Chronic obstructive pulmonary disease causes: Difference between revisions

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__NOTOC__
{{Chronic obstructive pulmonary disease}}
{{Chronic obstructive pulmonary disease}}
{{CMG}}; '''Associate Editors-In-Chief:''' {{CZ}}, [[Priyamvada Singh|Priyamvada Singh, MBBS]] [mailto:psingh13579@gmail.com]
{{CMG}}; '''Associate Editors-In-Chief:''' {{CZ}}, [[Priyamvada Singh|Priyamvada Singh, MBBS]] [mailto:psingh13579@gmail.com]


==Overview==
==Overview==
'''Chronic obstructive pulmonary disease''' ('''COPD'''), also known as '''chronic obstructive airway disease''' ('''COAD'''), is a group of [[disease]]s characterized by the pathological limitation of airflow in the [[airway]] that is not fully reversible. COPD is the umbrella term for chronic [[bronchitis]], [[emphysema]] and a range of other lung disorders. It is most often due to [[tobacco smoking]],<ref name="dev">Devereux G. ''ABC of chronic obstructive pulmonary disease. Definition, epidemiology, and risk factors.'' [[British Medical Journal|BMJ]] 2006;332:1142-1144. PMID 16690673</ref> but can be due to other airborne irritants such as coal dust, [[asbestos]] or solvents, [[congenital]] conditions such as [[alpha-1-antitrypsin deficiency]] and as well as preserved meats containing nitrites. In the United States, tobacco use is a key factor in the development and progression of COPD, but asthma, exposure to air pollutants in the home and workplace, genetic factors, and respiratory infections also play a role. In the developing world, indoor air quality is thought to play a larger role in the development and progression of COPD than it does in the United States.
Chronic obstructive pulmonary disease (COPD), is most often due to [[tobacco smoking]]; but can be due to other airborne irritants such as coal dust, [[asbestos]] or solvents, [[congenital]] conditions such as [[alpha-1-antitrypsin deficiency]] and as well as preserved meats containing [[Nitrite|nitrites]]. In the United States, [[tobacco]] use is a key factor in the development and progression of COPD, but [[asthma]], exposure to [[Pollutant|air pollutants]] in the home and workplace, genetic factors, and [[Respiratory tract infection|respiratory infections]] also play a role. In the developing world, indoor air quality is thought to play a larger role in the development and progression of COPD than it does in the United States.


==Causes==
==Causes==
Line 10: Line 11:


====Smoking====
====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>
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 [[Smoking|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 [[Cigarette|cigarettes]] smoked daily multiplied by the number of years of [[smoking]]. The likelihood of developing COPD increases with age and cumulative [[Smoking|smoke]] exposure, and almost all life-long smokers will develop COPD, provided that [[smoking]]-related, extra-[[pulmonary]] diseases ([[cardiovascular]], [[diabetes]], [[cancer]]) do not claim their lives beforehand.<ref>{{cite doi|10.1016/S0140-6736(06)68516-4}}</ref>


====Occupational Exposures====
====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
Intense and prolonged exposure to workplace dusts found in coal mining, [[gold]] mining, and the cotton textile industry and [[Chemical substance|chemicals]] such as [[cadmium]], iso-cyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in non-smokers.<ref>{{cite journal
  | pmid = 16690673
  | pmid = 16690673
  | pmc = 1459603
  | pmc = 1459603
Line 25: Line 26:
  | month = May
  | month = May
  | author = Devereux, Graham
  | 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>
}}</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 [[Pollution|pollutants]] on the [[Lung|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====
====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>
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 [[Lung|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.<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====
====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.
Some factor in addition to heavy [[Smoking|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 [[Smoking|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 [[Inflammation|inflammatory]] response to [[Tobacco smoking|tobacco smoke]].<ref>{{MedlinePlus|000091}}</ref>
[[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>


