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191 Cards in this Set
- Front
- Back
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What structures are included in the immune system? |
1) skin and mucuous membranes 2) mononuclear phagocyte system 3) lymphoid system (spleen, thymus gland, lymph nodes) 4) bone marrow |
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Inflammation |
response of a tissue to injury - any damage to tissue sets off a localized series of events known as acute inflammation |
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Whatdoes inflammation involve? |
immune cells blood vessels molecular mediators |
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What are the 3 general steps of the process of inflammation? |
1) Initiation 2) Amplification 3) Termination |
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What are leukocytes responsible for? |
locating and eliminating pathogens and foreign molecules |
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What kinds of chemical mediators aide leukocytes in their task of bodily defense? |
complement kinins clotting factors cytokines chemokines |
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What are innate defenses? |
Require no previous exposure to mount an effective response against an antigen, as well as a wide variety of different antigens are recognized |
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Examples of Natural Killer cells |
neutrophils and macrophages |
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What are specific defenses? |
Respond more effectively on second exposure to an antigen and are highly selective in the ability to recognize antigens |
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What are some examples of agents of specific immunity? |
B and T lymphocytes |
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What occurs during the Initiation phase of Inflammation? |
Injured cells release mediator molecules that attract fluids and leukocytes from the blood |
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What occurs during the Amplification phase of Inflammation? |
Damaging agents are removed, dead cells and debris are eliminated so that tissues can be repaired |
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What occurs during the Termination phase of Inflammation? |
After repair is finished, chemical inhibitors terminate the inflammatory process. - Mass apoptosis occurs |
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What are the 5 signs of acute inflammation? |
(PRISH) Pain Redness Immobility Swelling Heat |
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Why does swelling occur with inflammation? |
Accumulation of fluid to the site of injury enables the body to bring more components into the affected area |
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Why does heat occur with inflammation? |
The increased blood in the affected area is to enable the WBC's to move faster |
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What would happen if you had too little inflammation? |
Injury would never heal and would become infected - this occurs with pressure ulcers, "SCID", HIV |
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What would happen if you had too much inflammation? |
It can cause collateral damage, such as anaphylactic shock |
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Circulating cells |
neutrophils, eosinophils, basophils, lymphocytes, monocytes, platelets |
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Connective tissue cells |
macrophages, mast cells, fibroblasts, lymphocytes |
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What do circulating proteins include? |
Clotting factors, kininogens, complement proteins |
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Where are circulating proteins synthesized? |
Liver |
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What are the structural components that make up the extracellular matrix? |
Collagen, elastin, proteglycans, fibronectin |
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What are monocytes? |
Inactive forms of macrophages |
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How do monocytes become macrophages? |
Monocytes are circulating cells that get released into the cardiovascular system and travel to the site of inflammation where they become macrophages |
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In inflammation, swelling is due to ? |
Fluid and blood cells invading the site of injury |
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What is the purpose of inflammation? |
Limits damage Prevents infection Initiates and promotes healing Removes injury stimulus Cleans stuff up |
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What does histamine do? |
Causes vasodilation and increases permeability |
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Which immune system cells are the first to encounter a pathogen or antigen? |
Macrophages |
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What are some stimuli for acute inflammation? |
- Infections - Tissue necrosis - Foreign bodies - Immune reactions |
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Acute inflammation |
Rapid host response that delivers leukocytes and plasma proteins to sites of injury or infection - series of events, triggered and coordinated by locally-released chemical mediators |
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What are the 2 components of acute inflammation? |
1) Vascular changes 2) Recruitment of leukocytes |
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What are the 3 purposes of the inflammatory response? |
1) To neutralize and destory invading and harmful agents 2) To limit the spread of harmful agents to other tissues 3) To prepare any damaged tissue for repair |
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Which vasoactive chemicals are released during the inflammatory process? |
Histamine, prostaglandins, and leukotrienes |
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What does the process of acute inflammation begin with? |
Vasodilation of arterioles feeding the site of injury, followed by increased blood flow in capillary beds |
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What cells do the chemical mediators of acute inflammation act on? |
Smooth muscle |
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What happens as a result of increased vascular permeability? |
Pushes fluid out of the blood vessels and into the surrounding tissue, contributing to local swelling (edema) |
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What happens in response to the dilating of blood vessels and open capillaries ? |
