Understanding Inflammation

Inflammation

• Inflammation is a local defensive response of the body to tissue damage and is considered a syndrome
• Noxious stimuli of various kinds can trigger it
• Naming inflammation includes the suffix "-itis"
• It can cause death if developed in vital organs
• It limits the noxa and destroys it, but in some occasions, inflammatory process may be excessive and cause harm

Causes of Inflammation

• Physical: Traumas, heat, cold, burns, radiation, etc
• Chemical: Toxins, irritants, poisons, drugs, etc
• Biologic: Bacteria, viruses, fungi, etc

Inflammation and the Histion

• At the level of organization, inflammation occurs in the histion, the unit of inflammation
• Inflammation does not occur in cells, tissues or organs
• Examples of histiones include the nephron, hepaton, and pneumon

Signs of Inflammation

• Heat/Calor: Sign caused by increased blood flow in the inflammatory focus
• Erythema: Redness. Sign caused by increased blood flow in the inflammatory focus
• Swelling/Tumoración: Sign caused by increased cells and fluid in the inflammatory focus
• Pain/Dolor: A symptom due to the release and action of inflammatory mediators on the nerves in the focus and compression by the increase in the number of cells
• Loss of Functionality: Occurs on occasion

Aspects of the inflammatory process

• Focus of the Response: Inflammation tends to limit the injured area to prevent damage from spreading in the body. An inflammatory focus is formed in the lesion area
• Nonspecific Process: Responds to any insult and does not vary between tissues or individuals

Phases of the inflammatory response

• Vascular reaction
• Cell reaction

Vascular reaction

• A transient arterial vasoconstriction occurs first due to stimulation of the vasoconstrictor nerves in the inflammatory focus
• Aspirin and other analgesics inhibits substances that causes pain
• An arterial vasodilation and consequent increase in blood flow (active hyperemia) occurs secondly due to the release of vasodilating substances such as histamine (main vasodilator), serotonin, prostaglandins, quinines, etc
• Due to vasodilation and active hyperemia, erythema and heat are produced in the inflammatory focus
• An increase in vascular permeability then occurs as endothelial cells contract, leaving gaps, resulting in vascular filtration, which equates to a loss of blood elements such as plasma
• Inflammatory exudate accumulates in interstitial tissue, causing swelling, increased blood viscosity, and slower blood flow
• Stasis finally occurs: Decrease in the speed of blood flow

Cell Phases

• Margination: Leukocytes line up on the periphery of the blood vessel
• Adhesion: Leukocytes adhere to the endothelium
• Migration: Leukocytes migrate through the vessel wall to the interstitial tissue by diapedesis
• The leukocytes change their shape, lengthen, flatten, emit pseudopods upon passing through the space
• Chemotaxis- factors are inflammatory mediators
• Phagocytosis- Leukocytes that have extravasated and are in the tissue carry out phagocytosis, digesting foreign particles
• Leukocytes will release leukocidal products that help eliminate the damaging agent, but will also cause cellular injury

Other aspects of the inflammatory response

• Purulent exudate which exits a vessel and enters tissue is rich in leukocytes and contains the majority of dead neutrophils
• Pus can exit if the lesion is superficial or create an abscess if the lesion is internal
• Macrophages and mast cells travel from the connective of the histion to the focus, presenting specific receptors capable of recognizing the existence of foreign particles
• Macrophages release cytokines, such as IL-1 and TNF-α, which help trigger inflammation; mast cells release histamine and serotonin (vasodilators)
• Fibrin forms a network to limit the inflammatory focus, preventing the components from expanding to other areas of the body
• Inflammatory mediators include prostaglandins, quinines, histamine, serotonin, cytokines (IL-1, TNF-α), PAF (platelet activating factor), and heparin (which inhibits coagulation, thinning the blood so it better reaches the focus)

Types of Inflammation

• Acute: Begins abruptly with obvious symptoms and is short in duration and is characterized by an exudate in which leukocytes (mostly PMNs) and plasma (leading to edema) predominate. Appears in first contact with a particular insult
• Chronic: Installed gradually and slowly with dull symptoms and is long in duration, and is characterized by an exudate composed of lymphocytes (more abundant), macrophages and fibroblasts, and the presence of angiogenesis and fibrosis
• Necrosis may also appear and tissue formation prevails over the exudate

Exudate on Inflammation

• Serous Inflammation predominates blood serum, containing in turn a low concentration of cells and the blood lesion is represented by an inflammatory edema due to the liquid prevailing in the serum.

Types of inflammation cont.

• Purulent inflammation predominate leukocytes, especially acting PMN against foreign particles that produce pus. "While there is pus, there is no cure."
• Fibrinous inflammation predominates fibrin in the exudate which forms white-yellowish membranes
• Hemorrhagic inflammation predominates erythrocytes in the exudate, usually caused by severe infections

Other inflammations

• Mucosal: If the PMNs are dominant, a mucopurulent exudate is produced and therefore a mucopurulent inflammation is present. Typically acute, but can be chronic

Inflammatory response to infection cont.

• Suppurative Inflammation: characterized by increased vascular permeability and leukocyte infiltration mainly by polymorphonuclear neutrophils that are attracted to the site of infection by bacterial chemotactic substances, causing pus-filled abscesses.
• Mononuclear Inflammation: appears in the form of diffuse interstitial infiltrates, predominantly mononuclear (lymphocytes) that go to the focus in response to the infectious agent.
• Granulomatous Inflammation: accumulation of epithelioid cells (flattened macrophages as epithelium) and multinucleated giant cells that form a granuloma to isolate the microorganism and prevent it from expanding.
• With cytopathic-cytoproliferative inflammation viruses can produce stimulation of the cells forming a mass, and HPV/HSV may result
• Necrotizing Inflammation: Produced by microorganisms that secrete toxins that severely damage cells, causing death or necrosis without significant inflammatory infiltrate

Chronic Inflammation and Scarring

• Chronic inflammation can lead to total healing or fibrosis (repair, scarring) causing dysfunction.

Additional Notes

• Scarring is the repair of damaged tissue that has lost the capacity to regenerate
• Regeneration can be understood as the substitution of an injured tissue with an identical one, while repair or scarring is the substitution of the injured tissue with another different one
• Factors facilitating the development of tissue repair comprise of low regenerative capacity in the damaged tissue, great loss of substance, destruction of the parenchyma of the tissue
• All tissues release and secrete inflammation mediators, although the major ones come from mast cells, and cytokines