochondrial alterations during necrosis?

    <p>Increased ATP production</p> Signup and view all the answers

    What process describes the decay of a cell due to its own enzymes?

    <p>Autolysis</p> Signup and view all the answers

    What type of necrosis commonly results from focal bacterial infection?

    <p>Liquefactive necrosis</p> Signup and view all the answers

    Which nuclear change is characterized by nuclear shrinkage and increased basophilia?

    <p>Pyknosis</p> Signup and view all the answers

    What is gangrenous necrosis best associated with?

    <p>Ischemic coagulative necrosis with infection</p> Signup and view all the answers

    Which of the following describes a cheesy necrotic area typically observed in tuberculosis?

    <p>Caseous necrosis</p> Signup and view all the answers

    What is the primary characteristic of fatty change (steatosis) in parenchymal cells?

    <p>Abnormal accumulation of triglycerides</p> Signup and view all the answers

    Which organ is most commonly associated with fatty change (steatosis)?

    <p>Liver</p> Signup and view all the answers

    Which condition is NOT a potential cause of fatty change in cells?

    <p>Excessive exercise</p> Signup and view all the answers

    What is the appearance of the liver in cases of moderate to severe fatty change?

    <p>Enlarged and progressively yellow</p> Signup and view all the answers

    What are foamy cells associated with in the body?

    <p>Accumulation of cholesterol and cholesterol esters</p> Signup and view all the answers

    Melanin accumulation in the epidermis can lead to which skin condition?

    <p>Freckles</p> Signup and view all the answers

    Which pigment is derived from hemoglobin and is associated with iron accumulation?

    <p>Hemosiderin</p> Signup and view all the answers

    Pathologic calcification is characterized by the accumulation of which substances?

    <p>Calcium salts and minerals</p> Signup and view all the answers

    Which of the following is NOT a type of injury mediated by free radicals?

    <p>Nutritional deficiencies</p> Signup and view all the answers

    What is the primary reason for the instability of free radicals?

    <p>They have a single unpaired electron</p> Signup and view all the answers

    Which mechanism describes how chemicals become reactive and toxic within the body?

    <p>Conversion to reactive metabolites</p> Signup and view all the answers

    What type of cellular change is most characteristic of reversible cell injury?

    <p>Vacuolar degeneration</p> Signup and view all the answers

    Which of the following species is generated during the reduction of O2 in normal physiological conditions?

    <p>Hydroxyl radical</p> Signup and view all the answers

    How does carbon tetrachloride (CCl4) primarily cause injury in liver cells?

    <p>By forming toxic free radicals</p> Signup and view all the answers

    Which statement about free radicals is true?

    <p>They react with lipids, proteins, and DNA</p> Signup and view all the answers

    What is a common effect of oxidative stress on cellular structures?

    <p>Inhibition of mitochondrial function</p> Signup and view all the answers

    What is the primary characteristic of dystrophic calcification?

    <p>Occurs in dead or dying tissues with normal serum calcium levels</p> Signup and view all the answers

    Which condition is least likely to cause metastatic calcification?

    <p>Chronic dehydration</p> Signup and view all the answers

    What is a common physiological adaptation that cells may undergo?

    <p>Hypertrophy due to hormone stimulation</p> Signup and view all the answers

    Atrophy is primarily characterized by which of the following?

    <p>Shrinkage in cell size by loss of cell substance</p> Signup and view all the answers

    Which of the following is NOT a typical cause of atrophy?

    <p>Increased workload on the organ</p> Signup and view all the answers

    Which best describes hypertrophy?

    <p>Increase in cell size due to synthesis of structural proteins</p> Signup and view all the answers

    Metastatic calcification typically occurs in which of the following tissues?

    <p>Principally in interstitial tissues, kidneys, lungs, and gastric mucosa</p> Signup and view all the answers

    Which of the following conditions is associated with increased bone catabolism?

    <p>Primary hyperparathyroidism</p> Signup and view all the answers

    What happens if a cell's adaptive capability is exceeded?

    <p>Cell injury develops.</p> Signup and view all the answers

    Which of the following is a characteristic of necrosis?

    <p>Cell swelling</p> Signup and view all the answers

    Which of the following are causes of cell injury? (Select all that apply)

    <p>Hypoxia</p> Signup and view all the answers

    What are the four intracellular systems vulnerable to injury?

    <p>Cell membrane integrity, aerobic respiration, protein synthesis, and the genetic apparatus.</p> Signup and view all the answers

    Reversible injury is characterized by acute cellular swelling.

    <p>True</p> Signup and view all the answers

    Which type of necrosis is characterized by the preservation of the structural outlines of the coagulated cell?