More blood is carried to the injured area and contributes to redness, pain, heat, and swelling of inflammation |
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What physically happens to increase permeability? |
Contraction of endothelial cells increases spaces in the BV The endothelial cells shrink and create gaps, allowing for escape of fluid |
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The loss of fluid and increased vessel diameter leads to |
vascular congestion |
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Why all this fluid and proteins that occur during the initial stages of inflammation? |
1) Dilution of harmful substances or organisms - helps reduce damage 2) Antibodies arrive at site in exudate 3) Exudate also carries other immune-mediating molecules - enhances bacterial killing, phagocytosis 4) Pain forces limited use of affected area |
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Which leukocytes are the 1st responders? |
Neutrophils |
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Which leukocytes are involved in inflammation? |
- neutrophils - monocytes - endothelial cells - mast cells and basophils - eosinophils - platelets |
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How do neutrophils eliminate pathogens and damaged cells? |
Through phagocytosis or through release of powerful digestive enzymes |
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Do neutrophils move back into circulation after they exit the bloodstream? |
No |
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Once damaged cells and pathogens have been eliminated, what happens to neutrophils? |
Undergo apoptosis within 10-24 hours after exiting circulation |
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What is the main component of pus? |
Neutrophils |
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What do macrophages do? |
Clean up dead cells and pathogens through phagocytosis - can alert other cells of the immune system |
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After 48 hours, what is the predominant cell type at the site of inflammation? |
Macrophages |
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What do activated macrophages release? |
Different pro-inflammatory chemicals, and also release powerful enzymes/chemicals to assist in the destruction of pathogens - ex: prostaglandins, leukotrines, platelet activating factor, various inflammatory cytokines |
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What are hyper-activated macrophages? |
Very potent killing and signaling cells - play a major role in chronic inflammation |
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In inflammation, what is a vascular change that does not occur? |
Vasoconstriction |
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Fluid and proteins help: |
bring pathogens to site of injury |
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True/False: Are neutrophils recruited to the site of damage after 48 hours? |
False: Neutrophils are the first responders |
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True/False: Are neutrophils responsible for pain? |
False: Neutrophils are not responsible for pain |
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True/False: Do neutrophils undergo apoptosis as soon as they get to the site of injury? |
False: Neutrophils undergo apoptosis, 10-24 hours after exiting circulation, once pathogens and damaged cells have been eliminated |
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True/False: Neutrophils kill pathogens via phagocytosis and via the release of destructive enzymes |
True: Neutrophils kill pathogens via phagocytosis and activation of bactericidal mechanisms such as Macrophages |
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In acute inflammation, which cells are recruited to damaged tissues following neutrophil recruitment? |
Macrophages |
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Recuitment of leukocytes involves interactions between what? |
Between endothelial cells from the damaged area and circulating leukocytes |
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How are leukocytes recruited to the tissue? What does the series of events involve: |
- Leukocyte margination, rolling, adhesion to the endothelial wall - Leukocyte migration through the endothelium (extravasation) - Chemotaxis in the tissue towards the area of injury |
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Margination and adhesionare mediation by what? |
Cell adhesion molecules |
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What are some families of adhesion molecules that are involved in leukocyte recruitment? |
- selectins - integrins - immunoglobulin superfamily (ICAM, VCAM) |
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What is Margination? |
when leukocytes slow their migration, adhere to the endothelium and begin to move along the periphery of the blood vessels ("rolling") |
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Rolling of leukocytes is initiated by ___________ |
selectins |
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What do selectins do? |
- Maintains loose contact with endothelial cells |
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Under normal circumstances, do endothelial cells express selectins? |
No - there is little or no expression of selectins by endothelial cells |
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When does expression of selectins on both cells types occur? |
When cells are exposed to cytokines |
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When are cytokines released? |
Released upon injury |
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What occurs after leukocyte rolling? |
Adhesion and extravasation |
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What occurs during leukocyte adhesion? |
Bind more firmly to endothelium |
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Which surface molecules do endothelial cells express? |
Intercellular adhesion molecule-1 (ICAM) Vascular cell adhesion molecule-1 (VCAM) |
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What binds to ICAM-1 and VCAM-1? |
Integrins |
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What are ICAM-1 and VCAM-1 responsible for? |
Leukocyte adhesion |
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What occurs during leukocyte extravasation? |
Leukocytes tightly bind to the endothelium, and endothelial cells contract, creating a gap between them Leukocytes then squeeze between endothelial cells, and exit the blood vessel (called extravasation) |
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What do leukocytes use to get through the basement membrane? |
