Cell Injury and Death Overview
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Questions and Answers

What is cell injury?

Cell injury is a variety of stresses a cell encounters due to changes in the cell's internal and external environment.

What does the cellular response to injury depend on? (Select all that apply)

  • The cell's ability to revert back to normal after stress is removed
  • Type, extent, and adaptability of cell injury (correct)
  • The nature of injury, duration, and severity (correct)
  • The cell's ability to adapt to changes

    • Cellular adaptations are irreversible changes that occur in response to stress.

    False

    What are the two possible outcomes for an injured cell?

    <p>Reversible and irreversible injury</p> Signup and view all the answers

    What is fatty change (steatosis)?

    <p>Fatty change is the accumulation of neutral fat within parenchymal cells.</p> Signup and view all the answers

    What is the most common site for accumulation of fat in the body and why?

    <p>The liver is the most common site for accumulation of fat because it plays a central role in fat metabolism.</p> Signup and view all the answers

    Fatty change is always irreversible.

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

    What are some common causes of fatty liver disease? (Select all that apply)

    <p>Diabetes mellitus</p> Signup and view all the answers

    Match the following characteristics of a fatty liver with their description:

    <p>Size = Increased Surface = Smooth Border = Rounded Cut section = Bulges Color = Pale yellow Touch = Greasy</p> Signup and view all the answers

    What are the microscopic features of fatty change?

    <p>Numerous lipid vacuoles appear in the cytoplasm of hepatocytes. Initially small, these vacuoles become large, pushing the nucleus to the periphery of the cell, giving a signet ring appearance. Eventually, the cells rupture and lipid vacuoles coalesce to form fatty cysts.</p> Signup and view all the answers

    What are the effects of fatty change?

    <p>Mild accumulation of fat can be reversible. However, marked accumulation is irreversible and can lead to necrosis and cirrhosis.</p> Signup and view all the answers

    What are two major types of irreversible cell injury?

    <p>Necrosis and apoptosis are two major types of irreversible cell injury.</p> Signup and view all the answers

    What is necrosis?

    <p>Necrosis is a focal death of a group of cells within a living body, often caused by hydrolytic enzymes released by damaged cells, and accompanied by an inflammatory reaction.</p> Signup and view all the answers

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

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

    Necrosis is a programmed cell death process.

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

    What are the two essential changes that occur during necrosis?

    <p>Denaturation of proteins, which leads to characteristic nuclear changes in the necrotic cell, and cell digestion by lytic enzymes are the two essential changes.</p> Signup and view all the answers

    How does cell digestion occur during necrosis?

    <p>Cell digestion can occur through autolysis, the breakdown of the cell by its own lysosomal enzymes, or heterolysis, the breakdown by proteolytic enzymes released from surrounding inflammatory cells, such as neutrophils and monocytes.</p> Signup and view all the answers

    What is the morphological appearance of necrotic cells?

    <p>Homogeneous and eosinophilic cytoplasm</p> Signup and view all the answers

    Describe the gross appearance of necrotic tissue.

    <p>Necrotic tissue appears opaque yellow and may be swollen. Surrounding tissues often appear hyperemic due to inflammation.</p> Signup and view all the answers

    What are the nuclear changes that occur during necrosis? (Select all that apply)

    <p>Karyorrhexis: nuclear fragmentation</p> Signup and view all the answers

    Necrotic tissue can be repaired by regeneration.

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

    What are two main possibilities for architectural changes during necrosis?

    <p>Structureless tissue due to cell lysis</p> Signup and view all the answers

    What are structural ghosts?

    <p>Structural ghosts are the architectural outlines of the original tissue that are preserved in the necrotic cells.</p> Signup and view all the answers

    Necrotic tissue is always structureless.

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

    What happens to necrotic tissue?

    <p>Necrotic tissues undergo a process of inflammation, healing, and sometimes dystrophic calcification.</p> Signup and view all the answers

    Inflammation is an essential component of the healing process.

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

    How does healing begin following necrosis?

    <p>Healing begins with phagocytosis: removal of dead cells by macrophages, followed by drainage of liquefied necrotic tissue by lymphatics, aiding removal of cellular debris.</p> Signup and view all the answers

    What are the two ways healing can occur after necrosis? (Select all that apply)

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

    Fibrosis is a process of complete regeneration of dead cells.

