Prof Dr Sergülen...
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Prof Dr Sergülen Dervişoğlu
Tissue changes in revesible andirreversible injury
Necrosis and apoptosisPostmortem changes
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Cellular swelling
• Cells are incapable of maintaining ionicand fluid balance
• Acute infections• Toxic conditions• Physical injury• Anoxia• Malnutrition• Circulatory disturbances
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Hydropic/Vacuolardegeneration
• More severe than cellular swelling• Causes and gross pathology similar• Swollen, opaque organs ( cloudy )• Capsule is tense• Cut surface bulges
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Hydropic/Vaculardegeneration
• Clear vacules in the cytoplasm• Reversible• Water accumulation within cells• Cells are swollen, cytoplasm pale,
reticulated• Nuclei are unaffected• Increased water content of the
cytoplasm• Distertion of the endoplasmic reticulum
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Irreversible cell injury
• Cell membrane damage--- centralfactor
• Severe vacuolization of mitochondria• Swelling of lysosomes• Massive influx of calcium in cells• Loss of proteins, enzymes, RNAs• Injury to lysosomal membranes—enzyme
leakage—digestion of cell
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Necrosis• Sequence of changes• In a living tissue or organism• Most serious result of injury• Cell death• As a whole body---somatic death• Irreversible cell injury• Earliest change in nucleus• Progressive degradative activity of
enzymes
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• Autolysis---Catalytic enzymes arederived from the lysosomes of dead cells
• Heterolysis---Catalytic enzymesare derived from the lysosomes of immigrant leukocytes
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Macroscopy of dead tissue
• Opaque• The normal translucency is lost• Whitish or yellowish color
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Microscopy of dead tissue
• The dead cells shows increasedeosinophilia
• Glossy, homogenous appearance• Cytoplasm becomes vacuolated• Calcification of dead cells
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Nuclear changes
• Pyknosis---Nucleus shrinks, stainsmore intensely basophilic
• Karyorrhexis---Fragmentation of nucleus
• Karyolysis---Nucleus looses itsability to stain differentially withbasic dyes ( Hematoxylen)
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Types of necrosis
• Coagulation necrosis• Liquefactive necrosis• Fat necrosis• Caseous necrosis• Gangrenous necrosis
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Coagulation necrosis
• Cutting of blood supply ( INFARCTION)• Certain poisons ( Phenol, formaldehyde)• Most common form of necrosis• Loss of nuclei ( tombstone )• Preservation of basic outlines of cells• Recognition of tissue architecture• Sudden severe ischemia
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Myocardial infarct due to coronary occlusion
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Coagulation necrosis
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Demarcation line
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Fresh infarct in kidney
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Acute tubuler necrosis
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Splenic infarct
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Liquefaction necrosis
• Ischemic destruction of brain tissue• The dead area softens, liquefies• Bacterial lesions ( enzymes of bacteria
and leucocytes)• Action of powerfull hydrolytic enzymes• Cystic structure filled with debris and
fluid
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Liquefaction necrosis
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Fat necrosis• Acute pancreatic necrosis• Pancreatic enzymes ( Lipases)• Abdomen• Hydrolysis of the neutral fat• Shadowy outlines of necrotic fat cells• Inflammatory reaction• Released free fatty acids and calcium—
SOAPS—CHULKY/WHITE OPAQUE AREAS
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Fat necrosis 2
• Breast, subcutaneous tissue• Trauma• Traumatic fat necrosis• Inflammatory reaction• FOREIGN BODY TYPE• Resembling TUMOR
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Caseous necrosis• Soft, friable, whitish/gray debris• Clumped cheesy material• The cells are not totally liquefied nor
are their outlines preserved ( Coagulation and liquefaction )
• Amorphous, granular debris• Granuloma ( central necrosis, epithelioid
histiocytes,Langhans giantcells,fibroblasts,lymphocytes
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Caseous necrosis
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Gangrenous necrosis• Not a distinctive patern of necrosis• Surgical clinical term• Limb ( lower leg)• Lost its blood supply--ischemic cell
death,• Bacterial agents---modifies by
liquefaction• Coagulative patern—dry gangrene• Liquefactive patern—wet gangrene• Atherosclerosis / Diabetes mellitus
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Postmortem changes
• Rigor mortis• Livor mortis• Algor mortis• Postmortem clots• Autolysis• Putrification
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Rigor mortis
• Stiffening of the muscles• Precipitation of proteins• Chemical change• Involuntary muscle• 2-4 hours after death voluntary
muscles,• Completes in 12 hours• Gradually disappears in 24-48 hours
