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| Any organism capable of supporting the nutritional and physical growth requirements of another. Humans supporting the growth of microorganisms. |
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| If the host sustains injury or pathologic damage in response to a parasitic infection. The severity can range from mild to life-threatening,depending on many variables, including the health of the host at the time of infection and the virulence (disease-producing potential) of the microorganism. |
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| Used interchangeably with infection. Act of establishing a presence, a step required in the multifaceted process of infection. |
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| The presence and multiplication within a host of another living organism with subsequent injury to the host. |
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| Internal and external exposed surfaces of the human body are normally and harmlessly inhabited by a multitude of bacteria. |
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| Disease-producing potential. |
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| Group of microorganisms so virulent that they are rarely found in the absence of disease. |
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| Harmless, free-living organisms obtaining their growth from dead or decaying organic material in the environment. Can be opportunistic pathogens. |
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| All microorganisms, even saprophytes and members of the normal flora. Capable of producing an infectious disease when the health and immunity of the host have been severely weakened by illness, malnutrition, or medical therapy. |
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| Bodies main line of defense against injury and disease. Response to invasion, infection, immune reactions, trauma, physical or chemical agents, and tissue necrosis. "Wall off" injury and release cells to respond to injury and restore to normal function. Two part phase: vascular and cellular. Protective response intended to eliminate the initial cause of cell injury, remove the damaged tissue, and generate new tissue. Does this by diluting, destroying, or otherwise neutralizing the harmful agents. Interwoven with the repair process that replace damaged tissue or fill the residual defects with fibrous scar tissue. Reaction of vascularized tissue to injury. Characterized by the elaboration of inflammatory mediators and the movement of fluid and leukocytes from the blood into the extravascular tissues. Localizes and eliminates microbes, foreign particles, and abnormal cells and paves the way for repair of the injured tissue. |
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| Final stage of the cellular response, monocytes, neutrophils, and tissue macrophages are activated to engulf and degrade the bacteria and cellular debris. Involves three steps: recognition and adherence; engulfment; intracellular killing. Initiated by the recognition and binding of particles by specific receptors on the surface of phagocytic cells. |
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| Vary in terms of fluid type, plasma protein content, and the presence or absence of cells. Serous (plasma, WBC and some protein), hemorrhagic( occurs when there is severe tissue injury that damage blood vessels or when there is significant leakage of RBC from capillaries) , fibrinous (contains large amounts of fibrinogen and form thick and sticky mesh work), membranous(develop on mucous membranes surface and are composed of necrotic cells enmeshed in a fibro purulent exudate), or purulent (tissue debris, WBC, protein and plasma fluid, contains pus), catarrhal (thick mucous). Often composed of a combination of these types. |
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| Glistening red, moist connective tissue that contains newly formed capillaries, proliferating fibroblasts, and residual inflammatory cells. Development involves the growth of new capillaries (Angiogenesis), fibrogenesis, and I volition to the formation of scar tissue. Angiogenesis involves the generation and sprouting of new blood vessels from preexisting vessels. These sprouting capillaries tend to protrude from the surface of the wound as minute red granules. Bumpy texture, secrete chemicals to degrade existing clot. Proliferative phase. |
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| Key cell in the proliferative phase. Connective tissue cell that synthesizes and secretes collagen and other intercellular elements needed for wound healing. Produce a family of growth factors that induce angiogenesis and endothelial cell proliferation and migration. With vascular endothelial cells they begin proliferating to form the granulation tissue that serves as the foundation for scar tissue development. Most common cell which creates collagen. |
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| Development of strength in the healing wound site. Naturally occurring proteins, main component in connective tissue. In the form of elongated fibrils, mostly found in fibrous tissue. |