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

    What is dystrophic calcification?

    <p>Dystrophic calcification is the deposition of calcium salts in the tissues.</p> Signup and view all the answers

    What are the different types of necrosis? (Select all that apply)

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

    What is coagulative necrosis?

    <p>Coagulative necrosis is the most common form of necrosis, often due to ischemia, and less commonly due to bacterial and chemical agents.</p> Signup and view all the answers

    Where does coagulative necrosis typically occur?

    <p>Coagulative necrosis occurs in the infarction (death of tissue due to lack of blood supply) of most organs, except for the central nervous system (CNS).</p> Signup and view all the answers

    In coagulative necrosis, cell lysis precedes protein denaturation.

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

    Describe the gross appearance of coagulative necrosis.

    <p>In the early stages of coagulative necrosis, the affected areas are pale, firm, and slightly swollen, due to protein denaturation. As necrosis progresses, these areas become more yellowish, softer, and shrunken due to cell lysis.</p> Signup and view all the answers

    What are the microscopic features of coagulative necrosis?

    <p>Coagulative necrosis is characterized by the conversion of normal cells into 'tombstones' or structural ghosts, where the cell outlines are preserved but cytoplasmic and nuclear details are lost, resembling outlines of the original cells. Necrotic cells are also swollen and more eosinophilic than normal cells.</p> Signup and view all the answers

    Coagulative necrosis is characterized by the presence of structural ghosts, preserving the original shape of the cells.

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

    What is liquefactive necrosis?

    <p>Liquefactive necrosis is characterized by the complete enzymatic digestion of dead cells, resulting in a liquefied center.</p> Signup and view all the answers

    What are two examples of tissues where liquefactive necrosis commonly occurs?

    <p>Liquefactive necrosis commonly occurs in infarct brain due to its high lipid content and in abscess cavities (pus).</p> Signup and view all the answers

    Liquefactive necrosis involves more rapid lysis than protein denaturation.

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

    Describe the gross appearance of liquefactive necrosis in the brain.

    <p>The affected area in liquefactive necrosis of the brain appears soft, with a liquified center containing necrotic debris. Over time, a cyst wall forms around the affected area.</p> Signup and view all the answers

    What are the microscopic features of liquefactive necrosis?

    <p>The cystic space contains necrotic cell debris and macrophages filled with phagocytosed material. The cyst wall can be formed by proliferating capillaries, inflammatory cells, and remnants of glial cells in the case of brain damage or proliferating fibroblasts in the case of abscess formation.</p> Signup and view all the answers

    What is caseous necrosis?

    <p>Caseous necrosis is characterized by a cheesy, granular appearance and is commonly found in tuberculosis infections.</p> Signup and view all the answers

    Caseous necrosis typically occurs in areas of bacterial infection.

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

    How does caseous necrosis begin?

    <p>Caseous necrosis begins as ischemic coagulative necrosis, caused by endarteritis obliterans (inflammation and obstruction of arteries), leading to tissue death due to insufficient blood supply.</p> Signup and view all the answers

    Hypersensitivity to tuberculoprotein plays a role in creating the characteristic features of caseous necrosis.

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

    Describe the gross appearance of caseous necrosis.

    <p>Caseous necrosis appears as soft, granular, and yellowish foci that resemble dry cheese.</p> Signup and view all the answers

    What are the microscopic features of caseous necrosis?

    <p>Microscopically, the necrosed foci are structureless, eosinophilic, and contain granular debris. The surrounding tissue exhibits granulomatous inflammation, characterized by epithelioid cells with giant cells of Langhans and peripheral lymphocytes.</p> Signup and view all the answers

    Signup and view all the answers

    Signup and view all the answers

    Study Notes

    Cell Injury and Cell Death

    • Cell injury is a response to various stressors that arise from changes in the internal and external environment.
    • The cellular response to injury depends on the nature, duration, and severity of the injury, along with the cell's type, extent of injury, and adaptability.
    • Cells may adapt to the stress and revert to normal after the stress is removed (cellular adaptations)
    • Residual effects of injury may persist
    • Injured cells may recover (reversible cell injury), or die (irreversible cell injury).

