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Path2
Inflammation
| Question | Answer |
|---|---|
| What is inflammation? | Response to injury, including infection. Reaction of blood vessels causes accumulation of fluids and leukocytes in extravascular tissues. Destroys, dilutes or walls off the injurious agent and initiates the repair process. |
| Whata are potentially harmful inflammatory responses? | Hypersensitive reactions to bug bites, drugs or contrast media, chronic diseases such as arthritis and atherosclerosis, disfiguring scars and visceral adhesions. |
| What are the components of an inflammatory response? | 1) vascular reaction 2) cellular/exudative reaction |
| How does inflammation occur? | Via chemical mediators either derived from plasma proteins or cells from inside and outside of blood vessels. |
| What are the the different types of inflammation? | Acute, Chronic and granulomatous |
| Acute inflammation | Characterized by increased blood flow (causes redness and warmth), short duration, edema and emigration of neutrophils from microcirculation. Stimuli include infection, trauma, physical or chemical agents, foreign bodies, and immune reactions. |
| Chronic inflammation | Characterized by a longer duration, angiogenesis, fibrosis and an abundance of lymphocytes and macrophages |
| Granulomatous inflammation | This is a distinctive pattern of chronic inflammation where activated macrophages (epithelioid cells) predominate. |
| Four cardinal signs of inflammation | Rubor: vasodilation, redness. Tumor: swelling, extravascular accumulation of fluid. Calor: heat due to vasodilation. Dolor: pain. |
| Major components of acute reaction | 1)increased blood flow, blood vessel dilation and expansion of capillary bed 2)Deposition of fibrin and other plasma proteins 3)neutrophil emigration |
| Increased blood flow causes... | increased flow through the lymphatics, which increases antigen presentation and immune response. |
| Benefits of fluid accumulation at injury site | toxin dilution, pain decreases use and prevents further injury, antibodies in blood can kill microbes, plasma proteins can amplify response to injurious agent. |
| Increased vascular permeability due to enothelial contraction | Most common mechanism of increased vascular permeability. Occurs in venules via creation of gaps between endothelial cells by vasoactive mediators. FAST (minutes). |
| Increased vascular permeability due to direct injury | Occurs in arterioles, capillaries and venules via toxins, chemicals or burns. FAST and can be long-lived (hours to days) |
| Increased vascular permeability due to leukocyte-dependant injury. | Occurs mostly in venules but can happen in pulmonary capillaries. This a late and long-lived response (hours). |
| Increased vascular permeability due to increased transcytosis | Occurs in venules due to vascular endothelium-derived growth factor. |
| Increased vascular permeability due to angiogenesis | New leaky blood vessels persist until intercellular junctions are formed. |
| What is extravasation? | Delivery of leukocytes from the vessel lumen to the interstitium where they ingest offending agents via phagocytosis, kill microbes and degrade necrotic tissue and foreign antigens. In the lumen, margination, rolling and adhesion occur. |
| Diapedesis | Migration of leukocytes across the endothelium during extravasation |
| chemotaxis | Migration of leukocytes in the interstitial fluid toward the site of damage. |
| Leukocyte adhesion | Along with migration across the vessel wall, adhesion is determined by binding of complimentary adhesion molecules on the leukocyte and endothelia surfaces. Chemical mediators modulate the expression of the adhesion molecules. |
| Leukocyte emigration | 1) Fluid is released and causes edema2) 6-24 hours: Neutrophils3) 24-48 hours: monocytes4) Different adhesion molecules are induced/activated in different phases of inflammation |
| Serous inflamamtion | Outpouring of thin fluid that occurs with serous effusion and blisters. |
| Fibrinous Inflammation | Leakage of fibrin in body cavities that may lead to adhesions/scar tissue formation |
| Suppurative/Purulent inflammation | Pus or purulent exudate forms from neutrophils, debris and edema fluid, resulting in an abcess=localized collection of pus. |
| Ulcer | Sloughing of the inflammatory necrotic tissue causes a defect on the durfac of the organ or tissue. |
| Chronic inflammation | Prolonged duration (weeks or months). Active inflammation, tissue destruction and attempts at repair occur simultaneously. May follow acute inflammation or begin insidiously and often asymptomatically. |
| Causes of chronic inflammation | 1) persistent infections 2) exposure to endogenous or exogenous toxic agents 3) autoimmune (rheumatoid arthritis, lupus) |
| Histological features of chronic inflammation | Infiltration w/mononuclear cells (macrophages, lymphocytes and plasma cells), tissue destruction induced by inflammatory cells and healing by replacement of damaged tissue with CT (fibrosis) and new blood vessels (angiogenesis) |
