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==Overview==
==Overview==
[[Acute bronchitis]] is a self-limited inflammation of the large airways of the lung that is characterized by cough with or without sputum that last several days or weeks (10 days).  It is one of the commonest causes of outpatient admission worldwide.  Virus are thought to be the commonest cause of acute bronchitis.  [[Influenza]] A and B, [[parainfluenza]], [[respiratory syncytial virus]], [[coronavirus]] are the commonest involved pathogens.  Some atypical bacterias like [[mycoplasma]], [[chlamydiae]] and [[bordetella pertussis]] are also found to cause acute bronchitis.
Virus are thought to be the commonest cause of acute bronchitis.  [[Influenza]] A and B, [[parainfluenza]], [[respiratory syncytial virus]], [[coronavirus]] are the commonest involved pathogens.  Some atypical bacterias like [[mycoplasma]], [[chlamydiae]] and [[bordetella pertussis]] are also found to cause acute bronchitis.<br> Smoking,occupational exposures, air pollutants and genetic factors are etiologies of chronic bronchitis.


==Causes==
==Causes==
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::'''Bacteries:''' Mycoplasma pneumoniae and,Chlamydophila pneumoniae and Bordetella pertussis<ref name="pmid17108344">{{cite journal |vauthors=Wenzel RP, Fowler AA |title=Clinical practice. Acute bronchitis |journal=N. Engl. J. Med. |volume=355 |issue=20 |pages=2125–30 |year=2006 |pmid=17108344 |doi=10.1056/NEJMcp061493 |url=}}</ref>.
::'''Bacteries:''' Mycoplasma pneumoniae and,Chlamydophila pneumoniae and Bordetella pertussis<ref name="pmid17108344">{{cite journal |vauthors=Wenzel RP, Fowler AA |title=Clinical practice. Acute bronchitis |journal=N. Engl. J. Med. |volume=355 |issue=20 |pages=2125–30 |year=2006 |pmid=17108344 |doi=10.1056/NEJMcp061493 |url=}}</ref>.
::'''Environmental causes:''' Toxic fume inhalation, tobacco, dust and aerosol may result in acute bronchitis<ref name="pmid11106722">{{cite journal |vauthors=Irwin RS, Madison JM |title=The diagnosis and treatment of cough |journal=N. Engl. J. Med. |volume=343 |issue=23 |pages=1715–21 |year=2000 |pmid=11106722 |doi=10.1056/NEJM200012073432308 |url=}}</ref>.
::'''Environmental causes:''' Toxic fume inhalation, tobacco, dust and aerosol may result in acute bronchitis<ref name="pmid11106722">{{cite journal |vauthors=Irwin RS, Madison JM |title=The diagnosis and treatment of cough |journal=N. Engl. J. Med. |volume=343 |issue=23 |pages=1715–21 |year=2000 |pmid=11106722 |doi=10.1056/NEJM200012073432308 |url=}}</ref>.
*<font size="3.3">'''[[Chronic Bronchitis]]:'''</font> caused by ''smoking'',''Air Pollutions'',''Occupational Exposures'' and ''Genetic factors''
*<font size="3.3">'''[[Chronic Bronchitis]]:'''</font> caused by ''smoking'',''Air Pollutants'',''Occupational Exposures'' and ''Genetic factors''
::'''Smoking'''
:::The primary risk factor for COPD is chronic tobacco smoking. In the [[United States]], 80 to 90% of cases of COPD are due to smoking.<ref name="medcauses">[http://www.medicinenet.com/chronic_obstructive_pulmonary_disease_copd/page3.htm MedicineNet.com - COPD causes]</ref><ref>{{cite journal |author=Young RP, Hopkins RJ, Christmas T, Black PN, Metcalf P, Gamble GD |title=COPD prevalence is increased in lung cancer, independent of age, sex and smoking history |journal=Eur. Respir. J. |volume=34 |issue=2 |pages=380–6 |year=2009 |month=August |pmid=19196816 |doi=10.1183/09031936.00144208 }}</ref> Exposure to cigarette smoke is measured in [[pack-years]],<ref>{{cite web |url=http://www.cancer.gov/Templates/db_alpha.aspx?CdrID=306510 |title=Definition of pack year - NCI Dictionary of Cancer Terms |format= |work= |accessdate=}}</ref> the average number of packages of cigarettes smoked daily multiplied by the number of years of smoking. The likelihood of developing COPD increases with age and cumulative smoke exposure, and almost all life-long smokers will develop COPD, provided that smoking-related, extrapulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand.<ref>{{cite doi|10.1016/S0140-6736(06)68516-4}}</ref>
 
