Cell Death and Adaptations Quiz

Cell Death

• Cell injury occurs when cells are overly stressed. They are no longer able to adapt or they have been exposed to a harmful agent.
• Cell injury can be reversible if the stimulus is removed.
• If the stress is severe or persists, it leads to irreversible injury and cell death.
• Cell death is essential for normal cell function and development.

Cellular Adaptations to Stress

• Adaptations are reversible changes to cells that respond to environmental demands and stimuli.
• Physiological adaptations occur in response to normal stimuli like hormones and chemical mediators.
• Pathological adaptations occur in response to stress; cells change structure and function to avoid injury.
• Common pathological adaptation types include:
  • Hypertrophy: Increase in cell size.
  • Hyperplasia: Increase in cell number.
  • Atrophy: Decrease in cell size.
  • Metaplasia: Change in cell type.

Hypertrophy

• Increased cell size resulting in increased organ size.
• It is not a result of new cells, but the existing cells enlarging.
• Occurs due to the increase in structural proteins and organelles.
• Occurs when nondividing cells are exposed to stress or an increased functional demand.
• Examples include the myocardium and skeletal muscle cells.
• Weightlifting can cause hypertrophy of skeletal muscles.
• Cardiac enlargement due to constant strain from hypertension can cause hypertrophy.

Hyperplasia

• Increase in the number of cells, which increases organ size.
• Only occurs in cells capable of replication.
• May occur with hypertrophy in response to similar stimuli.
• Physiological hyperplasia:
  • Hormonal hyperplasia (e.g., breast development during puberty and pregnancy).
  • Compensatory hyperplasia (e.g., liver regeneration after a portion is removed).
• Pathological hyperplasia: Excessive hormone or growth factor stimulation (e.g., HPV causing skin warts).
• If hyperplasia becomes irreversible, it can lead to dysplasia and potentially cancer.

Atrophy

• Decrease in the cell size.
• A loss of cell substance leads to decreased organ size.
• Caused by decreased workload (e.g., limb immobilization) or reduced blood supply (e.g., aging).
• Cells have a reduced function but are not dead.
• Often accompanied by autophagy (self-eating).

Metaplasia

• Reversible change where a cell type is replaced by another cell type.
• Cells sensitive to a particular stress can be replaced by other more resistant cell types.
• Likely stems from genetic reprogramming of stem cells.
• Commonly occurs in epithelial cells that are continuously replaced by stem cells.
• May result in reduced function or increased susceptibility to further damage.
• Example: Squamous change in the respiratory epithelium of cigarette smokers.

Mechanisms of Cell Injury

• Major sites of damage from stimuli include:
  • ATP depletion
  • Membrane damage
  • Cytoskeletal damage
  • DNA damage including the accumulation of misfolded proteins.

Overview of Cell Injury and Cell Death: Reversible Cell Injury

• Early or mild forms of injury lead to functional and morphological changes than can be reversed if the stimulus is removed.
• Examples include swelling or changes to the cytoplasm or organelles (e.g., kidney tubules).
• DNA damage can cause the cell cycle checkpoint to arrest the cell in cycle until the damage is repaired; otherwise apoptosis occurs.

Overview of Cell Injury and Cell Death: Cell Death

• Continued damage causes cell death that is either necrosis or apoptosis; injury becomes irreversible.

• Types of cell death include:

  • Necrosis: Major pathway in many injuries, always a pathological process. The cell's integrity is lost.
  • Apoptosis: Activated by a tightly controlled suicide program. The cell’s integrity is maintained; no inflammatory response typically occurs.

• Changes in irreversible cell injury include:

  • DNA damage
  • Aging/senescence
  • Permanent cell-cycle arrest (G1)
  • Large flattened cells
  • Increased vacuoles
  • Cytoplasmic granularity

• Morphological changes in irreversible injury (e.g. loss of nuclei, cell fragmentation, and leakage of contents).

Cell Death: Necrosis

• Degradative actions of enzymes cause cellular damage, leading to cell death.
• Morphological alterations include nuclear shrinkage, fragmentation, and dissolution
• Breakdown of plasma and organelle membranes.
• Necrosis involves a collection of cells in a tissue or organ, leading to tissue death or sometimes the entire organ's death (e.g., brain, kidney, or lung).

Cell Death: Apoptosis

• Apoptosis is activated by a controlled suicide program (triggered by physiological or pathological conditions).
• Cell activation of enzymes occurs in a regulated manner to degrade itself, without harming neighboring cells.
• The plasma membrane has integrity, so there is no cell content spill into the surrounding area, and a no inflammatory response occurs.
• Morphological alterations of apoptosis include cell shrinkage and chromatin condensation, membrane blebbing and nuclear fragmentation. Apoptotic bodies are formed, which can then be phagocytosed by surrounding tissues.

Mechanisms of apoptosis

• Two main pathways exist; intrinsic (mitochondrial pathway) and extrinsic (death receptor pathway).
• Each has its own initiators, regulators, and executioners to activate a programmed cell death process.

Test your knowledge on cell injury, death, and adaptations to stress. This quiz covers essential concepts like reversible and irreversible cell changes, as well as common types of hypertrophy, hyperplasia, atrophy, and metaplasia. Enhance your understanding of cellular responses to different stimuli.