    <p>Coagulative necrosis</p> Signup and view all the answers

    What is apoptosis?

    <p>Programmed cell death.</p> Signup and view all the answers

    Which event is NOT typically associated with apoptosis?

    <p>Cellular swelling</p> Signup and view all the answers

    The abnormal accumulation of triglycerides within parenchymal cells is called _____ change.

    <p>fatty</p> Signup and view all the answers

    What is the main characteristic of metaplasia?

    <p>Replacement of one adult cell type with another</p> Signup and view all the answers

    Which of the following conditions can lead to aging and free radical damage?

    <p>All of the above</p> Signup and view all the answers

    Study Notes

    Cell Injury

    • Ischemia or toxins cause calcium influx into the cell
    • Mitochondrial calcium release triggers activation of enzymes like phospholipases, proteases, ATPases, and endonucleases
    • Oxygen free radicals play a crucial role in cell death

    Reversible Cell Injury

    • Hypoxia initially affects aerobic respiration, leading to reduced ATP
    • Reduced ATP causes influx of extracellular calcium and reduces the sodium pump function
    • This leads to sodium accumulation and potassium diffusion out of the cell
    • Cell swelling occurs due to isosmotic water gain
    • Accumulation of metabolites like phosphates, lactic acid, and purine nucleotides
    • Decreased ATP and AMP stimulates anaerobic glycolysis, depleting the glycogen stores
    • Lactic acid and inorganic phosphate buildup results in reduced intracellular pH
    • Ribosome detachment from the RER reduces protein synthesis
    • Continued hypoxia leads to cytoskeletal breakdown, causing loss of microvilli and formation of blebs on the cell surface

    Irreversible Cell Injury Signs

    • Severe mitochondrial vacuolization and calcium accumulation
    • Extensive plasma membrane damage
    • Swelling of lysosomes
    • Reperfusion injury mediated by calcium
    • Loss of proteins, coenzymes, and RNA through hyperpermeable membranes
    • Lysosomal enzymes leak into the cytoplasm, activated by the reduced pH, and degrade cellular components
    • Dead cells may be replaced by whorled masses of phospholipids called myelin figures

    Mechanisms of Irreversible Injury

    • Progressive loss of membrane phospholipids
    • Cytoskeletal abnormalities caused by proteases and increased calcium
    • Toxic oxygen radicals generated during reperfusion, releasing by neutrophils
    • Lipid breakdown products have detergent effects

    Free Radicals

    • Unstable chemical species with a single unpaired electron
    • React readily with organic and inorganic chemicals
    • Generated by absorption of radiant energy, redox reactions, and enzymatic catabolism of oxygenous chemicals
    • Can react with lipids, DNA, and proteins

    Chemical Injury

    • Combines with a critical molecular component or cellular organelle, e.g. mercury binds to sulfhydryl groups of the cell membrane, inhibiting ATP-dependent transport.
    • Chemicals converted to reactive toxic metabolites by P-450 oxidases in the SER, e.g. CCl4 to free radical CCl3, causing membrane peroxidation

    Patterns of Acute Cell Injury

    Reversible Cell Injury

    • Light microscopic changes include cell swelling and cytoplasmic eosinophilia
    • Ultrastructural changes include plasma membrane blebbing, mitochondrial swelling, and dilatation of the endoplasmic reticulum

    Necrosis

    • Morphologic changes following cell death due to irreversible exogenous injury
    • Results from enzyme digestion and protein denaturation
    • Cytoplasmic changes include eosinophilia, glassy appearance, vacuolation, and calcification
    • Nuclear changes include karyolysis, pyknosis, and karyorrhexis

    Types of Necrosis

    • Coagulative necrosis: Structural outlines preserved, cell hydrolysis blocked by injury and acidosis, characteristic of hypoxic death in most tissues except the brain
    • Liquefactive necrosis: Occurs due to bacterial or fungal infection, results in accumulation of white cells, also seen in hypoxic death in the CNS
    • Gangrenous necrosis: Ischemic coagulative necrosis with superimposed infection and liquefactive necrosis, commonly known as "wet gangrene"
    • Caseous necrosis: Characteristic of tuberculosis, cheese-like appearance

    Fatty Change (Steatosis)

    • Abnormal accumulation of triglycerides within parenchymal cells
    • Most common in the liver, reversible, but can also occur in other organs
    • Causes: toxins, diabetes mellitus, protein malnutrition, obesity, and anoxia
    • Excess triglyceride accumulation can result from defects in any stage of fatty acid entry to lipoprotein synthesis
    • Mild fatty change may have no effect on cellular function, severe changes can impair it

