Questions and Answers
What is the primary reason for surgically draining an abscess?
What is a fistula?
What is the primary characteristic of chronic inflammation?
Which of the following is NOT a constituent of exudate?
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What is the role of chemotactic factors in inflammation?
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Which of the following is NOT a vasoactive mediator?
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Which of the following factors contributes to the formation of exudate?
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What is the difference between a sinus and a fistula?
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What is the primary function of macrophages during the demolition phase of inflammation?
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What can occur if the demolition phase is delayed?
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Which mediators contribute to the termination of an acute inflammatory response?
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What characterizes suppuration in the context of inflammation?
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What is pus primarily composed of?
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What happens to a necrotic injury site due to neutrophil action?
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What is the role of the pyogenic membrane in an abscess?
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What indicates the ongoing inflammatory response in the development of an abscess?
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Study Notes
Demolition in Inflammation
- Achieved by macrophages, also known as scavenger cells, which remove all tissue debris from the site of inflammation.
- Delayed demolition can lead to the replacement of fibrin and dead tissue with fibrous tissue, resulting in adhesion.
Termination of Acute Inflammatory Response
- The inflammatory response must be actively terminated to prevent unnecessary tissue damage.
- This is achieved through:
- Cessation of chemical mediators, which have short half-lives and are degraded shortly after release.
- Production of anti-inflammatory lipoxins and cytokines, such as Transforming growth factor-beta (TGF-β).
- Cholinergic neural impulses that inhibit the production of TNF in macrophages.
Sequelae of Acute Inflammation
- Resolution: the injury is removed without residual tissue damage, and everything returns to normal.
Suppuration
- Commonly seen with pyogenic bacteria, characterized by marked infiltration of neutrophils.
- The injury site becomes necrotic and softens due to proteolytic enzymes released from dying neutrophils and autolysis induced by tissue lysosomal enzymes.
- Pus is formed, consisting of dead and dying neutrophils, dead and living bacteria, fluid exudate (fibrin), and tissue debris.
- The cavity containing the pus is called an abscess, lined by an extensively inflamed living tissue called the pyogenic membrane.
- Abscesses can become tense, leading to ischemic necrosis, and may eventually open into a surface, forming a sinus or fistula.
Chronic Inflammation
- Caused by the persistence of injury, with inflammatory and healing processes occurring simultaneously.
- Mechanisms involved in the formation of exudate include:
- Increased hydrostatic pressure.
- Increased vascular permeability.
- Breakdown of large tissue proteins.
- Increased fluidity of the ground substance, facilitating the flow of fluid into the injury site.
- Constituents of exudate include fibrin, cells (mainly neutrophils), immunoglobulins, complement components, water, electrolytes, and drugs.
Chemical Mediators
- Vasoactive mediators:
- Histamine.
- Serotonin.
- Bradykinin.
- Anaphylatoxins.
- Prostaglandins.
- Platelet-activating factors.
- Chemotactic factors:
- Complement components (C5a, C3a, etc.).
- Recruitment and stimulation of inflammatory cells.
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Description
Learn about the demolition process in inflammation, carried out by macrophages, and the importance of terminating the acute inflammatory response to prevent tissue damage.