Cell Injury 2 - Dental Students GU Part 2 PDF

CELL INJURY 2 By Prof. Dr. Marwa Abd El-Haq Professor of Pathology Department Faculty of Medicine Tanta University Irreversible cell injury Necrosis (cell death) Death of groups of cells within a living body. It occurs either d...

CELL INJURY 2 By Prof. Dr. Marwa Abd El-Haq Professor of Pathology Department Faculty of Medicine Tanta University Irreversible cell injury Necrosis (cell death) Death of groups of cells within a living body. It occurs either directly or following reversible injury. Membrane integrity is lost, and contents leak out causing inflammation. It is caused by the same causes of reversible injury, but the stimulus is severe or prolonged. Morphologic changes Gross features: Ø The necrotic tissue appears opaque whitish or yellowish. Ø The surrounding tissue is red due to inflammation.  Necrosis Microscopic picture: Ø Nuclear changes: due to breakdown of DNA - Pyknosis: shrunken deeply basophilic nucleus. - Karyorrhexis: the pyknotic nucleus breaks up into numerous small fragments. - Karyolysis: dissolved nucleus. 27 CHAPTER 2 Figure 2.20 Nuclear and cytoplasmic changes in necrosis. A, Normal cell. B, Cytoplasm is more pink and nucleus is shrunken (pyknosis). C, Cytoplasm Ø Cytoplasmic changes: is more pink and the nucleus is fragmented (karyorrhexis). D, The cytoplasm is intensely pink and nuclear material has disappeared (karyolysis). - The cytoplasm becomes swollen, deeply eosinophilic due to denaturation of cytoplasmic protein by its own enzymes Grossly, focus of coagulative necrosis in the early stage is pale, firm, and slightly swollen and is called infarct. With material. The cyst wall is formed by proliferating capillaries, inflammatory cells, and gliosis (proliferating glial cells) in Cell I progression, the affected area becomes more yellowish, the case of brain and proliferating fibroblasts in the case of softer, and shrunken. abscess cavity (Fig. 2.22). Necrosis Fate of necrosis: Ø Small necrotic area: undergo lysis by the action of lysosomal enzymes and then complete removal by phagocytosis by macrophages. Ø Large necrotic area: is usually surrounded by fibrous capsule + dystrophic calcification. Ø Putrefaction by certain bacteria leading to gangrene.  Patterns of Tissue Necrosis Coagulative Liquefactive Caseous Fat necrosis Fibrinoid Gangrenous  Coagulative necrosis Incidence Most common form of necrosis Causes Sudden and complete Ischemia Organs involved Solid organs (heart, kidney, spleen, liver) Major event Denaturation and coagulation of proteins (hence called coagulative) Features Grossly: necrotic area is firm, white Microscopically: cellular outlines are preserved but with no details, so the cell type can be recognized.  Coagulative necrosis Exercise (Kidney)16: Degenerations and Necrosis 81 FIGURE 16.4 Coagulative necrosis in infarct kidney. The affected area on right shows cells with intensely eosinophilic cytoplasm of tubular cells The necrotic cells show preserved outlines but the outlines of tubules are still maintained. The nuclei show granular debris. The junction of viable and non-viable area shows non-specific with loss of nuclei, and an inflammatory chronic inflammation and proliferating vessels. infiltrate is present M/E LIQUEFACTIVE NECROSIS (INFARCT) BRAIN i. The hallmark of coagulative necrosis kidney is that  Liquefactive necrosis Causes Ischemia (brain), bacterial infections (abscess) Organs involved Brain (Infarct brain), abscess Major event Enzymatic digestion of necrotic area Features The necrotic area is converted into a liquid mass which undergoes cystic change later. ii. The margin of infarct shows inflammatory reaction, example is infarct of the brain. initially by polymorphonuclear cells but later macro- (Fig. 16.4). Liquefactive G/A The necrosis phages, lymphocytes and fibrous tissue predominate affected area of the brain is soft with liquefied centre containing necrotic debris. Later, a cyst wall is formed.  Caseous necrosis Causes Mycobacterium tuberculosis Organs Lung, lymph node, skin and other tissues involed Major event A combination of denaturation of proteins and liquefaction necrosis. This is due to an immune mediated delayed hypersensitivity reaction to mycobacterium Features The necrotic area appears firm, dry and cheesy amorphous granular debris. The structure of the necrotic tissue is completely lost. Caseous necrosis  hypertension, peptic ulcer etc. Grossly, fat necrosis appears as yellowish-white and firm Microscopically, fibrinoid necrosis is identified by deposits. Formation of calcium soaps imparts the necrosed brightly eosinophilic, hyaline-like deposition in the vessel foci firmer and chalky white appearance. Caseous necrosis Microscopically, the necrosed fat cells have cloudy wall. Necrotic focus is surrounded by nuclear debris of neutrophils (leucocytoclasis) (Fig. 2.25). Local haemor- appearance and are surrounded by an inflammatory rhage may occur due to rupture of the blood vessel. Figure 2.23 Caseous necrosis lymph node. There is eosinophilic, amorphous, granular material, while the periphery shows granulomatous  Fat necrosis Causes Acute pancreatitis, trauma (breast) Organs Pancreas, breast, subcutaneous tissue Major event 1. Enzymatic digestion of peritoneal fat by the released lipase (in acute pancreatitis). 2. Non-enzymatic: rupture of fat cells (in trauma). The fatty acids combine with Ca+2 à Ca salt precipitates Features Grossly: necrotic area is firm, white (calcification) Microscopically: cellular outlines are preserved but with no details, so the cell type can be recognized. Necrosis Ø Grossly: necrotic fat appears as chalky white opaque deposits in the adipose tissue surrounding pancreas and in omentum  Fibrinoid necrosis Causes Immune mediated (Antigen-antibody reaction) Organs Blood vessels Major event The collagen fibers and media of BV are affected by fibrinoid deposition Features Deposition of pinkish substance in the blood vessels. Fibrinoid Necrosis  Gangrenous Necrosis Ø Gangrene is tissue necrosis followed by putrefaction Ø It is caused by certain bacterial infection (saprophytic) Ø Three types: 1. Dry: occur in limbs (e.g. senile) 2. Moist: occur mostly in internal organs as intestine and lung. 3. Gas gangrene  Dry gangrene Moist gangrene Usually occurs in the distal Occurs in moist organs like part of extremity due to small bowel, lung due to ischemia (arterial occlusion). obstruction to the venous Gradual in onset. outflow in addition to arterial supply. The affected part appears dry, shrunken and dark Rapid in onset. brown to black in color. The affected part appears The line of demarcation swollen and dark. present (between The line of demarcation is ill gangrenous and non- defined. gangrenous parts) Dry Gangrene  Dry Gangrene  Moist gangrene  Gas gangrene Special type of moist gangrene due to infection with anaerobic bacteria (Clostridia). The most common predisposing factor is lacerated wounds as in road traffic accidents contaminated with spores of the bacteria in the soil. The bacteria secretes powerful exotoxins causes muscle necrosis. The muscle carbohydrate is fermented into lactic acid, hydrogen and Co2 which accumulates in the affected tissue. The affected organ appears swollen, tense, greenish black, crepitant (due to gas accumulation) and foul smelling (due to formation of H2S). Gas gangrene THANK YOU