Term
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Definition
| natural or native immunity. includes barriers ([1st line of defense]physical, mechanical and biochemical) and inflammation [2nd line of defense]. Form the first line of defense at the body's surface and are in place to prevent damage by substances in the environment and thwart infection by pathogenic microorganisms. |
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Term
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Definition
| acquired or specific immunity. is induces in a relatively slower and more specific process and targets particular invading microorganisms for the purpose of eradicating them. Involves 'memory' |
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Definition
| are the first lines of defense that prevent damage to the individual and prevent invasion by pathogens; these include the skin and mucous membranes |
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Term
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Definition
| Antibacterial peptides (cathelicidins, defensins, collectins, and mannose-binding lectin) in mucous secretions, perspiration, saliva, tears, and other secretions provide a against pathogenic microorganisms. |
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Definition
| The skin and mucous membranes are colonized by commensal or mutualistic microorganisms that provide protection by releasing chemicals that facilitate immune responses, prevent colonization by pathogens, and facilitate digestion in the gastrointestinal tract. |
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Term
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Definition
| a spectrum of nonpathogenic microorganisms resides on the body's surface. These bacteria contribute to our innate protection against pathogenic microbes by competing for nutrients and blocking attachment to the epithelium. They also produce chemicals and toxic proteins that inhibit colonization by pathogenic microbes. |
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Definition
| The second line of defense, a rapid and nonspecific protective response to cellular injury from any cause. It can occur only in vascularized tissue. |
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Term
| manifestation of inflammation |
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Definition
*The macroscopic hallmarks of are redness, swelling, heat, pain, and loss of function of the inflamed tissues.
*The microscopic hallmarks of are vasodilation, increased capillary permeability, and an accumulation of fluid and cells at the inflammatory site. |
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Term
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Definition
(1) vasodilation and increased blood flow (erythema and warmth)
(2) Leakage of plasma proteins (edema)
(3) Leukocyte (neutrophil) recruitment and migration. |
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Term
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Definition
| The second line of defense, a rapid and nonspecific protective response to cellular injury from any cause. It can occur only in vascularized tissue. |
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Term
| manifestation of inflammation |
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Definition
*The macroscopic hallmarks of are redness, swelling, heat, pain, and loss of function of the inflamed tissues.
*The microscopic hallmarks of are vasodilation, increased capillary permeability, and an accumulation of fluid and cells at the inflammatory site. |
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Term
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Definition
(1) vasodilation and increased blood flow (erythema and warmth)
(2) Leakage of plasma proteins (edema)
(3) Leukocyte (neutrophil) recruitment and migration. |
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Term
| Inflammation is mediated by three key plasma protein systems |
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Definition
| the complement system, the clotting system, and the kinin system. The components of all three systems are a series of inactive proteins that are activated sequentially. |
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Term
| Steps of acute inflammatory response |
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Definition
(1) Cellular Injury/Pathogenic invasion
(2) Mast cell degranulation, the activation of three plasma systems, and the release of subcellular components from the damaged cells occur as a consequence (these systems are independent, so that induction of one can result in the induction of the other two).
(3)steps 1 and 2 results in vasodilation (erythema, warmth), Vascular permeability (edema), Cellular infiltration (pus), Thrombosis (clots), and Stimulation of nerve endings (pain) |
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Term
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Definition
| each of the plasma protein systems has there own specific function although similar to other ones. Each system consists of multiple proteins in the blood that can be activated during inflammation. Activation of these first components results in sequential activation of other components in the system leading to a biologic function that helps protect the individual. The sequential activation is referred to as a |
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Term
| Diagram the complement, clotting, and kinin systems, noting where they converge. |
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Definition
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Term
| The most biologically potent products of the complement system are |
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Definition
| C3b (opsonin), C3a (anaphylatoxin), and C5a (anaphylatoxin, chemotactic factor). |
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Definition
| is the most important product of the kinin system and causes vascular permeability, smooth muscle contraction, and pain. |
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Term
| Describe two control mechanisms for the protein systems, and explain how they provide a check and balance system for inflammation. |
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Definition
| Carboxypeptidase, histaminase, and C1 esterase inhibitor are inactivating enzymes, and the fibrinolytic system and plasmin facilitate clot degradation after bleeding is stopped. |
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Term
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Definition
| are the most common leukocytes and are classified by the type of stains needed to visualize enzyme-containing granules in their cytoplasm. (basophil, eosinophil, neutrophil) |
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Term
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Definition
| cytoplasmic fragments formed from megakaryocyte. They circulate in the bloodstream until vascular injury occurs. Activation results in (1) their interaction with components of the coagulation cascade to stop bleeding and (2) degranulation, releasing biochemical mediators such as serotonin, which has vascular effects similar to those of histamine. |
