Pulmo - COPD

November 9, 2017 | Author: Jorelyn Frias | Category: Chronic Obstructive Pulmonary Disease, Bronchitis, Lung, Cough, Pulmonology
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IM: PULMONOLOGY COPD (Dr. Pio T. Esguerra II, FPCP, FPCCP) Date: September 10, 2015 FEU-NRMF Institute of Medicine --------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------EMPHYSEMA BRONCHITIS Italicized – as said by Dr. Esguerra. Others taken from ppt, Castillo trans, and th Harrison’s 19 ed.


A preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Before, it was known to be a non-treatable disease. It is preventable because the risk factors for the development of COPD are all modifiable. It is treatable because when you ask a COPD patient early in the course of treatment, and is given appropriate treatment, you will be able to manage and control the symptoms as well as improve the quality of life of this patient. Its pulmonary component is characterized by airflow limitation that is not fully reversible. o In bronchial asthma, the airflow limitation is fully reversible. This disease is progressive, especially without treatment and is associated with an abnormal inflammatory response of the lungs to noxious particles and gases.

Asthenic Long history of exertional dyspnea Scanty mucoid sputum Prominent accessory muscles

Usually overweight Chronic cough Copious, purulent sputum Less dyspneic – d/t ↑ CO2

Physical Examination:

Physical Examination:

Pink puffer Barrel chest – by virtue of air trapping Tachypneic with purse lip breathing Decreased breath sound Hyperresonant Cor pulmonale - late in the course

Blue bloater Accessory muscles not prominent Crackles, wheezes Resonant Cor pulmonale - early in the course

NONPROPORTIONAL VENN DIAGRAM This is the Venn diagram, we know traditionally that COPD is composed of Chronic Bronchitis (CB) and Emphysema (E). But when it comes to COPD, not all patients with CB and E, even Bronchial Asthma (BA) will NOT be regarded as COPD; only those with significant airflow limitation that is NOT fully reversible. So, if your E,CB, or BA has NO airflow limitation that is NOT fully reversible → NOT COPD! (Remember this )


So much so that COPD can be diseases coming from patients w/ E, CB, BA, cystic fibrosis (CF) and any other diseases with airflow limitation. EMPHYSEMA vs Chronic BRONCHITIS It is difficult to look for a patient with exclusive E and CB. Most of the time it is overlapping. PREDOMINANTLY EMPHYSEMA The alveoli are destroyed, there is significant hyperinflation of the lungs. There is permanent abnormal distension of the air spaces distal to the terminal bronchiole. If proximal to airway involved, think of BXSIS or CB. In Emphysema, the involvement is the distal airway and the lung parenchyma.

PREDOMINANTLY CHRONIC BRONCHITIS There is cough that is productive for at least 3 months in a year for 2 consecutive years. In diagnosing, you usually DO NOT need CXR – only a GOOD history w/c reveals that the patient has been coughing for at least 3 months in a year for 2 consecutive years. Ulit-ulit na ‘to ha so do not forget  Excessie tracheobronchial mucus secretion

Exclude other causes of chronic cough s/a TB, BXSIS, CF.

NORMAL There are good and functioning alveolar attachment. They are interdependent with each other. If one alveolus is involved, the adjacent alveolus will ALSO be involved.

COPD AIRWAY The mucosa is thickened, there are mucus hypersecretions in the lumen, there are disruptions in the alveolar attachments, and there are thickenings and inflammation surrounding the airway wall. There is involvement of the mucosa, and the peribronchial area. There is inflammation as well as fibrosis.

There are a lot of patients in the world who have COPD, there are 9 out of 1000 in males, and 7 out of 1000 in females.  There are more male patients because of their occupational exposure.  Females are more susceptible to the effects of smoking than males. 4th leading cause of death 2.74 millions death worldwide COPD

Faith Angeli J. Ladia (3A)


Females may smoke about half a pack per day, while males smoke 1 pack per day, but the degree of lung involvement in lung diseases is the same.



Established Risk Factors o Cigarette Smoking o Alpha-1 Antitrypsin Deficiency > Emphysema o Emphysema Probable: Exposure to prim and sec smoke o Occupational Exposure Socioeconomic stat o Air Pollution Hyperreactive airways Probable and Possible Risk Factors Possible: o Low birth weight Low BW o IgA deficiency Childhood resp infections IgA deficiency

Please dwell on the ESTABLISHED causes of COPD.  ASTHMA vs COPD


ASTHMA Lymphocytes Eosinophils Macrophages

Mediators Effects on Airways Risk of malignancy T-cell involved Airflow Limitation Reversibility Response to Steroids

Mast cells

IL-4, IL-6, IL-13 Histamine ROS ALL airways Little fibrosis affected Epithelial shedding (-) CD4+ T cells Completely Reversible ++++ +++

TRIAD o o o

Chronic Cough Sputum production Exertional dyspnea

If you are thinking about COPD caused by cigarette smoking, look for these symptoms in patients who are >40 y/o. If you are thinking about emphysema cause by Alpha-1 Antitrypsin Deficiency, look for these symptoms in patients 65 y/o, once is enough. MANAGEMENT o Pharmacologic and Non-pharmacologic Interventions EVALUATION o Use of the Global Initiative for Chronic Obstructive Lung Disease (GOLD)  Assess symptoms

To evaluate for symptoms  Is there chronic cough?  Sputum production?  Coughing with sputum production? To assess degree of airflow limitation: do bronchodilator  FEV1/FVC 55%

For the management of Chronic Bronchitis: 

Mucolytics o N-acetylcysteine, Erdosteine, Ambroxol o Because there are a lot of secretions in the airways

Antibiotics o signs of bacterial infections s/a H. influenzae, S. pneumoniae, and M. catarrhalis. o A 7 to 10-day course is most often prescribed, although 5 days is probably sufficient.

at least 19 of 89%, you if there are

Bronchodilators o Β2 – agonist o Inhaled anti-cholinergics o Combination of the two (Ex. Combivent) o You can also use long-acting anti-cholinergic (once a day dosing)  Tiotropium  M3 inhibitor - blocking the action of acetylcholine on M3 muscarinic receptors, which induce contraction of airway smooth muscle. Methylxanthines o Oral: Theophylline and Doxophylline  Modest bronchodilator activity  Anti-inflammatory effects  Modest inotropic and diuretic effects  May augment skeletal muscle strength Steroids o Inhaled  Improvement in airflow obstruction: 50- to 100-mL increase in FEV1  Symptom relief  Exacerbation prevention: risk reduction of 20% to 25%  Alteration of disease progression: reduced hospitalization and reduced mortality o Systemic  If at all possible, should be avoided  associated with increased mortality (more likely due to underlying disease)  Randomized study demonstrated  No difference in FEV1, symptoms, or exacerbation frequency

sided Heart Surgical Bullectomy

Relieving exacerbations

Pulmonary ventilation MANAGEMENT: BULLOUS DISEASE This is seen in patients with emphysema. Giant bullae is described as occupying 1/3 of 1 lung.  Two mechanisms how the bullae impairs lung function o compression of nonbullous lung by a giant bulla whose internal pressure is high and whose volume does not change during respiration o impairment of ventilation because of the large amount of space occupied in the thorax by the bulla, with resultant loss of linkage between the chest wall and the nonbullous lung tissue.

Here’s a motivational photo from 9gag to get us through 2 weeks of the examination madness. Aral mabuti. 

Faith Angeli J. Ladia (3A)


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