Inflammation (Acute inflammation)

Inflammation (Acute inflammation). DR ANIMESH CHATTOPADHYAY TEAM NURSING EXTRA MILEAGE.

Definition and etiology. Definition Inflammation is defined as the reaction of living tissue to a sub lethal injury. It is fundamentally a protective response to get rid of the offensive injury; in severe condition it may be harmful Etiology Burns chemical irritants Frostbite Toxins.

Definition and etiology. infection by pathogens Physical injury Immune reactions due to hypersensitivity Ionizing radiation Foreign bodies.

Acute inflammation. Acute inflammation is a rapid and localized protective response that the body initiates against tissue injury, infection, or other harmful stimuli The primary purpose of acute inflammation is to eliminate the cause of cell injury, clear out necrotic cells and tissues damaged from the original insult, and initiate tissue repair Acute inflammation occurs immediately upon injury, lasting only a few days. Cytokines and chemokines promote the migration of neutrophils and macrophages to the site of inflammation.

Acute inflammation. Important events in acute inflammation Vascular events cellular events.

Acute inflammation (vascular events). The following are the vascular events that occur in acute inflammation. It includes Hemodynamic changes Altered vascular permeability a)Hemodynamic changes Transient vasoconstriction this occurs immediately after the injury Persistent progressive vasodilation Increase in local hydrostatic pressure- leads to transudate.

Acute inflammation (vascular events). Slowing or stasis of microcirculation as the protein rich plasma escapes out of the vessels, there will be accumulation of red cells, white cells and platelets within the vessel Leukocyte migration and emigration b) Altered vascular permeability Vascular permeability increases due to endothelial cell contraction due to histamine, bradykinin endothelial cell retraction due to interleukin 1 and tumor necrosis factor direct endothelial injury due to necrosis leukocyte mediated endothelial injury due to leukocyte activation.

Acute inflammation (vascular events). [image] Local effect of MCs on the vasculature during acute inflammation In this diagram activated MCs release inflammatory mediators which then induce changes along vascular endothelium Some of these mediators directly act on ECs and smooth muscle cells to promote vasodilation and vascular leakiness In addition vascular ECs up regulate many adhesion molecules and release WPBs to promote the rolling and extravasation of leukocytes into the inflamed tissue Concurrently increased vascular leakiness promotes the loss of fluid and blood proteins into the tissue or edema Additional MC derived mediators can limit clotting and these responses cumulatively act to increase vascular flow through the site of inflammation Presumably the compromised barrier function of the vascular ECs would also facilitate the dissemination of MC products systemically.

Acute inflammation (cellular events). Cellular events can be divided into two types….. Intravascular and extravascular events. Intravascular events includes margination, rolling and adhesion Extravascular events include diapedesis, chemotaxis and phagocytosis.

Acute inflammation (cellular events). [image] Cellular phase of acute inflammation YouTube.

Acute inflammation (cellular events). Chemotaxis Upon recognition of an activation by pathogens, resident macrophages in the affected tissue release cytokines such as interleukin one(IL-1), TNF alpha and chemokines. IL- and TNF alpha cause the endothelial cells of blood vessels near the site of infection to express cellular adhesion molecules, including selectins Circulating leukocytes are localized towards the site of injury or infection due to the presence of chemokines.

Acute inflammation (cellular events). Rolling and adhesion Carbohydrate ligands on the circulating leukocyte bind to selectin molecules on the inner wall of the vessel, with marginal affinity This causes the leukocyte to slow down and begin rolling along the inner surface of the vessel wall During this rolling motion, transitory bands are formed and broken between selectins and their ligands.

Acute inflammation (cellular events). Tight adhesion At the same time, chemokines released by macrophages activate the rolling leucocyte and cause surface integrin molecules to switch from the default low affinity state to a high affinity state In the activated state, integrins bind tightly to complementary receptors expressed on endothelial cells, with high affinity. This causes the immobilization of the leukocytes, despite the shear forces of the ongoing blood flow Adhesive molecules involved are selectins, integrin ligands and cytokines.

Acute inflammation (cellular events). Transmigration The cyto skeletons of the leukocytes are recognized in such a way that the leukocytes are spread out over the endothelial cells Transmission of leukocyte occurs as platelet endothelial cell adhesion molecule 1 (PECAM-1) PECAM-1 molecules found on the leukocyte and endothelial cell surfaces interact and effectively pull the cell through the endothelium Once through the endothelium, the leukocyte must penetrate the basement membrane The entire process of blood vessel escape is known as diapedesis..

Acute inflammation (cellular events). [image] Interaction of leukocytes and endothelial cells in the process of Download Scientific Diagram.

Acute inflammation (cellular events). Phagocytosis Phagocytosis is a vital cellular process by which certain cells engulf and digest foreign particles, such as bacteria, cellular debris or pathogen. Phagocytosis is one main mechanism of the innate immune defence. It is one of the first processes responding to infection, and is also one of the initiating branches of an adaptive immune response Steps involved in phagocytosis are-- Chemotaxis recognition and attachment.

Acute inflammation (cellular events). Engulfment Phagosome maturation Destruction and digestion Formation of residual bodies Anti-inflammatory signals.

Systemic effects of acute inflammation. Fever Endocrine and metabolic responses Autonomic responses such as increased blood pressure Behavioral responses like somnolence Leukocytosis Leukopenia Weight loss Loss of appetite.

Chemical mediators of inflammation. Plasma derived mediators Bradykinin C3C5a FactorXII membrane attack complex Plasmin Thrombin.

Chemical mediators of inflammation. Cell derived mediators Lysosome granules Histamine IFN-alpha IL-8 Leukotriene B4 Nitric oxide Prostaglandin TNF-ALPHA.

Morphological patterns of acute inflammation. Granulomatous inflammation where granuloma is formed like tuberculosis ,leprosy Fibrinous inflammation where there is large increase in vascular permeability which allows fibrin to pass through the blood vessels and fibrinous exudate is deposited like pericarditis, pleuritis. Sero-fibrinous Inflammation where the conversion of fibrinous exudate into a scar can occur between serous membranes like rheumatic pericarditis. Serous inflammation where copious effusion of non-viscous fluid occurs like blister in burns, pleural effusion Purulent inflammation where large amount of pus formation occurs. Ulcerative inflammation where inflammation occurring near an epithelium can result in the necrotic loss of tissue from the surface like acute peptic ulcers Pseudo membranous where deposition of a fibrinous membrane like material occurs like pseudomembranous colitis.

Fate of acute inflammation. Resolution complete restoration of the inflamed tissue back to a normal status fibrosis fibrous scarring occurs in these areas of damage, forming a scar composed primarily of collagen Abscess formation Chronic inflammation.

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