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.