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54 Cards in this Set
- Front
- Back
List the 3 lines of host defenses and an example of each |
1. 1st line- covering of the mucus membranes. Skin 2. 2nd line- inflammation and phagocytosis. Phagocytes 3. 3rd Line- Memory and specific immune system. Humoral immunity |
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List 3 components of the first line of defense |
1. Outer covering- skin 2. Flushing effect- sweat 3. Chemical barriers- acidity of sweat |
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What is the role of normal biota as a first line of defense? |
Normal biota prevents overgrowth of "bad" microbes |
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What is lysozyme and why is it important? |
This is an enzyme found in bodily fluids that is capable of destroying peptidoglycan, which is only found in bacteria. |
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Name two major body compartments that participate in immunity, what they do, and their function, |
1. Lymph nodes- collect pathogens that are killed off by the second line of defense and present it to the naive lymphocytes located there. 2. Respiratory- mucus brings pathogens out, nasal hairs trap large molecules |
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Name the 3 major lymphoid tissues we discussed |
1. Thymus- trains immature T cells 2. Bone marrow- matures B cells, produces T and B cells 3. Lymph nodes- concentrates dead pathogens and cells |
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What are PAMPs and PRRs? |
PAMPs- Pathogen Associated Molecular Patterns, a pattern on the outside of pathogens that our body is able to recognize PRRs- Pattern Recognition Receptor- identifies PAMPs |
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List 3 major differences in how the 3rd line of defense differs from the other 2 lines of defense |
1. Specific 2. Has memory 3. Life-long |
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List the 4 stages of a specific immune response |
1. Pathogen enters system 2. 2nd line kills the pathogen, brings it to lymph nodes 3. PMCs cut up the pathogen, put it on the outside of their cells, and present it to naive lymphocytes 4. Lymphocytes attempt to find a match, and when they do, they proliferate |
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Compare and Contrast T and B cells |
T- matured in thymus, part of cell-mediate immunity, not released as antibodies B- matured in bone marrow, part of humoral immunity, can be released as antibodies, need T cells for cell presentation |
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What is the difference between a naive and matured lymphocyte? |
Naive- has never seen an antigen before Matured- has seen and been matched to an antigen |
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Describe the structure of a T and B cell |
Both- Y shaped, has light chains matched up with heavy chains, has a variable and constant region B- can be attached to membrane, or secreted as an antibody T- embedded in membrane, unable to be secreted |
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List the characteristics of antigens that optimize their immunogenicity |
Able to be recognized as a pathogen by our immune system, composed of large molecules such as proteins that do not have repeating subunits (such as sugars) |
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Describe how the body reacts to a superantigen |
The body sees this antigen as much more severe than it actually is, and mounts an immune response 100-1000x bigger than normal, also releases cytokines which can result in cell death |
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Describe the steps of phagocytosis |
1. Phagocyte is attracted to bacteria 2. Bacteria adhere to phagocyte PRRs by their PAMPs 3. Vacuole is formed around bacteria during engulfment 4. Phagosome, a digestive vacuole results 5. Lysosomes fuse with phagosome, forming a phagolysosome 6. Enzymes kill and digest bacteria 7. Undigested particles are released |
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Describe the steps of inflammation |
1. Injury occurs, then vasoconstriction occurs 2. Vasodilation and increased blood flow occurs= increased permeability and leakage of fluid into tissues 3. Edema and infiltration of the skin by neutrophils 4. Macrophages and lymphocytes repair the tissues |
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What is diapedesis and why is it important in inflammation? |
AKA transmigration. The process of WBCs migrating out of the blood and into the tissues. This is important so WBCs can begin cleaning up the area |
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What is the mechanism of fever? |
Circulating substances called pyrogens reset the hypothalamic thermostat to a higher setting, causing increased heat production. Fever causes damage and stops the growth of bacteria |
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What are pyrogens, and where do they come from? |
These are molecules responsible for starting a fever during infection. Can be exogenous, and come from infectious agents, or endogenous, which are released during phagocytosis. |
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List four antimicrobial proteins |
1. Interferon: produced by WBCs for defense against viruses 2. Complement: a system that consists of 30 blood proteins that work to destroy bacteria and certain viruses 3. Iron binding proteins- keep iron bound so microbes can't use it 4. Antimicrobial peptides- AMPS, short proteins that insert themselves into bacterial membranes |
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What are the three major differences in the third line of defense versus the other defense mechanisms? |
The third line is: 1. Specific 2. Has Memory 3. Is life long |
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List the four stages of a specific immune response |
1. You are infected with a novel pathogen 2. Your second line of defense kills the pathogen 3. The dead pathogen gets taken to the lymph nodes, where they are chopped up and put on the outside of the APCs and shown to the naive lymphocytes 4. The naive lymphocytes attempt to match to the pathogens and if they do, they proliferate |