    Cellular Responses to Injury

    • Cells may adapt to changes and revert to normal when the stressor is removed (cellular adaptations).
    • Residual effects of injury may persist in the cell as evidence of the injury.
    • The injured cell may recover (reversible injury) or die (irreversible injury).

    Cell Injury: Overview

    • A normal cell in homeostasis can undergo adaptation to injury, leading to either reversible or irreversible injury.
    • Reversible injury leads to mild, transient conditions.
    • Irreversible injury, on the other hand, leads to severe, progressive conditions
    • Irreversible injury can result in necrosis or apoptosis.

    Nutritional Imbalance

    • Nutritional deficiency (starvation, protein-calorie malnutrition [marasmus, kwashiorkor], or mineral deficiency [anemia]) can cause diseases
    • Nutritional excess in affluent societies can result in obesity, atherosclerosis, heart disease, and hypertension.

    Aging

    • Cell aging decreases the ability of cells to replicate and repair, leading to cell death, and ultimately death of the individual.

    Psychogenic Diseases

    • Psychogenic diseases, such as depression and schizophrenia, do not have specific biochemical or morphological changes caused by mental stress.
    • Problems like drug addiction, alcoholism, and smoking result in various organic diseases.

    Free Radical Initiation

    • Exposure to energy sources like UV light and X-rays can initiate free radicals.
    • Conversion of exogenous chemicals/drugs (e.g., carbon tetrachloride) can also lead to free radical formation.
    • Oxygen-derived radicals are also a source of free radical formation.

    Idiopathic Diseases

    • Idiopathic diseases have unknown causes.
    • Essential hypertension (90% of cases) is an example of an idiopathic disease.

    Types of Cell Injury

    I. Reversible Cell Injury

    • Cellular changes can regress and disappear when the injurious agent is removed or altered.
    • The cell returns to normal function and morphology.
    • Example: Fatty change (steatosis)

    II. Irreversible Cell Injury

    • Occurs when the injury persists or is severe from the start.
    • Cells reach a point of no return and progression to death.
    • Example: Necrosis and apoptosis.

    Fatty Change (Steatosis)

    • Accumulation of neutral fat within parenchymal cells.
    • Commonly affects the liver, but can also occur in the heart, skeletal muscle, and kidneys.

    Fatty Liver

    • Liver is the prime site for fat accumulation due to its role in fat metabolism.
    • Imbalance in uptake, utilization, and secretion of fat causes fatty liver.
    • Fatty change may be mild and reversible or severe and irreversible, and induce death.
    • Excess alcohol intake, liver diseases, starvation, malnutrition, diabetes, chronic illnesses, hypoxia, hepatotoxins, and certain drugs can all cause fatty liver.

    Etiology of Fatty Liver

    • Excessive alcohol consumption is the most common cause.
    • Liver diseases, such as hepatitis C, can contribute significantly to fatty liver.
    • Starvation and malnutrition can cause fat mobilization.
    • Obesity, diabetes, chronic illnesses (e.g., tuberculosis), hypoxia (e.g., anemia), exposure to hepatotoxins (e.g., carbon tetrachloride, chloroform, aflatoxins), and certain drugs (e.g., estrogens, steroids, tetracycline) can also lead to fatty liver development.

    Gross Picture: Fatty Liver

    • Increased size.
    • Smooth surface.
    • Rounded border.
    • Bulging cut section.
    • Pale yellow color.
    • Greasy texture.

    Microscopic Picture: Fatty Liver

    • Numerous lipid vacuoles (microvesicular at the initial stage, enlarging into macrovesicular vacuoles), which displace the nucleus to the cell periphery (signet ring appearance).
    • Rupture of cells and merging of fat vacuoles ultimately form fatty cysts.

    Effects of Fatty Liver

    • Mild fat accumulation is reversible.
    • Significant fat accumulation is irreversible and may progress to necrosis and cirrhosis.

    Necrosis: Irreversible Cell Injury

    • Focal death of cells within a living body due to released hydrolytic enzymes.
    • Accompanied by an inflammatory response.
    • Causes include hypoxia, various chemical or physical agents, microbial agents, and immunological factors.

    Pathogenesis of Necrosis

    • Denaturation of proteins: characteristic nuclear changes occur in necrotic cells.
    • Cell disintegration by lytic enzymes: autolysis (by the cell's own lysosomal enzymes) and heterolysis (by proteolytic enzymes from surrounding inflammatory cells)
    • Morphologically: homogeneous and intensely eosinophilic cytoplasm.