::'''Occupational Exposures'''
:::Intense and prolonged exposure to workplace dusts found in [[coal mining]], [[gold mining]], and the cotton textile industry and chemicals such as [[cadmium]], [[isocyanates]], and fumes from [[welding]]  have been implicated in the development of airflow obstruction, even in nonsmokers.<ref>{{cite journal
| pmid = 16690673
| pmc = 1459603
| title = Definition, epidemiology, and risk factors
| year = 2006
| journal = BMJ
| volume = 332
| issue = 7550
| pages = 1142–4
| doi = 10.1136/bmj.332.7550.1142
| month = May
| author = Devereux, Graham
}}</ref> Workers who smoke and are exposed to these particles and gases are even more likely to develop COPD. Intense [[silica]] dust exposure causes [[silicosis]], a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition.<ref>{{cite journal |author=Hnizdo E, Vallyathan V |title=Chronic obstructive pulmonary disease due to occupational exposure to silica dust: a review of epidemiological and pathological evidence |journal=Occup Environ Med |volume=60 |issue=4 |pages=237–43 |year=2003 |month=April |pmid=12660371 |pmc=1740506 |doi=10.1136/oem.60.4.237}}</ref> The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking.<ref name="Harrisons">{{cite book |author=Loscalzo, Joseph; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser, Stephen L; Longo, Dan L. |title=Harrison's Principles of Internal Medicine |edition=17th |publisher=McGraw-Hill Professional |year=2008 |isbn=0-07-146633-9}}</ref>
 
::'''Air Pollution'''
:::Studies in many countries have found people who live in large cities have a higher rate of COPD compared to people who live in rural areas.<ref>{{cite journal |author=Halbert RJ, Natoli JL, Gano A, Badamgarav E, Buist AS, Mannino DM |title=Global burden of COPD: systematic review and meta-analysis |journal=Eur. Respir. J. |volume=28 |issue=3 |pages=523–32 |year=2006 |month=September |pmid=16611654 |doi=10.1183/09031936.06.00124605 }}</ref> Urban [[air pollution]] may be a contributing factor for COPD, as it is thought to slow the normal growth of the lungs, although the long-term research needed to confirm the link has not been done. Studies of the industrial waste gas and COPD/asthma-aggravating compound, [[sulfur dioxide]], and the inverse relation to the presence of the blue lichen ''[[Xanthoria]]'' (usually found abundantly in the countryside, but never in towns or cities) have been seen to suggest combustive industrial processes do not aid COPD sufferers. In many [[developing countries]], indoor air pollution from cooking fire smoke (often using [[biomass fuel]]s such as wood and animal dung) is a common cause of COPD, especially in women.<ref>{{cite journal |author=Kennedy SM, Chambers R, Du W, Dimich-Ward H |title=Environmental and occupational exposures: do they affect chronic obstructive pulmonary disease differently in women and men?|journal=Proceedings of the American Thoracic Society|volume=4 |issue=8 |pages=692–4 |year=2007 |month=December |pmid=18073405 |url=http://pats.atsjournals.org/cgi/content/full/4/8/692 |doi=10.1513/pats.200707-094SD}}</ref>
 
