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Definition
| a "pre-programmed" response of tissue to injury; involves the microcirculation plus cellular and acellular components of the blood. |
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| List of the Cellular components of inflammation |
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Definition
| polymorphonuclear leukocyte, monocyte, lymphocytes, eosinophils, basophils, and platelets |
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| Polymorphonuclear Leukocytes |
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Definition
| short-lived, "end-stage" phagocytic cell. |
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Definition
| Large phagocytic cell capable of reproduction; tissue monocytes are termed histiocytes or macrophages. |
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Definition
| source of antibody producing plasma cells; Humoral immunity. |
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Definition
Helpers [T4 helper cells induce Ab production], killers, suppressors
[T8 suppresses Ab production]; Cell-mediated immunity. |
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Definition
| molecule found early in antibody production; activates complement. |
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Definition
| smaller molecule (than IgM); is long-lived in the circulation |
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Definition
| mucosal antibody. Secretions found especially in Respiratory and GI Tracts. |
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Definition
| responsible for allergies and allergic reactions. [eg: mast cells -> anaphylactic reaction] |
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Definition
| granulocyte with eosinophilic cytoplasmic granules; capable of phagocytosis, especially antigen-antibody complexes. [eg: allergic and parasitic reaction] |
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Definition
| granulocyte with basophilic cytoplasmic granules containing vasoactive polypeptides, such as histamine. Basophils in peripheral circulation - Cf: mast cell in tissue] |
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Definition
fragments of the cytoplasm of megakaryocytes (located in bone marrow); cause stickiness of red cells and help initiate clotting within blood vessels.
[have phospholipids -> for clotting]
Clinical correlation: aspirin and/or ibuprofin affect ability of platelets to aggregate |
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Term
| List of the Acellular components of inflammation (chemical mediators) |
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Definition
| Histamine, Progtaglandins and leukotrines, Platelet activating factor, Cytokines, Nitric Oxide, Complement system, Kinins, clotting pathway and thrombolytic pathway |
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Term
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Definition
| a vasoactive polypeptide which causes increased short-term vascular permeability; released from mast cells, basophils and platelets. |
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Term
| Prostaglandins, leukotrines |
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Definition
| variety of effects- - including vascular constriction, dilation, permeability; leukocyte adhesion; pain. |
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Term
| Platelet-activating factor |
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Definition
| synthesized by mast cells, basophils, platelets, neutrophils, monocytes, endothelium. Causes vasoconstriction, increased vascular permeability and platelet aggregation. |
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Term
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Definition
| products released by activated lymphocytes and monocytes, some of which are capable of attracting other leukocytes; improving phagocytic activity; cause fever and anorexia.; stimulate fibroblasts. |
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Definition
| made by endothelium and macrophages. Causes vascular dilation and increasedvascular permeability; can mediate cell and bacterial killing. |
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Term
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Definition
| a circulating protein system of proenzymes which, when activated (usually by antigen-antibody complexes - esp. IgM), form several fragments, which augment the inflammatory process (for example - cause release of histamine from mast cells/platelets, chemotaxis, phagocytosis, and cell membrane damage). |
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Definition
| a series of small polypeptides derived from serum which, after enzymatic conversion, produce prolonged vascular permeability; causes pain; activates complement. |
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Definition
| results in coagulation of blood by formation of fibrin (a large clottable protein) from fibrinogen [fibrinogen is the only clottable protein in the body]. |
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Definition
| feedback mechanism to prevent excessive clotting. |
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Term
| List of the Cardinal Signs of inflammation (as described by Celsus) |
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Definition
| Rubor (redness), tumor (swelling), calor (heat), and dolor (pain) |
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Term
| What did Galen add to the cardinal signs of inflammation? |
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Definition
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Term
| Duration of acute inflammation |
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Definition
| Relatively short duration (few minutes, several hours, 1 or 2 days), nonspecific response to tissue damage. |
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Term
| Cell type of acute inflammation |
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Definition
| leukocytes, predominantly neutrophils (polymorphonuclear leukocytes - derived from bone marrow granulocyte; is an end-stage cell, ie, once outside of bone marrow, does not divide/proliferate). |
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Term
| Sequence of events of acute inflammation |
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Definition
| (1)Transient vasoconstriction of arterioles (2)Vasodilation resulting in increased blood flow (3)Increased permeability of the microvasculature (histamine then kinin) with slowing of the circulation, outpouring of protein-rich fluid (fibrinogen/fibrin and immunoglobulin) into extravascular tissues, stasis (dilated small vessels packed with red cells)(4) Leukocytic margination (neutrophils first, then smaller numbers of monocytes [tissue monocutes/histiocytes can replicate, as evidenced by mitosis] and lymphocytes) along the vascular endothelium, emigration (5) Phagocytosis, lysosomal activity |
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Term
| Outcomes of acute inflammation |
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Definition
| Resolution/restitution, healing by scarring, abscess formation, progression to chronic inflammation |
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Definition
| restoration to normal structure and function |
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Definition
| deposition of vascular granulation tissue; gradual progression to dense collagenous scar tissue with low vascularity |
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Definition
| [eg: clostridium - a gas-forming bacterium] |
