L20 Overview Of Inflammation Lecture Notes PDF

24 Overview of inflammation **ILOs** ***By the end of this lecture, students will be able to*** 1. Relate subtypes of inflammation to onset, duration, and aetiology. 2. Discuss nomenclature and cardinal signs of acute inflammation. 3. Differentiate between exudates and transudates. ***Defi...

24 Overview of inflammation **ILOs** ***By the end of this lecture, students will be able to*** 1. Relate subtypes of inflammation to onset, duration, and aetiology. 2. Discuss nomenclature and cardinal signs of acute inflammation. 3. Differentiate between exudates and transudates. ***Definition:*** Inflammation is the response of vascularized tissues to infections and tissue damage that brings cells and molecules of host defense from the circulation to the sites where they are needed, to eliminate the offending agents. ***Causes of inflammation:*** It may be caused by: 1. **Infection:** Different types of microorganisms (virus, bacterium, fungus, parasite) elicit different inflammatory responses. 2. **Tissue necrosis:** Ischemia, trauma, and toxins all elicit inflammation. 3. **Foreign bodies:** These include splinters, dirt, suture, prosthetic devices, urate crystals (gout), and cholesterol esters. 4. **Immune reactions** (hypersensitivity responses) can be directed against self *(autoimmunity)* or exogenous agents *(allergy).* ***Role of inflammation:*** Inflammation is intended to 1. Contain and isolate injury 2. Destroy invading microorganisms 3. Inactivate toxins 4. Prepare the tissue for healing and repair. ***Characteristics of inflammation:*** - Two main components, vascular wall response and inflammatory cell response. - Effects that are mediated by circulating plasma proteins and by chemical mediators produced locally by vessel wall or inflammatory cells. - Presents by local and systemic responses. - Termination when the offending agent is eliminated: the secreted mediators are removed; active anti-inflammatory mechanisms are also involved. - Tight association with healing. - Fundamental protective response. - Inflammation can be harmful, and can cause life-threatening hypersensitivity reactions, or relentless and progressive organ damage from chronic inflammation and subsequent fibrosis, in the following situations: 1. It is misdirected (e.g., against self-tissues in autoimmune diseases) 2. It occurs against normally harmless environmental substances that evoke an immune response (e.g., in allergies) 3. It is excessively prolonged (e.g., in infections by microbes that resist eradication). 4. It is too little. This typically manifests by increased susceptibility to infections. It is most often caused by either defective function or reduced number of leukocytes resulting from replacement of the bone marrow by cancers and suppression of the marrow by therapies for cancer and graft rejection. - Associated with five classic clinical signs of inflammation (most prominent in acute inflammation): 1. **Warmth (Latin: *calor*),** due to vascular dilation 2. **Erythema (Latin: *rubor*),** due to vascular dilation and congestion 3. **Edema (Latin: *tumor*),** due to increased vascular permeability 4. **Pain (Latin: *dolor*),** due to mediator release 5. ***Loss of function* (Latin: *functio laesa*),** due to pain, edema, tissue injury, and/or scar ***Types of inflammation:* Inflammation may be of two types, acute and chronic**. - ***Acute inflammation***: It is the initial, rapid response to infections and tissue damage. It typically develops within minutes or hours and is of short duration, lasting for several hours or a few days. Its main characteristics are the exudation of fluid and plasma proteins (edema) and the emigration of leukocytes, predominantly neutrophils. - When the offending agent is eliminated, the reaction subsides and residual injury is repaired. - If the initial response fails to clear the stimulus, the reaction progresses to a protracted type of inflammation that is called *chronic inflammation*. - ***Chronic inflammation*** may follow acute inflammation or arise de novo. It is of longer duration and is associated with more tissue destruction, the presence of lymphocytes and macrophages, the proliferation of blood vessels, and fibrosis. ***The typical inflammatory reaction develops through a series of sequential steps:*** - Recognition of the offending agent by host cells and molecules. - Recruitment of leukocytes and plasma proteins from the circulation to the site where the offending agent is located. - Removal of the agent by activated leukocytes and proteins. - Regulation and termination of the response. - Resolution: the damaged tissue is repaired. A picture containing graphical user interface Description automatically generated ***Acute inflammation** **has three major components:*** 1. Vascular dilation leading to increased blood flow 2. Structural changes in the microvasculature permitting plasma proteins and leukocytes to leave the circulation 3. Leukocyte emigration from blood vessels and accumulation and activation at the site of injury ***Reactions of Blood Vessels in Acute Inflammation:* The vascular reactions of acute inflammation consist of:** - **Changes in the flow of blood;** arteriolar vasodilatation. - **Changes in the permeability of vessels;** increased vascular permeability**.** Both lead to the movement of fluid, plasma proteins and leukocytes out of the circulation into the site of infection or injury into interstitial tissues or body cavities, a process known as ***edema***. - *Edema* denotes an excess of fluid in the interstitial tissue or serous cavities; it can be either an exudate or a transudate. - ***Exudate*** inflammatory Edema \[ exudation\] due to increased vascular permeability. It has high protein contents, high specific gravity and rich in cellular debris. - ***Transudate*** is an ultrafiltrate fo blood plasma resulting from increased hydrostatic pressure at arteriolar side of circulation. It has low protein contents, low specific gravity and little or no inflammatory cells. - ***Pus***, a *purulent* exudate, is an inflammatory exudate rich in leukocytes (mostly neutrophils), the debris of dead cells, and, in many cases, microbes. +-----------------------------------------------------------------------+ | **References:** | | | | 1. **Kumar, Abbas, Aster. Robbins Basic Pathology, 10^th^ ed. | | Elsevier.** | | | | 2. **Mitchell, Kumar, Abbas, Aster. Pocket Companion to Robbins and | | Cotran Pathologic Basis of Disease, 9^th^ ed. Elsevier.** | +-----------------------------------------------------------------------+