Collagenases |
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What do collagenases do? |
Digest some basement membrane away so that leukocytes can get through |
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Which blood vessels is leukocyte extravasation occuring in? |
Capillaries (pulmonary) and venules (systemic) |
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Selectins are expressed by which cells? |
Leukocytes and endothelial cells |
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Which receptors help neutrophils stick and roll along the capillary endothelial surface? |
Selectins and chemokines |
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Which receptor helps neutrophils with the binding to and subsequent movement through the capillary wall? |
Integrins |
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Neutrophils are attracted to the inflamed tissue by a process called ___________ |
chemotaxis |
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The process of passing through the blood vessel walls and migrating to the inflamed tissue is referred to as ___________ |
emigration |
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What are some examples of chemoattractants |
may be molecules of pathogen, complement (C5a), mitochondrial debris, chemokines |
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As cells approach the site of injury/infection, the concentration of chemoattractants _________(increases/decreases) |
increases |
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The binding of chemoattractant to receptor causes what? |
Reorganization of the cytoskeleton |
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Once leukocytes are activated, what occurs? |
They begin producing and releasing various digestive enzymes and ROS to kill bacteria |
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Once macrophages are activated, what do they do? |
Begin secreting cytokines, which recruits/alerts/activates other cells and phagocytotes begin phagocytosing |
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What are the 3 stages of phagocytosis? |
1) Recognition 2) Engulfment 3) Digestion |
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The different types of receptors on phagocytes allow them to respond to what? |
- molecules found on surface of microbes - bacterial DNA - bacterial proteins - mitochondrial proteins - some viral RNA - Molecules on surface of apoptotic cells - antibodies |
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Phagocytosis is greatly enhanced by __________ |
opsonization |
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Which molecules are common opsonins? |
antibodies and complement molecules |
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What do opsonins do? |
act as "handles" that phagocytes can grab - stick to bacteria - make it easier for WBC to grab onto |
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What occurs during the engulfment stage of phagocytosis? |
Once a particle is bound to the cell membrane of the phagocyte (macrophage, neutrophils), extensions form on either side of the particle, with the pseudopods eventually surrounding the particle - particle becomes engulfed |
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After a particle becomes engulfed, is it now enclosed in a vacuole called ____________ |
phagosome |
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The phagosome fuses with what? to produce what? |
Fuses with: lysosome Produces: Phagolysosome |
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What happens during the digestion phase of phagocytosis? |
Hydrogen ions are pumped into the phagolysosome, which lowers the pH - This activates lysosomal enzymes - Creates an oxidative burst which produces ROS - ROS kills invader and is digested |
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What causes leukocytes to slow down and adhere to endothelial cells in an inflammatory response? |
The presence of adhesion molecules on leukocytes and endothelial cells |
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Leukocyte rolling is mediated by ______ and leukocyte adhesion is mediated by ________ |
selectins; integrins |
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What are lysosomal hydrolases? What do they do? |
Enzymes contained in granules (neutrophils) and in lysosomes (macrophages) They digest bacterial coats, DNA, proteins, lipids, etc. |
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Bactericidal permeability-increasing protein (BPI) |
pokes holes in bacterial envelope |
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What is lysozyme? Where can it be found? |
Natural antibiotic. Found in tears, saliva, etc. |
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What does lysozyme do? |
Works against gram-positive bacteria |
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Neutrophils and macrophages specialize in what kind of degradation? |
Collagen and extracellular matrix |
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Lactoferin |
Binds iron, keeping it away from bacteria |
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Defensins |
kill a variety of pathogens - typically found on the surface of the skin |
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Which kind of mechanism is more effective in pathogen destruction? (non-oxidative vs oxidative) |
Oxygen dependent killing is more effective than enzymatic mechanisms |
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Prostaglandins contribute to what? |
pain and inflammation |
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What kind of destructive products do leukocytes release into intercellular spaces? |
- ROS, enzymes, prostaglandins, leukotrines |
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Release of leukocyte products can result in tissue injury. How? |
Leukocyte products destroy extracellular invaders, but can also damage healthy host cells. Collateral damage can be caused by inflammation |
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Where are mast cells stored? When are they synthesized? |
Granules, ready for secretion Can be synthesized when inflammatory response is triggered |
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What are some examples of plasma-derived mediators? |
Clotting system Kinin system Complement system |
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Where are plasma-derived mediators produced? |
Liver |
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What are some functions of the complement cascade? |
Promotes: - vascular changes - chemotaxis - opsonization - leukocyte activation |
