SHS 301 Lecture 5: Acute Inflammation PDF

COURSE CODE: 301 Dr.AYESHA ILYAS SEMESTER:5 (spring 2020) REFERENCE TEXT: (Robbins Pathology) Vinay Kumar, Abul K. Abbas, Jon C. Aster-Robbins and Cotran Pathologic Basis of Disease-Saunders (2015)  INTRACELLULAR ACCUMULATIONS TODAY’S TOPIC  INFLAMMATION, ACUTE INFLAMM...

COURSE CODE: 301 Dr.AYESHA ILYAS SEMESTER:5 (spring 2020) REFERENCE TEXT: (Robbins Pathology) Vinay Kumar, Abul K. Abbas, Jon C. Aster-Robbins and Cotran Pathologic Basis of Disease-Saunders (2015)  INTRACELLULAR ACCUMULATIONS TODAY’S TOPIC  INFLAMMATION, ACUTE INFLAMMATION : VASCULAR AND CELLULAR EVENTS -I  INTRODUCTION Survival of all living organisms requires that they should eliminate foreign invaders , such as infectious pathogens & damaged tissues. These functions are mediated by complex host immune response called as an Inflammation.  Inflammation is a protective attempt by the organism to remove the injurious stimuli and to initiate the healing process. Hence without inflammation, wounds and infections would never heal.  INFLAMMATION Definition – The word inflammation is derived from Latin word inflammare, which means “to set on fire.”  INFLAMMATION Inflammation is a response of vascularized tissues to infections and damaged tissues that brings cells and molecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offending agents.  INFLAMMATION is not harmful infact it is a protective response. MEDIATORS OF DEFENSE: 1. Phagocytic leukocytes 2. Antibodies 3. Complement proteins  The process of inflammation delivers these cells and proteins to damaged or necrotic tissues and foreign invaders, such as microbes, and activates the recruited cells and molecules, which then function to get rid of the harmful or unwanted substances.  HISTORICAL BACKGROUND 1. Word inflammation – Latin word inflammare ( meaning – to set on fire ) 2. CELSUS – A roman physician and medical writer (30 BC to 45 AD ) gave 4 cardinal signs of inflammation saying “ Rubor et tumor cum calore et dolore.” (meaning - Redness and swelling come 3. VIRCHOW added 5th Cardinal sign of inflammation in 1871 i.e. functio laesa (loss of function) 4. COHNHEIM gave First description of diapedesis in 1873. 5. LEWIS described Inflammation as the ‘‘triple response’’ to injury in 1927 * LEWIS TRIPLE RESPONSE - Inflammation is characterized by vascular events ,mediated by local chemicals and by axons.  STEPS OF INFLAMMATION 5R’s 1. Recognition of injurious agent 2. Recruitment of leukocytes 3. Removal of agent 4. Regulation of the response 5. Resolution  TYPES OF INFLAMMATION Acute Chronic  ACUTE INFLAMMATION Rapid response to injury or microbes and other foreign substances that is designed to deliver leukocytes and plasma proteins to sites of injury.  STIMULI Can be triggered by a variety of stimuli: Infections Trauma Physical & chemical agents Foreign bodies Immune reactions  COMPONENTS OF ACUTE INFLAMMATION Acute inflammation has two major components 1. Vascular changes 2. Cellular events  VASCULAR CHANGES Changes in Vascular Caliber and Flow Increased Vascular Permeability  CHANGES IN VASCULAR CALIBER AND FLOW Changes in blood vessels begin rapidly after infection or injury but may develop at variable rates, depending on the nature and severity of the original inflammatory stimulus.  The escape of fluid, proteins, and blood cells from the vascular system into the interstitial tissue or body cavities is known as exudation. An exudate is an extravascular fluid that has a high protein concentration and contains cellular debris. Its presence implies that there is an increase in the permeability of small blood vessels triggered by some sort of tissue injury and an ongoing inflammatory reaction. In contrast, a transudate is a fluid with low protein content (most of which is albumin), little or no cellular material, and low specific gravity.  INCREASED VASCULAR PERMEABILITY 1. Contraction of endothelial cells resulting in increased interendothelial spaces is the most common mechanism: It is carried out by: a. Histamine b. Leukotrienes c. Bradykinin 2. Endothelial injury, resulting in endothelial cell necrosis and detachement. Due to : a. Direct damage b. Microbes c. Microbial toxins d. Neutrophils that adhere to endothelium also amplify the reaction  RESPONSES OF LYMPHATIC VESSELS AND LYMPH NODES IN INFLAMMATION  INCREASED LYMPH FLOW  DRAIN EDEMA FLUID Lymphatic vessels proliferates to handle the increased load. Lymphatics becomes secondarily inflammed causing : 1. Lymphangitis 2. Lymphadenitis So show REDNESS and SWELLING PATHOPHYSIOLOGY OF INFLAMMATION  Inflammation  vasodilation  increased blood flow  RUBOR As microvasculature becomes more permeable , protein rich fluid moves into extravascular tissue. RBCs become more concentrated , thereby increasing blood viscosity.. slowing the circulation called as STASIS. as stasis develops leukocytes begin to accumulate along the endothelial surface….  NORMAL Arteriole Venule Capillary bed Inflammed (Vasodilatio  CELLULAR EVENTS An important function of the inflammatory response is to deliver leukocytes to the site of injury and to activate them Leukocyte Transmigration , Chemotaxis & Phagocytosis  Activating substances released by bacterial and dead tissues go and adhere to the vessel walls which facilitates adhesion and activation of leukocytes ………… 4 steps of leukocytic recruitment : 1.Margination 2. rolling. 3. Adhesion 4.transmigration or diapedesis 5. margination in interstitial tissue towards chemotactic nucleus. RESOLUTION OF INFLAMMATION  RESOLUTION OF INFLAMMATION When inflammation subsides Phagocytes or macrophages clear leukocytes and dead tissues. Fluid and proteins are removed by lymphatic drainage as well as macrophages … Macrophages also release growth factors to new blood vessels and fibroblasts to carry on fibrosis and scaring.  PHAGOCYTOSIS Consists of 3 distinct but interrelated steps 1. Recognition and attachment of the particle to the ingesting leukocyte 2. Engulfment, with subsequent formation of a phagocytic vacuole 3. Killing and degradation of the ingested material.  PATTERNS OF ACUTE INFLAMMATION PATTERNS OF ACUTE INFLAMMATION Vascular and cellular reactions that characterize acute inflammation are reflected in the morphologic appearance of the reaction. Serous inflammation  SEROUS FIBRINOUS SUPPURATI INFLAMMAT INFLAMMAT VE ION ION INFLAMMAT ION characterized by: occurs as a manifested by the the outpouring consequence of presence of large of a watery more severe amounts of relatively protein- injuries, purulent exudate poor fluid that, resulting in (pus) depending on the greater vascular consisting of site of injury permeability neutrophils, that allows large necrotic cells, and molecules (such edema fluid BLISTER, “Watery”, i.e.,  NEXT LECTURE INFLAMMATION, ACUTE INFLAMMATION : VASCULAR AND CELLULAR EVENTS - II  HOME TASK PRINCIPAL MEDIATORS OF INFLAMMATION