    Cholesterol And Cholesterol Esters

    • Macrophages engulf lipid debris of necrotic cells, leading to foamy cells
    • Atherosclerosis involves accumulation of cholesterol and cholesterol esters in smooth muscle cells and macrophages
    • Xanthomas are accumulations of fat within macrophages in subcutaneous connective tissue, appearing as white nodules

    Proteins

    • Accumulation less common, e.g., in glomerular diseases with proteinuria, accumulating in renal tubules

    Glycogen

    • Accumulation seen in cases of abnormal glucose or glycogen metabolism
    • Appear as vacuoles under the microscope

    Pigments

    • Melanin: Accumulates in basal cells of the epidermis, leading to freckles, or in dermal macrophages
    • Hemosiderin: Granular pigment, golden brown, accumulates when there is excess iron

    Pathologic Calcification

    • Abnormal accumulation of calcium salts
    • Dystrophic calcification: Occurs in dead or dying tissues, despite normal serum calcium, e.g., advanced atherosclerosis
    • Metastatic calcification: Occurs in normal tissues due to hypercalcemia, e.g., hyperparathyroidism, tumors, Vitamin D intoxication

    Cellular Adaptations of Growth and Differentiation

    • Physiological adaptations: Normal responses to hormonal or endogenous stimuli
    • Pathological adaptations: Allow cells to modulate their environment and escape injury

    Atrophy

    • Shrinkage of cells due to loss of cell substance
    • May involve entire organs
    • Causes: decreased workload, loss of innervation, diminished blood supply, inadequate nutrition, loss of endocrine stimulation, and aging
    • Biochemically, involves decreased synthesis, increased catabolism, or both

    Hypertrophy

    • Increase in cell size due to increased synthesis of structural proteins and organelles
    • Increases size of the organ

    Cell Injury

    • Cell injury occurs when the cell’s adaptive capability is exceeded.
    • Two principal patterns of cell death: necrosis and apoptosis.
    • Necrosis occurs after exposure to noxious conditions, characterized by cell swelling, protein denaturation, and organellar breakdown.
    • Apoptosis is a programmed cell death occurring in normal or physiologic conditions.

    Causes of Cell Injury

    • Hypoxia: Impinges on aerobic oxidative respiration.
    • Physical agents: trauma, extremes of temperatures, radiation, electric shock, and sudden changes in atmospheric pressure.
    • Chemicals and drugs.
    • Microbiologic agents: viruses to tapeworms.
    • Immunologic reactions: the immune system may cause cell injury.
    • Genetic defects.
    • Nutritional imbalances: protein-calorie insufficiency, vitamin deficiencies, diets rich in animal fat.
    • Aging: cell injury related to aging.

    Mechanisms of Cell Injury

    • Four intracellular systems vulnerable to injury: cell membrane integrity, aerobic respiration, protein synthesis, the genetic apparatus.
    • Cytosolic free calcium is maintained at extremely low levels.
    • Ischemia or toxins allow an influx of calcium from the extracellular space with a release of mitochondrial calcium, resulting in activation of various enzymes.
    • The generation of oxygen free radicals are important mediators of cell death.

    Ischemic and Hypoxic Injury

    • Reversible injury: the first effect of hypoxia is on aerobic respiration, reducing intracellular ATP, leading to influx of extracellular calcium, reduction of the plasma membrane sodium pump, and accumulation of intracellular sodium.
    • Irreversible injury: severe vacuolization of mitochondria and accumulation of calcium particles, extensive damage of the plasma membrane, swelling of lysosomes, reperfusion of oxygen results in calcium-mediated injury.

    Mechanisms of Irreversible Injury

    • Progressive loss of membrane phospholipids.
    • Cytoskeletal abnormalities: activation of proteases and increased calcium may result in detachment of the cell membrane.
    • Toxic oxygen radicals generated after reperfusion.
    • Lipid breakdown products have detergent effects.

    Free Radical Mediation of Cell Injury

    • Free radicals are implicated in chemical mediated injury, radiation mediated injury, oxygen toxicity, cellular aging, microbial killing, inflammatory damage, and tumor killing.
    • Free radicals may be generated by absorption of radiant energy, reduction-oxidation reactions, and enzymatic catabolism.
    • Oxygen free radicals react with lipid peroxidation of plasma membranes, deoxyribonucleic acid (DNA), and cross linking of proteins.

    Chemical Injury

    • Two main mechanisms: combining with a critical molecular component or cellular organelle, conversion to reactive toxic metabolites.

