Pathology Quiz: Necrosis and Apoptosis
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Questions and Answers

Which of the following is NOT a characteristic of necrosis?

  • Eosinophilia
  • Loss of membrane integrity
  • Cell shrinkage (correct)
  • Nuclear disintegration

    • Which cellular process can be triggered by both pathological and physiological conditions?

  • Apoptosis (correct)
  • Both necrosis and apoptosis
  • Neither necrosis nor apoptosis
  • Necrosis

    • What is the fate of cells undergoing apoptosis?

  • They burst and release their contents, triggering an inflammatory response
  • They are phagocytosed by neutrophils and macrophages
  • They remain intact and are eventually removed by the immune system
  • They are phagocytosed by neighboring cells and macrophages (correct)

    • What is the primary biochemical mechanism responsible for apoptosis?

    <p>Energy-dependent processes, such as endonuclease activity (B)</p> Signup and view all the answers

    Which of the following is a characteristic of both necrosis and apoptosis?

    <p>Phagocytosis by neighboring cells (B)</p> Signup and view all the answers

    Which of the following describes a direct mechanism of toxic injury?

    <p>A chemical binds to a critical molecular component, interfering with its function. (B)</p> Signup and view all the answers

    What is a consequence of the activation of the complement system during reperfusion?

    <p>Recruitment of neutrophils to the site of injury, exacerbating tissue damage. (A)</p> Signup and view all the answers

    How does ischemia contribute to tissue sensitivity to free radical damage?

    <p>Ischemia depletes the cells' antioxidant defense mechanisms. (C)</p> Signup and view all the answers

    What is the main consequence of impaired mitochondrial function in irreversibly injured cells?

    <p>Reduced ATP production, leading to energy depletion. (C)</p> Signup and view all the answers

    What is the primary mechanism by which CCl4 causes cell injury?

    <p>Conversion to toxic metabolites that cause membrane damage. (A)</p> Signup and view all the answers

    What is the primary type of necrosis observed in the gangrenous necrosis of the second and third toes, as described in the content?

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

    What is the most likely cause of the gangrenous necrosis of the toes described in the content?

    <p>Ischemia (A)</p> Signup and view all the answers

    Which of the following is NOT a reference listed in the content provided?

    <p>Human Anatomy and Physiology (2022) (B)</p> Signup and view all the answers

    In the context of the content, what does the term "chronic reversible adaptations" refer to?

    <p>Cellular responses to persistent injury that allow cells to survive but are often associated with altered function (C)</p> Signup and view all the answers

    According to the content provided, which of the following is a key publication used often in medical education?

    <p>Robbins &amp; Cotran Pathologic Basis of Disease (A)</p> Signup and view all the answers

    Which type of necrosis is characterized by the presence of 'ghost cells' and is often caused by ischemia?

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

    What is the defining characteristic of caseous necrosis?

    <p>Friable, white appearance with amorphous granular debris (A)</p> Signup and view all the answers

    Which type of necrosis is associated with pancreatitis and trauma to fat?

    <p>Fat necrosis (C)</p> Signup and view all the answers

    What is the process called where fatty acids released during fat necrosis combine with calcium?

    <p>Saponification (B)</p> Signup and view all the answers

    What is the characteristic microscopic appearance of fibrinoid necrosis?

    <p>Bright pink, amorphous appearance on H&amp;E staining (B)</p> Signup and view all the answers

    Which of the following is a common cause of fibrinoid necrosis?

    <p>Malignant hypertension (D)</p> Signup and view all the answers

    Dry gangrene is characterized by what type(s) of necrosis?

    <p>Coagulative necrosis followed by liquefactive necrosis (D)</p> Signup and view all the answers

    In which type of necrosis is the tissue architecture mostly preserved, although the cells are dead?

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

    Which of the following is NOT a mechanism through which cells respond to ER stress?

    <p>Decreased production of ATP (D)</p> Signup and view all the answers

    What is the primary difference between hypoxia and ischemia?

    <p>Hypoxia involves a lack of oxygen, while ischemia also involves compromised delivery of substrates for glycolysis. (D)</p> Signup and view all the answers

    What is the primary mechanism of ischemic cell injury?

    <p>Failure of oxidative phosphorylation and ATP depletion (B)</p> Signup and view all the answers

    What is the paradox of reperfusion injury?

    <p>Restoring blood flow to ischemic tissues can worsen cell injury and death. (A)</p> Signup and view all the answers

    Which of the following is NOT a mechanism of reperfusion injury?

    <p>Activation of the proteasome (A)</p> Signup and view all the answers

    What are the factors secreted by damaged mitochondria that trigger apoptosis?

