Pathology
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| Define inflammation | Response to injury (including infection)
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| Inflammatory reaction of blood vessels leads to: | Accumulation of fluid and leukocytes in extravascular tissues
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| 5 cardinal signs of inflammation | Rubor (erythema [redness]); Tumor (swelling); Calor (heat); Dolor (pain); functio laesa (loss of function)
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| 2 signs of inflammation characterized by vasodilatation & increased blood flow | Rubor (erythema [redness]); Calor (heat)
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| Under what circumstances is inflammation potentially harmful? | Hypersensitivity reactions to insect bites, drugs, contrast media in radiology; chronic diseases (arthritis, atherosclerosis); disfiguring scars, visceral adhesions
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| Components of inflammatory response | Vascular reaction; Cellular (exudative) reaction
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| Types of Inflammation | Acute inflammation; Chronic inflammation; Granulomatous inflammation
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| Characteristics of acute inflammation | Short duration, edema, and mainly neutrophils
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| Characteristics of chronic inflammation | Longer duration, lymphocytes & macrophages predominate, fibrosis, new blood vessels (angiogenesis)
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| Characteristics of granulomatous inflammation | Distinctive pattern of chronic inflammation; activated macrophages (epithelioid cells) predominate
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| Three major components of acute inflammation | Increase in blood flow (redness & warmth); Edema results from increased hydrostatic pressure (vasodilation) and lowered intravascular osmotic pressure (protein leakage); Leukocytes emigrate from microcirculation and accumulate in the focus of injury
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| Transudate vs. exudate | Transudate, SpGr <1.012; Exudate (cell- and protein-rich), SpGr >1.020
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| Benefits of Fluid Accumulation at Injury Site | Dilution of toxins; Pains decreases use and prevents additional injury; Antibodies in blood can kill microbes; Blood plasma proteins can amplify responses against the injurious agent
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| Definition of Extravasation | Delivery of leukocytes from the vessel lumen to the interstitium
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| Types/Examples of Extravasation | In the lumen: margination, rolling, and adhesion; Migration across the endothelium (diapedesis); Migration in the interstitial tissue (chemotaxis)
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| Diapedesis | Migration across the endothelium
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| Chemotaxis | Migration in the interstitial tissue
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| Role of Leukocytes | Ingest offending agents (phagocytosis); kill microbes; degrade necrotic tissue and foreign antigens
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| Leukocyte adhesion and migration across vessel wall are determined largely by ______ | Binding of complementary adhesion molecules on the leukocyte and endothelial surfaces
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| Morphologic Patterns of Acute Inflammation | Serous inflammation; Fibrinous inflammation; Suppurative (purulent) inflammation; Ulcers
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| Serous inflammation | Outpouring of thin fluid (serous effusion, blisters)
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| Fibrinous inflammation | In body cavities; leakage of fibrin; may lead to scar tissue (adhesions)
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| Suppurative (purulent) inflammation | Pus or purulent exudate (neutrophils, debris, edema fluid); abscess: localized collections of pus
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| Ulcers | Local defect of the surface of an organ or tissue produced by the sloughing (shedding) of inflammatory necrotic tissue
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| Chronic Inflammation | Inflammation of prolonged duration (weeks or months)
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| What is occurring during chronic inflammation? | Active inflammation, tissue destruction, and attempts at repair are proceeding simultaneously
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| Examples of chronic inflammation | Persistent infections (Treponema pallidum [syphilis], viruses, fungi, parasites); Exposure to toxic agents; Autoimmunity (Rheumatoid arthritis, systemic lupus erythematosus)
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| Exposure to toxic agents (leading to chronic inflammation) | Exogenous: silica (silicosis); Endogenous: toxic plasma lipid components (atherosclerosis)
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| Histological features of chronic inflammation | Infiltration with mononuclear cells (macrophages, lymphocytes, and plasma cells); Tissue destruction (induced by the inflammatory cells); Healing by replacement of damaged tissue by connective tissue (fibrosis) and new blood vessels (angiogenesis)
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| Macrophages predominate by _____ hours | 48 hours
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| Role of Lymphocytes in Chronic Inflammation | Produce inflammatory mediators; Participate in cell-mediated immune reactions; Plasma cells produce antibody; Lymphocytes and macrophages interact in a bi-directional fashion
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| Eosinophils in Chronic Inflammation | Immune reactions mediated by IgE; Parasitic infections (Eosinophil granules contain a protein that is toxic to parasites)
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| Mast cells in Chronic Inflammation | Release mediators (histamine) and cytokines
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| What characterizes Granulomatous Inflammation? | Predominant cell type is an activated macrophage with a modified epithelial-like (epithelioid) appearance; Giant cells may or may not be present
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| Foreign body granulomas form when ______ | Foreign material is too large to be engulfed by a single macrophage
