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27 Cards in this Set
- Front
- Back
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Susceptibility |
lackof resistance to a disease |
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Immunity
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abilityto ward off disease
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Innateimmunity
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defensesagainst any pathogen
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Adaptiveimmunity
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immunityor resistance to a specific pathogen |
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what are some mechanical factors of immunity |
Skin
Mucous membranes Ciliaryescalator-transportsmicrobes trapped in mucus away from the lungs Alimentary canal-•Peristalsis•Mucus layer protects epithelium Saliva-washesmicrobes off |
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chemical factors of immunity |
Fungistatic fatty acid in sebum (produced by sebaceous or oil glands inthe skin) LowpH (3–5) of skin Saltinessof the skin LowpH (1.2–3.0) of gastricjuice Alimentary canal - Cells in the innate immune system sensepathogen-associatedmolecular pattern (PAMPS) viaToll-likereceptors (TLRs) orother receptors |
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what is Microbialantagonism/competitive exclusion |
normalmicrobiota compete with pathogens or alterthe environment |
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Commensalmicrobiota |
oneorganism (microbe) benefits, and the other (host) is unharmed may be opportunistic pathogens |
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Fever |
Abnormallyhigh body temperature Hypothalamusis normally set at 37°C
Gram-negativeendotoxins cause phagocytes to release interleukin-1 (IL-1) Hypothalamusreleases prostaglandins that reset the hypothalamus to a high temperature Bodyincreases rate of metabolism, vasoconstriction, and shivering occurs, which raise temperature Vasodilationand sweating: body temperature falls (crisis) |
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Advantages of a fever |
Increases transferrins Produces interferon Can impede bacterial growth |
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Disadvantages of a fever |
Tachycardia Acidosis Dehydration 41.5C (106.7F) is considered a medical emergency |
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Phagocytosis |
Phago:from Greek, meaning eat Cyte:from Greek, meaning cell Ingestionof microbes or particles by a cell, performed by phagocytes has several immune cells: Neutrophils, fixed (tissue resident) macrophages, wandering macrophages |
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what are the process of phagocytosis |
Chemotaxis Adherence Ingestion Digestion |
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Chemotaxis
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The movement of the phagocyte toward themicrobes/inflammation Trust NetA |
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Adherence
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Attachment of the phagocytes plasmamembrane to the surface of the microbe
Opsonization (immune adherence): certain proteins (opsonins) coatthe surface of the microbe and provide a “handle” that helps phagocytes toadhere Some pathogens have a variety of means bywhich to block adherence |
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Ingestion
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Microbeis surrounded by pseudopods until it is completely enveloped in a phagocyticvesicle
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Digestion
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Vesicle (phagosome)pinches off from the plasma membrane, moves into the cytoplasm fuses withlysosome to form a phagolysosome microbe is digested byenzymes and oxidizing agents |
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steps of inflammation |
Activationof acute-phaseproteins (complement, cytokine, and kinins) Vasodilation (histamine, kinins,prostaglandins, and leukotrienes) Redness Swelling(edema) Pain Heat |
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what are some chemicals released by damaged cells |
Histamine
Kinins Prostaglandins Leukotrienes |
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Histamine
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Vasodilation
increased permeabilityof blood vessels |
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Kinins
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Vasodilation
increased permeabilityof blood vessels |
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Prostaglandins
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Intensify histamine and kinineffect
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Leukotrienes
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Increased permeability of blood vessels phagocytic attachment |
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Describethree pathways for the activation of complement |
Antigen–antibody complex on the surfaceof a microbe (classicalpathway) Complement proteins (B, D, and P) boundto PAMPS on the surface of a microbe (alternativepathway) Lectinbound to cell carbohydrates |
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what are the results of the compliment system |
C3b causes opsonization (acts as an opsonin) Makes it easier for phagocytes to holdonto microbes and take them up C3a + C5a cause inflammation Recruit phagocytes Binds to C3a receptor on mast cells Causesmast cells to secrete histamine this cause inflammation C5b - C9 cause cell lysis by forming amembrane attack complex (MAC) Opens a pore in the cell membrane Water gets in, electrolytes get out d |
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how does bacteria evade complement |
Capsulesprevent C activation Surfacelipid–carbohydrate complexes prevent formation of membrane attack complex (MAC) Enzymaticdigestion of C5a |
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Interferons(IFNs) a, b, and g |
Type-1 IFN (a and b)are produced in response to viral infection
Host-specific, but not virus-specific IFN-a and IFN-b: cause cells to produce antiviralproteins that inhibit viral replication IFN-g: activates neutrophils and macrophagesto phagocytize and kill bacteria |
