Term
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Definition
| Condition of being resistant to infection. |
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Term
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Definition
| Coordinated response of cells and molecules of the immune system |
|
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Term
| What are the two categories of immunity? |
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Definition
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Term
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Definition
| Consists of physical, chemical, molecular and cellular defenses. Prevents deeper tissue penetration of microorganisms. Includes components such as the skin, and mucous membranes |
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Term
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Definition
| The second line of defense. Less rapid than innate and consists of lymphocytes and their products. (antibodies) |
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Term
| What are the two subtypes of acquired immunity? |
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Definition
Humoral Immunity
Cell Mediated Immunity |
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Term
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Definition
| Involves antibodies produced by B-lymphocytes |
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Term
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Definition
| Involves T-lymphocytes and intracellular microbes |
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Term
| What attracts neutrophils to areas of injury? |
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Definition
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Term
| What is the most common type of WBC observed in a person with an infection? |
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Definition
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Term
| Neutrophils contain three types of granules and a lysosome group |
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Definition
Primary-enzymes with anti bacterial activity
Secondary-Enzymes associated with plasma membrane
Tertiary granules-Plasminogen activator
Lysosome-Acid hydrolyses |
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Term
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Definition
| Mononuclear cell that contains digestive vacuoles |
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Term
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Definition
| Phagocytic cells that are found in almost all tissues. Important first line of defense in innate immune response. Respond to chemotactic stimuli |
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Term
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Definition
| Release pro-inflammatory chemicals from granules when activated |
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Term
| What granules do basophils release? |
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Definition
Histamine
Platelet activating factor |
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Term
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Definition
| Found in connective tissue throughout the body. Mast cell degranulation is stimulated by injury, immune responses, complement C3a C5a and cytokines 1L-1 and 1L-8 |
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Term
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Definition
| Tissue and vascular reactions resulting from non-lethal injury. Delivery of fluid, dissolved substances and cells from the circulating blood and tissues to an area of injury or necrosis |
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Term
| What are some of the benefits of inflammation? |
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Definition
Localizes an area of injury
Neutralization of offending agent
Removal of necrotic tissue
Sets stage for repair process |
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Term
| What are some common causes if inflammation? |
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Definition
| Physical, chemical and biological agents |
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Term
|
Definition
| Almost immediate reaction of local tissues and blood vessels to injury |
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Term
| What is the primary goal of acute inflammation? |
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Definition
| Remove the injurious agent and limit extent of tissue damage |
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Term
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Definition
| Persists for a longer time frame than acute inflammation. Occurs when there is a persistence of the injurious agent |
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Term
| What are the cardinal signs of inflammation? |
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Definition
Rubor-Erythema
Calor-Heat
Dolor-Pain
Tumor-Edema
Function lasea-Altered function |
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Term
| What are the two stages of acute inflammation? |
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Definition
Vascular stage
Cellular stage |
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Term
| What occurs during the vascular stage? |
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Definition
| Vasodilation and increased vascular permeability |
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Term
| How is vasodilation induced? |
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Definition
| Several mediators such as histamine and nitric oxide |
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Term
| How does erythema and warmth occur? |
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Definition
| These processes occur during vasodilation because there is an increased blood flow which warms the area and makes it become congested. |
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Term
| What occurs during the cellular stage of acute inflammation? |
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Definition
| Emigration of leukocytes from microcirculation and accumulation at site of injury |
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Term
| What process immediately follows vasodilation? |
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Definition
| Increased vascular permeability |
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Term
| What does increased vascular permeability include? |
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Definition
| Outpouring if protein-rich fluid into extravascular spaces. This fluid loss results in an increased concentration of RBC's, WBC's, platelets and clotting factors in the blood. |
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Term
| Loss of plasma proteins reduces intracapillary osmotic pressure which causes |
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Definition
| Formation of endothelia gaps |
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Term
| What do histamine, bradykinin and leukotrites do? |
