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94 Cards in this Set
- Front
- Back
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Innate resistance aka as natural or native immunity,
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includes natural barriers (physical, mechanical and biochemical-1st defense) and inflammation(2nd defense.
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Inflammatory response
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protects the body from further injury, prevent infection of the injured tissue and promote healing.
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Adaptive immunity aka acquired or specific immunity
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is induced in a relatively slower and more specific process. Targets particular invading microbes for purpose of eradicating them. Involves memory which results in more rapid response during future exposures to same microbe.
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Antimicrobial peptides
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small proteins secreted by epi tissue that are toxic to certain bacteria, fungi and viruses.
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normal bacterial flora
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Inflammation
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A vascular reaction whose net result is the delivery of fluid, dissolved substances, and cells from the circulating blood into the interstitial tissues in an area of injury or surrounding an area of necrosis; it serves to localize, destroy, neutralize, or remove an injurious agent in preparation for the process of healing.
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Inflammation
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mast cell
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Connective tissue cells that contain histamine and heparin in their granules; important in cellular defense mechanisms needed during injury or inflammation.
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Degranulation
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Emptying out of vesicles containing histamine from mast cells and basophils.
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Histamine
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vasoactive amine, temporary,rapid constriction of smooth muscle and dilation of postcapillary venules resulting in increased blood flood, increased vascular permeability and increased adherence of leukocytes to endothelium.
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chemotactic factors diffuse from site of inflammation, 2 types. Name them.
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Neutrophil (kill bacteria) chemotactic factor esinophil (regulate inflammation) chemotactic factor of anaphylaxis
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Chemotaxis
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Directionally oriented movement of the leukocytes to a site of injury or to inflamed tissue in response to a variety of chemical “signals.”
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leukotriences (slow reacting substance of anaphyaxis)
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sulfur containing lipids that produce histamine like effects. Stim slower and more prolonged responsesthan histamines.
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Prostaglandins
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cause increased vascular permeability, neutraphil chemotaxis and pain by direct effect on nerves. Aspirin and nsaids block syntheses of prostaglandins, thereby inhibiting inflammation.
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platelet-activating factor
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mast cells are a major source of PAF, but can also be produced during inflammation by neutrophils, monocytes, endothelial cells and plateletes. Biologic activity: same as leukotrienes 1)increased vascular permeability 2) leukocyte adhesion to endothelial cells 3) platelet activation.
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Plasma protein systems
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includes the complement system, the clotting system and kinin system.
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Complement system can destroy pathogens directly or can
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activate or collaborate with every other component of the inflammatory system.
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complement system activation in 1 of 3 ways.
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1) classical pathway: activated by proteins of the acquired immune system (antibodies). 2) lectin pathway: activated by certain bacterial carbs. 3) alternative pathway: actived by gram- bacterial and fungla cell wall polysaccharides.
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Opsonins (C3b)
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molecules that coat bacteria and increase their susceptibility to being eaten and killed by inflammatory cells.
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Anaphylatoxins (C5a)
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molecules that induce rapid degranulation of mast cells thus increasing inflammation.
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Clotting (coagulation) system
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Kinin system
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activated thru factor XII or prekallikrein. Final product of kinin system is bardykinin which causes dilation of blood vessels, induces pain, causes smooth muscle contraction(more slowly than histamine) and increases vascular permeability.
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Plasmin
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enzyme limits clot formation by degrading fibrin and fibrinogen, can activate the complement cascade.
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Carboxypeptidase
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enzyme inactivates the anaphylatoxic activities of C3a and C5.
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C1 esterase inhibitor
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binds to C1 to inhibit further activation of classical complement pathway.
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Endothelial cells
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line vessels and cell sin the circulation
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adhesion molecules on leukocytes
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increases a cells stickiness, thus wbc and platelets accumulate on vessel wall.
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Nitric oxide NO released by endothelial cells has 2 effects on inflammation.
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1-causes vasodilation by inducing relaxation of vascular smooth muscle 2- supppress mast call release of inflammatory molecules and decrease platelet adhesion and aggregation.
