I. INTRODUCTION. NECROSIS, GANGRENE. ATROPHY.
Coagulativenecrosis
1. Recentmyocardialinfarction: Anexampleofcoagulativenecrosis. Actually, thisis not the most recentinfarction. Judgingfromthelackofstainingofthenucleiofcardiacmusclecells (withincreasedeosinophiliaofthecytoplasm) and thediffuseneurotrophilicinfiltrate in theinterstitium, ithas to bemorethan 24 hoursold. Subendocardiallayerssurvive (suppliedthroughdiffusionthroughtheendocardium). Notethecomcommitantendocarditis and pericarditis (leukocytes on theendocardialsurface and in thesubepicardial fat tissue) and thrombi in thearterialbranches.
Splenicinfarction:Triangularshapewiththe base underthecapsule, sometimesmultiple. Result – retrctedfibrousscar, haemosiderinpigmentation. Ischaemiccoagulationnecrosis, most oftencaused by arterialembolism.Possibilityofsecondaryifectionofthenecrotictissue.
2. Renalinfarct: Coagulativenecrosisofthekidneyusuallysecondary to arterialocclusion, caused by a thrombotic embolus. Notepreservationofthe basic architerctureofthenecroticrenalparenchyma. Necrotic area isusuallysurrounded by a zoneofleukocyticinfiltration, haemorrhage and a zoneofselectivenecrosiofepitheliumofproximaltubules, whichis most sensitive to hypoxia. In anolderinfarct, centralnecrosisissurrounded by a layeroffibrosingnonspecificgranulationtissue.
Liquefactivenecrosis
3. Cerebralinfarct (encephalomalacia):Ischamiccolliquativenecrosis, healing by formationof a pseudocyst. Cases: thrombosis, embolism. Haemorrhagicinfarct (ussuallycaused by embolism, small, cortical) through reflux ofbloodintothenecroticfocus. In ourslides, wehaveanolderinfarctionwithdisintegrationofthenecrotic center which has beenmostlyresorbed by activatedmicroglia (enlargedcellswithvacuolatedcytoplasm) and a markedcollateraloedema.
Caseousnecrosis
4. Caseous tbc lymphadenitis:Centralnecrosis in thelymph node issurrounded by a rimofthe so-calledepithelioidcells and largemultinucleatedgiantcellsoftheLanghans type. Notethecheomatindustfromthedestroyednuclei in someareasofnecrosis.
Specialformsofnecrosis
5. Zenker'snecrosis: in viraldiseases (severe courseofinfluenza), sepsis, typhoidfeveretc. Segmentalruptureofmyofibrils in musclefibers, hypercontractionofrupturedfibrils.
6. Lungtromboembolism and haemorrhagicinfarct:Pyramidalshape, note a branchofpulmonaryarteryoccluded by trombembolus. Developsonly in congestedlung.
7. Steaticytonecrosis (Balser'snecrosis):Yellow-whitefociundertheperitonealsurface, remnantsofmostlydissolvedfatty (acid crystals).
8. Chronicpepticofstomach:Tissuedefectwithraisedmargins. Notethreelayersatthe base oftheulcer – necroticdebriswithleukocytes, fibrinoidnecrosis, nonspecificgranulationtissuewithtransitionimtoperipheralfibrosis.
Modifiedformsofnecrosis
Atrophy
9. Atrophyoftheheartmuscle:Simpleatrophy – cardiacmusclecellsbecomesmaller but theirnumberdoes not decrease. Sudan B Black stainshowsaccumulationofthe lipid pigment lipofuscin in theperinuclearlysosomes (“wear and tear pigment”), PAS-positive, insoluble pigment resultingfrombreakdownofcellularmembranes. Elderlypatients, chronicwastingdiseases.
10. Fattyinfiltrationoftheheartmuscle: Fat cellsdispersed in themyocardialinterstitium. In obesepatients, physiologically in theanteriorwalloftherightventricle. No clinicalsignificance. Do not confusewithfattydegeneration (seebelow).
