History of study and classical signs
The history of the doctrine dates back to the works of Hippocrates. Classical pathology distinguishes five main signs of inflammation:
- Rubor (redness) — described by A. Celsus.
- Tumor (swelling) — identified by A. Celsus.
- Calor (heat) — noted by A. Celsus.
- Dolor (pain) — identified by A. Celsus.
- Functio laesa (loss of function) — added by C. Galen.
Etiology and causes of inflammation
Factors causing the pathological process are called phlogogens. They are divided into three large groups:
- Biological: various infectious agents ranging from viruses to parasites, as well as immunological factors and aseptic causes (e.g., breakdown of necrotic tissues).
- Physical: mechanical trauma, extreme temperatures (burns and frostbite), electrical and radiation energy.
- Chemical: exogenous poisons and toxins, as well as endogenous metabolic products formed inside the body under pathological conditions.
Mandatory components of the process
Full-blown inflammation consists of three inseparable local reactions:
- Alteration — primary tissue damage.
- Exudation — escape of the liquid part of blood and elements into the focus.
- Proliferation — cell multiplication for repair.
Diagnostic benchmark: isolated damage is called necrosis, exudation alone is edema, and pure proliferation is characteristic of tumors.
Biological significance
From a general biological standpoint, inflammation is evaluated as a perfect protective and adaptive reaction developed in the course of evolution. According to I.V. Davydovsky's concept, for humanity as a whole, it is the most important mechanism of adaptation and acquisition of immunity. However, for an individual with reduced reactivity, the inflammatory reaction may take on severe disease features and lead to a fatal outcome due to imperfect compensatory capabilities.
Briefly: answers to topical questions
Which specific substances belong to endogenous chemical phlogogens?
Endogenous chemical phlogogens include substances formed directly in the body:
- Toxins formed during uremia or azotemia.
- Excess enzymes.
- Reactive oxygen species.
What types of exudative inflammation are distinguished depending on the nature of the formed exudate?
Depending on the composition of the resulting exudate, four main types of exudative inflammation are distinguished. These include:
- Serous — main type.
- Fibrinous — main type.
- Purulent — main type.
- Putrid — main type.
Additionally, variants of inflammation are distinguished that are not independent types:
- Catarrhal (catarrh) — develops on mucous membranes, mucus is mixed into the exudate.
- Hemorrhagic — erythrocytes are mixed into the exudate.
- Mixed — combination of different exudates.
What types of productive (proliferative) inflammation exist?
Productive (proliferative) inflammation is classified into several main types. The following forms are distinguished:
- Interstitial (interstitial) — diffuse inflammation.
- Granulomatous — formation of granulomas.
- Inflammation around animal parasites and foreign bodies — aimed at walling off the irritant.
Inflammatory hyperplastic growths (polyps, condylomata acuminata) are not essentially productive inflammation, representing a hyper-regenerative epithelial reaction to chronic exudative inflammation.
Which inflammatory mediators are cellular and which are plasma-derived?
Inflammatory mediators are subdivided into cellular and plasma (humoral) depending on their origin.
| Mediator group | Representatives |
|---|---|
| Cellular | Histamine, heparin, serotonin, granulocytic factors, monokines, lymphokines. |
| Plasma-derived | Components of the complement system, plasmin system, and blood clotting system. |
These substances act together, providing chemical links between reactions in the inflammatory focus and concentrating efforts on removing damaging factors.
Which cells emigrate first from blood vessels into the focus during acute inflammation?
Neutrophilic leukocytes are the first to emigrate from blood vessels into the focus of acute inflammation. Their exit occurs in the first 6–24 hours from the onset of the inflammatory process. After 24–48 hours, the picture changes, and the emigration of monocytes and lymphocytes begins to predominate. After performing their digestive function, polymorphonuclear leukocytes die, and the synthesis of enzymes in macrophages increases in the focus to clear the inflammatory field.
The three pillars of inflammation: A-E-P (Alteration, Exudation, Proliferation). Without all three, the diagnosis of "inflammation" cannot be made!
Class and exam questions
How are the names of inflammatory processes correctly formed?
In most cases, the suffix "-itis" is added to the Latin or Russian name of the organ (e.g., myocardium — myocarditis, liver — hepatitis). Historical exceptions include angina, pneumonia, and empyema.
How does inflammation at the species level differ from that at the individual level?
At the level of humanity, inflammation acts as a flawless protective reaction, forming adaptation and immunity. In a specific patient, it can become a disease and lead to death due to individual insufficiency of defenses.
What are phlogogens?
These are pathogenic factors of exogenous or endogenous nature (biological, chemical, physical) capable of triggering an inflammatory response.
What else to study on this topic
- Nomenclature of inflammation and historical exceptions (angina, pneumonia, empyema)
- Contributions of scientists H. Boerhaave, K. Rokitansky, and R. Virchow to the doctrine of inflammation
- Debated questions on the relative teleological utility of inflammation and Charles Darwin's views
- Physiological analogues of inflammation: the menstrual cycle and dualistic processes
- Dependence of the inflammatory process course on the body's reactivity and localization
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