Morphologic Manifestations of Toxic Cell Injury

Matthew A. Wallig, Evan B. Janovitz

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Whatever causes injury to a cell—toxicant, toxin, infectious agent, or otherwise—the result is a simple or complex biochemical shift that generally results in a morphologic change which can be observed in some form. The pathologist must be able to recognize that such changes in morphology reflect a significant alteration in the cell's homeostasis, as sometimes altered morphology has no impact on cellular function. The first step is to determine whether the abnormal morphology is harmful to the cell or tissue. By determining whether the primary morphological change is one of degeneration, inflammation, or neoplasia, the next step is to determine whether this finding indicates reversible injury, irreversible injury, or adaptation to the new situation. Visible manifestations of disrupted function, whether ultrastructural, microscopic, or macroscopic, are lesions by definition, and lesions are still the primary means by which a toxicologic pathologist arrives at a diagnosis, hopefully one that includes the etiology as well as a description of the underlying morphologic alterations and a plausible pathogenesis of how the lesions came about. This chapter will serve as an overview of the basic histologic and ultrastructural features that reflect cell injury and death as well as the sequelae to such processes.

Original languageEnglish (US)
Title of host publicationHaschek and Rousseaux's Handbook of Toxicologic Pathology
EditorsWanda M Haschek, Colin G Rousseaux, Matthew A Wallig, Brad Bolon
PublisherAcademic Press
Pages113-148
Number of pages36
Volume1
Edition4
ISBN (Electronic)9780128210444
ISBN (Print)9780128218297
DOIs
StatePublished - Jan 1 2021

Keywords

  • Adaptation
  • Apoptosis
  • Atrophy
  • Autolysis
  • Autophagic cell death
  • Autophagy
  • Caspase(s)
  • Cell injury
  • Cell swelling
  • Cytochrome c
  • Endoplasmic reticulum
  • Ferroptosis
  • Fibrosis
  • Glutathione
  • High amplitude swelling
  • Homeostasis
  • Hyperplasia
  • Hypertrophy
  • Hypoxia
  • Lipidosis
  • Lysosome(s)
  • Macroautophagy
  • Macrophage
  • Metaplasia
  • Microautophagy
  • Mitochondria
  • NETosis
  • Necroptosis
  • Necrosis
  • Necrotic
  • Neutrophil
  • Parthanatos
  • Programmed cell death
  • Pyronecrosis
  • Pyroptosis residual bodies
  • Sequela(e)
  • Single-cell necrosis
  • Vacuolar change

ASJC Scopus subject areas

  • General Medicine

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