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10 Cards in this Set
- Front
- Back
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Particles bigger than >10um localize mainly where on inhalation?
What is the primary defense (gross) of the upper airways? |
nasal cavity.
mucociliary clearance. |
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Primary cilium serve what function?
Motile cilia beat 800-1500 times/min... do they respond to neurohumoral stim? mechanical stim? |
sensory, non-motile
yes, both. |
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Human cilia beat in which shape?
1/2 the pts with abnormal cilia (completely) will have what complication? |
in a plane
situs inversus totalis |
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Why do you only have ~4-6 hours to get bacteria out of the lung?
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the bacteria will otherwise evolve beyond the capacity of things like lysozyme and lactoferrin to control their growth.
- IgA is trying to stop the growth as well. |
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Is IgG actively transferred into the airway lumen? IgM? IgA?
Is Decreased serum IgA always a cause of chronic respiratory infection? |
No, only IgM and IgA
No. |
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In the more distal airways, what are the main defensive enactors? Do they just eat stuff?
Are there cilia and submucosal glands in the distal airway? |
aveolar macrophages.
No, they also secrete things! No. |
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Proximal airway defense mechanisms?
Distal airway defense mechanisms? |
Non opsonic secretory IgA
cilia liquid/mucus submucosal gland secretions (sIgA, lysozyme, lactoferrin, mucus) no cilia or submucosal glands aveolar macrophages - phagocytose stuff - chemotactic factors cytokines IgG opsonic |
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Is the study of rare dz irrelevant to the study of common dz?
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No: defects in these innate mechanisms illustrate their importance to everyday protection.
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Why aren't CF pts dead in a matter of hours/days?
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When you cough, your airways cells make ATP --> opens a different sort of Cl- channel --> rescue mechanism.... but, in CF pts they have endogenous ectonucleotidases that degrade free ATP.
- thus this mech doesn't help as much as it should - stuff is in the works that acts like ATP but isn't degradable. |
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Airway host defense innate mechanisms requires the coordination of multiple individual components of lung defense.
(T/F)? |
T
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