Local manifestations of inflammation
The classic picture of tissue inflammation consists of several interrelated processes.
Swelling (tumor) manifests as tissue edema and elevation. It arises due to a sharp increase in blood filling (arterial and venous hyperemia develop), enhanced lymph formation, fluid leakage of blood into the interstitium, and active cell proliferation in the focus.
Temperature elevation in the damage zone is caused by three factors:
- An influx of warmer arterial blood from the body core.
- A sharp activation of local metabolism.
- Uncoupling of oxidation and phosphorylation. Due to an excess of free fatty acids and calcium ions, energy is not stored in ATP molecules but is dissipated as heat.
Receptor irritation (the basis of the pain syndrome) is of chemical and mechanical nature. Nerve endings react to inflammatory mediators (histamine, serotonin, kinins, prostaglandins) and tissue acidosis caused by the accumulation of acidic metabolites (lactate and pyruvate). In addition, accumulating exudate compresses tissues mechanically.
Impaired function (functia laesa) is the fifth local sign. Function suffers both from the direct damaging action of the phlogistic factor and from subsequent vascular reactions, alteration, and exudation. The scale of the problem depends on localization: a specific organ usually suffers, but when inflammation occurs in vital structures (brain, heart, liver, endocrine glands), the vital activity of the entire organism is threatened.
Systemic reactions of the body
The response to injury is not limited to a single area. The sympathoadrenal system and the hypothalamus-pituitary-adrenal cortex axis are involved in the process, which is a classic component of the stress response.
Seven main general (systemic) signs of inflammation are distinguished:
- Leukocytosis (in rare cases, leukopenia).
- Fever.
- Elevated ESR (erythrocyte sedimentation rate).
- Dysproteinemia (a shift in the ratio of blood protein fractions).
- Dysfermentemia (changes in enzyme activity in biological fluids).
- Shifts in the hemostasis system (coagulation, anticoagulation, and fibrinolytic links).
- General disorders of vital activity (intoxication, general malaise).
Pathophysiology of key general signs
Leukocytosis is an increase in the number of white blood cells. The process is triggered by the phlogistic agent itself (especially of bacterial nature) and breakdown products of own tissues. These substances block proliferation inhibitors and stimulate the production of leukopoietins. Leukocytosis plays a crucial adaptive role: cells migrate to the focus, localize and destroy pathogens, clear away dead tissues, and secrete biologically active substances to regulate immunity. Evaluation of shifts in the leukocyte formula is critically important for diagnosis and prognosis.
Fever develops under the action of pyrogenic substances (interleukins 1 and 6, tumor necrosis factor alpha, prostaglandins). A moderate temperature rise is beneficial: it hinders microbial reproduction, reduces their resistance to drugs, activates the immune system, and spurs metabolism. However, excessive fever exhausts reserves and reduces the body's resistance.
Dysproteinemia reflects the restructuring of protein metabolism. The globulin fraction increases due to the activation of the humoral link of immunity, while albumin synthesis in the liver drops during severe inflammation.
ESR acceleration is associated with the appearance of substances with proaggregant action in the blood. The mechanism includes several links:
- Influence of high-molecular-weight proteins: acute-phase proteins (fibrinogen, C-reactive protein, ceruloplasmin, globulins) are adsorbed on erythrocytes, accelerating their sedimentation.
- Influence of cations: hydrogen, potassium, and calcium ions eliminate the natural negative charge of undamaged erythrocytes. Re-charging occurs, and oppositely charged cells are attracted to each other (Coulombic convergence).
- Influence of glycoproteins: adhesive transmembrane molecules additionally glue cells together (especially in immunopathological conditions and tumor growth).
Briefly: answers to topical questions
What are the 5 classic local signs of inflammation?
There are five classic local signs of inflammation, described by Latin terms:
- Redness (Rubor / Hyperemia) — caused by inflammatory hyperemia;
- Swelling (Tumor / Edema) — elevation, tissue edema;
- Pain (Dolor);
- Local temperature rise (Calor) — associated with arterial hyperemia, metabolic activation, and uncoupling of oxidation and phosphorylation;
- Impaired function (Functio laesa) — impairment of specific or nonspecific function.
An additional diagnostic sign in the presence of fluid, including pus, in the focus is fluctuation (waving).
Which inflammatory mediators cause arterial hyperemia in the focus?
Arterial hyperemia in the focus of inflammation is caused by the formation and action of vasoactive substances — inflammatory mediators. By origin, inflammatory mediators are subdivided into cellular and humoral.
These endogenous substances accumulate at the site of tissue alteration and suppress the automatism of the smooth muscle walls of microcirculatory vessels. As a result, relaxation of the vascular wall occurs (myoparalytic effect), leading to an increase in blood pressure in microvessels, an increase in blood flow volume, and an increase in the extent of blood flow through the capillary network.
To easily recall the main systemic signs of inflammation, divide them into three logical groups: Cells (leukocytosis), Plasma (dysproteinemia, dysfermentemia, ESR acceleration, hemostasis shifts), and General State (fever, intoxication).
Class and exam questions
Why does temperature locally rise in the focus of inflammation?
This happens due to the influx of warm arterial blood, a sharp acceleration of local metabolism, and the uncoupling of oxidation and phosphorylation processes, in which energy is dissipated as heat rather than stored in ATP.
Why does the body need a fever during inflammation?
Moderate fever is an adaptive response. It suppresses the reproduction of many microorganisms, makes them more vulnerable to drugs, and stimulates the immune system.
How do acute-phase proteins affect the erythrocyte sedimentation rate (ESR)?
High-molecular-weight proteins (fibrinogen, C-reactive protein, globulins) are adsorbed on erythrocyte membranes. This promotes their adhesion (aggregation) and faster sedimentation to the bottom of the test tube.
What causes receptor irritation and pain in the area of inflammation?
Receptors are irritated chemically (by inflammatory mediators and acidic metabolites causing tissue acidosis) and mechanically (due to compression of nerve endings by accumulating exudate).
What else to study on this topic
- Mechanisms of development of arterial and venous hyperemia in the focus of inflammation
- The role of specific mediators (histamine, serotonin, kinins) in pathogenesis
- The effect of tissue acidosis on the development of the inflammatory reaction
- Changes in the leukocyte formula and their clinical significance
- Pathogenesis of the stress response and the role of the endocrine system in tissue injury
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