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List the characteristics of antigens that increase their antigenicity |
Have large molecules that are not repeating- good= proteins, lipoproteins bad= sugars |
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What kinds of cells can act as antigen presenting cells? |
Dendritic cells, macrophages, and B cells |
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Explain the role of cytotoxic T cells in apoptosis |
Cytotoxic T cells get attracted to certain cells, and release perforins which punch holes in the cells, and then release granzymes, which cause apoptosis of the cell |
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Describe the titer in the first and second response |
In the first response, there is a latent period from infection to production of antibodies, then the antibodies build slowly and gradually, and then decrease. With the second response, there is a quick, sharp increase of antibodies |
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What is the main goal of antimicrobial treatment? |
To destroy the pathogen with minimal harm to the host cells |
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What is the perfect antimicrobial drug? |
No perfect drug- each has its own pros and cons |
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What are the sources of the most commonly used antimicrobial drugs? |
Bacillus, streptomyces, penicillin, and cephaloproium |
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Selective toxicity |
The idea that an antimicrobial drug can destroy the pathogen without harming the host |
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What are the five major targets of antimicrobial drugs? |
1. Cell walls/ Peptidoglycan 2. Proteins/ Ribosomes 3. DNA/ RNA 4. Folic Acid Synthesis 5. Cell Membranes |
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What are some broad spectrum antibiotics? And narrow spectrum antibiotics? |
Broad: Penicillin, Cipro Narrow: Polymyxins |
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Describe the role of beta-lactamases, and their role in antibiotic resistance |
Beta-lactamases cleave beta-lactam rings in half, rendering Penicillin useless. They are created naturally by other microbes to combat the antibiotics made naturally by penicillin. |
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What are examples of beta-lactam antibiotics? |
Penicillin and cephalosporins |
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What are common cell-wall antibiotics that are not in the beta-lactam class? |
Carbapenems |
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What are the ribosomal targets of antibiotics that target protein synthesis? |
They stop the substrate from moving within the ribosome, stops translation, distorts the ribosome, blocks tRNA entry |
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What is the cellular target of quinolones? |
DNA and RNA |
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Name two drugs that target the cell membrane |
Polymyxins and Daptomycin |
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How does competative inhibition figure into the activity of sulfa drugs? |
You must give a large amount of Sulfa drugs, because they bind to and block the site of an enzyme that produces folic acid. If you don't have enough sulfa, it doesn't block the site |
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What are two categories of Anti-fungal medication, and how do they work? |
1. Azoles- work by inhibiting ergosterol synthesis, which decreases membrane structural integrity 2. Griseofulvins- work by inhibiting cell division by messing with the microtubules |
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List four anti-protozoa drugs |
1. Quinine 2. Chloroquine 3. Artemisinin 4. Metronidazole |
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List three anti-Helminth drugs |
1. Mebendazole 2. Praziquantel 3. Albendazole |
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What are three major modes of action of anti-viral drugs |
1. Block penetration of virus into the host cell 2. Blocks transcription and translation of viral molecules 3. Prevent maturation of viral particules |
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What are the two types of antibiotic resistance? |
1. Acquired- bacteria are resistant to a drug which they were previously sensitive to, bacteria learn this from each other 2. Intrinsic- bacteria are resistant to any antibiotic that they produce |
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Where does resistance come from? |
Has been around for longer than humans, comes because bacteria make antibiotics naturally to kill off other competative bacteria, who in turn make chemicals to make themselves resistant to the antibiotic |
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What is a resistome? |
All antibiotic resistant genes |
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How does drug resistance develop? |
By not finishing antibiotics- bacteria who have some resistance don't die, and share the resistance with others Mass ABX prophylaxis in cattle Addition to household products, creating resistance on our household surfaces |
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Edema |
The leakage of vascular fluid into tissues |
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Diapedesis |
Passage of blood cells through intact blood vessel walls during inflammation |
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What process involves antibodies cross linking cells to make them bigger and easier to phagocytize? |
Agglutination |
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True or false- Resistance genes can be transferred during transformation, transduction, and conjugation? |
True |
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Are lymphocytes granulocytes? |
No |
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What group do neutrophils, eosinophils, and basophils belong to? |
Granulocytes |
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What lymphoid tissue has the function of filtering pathogens from the blood? |
Spleen |