The inflammatory Response Anticipated learning outcomes of this clinical presentation are: Become familiar with the vascular and cellular events that characterized both acute-chronic inflammation. Review the classic signs of acute inflammation Recognize common etiologies of inflammation and types of inflammatory disorders Be familiar with the general category of treatment modalities

The Inflammatory Response The cardinal signs of inflammation have been passed down from antiquity, they are rubor, calor, dolor and tumor. These signs are consequences of chemical mediators-induced effects on local blood flow, vascular permeability, infiltration of leucocytes, and release of pain inducing agents.

The Inflammatory Response It is important to note, that there are a number of different types of inflammation, which depend on the types of mediators and inflammatory cells that participate in the process, as well as triggering events. Inflammation can be either local or systemic. An acute inflammatory response is characterized by rapid onset and resolution of tissue changes with vascular and cellular activity over a brief period.

Paronychia

Upper Respiratory Infections

Upper Respiratory Infections

The Inflammatory Response Elimination of foreign antigen by cellular or humoral responses is an integral link to the inflammatory response. However, dysregulation of the system can perpetuate inflammatory processes that lead to tissue damage and organ dysfunction. Inflammation is also responsible for hypersensitivity reactions and for many of the effects of autoimmunity.

SLE

Vasculitis

Vasculitis

Osteoarthritis (DJD)

DJD

Rheumatoid Arthritis

Obstructive Lung Disease

The Inflammatory Response Vascular events triggered by either tissue injury (lacerations-contusions), noxious substances (insect bites, plants, toxins) Results in alterations in blood flow, transient arteriolar constriction, the arterioles dilate, allowing an influx of blood under increase pressure (hyperemia). Followed by increased vessel wall permeability, transudation of fluid into the perivascular spaces (edema).

The Inflammatory Response Concurrent cellular events by neutrophils (PMNs) are the primary effector cells in acute inflammation, i.e., there margination, activation, adhesion and transmigration to and through vascular endothelium Cell-derived chemical mediators such as histamine, arachidonic acid derivatives, chemokines, nitric oxide and cytokines account for the cascade of vascular-cellular events in acute inflammation

Neutrophil migration

The Complement System The complement system enhances phagocytosis and lyses microbes and infected cells. Microbes and acute phase proteins activate the complement system. Complement are plasma proteins synthesized by the liver. The classic pathway is activated by antigen-antibody complexes, the alternate pathway by microbial-cell walls (bacterial polysaccharides).

Complement

Cell-derived chemical mediators Levels of acute phase proteins increase in response to an infectious agent, burns, trauma, and neoplasm's (e.g, C- reactive protein, ESR, histamine,prostaglandins, and leukotrienes). Many of the symptoms associated with infection, such as fever, fatigue, and myalgia, are Attributed to cytokines.

The Inflammatory Response Elimination of foreign antigen by cellular or humoral responses is an integral link to the inflammatory response. However, dysregulation of the system can perpetuate inflammatory processes that lead to tissue damage and organ dysfunction. Inflammation is also responsible for hypersensitivity reactions and for many of the effects of autoimmunity.

Hypersensitivity Response Type I: IgE mediated anaphylactic or immediate hypersensitivity reactions,involves the binding of IgE to either basophils or mast cells with the release of histamine,leukotrienes,etc. Examples of type I reactions include atopy (allergic rhinitis-asthma, and atopic dermatitis) anaphylactic shock,and acute drug allergic reactions, insect venom,latex and foods. Isolate urticaria and angioedema are cutaneous forms of anaphylaxis.

IgE or complement

Type I IgE reaction

Hypersensitivity Response Type II: Cytotoxic or antibody mediated reactions involve the binding of either IgG or IgM to cell membrane-bound antigens. Antigen-Ab binding activates the complement cascade and results in cytolysis. Examples of tissue injury by this mechanism include hemolytic anemia, autoimmune hyperthyroidism and myasthenia gravis. The latter doesn’t involve cytolysis.

Hypersensitivity Response Type III: Immune complex mediated reactions occur when IgG or IgM bind to allergen or antigens and these complexes can be deposited in tissues. Their deposition in tissues activate complement. Clinical examples of type III reactions are serum sickness, certain types of nephritis and certain features of infective endocarditis.

Type III (immune complexes)

Rheumatoid Arthritis

Hypersensitivity Response Type IV: Cell-mediated or delayed hypersensitivity reactions occur through T-lymphocytes and usually occur 24-72 hours after exposure to the offending antigen. Classic examples are the tuberculin skin test reaction, arthrus reaction, and allergic contact dermatitis.

Type IV (contact dermatitis)

The Inflammatory Response SIRS Sepsis, sepsis syndrome, and septic shock are commonly used terms that represent a continuum of SIRS. Half of all cases of sepsis are caused by gram-negative rods; indeed, the sepsis syndrome may complicate infections with bacteria, viruses, fungi, rickettssiae, mycobacteria and parasites.

The Inflammatory Response Sepsis, sepsis syndrome, and septic shock are commonly used terms that represent a continuum of SIRS. Half of all cases of sepsis are caused by gram-negative rods; indeed, the sepsis syndrome may complicate infections with bacteria, viruses, fungi, rickettssiae, mycobacteria and parasites.

The Inflammatory Response Treatment modalities NSAIDS and Cox-inhibitors Topical, inhaled and systemic steroids Antibiotics for infection related disorders Immunosuppressives (Methotrexate-Cytoxan) Biologic agents (Enbrel-Humira)