    <p>Apoptosis inducing factor, Bak, Bax (A)</p> Signup and view all the answers

    What occurs as a result of the dimerization of Bak and Bax proteins?

    <p>Formation of channels that allow the release of Cytochrome C into the cytosol (C)</p> Signup and view all the answers

    Why does the tissue become firm after coagulative necrosis?

    <p>Due to the denaturation of structural proteins and lysosomal enzymes (D)</p> Signup and view all the answers

    Which of the following is a characteristic of liquefactive necrosis?

    <p>The tissue becomes soft and liquefies due to enzymatic digestion. (A)</p> Signup and view all the answers

    What is the primary cause of tissue liquefaction in liquefactive necrosis?

    <p>Activation of lysosomal enzymes (D)</p> Signup and view all the answers

    Coagulative necrosis is characterized by the initial swelling of the tissue. What causes this swelling?

    <p>Cellular acidosis and denaturation of proteins (B)</p> Signup and view all the answers

    What is the main reason why proteolytic disintegration does not occur immediately after coagulative necrosis?

    <p>The denaturation of lysosomal enzymes and structural proteins due to cellular acidosis (B)</p> Signup and view all the answers

    What is the primary role of caspase-9 in apoptosis?

    <p>Triggering the activation of other caspases in the apoptotic cascade (D)</p> Signup and view all the answers

    Flashcards

    Signaling Pathways

    Pathways that boost chaperone production and protein degradation while slowing translation.

    Calcium Changes

    Increased cytosolic Ca2+ can open mitochondrial pores, deplete ATP, and lead to cell injury.

    Ischaemic Cell Injury

    Cell injury from hypoxia plus reduced blood flow, leading to more severe damage.

    Mechanism of Ischaemic Injury

    Decreased oxygen leads to reduced ATP production due to failure of oxidative phosphorylation.

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    Ischemic-Reperfusion Injury

    Worsening injury when blood flow resumes after ischaemia due to oxidative stress.

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    Irreversible Cell Injury

    Cell death resulting from extreme damage or stress.

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    Necrosis

    Cell death caused by pathological conditions, affecting groups of cells.

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    Apoptosis

    Programmed cell death occurring in single cells, usually without inflammation.

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    Morphology of Necrosis

    Characterized by cell swelling, lysis, and nuclear disintegration.

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    Morphology of Apoptosis

    Involves cell shrinkage, chromatin condensation, and formation of apoptotic bodies.

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    Ischemia and Free Radicals

    Ischemia can increase tissue sensitivity to free radical damage by compromising antioxidant defenses.

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    Intracellular Calcium Overload

    Calcium overload occurs during ischemia and worsens during reperfusion due to membrane damage.

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    Inflammation in Reperfusion

    Inflammation caused by dead cells and cytokines recruits neutrophils, worsening tissue injury.

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    Complement System Activation

    During ischemia, antibodies deposit in tissue; on reperfusion, complement proteins bind, worsening injury.

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    Irreversibility of Cell Death

    Irreversibility is marked by mitochondrial dysfunction and severe membrane disturbances.

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    Coagulative necrosis

    A type of tissue death characterized by the preservation of tissue architecture but loss of cellular detail, commonly seen in ischemia.

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    Gangrenous necrosis

    A type of necrosis associated with the death of tissue due to a lack of blood supply, often leading to infection.

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    Chronic reversible adaptations

    Physiological changes that occur in response to prolonged stress, allowing cells to function under abnormal conditions without dying.

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    Cell injury

    Damage to cells that may result from various factors such as toxins, hypoxia, or infection, potentially leading to death.

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    Disease syndrome

    A collection of signs and symptoms that often occur together, signaling a specific disease or condition.

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    Caseous Necrosis

    Necrosis characterized by a 'cheese-like' appearance and presence of granular debris.

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    Fat Necrosis

    Necrosis of adipose tissue with a chalky-white appearance, often due to pancreatitis.

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    Saponification

    Process where fatty acids and calcium form chalky deposits, seen in fat necrosis.

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    Fibrinoid Necrosis

    Necrosis of blood vessel walls due to immune complexes and plasma proteins, appearing pink on H&E stain.

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    Dry Gangrene

    Coagulative necrosis with possible liquefactive necrosis, usually from ischaemia and bacterial infection.

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    Granulomas

    Inflammatory masses formed in response to caseous necrosis, surrounded by inflammation.

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    Ischaemia

    Insufficient blood supply to tissues, leading to cell injury or necrosis.

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    Mitochondrial damage

    A change in membrane potential or permeability leads to mitochondrial injury.

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    Apoptosis-inducing factors

    Factors secreted by damaged mitochondria that trigger apoptosis.

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    Bak and Bax

    Proteins that dimerize and form channels in the mitochondrial membrane during apoptosis.