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| Toxins: primarily with bacterial pathogens; these are substances that alter or destroy normal function of the hosts cells; these can be further divided into endotoxins (found in the cell wall of gram-negative bacteria and activate regulatory systems such as clotting, bleeding, or inflammation-while this sounds normal, it is actually "toxic" because just a little can overwhelm the body) and endotoxins (proteins released that modify host cells and cause cellular death). Adhesion: being able to adhere to a site and this can be specific to sites depending on the pathogen (sounds like a tick!). Evasive: allow the pathogen to evade the normal immune response; an example would be H. Pylori which produces a type of enzyme that neutralizes the acidic environment of the stomach-this allows H. Pylori to survive in the stomach. Invasive: allow penetration of anatomic barriers and host tissue; usually this is an. Enzyme that will destroy cell membranes, connective tissue, intercellular matrices, and protein complexes. |
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Vascular Phase
(Active Hyperemia) |
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| Brief vasoconstriction(below the area if injury) and then vasodilation; this is almost immediate with injury. Vasodilation is triggered by the release of histamine from the damaged cells. There are also chemical mediators released that contribute to changes in the permeability ( ability of fluid/cells to pass through vessel wall) of the capillary membrane. Purposes: increase blood flow to the area and raises the hydrostatic pressure of the blood in the vessel; this will cause fluid/proteins to push through the vessel wall into the surrounding tissue ( interstitial space). It concentrates what is left in the capillary ( blood vessel), this stagnation of flow will cause a clot to form. This walls off the area so that it prevents spread of a potential infection to the body. The increased fluid in the tissue will also help dilute the offending agent, whether it is chemical or a microorganism. |
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| Change in the lining of the vessel (adhesion) (the endothelium), due to release of chemical mediators such as mast cells, macrophages, and cytokines; these cause communication between the injured area and the endothelium. The endothelial cells attract leukocytes to the walls of the vessel, where they adhere (margination). The endothelial cells open enough to allow the leukocytes to migrate through and into the tissue spaces (chemotaxis). Once the leukocytes get to the area of damage, they engulf and degrade the damaged cells and bacteria. This is the 3rd stage of the inflammatory process. |
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| Immediate and early response to an injurious agent. The response serves to control and eliminate altered cells, microorganisms, and antigens. Occurs in two phases: vascular phase and cellular phase. Vascular phase: leads to an increase in blood flow and changes in the small blood vessels of the microcirculation. Cellular phase: leads to the migration of leukocytes from the circulation and their activation to eliminate the injurious agent. The primary function of inflammatory response is to limit the injurious effect of the pathogenic agent and remove the injured tissue components, allowing the tissue repair to take place. Time frame is hours to days, depending on the injury to tissue. Risk of scarring and deformity greater. Leukocyte activation and phagocytosis. |
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| Characterized by infiltration of lymphocytes, macrophages, and fibroblasts; this is what causes the scarring and deformity. Self-perpetuating and may last for weeks, months, or even years. May develop as the result of a recurrent or progressive acute inflammatory process or from low-grade, smoldering responses that fail to evoke an acute response. Involves the proliferation of fibroblasts instead of exudates. Causes: foreign bodies such as talc, silica, asbestos, and surgical suture materials; viruses, bacteria, fungi, and larger parasites of moderate to low virulence. Two patterns: nonspecific (chronic inflammation that involves a diffuse accumulation of macrophages and lymphocytes at the site of injury) and granulomatous (massing of macrophages surrounded by lymphocytes, these modified macrophages resemble epithelial cells, associated with foreign bodies (splinter, silica, asbestos, microorganism that causes TB, syphillis, sarcoidosis and deep fungal infections and brucellosis) . |
