What is chemotaxis?

After exiting the circulation, leukocytes move in the tissues toward the site of injury by a process called chemotaxis, which is defined as locomotion along a chemical gradient. 

Both exogenous and endogenous substances can act as chemoattractants. 

Exogenous agents are bacterial products, including peptides that possess an N-formylmethionine terminal amino acid and some lipids. 

Endogenous chemoattractants include several chemical mediators 

(1) Cytokines, particularly those of the chemokine family

(2) Components of the complement system, particularly C5a

(3) Arachidonic acid (AA) metabolites, mainly leukotriene B4.

Mechanism of Increased Vascular Permeability in Acute Inflammation

Several mechanisms involved in increased vascular permeability in acute inflammation:

1. Contraction of endothelial cells resulting in increased interendothelial spaces is the most common mechanism of vascular leakage.
2. Endothelial injury, resulting in endothelial cell necrosis and detachment.
3. Increased transport of fluids and proteins, called transcytosis, through the endothelial cell. This process may involve intracellular channels that may be stimulated by certain factors, such as vascular endothelial growth factor (VEGF), that promote vascular leakage.

What vascular changes occur in acute inflammation?

Vascular changes in acute inflammation are as follows:

1. Vasodilation is induced by the action of several mediators, mainly histamine, on vascular smooth muscle.
2. Vasodilation is quickly followed by increased permeability of the microvasculature.
3. Engorgement of small vessels with slowly moving red cells, a condition termed stasis,
   which is seen as vascular congestion and localized redness of the involved tissue.
4. As stasis develops, blood leukocytes, principally neutrophils, accumulate along the vascular endothelium.

What are the components of acute inflammation?

There are three components of acute inflammation:

1. Dilation of small vessels leading to an increase in blood flow, 
2. Increased permeability of the microvasculature enabling plasma proteins and leukocytes to leave the circulation.
3. Emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent

Define Inflammation. What are the cardinal features of acute inflammation?

Inflammation: Inflammation is a response of vascularized tissues to infections and damaged tissues that brings cells and molecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offending agents.

Cardinal features of acute inflammation:(Hallmark of acute Inflammation).

1. Rubor (Redness)
2. Tumor (Swelling)
3. Calor (Heat)
4. Dolor (Pain)
5. Functio laesa (Loss of function)

Dystrophic calcification.

Pathologic calcification is the abnormal tissue deposition of calcium salts, together with smaller amounts of iron, magnesium, and other mineral salts.
There are two form of pathologic calcification.

• Dystrophic calcifation: When the deposition occur locally in dying tissues it is known as dystrophic calcification. Here - 

• Normal serum calcium level.
• Absence of derangement in calcium metabolism.

• Metastatic calcification: Deposition of calcium salts in otherwise normal tissues.
• Almost always results from hypercalcemia secondary to some disturbance in calcium metabolism.

Example of dystrophic calcification:

1. In areas of necrosis whether they are of coagulative, caseous or liquefactive type and in foci of enzymatic necrosis of fat.
2. Atheromas of advanced atherosclerosis.

Although dystrophic calcification is a tell-tale sign of previous cell injury it is often a cause of organ dysfunction such in case of calcific valvular disease and atherosclerosis.