| Macrophages | Monocyte emigrate into tissue early in inflammation, where they grow and become phagocytic and immobile. These predominate by 48 hours. Injurious agent activates macrophages in the tissue so it secretes biologically active products. |
| How do macrophages get into the tissue? | Circulating monocytes are recruited via rolling, adhesion, diapedesis and then some are stimulated to divide. All are imobilized in the tissue. |
| How are macrophages activated? | Endotoxins (LPS on surface of bacteria), components of the cell matrix (nonimmune) or cytokines made by T cells. |
| What do macrophages do after they are activated? | Secrete toxic oxygen metabolites, proteases, neutrophilic chemotactic factors, coagulation factors, AA metabolites and nitric oxide (TISSUE INJURY) They also release growth factors, fibrogenic cytokines, angiogenesis factors and collagenesis (FIBROSIS) |
| Lymphocytes in chronic inflammation | produce inflammatory mediators, participate in cell-mediated immune reactions, interact with macrophages, produce antibodies in plasma. |
| Macrophage-lympohocyte interaction | Macrophages engulf bacteria and present antigens to T lymphocytes, and activate other inflammatory mediators |
| Eosinophils in chronic inflammation | Immune reactions are mediated by IgE. Eosinophil granules contain a protein that is toxic to parasites |
| Mast cells in chronic inflammation | Release mediators (histamine) and cytokines. |
| Cells involved in chronic inflammation | macrophages, lymphocytes, eosinophils and mast cells |
| Granulomatous inflammation | Distinctive pattern of chronic inflammation where the predominatn cell type is a macrophage with a modified epithelioid appearance. These cells often fuse to form giant multinucleated cells. |
| granuloma | focal area of granulomatous inflammation |
| foreing body granulomas | form when foreign material is too large to be engulfed by a single macrophage |
| immune granulomas | insoluble or poorly soluble particles elicit a cell-mediated immune response |
| endocrine and metabolic manifestations of inflammation | secretion of acute phase liver proteins, increased glucocorticoid production (stress response)and decreased secretion of vasopressin causing reduction of body fluid to be warmed. |
| What is the pupose of fever during inflamamtion? | Improves efficiency of leukocyte killing, impairs replication of offending organisms |
| Autonomic manifestations of inflammation | Redirection of blood flow from skin to deep vascular beds to minimize heat loss, increased pulse and BP, and decreased sweating |
| Behavioral manifestations of inflammation | Shivering (rigors), chills, anorexia, somnolence and malaise. |
| Leukocytosis | Increased leukocyte count in the blood due to inflammation. 1) Bacterial infections cause neutrophila, mono, mumps and measles cause lymphocytosis and parasites, asthma and hay fever cause eosinophila. |
| leukopoenia | reduced leukocyte count due to typhoid fever, some viruses, rickettsiae and protozoa |
| Where are chemical mediators of inflammation derived from? | plasma or cells |
| Wher do chemical mediators of inflammation bind? | Most bind to specific receptors on target cells |
| What do chemical mediators of inflammation stimulate? | The release of mediators by target cells, which can amplify or ameliorate the inflammatory response |
| Who do chemical mediators of inflammation act on? | One or a few target cells. They have widespread targets and may have differing effects depending on the cell and tissue types |
| How long do chemical mediators of inflammation last? | They are usually short-lived because the body wants to tightly control inflammatory response. |
| Do chemical mediators of inflammation have harmful affects? | Yes, most have the potential to cause harm |
| Preformed chemical mediators of inflammation | -contained in secretory granules, released by WBC's. Induce a rapid response. Examples: histamine, seratonin and lysosomal enzymes. |
| Newly formed chemical mediators of inflammation | -made by all types of leukocytes in the ER. Take longer than preformed mediators. Examples: Prostaglandins, leukotrienes, platelet-activating factors, activated oxygen species, nitric oxide and cytokines. |
| What organ is a major source of plasma mediators? | Liver |
| Vasoactive mediators of inflammation | histamine, bradykinin, complement (C3a, C5a), prostaglandins/leukotrienes, platelet activating factor, nitric oxide, neuropeptides |
| Chemotactic mediators of inflammation | C5a, leukotriene (B4), platelet activating factor, cytokines (IL-1, TNF), chemokines, nitric oxide |
| What cells release histamine? | Mast cells, basophils and platelets |
| How is histamine released? | Binding of antigen to IgE on mast cells causes the release of histamine containing granules. Cold, trauma or other chemical mediators can trigger release as well. |
