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Etiology1. Cigarette smoking

The primary cause of COPD is exposure to tobacco smoke. Overall, tobacco smoking

accounts for as much as 90 of COPD risk.

Cigarette smoking in!uces macrophages to release neutrophil chemotactic factors an!elastases, "hich lea! to tissue !estruction. Clinically significant COPD !evelops in #$

of cigarette smokers, although this number is believe! to be an un!erestimate. %ge of initiation of smoking, total pack&years, an! current smoking status pre!ict COPD

mortality.

People "ho smoke have an increase! annual !ecline in '()#* the physiologic normal!ecline in '()# is estimate! to be +0&0 ml-y, but the rate of !ecline in COPD patients is

generally 0 ml-y or greater.

/econ!han! smoke, or environmental tobacco smoke, increases the risk of respiratory

infections, augments asthma symptoms, an! causes a measurable re!uction in pulmonary

function.

% stu!y by agelmann et al conclu!e! that lung function !eviation an! lung structural

changes are present in people "ho smoke cigarettes before the clinical signs of air"ay

obstruction reveal them.1#92 These changes can be !etecte! by bo!y plethysmography an!!iffusing capacity measurement "ith routine spirometry.

2. Environmental factors

COPD !oes occur in in!ivi!uals "ho have never smoke!.1+02 %lthough the role of air 

 pollution in the etiology of COPD is unclear, the effect is small "hen compare! "ith that

of cigarette smoking. 3n !eveloping countries, the use of biomass fuels "ith in!oor 

cooking an! heating is likely to be a ma4or contributor to the "orl!"i!e prevalence of COPD. 5ong&term exposure to traffic&relate! air pollution may be a factor in COPD in

 patients "ith !iabetes an! asthma.1+#2

3. Airway hyperresponsiveness

%ir"ay hyperresponsiveness 6ie, Dutch hypothesis7 stipulates that patients "ho have

nonspecific air"ay hyperreactivity an! "ho smoke are at increase! risk of !evelopingCOPD "ith an accelerate! !ecline in lung function. onspecific air"ay hyperreactivity is

inversely relate! to '()# an! may pre!ict a !ecline in lung function.

The possible role of air"ay hyperresponsiveness as a risk factor for the !evelopment of COPD in people "ho smoke is unclear. 8oreover, bronchial hyperreactivity may result

from air"ay inflammation observe! "ith the !evelopment of smoking&relate! chronic bronchitis. This may contribute to air"ay remo!eling, lea!ing to a more fixe!obstruction, as is seen in persons "ith COPD.

4. Alpha1-antitrypsin deficiency

%lpha#&antitrypsin 6%%T7 is a glycoprotein member of the serine protease inhibitor 

family that is synthesie! in the liver an! is secrete! into the bloo!stream. The main

 purpose of this 9:&amino&aci!, single&chain protein is to neutralie neutrophil elastase in

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the lung interstitium an! to protect the lung parenchyma from elastolytic break!o"n.

/evere %%T !eficiency pre!isposes to unoppose! elastolysis "ith the clinical se;uela of 

an early onset of panacinar emphysema. To see complete information on %lpha#&%ntitrypsin Deficiency, please go to the main article by clicking here.

%%T !eficiency is the only kno"n genetic risk factor for !eveloping COPD an! accounts

for less than # of all cases in the

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car!iovascular abnormality. Pulmonary abnormalities, inclu!ing emphysema, have been

!escribe! in approximately #0 of patients.

(hlers&Danlos syn!rome refers to a group of inherite! connective tissue !isor!ers "ith

manifestations that inclu!e hyperextensibility of the skin an! 4oints, easy bruisability, an!

 pseu!otumors@ it has also been associate! "ith a higher prevalence of COPD.

&. 'alla disease

/alla !isease is an autosomal recessive storage !isor!er !escribe! in /can!inavia@ the!isease is characterie! by intralysosomal accumulation of sialic aci! in various tissues.

The most important clinical manifestations are severe mental retar!ation, ataxia, an!

nystagmus. Precocious emphysema has been !escribe! an! likely is secon!ary to

impaire! inhibitory activity of serum trypsin.

ClassificationThere is a !iscrepancy bet"een the value )(P# an! symptoms of patients , an! therefore

nee! to be consi!ere! other con!itions . /hortness of breath may not be pre!icte! "ith)(P#

Classification of (iseases 'ymptoms 'pirometry

8il!

8o!erate

& o symptoms of a breakor "hen the exercise

& o symptoms of a break

 but mil! symptoms inmo!erate exercise 6eg,

"alking fast, climbing

stairs7

& o symptoms of a break but began to be felt in

training- "ork light 6eg,

!ressing7& 8il! symptoms at rest

)(P A B0Pre!iction of )(P-)P

E$

)(P 0 & B0Pre!iction )(P-)P E$

/evere

& 8o!erate symptoms at

rest

& /evere symptoms at rest

& /igns of cor pulmonal

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