CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
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There are two types: chronic bronchitis and emphysema, but usually the condition is a mixture of the two types.
CHRONIC BRONCHITISIncidenceOnset usually after 40Etiology1. Cigarette smoking is the primary cause.2. Exacerbations may be brought on by infection due to Streptococcus pneumoniae or Hemophilus influenzae.Manifestations1. Chronic cough with sputum, wheezing, gradually worsening dyspnea and recurrent infections of the respiratory tract2. Auscultation - diminished breath sounds, wheezes, rhonchi3. With time, the symptoms become worse and use of accessory respiratory muscles is seen with cyanosis, right ventricular hypertrophy and polycythemia (as compensation for hypoxemia).4. pO2 is low, pCO2 high with partially compensated respiratory acidosis; pulmonary function tests show normal or increased TLC with decreased FEV1(%) and FEV1 .5. Patients with chronic bronchitis are nicknamed by medical students "blue bloaters" since they are cyanotic and edematous.DiagnosisDiagnosis is clinical - productive cough for over 3 months of the year for 2 or more yearsPrinciples of management1. Number one priority is to quit smoking, but patients are notoriously not compliant.2. Administering oxygen is first priority during acute exacerbations. Treat infection with antibiotics. Bronchodilators, ipatropium bromide and steroids are often helpful. Respiratory physiotherapy is useful in releasing excess sputum and preventing mucus plugs.3. Patients with COPD should receive immunizations for influenza and pneumococcus. EMPHYSEMAIncidenceEtiology1. Number one etiology is cigarette smoking2. A very rare congenital (autosomal codominant alleles) form is seen in persons with ?1antitrypsin deficiency.PathophysiologyTobacco causes chronic inflammation. There is constant activation of neutrophils and macrophages with the consequent secretion of proteases that destroy the alveoli and bronchioles. Manifestations1. Symptoms are dyspnea and wheezing of long standing.2. On physical examination, patient has a barrel-shaped chest. On auscultation, decreased breath sounds with rhonchi are heard and the expirium is longer than usual. It may also be difficult to hear heart sounds.3. Patients with ?1antitrypsin deficiency usually present with emphysema before age 50. There is also damage to the liver.4. Patients with emphysema are nicknamed by medical students as "pink puffers" since they are not cyanotic and tend to breathe in puffs.5. Changes in pulmonary function tests include low FEV1, low FVC and low FEV1(%). Arterial blood gases show low pO2 with low or normal pCO2. Hyperinflated lungs, lowered diaphragms and decreased vascularity, characterize chest radiograph. Small vesicles filled with fluid, called bullae, are often seen.Principles of management1. Number one priority is to quit smoking, but patients are notoriously not compliant.2. Treatment is symptomatic - mainly aerosolized bronchodilators.3. Patients with emphysema should avoid drugs that suppress respiratory drive, such as sedatives or hypnotics.4. There is no specific treatment for ?1antitrypsin deficiency. There is no proof that replacing the enzyme makes any difference.ASTHMADefinition1. Although asthma is an atopic disorder and is reversible, it is still similar enough to COPD to be discussed in that context.2. Reversible obstruction due to inflammation and hypersensitivity of bronchiManifestations1. Asthma is episodic; between attacks pulmonary function tests are usually normal and symptoms are absent or very mild. Triggers for attacks include environmental agents (cigarette smoke, dust, pollen), exercise, cold air and other allergens.2. Severity of asthma is based on the severity of individual attacks and on the frequency of attacks.3. Cough, dyspnea, wheezing and a feeling of tightness in the chest are the most common symptoms of asthma attacks.4. Severe asthma may cause cyanosis and severe dyspnea.5. Cough is not productive or produces a very small amount of white-yellow rubbery discharge.6. On auscultation, one hears wheezes, decreased movement of air and prolonged expirium.7. Pulmonary function tests show decreased FEV1 that increases after the use of a bronchodilator, showing reversibility of the disorder.8. Arterial blood gases show respiratory alkalosis with decreased pCO2 due to hyperventilation. Normal pCO2 is a bad prognostic sign, showing possibility of respiratory failure.DiagnosisDiagnosis is clinical and is confirmed by response to treatment.Principles of management1. All patients should undergo chest radiograph in order to rule out pneumonia, which may co-exist with asthma, or other pulmonary disorders. 