Classification by rate of development and course
The interaction of a phlogogenic (damaging) agent with tissues leads to the development of one of two forms of the inflammatory response. The classification is based on the speed of reaction unfolding and the overall duration of the process.
- Acute inflammation. It represents the classic, evolutionarily refined variant of the reaction. It develops intensively. With a normoergic course (adequate reactivity), the process takes 1–2 weeks. In the lesion, there are moderately pronounced phenomena of damage (alteration and destruction), fluid extravasation into tissues (exudation), and cell multiplication (proliferation).
- Chronic inflammation. Considered as a variant of inadequate development of the protective process.
The clinical picture is critically influenced by body reactivity:
- In a hypoergic course, all classic signs of inflammation are extremely weakly expressed, and the process proceeds sluggishly.
- In a hyperergic course, the reaction is excessive: severe alteration and massive destruction of own tissues come to the fore.
Features of chronic inflammation
Chronification of the process can follow two different scenarios:
- Primary chronic. Arises immediately after exposure to the phlogogenic agent, completely bypassing the acute phase. Initially distinguished by a persistent, prolonged, and sluggish character.
- Secondary chronic. Forms as an outcome of initially acute inflammation that did not resolve on time and acquired a protracted character.
Morphological markers of a chronic course:
- Appearance of areas of tissue necrosis.
- Pronounced monocytic and lymphocytic infiltration in the injury zone.
- Formation of specific structures — granulomas and protective capsules.
Main causes of chronification
There are five key groups of etiological factors that maintain prolonged inflammation:
- Persistence of infection (bacteria, protozoa, chlamydia, mycoplasmas, rickettsiae, spirochetes, fungi) with the parallel development of delayed-type hypersensitivity.
- Prolonged exposure of foreign factors to tissues (foreign bodies, organic and inorganic dust).
- Endocrine shifts, in particular — chronic stress with constantly high levels of catecholamines and glucocorticoids in the blood.
- Immune autoaggression (observed in systemic lupus erythematosus, rheumatoid arthritis).
- Phagocytic insufficiency (may be congenital, hereditary, or acquired).
Local signs of inflammation (LIRS)
Local manifestations of the inflammatory process are subdivided into local and general (systemic). Local signs were described in antiquity and are known as the classic Celsus-Galen pentad. In modern medical literature, this symptom complex is designated by the term LIRS (Local Inflammatory Response Syndrome).
The pentad includes:
- Rubor — redness;
- Tumor — swelling;
- Dolor — pain;
- Calor — heat (local temperature increase);
- Functio laesa — impairment of organ or tissue function.
Pathogenesis of redness (Rubor)
Visually, the sign manifests as hyperemia of the skin or mucous membranes directly over the inflammatory lesion. This is due to profound vascular changes:
- Arterial hyperemia develops.
- Dilation of precapillaries and an increase in their number occur.
- The number of functioning capillaries sharply increases, and they become engorged with arterial blood.
- Arterialization of venous blood is observed. Due to accelerated blood flow and reduced oxygen utilization by the damaged tissue, the content of oxyhemoglobin ($HbO_2$) in the venous bed is abnormally increased.
Briefly: answers to topical questions
What is the pathogenesis of the development of swelling (Tumor) in inflammation?
The pathogenesis of swelling (Tumor) development in inflammation lies in the exit of plasma and blood formed elements into tissues with the formation of exudate.
The process of inflammatory edema formation includes the following mechanisms:
- Exudation — the exit of the liquid part of the blood and cells from microvessels into tissues or body cavities.
- Action of mediators — release of histamine and bradykinin in response to injury.
- Vascular reactions — development of vasodilation and a sharp increase in vascular wall permeability.
As a result of these changes, enhanced filtration of fluid with a high protein content occurs outside the vascular bed, leading to an increase in tissue volume.
Which inflammatory mediators cause the development of pain syndrome (Dolor)?
The development of pain syndrome (Dolor) in inflammation is associated with the action of pain mediators.
Pain mediators include:
- Prostaglandins in a complex with histamine, serotonin, bradykinin, and substance P.
- Prostaglandins increase the sensitivity of pain receptors to algogens.
- Reduction of PGE₂ synthesis prevents the sensitization of pain receptors to chemical irritants such as bradykinin and histamine released in the inflammatory lesion.
Maximum release of pain mediators occurs during the exacerbation of a chronic inflammatory process.
The classic pentad of local signs is easy to remember as a rhythmic Latin tongue twister: “Rubor, tumor, calor, dolor et functio laesa” (Redness, swelling, heat, pain, and impairment of function).
Class and exam questions
What is the difference between primary and secondary chronic inflammation?
Primary chronic inflammation initially proceeds sluggishly and persistently, bypassing the acute stage. Secondary chronic develops as a continuation of an acute process that did not end in recovery and took on a protracted character.
Why does venous blood in the inflammation focus become "arterialized"?
This happens due to the acceleration of local blood flow and a decrease in oxygen consumption by damaged tissues. As a result, a high content of oxyhemoglobin ($HbO_2$) remains in the venous blood, which gives it a bright red color and causes the symptom of redness (Rubor).
How do hypoergy and hyperergy alter the picture of inflammation?
In a hypoergic course, the body's reactivity is reduced, so the signs of inflammation are weakly expressed. In a hyperergic course, the reaction is inadequately strong: the processes of alteration (damage) and tissue destruction predominate in the lesion.
What else to study on this topic
- Mechanisms of arterial hyperemia and exudation
- Pathogenesis of granuloma formation in chronic inflammation
- Role of delayed-type hypersensitivity in microbial persistence
- Types and causes of phagocytic deficiency
- Effects of glucocorticoids and catecholamines on the inflammatory response
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