| What does histamine do? | Dilates arterioles and increases permeability of venules (wheal and flare reaction) |
| Where is complement made? | It is made in the liver and released into the blood where it can become C5a, C3a, C3b or MAC |
| What do C5a and C3a (complement) do? | Recruit and activate leukocytes so that they can engulf and destroy microbes |
| What does C3b do? | Cause recognition and phagocytosis of microbe when bound. |
| What does MAC do? | MAC=membrane attack complex. Causes lysis of the microbe. |
| What is Bradykinin? | A small peptide released from plasma precursors that increases vascular permeability and dilates blood vessels. It causes pain and is rapidly inactivated. |
| How are clotting and inflammation interelated? | Thrombin, a major clotting enzyme, acts on protease-activated receptors to induce acute inflammation. |
| What are the two categories of arachidonic acid metabolites? | prostaglandins and leukotrienes |
| What do prostaglandins do? | Cause either vasodilation (prostacyclins) or vasoconstriction (thromboxane A2). PGE2 causes pain and fever. |
| What do leukotrienes do? | Increase vascular permeability and cause vasoconstriction (C4, D4 and E4).Also cause leukocyte adhesion and chemotaxis (B4, HETE and lipoxins) |
| Where is platelet-activating factor synthesized? | In stimulated platelets, leukocytes and endothelium. |
| What does platelet activating factor do? | Has inflammatory effects: platelet aggregation, V-constriction, V-dilation, bronchoconstriction, incresaed venular permeability, Leuk. adhesion chemotaxis degranulation and oxidative burst, increased synth of AA metabolites by leuk's and other cells. |
| What are cytokines | Proteins produced by many cell types (mostly activated macrophages and lymphocytes) that modualte other cells' function. |
| What are the major cytokines that mediate inflammation? | Interleukin-1 (IL-1) and tumor necrosis factor (TNF) |
| What are acute phase reactions to cytokines | sleep, decreased apettite, more acute-phase proteins, shock and neutrophilia |
| What are the endothelial effects of cytokines? | leukocyte adherence, PGI synthesis, procoagulent activity, decreased anticoagulant activity, increased IL-1, IL-8, IL-6 and PDGF |
| What are the fibroblast effects of cytokines? | Fibroblast proliferation, collagen synthesis, collegenase, protease and PGE sythesis |
| What is the leukocyte effect of cytokines? | Increased cytokine secretion |
| What are chemokines? | Small proteins that are chemoattractants for specific types of leukocytes. |
| What do chemokines do>? | Stimulate leukocyte recruitment during inflammation, and control normal migration of cells through tissues during organogenesis and organization of tissues. |
| What are some examples of chemokines? | IL-8, eotaxin and lymphotactin |
| What does nitric oxide do? | Relaxes smooth muscle, prevents platelet adhesion (keeping blood vessels open and patent) and enhances phagocytic killing. |
| Where are neuropeptides produced? | central and peripheral NS |
| What do neuropeptides do? | Cause vasodilation either directly or through mast cell degranulation, and increased vascular permeability |
| What are two important neuropeptides in inflammation? | Substance P and neurokinin A |
| Where does substance P act? | It stimulates vasodilation in the lungs and GI tract |
| What are neutrophil granules? | cationic proteins that increase vascular permeability, immobilize neutrophils, serve as chemotactic agents for mononuclear phagocytes |
| What are oxygen-derived free radicals? | Produced by neutrophil phagocytosis of bacteria, cause tissue damage. |
| What mediators cause vasodilation? | prostaglandins and nitric oxide |
| What mediators increase vascular permeability? | histamine, seratonin, complement, bradykinin, leukotrienes, PAF, nitric oxide, Substance P and oxygen metabolites |
| What mediators cause chemotaxis and leukocyte activation? | C5a, Leukotriene B4, chemokines, and nitric oxide |
| What mediators cause fever? | Interleukin-1, TNF, prostaglandins |
| What mediators cause pain? | prostaglandins and bradykinin |
| What mediators cause tissue damage? | neutrophils, macrophages, lusosomal enzymes, oxygen metabolites, nitric oxide |
| What are the steps of wound healing? | 1) acute inflammation 2) regeneration of parenchymal cells 3) migration/proliferation of parenchyma and CT cells 4) production of extracellular matrix 5) remodeling 6) Collagen deposition increases wound strength |
| What is granulation tissue? | The hallmark of healing. It is soft, pink and granular due to the proliferation of small blood vessels and fibroblasts. Edema is common. |
| What cells are pathognemonic for acute inflammation? | neutrophils |
| What cells are pathognemonic for chronic inflammation? | Plasma cells |
| What cells are pathognemonic for granulomatous inflammation? | epithelioid macrophages |
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