2. Treatment for asthma needs to be divided into emergency treatment, treatment of the acute attack and maintenance treatment.3. Acute attacks need to be treated with oxygen, bronchodilators (b-adrenergics) and/or inhaled steroids. Ipatropium bromide (anticholinergic) is also helpful and cromolyn sodium can be started as well. 4. Emergency situations may need intravenous theophylline and intravenous steroids, as well as oxygen. Very severe cases may even require intubation.5. Maintenance therapy consists of inhaled cromolyn sodium and bronchodilators, with or without oral theophylline. In some cases, the patient continues oral steroids for a period of time and then gradually decreases dose until he can stop.BRONCHIECTASISDefinitionDestruction of the cartilage and elastin that make up the airway walls, thus causing dilatation of the bronchi; due to progressive inflammatory disease of the bronchial treeEtiology1. May be due to congenital malformations2. Often follows infections, especially pneumonia, measles or pertussisManifestations 1. Episodes of coughing with copious sputum, exertional dyspnea and hemoptysis2. Clubbing is common. Recurrent fever, weakness and weight loss often occur.3. There may be signs of other lung disease such as COPD or fibrosis. 4. Bronchiectasis is associated with respiratory infections, immotile cilia syndrome, immunoglobulin deficiency and allergic aspergillosis.DiagnosisBronchogram or CTPrinciples of management1. Antibiotics as prophylaxis2. Bronchodilators, steroids and physical therapy are often helpful.INTERSTITIAL (RESTRICTIVE) LUNG DISEASEEtiology1. inorganic particles - silica, asbestos2. organic particles - fungi, animal proteins3. radiation therapy4. drugs - gold, cytotoxic drugs (especially bleomycin), antibiotics5. microorganisms6. associated with systemic disease - sarcoidosis, rheumatoid arthritis7. idiopathic pulmonary fibrosis8. pulmonary edema9. neoplasms - especially lymphomaManifestations1. Progressive dyspnea at first, with clubbing, cor pulmonale, dry cough and tachypnea appearing later2. Dry rales are heard over both lungs.3. Chest radiograph is usually not pathological, but may show nodular infiltrates at the bases of the lungs.4. Pulmonary function tests show decreased diffusing capacity and reduced lung compliance.DiagnosisLung biopsyComplicationsPneumothoraxSPECIFIC TYPES OF INTERSTITIAL DISEASESARCOIDOSISDefinitionNoncaseating granulomas found in many body systems, particularly the lungs, liver, spleen and bonesIncidence1. age of onset third and fourth decades2. More common in Blacks and ScandinaviansEtiologyUnknownManifestations1. nonspecific signs as of respiratory tract infection - fever, malaise, lymphadenopathy, dyspnea and cough - or may be asymptomatic2. Hypercalcemia and hypercalciuria are seen along with elevated ESR. Hypergammaglobulinemia is common.3. Red, tender nodules on lower legs and arms (erythema nodosum) are common. Other skin manifestations are plaques and nodules.4. Other manifestations include arthritis, arrythmias and cranial nerve palsies (especially of the optic nerve).5. Chest radiograph shows the pathognomonic bilateral hilar and paratracheal lymphadenopathy with characteristic "ground glass" appearance.DiagnosisBiopsy showing granulomasPrinciples of management1. Most resolve spontaneously2. Steroids may be useful for involvement of the eyes or severe systemic symptoms (particularly hypercalcemia); hydroxychloroquinine has been shown to help skin manifestations.PrognosisAbout one-third have chronic diseaseIDIOPATHIC PULMONARY FIBROSISAlso called interstitial pneumonitis, interstitial pulmonary fibrosis and fibrosing alveolitisEtiologyUnknownManifestations1. gradually progressing dyspnea with dry cough, and cyanosis2. Clubbing and Raynaud's phenomenon are common.3. Cor pulmonale is often seen.4. Chest radiograph shows diffuse interstitial infiltrates. Pulmonary function tests are restrictive.5. Antinuclear antibody titer is low.Principles of managementSteroids and cytotoxic drugs (azathioprine, cyclophosphamide) and symptomatic treatment (oxygen, diuretics) may help for the short term; long-term treatment is lung transplant.ASBESTOSISEtiology1. Occupational exposure to asbestos fibers2. Smoking exacerbates the condition.Manifestations1. Slowly-progressive dyspnea especially with effort and cough; may be asymptomatic at the beginning2. Auscultation yields inspiratory crackles.3. Clubbing may be seen.4. Chest radiograph is characteristic with diffuse opaque areas and