Irreversible Cell Injury and Necrosis
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Irreversible Cell Injury and Necrosis

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Questions and Answers

What is the primary consequence of irreversible cell injury?

  • Cells recover from damage
  • Cells undergo necrosis or apoptosis (correct)
  • Cells experience minor inflammation
  • Cells repair themselves without scarring
  • Which of the following is a common cause of necrosis?

  • Localized infection
  • Moderate exercise
  • Nutritional supplementation
  • Ischemia (correct)
  • Which characteristic is associated with necrotic cells?

  • Preserved nuclear integrity
  • Membrane damage (correct)
  • Decreased eosinophilia
  • Enhanced cellular respiration
  • What type of necrosis is characterized by the preservation of tissue architecture for a few days?

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

    How does liquefactive necrosis primarily affect tissue?

    <p>Dead cells are digested into a viscous liquid</p> Signup and view all the answers

    Which stage of gangrenous necrosis is commonly associated with the presence of pus?

    <p>Wet gangrene</p> Signup and view all the answers

    What happens to cellular proteins during necrosis?

    <p>Proteins undergo denaturation</p> Signup and view all the answers

    What is the role of pro-apoptotic proteins like BAX and BAK in the mitochondrial pathway of apoptosis?

    <p>They oligomerize to enhance mitochondrial outer membrane permeability.</p> Signup and view all the answers

    Which step is critical in the initiation of the extrinsic pathway of apoptosis?

    <p>Binding of Fas ligand to Fas death receptors.</p> Signup and view all the answers

    What is a key characteristic of apoptotic bodies in histological examination?

    <p>Intensely eosinophilic (pink) cytoplasm with nuclear fragments.</p> Signup and view all the answers

    Which proteins are considered anti-apoptotic members that help maintain mitochondrial integrity?

    <p>BCL2, BCL-XL, and MCL1</p> Signup and view all the answers

    What is the primary purpose of phagocytosing apoptotic bodies by neighboring cells?

    <p>To efficiently remove dying cells and prevent inflammation.</p> Signup and view all the answers

    What is the primary characteristic of caseous necrosis?

    <p>Presence of fragmented lysed cells within a granuloma</p> Signup and view all the answers

    Which type of necrosis is primarily caused by the release of pancreatic lipases?

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

    What distinguishes apoptosis from necrosis?

    <p>Membrane integrity is maintained during apoptosis</p> Signup and view all the answers

    Which of the following best describes the outcome of necrotic tissue resorption in the brain?

    <p>Development of a fluid-filled cyst</p> Signup and view all the answers

    What physiological role does apoptosis play during the menstrual cycle?

    <p>Removes superfluous endometrial cells</p> Signup and view all the answers

    What is the first step in the process of apoptosis?

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

    In which pathological condition is apoptosis particularly critical to prevent cancerous transformation?

    <p>DNA damage</p> Signup and view all the answers

    What microscopic feature is most distinctive of apoptosis?

    <p>Chromatin condensation</p> Signup and view all the answers

    Which of the following correctly describes the appearance of fibrinoid necrosis?

    <p>Bright pink fibrin-like deposits in vessel walls</p> Signup and view all the answers

    What outcome can occur as a result of dystrophic calcification in necrotic tissue?

    <p>Formation of calcium deposits</p> Signup and view all the answers

    Study Notes

    Irreversible Cell Injury

    • Irreversible cell injury results in cell death, which can occur in two primary forms: necrosis and apoptosis.

    Necrosis

    • Necrosis is a pathologic process that occurs due to severe cell injury.
    • Causes include ischemia (loss of blood supply), toxin exposure, physical injury (burns), and conditions like pancreatitis.
    • Characteristics:
      • Denaturation of proteins results in a firm texture.
      • Damaged membranes cause leakage of cellular contents, triggering local inflammation.
      • Enzymatic digestion breaks down dead cells.
      • Increased eosinophilia due to loss of RNA and protein accumulation.
      • Nuclear changes:
        • Karyolysis: Fading nucleus due to DNA degradation.
        • Pyknosis: Nuclear shrinkage and increased basophilia.
        • Karyorrhexis: Nuclear fragmentation.

    Patterns of Tissue Necrosis

    • Coagulative necrosis:
      • Tissue architecture is preserved for several days.
      • Firm texture with eosinophilic cells due to protein and enzyme denaturation.
      • Commonly caused by ischemia, leading to tissue infarction.
    • Liquefactive necrosis:
      • Digests dead cells, transforming the tissue into a viscous liquid.
      • Associated with bacterial or fungal infections and hypoxic brain death.
      • Necrotic material often appears as pus due to leukocyte presence.
    • Gangrenous necrosis:
      • Clinical term describing tissue (often limb) undergoing necrosis due to loss of blood supply.
      • Types:
        • Dry gangrene: Coagulative necrosis affecting multiple levels of tissue.
        • Wet gangrene: Bacterial infection superimposed on dry gangrene, leading to liquefactive necrosis.
    • Caseous necrosis:
      • Often seen in tuberculosis infections, characterized by cheese-like appearance.
      • Microscopic appearance: Fragmented or lysed cells in a distinctive inflammatory border called a granuloma.
    • Fat necrosis:
      • Localized fat destruction, typically due to pancreatic lipases released during acute pancreatitis.
      • Chalky-white areas are visible macroscopically, and histologically, necrotic fat cells show calcium deposits and an inflammatory reaction.
    • Fibrinoid necrosis:
      • Special form of necrosis occurring in immune reactions involving blood vessels.
      • Antigen-antibody complexes and plasma proteins leak into the wall, creating a pink fibrin-like appearance on H&E stains.

