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  • It was a amazing lecture, sir, took me 40minutes to study 7 types of Necrosis!
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  1. 1. Group Members
  2. 2. “Necrosis is the morphological changes that follow cell death in a living tissue or organ,Resulting from the progressive degenerative action of enzymes on the lethally injured cell.”So, Necrosis begins with an impairment of the cell’s ability to maintain homeostasis, leading to an influx of water and extracellular ions
  3. 3. Apoptosis vs NecrosisThe word apoptosis mean falling off.“Apoptosis is a process of programmed and targetedcause of cellular death”Necrosis is differ from apoptosis:
  4. 4. Apoptosis Necrosis Physiological or Always pathological pathological Cell shrinkage Cell swellingApoptotic bodies form Do not form Dna cleavage No DNA cleavage Beneficial DetrimentalCharacteristic nuclear Nuclei lost changesNo leak of lysosomal Leak of lysosomal enzymes enzymes
  5. 5.  Anoxia Ischemia Physical agents Chemical agents Biological agents Hypersenstivity
  6. 6. Necrotic changes in tissues are caused By Digestion of cell by enzymes Denaturation of proteinsDigestion of cell by enzymesThis digestion is of two types Autolysis: Digestion of cell by enzymes derived from their own lyosomes Heterolysis: Digestion of cell by enzymes derived from lysosmes of leukocytes.
  7. 7. Denaturation of proteins caused by intracellular acidosisand due to this result is that:Injury to the cell membraneSevere impairment of phosphorylation of cellIncrease permeability of the cellInflux of Na+ and Ca+ in the cellDecreased intracellular activity of the cell
  8. 8.  Changes inside the cell Changes in mitochondria Changes in Nucleus Changes in cytoplasm
  9. 9.  Endoplasmic reticulum is disorganized There is rupture of membrane Ribosomes are shed off Disorganization of polysomes & their structures Mitochondria become swallon Loss of interamitochondrial granules Loss of cristae & change their shape Rupture of outer membrane of Mitochondria
  10. 10.  Nucleus becomes smaller Chromatin loses & become clumpedNucleus shows following changes Pyknosis Karyorrhexis Karyolysis
  11. 11. PYKNOSIS“When the dna is broken down by endonucleasesfragments are formed & the nucleus becomes acidand stains basophillic”KARYORRHEXIS“The pyknotic nucleus may break up into fragmentsand disappear. This process is called karyorrhexis”KARYOLYSIS“The pyknotic nucleus may undergo lysis by theenzyme DNAse”
  12. 12.  Cytoplasm becomes more eosinophilic:Due to loss of Rna & denaturation of cytoplasmic proteins Cytoplasm becomes opaque.
  13. 13. Basic types Coagulative necrosis Liquefactive necrosis Caseous necrosisIn special sites Fat necrosis Fibrinoid necrosis Gangrenous necrosis
  14. 14. “In this type of necrosis, the necrotic cell retains its cellular outline for several days” Coagulative necrosis typically occurs in solid organs such as kidney, heart and adrenal gland usually as a result of deficient blood supply and anoxia.Examples Myocardial infarction
  15. 15.  Denaturation of protein is the basic mechanism of coagulative necrosis The injury and the subsequent increasing acidosis denatures not only the structural proteins but also the enzymic proteins, thus blocking the cellular proteolysis.Morphology Preservation of basic structural outline of the coagulated cells Appears as a mass of coagulated, pink staining homogenous cytoplasm
  16. 16. It is the type of necrosis that occurs due to autolytic andheterolytic actions of enzymes that convert the proteinsof cells into liquid. It is characterized by softening and liquifaction of tissue.Examples Ischemic necrosis of brain Suppurative inflammation.
  17. 17.  Enzymatic degradation of proteins is the basic mechanism of liquefactive necrosisMorphologyo Complete loss of cellular detailo Cellular outline is also destroyed
  18. 18.  Combination of coagulative and liquefactive necrosis Characterized by the presence of soft, dry, cheesy homogenous necrotic material. It is not liquifiedExamples Principaly in the center of tuberculous granulomaMorphology Microscopically the necrotic focus is composed of structureless amorphous granular debris enclosed within a ring of granulomatous inflammation.
