Inflammation - W3

INFLAMMATION DR ZAKARIA ELTAHIR 1  Outlines q Definition q Clinical signs q Etiology q Mechanisms q Cellular events q Classification q Pathogenesis q Acute Inflammation...

INFLAMMATION DR ZAKARIA ELTAHIR 1  Outlines q Definition q Clinical signs q Etiology q Mechanisms q Cellular events q Classification q Pathogenesis q Acute Inflammation q Chronic Inflammation q Inflammation outcomes q Post Inflammation, healing … q Acute v Chronic Inflammations q Diseases of inflammation q Case study q Workshop topics 1/26/25 2  Poll Question No. 1 Do you think inflammation is a disease condition? A. Yes B. No 1/26/25 3  What is inflammation? Ø “Inflame”: set on fire Ø Inflammation is a complex protective reaction Ø A dynamic response of vascularized to injury Ø Injurious agents to be destroyed, neutralized, diluted or walled off [Greek root + -itis] Ø Induced by endogenous/exogenous stimuli factors Ø Vital defense mechanism for survival Ø Could be harmful?! 1/26/25 4  Poll Question No. 2 How do we know some one has an inflammation? A. Fever B. Size increase C. Change in color D. All of the above E. Only A&C 1/26/25 5 1/26/25 6  Clinical signs v Rubor --- Redness v Calor --- Heat v Dolor --- Pain v Tumor --- Swelling v Functio laasa -- Loss of Function 1/26/25 7 1/26/25 8  Etiology € Microbial infections: bacterial, viral, fungal, etc. € Physical agents: burns, trauma--like cuts, radiation € Chemicals: drugs, toxins, battery acid € Immunologic reactions: rheumatoid arthritis 1/26/25 9  Mechanisms q Two types of mechanisms Ø Local Ø Systemic Ø Three major mechanisms: v Alteration: vascular changes v Exudation: Inflammatory exudate: a) liquid b) cellular v Proliferation: Formation of granulation and fibrous tissue 1/26/25 10 1/26/25 11  Mechanisms 1/26/25 12  Cellular events € Leukocytes margination ® rolling ® adhesion ® transmigration € Emigration of: neutrophils (1-2 days) monocytes (2-3 days) € Chemotaxis endogenous signaling molecules - lymphokines exogenous - toxins € Phagocytosis - lysosomal enzymes, free radicals, oxidative eruption € Passive emigration of RBC - no active role in inflamm. - hemorrhagic inflammation 1/26/25 13  Phagocytosis 1/26/25 14  Outlines 1/26/25 15  Phagocytosis Phagocytosis: is a process which involves the recognition , engulfment and digestion of microbes, dead cells an foreign bodies € Recognition, adhesion and invagination into cytoplasm € Engulfment € Lysosomes - destruction € In highly virulent microorganisms can kill the leucocyte and not the microbe € In highly resistant microorganisms - persistence within macrophage - activation after many years 1/26/25 16  Pathogenesis Three main processes occur at the site of inflammation, due to the release of chemical mediators: Ø Increased blood flow (redness and warmth) Ø Increased vascular permeability (swelling, pain & loss of function) Ø Leukocytic Infiltration 1/26/25 17  Poll Question No. 3 Chemomediators main goal in pathogenesis is to stop the inflammation? A. True B. False 1/26/25 18  Classification Classified according to; histology, causative & duration q Acute inflammation Acute Inflammation is a general pattern of immune response to cell injury characterized by rapid accumulation of immune cells at the site of injury q Chronic Inflammation A transition to a pattern of chronic inflammation develops following weeks of an unresolved inflammatory process and can last months or even years 1/26/25 19  Acute inflammation Ø Early onset – seconds to minutes – short duration – minutes to days, involving fluid exudation, plasma proteins, (edema) and cell emigration (neutrophils) to site of injury Ø Inflammation is terminated when the offending agent is eliminated, by activation of anti-inflammatory mechanisms Ø Inflammatory response is intertwined with repair process Ø Injured tissue is replaced through regeneration of native parenchymal cells, scarring or a combination of both 1/26/25 20  Main features of Acute Inflammation 1/26/25 21  Chronic Inflammation q In many cases the processes of acute inflammation are not sufficient to remove the source of injury q Additionally, the inflammatory processes themselves may initiate further injury which induces further inflammation, scenarios where inflammation lasts for a longer period 1/26/25 22  Characteristics of chronic inflammation Ø Infiltration with mononuclear cells, which include macrophages, lymphocytes and plasma cells Ø Tissue destruction, induced by the persistent offending agent or by the inflammatory cells Ø Attempts at healing by connective tissue replacement of damaged tissue, accomplished by proliferation of small blood vessels (angiogenesis) and, in particular, fibrosis 1/26/25 23  Inflammation outcomes! v Complete resolution - injury is limited or short lived - little tissue destruction, and - parenchymal cells can regenerate Removal of cellular debris and microbes Resorption of edema fluid by lymphatics v Healing by connective tissue replacement (fibrosis). - substantial tissue destruction - tissue involved is incapable of regeneration - abundant fibrin exudation in tissues or serous cavities 1/26/25 24 1/26/25 25  Poll Question No. 4 Why does acute inflammation continue to become chronic? A. No enough antibodies B. Failure of acute inflammation 1/26/25 26  Characteristics of acute inflammation 1/26/25 27  Characteristics of acute inflammation 1/26/25 28  Characteristics of acute inflammation 1/26/25 29  Characteristics of acute inflammation 1/26/25 30  Progression of acute inflammation 1/26/25 31  Characteristics of chronic inflammation 1/26/25 32  Characteristics of chronic inflammation 1/26/25 33  Characteristics of chronic inflammation 1/26/25 34  Giant cells in chronic inflammation HISTOLOGY: CARDIOVASCULAR: HEART: Boecks Sarcoid (sarcoidosis): Micro low mag H&E chronic 1/26/25 case region, giant cells chronic inflammatory cells no frank granulomas 35  Post inflammation: healing … Pulmonary vein completely obliterated by a thrombus with organization. The thrombus was replaced by an immature granulation tissue, rich in newly formed 1/26/25capillaries, fibroblasts, collagen and reduced inflammatory infiltrate. 36  Oesophagus??? 1/26/25 37  Lung … which type??? 1/26/25 38  Colon.. Which type??? 1/26/25 39  Acute versus Chronic Acute Chronic Pathogens that the body cannot break down, including some Harmful bacteria or types of virus, foreign Caused by tissue injury bodies that remain in the system, or overactive immune responses Onset Rapid Slow Duration A few days From months to years Inflammation Tissue death and the improves, turns into an thickening and Outcomes abscess, or becomes scarring of connective chronic tissue 1/26/25 40  Characteristics of acute versus Chronic Acute Inflammation Chronic Inflammation Infection: Neutrophils. Macrophages, Cells Allergy: eosinophils, lymphocytes mast cells Complement, kinins, prostaglandins, leukotrienes, cytokines Cytokines from (Interleukin 1, Chemical Mediators macrophages and T Interleukin 6) from lymphocytes various immune cells, interferon-gamma from T cells Rash, fibrosis, Lesion Rash, pus, abscess granuloma Autoimmune Abscesses (brain; conditions (lupus; Clinical Examples skin), allergic reaction rheumatoid arthritis), (anaphylaxis) 1/26/25 cystic fibrosis 41  Diseases of inflammations 1/26/25 42