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Term
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Definition
| Various forms participate in the innate immune response (natural killer [NK]cells) and the acquired immune response (B and T cells). |
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Term
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Definition
| a lymphocyte capable of killing target cells by binding specific receptors with or without the aid of antibodies and by releasing chemical toxic to the targeted cell. |
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Term
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Definition
| are precursors of macrophages that are found in the tissue. |
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Term
| How can phagocytosis actually promote the inflammatory process? |
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Definition
| Released lysosomal products also may contribute to inflammation by increasing vascular permeability, attracting additional monocyte, and activating the complement and kinin systems. |
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Term
| How can phagocytosis actually promote the inflammatory process? |
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Definition
| Released lysosomal products also may contribute to inflammation by increasing vascular permeability, attracting additional monocyte, and activating the complement and kinin systems. |
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Term
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Definition
| cooperation is achieved in innate and acquired immunity by secretions of a variety of molecules that affect other cells. These factors are referred to as |
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Term
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Definition
| classification of cytokines that are produced predominantly by macphages and lymphocytes in response to stimulation of PRR's or by other cytokines. |
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Term
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Definition
| members of a family of cytokines that protect against viral infections |
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Term
| pro-inflammatory cytokines |
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Definition
interleukins
transforming growth factor-beta (TGF-b)
chemokines |
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Term
| anti-inflammatory cytokines |
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Definition
| tumor necrosis factor-alpha TNF-a) |
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Term
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Definition
is a multistep cellular process for the elimination of pathogens and foreign debris. The steps include recognition and attachment, engulfment, formation of a phagosome
Chapter Summary Review 6-3
Copyright © 2017, Elsevier Inc. All rights reserved.
and phagolysosome, and destruction of pathogens or foreign debris. Phagocytic cells engulf microorganisms and enclose them in phagocytic vacuoles (phagolysosomes), within which toxic products (especially metabolites of oxygen) and degradative lysosomal enzymes kill and digest the microorganisms |
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Term
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Definition
is self-limiting and usually resolves within 8 to 10 days.
Local manifestations of inflammation are the result of the vascular changes associated with the inflammatory process, including vasodilation and increased capillary permeability. The symptoms include redness, heat, swelling, and pain. |
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Term
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Definition
can be a continuation of acute inflammation that lasts 2 weeks or longer. It also can occur as a distinct process without much preceding acute inflammation.
is characterized by a dense infiltration of lymphocytes and macrophages. The body may wall off and isolate the infection to protect against tissue damage by formation of a granuloma. |
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Term
| healing by primary intention |
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Definition
| Damaged tissue proceeds to resolution (restoration of the original tissue structure and function) if little tissue has been lost or if injured tissue is capable of regeneration. |
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Term
| healing by secondary intention |
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Definition
| Tissues that sustained extensive damage or those incapable of regeneration heal by the process of repair resulting in the formation of a scar. |
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Term
| Dysfunctional wound healing |
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Definition
| can be related to ischemia, excessive bleeding, excessive fibrin deposition, a predisposing disorder (such as diabetes mellitus), wound infection, inadequate nutrients, numerous drugs, or altered collagen synthesis. |
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Term
histologic characteristics of resolution
inflammatory phase |
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Definition
| usually lasts for 1 to 2 days, includes coagulation and the infiltration of cells that participate in wound healing, including platelets, neutrophils, and macrophages. The fibrin mesh of the blood clot acts as a scaffold for cells that participate in healing. Platelets contribute to clot formation and, as they degranulate, release, release growth factors. Neutrophils clear the wound of debris and bacteria and are later replaced by macrophages. Macrophages are essential because they are phagocytic, release wound healing mediators and growth factors, recruit fibroblasts, and help promote angiogenesis during the proliferative phase of wound healing. |
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Term
histologic characteristics of repair
proliferative phase |
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Definition
| begins 2-4 days after the injury and continues for as long as 2 weeks. The wound is sealed and the fibrin clot is replaced by normal tissue or scar tissue during this phase. Is characterized by macrophage recruitment of fibroblasts and fibroblast proliferation, followed by fibroblast collagen synthesis, epithelialization, contraction of the would and cellular differentiation. |
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Term
histologic characteristic of repair
remodeling and maturation |
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Definition
| begins several weeks after injury and is normally complete within 2yrs. during this phase, there is continuation of cellular differentiation, scar formation, and scar remodeling. The fibroblast is the major cell of tissue remodeling with the deposition of collagen into an organized matrix. |
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Term
Plasma protein systems in inflammation |
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Definition
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