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| Inflammation is usually the beginning of this process to restore the tissue back to normal structure and function. Tissue regeneration is possible as long as the cells are capable of mitotic division. There are some cells that do not do this- once destroyed, they are replaced with fibrous scar tissue. This can also occur when damage is extensive, fibrin persists in the wound, or infection results in abcess or granuloma formation. This is regulated by chemical mediators and growth factors. Chemical mediators are the same ones that are involved in the inflammatory response. Growth factors are specific to certain cells and are named in one of 3 ways: the tissue they originate in; their biologic activity;or the cells that they work on. These cells are the ones that regulate the entire process, from attracting cells to help with removal of cellular debris, repair and regeneration; stimulating angiogenesis; and building of an extra cellular matrix. |
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| Occurs by primary or secondary intention- primary is what normally occurs and what would also occur with wounds such as incisions with surgery or traumas such as lacerations (cuts) or abrasions-- these wounds may be closed with glue, staples, or sutures (stitches) and would heal from the outside in. With secondary healing by intention, there is more complexity in that these are larger wounds with more tissue damage, or potentially infection involved. These wounds would heal from the outside in with formation of granulation tissue and usually involve scarring. 3 phases: inflammatory, proliferatiive, and remodeling. Delay: malnutrition (particularly protein, vitamins A, C), aging (less collagen and fibroblast synthesis), poor blood flow to the area of injury, oxygen delivery (aids in collagen synthesis), infection and impaired immune responses. |
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| Hosts (people or animals), Infectious Agents (microbes, bacteria, viruses, fungi, protozoa, and rickettsia), Reservoirs(pooled sources which harbor infectious agents), Portals of Exit (secretions, excretions), Modes of Transmission (way in which the infectious agents get passed from one host to another), and Portals on Entry (avenues by which an infectious agent enters a new host). |
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| Serum marker for systemic inflammation elevated CRP associtated with vascular disease. Acute inflammatory phase reactant, major infections, trauma, or acute hospitalization canelevate levels performed whenpatient is clinically stable. Involved in the defense against infections. Produced in the liver after cytokine activation and function as opsonins as well as activators of the alternative complement pathway. Works mannose-binding ligand (MBL). The binding of MBL to mannose residues and CRP to phospholipids and sugars on microbes And their subsequent binding to their complementary receptors on leukocytes leads to phagocytosis and immune cell activation. Named because it precipitated with the C fraction (C-polypeptide) of pneumococci. |
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| Erythrocyte Sedimentation Rate (ESR) |
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| Screening test for monitoring the fluctuations in the clinical course of a disease. In anticoagulated blood, RBC aggregate and sediment to the bottom of a tube. The rate of fall of the aggregate is accelerated in the presence of fibrinogen and other plasma proteins that are often increased in inflammatory diseases. The ESR is the distance in mm that a red cell column travels in 1 hour. Normal values are 0-15 mm/hr for men and 1-20 mm/hr for women. |
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| Leukocytes is, or increased white blood cells, is a frequent sign of an inflammatory response, especially one caused by bacterial infection. Commonly increases from a normal value of 4,000-10,000 to 15,000-20,000 in acute inflammatory conditions. After being released from the bone marrow, circulating neutrophils have a life span of only about 10 hours and therefore must be constantly replaced if their numbers are to adequate. With excessive demand for phagocytes, immature forms of neutrophils (bands) are released from the bone marrow. Bacterial infections produce a relatively selective increase in neutrophils ( neutrophillia), whereas parasitic and allergic responses induce eosinophilia. Viral infections tend to produce a decrease in neutrophils ( neutropenia) and an increase in lymphocytes (lymphocytosis). A decrease in white blood cells (leukopenia) may occur with overwhelming infections or an impaired ability to produce white blood cells. Chemotaxis: direct movement of WBC, |
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| 3 Phases of Wound Healing |
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Definition
Inflammation: neutrophils die off then monocytes mature, macrophages eat dead neutrophils and cellular debris then the wound is cleaned.
Proliferation: clot is replaced with granulation tissue, new covering of epidermal cells, edges are appoximated, fibroblasts produces collagen which holds the wound together providing strength and structure (skin starting to grow back).
Maturation(Remodeling): several weeks after injury cells and capillaries begin to thin out, collagen is replaced with stronger collagen material, wound contracts and sealed with a collagen rich scar tissue |
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