====Autoimmune Disease====
====Autoimmune Disease====
{{Main|Autoimmunity}}
{{Main|Autoimmunity}}
There is mounting evidence that there may be an autoimmune component to COPD, triggered by lifelong smoking.<ref>{{cite journal |author=Agustí A, MacNee W, Donaldson K, Cosio M. |title=Hypothesis: Does COPD have an autoimmune component? |journal=Thorax |volume=58 |issue=10 |pages=832–4 |year=2003 |pmid=14514931 |doi=10.1136/thorax.58.10.832 |pmc=1746486}}</ref> Many individuals with COPD who have stopped smoking have active inflammation in the lungs.<ref name=Rutgers00>{{cite journal |author=Rutgers SR, Postma DS, ten Hacken NH, ''et al.'' |title=Ongoing airway inflammation in patients with COPD who do not currently smoke |journal=Thorax |volume=55 |issue=1 |pages=12–8 |year=2000 |month=January |pmid=10607796 |pmc=1745599 |doi= 10.1136/thorax.55.1.12|url=}}</ref> The disease may continue to get worse for many years after stopping smoking due to this ongoing inflammation.<ref name=Rutgers00/> This sustained inflammation is thought to be mediated by [[autoantibodies]] and [[autoreactive T cell]]s.<ref name=Rutgers00/><ref>{{cite journal |author=Feghali-Bostwick CA, Gadgil AS, Otterbein LE, ''et al.'' |title=Autoantibodies in Patients with Chronic Obstructive Pulmonary Disease |journal=Am. J. Respir. Crit. Care Med. |volume=177 |issue=2 |pages=156–63 |year=2008 |month=January |pmid=17975205 |doi=10.1164/rccm.200701-014OC |pmc=2204079 }}</ref><ref>{{cite journal |author=Lee SH, Goswami S, Grudo A, ''et al.'' |title=Antielastin autoimmunity in tobacco smoking-induced emphysema |journal=Nat. Med. |volume=13 |issue=5 |pages=567–9 |year=2007 |month=May |pmid=17450149 |doi=10.1038/nm1583 }}</ref>
There is mounting evidence that there may be an autoimmune component to COPD, triggered by lifelong smoking.<ref>{{cite journal |author=Agustí A, MacNee W, Donaldson K, Cosio M. |title=Hypothesis: Does COPD have an autoimmune component? |journal=Thorax |volume=58 |issue=10 |pages=832–4 |year=2003 |pmid=14514931 |doi=10.1136/thorax.58.10.832 |pmc=1746486}}</ref> Many individuals with COPD who have stopped smoking have active [[inflammation]] in the [[Lung|lungs]].<ref name="Rutgers00">{{cite journal |author=Rutgers SR, Postma DS, ten Hacken NH, ''et al.'' |title=Ongoing airway inflammation in patients with COPD who do not currently smoke |journal=Thorax |volume=55 |issue=1 |pages=12–8 |year=2000 |month=January |pmid=10607796 |pmc=1745599 |doi= 10.1136/thorax.55.1.12|url=}}</ref> The disease may continue to get worse for many years after stopping [[smoking]] due to this ongoing [[inflammation]].<ref name="Rutgers00" /> This sustained [[inflammation]] is thought to be mediated by [[autoantibodies]] and autoreactive T cells.<ref name="Rutgers00" /><ref>{{cite journal |author=Feghali-Bostwick CA, Gadgil AS, Otterbein LE, ''et al.'' |title=Autoantibodies in Patients with Chronic Obstructive Pulmonary Disease |journal=Am. J. Respir. Crit. Care Med. |volume=177 |issue=2 |pages=156–63 |year=2008 |month=January |pmid=17975205 |doi=10.1164/rccm.200701-014OC |pmc=2204079 }}</ref><ref>{{cite journal |author=Lee SH, Goswami S, Grudo A, ''et al.'' |title=Antielastin autoimmunity in tobacco smoking-induced emphysema |journal=Nat. Med. |volume=13 |issue=5 |pages=567–9 |year=2007 |month=May |pmid=17450149 |doi=10.1038/nm1583 }}</ref>


====Other Risk Factors====
====Other Risk Factors====
A tendency to sudden airway constriction in response to inhaled irritants, bronchial hyperresponsiveness, is a characteristic of asthma. Many people with COPD also have this tendency. In COPD, the presence of bronchial hyperresponsiveness predicts a worse course of the disease.<ref name="Harrisons" /> It is not known if bronchial hyperresponsiveness is a cause or a consequence of COPD. Other risk factors such as repeated lung [[infection]] and possibly a diet high in cured meats (possibly due to the preservative [[sodium nitrite]]) may be related to the development of COPD.
A tendency to sudden [[airway constriction]] in response to inhaled irritants, bronchial hyperresponsiveness, is a characteristic of [[asthma]]. Many people with COPD also have this tendency. In COPD, the presence of bronchial hyperresponsiveness predicts a worse course of the disease.<ref name="Harrisons" /> It is not known if bronchial hyperresponsiveness is a cause or a consequence of COPD. Other risk factors such as repeated lung [[infection]] and possibly a diet high in cured meats (possibly due to the preservative [[sodium nitrite]]) may be related to the development of COPD.


