Phase 1: Ischemia and metabolic shift
The primary response to injury is a brief vascular spasm. It is triggered by the release of vasoconstrictors (endothelin, thromboxane, catecholamines) and a reflex response.
Biological significance: localization of the focus.
Consequences:
- Slowing of blood flow and erythrocyte stasis.
- Increased glycolysis leading to acidosis.
- Activation of lipid peroxidation, which damages cell membranes.
- Increase in osmotic pressure causing tissue swelling.
Phase 2: Arterial hyperemia
Spasm is replaced by vasodilation due to the accumulation of mediators: kinins, prostaglandins, adenosine. Vessels lose their sensitivity to nerve impulses ("paralysis"). This creates conditions for plasma leakage and the activation of plasma cascades (complement, fibrinolysis, coagulation).
Stage of exudation
A key stage characterized by the release of exudate — a fluid with a high protein content (over 2.5 g/L), formed elements, and decay products.
Mechanism:
- Increased vascular wall permeability under the influence of cytokines and mediators.
- Enhanced transendothelial transport.
- Destruction of the vascular basement membrane.
Venous hyperemia and hypoxia
Impaired blood outflow (passive hyperemia) is caused by microthrombosis, sludge phenomenon, and compression of venules by edematous tissue. This leads to hypoxia in the lesion, which further isolates the inflammatory zone and prevents the spread of toxins into the systemic circulation.
Briefly: answers to topical questions
What are the mechanisms of exudate extravasation?
The main factor in exudate leakage is an increase in vascular wall permeability. This process is mediated through the following mechanisms:
- Action of mediators — histamine, serotonin, bradykinin, and prostaglandins enlarge interendothelial gaps.
- Changes in endotheliocytes — a sharp increase in micropinocytosis and enhanced transendothelial plasma transport occur.
- Structural changes — destruction of glycosaminoglycans and basement membrane proteins, as well as contraction of endothelial cells driven by leukocyte enzymes.
- Direct endothelial damage — occurs upon exposure to physical, chemical, and biological factors.
How does exudate differ from transudate?
The key differential diagnostic criteria are protein content and the presence of blood cells.
| Parameter | Transudate | Exudate |
|---|---|---|
| Nature of the fluid | Non-inflammatory edema fluid | Inflammatory fluid |
| Protein content | Protein-poor fluid | Protein-rich fluid |
| Formed elements | Generally absent or solitary | Frequently contains leukocytes and erythrocytes |
| Formation mechanism | Hemodynamic and colloid-osmotic pressure disorder without endothelial damage | Increased vascular permeability due to alteration and inflammation |
| Specific gravity | Below 1.015–1.018 | Above 1.018 |
| Rivalta test | Negative | Positive |
| Properties | Transparent, does not clot spontaneously | Usually turbid, may clot if fibrin content is high |
What types of exudate are distinguished based on cellular and protein composition?
Depending on composition, four main types of exudative inflammation determine the nature of the exudate: serous, fibrinous, purulent, and putrefactive. Additional variants are distinguished that are not independent types:
- Catarrhal — mucus is mixed into the exudate (develops on mucous membranes).
- Hemorrhagic — erythrocytes are mixed into the inflammatory fluid.
- Mixed — represents a combination of different exudates.
Cellular and protein composition also determines fluid properties: a predominance of neutrophils is characteristic of purulent inflammation, lymphocytes for immune inflammation, and a high fibrin content leads to the clotting of fibrinous exudate.
Which cells emigrate into the acute inflammation focus first?
Neutrophilic leukocytes typically emigrate into the acute inflammation focus first (within 6–24 hours). However, the exact order of cell emigration primarily depends on the etiological factor:
- Neutrophilic leukocytes — arrive first in bacterial infections.
- Lymphocytes — migrate earlier than others in viral diseases and tuberculosis.
- Eosinophils — characteristic of immune-mediated inflammation.
After 24–48 hours, monocyte and lymphocyte emigration begins to predominate in the focus.
SAVE: Spasm -> Arterial hyperemia -> Venous hyperemia -> Exudation.
Class and exam questions
How does exudate differ from transudate?
Exudate is an inflammatory fluid with a high protein content (over 2.5 g/L), formed elements, and tissue decay products.
Why does acidosis occur in inflammation?
Due to ischemia, tissue respiration is impaired, forcing cells to switch to anaerobic glycolysis, producing lactic acid as a byproduct.
What is the role of venous hyperemia in inflammation?
It slows down blood flow, facilitating focal isolation, mediator accumulation, and creating conditions for leukocyte emigration.
What else to study on this topic
- The role of the complement system in inflammation activation.
- Mechanisms of leukocyte emigration (margination, adhesion, diapedesis).
- Biochemical properties of inflammatory mediators.
- Comparative characteristics of exudate types (serous, fibrinous, purulent).
- The effect of lymphostasis on the dynamics of inflammatory edema.
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