•Fat necrosis referstofocalareasoffatdestruction,typicallyresultingfromthereleaseofactivatedpancreaticlipasesintothesubstanceofthepancreasandtheperitonealcavity.Thisoccursinthecalamitousabdominalemergencyknownasacutepancreatitis(Chapter17).Inthisdisorder,pancreaticenzymesthathaveleakedoutofacinarcellsandductsliquefythemembranesoffatcellsintheperitoneum,andlipasessplitthetriglycerideesterscontainedwithinfatcells.Thereleasedfattyacidscombinewithcalciumtoproducegrosslyvisiblechalkywhiteareas(fatsaponification),whichenablethesurgeonandthepathologisttoidentifythelesions(
Fig.2.9 ).Onhistologicexamination,thefociofnecrosiscontainshadowyoutlinesofnecroticfatcellssurroundedbybasophiliccalciumdepositsandaninflammatoryreaction.
Fig. 2.9 Fatnecrosisinacutepancreatitis.Theareasofwhitechalkydepositsrepresentfocioffatnecrosiswithcalciumsoapformation(saponification)atsitesoflipidbreakdowninthemesentery.
Fig. 2.10 Fibrinoidnecrosisinanarteryinapatientwithpolyarteritisnodosa.Thewallofthearteryshowsacircumferentialbrightpinkareaofnecrosiswithproteindepositionandinflammation.
•Fibrinoid necrosis isaspecialformofnecrosis.Itusuallyoccursinimmunereactionsinwhichcomplexesofantigensandantibodiesaredepositedinthewallsofbloodvessels,butitalsomayoccurinseverehypertension.Depositedimmunecomplexesandplasmaproteinsthatleakintothewallofdamagedvesselsproduceabrightpink,amorphousappearanceonH&Epreparationscalledfibrinoid(fibrinlike)bypathologists(
Fig.2.10 ).Theimmunologicallymediateddiseases(e.g.,polyarteritisnodosa)inwhichthistypeofnecrosisisseenaredescribedinChapter5.
Leakage of intracellular proteins through the damaged cell membrane and ultimately into the circulation provides a means of detecting tissue-specific necrosis using blood or serum samples. Cardiac muscle, for example, contains a unique isoform of the enzyme creatine kinase and of the contractile protein troponin, whereas hepatic bile duct epithelium contains the enzyme alkaline phosphatase, and hepatocytes contain transaminases. Irreversible injury and cell death in these tissues elevate the serum levels of these proteins, which makes them clinically useful markers of tissue damage.
Apoptosis is a pathway of cell death in which cells activate enzymes that degrade the cells’ own nuclear DNA and nuclear and cytoplasmic proteins (
Fig. 2.11 ). Fragments of the apoptotic cells then break off, giving the appearance that is responsible for the name (apoptosis, “falling off”). The plasma membrane of the apoptotic cell remains intact, but the membrane is altered in such a way that the fragments, called apoptotic bodies, become highly “edible,” leading to their rapid consumption by phagocytes. The dead cell and its fragments are cleared with little leakage of cellular contents, so apoptotic cell death does not elicit an inflammatory reaction. Thus, apoptosis differs in many respects from necrosis (
Table 2.1
Causes of Apoptosis
Apoptosis occurs in many normal situations and serves to eliminate potentially harmful cells and cells that have http://ebooksmedicine.net
Fig. 2.11 Apoptosis.Thecellularalterationsinapoptosisareillustrated.Contrastthesewiththechangesthatcharacterizenecroticcelldeath,shownin