::'''Genetics'''
:::Some factor in addition to heavy smoke exposure is required for a person to develop COPD. This factor is probably a [[gene]]tic susceptibility. COPD is more common among relatives of COPD patients who smoke than unrelated smokers.<ref>{{cite journal |author=Silverman EK, Chapman HA, Drazen JM, ''et al.'' |title=Genetic epidemiology of severe, early-onset chronic obstructive pulmonary disease. Risk to relatives for airflow obstruction and chronic bronchitis |journal=Am. J. Respir. Crit. Care Med. |volume=157 |issue=6 Pt 1 |pages=1770–8 |year=1998 |month=June |pmid=9620904 |url=http://ajrccm.atsjournals.org/cgi/pmidlookup?view=long&pmid=9620904}}</ref> The genetic differences that make some peoples' lungs susceptible to the effects of tobacco smoke are mostly unknown.[[Alpha 1-antitrypsin deficiency]] is a genetic condition that is responsible for about 2% of cases of COPD. In this condition, the body does not make enough of a protein, [[alpha 1-antitrypsin]]. Alpha 1-antitrypsin protects the lungs from damage caused by [[protease]] [[enzymes]], such as [[elastase]] and [[trypsin]], that can be released as a result of an inflammatory response to tobacco smoke.<ref>{{MedlinePlus|000091}}</ref>
===Common Causes===
===Common Causes===
*[[Adenovirus]]
*[[Adenovirus]]

Revision as of 15:52, 14 September 2016

Bronchitis Main page

Patient Information

Overview

Causes

Classification

Acute bronchitis
Chronic bronchitis

Differential Diagnosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogheneochuko Ajari, MB.BS, MS [2]

Overview

Virus are thought to be the commonest cause of acute bronchitis. Influenza A and B, parainfluenza, respiratory syncytial virus, coronavirus are the commonest involved pathogens. Some atypical bacterias like mycoplasma, chlamydiae and bordetella pertussis are also found to cause acute bronchitis.
Smoking,occupational exposures, air pollutants and genetic factors are etiologies of chronic bronchitis.

Causes

  • Acute Bronchitis: may be caused by either viral, bacterial or environmental causes.
Viruses: Influenza Virus,parainfluenza virus,respiratory syncytial virus, coronavirus, adenovirus, enterovirus, rhinovirus, coxsackievirus, and human metapneumovirus[1][2][3].
Bacteries: Mycoplasma pneumoniae and,Chlamydophila pneumoniae and Bordetella pertussis[4].
Environmental causes: Toxic fume inhalation, tobacco, dust and aerosol may result in acute bronchitis[5].
  • Chronic Bronchitis: caused by smoking,Air Pollutants,Occupational Exposures and Genetic factors
Smoking
The primary risk factor for COPD is chronic tobacco smoking. In the United States, 80 to 90% of cases of COPD are due to smoking.[6][7] Exposure to cigarette smoke is measured in pack-years,[8] the average number of packages of cigarettes smoked daily multiplied by the number of years of smoking. The likelihood of developing COPD increases with age and cumulative smoke exposure, and almost all life-long smokers will develop COPD, provided that smoking-related, extrapulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand.[9]
Occupational Exposures
Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry and chemicals such as cadmium, isocyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in nonsmokers.[10] Workers who smoke and are exposed to these particles and gases are even more likely to develop COPD. Intense silica dust exposure causes silicosis, a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition.[11] The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking.[12]
Air Pollution
Studies in many countries have found people who live in large cities have a higher rate of COPD compared to people who live in rural areas.[13] Urban air pollution may be a contributing factor for COPD, as it is thought to slow the normal growth of the lungs, although the long-term research needed to confirm the link has not been done. Studies of the industrial waste gas and COPD/asthma-aggravating compound, sulfur dioxide, and the inverse relation to the presence of the blue lichen Xanthoria (usually found abundantly in the countryside, but never in towns or cities) have been seen to suggest combustive industrial processes do not aid COPD sufferers. In many developing countries, indoor air pollution from cooking fire smoke (often using biomass fuels such as wood and animal dung) is a common cause of COPD, especially in women.[14]
Genetics
Some factor in addition to heavy smoke exposure is required for a person to develop COPD. This factor is probably a genetic susceptibility. COPD is more common among relatives of COPD patients who smoke than unrelated smokers.[15] The genetic differences that make some peoples' lungs susceptible to the effects of tobacco smoke are mostly unknown.Alpha 1-antitrypsin deficiency is a genetic condition that is responsible for about 2% of cases of COPD. In this condition, the body does not make enough of a protein, alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke.[16]