thickening of the pleura. Pulmonary functions are restrictive.Principles of managementNo treatment is effective. Quitting smoking makes the disease milder. Exposure to asbestos should be avoided as much as possible and protective clothing is recommended.PrognosisIncreased risk of lung cancer and mesothelioma (cancer of the mesothelial cells of the pleura)SILICOSISEtiologyOccupational exposure to silicon dioxide, usually over 20-30 yearsManifestations1. Often asymptomatic; may present with chronic cough and/or difficulty in breathing2. Later, pulmonary hypertension and right congestive heart failure may appear3. Chest radiograph demonstrates calcified lymph nodes at the hilus and many small nodules in the upper lobes and is diagnostic.4. Pulmonary function tests show decreased volumes and a diminished diffusing capacity.Principles of managementNo treatment is effective. Best is to avoid exposure as much as possible and use protective clothing.PrognosisIncreased risk of tuberculosisCYSTIC FIBROSISDefinitionViscous exocrine secretions caused by a defect in the chloride pumpEtiologyAutosomal recessivePathophysiologyBronchial secretions are viscous and cause obstruction. This leads to destruction of lung parenchyma and recurrent respiratory infections, particularly by Staphlycoccus and Psuedomonas.Pulmonary manifestations1. Persistent cough and recurrent lower respiratory tract infections2. Pulmonary function tests show obstructive response.3. Chest radiograph demonstrates hyperinflated lungs with increased size of pulmonary arteries, bronchiectasis and cystic formations.Principles of management1. Treatment is aimed at dilating airways and reducing mucus secretion - bronchodilators, mucolytic drugs and physical therapy (postural drainage and chest percussion).2. Antibiotics and immunizations are usually necessary.3. Some children benefit from a heart-lung transplant.
For more information on Clinical Research Career Training and Clinical Trials Services please contact Kriger Research Group ( www.kriger.com ) at info@kriger.com or call (866) 757-9791 (USA and Canada) or + 1(416) 630-0038 (Internationally)
The project is sponsored by Kriger Research - CRO and Training Services ( www.kriger.com ) and ClinQua CRO (www.clinqua.com )
Start your Clinical Research Career Now:
Clinical Research Associate Program
Data Management Program
Quality Assurance Program
Marketing & Management Program
Clinical Investigator Program
SAS Programming Trainig Program
Recruitment for the Bio Pharmaceutical Industry Program
MedicalTerminology Program
There are two types: chronic bronchitis and emphysema, but usually the condition is a mixture of the two types.
CHRONIC BRONCHITISIncidenceOnset usually after 40Etiology1. Cigarette smoking is the primary cause.2. Exacerbations may be brought on by infection due to Streptococcus pneumoniae or Hemophilus influenzae.Manifestations1. Chronic cough with sputum, wheezing, gradually worsening dyspnea and recurrent infections of the respiratory tract2. Auscultation - diminished breath sounds, wheezes, rhonchi3. With time, the symptoms become worse and use of accessory respiratory muscles is seen with cyanosis, right ventricular hypertrophy and polycythemia (as compensation for hypoxemia).4. pO2 is low, pCO2 high with partially compensated respiratory acidosis; pulmonary function tests show normal or increased TLC with decreased FEV1(%) and FEV1 .5. Patients with chronic bronchitis are nicknamed by medical students "blue bloaters" since they are cyanotic and edematous.DiagnosisDiagnosis is clinical - productive cough for over 3 months of the year for 2 or more yearsPrinciples of management1. Number one priority is to quit smoking, but patients are notoriously not compliant.2. Administering oxygen is first priority during acute exacerbations. Treat infection with antibiotics. Bronchodilators, ipatropium bromide and steroids are often helpful. Respiratory physiotherapy is useful in releasing excess sputum and preventing mucus plugs.3. Patients with COPD should receive immunizations for influenza and pneumococcus. EMPHYSEMAIncidenceEtiology1. Number one etiology is cigarette smoking2. A very rare congenital (autosomal codominant alleles) form is seen in persons with ?1antitrypsin deficiency.PathophysiologyTobacco causes chronic inflammation. There is constant activation of neutrophils and macrophages with the consequent secretion of proteases that destroy the alveoli and bronchioles. Manifestations1. Symptoms are dyspnea and wheezing of long standing.2. On physical examination, patient has a barrel-shaped chest. On auscultation, decreased breath sounds