Inflammation: Causes and Types

• Inflammation is a local response of living vascularized tissues to irritants, involving local vascular and cellular changes.

Aim of Inflammation

• Elimination of the irritant is the main goal.
• It involves the destruction of invading organisms.
• Toxins are inactivated during inflammation.
• The process prepares tissue for healing and repair.

Causes of Inflammation

• Physical agents like electricity, excess heat or cold, and radiation cause inflammation.
• Chemical agents, including concentrated acids and alkalies, are causes.
• Infectious agents such as viruses, bacteria, fungi, and parasites can be causative.
• Mechanical causes like crushing injuries, fractures, and foreign bodies induce inflammation.
• Necrotic tissue itself can trigger inflammation.

Types of Inflammation

• Acute inflammation is characterized by a rapid onset and short duration.
• It is associated with a high dose of irritant and involves acute inflammatory cells like neutrophils and macrophages.
• Chronic inflammation has a gradual onset and long duration.
• This type is related to a low dose of irritant and involves chronic inflammatory cells like lymphocytes, macrophages, giant cells, and eosinophils.
• Subacute inflammation grades in-between acute and chronic, indicating a level of severity and duration between the two.

Nomenclature of Inflammation

• Generally, inflammation naming convention includes the organ name with the suffix "itis".
• Gastritis refers to inflammation of the stomach.
• Orchitis refers to the inflammation of the testis.
• Glossitis refers to inflammation of the tongue.
• Hepatitis refers to inflammation of the liver.
• Appendicitis refers to inflammation of the appendix.
• Exceptions to the general rule include Pneumonia, which is inflammation of the lung, and Pleurisy, which is inflammation of the pleura.

Acute Inflammation

• An immediate response of living vascularized tissue to an irritant.
• The purpose is to deliver leukocytes and mediators from blood to the site of inflammation.

Pathogenesis of Acute Inflammation

• Local tissue damage occurs initially.
• A vascular response involves transient vasoconstriction followed by permanent vasodilation.
• There is increased vascular permeability and a slowing of blood stream.
• Dilatation of lymphatics also occurs.
• Cellular responses include exudation of leukocytes and phagocytosis.

Local Tissue Damage

• Irritants cause tissue damage and necrosis, which are maximum in the center around the irritant.
• This process releases chemical mediators.
• Mediators initiate and promote vascular and cellular changes.

Vascular Responses

• Transient vasoconstriction happens due to the direct effect of irritant on the vessel wall.
• Permanent vasodilation is due to the release of vasodilator chemical mediators like histamine.
• Increased vascular permeability is due to widened inter-endothelial gaps.
• This leads to the escape of protein-rich plasma fluid to the site of inflammation, forming inflammatory fluid exudate.
• Slowing of blood flow is due to vasodilation.
• Increased capillary permeability leads to the escape of plasma fluid, increasing blood viscosity (hemoconcentration).
• Resistance to blood flow by the swollen endothelium.
• Opening of new capillary buds.
• Dilatation of lymphatics leads to increased lymph flow, draining excess fluid back to blood.

Inflammatory Fluid Exudate

• Increased capillary hydrostatic pressure is a mechanism.
• Increased capillary permeability plays a major role.
• Increased osmotic pressure of interstitial tissue occurs due to the escape of plasma protein to tissue.
• High protein content (4-8gm%).
• Has a high specific gravity (above 1018).
• Appears turbid and yellowish due to the presence of many leukocytes and plasma protein, mainly fibrin.
• Dilutes toxins to minimize their effects on cells.
• Brings fibrinogen that changes into a fibrin network.
• Helps movement of acute inflammatory cells to the irritant site and surrounds the area of inflammation to localize infection.
• Acts as a framework for repair cells.
• Transports different types of antibodies to the site of inflammation.

Cellular Responses

• Cellular responses involve exudation of leukocytes and phagocytosis.

Exudation of Leukocytes

• Margination occurs due to stasis.
• Leukocytes leave the axial zone and adhere to the endothelial wall.
• Rolling is when leukocytes transiently stick along the endothelial cells.
• Adhesion is when leukocytes firmly stick to endothelial cells with the help of certain adhesion molecules.
• Emigration refers to the passage of WBCs through widened inter-endothelial gaps exiting the capillaries by ameboid movement.
• Neutrophils predominate for 24 - 48 hours, followed by macrophages.
• Chemotaxis is the attraction of leukocytes to the irritant site.
• This movement occurs along a concentration gradient of chemotactic substances, such as bacterial products, cytokines, C5a, and Leukotriene B4 (LT-B4).

Phagocytosis

• Phagocytosis is the recognition, engulfment, and destruction of irritants by phagocytic cells.
• Recognition and attachment occurs when leukocytes (neutrophils, macrophages) use cell surface receptors to recognize and attach to bacteria using specific antibodies (opsonins).
• Engulfment involves phagocytic cells forming cytoplasmic pseudopods around bacteria, enveloping it in a phagocytic vacuole (phagosome).
• The phagosome membrane fuses with the lysosome membrane, releasing lysosomal granules (phagolysosome).
• Killing and destruction happen through the release of lysosomal enzymes or oxygen-derived free radicals.