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| Immune granulomas | Insoluble or poorly soluble particles elicit a cell-mediated immune response
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| Endocrine and Metabolic Manifestations of Inflammation | Secretion of acute phase proteins by the liver; Increased production of GCs (stress response); Decreased secretion of vasopressin leads to reduced volume of body fluid to be warmed
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| Role of Fever in Inflammation | Improves efficiency of leukocyte killing; Impairs replication of many offending organisms
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| Autonomic Nervous System Manifestations of Inflammation | Redirection of blood flow from skin to deep vascular beds minimizes heat loss; Increased pulse and blood pressure; Decreased sweating
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| Behavioral Manifestations of Inflammation | Shivering (rigors), chills (search for warmth), anorexia (loss of appetite), somnolence, and malaise
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| Leukocytosis | Increased leukocyte count in the blood
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| Neutrophilia seen in inflammatory response to ______ | Bacterial infections
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| Lymphocytosis seen in inflammatory response to ______ | Infectious mononucleosis, mumps, measles
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| Eosinophilia seen in inflammatory response to ______ | Parasites, asthma, hay fever
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| Leukopenia seen in inflammatory response to ______ | Typhoid fever, some viruses, rickettsiae, protozoa
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| Predisposing factors to orbital mucormycosis | Diabetic ketoacidosis; Leukemia
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| Vasoactive mediators | Histamine; Bradykinin; Complement (C3a, C5a); Prostaglandins/leukotrienes; Platelet activating factor; Nitric oxide; Neuropeptides
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| Chemotactic factors | Complement (C5a); Leukotriene (B4); Platelet activating factor; Cytokines (IL-1, TNF); Chemokines; Nitric oxide
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| Action of histamine | Dilates arterioles and increases permeability of venules (wheal and flare reaction)
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| Release mechanisms of histamine | Binding of antigen (allergen) to IgE on mast cells releases histamine containing granules; Release by nonimmune mechanisms such as cold, trauma, or other chemical mediators; Release by other mediators
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| Bradykinin | Small peptide released from plasma precursors; Increases vascular permeability; Dilates blood vessels; Causes pain; Rapid inactivation
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| Arachidonic Acid Metabolites | Prostaglandins; Leukotrienes
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| Actions of Prostaglandins | Vasodilatators (prostacyclin); Vasoconstrictors (thromboxane A2); produce pain (PGE2 makes tissue hypersensitive to bradykinin) and fever
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| Actions of Leukotrienes | Increase vascular permeability; Vasoconstriction; Leukocyte adhesion & chemotaxis
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| Platelet Activating Factor is synthesized by ______ | Stimulated platelets, leukocytes, endothelium
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| Proteins produced by many cell types (principally by activated lymphocytes and macrophages) = | Cytokines
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| _____ and ______ are the major cytokines that mediate inflammation | Interleukin-1 (IL-1) and tumor necrosis factor (TNF)
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| Inflammatory effects of Platelet Activating Factor | Stim plt aggregatn; Vasoconstrictn & bronchoconstrictn; Vasodilatn & inc’d ven. permeability; Inc’d leukocyte adhesion to endothel., chemotaxis, degranulatn, & oxidative burst; Inc. synthesis of arachid. acid metabolites by leukocytes etc
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| Chemokines | Small proteins that act primarily as chemoattractants for specific types of leukocytes
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| Actions of Chemokines | Stimulate leukocyte recruitment in inflammation; Control the normal migration of cells through tissues (organogenesis and maintenance of tissue organization)
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| Substance P and neurokinin A are _______ | Neuropeptides
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| Substance P nerve fibers are prominent in the _______ | Lung and gastrointestinal tract
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| Neuropeptides are produced in the __________ nervous system | Central and peripheral nervous systems
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| Effects of neuropeptides | Vasodilation (direct and through mast cell degranulation); Increased vascular permeability
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| Other chemical mediators of inflammation | Neutrophil granules; Oxygen-Derived Free Radicals
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| Steps in Wound Healing | Injury induces acute inflamn; Parenchymal cells regenerate; parenchymal & conn. tissue cells migrate and proliferate; Extracellular matrix produced; parenchymal & conn. tissue matrix remodel; Increase in wound strength due to collagen deposition
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| The hallmark of healing is ______ | Granulation tissue
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| Histology of granulation tissue | Proliferation of small blood vessels and fibroblasts; tissue often edematous
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| Neutrophils are pathognomonic for _______ | Acute Inflammation
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| Plasma cells are pathognomonic for ________ | Chronic inflammation
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| Granulomatous inflammation for _______ | Epithelioid macrophages are pathognomonic
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| Function of cytokines | Modulate the function of other cell types
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