with rhonchi are heard and the expirium is longer than usual. It may also be difficult to hear heart sounds.3. Patients with ?1antitrypsin deficiency usually present with emphysema before age 50. There is also damage to the liver.4. Patients with emphysema are nicknamed by medical students as "pink puffers" since they are not cyanotic and tend to breathe in puffs.5. Changes in pulmonary function tests include low FEV1, low FVC and low FEV1(%). Arterial blood gases show low pO2 with low or normal pCO2. Hyperinflated lungs, lowered diaphragms and decreased vascularity, characterize chest radiograph. Small vesicles filled with fluid, called bullae, are often seen.Principles of management1. Number one priority is to quit smoking, but patients are notoriously not compliant.2. Treatment is symptomatic - mainly aerosolized bronchodilators.3. Patients with emphysema should avoid drugs that suppress respiratory drive, such as sedatives or hypnotics.4. There is no specific treatment for ?1antitrypsin deficiency. There is no proof that replacing the enzyme makes any difference.ASTHMADefinition1. Although asthma is an atopic disorder and is reversible, it is still similar enough to COPD to be discussed in that context.2. Reversible obstruction due to inflammation and hypersensitivity of bronchiManifestations1. Asthma is episodic; between attacks pulmonary function tests are usually normal and symptoms are absent or very mild. Triggers for attacks include environmental agents (cigarette smoke, dust, pollen), exercise, cold air and other allergens.2. Severity of asthma is based on the severity of individual attacks and on the frequency of attacks.3. Cough, dyspnea, wheezing and a feeling of tightness in the chest are the most common symptoms of asthma attacks.4. Severe asthma may cause cyanosis and severe dyspnea.5. Cough is not productive or produces a very small amount of white-yellow rubbery discharge.6. On auscultation, one hears wheezes, decreased movement of air and prolonged expirium.7. Pulmonary function tests show decreased FEV1 that increases after the use of a bronchodilator, showing reversibility of the disorder.8. Arterial blood gases show respiratory alkalosis with decreased pCO2 due to hyperventilation. Normal pCO2 is a bad prognostic sign, showing possibility of respiratory failure.DiagnosisDiagnosis is clinical and is confirmed by response to treatment.Principles of management1. All patients should undergo chest radiograph in order to rule out pneumonia, which may co-exist with asthma, or other pulmonary disorders. 2. Treatment for asthma needs to be divided into emergency treatment, treatment of the acute attack and maintenance treatment.3. Acute attacks need to be treated with oxygen, bronchodilators (b-adrenergics) and/or inhaled steroids. Ipatropium bromide (anticholinergic) is also helpful and cromolyn sodium can be started as well. 4. Emergency situations may need intravenous theophylline and intravenous steroids, as well as oxygen. Very severe cases may even require intubation.5. Maintenance therapy consists of inhaled cromolyn sodium and bronchodilators, with or without oral theophylline. In some cases, the patient continues oral steroids for a period of time and then gradually decreases dose until he can stop.BRONCHIECTASISDefinitionDestruction of the cartilage and elastin that make up the airway walls, thus causing dilatation of the bronchi; due to progressive inflammatory disease of the bronchial treeEtiology1. May be due to congenital malformations2. Often follows infections, especially pneumonia, measles or pertussisManifestations 1. Episodes of coughing with copious sputum, exertional dyspnea and hemoptysis2. Clubbing is common. Recurrent fever, weakness and weight loss often occur.3. There may be signs of other lung disease such as COPD or fibrosis. 4. Bronchiectasis is associated with respiratory infections, immotile cilia syndrome, immunoglobulin deficiency and allergic aspergillosis.DiagnosisBronchogram or CTPrinciples of management1. Antibiotics as prophylaxis2. Bronchodilators, steroids and physical therapy are often helpful.INTERSTITIAL (RESTRICTIVE) LUNG DISEASEEtiology1. inorganic particles - silica, asbestos2. organic particles - fungi, animal proteins3. radiation therapy4. drugs - gold, cytotoxic drugs (especially bleomycin), antibiotics5. microorganisms6. associated with systemic disease - sarcoidosis, rheumatoid arthritis7. idiopathic pulmonary fibrosis8. pulmonary edema9. neoplasms - especially lymphomaManifestations1. Progressive dyspnea at first, with clubbing, cor pulmonale, dry cough and tachypnea appearing later2. Dry