Cellular Adaptation and Injury Quiz

Cellular Adaptation

• Cells adjust their structures and functions to respond to physiological or pathological changes.
• Atrophy: Reduction in cell size.
• Hypertrophy: Increase in cell size, leading to organ enlargement.
• Hyperplasia: Increase in cell number in an organ or tissue.
• Metaplasia: Replacement of one mature cell type by another.

Cell Injury

• Occurs when cells fail to adapt to stress.
• Causes: Anoxia (O₂ deprivation), hypoxia, ischemia, physical agents (trauma, heat/cold, radiation, electricity), chemical agents, microbial agents, immunological reactions, genetic defects, nutritional imbalances.
• Reversible injury: Initial response to stress, potentially reversible to normal if stress removed. Characterized by acute cell swelling.
• Irreversible injury: Cell cannot recover, marked by loss of mitochondrial function and impaired membrane integrity.

Cell Death

• Necrosis: Local death of cells and tissue within a living organism. Distinguished from apoptosis.
• Causes of necrosis: Poisons, lack of blood/nerve supply, pressure, thermal/mechanical injury.
• Apoptosis (Necrobiosis): Programmed cell death, a vital process removing unwanted cells. Examples include epithelial cells in epidermis and intestines.

Inflammation

• Complex protective reaction to harmful stimuli (bacteria, damaged cells, irritants).
• Classification (duration): Acute vs. Chronic
• Classification (causative agents): Aseptic (sterile) vs. Septic (caused by living organisms)
  • Aseptic inflammation often has a reparative goal, while septic inflammation is protective.
• Local signs and symptoms: Heat, redness, swelling, pain, loss of function (the "5 classic signs").
• Systemic symptoms: Fever (altered thermoregulation center), increased white blood cell count (leukocytosis, specific types increase with different infections)—neutrophils for bacteria, eosinophils for parasites, lymphocytes for viruses; alternatively, decreased white blood cell count (leukopenia)
• Vascular changes: Dilation of blood vessels, increase in vessel permeability. Mediated by molecules like histamine, VEGF, and bradykinin.
• Cellular changes:
  • Emigration of neutrophils (1-2 days), monocytes (2-3 days).
  • Chemotaxis (movement of cells toward inflammation).
  • Phagocytosis (removal of invaders/damaged cells) by leukocytes.
• Outcomes of acute inflammation:
  • Resolution (restoration to normal): Limited injury, chemical neutralization, vascular normalization, apoptotic inflammatory cells.
  • Healing by scar: Tissue damage, fibrous inflammation, purulent inflammation (formation of pus, abscess), resolution (weeks-months).
  • Progression into chronic inflammation: Persistent infections/irritants, repeated acute inflammations, autoimmune diseases.

Chronic Inflammation

• Long-lasting inflammation.
• Causes: Persistence of infection, prolonged exposure to irritants, repeated acute inflammation, autoimmune diseases.
• Cellular features: Infiltrations of chronic inflammatory cells ("round cell" infiltrate): lymphocytes, plasma cells (produce antibodies), monocytes/macrophages, cytotoxic/NK cells; coordination with immune system.
• Examples of diseases: Syphilis, tuberculosis, leprosy, rheumatoid arthritis, glomerulonephritis, multiple sclerosis.

Test your knowledge on cellular adaptation, injury, and death. This quiz covers key concepts such as atrophy, hypertrophy, hyperplasia, and the types of cell injuries including reversible and irreversible injury. Dive into the mechanisms that lead to cellular responses and their implications in health and disease.