Inflammation: A Vital Defense Mechanism

Study Notes

Inflammation: A protective response to injury or infection.
Goals of Inflammation:
- Eliminate the cause of injury
- Initiate repair of damaged tissue
Two Major Components:
- Vascular Response
- Cellular Response

Initial Vasoconstriction: Brief narrowing of blood vessels
Vasodilation: Dilation of blood vessels, leading to increased blood flow, heat, and redness
Increased Vascular Permeability: Leakage of fluid (exudate) from blood vessels into interstitial spaces, leading to swelling
- Mechanisms:
  - Endothelial Cell Contraction: Histamine, bradykinin, leukotrienes cause gaps in venules
  - Direct Endothelial Injury: From burns, infections, or toxins
Edema: Excess fluid in interstitial spaces or body cavities

Exudate: High protein content, cellular debris. Implies increased vascular permeability
Transudate: Low protein content, caused by increased hydrostatic pressure or decreased osmotic pressure. Non-inflammatory

Leukocytes: White blood cells, essential for fighting infection and clearing debris
Leukocyte Recruitment: The journey of leukocytes from blood vessels to the site of inflammation
- Margination and Rolling: Leukocytes slow down and attach loosely to the endothelium. Selectins play a role.
- Adhesion: Leukocytes bind firmly to the endothelium. Integrins play a role.
- Transmigration (Diapedesis): Leukocytes move across the endothelium and into the tissue.
Leukocyte Activation: Leukocytes respond to signals (like microbes, necrotic cells, or inflammatory mediators) and perform their functions.

Engulfment: Neutrophils and macrophages "eat" bacteria, cell debris, and other foreign particles.
Steps in Phagocytosis:
- Recognition and Attachment: Leukocytes recognize and bind to the target. Opsonins (like antibodies and complement) enhance binding.
- Engulfment: The leukocyte wraps its cytoplasm around the target, forming a vesicle (phagosome).
- Killing and Degradation: The phagosome fuses with lysosomes containing enzymes and reactive oxygen & nitrogen species that destroy the engulfed particles.

Resolution: Complete restoration of normal tissue structure and function (ideal outcome)
Progression to Chronic Inflammation: Persistent inflammation that can lead to tissue damage and scarring. Occurs when the offending agent is not removed or inflammation continues.
Suppuration (Pus Formation): A thick, creamy yellow fluid containing neutrophils, dead cells, microbes, and cellular debris. Common in bacterial infections.

Serous Inflammation: Outpouring of thin fluid (plasma or mesothelial secretion) eg. Pleural effusion
Fibrinous Inflammation: Deposition of fibrin (a clotting protein) in body cavities. More severe injury than serous inflammation. eg. Pericarditis
Suppurative (Purulent) Inflammation: Formation of pus, with neutrophil infiltration. Caused mostly by bacteria. eg. Appendicitis
Pseudomembranous Inflammation: Formation of a white-creamy, false membrane on mucous membranes, composed of fibrin, dead epithelium, neutrophils, red cells, and bacteria. eg. Diphtheria

Abscess: Localized collection of pus. A central necrotic area surrounded by neutrophils and a zone of dilated blood vessels. Can be walled off by connective tissue.
Ulcer: Localized defect or excavation of the surface of an organ. Typically occurs in mucous membranes or subcutaneous tissue.

Beneficial Effects: Dilutes toxins, produces antibodies, forms a fibrin network to limit infection spread
Harmful Effects: Swelling, increased tissue pressure, tissue necrosis, severe damage in allergic reactions, generalized vascular permeability leading to shock (anaphylactic shock).