Common Causes

Causes by Organ System

Cardiovascular Heart disease
Chemical / poisoning Acenaphthene, acetaldehyde, acetic acid, acetic anhydride, biphenyl, chlorine dioxide, ethyleneamine, hexamethylene diisocyanate, nitric acid, phosphine, polychlorinated dibenzofurans, selenium poisoning, silver, sulfuric acid, toluene diisocyanate, vanadium poisoning
Dermatologic Yellow nail syndrome
Drug Side Effect Albuterol, alferon N, alfuzosin, artemether and lumefantrin, belimumab, benazepril, budesonide, butorphanol, candesartan, captafol, cardura, cevimeline, ciclesonide, citalopram, clopidogrel, crofelemer, doxazosin, enalapril maleate, escitalopram, exemestane, febuxostat, felodipine, fingolimod, fluoxetine, fluvoxamine, goserelin, ibandronate, infliximab, interferon, ipratropium, irbesartan, isosorbide dinitrate, isosorbide mononitrate, itraconazole, lamotrigine, latanoprost, leflunomide, lumigan, methotrexate, metipranolol, metronidazole topical, minoxidil, moexipril, mycophenolate, mycophenolic acid, nateglinide, nitisinone, oseltamivir, oxcarbazepine, paroxetine, pentamidine isethionate, pirbuterol, pramipexole, repaglinide, risedronate, ropinirole, rosuvastatin, sertraline, sibutramine, simvastatin, tacrolimus, tamsulosin, tarka (medication), telmisartan, thalidomide, tiagabine, tobramycin, tolterodine, topiramate, trandolapril, travoprost, unoprostone, zanamivir
Ear Nose Throat Pharyngitis, sinusitis
Endocrine No underlying causes
Environmental Air pollution, aluminium lung, anthracosis, coal dust, coal worker's pneumoconiosis, farmer's lung, mesothelioma, pneumoconiosis, silicosis, smoking
Gastroenterologic Alpha 1-antitrypsin deficiency, cystic fibrosis, gastroesophageal reflux disease, inflammatory bowel disease
Genetic Alpha 1-antitrypsin deficiency, ataxia telangiectasia, cystic fibrosis, Gulf War syndrome, Klinefelter syndrome
Hematologic No underlying causes
Iatrogenic Lung transplantation
Infectious Disease Acute viral nasopharyngitis (common cold), adenovirus, aspergillosis, bordetella pertussis, chickenpox, chlamydia pneumonia, common cold, coronavirus, coxsackievirus, echovirus, encephalitozoon cuniculi infection, enterovirus, flu, group A streptococcal infection, HIV, influenza, measles, moraxella catarrhalis, mycoplasma pneumonia, orthomyxovirus, paragonimiasis, parainfluenza, paramyxovirus, pharyngitis, pneumococcus, respiratory syncytial virus, rhinovirus, trichinellosis
Musculoskeletal / Ortho Prune belly syndrome
Neurologic Ataxia telangiectasia, Gulf War syndrome
Nutritional / Metabolic Hypoglycemia
Obstetric/Gynecologic No underlying causes
Oncologic Lung cancer, mesothelioma
Opthalmologic No underlying causes
Overdose / Toxicity Marijuana abuse, nicotine addiction
Psychiatric No underlying causes
Pulmonary Acute viral nasopharyngitis (common cold), alpha 1-antitrypsin deficiency, aluminium lung, anthracosis, aspergillosis, asthma, blue and bloated syndrome, bronchiectasis, bronchiolitis, coal worker's pneumoconiosis, common cold, COPD, farmer's lung, flu, influenza, lung cancer, lung transplantation, mesothelioma, yellow nail syndrome
Renal / Electrolyte No underlying causes
Rheum / Immune / Allergy Asthma, Felty's syndrome, Gulf War syndrome, IgG deficiency, Immunoglobulin G subclass deficiency, MHC class I deficiency, primary immunodeficiency, Sjogren's syndrome
Sexual No underlying causes
Trauma No underlying causes
Urologic Prune belly syndrome
Miscellaneous Tobacco smoking

Causes in Alphabetical Order

The unnamed parameter 2= is no longer supported. Please see the documentation for {{columns-list}}.
3

Causes Based on Classification

Acute Bronchitis

The following things can make bronchitis worse:

Chronic Bronchitis

Chronic bronchitis is a long-term condition. People have a cough that produces excessive mucus. To be diagnosed with chronic bronchitis, you must have a cough with mucus most days of the month for at least 3 months.

