Events of inflammation in the synopsis
The local reaction of living mammalian tissues to harm caused by any substance is known as inflammation. The clearance of the necrosed cells and tissues follows the body’s defensive reaction to stop or slow the spread of the harmful toxin.
Agents causing inflammation
Inflammatory agents include the following:
- Infectious agents, such as bacteria, viruses and their poisons, fungi, and parasites.
- Immunological substances, such as cell-mediated and antigen-antibody responses.
- Physical agents including heat, cold, radiation, and physical harm.
- Chemical substances, such as organic and inorganic toxins.
- Inert substances like foreign bodies
Signs of inflammation
There are four signs of inflammation,
- Rubor (redness)
- Tumor (swelling)
- Calor (heat)
- Dolor (pain)
- Functio laesa (loss of function)
Acute inflammation is a continuous process even though the event can be divided into two major divisions,
- Vascular events
- Cellular events
The first reaction to tissue injury is alteration in the microvasculature (arterioles, capillaries, and venules). This set of events includes haemodynamic changes and changes on vascular permeability.
Changes in the vascular flow and size of tiny blood vessels in the wounded tissue provide the initial characteristics of the inflammatory response. The sequence of such changes is as follows.
- Transient vasoconstriction
- Progressive vasodilation
- Elevation of local hydrostatic pressure
- Slowing or stasis
- Leucocytic margination
Altered vascular permeability
Oedema fluid from blood plasma, which escapes through the endothelium wall of the peripheral vascular bed, accumulates in and around the inflamed tissue in the interstitial compartment. Vasodilatation causes fluid to leave in the first stage. This is transudate by nature. The inflammatory oedema, or exudate, subsequently occur due to increased vascular permeability of microcirculation.
Mechanisms of increased vascular permeability
Contraction of endothelial cells:
This is the most frequent mechanism of increased leakiness, which only affects venules and not the capillaries and arterioles. Vascular leakiness is caused by the endothelial cells’ brief gaps between them, which they generate during contraction. Histamine, bradykinin, and other chemical mediators are released to mediate it. The response starts right away after damage, is typically reversible, and lasts only briefly (15-30 minutes)
Retraction of endothelial:
In this mechanism, endothelial cells’ cytoskeleton undergoes structural reorganisation, which results in reversible retraction at the intercellular connections. Interleukin-1 (IL-1) and tumour necrosis factor (TNF)- are cytokines that are involved in mediating this shift, which also impacts venules. After injury, the response begins to manifest 4-6 hours later and lasts for at least 2-4 hours.
Direct injury to endothelial cells:
At the areas of detached endothelial cells, direct damage to the endothelium results in cell necrosis and the formation of physical gaps. The beginning of the thrombosis process occurs where the endothelial cells are injured. The modification impacts the microvasculature at all levels (venules, capillaries and arterioles). After an injury, there may be a rapid increase in permeability that lasts for several hours or days.
Endothelial injury mediated by leucocytes:
Leucocytes may become activated if they adhere to the endothelium at the site of inflammation. The proteolytic enzymes and hazardous oxygen species released by the activated leucocytes have the potential to damage endothelial cells and promote vascular leakiness. This type of late reaction increased vascular leakiness mostly impacts venules.
Leakiness in neovascularisation:
Additionally, throughout the healing process, newly created capillaries under the influence of vascular endothelial growth factor (VEGF) are abnormally leaky.
The cellular events of inflammation consists of two important processes,
- Exudation of leucocytes
Exudation of leucocytes
The most significant aspect of an inflammatory response is the escape of leucocytes into the interstitial tissue from the lumen of the microvasculature. Polymorphonuclear neutrophils (PMNs) are the body’s initial line of defence during acute inflammation, followed by monocytes and macrophages.
The changes leading to migration of leucocytes are as follows
Changes in the formed elements of blood
Vasodilatation causes an increase in blood flow rate during the initial stages of inflammation. Stasis of blood after some time causes disruptions to the axial flow of blood that normally occurs in the microcirculation. Leucocytes and RBCs make up the primary stream of cells in the normal axial flow, which also includes a peripheral layer of cell-free plasma near to the vessel wall. The centre stream of cells widens as a result of slowing and stasis, and the peripheral plasma zone shrinks as a result of plasma loss through exudation. This phenomenon is known as margination. Pavementing occurs when the neutrophils of the central column move closer to the vessel wall as a result of this redistribution
Rolling and adhesion
The endothelial cells lining the artery wall are gently rolled over by peripherally marginated and pavemented neutrophils (rolling phase). After afterwards, the temporary link between the leucocytes and endothelial cells solidifies (adhesion phase). Selectins, integrins and immunoglobulin gene superfamily adhesion molecule are the important molecules that bring about rolling and adhesion phases.
After adhering to the endothelium, neutrophils travel along its surface until they locate an appropriate location between endothelial cells.
Emigration is the process by which neutrophils between the endothelial cells and the basement membrane cross the barrier by locally destroying it with collagenases produced from their bodies. The damaged basement membrane is nearly instantly healed. Diapedesis, the movement of red cells via spaces between endothelial cells, occurs. RBCs are pushed out passively, either by increased hydrostatic pressure or possibly through endothelial flaws left behind by leucocyte emigration. The inflammatory exudate has a hemorrhagic appearance due to diapedesis.
Chemotaxis is the process by which leucocytes move through a number of barriers (including the endothelium, basement membrane, perivascular myofibroblasts, and matrix) in order to reach the interstitial tissues. The following agents acts as the chemotactic substances for neutrophils
- Leukotriene B4
- Components of complement system
- Soluble bacterial products
Phagocytosis is the mechanism by which cells take in solid particle material (cell-eating). The cells carrying out this action are referred to as phagocytes. The two primary categories of phagocytic cells are:
- Polymorphonuclear neutrophils (PMNs), also known as microphages, first emerge during an acute inflammatory reaction.
- Fixed tissue mononuclear phagocytes, also known as macrophages, and circulating monocytes.
Upon entering the tissue spaces, neutrophils and macrophages release a variety of proteolytic enzymes, including lysozyme, protease, collagenase, elastase, lipase, proteinase, gelatinase, and acid hydrolases. These enzymes break down extracellular matrix and collagen. The following three processes are involved in the phagocytosis of the microorganism by polymorphs and macrophages.
A – Opsonisation of the particle
B – Pseudopod engulfing the opsonised particle.
C – Incorporation within the cell (phagocytic vacuole) and degranulation
D – Phagolysosome formation after fusion of lysosome of the cell.
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