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Pathological Anatomy · Inflammation

Stages of acute inflammation

*Inflammatio acuta*

Acute inflammation is a protective and adaptive bodily reaction triggered by tissue damage and culminating in repair. The process begins with the alteration phase, which engages vascular and immune defense mechanisms.

Trigger mechanismAlteration is the initial stage during which inflammatory mediators are released.
Biochemical shiftThe predominance of catabolism leads to acidosis and the activation of lysosomal hydrolases.
Biological purposeNecrosis in the inflammation focus helps localize and destroy the pathogenic factor.
Duration of the acute processAcute inflammation typically lasts from 1.5 to 2 weeks, up to a maximum of 6 weeks.
4 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Alteration stage: onset of the process

Alteration is tissue damage that serves as a trigger for the entire cascade of inflammatory reactions. It proceeds in two phases:

  1. Biochemical phase: in the damage zone, metabolism shifts toward catabolism. The breakdown of proteins, fats, and carbohydrates leads to the accumulation of metabolic products and the development of acidosis. Medium acidification activates lysosomal enzymes, causing secondary cell damage.
  2. Morphological phase: characterized by the formation of "cellular cooperation". This is coordinated cell work with a division of functions that ensures the cyclicity and regulation of the inflammatory response.

Role of necrosis in inflammation

Contrary to the negative perception, the development of necrosis in the inflammation focus is a biologically purposeful process. Its task is to isolate and destroy the aggressor as quickly as possible.

  • Mechanism: cells release hydrolases, and thrombi form in the small vessels around the focus. This creates a barrier limiting the spread of damage.
  • Outcome: after pathogen elimination, the dead tissue is replaced during repair, restoring the original function of the organ.
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Clinical and anatomical forms

Depending on which process predominates, two main forms of inflammation are distinguished:

MorphologyLeading process
ExudativeExudation (fluid and cell extravasation)
ProductiveProliferation (cell multiplication)

Important: "Alterative inflammation" is not distinguished as a separate type in modern classification, as it represents merely necrosis without a full-fledged vascular-mesenchymal reaction.

Briefly: answers to topical questions

Which inflammatory mediators are released during the alteration stage?

During the alteration stage, cellular and plasma (humoral) inflammatory mediators are released. Substances with vasodilatory action accumulate in the damage zone:

  • Kinin — 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 form local and systemic signs of the inflammatory process.

Which cells participate in the formation of "cellular cooperation" in the morphological phase of alteration?

The formation of primary cellular cooperation involves resident producer cells of mediators that enter the damage zone first. These include:

  • Resident macrophages — occupy a central place, produce colony-stimulating factors, and participate in creating primary cooperation.
  • Labrocytes (mast cells) — initiate the process by releasing biologically active substances.
  • Eosinophils — participate in the initiation of inflammation.
  • NK cells (natural killers) — are also present at the initial stage.

As a result of their interaction, autoregulatory mechanisms arise and a division of functions occurs among the cells.

What microcirculatory changes occur following the alteration stage?

Following the alteration stage, a vascular reaction is engaged, marking the launch of the exudation stage. The following changes develop in the microvasculature:

  • Short-term spasm — rapidly replaced by vessel expansion.
  • Arterial hyperemia — occurs due to the accumulation of vasodilatory mediators and increased parasympathetic influences.
  • Vessel "paralysis" — loss of ability to respond to neural and humoral influences.
  • Increased permeability — leads to increased blood plasma output from the vessel followed by the emigration of formed blood elements.

Which etiological factors can cause primary tissue alteration?

Primary tissue alteration is caused by the direct action of exogenous and endogenous phlogistic agents. The main etiological factors include:

  • Biological factors — viruses, animal 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 formed in the body, e.g., in uremia).

The action of these factors leads to tissue structure damage and gross physical and chemical disturbances at the site of direct contact.

What are the possible outcomes of acute inflammation?

The possible outcomes of acute inflammation are:

  • Recovery — the most frequent outcome.
  • Death or disability — possible.
  • Inflammation culminates in repair after the destruction and elimination of the damaging factor.
How to memorize

A-B-C: Alteration triggers Biochemistry, which leads to Inflammation (exudation and proliferation).

Class and exam questions

Why is alterative inflammation no longer considered an independent type?

Because it lacks a full-fledged vascular-mesenchymal reaction, and the process is limited solely to tissue necrosis.

How does acidosis affect the development of inflammation?

Acidosis activates lysosomal hydrolases, which enhance secondary cell damage and irritate nerve endings, causing pain.

How does acute inflammation differ from chronic inflammation in terms of duration?

Acute inflammation lasts up to 6 weeks (more often 1.5–2 weeks), whereas chronic inflammation lasts more than 6 months.

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What else to study on this topic

  • Mechanisms of vascular tone regulation in inflammation.
  • Classification of exudates and their morphological differences.
  • Features of proliferative inflammation in infectious diseases (typhus, rabies).
  • Relationship between the immune system and the alteration phase.
  • Pathogenesis of pain syndrome in the inflammation focus.

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