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43 Cards in this Set
- Front
- Back
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What is the effector response? How long does it last? |
The body trying to get rid of the pathogen. It lasts about 2 weeks. |
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What is target differentiation? |
The immune system triggers the appropriate response for the invading pathogen |
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What sorts of barriers does the humanbody have to try and prevent pathogens from gaining entry?
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Skin, mucous membranes |
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What does anatomic mean? Break it down into parts. |
ana: up tom: to cut ic: pertaining to Anatomic: pertaining to being able to be cut up (AKA physical structures) |
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Describe the overall properties of skin that make it an effective barrier against the entry of bacteria
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Dry, tight connections, antimicrobial substances, acidic, waterproof |
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Where are mucous membranes found? |
GI tract, urogenital tract, respiratory tract, conjunctiva |
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What make mucous membranes different than skin? |
Moist, more intimate relationship with environment, selectively permeable for absorption/secretion of fluids/nutrients |
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How do cilia work? Where are they in the body? |
The move in a synchronous motion to push bacteria (trapped in mucous) up and out. They are found in the lower respiratory tract. |
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How do we know that the normal flora are protective?
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If we disrupt the normal flora, we can get diseases like flush, C. diff., yeast infections, etc. |
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How do our mucous membranes protect us? |
Mucous traps bacteria, cilia wash bacteria out, normal flora out-compete pathogens, chemical agents prevent infection (lysozyme and antimicrobial peptides) |
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What does physiological mean? |
Traits associated with life |
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What are the physiological barriers of the immune system? |
Temperature, pH, chemical factors, and iron sequestration |
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Why don't you feed babies, who are less than 1 year old, honey? |
Their stomachs are not acidic enough to kill the bacteria in honey (lots of Chlostridia). |
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Which chemical factors does the body use in the innate immune system? |
Fatty acids, lactic acid, HCl, lysozyme and complement |
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What does phagocytosis mean? Break it up into parts. |
Phago: to eat Cyt: cell osis: the process of --> the process of eating cells |
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Describe phagocytosis |
The pseudopodia attach to the bacteria, bacteria is ingested to form the phagosome, phagosome fuses with the lysosome, lysosomal ATPases pump protons in to activate the hydrolytic enzymes, bacteria are digested, digested products are released through exocytosis |
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Which are the "professional" phagocytes? |
Monocytes, macrophages, dendritic cells, activated B cells, and neutrophils. |
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What does lysosome mean? Break it up into parts. |
Lys: to break some: body --> body that breaks |
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Which are the non-professional phagocytes (those that need to be induced)? |
Fibroblasts and epithelial cells |
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What does macrophage mean? Break it up into parts. |
Macro: large phage: eat --> large eater |
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What causes inflammation? |
Tissue damage (from a wound or an invading pathogen) |
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What are the functions of inflammation? |
Deliver/recruit cells and effector molecules to site, form a physical barrier at site, promote wound healing and tissue repair (lots of growth factors). |
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What are the clinical signs of inflammation? |
Heat, redness, swelling, loss of function, and pain. |
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Describe the major events of the inflammatory response. |
Bacteria enters the body through a cut, triggers release of vasodilators (histamine, prostaglandins, and serotonin), vasodilation to the site and vasoconstriction away from the site increase --> swelling, bacteria replicate, [vasodilators] increase, antibodies and complement bind bacteria, phagocytic cells leave the blood vessel and clean up the bacteria, blood clotting occurs to stop additional bacteria from entering. |
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What is extravasation? |
During inflammation, phagocytic cells are able to exit the bloodstream. |
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What is margination? |
During inflammation, white blood cells adhere to the wall of the blood vessels. |
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What does PAMP stand for? |
Pathogen-associated molecular pattern |
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What is a PAMP? |
Broad-basedmolecular signatures or motifs commonly found in many pathogens but notcommonly found in the host |
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What are examples of PAMPs? |
Lipoteichoic acid and teichoic acid (Gram-positive), lipopolysaccharides (Gram-negative), and mannose. |
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What are PRRs? What do they have to do with PAMPs? Give an example of a PRR? |
Pattern Recognition Receptors. They are receptors on host cells that recognize the PAMPs on pathogens to let the body know it's been infected. Toll-like receptors are an example. |
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How do toll-like receptors work? |
PAMPs bind to the extracellular domain of the TLR. This triggers the cytoplasmic domain of the TLR to activate distinct signalling pathways and transcription factors that cause changes in gene expression leading to cytokine production which triggers inflammation. |
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What did Jules Bordet discover and how did he do it? |
Antibodies are heat-stable and complement is heat-labile. Inoculated sheep blood kills bacteria unless you heat it up. Normal sheep blood doesn't kill bacteria. Heated inoculated sheep blood mixed with normal sheep blood does kill bacteria. Normal sheep have complement, but not the right antibodies. Inoculated sheep have both. |
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Describe the roles of complement and antibodies. |
Antibodies tag bacteria as foreign and complement kills tagged bacteria. |
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How does complement work? |
Complement is inactive in the blood until enzymatic cleavage causes an activation cascade which results in the formation of the membrane attack complex (MAC) which lyses tagged bacteria by forming a pore in the membrane. |
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What are the functions of complement? |
Opsonization, activate the inflammatory response, bacterial cell lysis. |
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Describe the classical pathway. |
2 antibodies bind to the pathogen's membrane. C1 binds to the antibodies. This cleaves C2 and C4 which combine to form C3 convertase (C2a4b) which cleaves C3. C3 binds with C3 convertase to form C5 convertase (C2a4b3b) which cleaves C5 which then (just C5b) forms the MAC with C6-9. |
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Describe the lectin pathway. |
Mannose-binding lectin binds to mannose on the bacterial cell membrane. MASP 1 and 2 bind to mannose-binding lectin. This complex cleaves C2 and C4 which combine to form C3 convertase (C2a4b) which cleaves C3. C3b combines with C3 convertase to form C5 convertase which cleaves C5. C5b then forms the MAC with C6-9. NO ANTIBODIES REQUIRED. |
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Describe the alternative pathway. |
Low levels of C3 get cleaved spontaneously. C3b then binds with Factor B. Factor B is then cleaved by Factor D which allows another C3 to bind to Factor Bb. This complex is called Alternative C3 convertase. C3 convertase cleaves another C3, and the resulting C3b binds to a C3 convertase to form C5 convertase which cleaves C5. C5b then forms the MAC with C6-9. |
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What is Mannose-Binding Lectin? |
A secreted protein that binds mannose found on the surface of bacteria and yeasts. It results in opsonization which activates complement proteins and binds to macrophages' receptors which promotes phagocytosis. |
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Describe necrosis. |
Physical of chemical trauma occurs to a cell. The cell membrane is damaged. The contents of the cell leak into the surrounding tissues. Nearby cells may be damaged by the released cell contents. Inflammation results. |
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What are the two main functions of the vertebrate immune system? Explain the two sub-points of each. |
Recognition and Response. Recognition: self vs non-self and target differentiation (generate an appropriate response to the specific pathogen). Response: effector response (eliminating the pathogen the first time you're exposed to it) and memory response (adapted effector response). |
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Explain the two main components of the vertebrate immune system. |
Innate (present at birth, first line of defense, non-specific immunity, no immunological memory, no adaptation) and adaptive (learns from previous encounters, improves ability to fight disease). |
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