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Neutrophil or polymorphonuclear neutrophil (PMN)
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predominant phagocyte in early inflammation (6-12hrs after injury).
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Monocytes
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the immature form of wbc? In the blood
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macrophages
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mature cell in the tissues.
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Cytokines
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family of proteins that are secreted and activate other inflammatory cells
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Esinophils
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only mildly phagocytic, defend against parasites, help regulate vascular mediators released from mast cells.
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Natural killer cells
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recognize and eliminate cells infected w/ viruses and abnorm host cells (cancer)
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Platelets (thrombocytes)
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Nonnucleated cell fragments (1-4 µm in diameter) from megakaryocytes, which stain light blue with red-purple granules. Platelets have a lifespan of 9 to 10 days; 80% circulate in the blood and 20% are sequestered in the spleen. Platelets play a vital role in primary hemostasis (temporary platelet plug), secondary hemostasis (formation of the stable fibrin clot), and in clot retraction; thus in thrombocytopenia all these functions are abnormal. The normal serum platelet count is 150,000 to 400,000/mm3.
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Phagocytosis
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Process of ingestion (engulfment) and digestion of bacteria and foreign materials by certain cells, especially polymorphonuclear neutrophils and macrophages.
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margination or pavementing
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Diapedesis
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The passage of leukocytes by ameboid movement through the unruptured wall of a capillary into an area of inflammation (emigration).
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pattern recognition receptors
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pathogen-associated molecular patterns
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toll-like receptors
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complement receptors
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Fc receptors
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phagosome
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phagolysosome
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Vacuoles formed by fusion of lysosomes with phagosomes
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hexos-monophosphate shunt
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a1-antitrypsin
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interleukins IL
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interleukin-1 IL-1
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interleukin-6 IL-6
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interleukin-10 IL-10
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Interferons
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tumor necrosis factor-alpha
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transforming growth factors
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colony stimulating factors
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chemokines
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exudate
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serous exudate
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fibrinous exudate
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purulent (suppurative ) exudate
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An exudate containing pus; usually formed in response to bacterial infection; also seen in response to many aseptic injuries and is prominent almost anywhere in the body that tissues have come necrotic.
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Cysts
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abscesses
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hemorrhagic exudate
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fever
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endogenous pyrogens
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exogenous pyrogens
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pyrogens
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Leukocytosis
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An increase in the WBC (>10,000/mm3)—a common reaction in a variety of inflammatory states. Most commonly occurs as a response to bacterial infection or as a response to tissue necrosis (infarction).
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acute phase reactants
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Granulomas
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A granular tumor or growth consisting of the massing of large numbers of macrophages and their aggregation; formed in reaction to an infectious agent or chronic infectious agent.
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epithelioid cells
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giant cells
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Regeneration
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A process involving proliferation of parenchymal elements identical to those lost, the net result being replacement of those lost elements by the same type of cells.
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Resolution
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repair
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scar tissue
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debridment
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Removal of foreign material and dead or damaged tissue from a wound.
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Epithelialization
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contraction
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primary intention
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reconstructive phase
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maturation phase
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transforming growth factor-beta
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angiogenesis factors
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matrix metalloproteinases
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Granulation tissue
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Young, vascular connective tissue consisting of newly formed capillary buds mixed with proliferating fibrocytes, the spaces between them containing an inflammatory exudate, representing a stage in repair of tissue damage associated with inflammation.
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Fibroblasts
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wound contraction
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myofibroblasts
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Keloid
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Excessive scar tissue that extends beyond the bounds of the original wound, most commonly occurring around the face, neck, and shoulders. The cause is abnormal collagen synthesis and degradation.
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hypertrophic scar
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Dehiscence
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Breaking open of a wound; a serious complication when an abdominal incision is involved.
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Contracture
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Condition occurring when scar tissue shortens and becomes more dense and compact over time; scar tissue contracture over a joint may cause deformity or abnormal limitation of movement of the joint.
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Never Let Monkeys Eat Bananas:
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Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils
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