    Gross Picture: Necrosis

    • Necrotic tissue appears opaque yellow and may be swollen.
    • Surrounding tissues are hyperemic due to inflammation.

    Microscopic Picture: Necrosis

    • Cytoplasm appears homogeneous and eosinophilic.
    • Nuclear changes due to protein denaturation include: pyknosis (small, dark nucleus); karyorrhexis (nuclear fragmentation); and karyolysis (faintly dissolved nucleus).

    Liver - Hepatocellular Necrosis

    • Microscopic descriptions of the features of hepatocellular necrosis include: pyknosis, karyorrhexis, and karyolysis

    Architectural Changes in Necrosis

    • Necrotic tissue appears rapidly structureless due to cell lysis (autolysis, heterolysis).
    • Protein denaturation (coagulation) can precede cell lysis, especially in ischemia.
    • Necrotic tissue can retain the architectural outlines of the original tissue (structural ghosts).
    • Tissue structure rapidly disintegrates.

    Fate of Necrotic Tissue

    • Inflammation surrounds the necrotic area due to released chemical mediators.
    • Healing involves phagocytosis of necrotic tissue by phagocytes, such as macrophages and lymphocytes.
    • Regeneration or fibrosis (tissue in the area) can occur.
    • Dystrophic calcification can follow some types of necrosis due to the tissue's altered chemical environment.

    Types of Necrosis

    • Coagulative necrosis
    • Liquefactive necrosis
    • Caseous necrosis
    • Fat necrosis
    • Fibrinoid necrosis

    1. Coagulative Necrosis

    • Most common type.
    • Results from ischemia (reduced blood flow) and less frequently from bacterial or chemical agents.
    • Occurs in infarcts of most organs except the central nervous system (CNS).
    • Organs commonly affected are the heart, kidney, and spleen
    • Protein denaturation precedes cell lysis.
    • Cell outlines persist for several days.
    • Gradual nuclear degeneration.

    Gross Picture: Coagulative Necrosis

    • Early stage: Pale, firm, and slightly swollen foci.
    • Late stage: Yellowish, softer, and shrunken necrotic area.

    Microscopic Picture: Coagulative Necrosis

    • Conversion of normal cells into their 'tombstone' forms (structural ghosts), preserving the outlines of cells.
    • Swollen cells that appear more eosinophilic.
    • Nuclear changes.
    • Necrotic tissue becomes structureless later.
    • Acute inflammation in the surrounding tissue.

    2. Liquefactive Necrosis

    • Due to ischemia and bacterial or fungal infections.
    • Degradation of tissue by powerful hydrolytic enzymes. Cell lysis exceeds protein denaturation.
    • Examples include brain infarcts (due to high lipid content) and abscess cavities (pus).

    Gross Picture: Liquefactive Necrosis

    • Affected area is soft with a liquefied center containing necrotic debris.
    • Cyst wall eventually forms.

    Microscopic Picture: Liquefactive Necrosis

    • Cystic space contains necrotic cell debris and macrophages.
    • Cyst wall composed of proliferating capillaries, inflammatory cells, and glial cell ghosts (brain).
    • Proliferating fibroblasts (abscess cavity).

    3. Caseous Necrosis

    • Found in the center of foci associated with tuberculosis infections.
    • Exhibits features of both coagulative and liquefactive necrosis.
    • Begins as ischemic coagulative necrosis caused by endarteritis obliterans.
    • Hypersensitivity to tuberculoprotein releases cytotoxins causing partial liquefaction of the necrotic cells.

    Gross Picture: Caseous Necrosis

    • Foci resemble dry cheese, appearing soft, granular, and yellowish.

    Microscopic Picture: Caseous Necrosis

    • Structureless, eosinophilic necrotic foci with granular debris.
    • Characteristic granulomatous inflammation with epithelioid cells, giant cells (e.g., Langhans cells), and peripheral lymphocytes.

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    Description

    This quiz explores the concepts of cell injury and death, focusing on the cellular responses to various stressors. It details how cells can adapt to injury, recover, or face irreversible damage. Understand the factors influencing these outcomes and the implications for cellular health.

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