rales are heard over both lungs.3. Chest radiograph is usually not pathological, but may show nodular infiltrates at the bases of the lungs.4. Pulmonary function tests show decreased diffusing capacity and reduced lung compliance.DiagnosisLung biopsyComplicationsPneumothoraxSPECIFIC TYPES OF INTERSTITIAL DISEASESARCOIDOSISDefinitionNoncaseating granulomas found in many body systems, particularly the lungs, liver, spleen and bonesIncidence1. age of onset third and fourth decades2. More common in Blacks and ScandinaviansEtiologyUnknownManifestations1. nonspecific signs as of respiratory tract infection - fever, malaise, lymphadenopathy, dyspnea and cough - or may be asymptomatic2. Hypercalcemia and hypercalciuria are seen along with elevated ESR. Hypergammaglobulinemia is common.3. Red, tender nodules on lower legs and arms (erythema nodosum) are common. Other skin manifestations are plaques and nodules.4. Other manifestations include arthritis, arrythmias and cranial nerve palsies (especially of the optic nerve).5. Chest radiograph shows the pathognomonic bilateral hilar and paratracheal lymphadenopathy with characteristic "ground glass" appearance.DiagnosisBiopsy showing granulomasPrinciples of management1. Most resolve spontaneously2. Steroids may be useful for involvement of the eyes or severe systemic symptoms (particularly hypercalcemia); hydroxychloroquinine has been shown to help skin manifestations.PrognosisAbout one-third have chronic diseaseIDIOPATHIC PULMONARY FIBROSISAlso called interstitial pneumonitis, interstitial pulmonary fibrosis and fibrosing alveolitisEtiologyUnknownManifestations1. gradually progressing dyspnea with dry cough, and cyanosis2. Clubbing and Raynaud's phenomenon are common.3. Cor pulmonale is often seen.4. Chest radiograph shows diffuse interstitial infiltrates. Pulmonary function tests are restrictive.5. Antinuclear antibody titer is low.Principles of managementSteroids and cytotoxic drugs (azathioprine, cyclophosphamide) and symptomatic treatment (oxygen, diuretics) may help for the short term; long-term treatment is lung transplant.ASBESTOSISEtiology1. Occupational exposure to asbestos fibers2. Smoking exacerbates the condition.Manifestations1. Slowly-progressive dyspnea especially with effort and cough; may be asymptomatic at the beginning2. Auscultation yields inspiratory crackles.3. Clubbing may be seen.4. Chest radiograph is characteristic with diffuse opaque areas and thickening of the pleura. Pulmonary functions are restrictive.Principles of managementNo treatment is effective. Quitting smoking makes the disease milder. Exposure to asbestos should be avoided as much as possible and protective clothing is recommended.PrognosisIncreased risk of lung cancer and mesothelioma (cancer of the mesothelial cells of the pleura)SILICOSISEtiologyOccupational exposure to silicon dioxide, usually over 20-30 yearsManifestations1. Often asymptomatic; may present with chronic cough and/or difficulty in breathing2. Later, pulmonary hypertension and right congestive heart failure may appear3. Chest radiograph demonstrates calcified lymph nodes at the hilus and many small nodules in the upper lobes and is diagnostic.4. Pulmonary function tests show decreased volumes and a diminished diffusing capacity.Principles of managementNo treatment is effective. Best is to avoid exposure as much as possible and use protective clothing.PrognosisIncreased risk of tuberculosisCYSTIC FIBROSISDefinitionViscous exocrine secretions caused by a defect in the chloride pumpEtiologyAutosomal recessivePathophysiologyBronchial secretions are viscous and cause obstruction. This leads to destruction of lung parenchyma and recurrent respiratory infections, particularly by Staphlycoccus and Psuedomonas.Pulmonary manifestations1. Persistent cough and recurrent lower respiratory tract infections2. Pulmonary function tests show obstructive response.3. Chest radiograph demonstrates hyperinflated lungs with increased size of pulmonary arteries, bronchiectasis and cystic formations.Principles of management1. Treatment is aimed at dilating airways and reducing mucus secretion - bronchodilators, mucolytic drugs and physical therapy (postural drainage and chest percussion).2. Antibiotics and immunizations are usually necessary.3. Some children benefit from a heart-lung transplant.
For more information on Clinical Research Career Training and Clinical Trials Services please contact Kriger Research Group ( www.kriger.com ) at info@kriger.com or call (866) 757-9791 (USA and Canada) or + 1(416) 630-0038 (Internationally)
posted by Kriger Research Group International @ 3:41 PM
