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[[Cough]], together with [[mucociliary clearance]], prevent pathogens from entering the lower [[respiratory tract]]. Cough suppression or [[cough reflex]] inhibition seen in patients with [[cerebrovascular accident]]s and [[overdose|drug overdosage]]s is associated with an enhanced risk for [[aspiration pneumonia]]. Another relation to [[cough]] is [[genetic polymorphism]]s in the [[angiotensin-converting enzyme|angiotensin-converting enzyme (ACE)]] gene. The role of [[cough]] in preventing [[pneumonia]] may be explained by a higher risk for developing [[pneumonia]] in [[homozygote]]s carrying [[deletion]]/[[deletion]] (DD) [[genotype]] who are found to have lower levels of [[bradykinin]] and [[tachykinins]] such as [[substance P]].<ref name="Morimoto-2002">{{Cite journal | last1 = Morimoto | first1 = S. | last2 = Okaishi | first2 = K. | last3 = Onishi | first3 = M. | last4 = Katsuya | first4 = T. | last5 = Yang | first5 = J. | last6 = Okuro | first6 = M. | last7 = Sakurai | first7 = S. | last8 = Onishi | first8 = T. | last9 = Ogihara | first9 = T. | title = Deletion allele of the angiotensin-converting enzyme gene as a risk factor for pneumonia in elderly patients. | journal = Am J Med | volume = 112 | issue = 2 | pages = 89-94 | month = Feb | year = 2002 | doi = | PMID = 11835945 }}</ref><ref>{{Cite journal | last1 = Rigat | first1 = B. | last2 = Hubert | first2 = C. | last3 = Alhenc-Gelas | first3 = F. | last4 = Cambien | first4 = F. | last5 = Corvol | first5 = P. | last6 = Soubrier | first6 = F. | title = An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels. | journal = J Clin Invest | volume = 86 | issue = 4 | pages = 1343-6 | month = Oct | year = 1990 | doi = 10.1172/JCI114844 | PMID = 1976655 }}</ref> | [[Cough]], together with [[mucociliary clearance]], prevent pathogens from entering the lower [[respiratory tract]]. Cough suppression or [[cough reflex]] inhibition seen in patients with [[cerebrovascular accident]]s and [[overdose|drug overdosage]]s is associated with an enhanced risk for [[aspiration pneumonia]]. Another relation to [[cough]] is [[genetic polymorphism]]s in the [[angiotensin-converting enzyme|angiotensin-converting enzyme (ACE)]] gene. The role of [[cough]] in preventing [[pneumonia]] may be explained by a higher risk for developing [[pneumonia]] in [[homozygote]]s carrying [[deletion]]/[[deletion]] (DD) [[genotype]] who are found to have lower levels of [[bradykinin]] and [[tachykinins]] such as [[substance P]].<ref name="Morimoto-2002">{{Cite journal | last1 = Morimoto | first1 = S. | last2 = Okaishi | first2 = K. | last3 = Onishi | first3 = M. | last4 = Katsuya | first4 = T. | last5 = Yang | first5 = J. | last6 = Okuro | first6 = M. | last7 = Sakurai | first7 = S. | last8 = Onishi | first8 = T. | last9 = Ogihara | first9 = T. | title = Deletion allele of the angiotensin-converting enzyme gene as a risk factor for pneumonia in elderly patients. | journal = Am J Med | volume = 112 | issue = 2 | pages = 89-94 | month = Feb | year = 2002 | doi = | PMID = 11835945 }}</ref><ref>{{Cite journal | last1 = Rigat | first1 = B. | last2 = Hubert | first2 = C. | last3 = Alhenc-Gelas | first3 = F. | last4 = Cambien | first4 = F. | last5 = Corvol | first5 = P. | last6 = Soubrier | first6 = F. | title = An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels. | journal = J Clin Invest | volume = 86 | issue = 4 | pages = 1343-6 | month = Oct | year = 1990 | doi = 10.1172/JCI114844 | PMID = 1976655 }}</ref> | ||
====Defects in Immnue System==== | |||
[[Pathogen-associated molecular pattern|Pathogen-associated molecular patterns (PAMPs)]] are microbial components initially recognized by [[Toll-like receptor|Toll-like receptors (TLRs)]] and other [[pattern recognition receptor|pattern-recognition receptors (PRRs)]] of the [[innate immune system]]. Effectors in the [[acquired immunity|acquired immune system]] are involved in elimination of microorganisms and generation of immunological memory. Patients with defective innate or acquired immunity are mroe susceptible to pneumonia. | |||
==References== | ==References== | ||
Revision as of 18:20, 17 February 2014
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Community-Acquired Pneumonia Microchapters |
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Differentiating Community-acquired pneumonia from other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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Sandbox/cap On the Web |
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American Roentgen Ray Society Images of Sandbox/cap |
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Directions to Hospitals Treating Community-acquired pneumonia |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chetan Lokhande, M.B.B.S [2]
Pathophysiology
Diminished Mucociliary Clearance
The cilia lining the respiratory epithelium serve to move secreted mucus containing trapped foreign particles including pathogens towards the oropharynx for either expectoration or swallowing. Elevated incidence of pneumonia in patients with genetic defects affecting mucociliary clearance such as primary ciliary dyskinesia suggests its role in the pathogenesis of community-acquired pneumonia.
Cough Suppression
Cough, together with mucociliary clearance, prevent pathogens from entering the lower respiratory tract. Cough suppression or cough reflex inhibition seen in patients with cerebrovascular accidents and drug overdosages is associated with an enhanced risk for aspiration pneumonia. Another relation to cough is genetic polymorphisms in the angiotensin-converting enzyme (ACE) gene. The role of cough in preventing pneumonia may be explained by a higher risk for developing pneumonia in homozygotes carrying deletion/deletion (DD) genotype who are found to have lower levels of bradykinin and tachykinins such as substance P.[1][2]
Defects in Immnue System
Pathogen-associated molecular patterns (PAMPs) are microbial components initially recognized by Toll-like receptors (TLRs) and other pattern-recognition receptors (PRRs) of the innate immune system. Effectors in the acquired immune system are involved in elimination of microorganisms and generation of immunological memory. Patients with defective innate or acquired immunity are mroe susceptible to pneumonia.
References
- ↑ Morimoto, S.; Okaishi, K.; Onishi, M.; Katsuya, T.; Yang, J.; Okuro, M.; Sakurai, S.; Onishi, T.; Ogihara, T. (2002). "Deletion allele of the angiotensin-converting enzyme gene as a risk factor for pneumonia in elderly patients". Am J Med. 112 (2): 89–94. PMID 11835945. Unknown parameter
|month=ignored (help) - ↑ Rigat, B.; Hubert, C.; Alhenc-Gelas, F.; Cambien, F.; Corvol, P.; Soubrier, F. (1990). "An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels". J Clin Invest. 86 (4): 1343–6. doi:10.1172/JCI114844. PMID 1976655. Unknown parameter
|month=ignored (help)