Inflammation: Types, Causes and Nomenclature

• Inflammation is a local response of living vascularized tissues to irritants, involving local vascular and cellular changes
• The aim of inflammation is to eliminate irritants, destroy invading organisms, inactivate toxins, and prepare tissue for healing and repair
• Inflammation can be caused by physical agents like electricity or radiation, chemical agents like concentrated acids, infectious agents like bacteria, mechanical causes like fractures, or necrotic tissue

Types of Inflammation

• Acute: Rapid onset, short duration, high irritant dose, involves neutrophils and macrophages
• Chronic: Gradual onset, long duration, low irritant dose, involves lymphocytes, macrophages, giant cells, and eosinophils
• Subacute: Grades in-between acute and chronic inflammation

Nomenclature of Inflammation

• Inflammation is named using the organ name plus the suffix "itis"
• Gastritis: inflammation of the stomach
• Orchitis: inflammation of the testis
• Glossitis: inflammation of the tongue
• Hepatitis: inflammation of the liver
• Appendicitis: inflammation of the appendix
• Exceptions include Pneumonia (inflammation of the lung) and Pleurisy (inflammation of the pleura)

Acute Inflammation

• Immediate response of living vascularized tissue to an irritant
• Aims to deliver leukocytes and mediators from blood to the site of inflammation

Pathogenesis of Acute Inflammation

• Local tissue damage
• Vascular response
• Cellular responses

Local Tissue Damage

• Irritants cause tissue damage and necrosis, which is greatest at the center around the irritant
• This process releases chemical mediators that initiate and promote vascular and cellular changes

Vascular Responses

• Transient vasoconstriction occurs due to the direct effect of the irritant on the vessel wall
• Permanent vasodilation results from the release of vasodilator chemical mediators such as histamine
• Increased vascular permeability occurs due to widened inter-endothelial gaps leading to the escape of protein-rich plasma fluid to the site of inflammation with the formation of inflammatory fluid exudate
• Slowing of blood flow is due to vasodilation, increased capillary permeability, hemoconcentration, swollen endothelium resistance, and the opening of new capillary beds
• Dilation of lymphatics increases lymph flow in inflammation, which helps drain excess fluid back to the blood

Inflammatory Fluid Exudate

• Formation: Increase capillary hydrostatic pressure, increase capillary permeability, increased osmotic pressure of interstitial tissue due to plasma protein escape
• Composition: High protein content (4-8%), high specific gravity (above 1018), turbid and yellowish due to leukocytes and plasma protein (fibrin)
• Functions: Dilutes toxins, brings fibrinogen to form a fibrin network to aid cell movement/localize infection/act as framework, transports antibodies

Cellular Responses

• Exudation of leukocytes
• Phagocytosis

Exudation of Leukocytes

• Margination: Leukocytes leave the axial zone and adhere to the endothelial wall due to stasis
• Rolling: Leukocytes stick transiently along the endothelial cells
• Adhesion: Leukocytes firmly stick to endothelial cells with the help of adhesion molecules
• Emigration: White blood cells pass through widened inter-endothelial gaps and outside the capillaries via ameboid movement; neutrophils predominate for 24-48 hours, then macrophages predominate
• Chemotaxis: Leukocytes are attracted to the site of irritant along a concentration gradient of chemotactic substances (bacterial products, cytokines, C5a, Leukotriene B4)

Phagocytosis

• Recognition, engulfment, and destruction of irritants by phagocytic cells

Steps of Phagocytosis

• Recognition and Attachment: Leukocytes (neutrophils, macrophages) use cell surface receptors to recognize and attach to bacteria with the help of opsonins
• Engulfment: Phagocytic cells form cytoplasmic pseudopods around the bacteria, enveloping it in a phagocytic vacuole (phagosome); the phagosome membrane fuses with the lysosome membrane, releasing lysosomal granules (phagolysosome)
• Killing and Destruction: Achieved through the release of lysosomal enzymes or oxygen-derived free radicals