Chapter 1: Cell Injury, Cellular Adaptation, and Cell Death · 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.

0 of 8 topics studied0 of 53 questions correct

1.116 minUp nextHow cells respond to stressA cell under stress either adapts, is injured and recovers, or dies. This section sets out that spectrum, the causes that push cells along it, and the organelles that decide which way they go.Four lenses on one diseaseFrom normal to deathCauses of cell injuryOrganelles in the story+1
1.224 minCellular adaptations and related changesCells adapt to sustained demand or stress by growing, multiplying, shrinking or changing type. Each response depends on what the cell can do, and each has limits that lead back to injury.HypertrophyHyperplasiaRegenerative capacityAtrophy+4
1.328 minHypoxia, ischemia and oxygen deliveryOxygen travels from inspired air to the alveolus, into arterial blood, onto hemoglobin, through tissue blood flow and into the mitochondrion. Each disorder in this section breaks the chain at a different link.Hypoxia, anoxia, hypoxemia, ischemiaFind where oxygen failsFive causes of hypoxemiaWho responds to supplemental oxygen+4
1.422 minReversible and irreversible cell injuryFollow the energy: falling ATP explains the early, reversible changes; sustained loss brings calcium overload and the membrane and mitochondrial damage that cannot be undone.ATP depletion: the first casualtyReversible injury: why the cell swellsCell on a ClockInjury simulator: set the dose, then restore oxygen+4
1.520 minFree radicals and reperfusion injuryReactive oxygen species come from normal metabolism, inflammation, radiation, metals and drug metabolism. They attack lipids, proteins and DNA unless the cell's defenses keep up, and they are why restoring flow can harm already injured tissue.Radicals and reactive speciesWhere they come fromWhat they damageDefenses+2
1.626 minNecrosis and infarctionNecrosis is the death of groups of cells with membrane rupture and inflammation. Its pattern depends on whether proteins denature or enzymes digest, and an infarct is necrosis caused by loss of blood supply.Patterns at a glanceCoagulative necrosisLiquefactive necrosisCaseous necrosis+5
1.720 minApoptosisApoptosis is programmed, energy-dependent, caspase-driven cell death. Single cells shrink and are quietly eaten, without inflammation. Three routes lead to the same executioner caspases.When cells are meant to dieIntrinsic (mitochondrial) pathwayExtrinsic (death receptor) pathwayCytotoxic T cells+2
1.820 minCalcification, accumulations and amyloidInjured and stressed tissues collect abnormal material. Ask three questions of any deposit: what accumulates, where does it go, and why.What, where and whyIntracellular accumulationsDystrophic and metastatic calcificationAmyloid+2

Practice

Interactive labThe injury simulator, Cell on a Clock, 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 stroke, from minutes to weeks, then 15 mixed case-based questions with explanations.Case and source mapWhat each supplied case and lecture question tests (20 items), linked to where it is practised, with the source page map.

How the ideas connect

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