References

  1. Jonsson JS, Sigurdsson JA, Kristinsson KG, Guthnadóttir M, Magnusson S (1997). "Acute bronchitis in adults. How close do we come to its aetiology in general practice?". Scand J Prim Health Care. 15 (3): 156–60. PMID 9323784.
  2. Boivin G, Abed Y, Pelletier G, Ruel L, Moisan D, Côté S, Peret TC, Erdman DD, Anderson LJ (2002). "Virological features and clinical manifestations associated with human metapneumovirus: a new paramyxovirus responsible for acute respiratory-tract infections in all age groups". J. Infect. Dis. 186 (9): 1330–4. doi:10.1086/344319. PMID 12402203.
  3. Louie JK, Hacker JK, Gonzales R, Mark J, Maselli JH, Yagi S, Drew WL (2005). "Characterization of viral agents causing acute respiratory infection in a San Francisco University Medical Center Clinic during the influenza season". Clin. Infect. Dis. 41 (6): 822–8. doi:10.1086/432800. PMID 16107980.
  4. Wenzel RP, Fowler AA (2006). "Clinical practice. Acute bronchitis". N. Engl. J. Med. 355 (20): 2125–30. doi:10.1056/NEJMcp061493. PMID 17108344.
  5. Irwin RS, Madison JM (2000). "The diagnosis and treatment of cough". N. Engl. J. Med. 343 (23): 1715–21. doi:10.1056/NEJM200012073432308. PMID 11106722.
  6. MedicineNet.com - COPD causes
  7. Young RP, Hopkins RJ, Christmas T, Black PN, Metcalf P, Gamble GD (2009). "COPD prevalence is increased in lung cancer, independent of age, sex and smoking history". Eur. Respir. J. 34 (2): 380–6. doi:10.1183/09031936.00144208. PMID 19196816. Unknown parameter |month= ignored (help)
  8. "Definition of pack year - NCI Dictionary of Cancer Terms".
  9. Template:Cite doi
  10. Devereux, Graham (2006). "Definition, epidemiology, and risk factors". BMJ. 332 (7550): 1142–4. doi:10.1136/bmj.332.7550.1142. PMC 1459603. PMID 16690673. Unknown parameter |month= ignored (help)
  11. Hnizdo E, Vallyathan V (2003). "Chronic obstructive pulmonary disease due to occupational exposure to silica dust: a review of epidemiological and pathological evidence". Occup Environ Med. 60 (4): 237–43. doi:10.1136/oem.60.4.237. PMC 1740506. PMID 12660371. Unknown parameter |month= ignored (help)
  12. Loscalzo, Joseph; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser, Stephen L; Longo, Dan L. (2008). Harrison's Principles of Internal Medicine (17th ed.). McGraw-Hill Professional. ISBN 0-07-146633-9.
  13. Halbert RJ, Natoli JL, Gano A, Badamgarav E, Buist AS, Mannino DM (2006). "Global burden of COPD: systematic review and meta-analysis". Eur. Respir. J. 28 (3): 523–32. doi:10.1183/09031936.06.00124605. PMID 16611654. Unknown parameter |month= ignored (help)
  14. Kennedy SM, Chambers R, Du W, Dimich-Ward H (2007). "Environmental and occupational exposures: do they affect chronic obstructive pulmonary disease differently in women and men?". Proceedings of the American Thoracic Society. 4 (8): 692–4. doi:10.1513/pats.200707-094SD. PMID 18073405. Unknown parameter |month= ignored (help)
  15. Silverman EK, Chapman HA, Drazen JM; et al. (1998). "Genetic epidemiology of severe, early-onset chronic obstructive pulmonary disease. Risk to relatives for airflow obstruction and chronic bronchitis". Am. J. Respir. Crit. Care Med. 157 (6 Pt 1): 1770–8. PMID 9620904. Unknown parameter |month= ignored (help)
  16. MedlinePlus Encyclopedia 000091


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