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Definition
| Bind to endothelia receptors causing contraction of endothelial cells and separation of intracellular junctions. |
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Term
| Increased vascular permeability occurs where? |
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Definition
| The venular end of the capillary bed. |
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Term
| Immediate Transient Response |
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Definition
| Involves a minor injury, develops rapidly, lasts for a short duration (15-30 minutes), affects venules and is mediated by hisatmine acting on endothelium. |
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Term
| Immediate sustained response |
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Definition
| Occurs with more serious types of injuries, continues for several days, direct damage of the endothelium by injurious stimuli such as burns and bacterial infections. |
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Term
| Delayed hemodynamic response |
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Definition
| Increased permeability begins after 2-12 hours and lasts several hours or days. Occurs with injuries resulting from radiation. Involves venules and capillaries |
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Term
| What is a delayed hemodynamic response mediated by? |
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Definition
| Bradykinin, factors derived from complements and factors from dead neutrophils in exudate |
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Term
| What are the three classes of inflammatory mediators? |
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Definition
Vasoactive amines
Plasma enzyme systems
Arachidonic acid metabolites |
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Term
| What four processes is histamine involved in? |
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Definition
| Vasodilation, increased vascular permeability, physical injuries and immunologic reactions. |
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Term
| Histamine is a granule of what types of cells? |
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Definition
| Mast cells, basophils and platelets |
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Term
|
Definition
| Mediators formed through the action of proteolytic enzymes |
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Term
| Arachidonic acid metabolites |
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Definition
| Derived from phospholipids of cell membranes. Involved in both the cyclooxygenase and lipoxygenase pathways. |
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Term
|
Definition
| Oxygen metabolites and lysosomal contents of neutrophils and macrophages. |
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Term
| What are two types of cytokines? |
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Definition
Interleukins 1 and 8 (1L-1 and 1L-8)
Tumor necrosis factor (TNF) |
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Term
|
Definition
| Complementary adhesion molecules |
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Term
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Definition
| Selectins, endothelial adhesion molecules, integrins. |
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Term
| What events triggers leukocyte extravision? |
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Definition
| When leukocytes are activated, integrins on their surface interact with endothelial adhesion molecules and lead to leukocyte extravision. |
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Term
| What is leukocyte extravision? |
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Definition
| Emigration of leukocytes from microcirculation and accumulation at the site of an injury (extravision) |
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Term
| Leukocyte extravision is involved in what stage of acute inflammation? |
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Definition
|
|
Term
| What are the events of leukocyte extravision? |
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Definition
Margination
Rolling
Adhesion
Pavementing
Transmigration |
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Term
|
Definition
| Accumlation of WBC's along the endothelial surface |
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Term
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Definition
| Tumbling of WBC's along the endothelial surface |
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Term
|
Definition
| Firm adhesion of WBC's to endothelial surface |
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Term
|
Definition
| Lining of adhered WBC's along the endothelial surface |
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Term
|
Definition
| WBC's move across endothelium (diapedesis) |
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Term
| Rolling, adhesion and transmigration involve |
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Definition
| Selectins, mucin-like glycoproteins, immunoglobulins and integrins. |
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Term
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Definition
| Transmembrane glycoproteins, expressed o the surface of WBC's and activated endothelial cells. 1L-1 and TNF |
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Term
| Binding of selectins is dependent upon what? |
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Definition
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Term
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Definition
| Expressed on endothelial cells and bind to oligosaccharides (Sialyl-Lewis X antigen) found on surface of WBC's. |
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Term
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Definition
| Expressed on neutrophils and bind to endothelial mucin-like molecules (Gly CAM-1) |
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Term
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Definition
| Molecules on the surface of WBC's that must be activated for tight adhesion to occur |
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Term
| What are integrins induced by? |
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Definition
| Platelet Activating Factor |
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Term
| Activation integrin binds to what? |
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Definition
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Term
|
Definition
| Process by which WBC's emigrate in tissues toward the site of an injury. (Move along chemical gradient) |
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Term
| Types of chemotactic agents |
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Definition
Exogenous (Bacterial products)
Endogenous (Damages tissue, C5a, leukotrine B4 and interleukin 8) |
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Term
| How do chemotactic agents work? |
|
Definition
Activation of phospholipase C (via G protein) causes release of Ca2+.