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    Cytochrome c

    A protein released into the cytosol that activates caspase-9 initiating apoptosis.

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    Caspase-9

    An enzyme activated by cytochrome c that plays a crucial role in apoptosis.

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    Liquefactive necrosis

    Type of necrosis where tissue becomes liquefied due to proteolytic enzymes.

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    Granulation tissue

    New connective tissue and tiny blood vessels that form during healing of the necrotic area.

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    Study Notes

    General Pathology: Cell Injury & Cell Death

    • Cell injury and cell death are the basis of all diseases.
    • Reversible injuries result in cell adaptation, repair, and healing.
    • Irreversible injuries lead to cell death.
    • The lectures cover pathology, pathogenesis, and physiology of cell death associated with various injuries.

    Topic Outline

    • General Features of Cell Injury:

      • Causes of cell injury: The factors/stimuli that damage cells
      • Progression of cell injury and death: Steps involved in cell injury

    • Reversible Cell Injury vs Cell Death:

      • Reversible cell injury: Early stages of cell injury (damage is potentially repairable)
      • Cell death: Necrosis vs. Apoptosis, Other mechanisms, Autophagy

    • Mechanisms and Selected Clinicopathologic Examples of Cell Injury:

      • Cellular targets of injurious stimuli: Factors targeted by injury (e.g., mitochondria, membranes, DNA)
      • Biochemical alterations in involved pathways: Changes in pathways affected by the injurious stimulus (e.g., oxidative stress, calcium homeostasis, ER stress)
      • Clinicopathologic examples: Specific examples of injury and death (e.g. hypoxia, ischemia, toxic injury, ischemic-reperfusion injury)

    Learning Outcomes

    • Discuss the aetiopathogenesis of cell injury and cell death
    • Differentiate apoptosis and necrosis
    • Compare the different types of necrosis with respect to aetiology, site, macroscopic and microscopic features
    • Define sublethal cell injury, list the causes and sequelae thereof
    • Describe the subcellular alterations (e.g. lysosomes, ER, mitochondria, cytoskeleton) resulting from cell injury
    • Explain the significance of reperfusion injuries, free radical-induced injury (referencing relevant textbook pages)
    • Distinguish between disease and non-disease states (referencing relevant textbook pages)

    Glossary

    • Aetiology: Refers to cause or inciting agent.
    • Pathogenesis: Describes the mechanism of a disease.
    • Morphological changes: Structural alterations indicative of a disease.
    • Hyaline: A descriptive histological term for a glassy, homogenous and eosinophilic appearance of material, non-specific.
    • Hydropic change: Cell and organelle swelling.
    • Adaptations: Mechanisms that allow cells to cope with stresses.
    • Reversible injury: Structural and functional abnormalities that are potentially correctable if the insult is removed.
    • Cell death: Irreversible degeneration of vital cellular functions

    Cell Injury Mind Map

    • Response to injury, duration, severity, consequences depend on the cell type and pre-existing state play a significant role.
    • Mechanisms of injury are diverse, including mechanical disruption, failure of membrane integrity, altered metabolic pathways, and DNA damage.
    • Injury can be reversible or irreversible, with different consequences for each.

    Categories of Cell Injury

    • Reversible cell injury: Acute & self-limited (complete resolution) or adaptive (functional & morphological).
    • Mild chronic injury: Subcellular alterations in organelles.
    • Progressive & severe irreversible injury leads to cell death by necrosis or apoptosis.

    Aetiology, Forms and Sites of Damage of Cell Injury

    • Injury can be caused by hypoxia/ischemia, or other injurious agents, ROS, or mutations.
    • Mitochondrial damage, damage to cellular membranes, nucleus damage can result in cell injury.

    Pathogenesis of Cell Injury

    • ATP depletion, mitochondrial damage, calcium influx, ROS production, membrane damage are major processes within cell injury.

    Reversible Injury

    • The cellular response to injury depends on the type of injury, duration, severity, the type of cell injured, the cell's metabolic state, and its ability to adapt.
    • Cell swelling, and impaired cellular regulation of mitochondria and endoplasmic reticulum and detachment of ribosomes from the RER, surface blebs and loss of microvilli structure are characteristic reactions during reversible injury.

    Mild Chronic Injury

    • Subcellular morphologic alterations are characteristic of this injury, such as cellular swelling (e.g., vacuolar change), increased influx of water into the cytoplasm, membrane bound vacuoles from invaginations of the plasma membrane and ER.
    • Other characteristics include plasma membrane blebbing, loss of microvilli, cytoplasmic changes, accumulation of small amorphous deposits, dilation of ER and detachment/disassociation of ribosomes, and nuclear alterations (chromatin clumping)

    Irreversible Cell Injury

    • Plasma membrane damage leads to cytoplasmic enzyme leakage (e.g. cardiac troponin) and calcium influx.
    • Mitochondrial membrane damage leads to the loss of the electron transport chain and cytochrome c leakage, activating apoptosis.
    • Lysosome membrane damage results in leakage of hydrolytic enzymes into the cytosol, and activation by high intracellular calcium.
    • Extensive membrane damage and increased calcium ions cause cell death.

