Unit 1: Cell Injury & Inflammation

February 21, 2026

Semester 2
BP204T

Introduction to Cell Injury & Inflammation

Unit 1 is the foundation of pathophysiology. It explains how cells respond to stress and injury – from reversible adaptation to irreversible death. The second major topic is Inflammation, the body’s defense response. Understanding these processes is essential to understanding every disease state covered in subsequent units.

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Syllabus & Topics

  • 1Basic principles of Cell Injury: Introduction, definitions, and Homeostasis.
  • 2Components and Types of Feedback systems (Negative and Positive feedback).
  • 3Causes of cellular injury (Hypoxia, Physical agents, Chemical agents, Microorganisms, Immunological).
  • 4Pathogenesis: Cell membrane damage, Mitochondrial damage, Ribosome damage, Nuclear damage.
  • 5Morphology of Cell Injury – Adaptive changes: Atrophy, Hypertrophy, Hyperplasia, Metaplasia, Dysplasia.
  • 6Cell Swelling (Reversible), Intracellular Accumulation (Fatty change), Calcification.
  • 7Electrolyte imbalance, Enzyme leakage, and Cell Death (Necrosis vs Apoptosis).
  • 8Acidosis and Alkalosis (Respiratory and Metabolic types).
  • 9Basic mechanism of Inflammation and Repair: Cardinal signs of inflammation (Rubor, Tumor, Calor, Dolor, Functio Laesa).
  • 10Different types of Inflammation: Acute vs Chronic.
  • 11Mechanism of Inflammation: Alteration in vascular permeability and blood flow.
  • 12Migration of WBCs (Chemotaxis, Margination, Pavementing, Emigration).
  • 13Mediators of Inflammation: Histamine, Prostaglandins, Bradykinin, Cytokines (TNF-α, IL-1).
  • 14Basic principles of Wound Healing in the skin: Primary vs Secondary intention.
  • 15Pathophysiology of Atherosclerosis: Step-by-step progression.

Learning Objectives

Classify Adaptations: Differentiate between Hypertrophy and Hyperplasia with examples.
Distinguish Necrosis vs Apoptosis: Compare the two types of cell death.
List Cardinal Signs: Give the 5 cardinal signs of inflammation and their pathological basis.
Know Mediators: Name 3 chemical mediators of inflammation and their source/action.
Explain Wound Healing: Distinguish between Primary and Secondary intention healing.

Frequently Asked Questions (FAQs)

Q1. What is the difference between Necrosis and Apoptosis?

Necrosis is pathological, passive cell death caused by injury. It triggers inflammation. Apoptosis is programmed, physiological cell death (like removing webbing between fingers in a fetus). It does not trigger inflammation.

Q2. What is the difference between Hypertrophy and Hyperplasia?

Hypertrophy is an increase in cell size (e.g., cardiac muscle in hypertension). Hyperplasia is an increase in cell number (e.g., liver cell regeneration).

Q3. What are the key mediators of Acute Inflammation?

Histamine (from mast cells), Prostaglandins (COX pathway, target of NSAIDs/Aspirin), Bradykinin (pain), and Cytokines like TNF-α and IL-1 (systemic effects: fever, acute phase response).

Q4. What is Atherosclerosis?

It is a chronic inflammatory disease of arteries involving accumulation of lipids, macrophages (forming “foam cells”), and fibrous tissue in the arterial wall. Fatty streaks → Plaques → Rupture → Thrombosis → Heart Attack/Stroke.

Q5. What is Acidosis and Alkalosis?

Acidosis is a fall in blood pH (<7.35). Alkalosis is a rise in blood pH (>7.45). Both can be Respiratory (CO₂ change) or Metabolic (HCO₃⁻ change) in origin.