Pathology

• Acute inflammation is defined as a response of vascularized tissues to infections and damaged tissues, bringing cells and molecules of host defense from circulation to the sites where they are needed to eliminate the offending agents.
• Inflammation is a harmful reaction but also a protective response important for survival.
• The purpose of inflammations is to limit and isolate injury, destroy the invading microorganism and inactivate toxin, prepare the tissue for healing and repair, and to regulate the response.
• The steps of the inflammatory response include recognition of offending agents, recruitment of leukocytes and plasma proteins, removal of the agent, regulation of the response, and resolution (repair).
• Chemical mediators and their functions in inflammation are also listed below:
• Differences between acute and chronic inflammation are also listed below:
• Persistence of chronic inflammation can lead to sinus formation with pus, stricture/contraction of scar, obstruction, and development of cancer in scar tissue.
• Chronic inflammation has an aetiology, pathogenesis, and morphology.
• Acute inflammation is a vascular and cellular response.
• The cardinal signs of acute inflammation and their corresponding morphology are listed below:
• The outcomes of acute and chronic inflammation are different.
• Inflammatory cells are a crucial part of the inflammatory process.
• Special types of chronic inflammation include chronic granulomatous inflammation.
• Inflammation is terminated when the causing agents are eliminated or destroyed, secreted chemical mediators are broken down or dissipated, and there are active anti-inflammatory mechanisms which serve to control the response and prevent it from causing excessive damage to the host.
• The triggering factors (aetiology) of inflammation include microbial infections, tissue necrosis, foreign bodies, and immune reaction.
• During inflammation, plasma fluid goes out from circulation into surrounding tissues, called exudate.
• Exudate is an inflammatory extravascular fluid, while transudate is an ultrafiltrate of blood plasma produced as a result of osmotic or hydrostatic imbalance across the vessel wall without increase in permeability.
• The two major components of inflammation are vascular reaction and cellular response.
• Vascular reaction involves vessels dilating to slow down blood flow with increasing permeability to allow circulating cells and proteins to enter the damaged site.
• PAF, Kinins, Neuropeptides are other mediators of inflammation.
• Reactions of inflammation include vasodilatation, increase in vascular permeability, chemotaxis, leukocyte recruitment and activation, and tissue damage.
• Morphological features of chronic inflammation include infiltration by mononuclear cells, which include macrophages, lymphocytes and plasma cells.
• Morphologic patterns of inflammation include serous inflammation, fibrinous inflammation, suppurative or purulent inflammation, and ulcers.
• Chronic inflammation is of prolonged duration, has a slow onset and lasts for weeks or months or years, and may arise from acute inflammation.
• Vasoactive amines, complement systems, arachidonic acid metabolites, cytokines, PAF, Kinins, Neuropeptides are mediators of inflammation.
• Outcomes of acute inflammation can be complete resolution, regeneration, healing by connective tissue replacement (fibrosis), or progression to chronic inflammation.
• Characteristics of chronic inflammation include on going tissue damage and inflammation, and attempts at repair.
• Cellular response involves activated leukocytes ingesting and destroying microbes etc.
• Chronic inflammation can be caused by persistent infections by microorganisms difficult to eradicate, such as mycobacteria or certain virus, fungi, prolonged exposure to potentially toxic agents either exogenous or endogenous, or hypersensitivity diseases.
• Mediators of inflammation can be produced by inflammatory cells, platelets, neutrophils and endothelial cells, or derived from plasma.
• Neutrophils are a type of inflammatory cell with cytoplasmic lysosomal granules rich in proteolytic enzymes capable of breaking down micro-organisms and tissues, and they are short-lived, surviving only for a few hours.
• Damaged area contains both viable neutrophils and dead neutrophils.
• Mediators of inflammation are substances that initiate and regulate inflammatory reactions.
• Macrophages are diffusely scattered in connective tissue and are clustered in organs such as the liver (Kuppfer cells), spleen and lymph nodes (sinus histiocytes) and lungs (alveolar macrophages).
• Eosinophils are involved in immune reactions mediated by IgE (allergic reactions) and in parasitic infections.
• Vasodilation in acute inflammation is induced by the action of several chemical mediators, such as histamine on vascular smooth muscle (heat and redness), and increase permeability is induced by histamine, kinins results from contraction of endothelial cells, increase inter endothelial space, endothelial injury, leukocytes emigration mediated by adhesion molecules and cytokines called chemokines (selectins, integrins).
• Macrophages are also found in bone (osteoclasts).
• Macrophages produce cytokines to activate B cells and transform them into plasma cells.
• Phagocytosis in acute inflammation involves three steps: recognition and attachment of particle to be ingested by leukocytes, engulfment with formation of phagocytic vacuole, and killing and degradation of ingested material by lysosomal enzymes and free radicals such as ROS and NO.
• The breakdown products of inflammation form a thick yellow fluid, pus.