    Biochemical Alterations in Cell Injury

    • Oxidative stress due to free radical accumulation results in lipid peroxidation, protein modifications, and DNA damage.
    • ER stress (unfolded protein response) leads to protein accumulation and activation of cellular signaling pathways involving chaperones, proteasomal degradation, and slow protein translation.

    Calcium Changes

    • Excessive increase in cytosolic calcium (Ca2+) accumulation in the mitochondria leads to opening of mitochondrial permeability transition pore and ATP depletion.

    Ischaemic Injury

    • Hypoxia (lack of oxygen) leads to ATP depletion and anaerobic glycolysis, whilst ischemia (reduced blood flow) and accumulation of toxic metabolites further damage tissue.
    • Ischaemic cell injury results from decreased cellular oxygen, ATP depletion, and subsequent damage.

    Ischemic-Reperfusion Injury

    • Reestablishment of blood flow can paradoxically exacerbate cell injury.
    • Oxidative stress, intracellular calcium overload, inflammation, and complement activation mechanisms contribute to further tissue damage.

    Chemical (Toxic) Injury

    • Direct toxicity occurs when chemicals bind to critical molecule components.
    • Chemicals can also be converted to toxic metabolites causing membrane damage and free radical formation.

    Cell Death - Point of No Return

    • Irreversible cell death is characterized by an inability to reverse mitochondrial dysfunction and profound disturbances in membrane function.

    Apoptosis

    • Activation of caspases orchestrates cell fragmentation.
    • Regulated by a balance of pro-apoptotic and anti-apoptotic proteins.
    • Intrinsic and extrinsic pathways regulate apoptosis.
    • Mitochondria release cytochrome c and activation of effector caspases lead to cellular breakdown and phagocytosis.

    Morphological Features of Apoptosis

    • (A) apoptosis of an epidermal cell in an immune reaction.
    • (B) Electron micrography of cultured cells undergoing apoptosis showing condensed or fragmented nuclei.

    Changes Leading to Necrosis

    • Prolonged ischemia causes depletion of ATP, and increased Ca2+ in the cytosol.
    • Activation of enzymes (phospholipase, protease, nuclease) contribute to cell membrane damage and protein damage leading to cell necrosis.

    Types of Necrosis

    • Coagulative: Common in tissues like kidney, heart, and liver (loss of nuclei and preservation of the cellular tissue outline).
    • Liquefactive: Characterised by enzymatic destruction of cell components (brain).
    • Caseous: A mix of coagulative and liquefactive (tuberculosis).
    • Fat: Lipases cause destruction of fat cells (pancreatitis).
    • **Fibrinoid:**Immune complexes deposit in vessel walls (malignant hypertension and vasculitis).
    • Gangrenous: Extensive coagulative necrosis often with bacterial superimposed infection.

    Liquefactive Necrosis-proteolytic Enzymes

    • Proteolytic enzymes cause cell lysis and liquefaction.
    • Necrosed tissue forms cystic spaces filled with cell debris in the surrounding areas.

    Coagulative Necrosis

    • Initial injury causes cellular acidosis and denaturation of proteins.
    • Tissue architecture initially maintains its form, and the outlines of dead cells remain visible, later becoming soft due to digestion by macrophages.
    • Typically associated with ischemia.

    Caseous Necrosis

    • Friable, white gross appearance; microscopic presentation is characterised by amorphous granular debris surrounded by inflammation, often in granulomas.

    Fat Necrosis

    • Necrotic adipose tissue with a chalky-white appearance due to calcium deposition.
    • Characterised by trauma to fat cells and/or pancreatitis.
    • Fatty acids released from dead fat cells combine with calcium to form soaps.

    Fibrinoid Necrosis

    • Characterized by immune complexes and exudated plasma proteins in artery walls.
    • Appears as bright pink amorphous material on H&E staining.
    • Typically associated with immunologically mediated vasculitis or malignant hypertension.

    Dry Gangrene

    • Coagulative necrosis usually with bacterial infection associated with ischemia of the lower extremities.
    • The skin is dry, dark, and wrinkled.

    Relationship of Cell Injury to Disease

    • Injurious stimuli can trigger reversible or irreversible cell injury.
    • Severe and progressing irreversible injury leads to necrosis or apoptosis, ultimately leading to disease.

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