  19. 19. Necrosis in special sitesIt occurs in two forms: Enzymatic fat necrosis Traumatic fat necrosis
  20. 20.  Most commenly seen in acute pancreatitis.“Refers to the necrosis in adipose tissue, induced by theaction of pancreatic enzymes which are lead due totrauma to the pancreas”Morphology Chalky white opaque spots surrounded by inflammatory margins are seen Necrotic area shows acute inflammatory changes with dissolved fat cells
  21. 21. It occur following severe injury to the tissues with highfat content such as the breast, subcutaneous tissue andabdomen.Morphology Foam cells and gaint cells are seen. necrotic foci contain a lot of phagocytes containing fat known as foam cells
  22. 22.  Type of connective tissue necrosis especially affecting arterial walls. Mostly seen in two conditions Auto immune diseases e.g Rheumaic fever SLE Malignant hypertension
  23. 23.  Gangrene is the necrosis of tissue with superadded putrefaction (enzymatic decomposition). It is the clinical condition in which extensive tissue necrosis is complicated to a variable degree by secondary bacterial infection. Gangree= Necrosis + infection + putrefaction
  24. 24.  Arterial obstructon due to: Thrombosis of atherosclerotic artery Embolus Diabetes:- atherosclerotic artery , loss of sensation results reapeted trauma & increase chances of infection Infection Gas gangrene Gangrene of scrotum Trauma Crush injuries Physical agents Burns Chemicals
  25. 25.  Dry gangrene Wet gangrene Gas gangrene
  26. 26. It is usually secondary to slow occlusive vascular diseaseEtiologyGradual loss of arterial supply to an organ or tissue ashappens inArteriosclerosisAtherosclerosisTraumaErgot poisoningCommon sites limbs; especially foot
  27. 27. Pathogenesis It is a traditional term used to describe the infarction of the limbs. It is not true gangrene because the infection in necrotic tissue is insignificant and putrefaction is absent or minimal. The necrotic area becomes black due to breakdown of hemoglobin and formation of iron sulfide
  28. 28.  It is a type of gangrene in which tissue appears moist. It results from severe bacterial infection superimposed on necrosisPathogenesis It is a true gangrene because it shows the severe infection and putrefaction of tissue with edema and foul smell. Arterial obstruction present. blackening of the tissue is due to formation of iron sulphide It is not clearly demarcated from adjacent healthy tissues.Common sites Intestine Appendix Limbs
  29. 29. Wet gangrene of intestineWet gangrene of appendix
  30. 30. “In this type of gangrene bacterial infection causes necrosisand then gangrene with abundant gas formation in the tissue” Gas gangrene=wet gangrene + gas formationPredisposing factors Foreign bodies in wound cause tissue ischemia Foreign bodies favour infection Contamination of wound by soil is dangerous bqz its ionisable calcium salts and silicic acid may lead to tissue necrosis. Infection by aerobic organisms at the same time serve to produce anaerobic environment that is favourable for anaerobic clostridia.
  31. 31. Two groups of clostridia cause gas gangrene Saccharolytic: Clostridia profringes Proteolytic: Clostridia isolyticumPathogenesis Deep wound----anerobic condition---caused by spores of clostridia Necrosis of muscle fiber occur Fermentation of muscle carbohydrate occur with formation of lactic acid and gas. Arterial supply of the area is cut down Muscles become greenish- black due to iron sulphide & foul smell
  32. 32.  Muscles LiverComplicatons Rapidly spreading gangrene Shock and hemolytic anemiaTreatment of gangrene Treatment of predisposing factor: Amputation:Surgical removal of gangrene tissue to prevent spreading ofthe infection to the healthy tissue.
  33. 33. Gas gangrene of muscles Gas gangrene of Liver
  34. 34. “It is wet type of gangrene in which necrosis is superadded by infection and putrefaction”Predisposing factors: Sensory neuropathy Ischemia Lower resistance to infectionManagement: Control diabetes Keep the tissue dry and clean Antibiotics Surgical drainage of necrotic tissue
  35. 35. Referances: http://www.diffen.com/difference/Apoptosis_vs_Necr osis http://www.qub.ac.uk/cm/pat/undergraduate/Basicca ncer/necrosis_v_apoptosis.htm www.roche-applied-science.com http://en.wikipedia.org/wiki/Necrosis Gross pathology By Dr. jawad ahmed. Text book of pathology by inam danish Text book illustrated pathology by peter s.macfarlane/robin reid/robin callander.
  36. 36. Hope you allget it…