    Sequelae (Outcomes) of Necrosis

    • Complete resolution: Some tissues, like the liver and kidney, can regenerate and repair fully.
    • Repair by fibrous scarring: In organs like the heart, necrotic tissue is replaced by scar tissue.
    • Resorption of necrotic tissue: In the brain, necrotic tissue is removed by macrophages leaving a fluid-filled cyst (pseudocyst).
    • Calcification: Dystrophic calcification can occur in necrotic tissues, leading to calcium deposits.

    Apoptosis

    • Apoptosis is programmed cell death occurring when cells activate enzymes that degrade their DNA and proteins.
    • It’s tightly regulated, essential for tissue homeostasis, and involves cell breakdown into membrane-bound fragments called apoptotic bodies.
    • Membrane integrity remains intact, but surface alterations attract phagocytes.
    • Rapid engulfment and digestion of the apoptotic body prevents inflammatory response.

    Historical Context

    • Apoptosis was first recognized in 1972, named after the Greek word for "falling off" due to the orderly nature of this cell death process.

    Causes of Apoptosis

    • Physiological situations:
      • Developmental cell removal: Eliminates excess cells, involution of primordial structures, and remodeling maturing tissues.
      • Involution of hormone-dependent tissues: Breakdown of endometrial cells during menstruation, ovarian follicular atresia during menopause, and regression of lactating breast after weaning.
      • Cell turnover in proliferating populations: Maintains constant cell numbers in tissues with high turnover rates (e.g., lymphocytes, intestinal epithelial cells).
      • Elimination of self-reactive lymphocytes: Prevents autoimmune reactions.
    • Pathological conditions:
      • DNA damage: Resulting from radiation, chemotherapy, or free radicals. Apoptosis prevents survival of mutation-carrying cells that could become cancerous.
      • Accumulation of misfolded proteins: Misfolded proteins trigger ER stress, a defense mechanism against accumulation of harmful proteins.
      • Infections: Induced by viral infections, directly by the virus or as a result of the host’s immune response.
      • Pathologic atrophy: Contribute to atrophy after duct obstruction, causing cell loss and tissue shrinking.

    Morphologic and Biochemical Changes in Apoptosis

    • Cell shrinkage: Cell becomes smaller, with densely packed cytoplasm.
    • Chromatin condensation: Distinctive feature of apoptosis, chromatin aggregates beneath the nuclear membrane.
    • Nuclear fragmentation: Nucleus breaks into fragments as apoptosis progresses.
    • Formation of cytoplasmic blebs and apoptotic bodies: Cell membrane forms blebs that break off into apoptotic bodies containing cytoplasmic and nuclear material. Eosinophilic appearance.
    • Absence of inflammation: Rapid clearance of apoptotic bodies by phagocytes prevents the release of cell contents and prevents inflammation. Difficult to detect with light microscopy.

    Mechanism of Apoptosis

    • Apoptosis is orchestrated by caspases, activated through two main pathways:
      • **Mitochondrial (intrinsic) pathway : **
        • Initiated by increased permeability of the mitochondrial outer membrane.
        • Cytochrome c released into the cytoplasm triggers apoptosis.
        • Controlled by BCL2 family of proteins:
          • Anti-apoptotic proteins: BCL2, BCL-XL, and MCL1 maintain membrane impermeability.
          • Pro-apoptotic proteins: BAX and BAK increase membrane permeability when activated.
          • Regulated apoptosis initiators: BAD, BIM, and BID initiate apoptosis when upregulated.
      • **Death receptor (extrinsic) pathway: **
        • Initiated by engagement of death receptors on the plasma membrane.
        • Death receptors belong to the TNF receptor family with a cytoplasmic death domain.
        • Key death receptors: TNFR1 and Fas (CD95).
        • Fas ligand (FasL) expressed on T cells recognizes self-antigens and eliminates self-reactive lymphocytes.
        • FasL is also expressed on cytotoxic T lymphocytes (CTLs).
        • Upon binding of FasL to Fas, a binding site for the adaptor protein FADD is formed.
        • FADD recruits inactive caspase-8, leading to its activation.
        • Active caspase-8 initiates activation of executioner caspases.

    Execution Phase of Apoptosis

    • Both pathways lead to caspase cascade activation.
    • Initiator caspases (caspase-9 for intrinsic, caspase-8 and caspase-10 for extrinsic) activate executioner caspases (caspase-3 and caspase-6).

    Removal of Dead Cells

    • Formation of cytoplasmic buds containing cell components.
    • Formation of apoptotic bodies, encapsulating fragmented cellular contents.
    • Phagocytosis of apoptotic bodies by neighboring cells or macrophages, ensuring safe and efficient removal and preventing inflammation.

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    Description

    This quiz explores aspects of irreversible cell injury, including necrosis and apoptosis. It covers the causes, characteristics, and patterns of tissue necrosis, detailing the various nuclear changes associated with cell death. Ideal for students studying pathology or related fields.

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