LEC INFLAMMATION, TISSUE HEALING AND REPAIR Flashcards
composed of a series of physiologic and morphological changes in the blood vessels, blood components and surrounding connective tissue for the purpose of protecting the body against injury
INFLAMMATION
CARDINAL SIGNS OF INFLAMMATION
Calor- heat
Rubor- redness
Tumor- swelling
Dolor- pain
Functio Laesa- loss of function
Sequence of events in an inflammatory reaction
Offending agent is recognized by host cells
Leukocytes and Plasma proteins are recruited from the circulation to the site where the offending agent is located
Leukocytes and Protein are activated to eliminate offending substance
Reaction is controlled and terminated
Damaged tissues is repaired
2 types of inflammation
Acute- Fast mins or hrs, mainly neutrophils, self limiting and mild, prominent
Chronic- Slow days, monocytes, macrophages and lymphocytes, severe and progressive, less prominent
2 Major Components of Inflammation
Vascular Changes- dilation of small vessels leading to an increase in blood flow
Cellular Events- emigration of leukocytes from the microcirculation, accumulation in the injury and activation to eliminate offending agent
Stimuli for Acute Inflammation
Infections
Tissue Necrosis
Foreign Bodies
Immune Reactions
Hallmarks of Morphologic Patterns of Acute Inflammation
Dilation of small blood vessels
Accumulation of leukocytes and fluid in the extravascular tissue
Type of inflammation in which is marked by exudation of protein-poor fluid into spaces created by cell injury
Serous Inflammation
Samples of Serous Inflammation
Skin Blisters due to burns
Type of inflammation that has large molecules pass out of the blood and fibrin is formed and deposited in the extracellular space
Fibrinous Inflammation
This inflammation is caused by infection with bacteria that cause liquefactive tissue necrosis
Purulent/Suppurative Inflammation
Sample of Purulent/Suppurative Inflammation
Acute Appendicitis
A local defect or excavation of the surface of an organ or tissue
Ulcers
A mediator which causes vasodilation, increase vascular permeabiliy and endothelial activation
Histamine
This mediator acts by vasodilation, pain, fever
Prostaglandins
This mediator acts by increasing vascular permeability, chemotaxis, leukocyte adhesion and activation
Leukotrienes
This mediator acts by activation of adhesion molecules in systemic fever, metabolic abnormalities and hypotension
Cytokines
This mediator action is chemotaxis and leukocyte activation
Chemokines
This mediator acts as a vasodilator, degranulation, increased vascular permeability, leukocyte adhesion, chemotaxis and oxidative burst
Platelet Activating Factor
This mediator acts by activating leukocyte and its chemotaxis, vasodilation
Complement
This mediator acts by increasing vascular permeability, smooth muscle contraction activation, vasodilation, pain
Kinins
Properties of cell mediators
Cell-derived- sequestered in IC granules and can be rapidly secreted by granule exocytosis
Plasma-derived- produced mainly in the liver and present in the circulation as inactive precursor
2 Vasoactive amines
Histamine
Serotonin
2 Arachidonic Acid metabolites
Prostaglandins
Leukotrienes
This is the response of prolonged duration in which inflammation, tissue injury and attempts at repair coexists
Chronic Inflammation
Causes of Chronic Inflammation
Persistent infections
Hypersensitivity diseases
Prolonged exposure to potentially toxic agents
A form of Chronic Inflammation that is characterized by collections of activated macrophages and sometimes associated with central necrosis
Granulomatous inflammation
2 types of Granulomatous Inflammation
Foreign Body Granuloma- driven by inert foreign bodies in the absence of T cell-mediated immune response
Immune Granuloma- by persistent microbe or self antigen
Samples of diseases under Granulomatous Inflammation
Tuberculosis, Leprosy, Syphilis, Cat-scratch disease, Sacoidosis, Crohn Disease
Major causes of granulomatous inflammation
Bacterial: Tuberculosis, Syphilis, Cat-Scratch
Fungal: Histoplasmosis, Cryptococcus, Coccidioidomycosis, Blastomycosis
Helminthic: Schistosomiasis
Protozoal: Leishmaniasis, Toxoplasmosis
Chlamydia: Lymphogranuloma venerum
Systemic Effects of Inflammation
Fever
Acute Phase proteins
Leukocytosis
Increase pulse and BP, decrease sweating
It refers to the repair of tissue architecture and its function
Tissue Repair/Healing
2 Types of reaction under tissue repair
Regeneration
Scar formation
Factors influencing tissue repair
Infection
DM
Nutritional Status
Glucocorticoids
Mechanical Factors
Poor perfusion
Foreign bodies
Type and extent of tissue injury
Location of injury
What are the episodes in first intention of Skin wound healing
Clot forms within 24 hours
Fast healing
By 3-5 days macrophages come in
Week after granulation tissue is gone
What are the episodes in second intention of Skin wound healing
Fibrosis predominates over
Healing is slower with more inflammation and granulation
more scarring
