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50 Cards in this Set
- Front
- Back
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What are the 3 purposes of the inflammatory responses?
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1. Neutralize and destroy invading and harmful agents. 2. Limit the spread of harmful agents to other tissue. 3. Prepare any damaged tissue for repair.
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What are the 5 cardinal signs of inflammation?
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1. Redness (rubor) 2. Swelling (tumor) 3. Heat (calor)
4. Pain (dolor) 5. Loss of function (functio laesa) |
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The suffix -itis
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commonly used to describe conditions associated with inflammation. example appendicitis; inflammation of the appendix.
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Exogenous injuries that will evoke an inflammatory response.
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From sources outside the body; surgery, trauma, burns, and skin injury from chemicals.
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Endogenous injuries that will evoke an inflammatory response.
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From sources inside the body; tissue ischemia such as myocardial infarction or pulmonary embolism.
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Acute inflammation
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Short in duration, lasting less than 2 weeks, and involves a discrete set of events.
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Chronic inflammation
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More diffuse, lasting more than 2 weeks, and may result in the formation of scar tissue and deformity.
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Inflammatory process.
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Tissue injury stimulates the release of a number of chemical mediators that promote vasodilation, chemotaxis, and binding of neutrophils and macrophages to area capillaries. These events facilitate the emigration of neutrophils and macrophages into the tissue, where they begin phagocytosis.
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Vasoactive chemicals released during the inflammatory process.
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Histamine, prostaglandins, and leukotrienes.
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Mast cells.
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An important source of the inflammatory chemicals. In the area of injury degranulate and release packets of histamine and other inflammatory chemicals.
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Histamine.
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Early mediator of the inflammatory response. A potent vasodilator that can cause significant reductions in blood pressure when released in excessive amounts. Also causes bronchial constriction and mucus production.
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Prostaglandins.
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Involved in inflammation contribute to vasodilation and increased permeability. Cause pain by enhancing the sensitivity of pain receptors.
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What do platelets do during the early phase of inflammation?
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Move into the site and adhere to exposed vascular collagen. And release fibronectin to form a meshwork trap and stimulate the intrinsic clotting cascade to help reduce bleeding.
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Lymphatic blockage.
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Caused by fibrin deposited in the lymph system and "walls off" the area of inflammation from the surrounding tissue and delays the spread of toxins.
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Margination or pavementing.
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As blood flows through areas of inflammation, neutrophils move to the sides of the blood vessels and roll along the endothelium of the vessel wall.
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Selectins.
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Receptors which help neutrophils stick and roll along the capillary endothelial surface.
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Integrins.
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Receptors which bind to and subsequent movement through the capillary wall.
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Emigration or diapedesis.
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The process of passing through the blood vessel walls and migrating to the inflamed tissue.
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Chemotaxis.
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The movement of cells according to chemical gradients (chemotaxins) that attract them.
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Phagocytosis.
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Ingestion and destruction of pathogens by leukocytes.
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Oxidizing agents.
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The most destructive of the inflammatory cell products. Include the following oxygen radicals; superoxide, hydrogen peroxide, and hydroxyl ions.
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Antiprotease.
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An important inhibitor of inflammatory damage. Made in the liver and circulates continuously in the bloodstream.
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Pus.
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Formed when phagocytosis is incomplete; it is a collection of dead neutrophils, bacteria, and cellular debris.
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Granuloma.
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Tissue that forms into a nodular mass as a result of inflammation, infection, or injury.
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Macrophages.
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Essential for wound healing because of their phagocytic and debridement functions.
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When does the healing phase occur?
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Reconstructive phase usually begins 3 to 4 days after injury and persists for 2 weeks. Major cells involved in phase are fibroblasts, endothelial cells, and myofibroblasts.
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Fibroblast.
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A cell that produces components of collagen fibers, which compose the bulk of the dermis.
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Which cell type regenerate poorly?
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Neurons and muscle cells.
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Wound healing.
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Occurs several weeks after the injury and may last for 2 years or more. It is the process of collagen deposition and lysis with debridement of the wound edges.
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Exudate.
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Fluid that leaks out of blood vessels, combined with neutrophils and the debris from phagocytosis.
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Functions of exudate.
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1. Transport of leukocytes and antibodies. 2. Dilution of toxins and irritating substances. 3. Transport of the nutrients necessary for tissue repair.
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Serous exudate.
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Watery, low protein content, similar to the fluid that collects under a blister. Generally accompanies mild inflammation.
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Serosanguineous drainage.
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A pink-tinged drainage resulting from small amounts of red blood cells that may leak into the serous fluid with capillary injury.
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Fibrinous exudate.
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Sticky and thick. May need removal in order to allow healing to occur otherwise scar tissue and adhesions may develop.
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Purulent exudate.
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Pus. Generally occurs in severe inflammation accompanied by bacterial infection. Primarily composed of neutrophils, protein, and tissue debris.
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Abscess.
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Large pockets of purulent exudate, must generally be removed or drained for healing to take place.
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Hemorrhagic exudate.
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Large component of red blood cells; usually present with the most severe inflammation, severe leakage from blood vessels or after necrosis or breakdown of blood vessels.
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Systematic responses.
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Fever, neutrophilia (increased blood neutrophil count), lethargy, and muscle catabolism.
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IL-1, IL-6, and TNF-α
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Three macrophage-derived cytokines responsible for most of the systemic effects of inflammation.
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C-reactive protein (CRP) and serum amyloid A.
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Two of the most important acute phase proteins; which are released by the liver.
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Erythrocyte sedimentation rate (ESR, "sed. rate")
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A blood test that provides a simple measure of the level of inflammation in an individual.
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Specific immune system of B cells.
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B cells are said to provide "humoral" immunity because the antibodies they produce are found in body fluids, or "humors."
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Specific immune system of T cells.
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T cells provide "cell mediated" immunity because they recognize antigen presented on the surface of cells.
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What must B and T lymphocytes be capable of doing to achieve immunity against specific antigens.
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B and T lymphocytes must be capable of recognizing an enormous range of foreign antigen yet not be reactive to self tissues. Differentiation between self and nonself.
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Major histocompatibility complex (MHC) in humans also known as human leukocyte antigen (HLA)
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The gene regions on chromosome 6 that contain the genes for MHC proteins. Class I proteins are present on virtually all nucleated cells. Class II proteins are found mainly on antigen-presenting cells: B cells, macrophages, and dendritic cells.
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Polymorphism.
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Inherited structural differences in proteins as a result of many alleles for a particular gene locus.
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Transporters associated with antigen processing (TAPs)
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Located near the MHC I complexes on the ER membrane and target the peptides to the MHC I binding cleft.
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T-cell receptors (TCRs)
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Specialized receptors which enable T cells to recognize foreign antigen displayed on the surface of antigen-presenting cells.
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Two major types of T cells.
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T helper cells and cytotoxic T cells (locate and lyse abnormal cells through the actions of perforins).
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What is the result of the activation of T helper cells?
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Results in secretion of the cytokines necessary for clonal expansion of T and B lymphocytes.
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