Acute Inflammation: Vascular and Cellular Events PDF

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AffectionateMoldavite6680

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acute inflammation vascular events cellular events inflammation

Summary

These lecture notes provide an overview of acute inflammation, focusing on vascular and cellular events. They detail the process of inflammation, including the initial vascular changes (e.g., vasoconstriction and vasodilation) and the subsequent cellular responses (e.g., margination, diapedesis, and phagocytosis). The notes also introduce key concepts like Starling's hypothesis and types of phagocytic cells.

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# **1. VASCULAR EVENTS** - Alteration in the microvasculature (arterioles, capillaries and venules) is the earliest response to tissue injury. - These alterations include: - A. Haemodynamic changes. - Changes in vascular permeability. # **A. Haemodynamic changes.** - The earliest features of...

# **1. VASCULAR EVENTS** - Alteration in the microvasculature (arterioles, capillaries and venules) is the earliest response to tissue injury. - These alterations include: - A. Haemodynamic changes. - Changes in vascular permeability. # **A. Haemodynamic changes.** - The earliest features of inflammatory response result from changes in the vascular flow and calibre of small blood vessels in the injured tissue. Such as - # **1. Vasoconstriction of arterioles** - Irrespective of the type of injury, immediate vascular response. - i.e. transient vasoconstriction of arterioles. - The blood flow may be re-established in 3-5 seconds. - With more severe injury, the vasoconstriction may last for about 5 minutes. # **2. Persistent progressive vasodilatation:** - Involves mainly the arterioles. - Affects other components of the microcirculation like venules and capillaries. - This change is obvious within half an hour of injury. - Vasodilatation results in increased blood volume. - "Responsible for redness and warmth at the site of acute inflammation." # **3. Local hydrostatic pressure:** - Progressive vasodilatation, in turn, may elevate the **Local hydrostatic pressure** resulting in transudation of fluid into the extracellular space. - "This is responsible for swelling at the local site of acute inflammation." # **4. Emigration:** - Stasis or slowing is followed by leucocytic margination (mainly neutrophils). - The leucocytes stick to the vascular endothelium briefly, and then move and migrate through the gaps between the endothelial cells into the extravascular space. # **B. Changes in vascular permeability.** - In and around the inflamed tissue, there is accumulation of oedema fluid in the interstitial compartment. - Which comes from blood plasma by its escape through the endothelial wall of peripheral vascular bed. - In the initial stage, the escape of fluid is due to vasodilatation and consequent elevation in hydrostatic pressure. - Increased vascular permeability of microvascular bed is explained on the basis of **Starling's hypothesis.** - "In normal circumstances, the fluid balance is maintained by two opposing sets of forces:" - **1. Forces that cause outward movement of fluid from microcirculation are intravascular hydrostatic pressure and colloid osmotic pressure of interstitial fluid.** - **2. Forces that cause inward movement of interstitial fluid into circulation are intravascular colloid osmotic pressure and hydrostatic pressure of interstitial fluid.** - However, in inflamed tissues, the endothelial lining of microvasculature becomes more leaky. - Consequently, intravascular colloid osmotic pressure decreases and osmotic pressure of the interstitial fluid increases. - Resulting in excessive outward flow of fluid into the interstitial compartment. - Which is exudative inflammatory oedema. *** # **ACUTE INFLAMMATION** A diagram of an acute inflammation process describes an inflammation pathway, beginning with vascular events, then separating into two branches. - The **vascular events** branch of the diagram includes: - **Arteriolar Changes** - Vasodilatation leads to hyperemia (redness). - **Venular Changes** - Increased Venular Permeability leads to swelling (oedema). - This leads to **Exudative Edema**. - The **cellular events** branch of the diagram includes: - **Neutrophilic influx in vessels** - **Margination** - **Rolling** - **Adhesion** - **Transmigration (Diapedesis)** - **Chemotaxis** - **Opsonophagocytic Destruction** *** A diagram depicting a section of inflamed tissue. The diagram includes: - A description of the process as **INFLAMMATION: VASCULAR EVENTS + LEUKOCYTE MIGRATION** - Red blood cells moving through the vessels. - White blood cells migrating through the gaps in the vessel walls to the outside of the vessel. - White blood cells moving toward a stimulus at the top of the diagram. # **2. CELLULAR EVENTS** - The cellular phase of inflammation consists of 2 processes: - I. Exudation of leucocytes. - II. Phagocytosis. # **I. Exudation of leucocytes.** - A diagram depicting a section of inflamed tissue. The diagram shows: - **A. Normal axial flow** of red and white blood cells in the vessel. - **B. Margination and pavementing** of white blood cells against the vessel's edge. - **C. Rolling and adhesion** of the white blood cells as they adhere to the vessel wall. - **D. Emigration and diapedesis** of white blood cells that have moved through the gaps between the endothelial cells on the vessel wall. - The most important feature of inflammatory response is escape of leucocytes from the lumen of microvasculature to the interstitial tissue. - "In acute inflammation, polymorphonuclear neutrophils (PMNs) comprise the first line of body defense. Followed later by monocytes and Macrophages." - The changes leading to migration of leucocytes are as follows: - **1. MARGINATION:** As a result of this redistribution, the neutrophils of the central column come close to the vessel wall; this is known as pavementing. - **2. ROLLING AND ADHESION:** - Peripherally marginated and pavemented neutrophils slowly roll over the endothelial cells lining the vessel wall (rolling phase). - This is followed by the transient bond between the leucocytes and endothelial cells becoming firmer (adhesion phase). - **3. EMIGRATION:** After sticking of neutrophils to endothelium, the former move along the endothelial surface till a suitable site between the endothelial cells is found where the neutrophils throw out cytoplasmic pseudopods. # **II. Phagocytosis.** - "Phagocytosis is defined as the process of engulfment of solid particulate material by the cells (cell-eating)." - The cells performing this function are called phagocytes. - There are 2 main types of phagocytic cells: - i. Polymorphonuclear neutrophils (PMNs): commonly called **Microphage**. - ii. Circulating monocytes: commonly called **Macrophage**. # **Steps of Phagocytosis** - The microbe undergoes the process of phagocytosis by polymorphs and macrophages involves the following 3 steps: - 1. Recognition and attachment - 2. Engulfment - 3. Killing and degradation - A diagram of 4 stages of phagocytosis shows: - **A. Opsonisation of the particle:** a microbe is attached by an IgG opsonin, a C3b opsonin, and a Lectin to the Fc receptor on the surface. - **B. Pseudopod engulfing the opsonised particle:** the microbe has been pulled into the cell while attached to the receptor. - **C. Incorporation within the cell (phagocytic vacuole) and degranulation:** the microbe is completely enclosed in the cell with pseudopods surrounding it. - **D. Phagolysosome formation after fusion of lysosome of the cell:** the microbe has been broken down within the phagolysosome. # **Thanks.**

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