Acute inflammation is a protective and adaptive host response triggered by tissue injury and culminating in repair. The process begins with the alteration phase, which activates vascular and immune defense mechanisms.
Triggering mechanismAlteration is the initial stage, during which inflammatory mediators are released.
Biochemical shiftPredominance of catabolism leads to acidosis and the activation of lysosomal hydrolases.
Biological purposeNecrosis in the inflammatory focus helps localize and destroy the pathogenic factor.
Duration of the acute processAcute inflammation typically lasts from 1.5 to 2 weeks, with a maximum of up to 6 weeks.
Alteration Stage: Initiation of the Process
Alteration is tissue damage that serves as the trigger for the entire cascade of inflammatory reactions. It proceeds in two phases:
Biochemical phase: metabolism in the injury zone shifts toward catabolism. The breakdown of proteins, fats, and carbohydrates leads to the accumulation of metabolic products and the development of acidosis. Acidification of the environment activates lysosomal enzymes, causing secondary cell damage.
Morphological phase: characterized by the formation of "cellular cooperation." This is a coordinated effort of cells with a division of labor that ensures the cyclicity and regulation of the inflammatory response.
The Role of Necrosis in Inflammation
Despite its negative perception, the development of necrosis in the inflammatory focus is a biologically purposeful process. Its goal is to isolate and destroy the aggressor as quickly as possible.
Mechanism: cells release hydrolases, and thrombi form in small vessels around the focus. This creates a barrier limiting the spread of damage.
Outcome: following pathogen elimination, the dead tissue is replaced through repair, restoring the original function of the organ.
Clinico-Anatomical Forms
Depending on which process predominates, two main forms of inflammation are distinguished:
Form
Leading Process
Exudative
Exudation (fluid and cellular extravasation)
Proliferative
Proliferation (cell multiplication)
Note: "Alterative inflammation" is no longer distinguished as a separate type in modern classification, as it merely represents necrosis without a full vascular-mesenchymal reaction.
Mnemonic
A-B-C: Alteration triggers Biochemistry, which leads to Circulation changes (exudation and proliferation).
Frequently asked questions
Which inflammatory mediators are released during the alteration stage?
Cellular and plasma (humoral) inflammatory mediators are released during the alteration stage. Substances with vasodilatory effects accumulate in the injury zone:
Kinin system components — cause vasodilation.
Prostaglandin E2 — promotes vasodilation.
Adenosine — participates in vascular reactions.
Complement components — activated by tissue mediators.
These biologically active substances provide chemical links between reactions in the focus, alter metabolism, and shape local and systemic signs of the inflammatory process.
Which cells participate in the formation of "cellular cooperation" during the morphological phase of alteration?
Resident mediator-producing cells that are the first to enter the injury zone participate in primary cellular cooperation. These include:
Resident macrophages — occupy a central place, produce colony-stimulating factors, and participate in establishing primary cooperation.
Mast cells — initiate the process by releasing biologically active substances.
Eosinophils — participate in initiating inflammation.
NK cells (natural killers) — also present at the initial stage.
As a result of their interaction, autoregulatory mechanisms emerge and functions are divided among the cells.
What microcirculatory changes occur following the alteration stage?
The alteration stage is followed by the vascular reaction, which marks the onset of the exudative stage. The following changes develop in the microvasculature:
Transient vasoconstriction — quickly replaced by vasodilation.
Hyperemia (arterial) — occurs due to the accumulation of vasodilatory mediators and enhanced parasympathetic influences.
Vascular "paralysis" — loss of the ability to respond to neural and humoral influences.
Increased permeability — leads to increased escape of blood plasma from the vessel and subsequent emigration of formed blood elements.
Which etiologic factors can cause primary tissue alteration?
Primary tissue alteration is caused by the direct action of exogenous and endogenous phlogistic agents. The main etiologic factors include:
Biological factors — viruses, parasites, bacteria, as well as immune complexes and antibodies.
Physical factors — radiation and electrical energy, high and low temperatures (burns, frostbite), mechanical trauma.
Chemical factors — exogenous (poisons, toxins, chemicals) and endogenous (toxins produced within the body, e.g., in uremia).
The impact of these factors leads to tissue structure damage and severe physical and chemical disruptions at the site of direct contact.
What are the possible outcomes of acute inflammation?
The possible outcomes of acute inflammation include:
Resolution/Healing — the most common outcome.
Death or disability — possible depending on severity and organ involvement.
Inflammation terminates via repair after the damaging factor is destroyed and eliminated.
Why is alterative inflammation no longer considered an independent type?
Because it lacks a full vascular-mesenchymal reaction, and the process itself is limited strictly to tissue necrosis.
How does acidosis affect the development of inflammation?
Acidosis activates lysosomal hydrolases, which exacerbate secondary cell damage, and stimulates nerve endings, causing pain.
How does acute inflammation differ from chronic inflammation in duration?
Acute inflammation lasts up to 6 weeks (most commonly 1.5–2 weeks), whereas chronic inflammation lasts longer than 6 months.
Go deeper
Mechanisms of vascular tone regulation during inflammation.
Classification of exudates and their morphological differences.
Features of proliferative inflammation in infectious diseases (typhoid, rabies).
Interrelation between the immune system and the alteration phase.