Inflammation And Wound Healing
DIAGNOSTIC RADIOGRAPHY · NTA LEVEL 4 · SEMESTER ONE Inflammation And Wound Healing CRT04101 · Anatomy, Physiology and Pathology START READING NOTES Study Inflammation And Wound Healing using the sections below. Use the topic navigation to continue through Anatomy, Physiology and Pathology. Contents of This Topic INFLAMMATION AND WOUND HEALING Definition Cardinal signs of inflammation How to name the inflammation Acute inflammation Persistent arteriolar dilatation to increase blood flow in the affected site; leads to heat and redness( erythema) 2. Cellular phase After adhesion, leukocytes move to the extracellular space through the gap in the endothelial cells (emigration) The steps of the inflammatory response SPECIAL TYPES OF INFLAMATION CHRONIC INFLAMMATION Two major characteristic features of chronic inflammation causes ii. Persistent indigestible material. iv. Hypersensitivity reactions; inappropriate immune response to generally harmless antigen. MACROPHAGE IN CHRONIC INFL. Diseases involving chronic inflammation. Management WOUND HEALING Angiogenesis : formation of new blood vessels to supply oxygen and nutrients to the healing tissue Pathological issues in wound healing Key players Bone healing involves several stages Systemic factors INFLAMMATION AND WOUND HEALING Ms.Happy.BscMIR.2025. Definition Inflammation is dynamic process by which living vascularized tissues reacts to injury. Causes Physical e.g. trauma, temperature, radiation Infection e.g. bacteria, viruses, parasites Chemical e.g. acids, organic compounds Immunological e.g. antigen-antibody Under normal circumstances inflammation is a protective response, a goal of which is to eliminate the initial cause of injury, however if triggered or directed inappropriately, inflammatory response itself can be harmful and cause tissue and organ destruction. Cardinal signs of inflammation Rubor(redness): dilatation of small blood vessels in damaged area. Calor(heat): increased blood flow(hyperemia) Tumor(swelling): accumulation of fluid in interstitial space(edema) Dolor(pain):distortion of tissue from edema especially pus. Loss of function: movement hindered How to name the inflammation Using suffix – itis after the name of the organs/site involved Eg Pancreatitis Hepatitis Encephalitis Meningitis Peritonitis Myocarditis This is not applicable to other organs/sites,eg:- Pleurisy- inflammation of the pleura Pneumonia- inflammation of the lungs Acute inflammation Is a rapid response to injurious stimuli, short acting, minutes to days. Pathogenesis of events Vascular phase Tissue injury Release of chemical for local response (histamine, prostaglandin, bradykinin, leukotriene etc) The immediate response is vasoconstriction, it may last about 3-5 sec, even 5 min depends on severity. Persistent arteriolar dilatation to increase blood flow in the affected site; leads to heat and redness( erythema) When the volume of blood increases, it increases intravascular hydrostatic pressure, so fluid from capillaries migrate to the tissue (exudate) 2. Cellular phase It is marked by two major events Leukocyte (WBC) movement Plasma or fluid gets discharged from the blood due to increased permeability(migration) The leukocyte in the surface contain integrin protein and endothelial cell of blood capillary consists of selectins( P&E) proteins on their surface. During the leukocyte rolling on to the endothelial cell, integrin and selectin get activated. They produce adhesion on the capillary of endothelial cell. After adhesion, leukocytes move to the extracellular space through the gap in the endothelial cells (emigration) At the site of injury several mediators get released which attract the leukocytes.( chemotaxis process) Phagocytosis Engulfment of solid particle or an agent ( cell eating) After the engulfment phagocyte release the lysosomes or degrading enzymes. This process fails to kill bacteria like m.tuberculosis The steps of the inflammatory response can be remembered as the five Rs: (1) Recognition of the injurious agent (2) Recruitment of leukocytes, (3) Removal of the agent, (4) Regulation (control) of the response, (5) Resolution (repair). SPECIAL TYPES OF INFLAMATION Catarrhal inflammation- exudative inflammation occurring exclusively on the mucous membranes of respiratory and gastrointestinal tracts and producing watery exudate of serum and mucus. Hemorrhagic inflammation:-when damage is severe there is rupture of blood vessel where hemorrhage is most striking feature, eg hemorrhagic pneumonia in fatal cases of influenza Suppurative inflammation; production of pus is the main characteristics eg abscess, peritonitis following rupture of appendix Peritonitis- purulent inflammation CHRONIC INFLAMMATION Chronic inflammation is a long term inflammatory response that can last for months or even years. Its different from acute inflammation, which is the body’s normal response to an injury or infection and resolves over time. Chronic inflammation occurs when the body continues sending out inflammatory cells and substances, even though there is no infection or injury; persistent immune response. Two major characteristic features of chronic inflammation Ongoing tissue destruction Attempt to repaire by fibrosis( with or without cell regeneration) May develop soon after an acute reaction May be insidious in onset causes Persistent infection Some organisms may be difficult to be eradicated. M. tuberculosis- tuberculosis M. leprae-leprosy T. pallidum- syphilis Fungi parasites ii. Persistent indigestible material. Endogenous- necrotic bone, necrotic adipose tissue, calcium and uric acid deposits. Exogenous- silica, asbestos fibers, suture materials. iii. Immune mediated reactions Autoimmune reactions (Rheumatoid arthritis, Systemic lupus erythromatosus(SLE), Hashimoto’s thyroiditis, Chronic autoimmune gastritis) Organ transplant rejections Unregulated immune responses ( inflammatory bowel disease e.g. ulcerative colitis) iv. Hypersensitivity reactions; inappropriate immune response to generally harmless antigen. bronchial asthma hypersensitivity pneumonitis Following acute inflammation; persistent abscess. Predominant cell type in — acute inflammation; neutrophil –chronic inflammation; macrophage Macrophages are a type of wbc of the innate immune system that engulf and digest pathogens, such as cancer cells, microbes, cellular debris and foreign substances. MACROPHAGE IN CHRONIC INFL. Continuous recruitment from blood -blood is most important source of macrophage -Mediated by: TGF &PDGF Proliferation of macrophage at the site of inflammation. Immobilization of macrophage at the site of inflammation. mediated by migration inhibition factor (MIF) secreted by activated T. lymphocytes. Diseases involving chronic inflammation. Autoimmune diseases (e.g. lupus, rheumatoid arthritis) Cardiovascular diseases (e.g. heart disease, high blood pressure) Several cancers Gastrointestinal diseases (e.g., Crohn’s disease, inflammatory bowel disease) Lung diseases (e.g., asthma, chronic obstructive pulmonary disease) Management Eating an anti-inflammatory diet rich in fruits, vegetables and health fats. Regular exercise Managing stress Avoid smoking and excessive alc consumption. Taking medications as described by a healthcare professional. WOUND HEALING Wound healing is a complex, dynamic process that involves a series of overlapping phases to restore