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What is the complement system? |
Consists of about 20 proteins that interact to enhance inflammation, chemotaxis, and lysis of target cells |
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How is the complement system activated? |
Binding to microorganisms, either via direct binding to microbes or by binding to antibody antigen complex which are bound to microbes |
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After the complement system has been activated, what occurs? |
Leads to formation of C3 convertase, which cleaves C3 into C3a and C3b, starting the cascade |
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What is an important feature of the complement system? |
Amplification capacity |
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Which complement protein initiates the next step in the cascade? |
C3b, which cleaves C5 into its active fragments C5a and C5b |
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How is the alternative pathway of the complement system triggered? |
Can be activated on first exposure to an antigen |
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Which proteins in the complement system or proinflammatory? |
C3a and C5a |
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C3a and C5a cause mast cells to release _________ |
histamine |
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What does C5a do? |
- activates leukocytes - chemoattractant - enhances adhesion of leukocytes to endothelium |
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C3b acts as __________ to make phagocytosis easier |
opsonin |
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What does the membrane attack complex do? |
Pokes holes in cell membrane and disrupts the lipid bilayer. This allows for free movement of sodium and water into the cell, causing it to rupture (lysis) |
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Brief summary of complement system |
Results in vasodilation, increased permeability, chemotaxis, and activation of neutrophils |
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Thrombin leads to |
- production of chemokines - expression of adhesion molecules - expression of inflammatory mediators |
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What triggers the Kinin system? |
the Coagulation system |
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What is the kinin system? |
Consists of plasma proteins that play a role in inflammation, BP control, coagulation and pain |
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What are kinins? |
small polypeptides that cause powerful vasodilation |
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What are the important mediators of the kinin system? |
Bradykinin and kallidin |
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What does Factor XII convert? |
activates prekallikreins into kallikreins |
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What are the functions of bradykinin? |
- vascular permeability - vasodilation - smooth muscle contraction - pain |
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Where are mast cells found? |
Connective tissues, especially around blood vessels and under mucosal surfaces |
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What happens to mast cells and basophils when antigens bind to IgE antibodies? |
They degranulate, releasing proinflammatory chemicals (histamine, platelet activating factor) beginning the inflammatory response that usually occurs with allergic reactions |
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What does Thromboxane do? |
causes vasoconstriction, promotes platelet aggregation |
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What does leukotrine D4 do? |
vasoconstriction bronchospasm increased vascular permeability |
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What is arichidonic acid? |
phospholipid derived mediator - 20 carbon polyunsaturated fatty acid |
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What is thromboxane (TxA2) involved in? |
Healing process |
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What is prostacyclin (PGI2) involved in? |
Inflammatory response |
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What does PGD2 do? |
causes vasodilation increased permeability - resulting in edema potent chemoattractant |
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COX-1 prostaglandins do what? |
Part of normal cell function, they're always on - i.e. production of protective mucus in GI tract |
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Prostaglandins produced by COX-2 are related to what? |
Inflammation |
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What are some non-selective COX inhibitors? |
aspirin tylenol NSAIDs |
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What is the problem with non-selective COX inhibitors? |
Because non-selective, block "good" functions as well as bad - inhibit Gi mucus production, leading to ulceration - adversely affect kidney perfusion - inhibit clotting |
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What are the phospholipid compounds formed from arachidonic acid? |
Prostaglandins and leukotrienes |
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What are cytokines? |
polypeptide signaling molecules that affect the function of other cells by stimulating surface receptors |
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What are the main sources of cytokines? |
Macrophages and lymphocytes |
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What are the functions of cytokines? |
- inflammatory mediators - chemotaxins - intercellular communication signals - growth factors - growth inhibitors |
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Autocrine |
The same cell that produces hormones or chemical messages, also responds to those same hormones, leading to changes in that cell |
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Paracrine |
form of cell-cell communication in which a cell produces a signal to induce changes in nearby cells, resulting in differentiation of those cells |
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What 2 major inflammatory cytokines are released by macrophages in response to inflammatory stimuli? |
Interluekin-1 (IL-1) and Tumour necrosis factor (TNF) |
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What do both TNF and IL-1 do? |
- Activate endothelial cells - activate fibroblasts leading to tissue repair - Cause systemic acute-phase responses (fever, lethargy, cachexia, neutrophil release) |
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True/False: Arichidonic acid is derived from membrane phospholipids |