This causes the assembly of contractile elements within the cell (actin and myosin)
Once the assembly of the contractile elements has been completed, locomotion along a chemical gradient occurs. |
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Term
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Definition
| Recognition and attachment of particle to be ingested by a WBC |
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Term
| What does the process of phagocytosis involve? |
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Definition
Adherence/Binding
Engulfment/Ingestion
Fusion
Degradation or killing of ingested material |
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Term
| What does the neutrophilic kill mechanism require? |
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Definition
| It requires O2, NADPH and NADPH oxidase |
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Term
|
Definition
| Elevation in body temperature caused by cytokine-induced increase in hypothalamic set-point |
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Term
| What are the systemic responses of inflammation? |
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Definition
| Fever, leukocytosis and an increase in circulating proteins. |
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Term
| How does a fever initiate? |
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Definition
| Pyrogens (fever producing mediators) along with cytokine 1L-1 act on the hypothalamus by exciting the neuron in the anterior hypothalaus. This excitation causes the hypothalamus tp produce prostaglandins which cause the thermoregulatory set point to rise. The body then initiates heat-promoting mechanisms and initiates a fever |
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Term
| What are the four fever patterns? |
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Definition
Intermittent
Remittent
Sustained
Recurrent/Relapsing |
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Term
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Definition
| Temperature returns to normal at least once every 24 hours |
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Term
|
Definition
| Temperature does not return to normal, varies a few degrees up or down |
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Term
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Definition
| Temperature remains above normal, not much variation |
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Term
|
Definition
| One or more episodes of fever lasting several days with one or more days of normal temperature in between episodes |
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Term
| What are the benefits of a fever? |
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Definition
Improves the efficiency of leukocyte killing
Impairs replication of microorganisms |
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Term
| What are the disadvantages of a fever? |
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Definition
| May enhance the host's susceptibility to the effects on endotoxins |
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Term
|
Definition
| Increased release of white blood cells above the normal range. (15-20,000/uL in acute inflammation) |
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Term
| What is the cause of leukocytosis |
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Definition
| 1L-1 and TNF signal bone marrow to increase rate of cell release |
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Term
|
Definition
|
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Term
|
Definition
Infectious mononucleosis
German measles |
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Term
|
Definition
Bronchial asthma
Allergies
Parasitic infection |
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Term
|
Definition
| Decreased number of leukocytes below the normal reference range. Associated conditions are typhoid fever, viral infections, Rickettsial infections and some protozoa |
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Term
| Circulating plasma proteins |
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Definition
| Increase in acute phase reactants (APR) |
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Term
| When does a leukocyte induced injury occur? |
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Definition
| When activated WBC mechanisms do not distinguish between offending agent and host |
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Term
| Chronic inflammation is characterized by what? |
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Definition
| Infiltration of monoculear cells. It is an attempted connective tissue repair that is self-perpetuating and lasts for weeks, months and years. |
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Term
| Chronic inflammation develops from a recurrent acute inflammatory response or low-grade response that does not evoke |
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Definition
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Term
| The fate of an inflammation reaction can produce which two outcomes? |
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Definition
Resolution-Restoration of original structure and function
Repair- Replacement of damaged tissue with scar tissue. |
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Term
| The ability of tissues to regenerate is limited to only cells that are able to undergo |
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Definition
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Term
| Which tissues can regenerate easily? |
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Definition
|
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Term
| Which tissues can regenerate well? |
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Definition
| Cells of the liver, renal tubule and secretory elements of certain glands |
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Term
| Which tissues regenerate poorly or not at all? |
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Definition
Renal glomeruli
Skeletal muscle
Heart
CNS |
|
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Term
| What is the first step of repair? |
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Definition
Preparation of the injure site for either regeneration or repair
Debridgement
Drainage or exudate
Vascular dilation and permeability are reversed |
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Term
| Reconstructive phase begins 3-4 days past initial injury and continues for as long as two weeks. The steps in reconstructive phase include |
|
Definition
Epitheliazation
Angiogenesis
Proliferation of fibroblasts
Synthesis of Collagen
Cellular differentiation |
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Term
| For healing to proceed after the would has been initially sealed off by the primary/secondary platelet plugs what must occur? |
