Inflammation Question And Answers

Inflammation

Question 1. Define inflammation and describe cardinal signs of inflammation. Describe vascular events of inflammation.
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Describe in brief cardinal signs and vascular changes in inflammation.
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Discuss the pathogenesis of vascular phenomenon in acute inflammation.  
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Describe the vascular and cellular response of acute inflammation.
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Write a short note on vascular events of acute inflammation.
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Enumerate cardinal signs of inflammation and describe in brief vascular events of acute inflammation.
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Describe vascular events in acute inflammation.
Answer:

Definition: Inflammation is defined as the local response of living mammalian tissues to injury due to any agent. It is a body defense reaction to eliminate or limit the spread of injurious agents as well as to remove the consequent necrosed cells and tissues.

Cardinal Signs of Inflammation

The four cardinal signs of inflammation proposed by Celsus in the first century AD are as follows:

• Rubor or redness
• Tumor or swelling
• Calor or heat
• Dolor or pain.

Read And Learn More: Pathology Questions andd Answers

To these above four signs, the fifth sign is added by Virchow, i.e., function laksa or loss of function.

Vascular Events of Inflammation

Alteration in the microvasculature (arterioles, capillarie,,s and venules). These alterations include:

• Hemodynamic changes
• Changes in vascular permeability.

Hemodynamic Changes

• Transient vasoconstriction: Irrespective of the type of cell injury, the immediate vascular response transient vasoconstriction of arterioles. With the mild form of injury, the blood flow may be re-established in 3 to 5 seconds,, while with more severe injur,y the vasoconstriction may last for about 5 minutes.
• Persistent progressive vasodilatation: Next follows persistent progressive vasodilatation,, which involves mainly the arterioles, but to a lesser extent, 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 in the microvascular bed of the area, which is responsible for redness and warmth at the site of acute inflammation.
• Local hydrostatic pressure: Progressive vasodilatation, in turn, may elevate the local hydrostatic pressur,,e resulting in the transudation of fluid into the extracellular space. This is responsible for swelling at the local site of acute inflammation.
• Slowing or stasis: Slowing or stasis of microcirculation follows,, which causes an increased concentration of red cells and thus, raised blood viscosity.
• Leucocyte margination: Stasis or slowing is followed by leucocytic margination or peripheral orientation of leucocytes (mainly neutrophils) along the vascular endothelium. The leucocytes stick to the vascular endothelium briefly, and then move and migrate through the gaps between the endothelial cells into the extravascular space. This process is known as emigration.

Patterns of Increased Vascular Permeability:

Increased vascular permeability in acute inflammation by which normally non-permeable endothelial layer of microvasculature becomes leaky can have the following patterns and mechanisms which may be acting singly or more often in combination:

• Contraction of endothelial cells: This is the most common mechanism of increased leakiness that affects venules exclusively while capillaries and arterioles remain unaffected. The endothelial cells develop temporary gaps between them due to their contraction resulting in vascular leakiness. It is mediated by the release of histamine, bradykinin, and other chemical mediators. The response begins immediately after injury, is usually reversible, and is for a short duration (15-20 minutes). An example of such an immediate transient response is a mild thermal injury of the skin of the forearm.
• Contraction or mild endothelial damage: In this mechanism, there is a structural reorganization of the cytoskeleton of endothelial cells that causes reversible retraction at the intercellular junctions or mild forms of endothelial damage. This change affects venules and capillaries and is mediated by cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF)-a. The onset of response occurs after delay of 4-6 hours following injury and lasts for several hours to days. A classic example of delayed and prolonged leakage is the appearance of sunburns mediated by ultraviolet radiation.
• Direct injury to endothelial cells: Direct injury to the endothelium causes cell necrosis and the appearance of physical gaps at the sites of detached endothelial cells. The process of thrombosis involving platelets and firin is initiated at the site of damaged endothelial cells. The change affects all levels of microvasculature (venules, capillaries and = arterioles). The increased permeability may either appear immediately after injury and last for several hours or days (immediately sustained leakage), or may occur after a delay of 2-12 hours and last for hours or days (delayed prolonged leakage). Examples of immediate sustained leakage are severe bacterial infections while delayed prolonged leakage may occur following moderate thermal injury and radiation injury.
• Leucocyte­mediated endothelial injury: Adherence of leucocytes to the endothelium at the site of inflammation may result in activation of leucocytes. The activated leucocytes release proteolytic enzymes and toxic oxygen species which may cause endothelial injury and increased vascular leakiness. This form of increased vascular leakiness affcts mostly venules and is a late response. The examples are seen in sites where leucocytes adhere to the vascular endothelium, For Example. in pulmonary venules and capillaries.
• Leakiness in neovascularization: In addition, the newly formed capillaries under the influence of vascular endothelial growth factor (VEGF) during the process of repair and in tumors are excessively leaky.

Question 2. Describe characteristic features of acute inflammation.
Answer:

Characteristic Features of Acute Inflammation

• The main characteristic features of acute inflammation are:
• Accumulation of fluid and plasma at the affected side.
• Intravascular activation of platelets.
• PMN as inflammatory cells.