In the grand newsroom of human physiology, not every story is about growth and balance. Sometimes, the headlines are about damage, defense, and repair. Unit 1 takes readers behind the scenes of cell injury, adaptation, inflammation, and healing — processes that determine whether tissues survive a crisis or spiral into disease.
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Homeostasis: The Balancing Act of Life
At the heart of every healthy cell lies homeostasis — the delicate equilibrium that keeps internal conditions stable despite external changes. This balance is maintained by feedback systems:
Negative feedback acts like a fact-checker, correcting deviations (e.g., regulating blood glucose).
Positive feedback, though rarer, amplifies processes (like uterine contractions during childbirth).
When this stability is disrupted, the newsroom of the body reports a breaking story: cellular injury.
Causes and Pathogenesis of Cell Injury
Cell injury arises from diverse causes — hypoxia, toxins, infections, immune reactions, genetic defects, and nutritional imbalances. The damage often strikes the body’s vital structures:
Cell membrane damage: disrupting the protective barrier.
Mitochondrial injury: halting ATP production, the cell’s energy currency.
Ribosomal damage: impairing protein synthesis.
Nuclear damage: threatening the genetic blueprint itself.
Each form of injury sets the stage for morphological changes that can be seen under the microscope — the “crime scene photos” of pathology.
Adaptive Changes: How Cells Respond
When under stress, cells don’t always surrender. They adapt, reshaping themselves like seasoned survivors:
Atrophy: shrinking in size to conserve energy.
Hypertrophy: bulking up in response to demand, as seen in athlete’s muscles.
Hyperplasia: multiplying in number, often seen in hormonal stimulation.
Metaplasia: switching identity, like respiratory cells changing in smokers.
Dysplasia: disordered growth, often a warning signal for cancer.
Other markers of injury include cell swelling, intracellular accumulation of lipids and proteins, pathological calcification, and enzyme leakage, which often serve as laboratory indicators of disease.
The end of this road is cell death, occurring either by necrosis (accidental, messy death) or apoptosis (a clean, programmed exit).
Acidosis, Alkalosis, and Electrolyte Imbalance
Cells thrive only within a narrow chemical window. Disturbances like acidosis (excess acidity), alkalosis (excess alkalinity), or electrolyte imbalance (sodium, potassium, calcium shifts) can destabilize cellular functions. These imbalances often headline critical care units, signaling severe underlying disorders.
Inflammation: The Body’s Emergency Response
If injury makes the headlines, inflammation is the breaking news team rushing to the scene. Defined as the body’s protective response to injury, it comes with five clinical signs: redness, heat, swelling, pain, and loss of function.
Types of Inflammation
Acute inflammation is short-lived but dramatic — the equivalent of live breaking coverage.
Chronic inflammation is slow, smoldering, and often linked to long-term diseases.
Mechanisms in Action
The inflammatory process unfolds in stages:
Altered vascular permeability lets plasma and immune cells flood the area.
Changes in blood flow direct more defenses to the site.
Migration of white blood cells ensures pathogens or debris are neutralized.
Mediators of inflammation — chemical messengers like histamine and prostaglandins — amplify the response.
Wound Healing and Atherosclerosis
When the dust settles, the body turns to repair and healing. In the skin, wounds heal through a structured process: inflammation, proliferation of new tissue, and remodeling. This ensures damaged tissue regains both strength and function.
But not every repair story ends well. In blood vessels, chronic inflammation can trigger atherosclerosis — the buildup of fatty plaques that narrow arteries. This “long-running investigation” often leads to heart attacks and strokes, making it one of the most serious consequences of unchecked cellular injury and repair.