Morphological Features of Cell Injury

• Morphological Features of Cell Injury are structural changes in cells caused by harmful stimuli.
• In reversible injury, cells may swell, accumulate fat, and show mild organelle damage.
• In irreversible injury, more severe changes occur, such as membrane rupture and nuclear alterations like pyknosis, karyorrhexis, and karyolysis, often leading to necrosis or apoptosis.
• Morphological Features help pathologists assess the type and severity of cell damage under a microscope.

Cell Swelling

• Cell swelling, also known as hydropic change or vacuolar degeneration, is one of the earliest signs of cellular injury.
• It occurs when cells lose their ability to maintain ionic and fluid homeostasis due to damage to the plasma membrane, leading to an influx of water.

• Causes:

  • Malfunction of energy-dependent ion pumps caused by hypoxia, toxins, or other disruptions to energy production.

• Mechanism:

  • ATP depletion impairs the function of membrane ion pumps, leading to sodium and water influx, which causes the cell to swell.
  • Organelles like mitochondria and the endoplasmic reticulum also swell, which may disrupt cellular functions further.

• Microscopy:

  • Enlarged, pale, and turgid cells.

• Outcome:

  • Reversible if the stressor is removed; may progress to irreversible injury and cell death if persistent.

Intracellular Accumulation

• Abnormal build-up of substances within the cell, which can be endogenous (proteins, lipids, carbohydrates) or exogenous (infectious agents, minerals, pigments).

• Types of Accumulations:

  1. Lipids: Fatty change (steatosis) in the liver due to excessive fat deposition (e.g., from alcohol, diabetes, or obesity).
  2. Proteins: Accumulation of misfolded proteins (e.g., neurodegenerative diseases like Alzheimer’s).
  3. Pigments: Accumulation of endogenous pigments (e.g., melanin, bilirubin, lipofuscin) or exogenous pigments (e.g., carbon in anthracosis).
  4. Glycogen: Abnormal accumulation in glycogen storage diseases.
  5. Calcium: Pathological calcification, discussed below.

• Mechanism:

  • Accumulation may result from increased production, reduced degradation, or an inability to metabolize certain substances, leading to their deposition in the cytoplasm or organelles.

• Examples:

  1. Fatty Change: Lipid accumulation.
  2. Hyaline Change: Protein accumulation.
  3. Hemosiderin Deposition: Iron accumulation.

• Outcome:

  • Can cause cellular dysfunction, injury, or death depending on the nature and severity of the accumulation.

Calcification

• Calcification is the abnormal deposition of calcium salts in tissues. It can be classified as dystrophic or metastatic.

• Mechanism:

  • In dystrophic calcification, dead or damaged cells release intracellular contents that act as a nidus for calcium deposition.
  • In metastatic calcification, elevated blood calcium levels cause calcium to be deposited in otherwise normal tissues.

• Types:

  • Dystrophic Calcification: Localized deposition in injured or dead tissues (e.g., necrotic areas, heart valves, atherosclerotic plaques), unrelated to calcium metabolism disturbances.
  • Metastatic Calcification: Occurs in normal tissues due to hypercalcemia or calcium metabolism disturbances, affecting organs such as kidneys, lungs, blood vessels, and stomach.

• Outcome:

  • Impairs organ function and may lead to further tissue injury or inflammation.

Enzyme Leakage

• Enzyme leakage occurs when damaged cells, particularly those undergoing necrosis, release intracellular enzymes into the extracellular space and eventually into the bloodstream.
• These enzymes can be measured as markers of cell injury or death.

• Mechanism:

  • When the plasma membrane is damaged due to injury or cell death, cellular enzymes leak out.
  • These enzymes can be detected in blood tests and are used to diagnose tissue damage.

• Causes:

  • Mechanical trauma, toxins, ischemia.

• Clinical Relevance:

  • Measurement of specific enzymes in the blood (e.g., creatine kinase for myocardial infarction, alanine aminotransferase for liver injury) helps diagnose and monitor tissue damage.

• Outcome:

  • Indicator of cell injury or death, reflecting loss of membrane integrity.

Cell Death

• Cell death can occur by two main processes: necrosis and apoptosis.

Forms:

1. Apoptosis

   • Necrosis is uncontrolled cell death that occurs due to severe injury, often associated with inflammation.
   • It is a pathological process in which cell membranes rupture, leading to the release of cellular contents that cause inflammation in the surrounding tissue.
   • Features:
     • Cell shrinkage
     • Chromatin condensation
     • Nuclear fragmentation
     • Formation of apoptotic bodies
     • Phagocytosis by neighbouring or immune cells
   • Outcome: Typically, does not induce an inflammatory response.

2. Necrosis

   • Apoptosis is a tightly regulated, programmed cell death that is often physiological and does not elicit an inflammatory response.
   • It is crucial for tissue homeostasis, development, and the elimination of damaged cells.
   • Features:
     • Cell swelling
     • Membrane rupture
     • Leakage of cellular contents
     • Inflammation in surrounding tissues
   • Subtypes: Coagulative necrosis and other types with distinct morphological features.
   • Outcome: Final consequence of irreversible cell injury.

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