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INFLAMMATION

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A complex reaction to various injurious agents
Consists of vascular responses, migration and activation of leukocytes, and systemic
reactions
A protective response
 Ultimate goal:
 Remove initial cause of injury
 Remove consequences of injury
Important in tissue repair
 Destroy, dilute, wall of infectious process
 Sets in motion tissue repair
 Regeneration
 Scarring
Unique features
 Reaction of blood vessels
 Accumulation of fluids and electrolytes in extravascular space
Tissues and cells are involved in this reaction
 Fluid and plasma proteins, blood vessels, circulating cells (WBCs), CT cells (mast
cells, fibroblasts, macrophages), extracellular matrix (collagen, elastin), adhesive
glycoproteins
Inflammation is terminated when the inciting agent is eliminated and the mediators have
degenerated

Components of inflammatory response
1. Vascular reaction
 Vasodilation
 Increased permeability
2. Cellular reaction
 Margination
 Rolling
 Adhesion
 Transmigration
 Migration

ACUTE INFLAMMATION
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Predominating WBC: Neutrophils
A rapid response to an injurious agent that aims to rapidly bring mediators of
inflammation to the site of injury
 Alterations in blood flow
 Increased vascular permeability
 Emigration, accumulation, and activation of neutrophils
Infiltration by polymorphonuclear cells (BEN)
Resolve in 1-2 wks.

TNF) Hallmark of Acute Inflammation: . Cytokines (Interleukins.Stimuli for acute inflammation . tissue debris.Tissue necrosis . D4.Physical and chemical agents . Purulent or Suppurative . heart failure. pleural effusions 2. proteins and blood cells from the vascular system into interstitial tissue or body cavities .Vascular dilatation may be apparent to the naked eye . proteins.020 None An exudate rich in inflammatory cells (leukocytes) and cellular debris MORPHOLOGIC PATTERNS 1.Caused by pyogenic bacteria .Vasoactive amines (histamine and serotonin) .Trauma . Platelet aggregating factor 4.Infections .The pus may become walled-off by granulation tissue or fibrous tissue or produce an abscess (a localized collection of pus in a tissue .Escape of fluid.Empyema . Thromboxane A2.Plasma-like effusion with no cells . E4) 2.Clotting system 1. C4. acute synovitis . Nitric oxide 5.There is abundant protein-rich fluid exudate with a relatively low cellular content .Contains dying and degenerate neutrophils.Kinins (Bradykinin) .Increased vascular permeability Edema . Prostacyclin. Serous . Leukotrienes (B4. such as peritonitis.Foreign bodies .020 Inflammatory cells. Oxygen metabolites 3.Swelling due to tissue fluid accumulation Exudation: .Early inflammation. infecting organisms .Inflammation of the serous cavities.Immune rxns Mediators of acute inflammation . and inflammation of a synovial joint. Arachidonic acid metabolites: Prostaglandin.Complement system (C3a and C3a) .The term suppurative and purulent denote the production of pus .Two types  Exudate  Transudate Protein content Sp Gr Cellular components Pus - Exudate High >1. cellular debris Transudate Low (Albumin) <1.

Caused by bleeding.Acute pancreatitis due to proteolytic destruction of vascular walls. desquamated epithelial cells and inflammatory cells .Damaged or vascular injury or permeable blood vessels or depletion of coagulation factors .Contains both serous and hemorrhagic materials . Abscess .An epithelium becomes coated by fibrin.Contains large amounts of fibrinogen .Thick mucous and WBCs 4.Often seen in acute pericarditis giving the parietal and visceral pericardium a bread and butter appearance 4.Formed by the fibrin and necrotic surface epithelium .Inflammatory conditions like allergic rhinitis.Often found in mucous membranes.Mucosal surface . surrounded by an inflamed area . Fibrinous . Membranous .Localized collection of pus in a part of the body.Forms thick stick meshwork that may cause areas to stick together .A structure which resembles the luminal surface of tissue (looks like the affected tissue is covered by a membrane) . often caused by an initial abrasion and generally maintained by an inflammation and/or an infection 3.An example is the grey membrane seen in pharyngitis laryngitis due to Corynebacterium diphtheriae 5.Contains fibrinous or fibrinopurulent material with necrotic cells . Hollow viscus fills with pus (empyema of the gall bladder or the appendix) 3. serous exudation like injury and burns Exudates in Inflammatory Process 1. Mucinous or Catarrhal . Serosanguinous . Hemorrhagic .Contains large amount of RBC and other cells . Ulcer .Thick fibrin coating .The area will most likely look like a giant boil or cyst that can become extremely red and infected 2.Contains large amount of mucous and epithelial cells . Membranous . eyes or mucous membrane.An open sore of the skin. and in meningococcal septicemia due to disseminated intravascular coagulation 2. Pseudomembranous . common Types of Inflammation According to Location 1.When mucus hypersecretion accompanies acute inflammation of a mucous membrane . Catarrhal . some microbial infection 5.

