Human Pathology Inflammation and Repair

Acute Inflammation: Vascular and Cellular Responses​

Topic overview

Start with the big picture

The lesson follows acute inflammation from arteriolar vasodilation and increased vascular permeability to fluid loss, stasis, and leukocyte margination. It explains how endothelial gaps and other permeability mechanisms produce protein-rich exudate and edema, and how these changes contribute to redness, heat, swelling, pain, and impaired function. The cellular response is organized as leukocyte rolling, firm adhesion, transmigration, and chemotaxis, with selectins, integrins, and other signals guiding each stage. The topic then introduces phagocytosis: recognition through opsonins, engulfment, and intracellular killing using reactive oxygen species and other mechanisms. It also identifies key inflammatory mediators and connects these vascular and cellular events into a coordinated response.

Learning objectives

What you'll learn

  • Relate vascular and cellular changes to the cardinal signs of acute inflammation.
  • Describe how vasodilation and increased permeability produce exudate, edema, stasis, and margination.
  • Outline leukocyte recruitment from rolling through chemotaxis.
  • Summarize phagocytosis, opsonins, and intracellular killing mechanisms.
  • Identify major mediators involved in acute inflammation.
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