PPT-CELL INJURY & Inflammation - II

PRACTICAL 2 I Acute Inflammation Foundation Block Pathology Dept KSU Pathogenesis of Exudation The diagram shown here illustrates the process of exudation aided by endothelial cell contraction and vasodilation which typically is most pronounced in venules. 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. A Medical/Legal Perspective. OSIA Winter Conference – January 24, 2013. John Klor. Wallace Klor & Mann, P.C.. and. Stephen Fuller, M.D.. Impartial Medical Opinions, Inc.. Combined Conditions. 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. 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. rubor. (redness), . calor. (heat), tumor (swelling), dolor (pain), and loss of function. Seen here is skin with . erythema. , compared to the more normal skin at the far right.. The arm at the bottom is swollen (edematous) and reddened (. 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. . Acute. – quick onset, short duration. Adhesion. – a sticking together or binding of tissue fibers. Antiseptic. – a substance which prevents the growth of bacteria. Avascular. – without blood or . J. Matthew Velkey. matt.velkey@duke.edu. 454A Davison, Duke South (green zone). Cellular Adaptation to Injury or Stress. Injury or Stress. Increased demand. Decreased stimulation or lack of nutrients. Olivia Stevens and Judith Scott. What we’ll cover:. Inflammation . Thrombosis and emboli. Infarction. Cell growth and death . Classification of tumours. Mechanisms of carcinogenesis . Main tumour types. ASSISTANT PROFESSOR. WEST MEDICAL WARD. MAYO HOSPITAL/K.E.M.U. 1. DEFINITION OF INFLAMMATION. . Inflammation is a defensive process that a living body initiates against local tissue damage. It takes the form of a complex reaction of blood vessels, certain plasma components and blood cells, and cellular and structural components of connective tissue. . 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).. 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.”.