Chronic Inflammation and Tissue Repair

Study Notes

The lecture material covered inflammation and repair, a refresher for students previously taught the topic in a different course.
This lecture serves as a refresher, focusing on application in systematic pathology.
Inflammation is a multifaceted response to injury, observed in various tissues and systems, thus warranting a review of basic principles.

Understand the purpose of the inflammatory response and its primary causes.
Recall the five fundamental aspects (5 Rs) of the inflammatory response.
Recall the cardinal signs of inflammation and their associated pathophysiology.
Distinguish between acute and chronic inflammation based on onset, duration, and cell types involved.
Describe the basic vascular and cellular responses underlying acute inflammation.
Detail the helpful and harmful effects of inflammation.
Define the different morphological patterns of acute inflammation.
Outline the possible outcomes of acute inflammation.
Describe chronic inflammation, including the causes and general pathological features.
Explain granulomatous inflammation, encompassing associated diseases and providing examples.
Define healing and repair processes, including regeneration, resolution, organization, and fibrosis.
Describe the stages of scar tissue formation.
Identify conditions arising from irregularities in wound healing and repair.

Inflammation is the body's response to injury in vascularized tissues.
Its purpose is multifaceted, encompassing isolating the injury site, recruiting necessary components, eliminating microbes/toxins, and preparing for repair.
Inflammation is critical for maintaining normal tissue health but can also be harmful if poorly controlled.
Misdirected responses to allergens, autoimmune disorders, or persistent stimuli can lead to detrimental effects.

Acute inflammation is characterized by rapid onset, short duration, and prominent edema, with neutrophils as the predominant cell type.
Chronic inflammation features a later onset, longer duration, and a predominance of lymphocytes and macrophages.

Defined as a rapid host response delivering leukocytes and plasma proteins to infection or tissue injury/necrosis.
Characterized by changes in vascular flow/vessel calibre, increased vascular permeability (fluid exudate), and recruitment of leukocytes, leading to cardinal signs of inflammation.
Two main components: vascular and cellular reactions.

Vasodilation (initial brief vasoconstriction followed by increased blood flow, erythema)
Increased vascular permeability (retraction of endothelial cells, endothelial injury, leukocyte-mediated vascular injury), leading to fluid exudate (edema) escape of proteins.

Extravasation/emigration of leukocytes from vessels and into the injured area.
Steps include margination, rolling, adhesion, migration (diapedesis), and chemotaxis.
Chemotaxis is the directed migration of leukocytes along a chemical gradient to the site of injury.

Beneficial: dilution of toxins, entry of antibodies, enhanced drug delivery, fibrin formation, delivery of nutrients/O2, stimulation of the immune response.
Harmful: digestion of normal tissues, swelling, and inappropriate or exaggerated immune responses (severe cases).

Characterized by prolonged duration, tissue destruction, and mononuclear inflammatory response (macrophages, lymphocytes, plasma cells).
Causes include progression from acute inflammation, persistent infection, prolonged exposure to toxins, and autoimmune responses.
Described by pathological features like cellular infiltration, immune response, and persistent attempts to heal.

A distinct chronic inflammatory pattern characterized by aggregated macrophages (epithelioid macrophages) and a rim of lymphocytes.
Results from persistent agents or foreign material that cannot be easily eliminated.
Includes various conditions (e.g., tuberculosis, leprosy, syphilis).

Regeneration: restoration of normal tissue architecture without scarring, through either cell proliferation or stem cell activity.
Organisation: Replacement by granulation tissue in tissues unable to regenerate, resulting in scar formation.
Fibrosis: excessive collagen deposition in response to chronic inflammation/tissue necrosis.
Detailed steps of scar tissue formation, including inflammation, cellular proliferation, granulation tissue formation, and wound contraction.
Different types of wound healing (primary and secondary intention).