===Causes by Organ System===
===Causes by Organ System===


{|style="width:75%; height:100px" border="1"
{| style="width:75%; height:100px" border="1"
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
| style="width:25%" bgcolor="LightSteelBlue" ; border="1" | '''Cardiovascular'''
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | [[Congestive heart failure]]
| style="width:75%" bgcolor="Beige" ; border="1" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Chemical / poisoning'''
| '''Chemical / poisoning'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" |[[Silicosis]], Isocyanates, [[Cigarette smoking]], [[Cadmium]], [[Sulfur dioxide]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Dermatologic'''
| '''Dermatologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Drug Side Effect'''
| '''Drug Side Effect'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | [[Goserelin]], [[Pramipexole]], [[Zanamivir]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Ear Nose Throat'''
| '''Ear Nose Throat'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Endocrine'''
| '''Endocrine'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Environmental'''
| '''Environmental'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" |Use of biomass fuels for cooking, Second hand [[smoking]], Occupational pollution exposure to dusts and [[chemicals]], [[Fumes]] from welding, Environmental [[air pollution]] such as coal, grain
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Gastroenterologic'''
| '''Gastroenterologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Genetic'''
| '''Genetic'''
|bgcolor="Beige"| [[Alpha1-Antitrypsin Deficiency]]
| bgcolor="Beige" |[[Tumor necrosis factor-alpha]] (TNF-a) gene polymorphisms, Several SNPs of the [[leptin receptor]] (LEPR) [[gene]],
Several [[gene polymorphisms]] of [[Transforming growth factor]] beta 1, [[Metalloproteinase]] dysregulation, Increased Matrix [[metalloproteinases]] ( MMP)-9 (gelatinase B), Increased [[Matrix metalloproteinases]] (MMP)-8 (Collagenase 2), Increased [[Matrix metalloproteinases]] (MMP)-2 (gelatinase A), [[Heredity]], [[Genetic]] influences, Excess [[elastase]], Decreased [[glutathione]] S-transferase P1 activity, Decreased [[glutathione]] levels, Decreased function of [[microsomal epoxide hydrolase]], Decreased function of [[microsomal epoxide hydrolase]], [[Alpha-1-antitrypsin deficiency]], Abnormal activity of tissue inhibitors of [[metalloproteinase]] (TIMP-1)
 