    Patterns of Acute Cell Injury

    • Reversible Cell Injury: cell swelling, cytoplasmic eosinophilia, fatty change.
    • Necrosis: refers to a sequence of morphologic changes that follow cell death in living tissue.
    • Cytoplasmic changes: eosinophilia and glassy appearance due to loss of glycogen, cytoplasmic vacuolation, and calcification.
    • Nuclear changes: karyolysis, pyknosis, karyorrhexis.

    Types of Necrosis

    • Coagulative necrosis: preservation of the structural outlines of the coagulated cell or tissue.
    • Liquefactive necrosis: caused by focal bacterial or fungal infection.
    • Gangrenous necrosis: ischemic coagulative necrosis with superimposed infection.
    • Caseous necrosis: seen in tuberculous infection.
    • Fat necrosis: focal areas of fat destruction following acute pancreatitis.

    Apoptosis

    • Responsible for programmed cell death in physiologic and pathologic conditions.
    • Apoptosis usually involves single cells or clusters of cells appearing as round masses with intensely eosinophilic cytoplasm.
    • Apoptosis is initiated by withdrawal of growth factors or hormones, engagement of specific receptors, injury by radiation, toxins, and free radicals, intrinsic protease activation.

    Intracellular Accumulations

    • Normal cells may accumulate abnormal substances in various circumstances.
    • Three categories: normal endogenous substance produced at a normal or increased rate with inadequate metabolism, normal or abnormal endogenous substance which can not be metabolized, abnormal exogenous substance deposit.

    Fatty Change (Steatosis)

    • Abnormal accumulation of triglycerides within parenchymal cells.
    • Most often seen in the liver.
    • Caused by toxins, diabetes mellitus, protein malnutrition, obesity, and anoxia.
    • Excess accumulation of triglycerides may result from defects at any step from fatty acid entry to synthesis of lipoproteins.

    Cholesterol and Cholesterol Esters

    • Macrophages in contact with lipid debris of necrotic cells may become stuffed with lipid.
    • In atherosclerosis, smooth muscle cells and macrophages are filled with lipid vacuoles composed of cholesterol and cholesterol esters.
    • Xanthomas are accumulation of fat within macrophages of subcutaneous connective tissues.

    Proteins

    • Less commonly seen: e.g., in glomerular diseases with proteinuria, accumulating in proximal convoluted tubules.

    Glycogen

    • Seen in cases of abnormal metabolism of glucose or glycogen, appearing as vacuoles.

    Pigments

    • Colored substances either exogenous or endogenous.
    • Melanin accumulates in basal cells of the epidermis.
    • Hemosiderin is a hemoglobin-derived granular pigment, golden brown, accumulates in tissues when there is local or systemic excess iron.

    Pathologic Calcification

    • Abnormal accumulation of calcium salts, with smaller amounts of iron, magnesium, and other minerals.
    • Dystrophic calcification: occurs in dead or dying tissues.
    • Metastatic calcification: occurs in normal tissues whenever there is hypercalcemia.

    Causes of Hypercalcemia

    • Primary endocrine dysfunction (e.g., hyperparathyroidism).
    • Tumors associated with increased bone catabolism.
    • Ingested exogenous substances resulting in vitamin D intoxication or milk alkali syndrome.
    • Sarcoidosis.
    • Advanced renal failure.

    Cellular Adaptations of Growth and Differentiation

    • Physiologic adaptations usually represent responses of cells to normal stimulations by hormones or endogenous chemicals.
    • Pathologic adaptations often share the same underlying mechanisms, but they allow the cells to modulate their environment and hopefully escape injury.

    Atrophy

    • Shrinkage in the size of the cell by loss of cell substance.
    • May involve the entire organ.
    • Atrophic cells have diminished function but are not dead.
    • Causes: decreased workload, loss of innervation, diminished blood supply, inadequate nutrition, loss of endocrine stimulation, aging.

    Hypertrophy

    • Increase in the size of cells by increased synthesis of structural proteins and organelles, leading to an increase in the size of the organ.
    • Can be physiologic or pathologic, caused by increased functional demand or specific hormonal stimulation.

    Hyperplasia

    • Increase in the number of cells in an organ or tissue.
    • Hypertrophy and hyperplasia are closely related and often develop concurrently in tissues.
    • Hyperplasia can be physiologic or pathologic.

    Metaplasia

    • Reversible change in which one adult cell type is replaced by another adult cell type, another cellular adaptation where cells sensitive to a particular stress are replaced by other cell types able to withstand the adverse environment.

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    Cell Injury PDF

    Description

    Explore the critical concepts of cell injury, focusing on mechanisms such as calcium influx and the role of oxygen free radicals. Learn how reversible cell injury affects ATP production, leading to metabolic changes and cellular damage. This quiz will test your understanding of these biological processes.

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