11. Hydronefrosis: Severe pressureatrophyoftherenalparanchymacaused by obstructionoftheourflowofurine (renalstones, uroteralobstruction by stones, tumourscompressingtheuritnaryoutflowtract, diseasesoftheurinarybladder, in malesoftenhypertrophyofprostate). May becomplicated by (usuallyascending) infection – hydropyelonephritis. Numeroushyalinecasts in theatrophictubules, glomerularfibrosis, thickeningofarterialwalls.
12. Pancreaticatrophy and sclerosis:Oftenresultsfromlithiasis (obstructionof a major pancreaticduct by stones).Frequentlycomplicated by diabetes. Disappearingexocrineparenchmereplaced by thenewlyformedconnectivetissue. Sometimesincreased fat tissue – lipomatousatrophy. IsletsofLangerhansoftenwellpreserved.
II. CELLULAR AND TISSUE DYSTROPHIES
A/ Protein dystrophy
1. Cytomegaloviralsialoadenitis:Anexampleofpredominantlyalterativeinfiltration, mostly in smallinfants (cytomegaloviralinfection in HIV patientsusuallyinvolvesotherorgansthanthesalivaryglands). Typicalbasophilicintranuclearinclusions in themarkedlyenlargedductalliningcells.
2. Follicularamyloidosisof spleen: AA amyloid, Congo-positive, apple green fluorescence in polarizedlight. Depositionmostly in thewhite pulp (in follicles).
3. Diffuseamyloidosisof spleen:Diffuseinvolvementofbothred and white pulp.
4. Amyloid nephropathy:Depositionof amyloid in thewallsofarteries and arterioles, less in theglomeruli and underthetubularepithelium. Both in the AA and AL amyloidosis, morphologicallyindistinguishable.
5. Erdheim'scysticmedionecrosis:Multifocalnecrosisofmusclecellswithdisappearanceofelasticfibers (pale areas) and accumulationof acid mucopolysaccharides (smallbasophilicareas) (chondroitin-6-supl- hate) in theaortic media. Notemultifocallaminarsplittingofaortic media, theoriginofaorticdissection.
6. Rheumatismusnodosum:Centraleosinophilic (fibrinoid) necrosiswith a rimofpalisadinghistiocytes. Disperse lymphocyticinfiltratecanalsobeseen.
7. Fibrocartilaginousperisplenitis:Thespleniccapsuleisthickened by thenewlyformed, relativelyacellularhyalineeosinophilicmass, grosslyresemblingcartilage.
B/ Fattydystrophy, steatosis
Myocardialsteatosis
8. Fattychangeofthe liver:Intracellularaccumulationofneutraltriglycerides in largevacuoles in the liver cells. Variouscauses: hypoxia, toxiceffects (mushroompoisoning, carbon tetrachloride), starvationetc.
9. Atherosclerosis:Principalmorphologicalenvents: fattystreaks, fibrousplaques, atheromas, ulceration, dystrophiccalcification. Mostlyintimalinvolvement. Thesectionshowspoplitealarterywith a largeatheromatousplaque. The lumen ispartlyfilledwithredthrombus (amputationspcimen, gangreneofthe leg caused by arterialobstuction).
Fattyinfiltrationoftheheartmuscle: Fat cellsdispersed in themyocardialinterstitium. In obesepatients, physiologically in theanteriorwalloftherightventricle. No clinicalsignificance. Do not confusewithfattydegeneration (seebelow).
C/ Glycogendystrophy
10. Armani'scells: In parsrectaofproximaltubules, depositionofglycogen in thewater-clearcytoplasm, Glycogenis PAS-positive, amylase-digestible.
11. Renal cell carcinoma (tumor ofGrawitz):Assesmentofmalignancyisunreliable on morphologicalgrounds, sincemalignanttumoursmayappeardifferentiated and encepsulated. Smalltumours (under 2cm in diameter) consideredbenign (clear cell adenoma). Vascular, sometimescystic, consistingmostlyofcelarcellscontainingglycogen. Sometimeswithoxyphiliccells, sarcomatoid variant.