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Hematologic'''
| '''Hematologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Iatrogenic'''
| '''Iatrogenic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Infectious Disease'''
| '''Infectious Disease'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" |[[Pulmonary tuberculosis]], History of childhood [[respiratory infections]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Musculoskeletal / Ortho'''
| '''Musculoskeletal / Ortho'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Neurologic'''
| '''Neurologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Nutritional / Metabolic'''
| '''Nutritional / Metabolic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" |[[Vitamin C]] deficiency, Deficiency of [[antioxidant]] [[vitamins]], [[Vitamin E]] deficiency
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Obstetric/Gynecologic'''
| '''Obstetric/Gynecologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Oncologic'''
| '''Oncologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Opthalmologic'''
| '''Opthalmologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Overdose / Toxicity'''
| '''Overdose / Toxicity'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Psychiatric'''
| '''Psychiatric'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Pulmonary'''
| '''Pulmonary'''
|bgcolor="Beige"|[[Bronchitis]], [[Emphysema]], [[Pulmonary embolism]], [[Chronic Asthma]], [[Bronchiectasis ]], [[Bronchiolitis obliterans]], [[Lung tumor]], [[Pneumonia]], [[Silicosis]], [[Lymphangioleiomyomatosis]]
| bgcolor="Beige" |[[Bronchitis]], [[Bronchiectasis]], [[Bronchiolitis obliterans]], Early childhood recurrent [[Pneumonia]], [[Silicosis]], Increased airway responsiveness, [[Bronchopulmonary dysplasia]], [[Asthma]] (controversial), [[Pulmonary tuberculosis]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Renal / Electrolyte'''
| '''Renal / Electrolyte'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Rheum / Immune / Allergy'''
| '''Rheum / Immune / Allergy'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | [[Atopy]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Sexual'''
| '''Sexual'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" |[[Gender]] (controversial), more common in male
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Trauma'''
| '''Trauma'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Urologic'''
| '''Urologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Miscellaneous'''
| '''Miscellaneous'''
|bgcolor="Beige"| [[Nicotine addiction]]
| bgcolor="Beige" | [[Nicotine addiction]], Low socioeconomic status, First-degree relatives with severe premature [[COPD]], [[Age]]
|-
|-
|}
|}
===Causes in Alphabetical Order===
*Abnormal activity of tissue inhibitors of [[metalloproteinase]] (TIMP-1)
*[[Age]]
*[[Alpha-1-antitrypsin deficiency]]
*[[Asthma]] (controversial)
*[[Atopy]]
*[[Bronchopulmonary dysplasia]]
*[[Cadmium]]
*[[Cigarette smoking]]
*Decreased function of [[microsomal epoxide hydrolase]]
*Decreased function of [[microsomal epoxide hydrolase]]
*Decreased [[glutathione]] levels
*Decreased [[glutathione S-transferase]] P1 activity
*Deficiency of [[antioxidant]] [[vitamins]]
*Environmental [[air pollution]] such as coal, grain
*Excess [[elastase]]
*First-degree relatives severe premature [[COPD]]
*[[Fumes from welding]]
*[[Gender]] (controversial)
*[[Genetic]] influences
*[[Heredity]]
*History of childhood [[respiratory infections]]
*Increased airway responsiveness
*Increased [[Matrix metalloproteinases]] (MMP)-2 (gelatinase A)
*Increased [[Matrix metalloproteinases]] (MMP)-8 (Collagenase 2)]]
*Increased [[Matrix metalloproteinases]] ( MMP)-9 (gelatinase B)]]
*Isocyanates
*Low socioeconomic status
*[[Metalloproteinase]] dysregulation
*Occupation pollution exposure to dusts and [[chemicals]]
*[[Pulmonary tuberculosis]]
*Second hand [[smoking]]
*Several [[gene polymorphisms]] of [[Transforming growth factor]] beta 1
*Several SNPs (Several gene polymorphisms) of the [[leptin receptor]] (LEPR) gene
*[[Silicosis]]
*[[Sulfur dioxide]]
*[[Tumor necrosis factor-alpha]] (TNF-a) gene polymorphisms
*Use of biomass fuels for cooking
*[[Vitamin C]] deficiency
*[[Vitamin E]] deficiency
*[[Zanamivir]]


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Latest revision as of 20:58, 29 July 2020

Chronic obstructive pulmonary disease Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Chronic obstructive pulmonary disease from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

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MRI

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Treatment

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Secondary Prevention

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Cafer Zorkun, M.D., Ph.D. [2], Priyamvada Singh, MBBS [3]

Overview

Chronic obstructive pulmonary disease (COPD), is most often due to tobacco smoking; but can be due to other airborne irritants such as coal dust, asbestos or solvents, congenital conditions such as alpha-1-antitrypsin deficiency and as well as preserved meats containing nitrites. In the United States, tobacco use is a key factor in the development and progression of COPD, but asthma, exposure to air pollutants in the home and workplace, genetic factors, and respiratory infections also play a role. In the developing world, indoor air quality is thought to play a larger role in the development and progression of COPD than it does in the United States.

Causes

Common Causes

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.[1][2] Exposure to cigarette smoke is measured in pack-years,[3] 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, extra-pulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand.[4]

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, iso-cyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in non-smokers.[5] 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.[6] The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking.[7]

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.[8] 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.[9]

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.[10] 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.[11]

Autoimmune Disease

Main article: Autoimmunity

There is mounting evidence that there may be an autoimmune component to COPD, triggered by lifelong smoking.[12] Many individuals with COPD who have stopped smoking have active inflammation in the lungs.[13] The disease may continue to get worse for many years after stopping smoking due to this ongoing inflammation.[13] This sustained inflammation is thought to be mediated by autoantibodies and autoreactive T cells.[13][14][15]

Other Risk Factors

A tendency to sudden airway constriction in response to inhaled irritants, bronchial hyperresponsiveness, is a characteristic of asthma. Many people with COPD also have this tendency. In COPD, the presence of bronchial hyperresponsiveness predicts a worse course of the disease.[7] It is not known if bronchial hyperresponsiveness is a cause or a consequence of COPD. Other risk factors such as repeated lung infection and possibly a diet high in cured meats (possibly due to the preservative sodium nitrite) may be related to the development of COPD.