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Livor mortis
• Reddish discoloration• Resulting from the gravitationalsinking of blood
• Lungs, skin• Hemolysis of red cells• Hemolytic organisms• Hb stains the intimal lining andserous surfaces
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Algor mortis
• Cooling of the body• Until the temperature of theenvironment
• Environmental temperature affects• Clothing• State of nutrition
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Postmortem clots
• Moist• Elastic, homogenous• Not adherent to the liningendothelium
• Forms a cast of the vessel and itsbranches
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Autolysis• Self-digestion/breakdown of tissues• Caused by ferments released after
death• Stomach, gall bladder rapidly• Highly differentiated tissues(ganglion
cells, glandular epithelium more rapidthan connective tissue)
• NO INFLAMMATORY REACTION• NECROSIS WITH INFLAMMATORY
RX
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autolysis
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Putrification
• Entrance of saprophytes fromintestinal tract
• Production of gases• Greenish discoloration of tissues• Gas producing bacteria• Foamy or spongy appearance of tissues (LIVER)
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APOPTOSİS
• Genetically determined• Internal• Self destruct mechanism of celldeath
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Apoptosis
• Physiologic/pathologic events• Programmed destruction of cells• During embryogenesis• Hormone dependent involution in the
adults• Cell deletion in proliferating cell
population intestinal epithelium)• Cell death in tumors ( during regression)
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Apotosis 2• Death of immune cells• Pathologic atrophy in parenchymal
organs after duct obstruction ( pancreas, parotis)
• Atrophy of hormone dependent tissues• Cell death induced by cytotoxic T cells• Cell injury in certain viral disease• Mild thermal injury, radiation, cytotoxic
cancer drugs
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Apoptosis viral hepatitis
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Apoptosis/ morphology• Cell shrinkage ( small size, dense
cytoplasm)• Chromatin condensation ( most
characteristic)• Formation of cytoplasmic blebs—
apoptotic bodies------ fragmantation• Phagocytosis of apoptotic cells or bodies• Single cell or cluster of cells• Does not elicit inflammation• DISTINCT FORM OF CELL DEATH
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Mechanism of apoptosis
• Cell death by stimuli---necrosis• Low doses---apoptosis• Apotosis may occure beforeapparent
• Plasma membranes intact until laststage
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Biochemical features• Protein cleavage ( activation of cysteine
protease) Caspase—triggersendonuclease activitiy
• Protein-cross linking ( transglutaminaseactivation)---covalently linked shrunkenshells
• DNA breakdown-( not specific , endonuclease activity-late autolyticphenomenon
• Phagocytic recognition—early reco. of dead cell
• Macrophage/adjacent cells
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Mechanisms
• Signaling pathways--- Initiateapoptosis—transmembrane signals---negatif/positive determinants ( certain hormones, growthfactors,cytokins )
• Intracellular signaling ( glukocorticoids, physicochemicalagents,hypoxia,viral enfections)
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Control and integratingstage
• Specific proteins• Connect death signals to executionprogram
• Commitment or abortion of potentially lethal signals
• Bcl-2 family of proteins—apoptoticregulations ANTIAPOPTOTIC—regulating mitochondrial function
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Apoptotic signals
• Mitochondrial permeabilty formation of pores mitochondrial swelling
• Increased permeability of outermembrane
• Releasing cytochrome C (apoptotictrigger)
• Cytochrome C release– preceeds themorphologic changes of apoptosis
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Execution Phase
• Final pathways of apoptosis• Proteolytic cascade• Caspase– disrupts cytoskeleton, nuclear matrix proteins
• Proteins involved in transcription, DNA replication, DNA repair
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Removal of dead cell
• Apoptotic cells– marker moleculeson their surfaces
• Early recognition by adjacent cellsand phagocytes
• Phagocytic uptake• Dead cells disappear withoutleaving a trace
• NO INFLAMMATION
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Features of necrosis vs apoptosis
• Hypoxia,toxins• Cellular
swelling,coagulationnecrosis, disruptionof organalles
• Random, diffuseDNA damage,ATP depletion,membraneinjury,free radicaldamage
• Inflammation
• Physiologic/pathologic• Single cell, chromatin
condensation, apoptotic bodies
• Internucleosomal, gene activation, endonuclease
• No inflammation, phagocytosis of apoptotic bodies
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References and furtherreading
• Robbins Pathologic Basis of Disease, Cotran, Kumar 2004
• Pathology Illustrated, Macfarlane, Reid,Callande2000
• Sandritters Color Atlas and Textbook of Macropathology, Thomas, Kirstn, 1984
• Basic Pathology, 6th ed, Kumar, Kotran, Robbins• Pathology Rubin, Farber, 1999• Mohan Harsh Textbook of Pathology, 2005• Cerrahpaşa Pathology archieves• Internet (various medical web sites)