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Definition
| Longer duration; may follow acute inflammation |
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Term
| Mechanisms that can lead to Chronic inflammation |
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Definition
| repeated bouts of acute inflammation, or may be due to specific agents that classically cause a chronic inflammatory response (such as tubercle bacilli, virus); indicates activation of the immune system. |
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Term
| cell types characteristic of chronic inflammation |
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Definition
| macrophages, lymphocytes, plasma cells. [B cells: antigen; T cells: control] |
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Term
| tissue reaction characteristic of chronic inflammation |
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Definition
| proliferation of blood vessels and connective tissue, scar. [Cf: granulation tissue; keloid - an exuberant collagen build-up] |
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Term
| Chronic Granulomatous Inflammation |
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Definition
| Specific type of chronic inflammation, |
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Term
| Four diseases characteristic granulomatous inflammation |
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Definition
| with tuberculosis, leprosy, deep fungal infections, sarcoidosis, etc. |
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Term
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Definition
| Granulomas are small collections of modified macrophages ("epithelioid cells"), usually surrounded by a rim of lymphocytes. Epithelioid cells have abundant pale-pink, plump cytoplasm. Langhans' or foreign body-type giant cells may be present (represent fusion of macrophages). |
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Term
| cell types composing a granulomas |
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Definition
| macrophages, lymphocytes, and giant type cells |
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Term
| Factors involved in the formation of granulomas |
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Definition
(1.)Presence of indigestible organisms or particles.
(2.)Presence of cell-mediated immunity to the inciting agent (delayed hypersensitivity). |
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Term
| Serous inflammation/transudate |
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Definition
- outpouring of a thin fluid, derived from the blood serum or the secretions of serous mesothelial cells. (E.g. skin blister resulting from a burn.)
[Exudation - the escape of fluid, proteins, and blood cells from the vascular system into the interstitial tissue or body cavities.] |
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Term
| Fibrinous inflammation/exudate |
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Definition
| - exudate of large amounts of plasma proteins, including fibrinogen. Histologically fibrin is identified by its tangled, threadlike eosinophilic meshwork. |
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| Suppurative or purulent inflammation/exudate |
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Definition
| production of large amounts of pus. |
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Term
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Definition
| refers to excessive elaboration of mucin encountered in inflammatory states affecting any mucus-secreting mucosa. (E.g. common cold.) |
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Definition
| characterized by a bloody exudate. |
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Term
| Pseudomembranous inflammation |
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Definition
| formation of a membrane, usually made up of precipitated fibrin necrotic epithelium, and inflammatory white cells. Encountered only on mucosal surfaces, most commonly in the pharynx, larynx, respiratory passages, and intestinal tract. (E.g. diphtheria exotoxin causes necrosis of surface epithelial cells and their desquamation; clostridium toxin affects the intestinal mucosa and is related to patients receiving broad- spectrum antibiotics.) |
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Term
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Definition
| a focal accumulation of neutrophils and liquefactive necrosis. |
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Term
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Definition
| a localized collection of pus. |
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Term
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Definition
| - a local defect of the surface of an organ or tissue, which is produced by the sloughing of inflammatory necrotic tissue. |
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Term
| Systemic effects of inflammation |
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Definition
| Fever, chills, leukocytosis, altered sleep patterns, decreased appetite, etc. |
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Term
| general characteristic of acute inflammation |
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Definition
| short duration, PMN leukocytes, inflammation, and phagocytosis |
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Term
| Tissue reaction to injury, characterized by polymorphonuclear leukocytes, is called |
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Definition
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Term
| : Which of the following is the chemical mediator responsible for increased permeability of endothelial cells? |
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Definition
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| Which of the following is NOT considered a cardinal sign of inflammation? |
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Definition
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| Which immunoglobulin is associated with allergic reactions? |
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Definition
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| Which inflammatory cell is normally more common in tissues than in peripheral blood, and is capable of reproduction and phagocytosis? |
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Definition
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Term
| Which cellular component of the inflammatory process is required to form a blood clot? |
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Definition
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Term
| Exudation of plasma & leukocytes in acute inflammation is from the |
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Definition
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Term
| Which of the following mediators of inflammation causes pain? |
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Definition
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| : A 45-year-old man has had a fever and dry cough for 3 days, and now has difficulty breathing and a cough productive of sputum. On physical examination his temperature is 38.5 C. Diffuse rales are auscultated over lower lung fields. A chest radiograph shows a right pleural effusion. A right thoracentesis is performed. The fluid obtained has a cloudy appearance with a cell count showing 5500 leukocytes per microliter, 98% of which are neutrophils. Which of the following terms best describes his pleural process? |
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