Pa Tho Physiology of COPD

8/2/2019 Pa Tho Physiology of COPD

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Pathophysiology of Chronic

Obstructive Pulmonary Disease


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COPD types

Chronic Bronchitis

Emphysema

Bronchiectasis

destruction and widening oflarge airways

Asthma


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General COPD Progression

Most cases are a result of exposure to noxious

stimuli, most often cigarette smoke.

Pathogenic mechanisms are unclear

Increased numbers of PMN leukocytes and

macrophages release elastases in a manner

that cannot be counteracted effectively by

anti-proteases, resulting in lung destruction.


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Chronic Bronchitis

Defined as presence of a chronic productivecough for 3 months during each of 2consecutive years

Mucous gland hyperplasia is the histologichallmark

Damage to endothelium impairs mucociliary

response Contrast to emphysema, has relatively

undamaged pulmonary capillary bed.


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Histologic hallmark


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Emphysema

Defined as abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied bydestruction of their walls and without obvious fibrosis.

Airway limitation is due to loss in elastic recoil and increase

in airway resistance. Permanent enlargement of airspaces distal to the terminal

bronchioles.

Gradual destruction of alveolar septae and pulmonarycapillary bed leads to decreased ability to oxygenate blood

2 mechanisms of airflow limitation Loss of alveolar walls results in decrease in elastic recoil

Loss of alveolar supporting structure leads to airway narrowing.


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Chronic Bronchitis Emphysema

inflammation, or irritation, in the

bronchioles of the lungs.

permanent enlargement of the airways in

your lungs, accompanied by alveoli

destruction

Body responds by decreasing ventilation

and increasing cardiac output

Body responds by hyperventilation and

decreasing cardiac output

V/Q mismatch leading to hypoxemia(blue)

and polycythemia

V/Q mismatch leads to hypoxia(relatively

pink)

Hypercapnia and respiratory acidosis Lack of radial traction on bronchioles

leads to marked tendency to collapse

during expiration due to expiratory

positive pleural pressures

Pulmonary artery vasoconstriction and

Cor Pulmonale(alteration in the structure

and function of the right ventricle causedby a primary disorder of the respiratory

system)

Patient breathes through mouth with

gradual release of pressure so there is

more intra bronchial pressure to preventairway collapse(Purse lip breathing)

Right heart fibrillation leading to

edema(bloaters)

In other words, patient puffs breathing.


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References

http://emedicine.medscape.com/article/2976

64-overview#showall

http://www.prep4usmle.com/forum/thread/7

4374/
http://emedicine.medscape.com/article/297664-overviewhttp://emedicine.medscape.com/article/297664-overviewhttp://www.prep4usmle.com/forum/thread/74374/http://www.prep4usmle.com/forum/thread/74374/http://www.prep4usmle.com/forum/thread/74374/http://www.prep4usmle.com/forum/thread/74374/http://www.prep4usmle.com/forum/thread/74374/http://www.prep4usmle.com/forum/thread/74374/http://emedicine.medscape.com/article/297664-overviewhttp://emedicine.medscape.com/article/297664-overviewhttp://emedicine.medscape.com/article/297664-overviewhttp://emedicine.medscape.com/article/297664-overview

Pa Tho Physiology of COPD

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