Causes by Organ System

Cardiovascular No underlying causes
Chemical / poisoning Silicosis, Isocyanates, Cigarette smoking, Cadmium, Sulfur dioxide
Dermatologic No underlying causes
Drug Side Effect Goserelin, Pramipexole, Zanamivir
Ear Nose Throat No underlying causes
Endocrine No underlying causes
Environmental Use of biomass fuels for cooking, Second hand smoking, Occupational pollution exposure to dusts and chemicals, Fumes from welding, Environmental air pollution such as coal, grain
Gastroenterologic No underlying causes
Genetic Tumor necrosis factor-alpha (TNF-a) gene polymorphisms, Several SNPs of the leptin receptor (LEPR) gene,

Several gene polymorphisms of Transforming growth factor beta 1, Metalloproteinase dysregulation, Increased Matrix metalloproteinases ( MMP)-9 (gelatinase B), Increased Matrix metalloproteinases (MMP)-8 (Collagenase 2), Increased Matrix metalloproteinases (MMP)-2 (gelatinase A), Heredity, Genetic influences, Excess elastase, Decreased glutathione S-transferase P1 activity, Decreased glutathione levels, Decreased function of microsomal epoxide hydrolase, Decreased function of microsomal epoxide hydrolase, Alpha-1-antitrypsin deficiency, Abnormal activity of tissue inhibitors of metalloproteinase (TIMP-1)

Hematologic No underlying causes
Iatrogenic No underlying causes
Infectious Disease Pulmonary tuberculosis, History of childhood respiratory infections
Musculoskeletal / Ortho No underlying causes
Neurologic No underlying causes
Nutritional / Metabolic Vitamin C deficiency, Deficiency of antioxidant vitamins, Vitamin E deficiency
Obstetric/Gynecologic No underlying causes
Oncologic No underlying causes
Opthalmologic No underlying causes
Overdose / Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary Bronchitis, Bronchiectasis, Bronchiolitis obliterans, Early childhood recurrent Pneumonia, Silicosis, Increased airway responsiveness, Bronchopulmonary dysplasia, Asthma (controversial), Pulmonary tuberculosis
Renal / Electrolyte No underlying causes
Rheum / Immune / Allergy Atopy
Sexual Gender (controversial), more common in male
Trauma No underlying causes
Urologic No underlying causes
Miscellaneous Nicotine addiction, Low socioeconomic status, First-degree relatives with severe premature COPD, Age

Causes in Alphabetical Order

External Links

http://www.cdc.gov/copd/index.htm

References

  1. ↑ MedicineNet.com - COPD causes
  2. ↑ 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)
  3. ↑ "Definition of pack year - NCI Dictionary of Cancer Terms".
  4. ↑ Template:Cite doi
  5. ↑ 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)
  6. ↑ 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)
  7. ↑ 7.0 7.1 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.
  8. ↑ 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)
  9. ↑ 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)
  10. ↑ 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)
  11. ↑ MedlinePlus Encyclopedia 000091
  12. ↑ Agustí A, MacNee W, Donaldson K, Cosio M. (2003). "Hypothesis: Does COPD have an autoimmune component?". Thorax. 58 (10): 832–4. doi:10.1136/thorax.58.10.832. PMC 1746486. PMID 14514931.
  13. ↑ 13.0 13.1 13.2 Rutgers SR, Postma DS, ten Hacken NH; et al. (2000). "Ongoing airway inflammation in patients with COPD who do not currently smoke". Thorax. 55 (1): 12–8. doi:10.1136/thorax.55.1.12. PMC 1745599. PMID 10607796. Unknown parameter |month= ignored (help)
  14. ↑ Feghali-Bostwick CA, Gadgil AS, Otterbein LE; et al. (2008). "Autoantibodies in Patients with Chronic Obstructive Pulmonary Disease". Am. J. Respir. Crit. Care Med. 177 (2): 156–63. doi:10.1164/rccm.200701-014OC. PMC 2204079. PMID 17975205. Unknown parameter |month= ignored (help)
  15. ↑ Lee SH, Goswami S, Grudo A; et al. (2007). "Antielastin autoimmunity in tobacco smoking-induced emphysema". Nat. Med. 13 (5): 567–9. doi:10.1038/nm1583. PMID 17450149. Unknown parameter |month= ignored (help)

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