PPT-Cell Injury, Death, Inflammation, and Repair

J Matthew Velkey mattvelkeydukeedu 454A Davison Duke South green zone Cellular Adaptation to Injury or Stress Injury or Stress Increased demand Decreased stimulation or lack of nutrients. Grace Denton & Stephanie . Tristram. G.E.Denton@warwick.ac.uk. S.C.Tristram@warwick.ac.uk. What are some of the causes of cell injury and cell death?. Causes of cell injury .  . CHIPING: C. Jeffrey Bryan, DVM, MS, PhD, DACVIM(Oncology). bryanjn@missouri.edu. Cellular Radiation Effects . Cell membrane - Alteration in permeability. Cellular organelles - Functional Aberrations . Nuclear membrane - Altered permeability & Function . NST110, Toxicology. Department of Nutritional Sciences and Toxicology. University of California, Berkeley. Mechanisms of Toxicity. Delivery: Site of Exposure to the Target. Reaction of the Ultimate Toxicant with the Target Molecule. Immune . Response. and Inflammation. Inflammation-definition. R. eaction of . vascularized. living tissue to local injury. Acute inflammation. Chronic inflammation. Repair. Resolution. Abscess. Injury. Department of Nutritional Sciences and Toxicology. University of California, Berkeley. Mechanisms of Toxicity. Delivery: Site of Exposure to the Target. Reaction of the Ultimate Toxicant with the Target Molecule. . (Adaptations, injury and death). (. 2 of 5). Ali Al Khader, M.D.. Faculty of Medicine. Al-Balqa’ Applied University. Most injurious stimuli are grouped into:. Oxygen deprivation. Chemical agents. Four Stages in Skin Healing. Inflammation. Blood flow increases. Phagocytes attracted. Scab formation. Cell division and migration. Scar formation. Bleeding occurs at the site of injury immediately after the injury, and mast cells in the region trigger an inflammatory response.. Safety in the . Histotechnique. Laboratory . PEL – Permissible Exposure Limit . TLV – Threshold Limit Value . OEL – Occupational Exposure Limit . *Complete penetration by alcohol will destroy all infectious agents except prions. . DR. AYSER HAMEED. LEC.4. This is a distinctive pattern of chronic inflammatory reaction characterized by focal accumulations of activated macrophages, which often develop an . epithelioid. (epithelial-like) appearance. . Dr. . Shakir. H. Mohammed . Al_Alwany. LEC 2,3,4. Hyperplasia & Physiologic . Hyperplasia. HYPERPLASIA . Increase . in the number of cells . results in increase in size of the . organ. Lecture 2. Dr. Mohanad Al-Hindawi. 2022. Cellular changes of acute inflammation.. A critical function of inflammation is to deliver leukocytes to sites of injury (recruitment), especially those cells capable of phagocytosing microbes and necrotic debris (e.g., neutrophils and macrophages).. Cellular injury. Cellular injury . can occur in a number of different ways. The extent of injury that cells experience is often related to the intensity and duration of exposure to the injurious event or substance. Cellular injury may be a reversible process, in which case the cells can recover their normal function, or it may be irreversible and lead to cell death. . . Cellular. . Responses. . to. Stress and . Noxious. . Stimuli. Sequence. . of. . reversible. . cell. . injury. and . cell. . death. . . Necrosis. and . apoptosis. are the . two. major . Associate Professor. University of Kansas School of Medicine. Inflammation. Definition. . “. Inflammation is a reaction of a tissue and its microcirculation to a pathogenic insult. It is characterized by the generation of inflammatory mediators and movement of fluid & leukocytes from the blood into extravascular tissues.”.