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4.Necrosis and gangrene
Terms in this set (34)
Death of cells and tissues in living organism, failure of membrane integrity. Pathological process following cell injury. Inflammatory reaction evoked by the dead tissue - vital rection (hyperemia, inflammatory cells). Cell swells and nucleus undergo pyknosis, karohexis or karyolysis. Surrounding tissue are still living.
Apoptosis is programmed, controlled cell death, without inflammatory reaction. Membrane is kept intact, and energy is used. Later divided into apoptotic bodies. Physiological process.
Dystrophy, atrophy, necrosis - irreversible.
Causes of necrosis
Hypoxia, ischemia (vascular changes, atherosclerosis), trauma, allergies, viruses, microbes, burns, radiation, physical and chemical agents.
Most important etiological agent of necrosis. Reduced oxygen supply most commonly due to vascular changes. However, also can be caused by chemical damage, CO poisoning.
Macroscopical, microscopical, vital reaction
Tissue is paler than normal, later becomes sharply defined, yellow and softened. End of first week - rimmed by hyperaemic zone. Later replaced by fibrous vascular scar tissue. Scarring well advanced by end of 6th week.
Cytoplasm (bright red eosinophilic) - organelles die, swelling of ER and mitochondria. Homogenous glassy appearance (loss of glycogen particles), calcification may occur.
Pycnosis - nucleus shrink and chromatin is condensed. Karyorrhexis - fragmentation of nucleus. Karyolysis - nucleus dissolute.
Accumulation of leukocytes, inflammation, hyperaemia to prevent spreading (stagnation of blood).
Types of necrosis
Coagulative and liquefactive necrosis is most common. Rest are subgroups of coagulative necrosis. Also find caseous necrosis. Most important reason for different types - different proteins.
Firm and pale. First has dark red color which changes to yellow. It becomes marked by zone of hyperemia, which limits necrotic site -> macrophages present. Shape of cells conserved. It is seen in tissue rich in proteins. Necrosis heals from granulation tissue -> scar. Example - heart and kidney (infarct).
Liquefactive (Colliquative) necrosis
Small amount of proteins, high amount of fats. Dead tissue appears as semi liquid as result of dissolution of tissue by hydrolytic enzymes. Disintegration of all affected structures. Often occurs in tissue rich in lipids - brain or spinal cord. Shape of cells are lost. If area is big -> heal by pseudocyst, small = glial scar.
Translucency and shape lost. Most typical for tuberculosis. Mcroscopically -> cheese appearance. It is healed by calcification.
Subtypes of coagulative necrosis
Gummatous, Hemorrhagic, Fat, Fibrinoid
Restricted to necrosis involving spirochaetal infections (syphilis). Aooears firm and rubbery.
Typical for organs with dual blood supply - lungs, liver, intestine. Necrotic tissue filled with RBC's. May be due to blockage of venous drainage.
Areas of fat destruction - release of pancreatic enzymes (ipases) into abdominal cavity or pancreas. Can also be due to trauma. Appears hard and yellow (acute pancreatitis).
Most common in autoimmune diseases, affects connective tissue. Loss of fibrillary structure.
Sequels of necrosis
Small nr of cells - necrosis removed by phagocytosis. Large nr of cells - inflammatory response with organization and fibrous repair - scar. Necrotic tissue too big - deposition of calcium (tuberculosis).
(Red or white infarct) Ischemic necrosis by occlusion of coronary arteries and anoxia. Coagulative necrosis, infiltration of neutrophils.
(White infarct) Occlusion of renal arteries and anoxia. Coagulative necrosis!, infiltration of neutrophils.
(red or white) Liquefactive necrosis, neutrophils and edema.
(red infract) Occlusion of pulmonary artery, hemmorhagic, alveoli filled with blood. Coagulative necrosis.
Caseous necrosis, granulomatous inflammation. Rimming the necrotic area is epitheloid cells, histocytes, lymphocytes. Langhan's giant cells.
Secondary altered necrosis. Necrosis with putrefaction of tissue, may be caused by certain bacterias. Gangrene is a complication of necrosis. Tissue becomes black and malodorous. Bacteria decompose dead tissue - release of hydrogen sulphide and iron -> iron sulphide = black. Caused by infection or ischemia. Often associated with diabetes. Most common in lower extremitites.
Causes of gangrene
Ischemia (athero, trhombus, embolism), DM, Buerger's disease (vascular inflammation, heavy smoking), Raynaud's disease (spasm affecting small arteries and arterioles in response to cold), Frost bite.
Dry, wet, gas
In limbs due to arterial occlusion. Dry because limbs are not rich in tissue fluids due to surface evaporation. Veins are patent, fluids can be removed. Diabetic foot, Raynauds, buergers.
Distal to occlusion
Cold, pale, later red due to escape of blood from necrotic capillarieas - black-brown.
Line of demarcation
red zone of acute inflammation at margin of gangrenous area - caused by irritants from gangrenous tissue
Line of separation
groove near line of demarcation - gadually deepens as dead part separates from viable tissues.
Bacterial infection as secondary complication. It spreads proximally - sepsis occurs. Diabetic gangrene + infection (dry + infection = wet). Usually devolops rapidly due to blockage of venous and/or arterial blood flow = stagnant blood -> rapid growth for bacteria. Toxic products from bacteria absorbed -> sepsis and death. Macroscopically - edamatous, soft, putrid, rotten, dark.
Ischemic tissues infected with anaerobic bacterias producing gas - clostridia f ex. Spreads rapidly, gases expand and infiltrate healthy tissue nearby. It is a medical emergency.
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