What happens in the focus of inflammation
The term alteratio literally means "change". In the zone of inflammation, damage affects five key aspects:
- Structure: destruction of cellular and tissue elements.
- Metabolism: restructuring of metabolic processes.
- Physicochemical properties: alteration of the microenvironment in the focus.
- Spectrum of biologically active substances: synthesis of mediators of inflammation, pain, and hemostasis.
- Functions: impairment of the normal activity of the damaged area.
Zones of alteration
The damage process is heterogeneous and divided into two zones:
- Primary alteration: occurs instantaneously at the site of direct contact with the phlogistic agent. It is characterized by gross, often irreversible structural abnormalities.
- Secondary alteration: encompasses the periphery of the focus. It develops seconds or minutes later under the influence of metabolic disorders, inflammatory mediators, and impaired neural regulation. These changes are generally reversible.
Metabolic dynamics
Metabolic shifts during alteration go through two stages:
- Catabolic: prevails at the beginning of the process in both zones of alteration.
- Anabolic: dominates during the development of arterial hyperemia and proliferation. This is necessary to ensure local adaptive reactions aimed at destroying the agent and restoring tissue.
Briefly: answers to topical questions
What physicochemical changes occur in the focus of inflammation during alteration?
Pronounced shifts in physicochemical parameters occur in the focus of inflammation during alteration. The main ones include:
- Acidosis — a shift in pH towards the acidic side due to the accumulation of excess acidic metabolites.
- Hyperosmolarity — an increase in osmotic pressure resulting from the destruction of large organic molecules and salt hydrolysis.
- Hyperoncria — an increase in oncotic pressure due to an increased protein concentration and enhanced colloid hydrophilicity.
- Change in electrical properties — a decrease in surface charge, electrogenesis disorder, and alteration of cellular membrane potentials.
- Decrease in surface tension — affects cell membranes.
- Change in the colloidal state — occurs in the cell cytoplasm.
Which specific inflammatory mediators are synthesized at the stage of alteration?
At the stage of alteration, the spectrum of biologically active substances in the focus of inflammation changes: inflammatory mediators are formed. Sources list the following among cellular inflammatory mediators:
- Fatty acid derivatives and lipids — prostaglandins, leukotrienes, lipoperoxides.
- Biogenic amines — histamine, serotonin.
- Neuropeptides and neurotransmitters — norepinephrine, epinephrine, acetylcholine.
- Peptides and proteins — leukokinins, cytokines, enzymes.
- Nucleotides and nucleosides — adenine nucleosides, cyclic nucleotides, free nucleotides.
- Nitric oxide.
Sources also mention heparin, granulocytic factors, monokines, and lymphokines among cellular inflammatory mediators. Prostaglandins in combination with histamine, serotonin, bradykinin, and substance P are classified as pain mediators in inflammation.
A-A-A: Alteration — Agent (cause) — Adaptation (goal). Primary — direct, Secondary — surrounding.
Class and exam questions
What is the difference between primary and secondary alteration?
Primary alteration is caused by the direct action of a phlogistic factor, while secondary alteration is mediated by the indirect influence of mediators, metabolic shifts, and blood flow disturbances on surrounding tissues.
When does secondary alteration begin?
It develops a few seconds or minutes after exposure to the damaging factor.
Are structural changes mandatory during alteration?
Yes, structural changes in tissues and cells are an obligatory component of alteration, arising both from the direct action of the agent and the combined influence of secondary factors.
What else to study on this topic
- The role of inflammatory mediators in the formation of secondary alteration.
- Mechanisms of axonal transport impairment in inflammation.
- The relationship between physicochemical shifts and enzyme activity in the focus.
- The impact of microcirculatory disorders on the depth of tissue damage.
- Mechanisms of transition from catabolic to anabolic processes.
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