True |
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IL-1 and TNF are released by __________ |
macrophages |
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What cellular components are responsible for the process of chemotaxis? |
Cell surface receptors and the cytoskeleton |
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Chemokines |
Chemotactic cytokines - function in chemotaxis |
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What are chemokines important for? |
Guiding inflammatory cells to site of damage |
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Why do cells move towards the side of the cell membrane that is binding the most chemokine? |
Activation of receptors will induce a reorganization of cytoskeleton |
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Exudate |
fluid emitted by an organism through pores or a wound |
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Serous inflammation |
Minor increase in vascular permeability - only fluid escapes (no protein) fluid is watery i.e. blister |
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Purulent inflammation |
Exudate contains many dead neutrophils and bacteria - thick, white/yellowish/greenish - pus |
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What are the 2 general forms of purulent inflammation? |
1) Localized (abscess) 2) Diffuse (cellulitis) |
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When does an abscess form? |
If the inflammatory mechanisms fail to clear the debris |
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What occurs when an abscess forms? |
Sac of pus becomes walled off by collagen fibres (protective) |
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What is cellulitis usually due to? |
Bacterial infection of the dermis and subcutaneous layers |
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What happens when an abscess is not resolved? |
- may spread - grow larger - pull in more fluids - may get leaking of RBC's into tissue |
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Activating signals for the inflammatory response are ____________ |
short-lived |
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What are the 3 outcomes of acute inflammation? |
1) Complete resolution 2) Healing by connective tissue replacement (scarring) 3) Progression to chronic inflammation |
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What can chronic inflammation result in? |
Stromal hyperplasia Scarring Destruction of healthy tissue |
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What are some causes of chronic inflammation? |
- pathogens hard to eliminate - foreign material remains in tissues (asbestos, cant be broken down) - cancer |
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What is an example of an autoimmune disease that is characterized by chronic inflammation? |
Rheumatoid arthritis |
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How do cytokines and chemokines contribute to chronic inflammation? |
- keep the inflammatory response going |
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How do macophages contribute to chronic inflammation? |
- secrete various inflammatory mediators - secrete ROS and NO - secrete acids and proteinases that digest healthy tissue - release components of complement, leading to MAC formation and opsonization - display antigen to lymphocytes - secrete factors affecting proliferation of fibroblasts and endothelial cells |
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What are the 2 kinds of macrophages? |
Classicaly activated macrophages Alternatively activated macrophages |
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How do alternatively activated macrophages promote tissue repair and fibrosis? |
- Produce growth factors to stimulate proliferation of endothelial cells fibroblasts - Promote synthesis of collagen and enzymes that remodel CT |
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Granuloma |
An accumulation of macrophages, fibroblasts and collagen as a result of prolonged inflammation |
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Why would chronic inflammation lead to cancer? |
Rounds and rounds of cell division, build up of ROS, mutations accumulate |
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True/False: Chronic inflammation is generally short lived |
False: Chronic inflammation can last for days, months, or years. |
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True/False: Chronic inflammation primarily involves neutrophils |
False: Chronic inflammation primarily involves macrophages |
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True/False: Chronic inflammation often involves tissue damage and scar tissue |
True: Chronic inflammation results in collateral damage and scarring |
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What is SIRS |
Systemic inflammatory response syndrome - characterized by acute-phase response |
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What occurs during SIRS |
- increase in Temp - Increase in HR - Increase in Respiratory Rate - Increase in WBCs - induces lack of appetite - disturbed sleep - malaise - hypotension - atrophy |
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What is the purpose of a fever? |
Speeds up movement of WBC |
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What is a fever induced by? |
Pyrogens |
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What is the most well-known exogenous pyrogen? |
Lipopolysaccharide (LPS) |
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What are endogenous pyrogens? |
TNF, various interleukins |
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Which inflammatory mediators sensitize pain? |
TNF, interleukins, kinins, prostaglandins |
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Disseminated intravascular coagulation |
Increases risk of hemorrhages due to depletion of clotting factors in the formation of blood clots |
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When can the whole body become involved in an inflammatory response? |
- pathogen escapes original invasion site, enters general circulation - injury is so severe that a large quantity of mediators that have been released are carried away from the original site, setting off systemic responses |
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Symptoms of Sepsis |
Shivering, fever, cold Extreme pain Pale skin Sleepy, confused "I feel like I might die" Short of breath |
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True/False: Pain is associated with pyrogens |
False: Pain occurs with stimulation of nociceptors Pyrogens induce fever |
