Cellular Adaptations in Biology

Cellular Adaptations

• Cells adapt growth and differentiation to body changes.
• Normal adaptations include increased breast/uterine tissue in pregnancy.
• Tissue modifications often reverse after stimulus removal.
• Disease develops when cells change, preventing homeostasis.
• Irreversible changes signal DNA structure/function alterations.
• Abnormal changes aren't always cancerous, monitor for issues.
• Cell damage can result from metabolic shifts, ATP reduction, pH changes, or membrane/receptor damage.

Types of Cellular Adaptations

• Atrophy: Decrease in cell size, reduced tissue mass.

  • Causes: reduced use, insufficient nutrition, decreased hormonal/neurological stimulation, aging.
  • Example: immobilized limb muscle shrinkage.

• Hypertrophy: Increase in cell size, enlarged tissue mass.

  • Causes: increased tissue work, demands (e.g., enlarged heart muscle).
  • Example: Exercise-induced skeletal muscle enlargement.

• Hyperplasia: Increased cell number, enlarged tissue mass.

  • Causes: compensatory mechanisms to meet demands, hormonal imbalances.
  • Example: Uterine enlargement during pregnancy.
  • Potential link to cancer risk in some cases.

• Metaplasia: One mature cell type replaces another.

  • Causes: Vitamin A deficiency or environmental stimuli (e.g., cigarette smoke in respiratory tract).
  • Example: stratified squamous epithelium replacing ciliated columnar in smokers.
  • Reduced lung defenses due to loss of cilia.

• Dysplasia: Tissue cells with varied size/shape, large nuclei, increased mitosis.

  • Causes: chronic irritation/infection, potential precancerous change.
  • Diagnosis: Routine screening, such as Pap smear (cervical cells).

• Anaplasia: Undifferentiated cells with variable nuclear/cell structures, numerous mitotic figures.

• Sign of aggressive tumor growth. Common in malignant tumors. Basis for tumor grading.

• Neoplasia: New growth, aka tumor.

  • Types: Benign (less serious, usually do not spread)
  • Types: Malignant (cancerous, can spread)
  • Characteristics vary depending on cell origin.
  • Further discussion in Chapter 20

Cell Damage and Necrosis

• Apoptosis: Programmed cell death (normal).

  • Increases with abnormal development, excessive cell numbers, or injury/aging.
  • Cells self-digest into apoptotic bodies, engulfed without inflammation.

• Necrosis: Cell/tissue death from irreversible damage (not programmed).

  • Causes: ischemia, physical/chemical agents, mechanical damage, infection, metabolic imbalance, nutritional/electrolyte deficiencies.
  • Hypoxia: Reduced oxygen in tissue, a significant cause of cell damage. Can lead to cell swelling and rupture.

• Cell Injury Stages: Initial alteration in metabolic reaction leading to loss of function (reversible if damage factor removed). Increased damage leads to structural/morphological changes.

• Types of Necrosis:

  • Liquefactive: Dead cells liquefy (e.g., brain infarction, infections).
  • Coagulative: Protein alteration (denaturation), cells maintain structure for a while (e.g., heart attack).
  • Fat: Fatty tissue breakdown into fatty acids (e.g., infection).
  • Caseous: Thick, yellowish, "cheesy" substance (e.g., TB).
  • Infarction: Area of dead cells from lack of oxygen (e.g., heart attack).

• Gangrene: Necrotic tissue, often due to poor blood supply and infection.

  • Types: Dry (coagulative necrosis, tissue dries, shrinks, blackens)
  • Types: Wet (liquefaction necrosis, tissue becomes cold, swollen, black)
  • Gas gangrene: Build-up of gases further reduces blood supply.
  • Frequently requires surgical removal (amputation).

Diagnostic Findings

• Cell/tissue death can lead to enzyme release into the blood. The presence of specific enzymes can identify the damaged tissue type (e.g., cardiac enzymes indicating heart attack).