Multifocal . eosinophils) 2. lymphocytes. Follows an acute inflammation 2.Possible origin o Several local reactions that spread into adjacent tissue o Coalescence of foci in a multifocal reaction 4. Locally Extensive .Size is variable .Healing (by CT replacement or scarring) .Arising from or pertaining to many foci (several foci separated from one another) .Interstitial pneumonia Outcome of Acute Inflammation . asbestosis) C. principally lymphocytes and occasional plasma cells.Types of Inflammation According to Distribution/Location of Lesion in an Organ 1.Mononuclear cells Morphology 1. Focal .Each focus of inflammation is separated from the other inflamed foci by an intervening relatively normal zone of tissue 3.Also known as Focally Extensive .Single abnormality or inflamed area within a tissue .Size varies from 1 mm to several cms in diameter 2. mast cells. Repeated bouts of acute inflammation A. Diffuse . Attempts at healing by CT replacement (angiogenesis and fibrosis) Granulomatous Inflammation - A distinctive chronic inflammatory reaction in which the predominant cell type is an activated macrophage with a modified epithelial-like (epithelioid) appearance. In the focus of inflammation (granuloma). microscopic aggregations of macrophages are transformed into epithelioid cells surrounded by collar of mononuclear leukocytes.Abscess formation . Persistent infections of intracellular microbes (tubercle bacilli.Involvement of considerable area within an organ . plasma cells) Causes 1.Progression to chronic inflammation CHRONIC INFLAMMATION - Predominating WBC: Lymphocytes An inflammation of prolonged duration Infiltration by mononuclear cells (macrophages. lymphocytes. viral infections) B.Involve all the tissue or organ in which the inflammation is present . Prolonged exposure to nondegradable but potentially harmful substances (silicosis. Immune reactions (autoimmune disease) Hallmark of Chronic Inflammation: .Variations in severity may exist .Complete resolution . Such epithelioid cells often fuse to form giant cells comprising of a large mass of cytoplasm with 20 or more small nuclei . plasma cells. Tissue destruction 3. Infiltration of mononuclear cells (macrophages.

have an abundant pink cytoplasm.Vessels return to their normal permeability state . Characterized by formation of granulomas Granuloma  Focal aggregation of activated macrophages which are transformed in an epithelial-like (epithelioid histiocytes) cells.Fever. syphilis Two types of granuloma 1. serum amyloid A protein) .Cicatrization  Formation of the mature scar Cicatrix o Scar o Less vascular. sutures . lymphadenopathy .The intact. decreased in sweating.Offending agent is neutralized .Presence or absence of infection . chills.- - - arranged peripherally in a horseshoe shape (Langhan's Giant Cell) or haphazardly (body-type).Leukocytosis .Adequacy of blood supply .Shock Factors Modifying the Inflammatory-Reparative Response .Migration and proliferation of fibroblasts (laying down collagen) .Inflammatory reactions present Resolution Inflammation (Healing) Simple Resolution . contracting scar tissue . malaise.No inflammatory or immune reactions present 2.Caused by immune T cell-mediated reactions .Increase plasma levels of acute phase proteins (CRP. anorexia. leprosy.Replacement of lost or necrotic tissue with a new tissue that is structurally and functionally similar to those that were destroyed .Nutritional status of patient .Remodeling .Angiogenesis . somnolence. contraction of wound edges . healthy neighboring cells surrounding the dead cells will proliferate to replace the affected cells Replacement by a CT scar .Epithelialization Systemic Effects: Inflammation .Insoluble particles (microbial parts) . and are surrounded by numerous lymphocytes and plasma cells Histiocytes  Surround foreign body  Multinucleated giant cells that try to eat the foreign body. no arrangement Tuberculosis.Excess fluid is reabsorbed . rigors. pale.Clearance of mediators and inflammatory cells Regeneration .No destruction of normal tissue .Reorganization of the fibrous tissue.Formation of a new type of tissue that caused fibrous scar production with some loss of tissue function . Foreign body granuloma .Sepsis .Caused by inert foreign bodies . Immune granuloma . increase in pulse and BP.Deposition of extracellular matrix .Material (talc).

g. normal functioning WBCs . glucocorticosteroids) Adequate levels of circulating.- Presence or absence of DM Presence of absence of immunosuppressive drugs (e.