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Definition
The fibrin clot must be dissolved (fibrinolysis)
Macrophages clean up the area and secrete chemicals which attract fibroblasts to the area
Granulation tissue forms in the wound area. |
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Term
|
Definition
| Epithelial cells migrate under the clot or scab and connect to form a seal |
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Term
|
Definition
| Production of new blood vessels from preexisting vessels. |
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Term
| What is angiogensis stimulated by? |
|
Definition
| Vascular Endothelial Growth Factor (VEGF) |
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|
Term
| Proliferation of fibroblasts involves |
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Definition
| VEGF increases vascular permeability which leads to the deposition of fibrinogen and fibronectin which leads to the creation of a framework. Migration of fibroblasts then migrate to the site of injury and proliferate |
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|
Term
| What stimulates fibroblasts to proliferate and enter lesions? |
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Definition
| Fibroblastic-activating fator |
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Term
|
Definition
| A system in the body that complements the abilities and phagocytic cells to clear pathogens from an organism. |
|
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Term
|
Definition
| A process in which a pathogen is marked for ingestion and destruction by a phagocyte. It involves the binding of an opsonin, or antibody to an epitope on an antigen. After opsonin binds to the membrane, phagocytes are attracted to the pathogen. |
|
|
Term
| The Fab portion of the antibody binds to the |
|
Definition
|
|
Term
| The Fc portion of the antibody binds to the |
|
Definition
| Fc receptor on the phagocyte. This facilitates phagocytosis. |
|
|
Term
| Erythrocyte Sedimentation Rate |
|
Definition
| The rate of which red blood cells sediment in a period of one hour. Measured in mm/hour and it the results are increased in inflammation. Useful to diagnose diseases such as multiple myeloma, temporal arteritis and polymyalgia rheumatica |
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Term
|
Definition
| Cell that makes extracellular matrix and collagen |
|
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Term
|
Definition
| Swelling caused by vasodilation and increased blood vessel wall permeability in inflammation. |
|
|
Term
| What are the causes of the cardinal signs of inflammation? |
|
Definition
Erythema-Vasodilation
Heat-Vasodilation
Pain-Cytokines, edema
Edema-Increased vascular permeability
Altered Function- Increased vascular permeability |
|
|
Term
| What are the three pathways of the complement cascade? |
|
Definition
Classic Pathway
Alternative Pathway
Lectin Pathway |
|
|
Term
| What complement proteins are involved in the classical pathway? |
|
Definition
|
|
Term
| What complement proteins are involved in the alternative pathway? |
|
Definition
| Factor D, Factor B, Properdin and C3 |
|
|
Term
| What complement proteins are involved in the lectin pathway? |
|
Definition
| MBL, Ficolin, MASP-2, C4 and C2 |
|
|
Term
| What is the ultimate goal of the complement cascade? |
|
Definition
| The activation of C3 to make C3a and C3b |
|
|
Term
|
Definition
| Enhance Inflammation with other compliment proteins such as C5a |
|
|
Term
|
Definition
| Opsonization and lysis of cell to create membrane attack complex |
|
|
Term
| Compliment proteins are activated when they are |
|
Definition
|
|
Term
| Classical pathway is initiated when |
|
Definition
| Antibodies bind to the antigens of a pathogen. C1q c1s and C1r all bind to the antibody and form another complex known as C4b2a or C3 covertase |
|
|
Term
| Lectin pathway is initiated when |
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Definition
| Proteins bind to carbohydrates on the pathogen. Ficolin binds to oligosaccharides and MBL binds to mannose |
|
|
Term
| Ficolin and MBL, along with their associates, form a |
|
Definition
| Compliment protein complex known as C4b2a or C3 convertase |
|
|
Term
| What are the first two pathways that are activated? |
|
Definition
| Classical pathway and lectin pathway. The alternative pathway isn't activated until the C3 convertase (product of the other two pathways) has been formed |
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|
Term
| What does C4b2a or C3 convertase do? |
|
Definition
| C3 convertase, which is located on the surface of a pathogen, activates C3 and cleaves it into C3a and C3b |
|
|
Term
| When is the alternative pathway initiated? |
|
Definition
| It is initiated when the C4b2a activates C3b. |
|
|
Term
| How is the alternative pathway initiated from the classical pathway? |
|
Definition
| C3b formed from the classical pathway binds to the surface of the pathogen along with Factors D and B. It then forms an alternative C3 Convertase known as C3bBb |
|
|
Term
| How is the alternative pathway initiated from the lectin pathway? |
|
Definition
| C3b activated by the lectin pathway combines with a protein known as properdin to form the compliment protein complex C3bBb. |
|
|
Term
| All compliment proteins with a small "a" after them will performs what type of process? |
|
Definition
|
|
Term
| C3a and C5a stimulate what? |
|
Definition
| Mast cells to release histamine |
|
|
Term
|
Definition
| Enhances inflammation by increasing vascular permeability allowing leukocytes to pass through more easily. It also attracts leukocytes |
|
|
Term
|
Definition
| The pathogen surface using a thioester bond. Opsonization is said to have occurred after the surface of the pathogen is coated with C3b proteins. |
|
|
Term
| Macrophages have what types of receptors? |
|
Definition
|
|
Term
| C5a receptors cannot bind to the C3b without what compliment protein that will help bind the C3b to the CR1 receptors on the macrophage. |
|
Definition
|
|
Term
| Once the C3b proteins on the surface of a pathogen have bound to the CR1 receptors on a macrophage what process occurs? |
|
Definition
|
|
Term
| C3b can also bind to what, producing what effect? |
|
Definition
| C4b2a complex forming a C4b2a3b complex also known as C3/C5 convertase |
|
|
Term
| What does the C3/C5 convertase do? |
|
Definition
It can split to activate C3 and form C3a and C3b.
It can also cleave and activate C5 to form C5a and C5b |
|
|
Term
| C5a can perform what functions? |
|
Definition
| Enhance inflammation or bind to macrophages receptor |
|
|
Term
| C5b initiates the formation of what? |
|
Definition
| The terminal stage, the membrane attack complex (MAC) |
|
|
Term
| What compliment proteins form the MAC? |
|
Definition
|
|
Term
| Formation of a membrane attack complex on the surface of a pathogen will cause what? |
|
Definition
| It will cause the membrane to lyse, making the cell burst and destruct. |
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