Chapter 2: Inflammation and Tissue Repair · Pathology

Study path

Follow the order or jump to the concept you need. Every topic has a Deep Learning and a High-Yield view of the same facts, and ends with a short knowledge check.

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2.124 minUp nextFrom injury to acute inflammationSomething harmful is recognized, and within minutes the local vessels change: arterioles dilate, venules leak, flow slows. Those vascular changes explain four of the five cardinal signs and set the stage for neutrophils.What sets inflammation offFive cardinal signs, five mechanismsThe vascular sequenceExudate versus transudate+1
2.226 minLeukocyte recruitmentA neutrophil leaves the blood in four steps: it rolls on selectins, stops on integrins, squeezes between endothelial cells, and follows a chemical gradient to the target. Break any step and the cells pile up in the blood instead of the tissue.Margination: two pools of neutrophilsRolling and tight adhesionTransmigration (diapedesis)Chemotaxis: following the gradient+2
2.328 minPhagocytosis and killingOnce in the tissue, the neutrophil recognizes a coated microbe, swallows it into a phagosome, fuses that with its granules, and kills inside the sealed compartment with an oxygen-driven chain that ends in hypochlorous acid. Each link has an inherited disease that shows what it does.Recognition and opsoninsThe oxidative burstLysosomal enzymes, collateral injury and abscessesChédiak–Higashi syndrome: granules that cannot move+3
2.432 minMediators and the systemic responseEvery step so far was ordered by a chemical: amines and kinins open vessels in minutes, arachidonic acid products shape pain, leak and chemotaxis, complement tags and attracts, and cytokines carry the alarm to the brain, liver and marrow.Fast mediators: histamine, bradykinin and nitric oxideArachidonic acid: two enzymes, many mediators, four drug targetsComplement: split products with three jobsCytokines: the long-range signals+2
2.524 minPatterns and outcomes of acute inflammationWhat the exudate looks like depends on how much leaks, whether fibrinogen gets out, whether neutrophils pile up and whether a surface is lost. How the episode ends depends on how much tissue was destroyed and whether the cause is gone.Morphologic patterns: what the exudate looks likeAbscess versus cellulitisFour ways acute inflammation can endHow the response switches off
2.630 minChronic and granulomatous inflammationWhen the cause will not go away, the response changes character: macrophages and lymphocytes replace neutrophils, and injury and repair run side by side. When the cause is hard to digest, activated macrophages wall it off as a granuloma.What makes inflammation chronicAnatomy of a granulomaCaseating, non-caseating and foreign-body granulomasThe granuloma loop: IL-12, IFN-γ and TNF+1
2.732 minRegeneration and repairDamaged tissue is restored in one of two ways: surviving cells divide and rebuild the original (regeneration), or new vessels and fibroblasts fill the gap with collagen (repair by scar). Which one happens depends on whether the cells can divide and whether the framework survived.Regeneration or scar: cells and scaffoldThe wound-healing sequenceGranulation tissue and angiogenesisGrowth factors that drive repair+4

Practice

Interactive labThe recruitment and killing lab, The Missing Arrow, Almost Twins and One Fact Changes. Each also appears inside the topic where it helps most.High-yield cards40 cards on clues, comparisons and mechanisms worth recalling.Chapter reviewBringing it together: one thorn, from minutes to weeks, then 16 mixed case-based questions with explanations.Case and source mapWhat each supplied case and lecture question tests (62 items), linked to where it is practised, with the source page map.

How the ideas connect

18 bridges carry one concept into the next, within this chapter and across chapters. Each is taught where you first need it.