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81 Cards in this Set
- Front
- Back
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Acute Bronchitis |
Inflammation of the bronchial mucus membrane resulting from infectious agents |
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Etiology |
Viruses which cause upper respiratory infections |
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Clinical Manifestation |
- Cough (initially dry) - Inflammation of bronchial mucosa |
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Management of symptomatic Acute Bronchitis |
- Hydration - Cough suppressants |
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Obstructive disorders |
Most common - Chronic Bronchitis - Emphysema - Asthma Less common - Bronchiectasis - Cystic Fibrosis |
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Pathophysiology of Obstructive Lung Diseases |
1. Bronchial inflammation 2. Excessibe airway secretions 3. Mucous plugging 4. Bronchospasm 5. Distal airway weakening ** These factors can cause reduction of airflow ** |
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COPD |
A disease characterized by persistent airflow limitations, respiratory symptoms that usually progress, and not fully reversible |
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COPD is a mixture of two lung diseases |
1. Chronic Bronchitis 2. Emphysema |
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Epidemiology |
- 10-15 million people in the US suffer from COPD (more have chronic bronchitis than Emphysema) - 3rd leading cause of death in the US |
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Risk factors for COPD |
1. Exposure to tabacco smoke, and indoor/outdoor pollution 2. Genes 3. Age 4. Poor lung growth or development 5. Low socioeconomic status 6. Respiratory infections 7. Asthma |
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ACOS |
Persistent airflow limitaltion that includes features associated with both asthma and COPD. |
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Key features of ACOS |
- Persistent airflow limitation in patients 40 or older - Documented history of asthma - Exposure history to cigarette or air pollutions |
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ACOS compared to Asthma and COPD alone |
- More exacerbations - Poor quality of life - More rapid decline in lung function - Higher mortality |
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Diagnosing ACOS |
1. Evaluate symptoms 2. Patient history 3. Smoking history 4. Spirometry |
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Diagnostic tests for ACOS |
1. DLCO 2. high resolution CT scan 3. Skin testing for atopy 4. FeNO 5. Blood eosinophilia 6. Sputum |
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ACOS: if diagnosis is COPD |
Follow GOLD guidlines for therapy |
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ACOS: If diagnosis is ASTHMA |
Follow GINA guidlines for therapy |
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Managing ACOS |
- Start therapy according to asthma guidelines - Smoking cessation - Pulmonary rehab - Vaccinations - Treatment of comorbidities |
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Clinical Indications for COPD |
1. Dyspnea that is progressive, worse with exercise, and persistent 2. Chronic cough 3. Chronic sputum production 4. History of exposure to risk factors 5. Family history of COPD |
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3 main spirometry tests for COPD |
1. FVC 2. FEV1 3. FEV1/FVC |
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Diagnosis of COPD - Spirometry |
- FEV1/FVC < 70% determines airflow obstruction - Severity of obstruction is then determined |
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Stage I: Mild COPD |
- FEV1/FVC (or FEV1%) < 70% - FEV1 > or equal to 80% of predicted |
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Stage II: Moderate COPD |
- FEV1/FVC (or FEV1%) < 70% - FEV1 between 50 and 79% of predicted |
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Stage III: Severe COPD |
- FEV1/FVC (or FEV1%) < 70% - FEV1 between 30 and 49% of predicted |
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Stage IV: Very severe COPD |
- FEV1/FVC (or FEV1%) < 70% - FEV1 < 30% of predicted (Or FEB1 < 50% and chronic respiratory failure with PO2 < 60 mmHg and hypercapnia) |
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Group A |
- Low risk - Less symptoms - 0-1 exacerbation/year - FEV1 > 50% |
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Group B |
- Low risk - More symptoms - 0-1 exacerbation/year - FEV1 > 50% |
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Group C |
- High risk - Less symptoms - > 2 exacerbations/year - FEV1 < 50% |
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Group D |
- High risk - More symptoms - > 2 exacerbations/year - FEV1 < 50% |
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Chest Xray findings |
- Increased radiolucency - Decreased vascular markings - Long distended heart shadow - Increased intercostal spaces - Flattened rib angles |
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COPD what are their stimulus for breathing |
Hypoxemia - peripheral chemoreceptors fire impulses to medulla to stimulate ventilation |
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Over-oxygenation may: |
Decreased their stimulus to breathe (As PaO2 increase > 60 mmHg, drive to breathe may decrease and PaCO2 will increase) & ** NEVER withhold O2 from axutely hypoxemic pt with COPD ** |
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ABG: Severe but stable COPD |
- Normal pH - High PaCO2 (normally high for COPD pts. 55-65 mmHg or higher) - Some degree of hypoxemia |
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ABG: Impending Ventilatory Failure |
- Elevated pH (Normal for COPD is 7.35-7.39) - High PaCO2 ( normally high for COPD pts. 55-65 mmHg or higher) - Hypoxemia |
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ABG: Acute Ventilatory Failure |
- Low pH (Normal is 7.35-7.39 for COPD) - Higher than COPD normal PaCO2 ( normally high for COPD pts. 55-65 mmHg or higher) - Advanced Hypoxemia |
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Most important steps in management of COPD |
1. Assess and reduce symptoms 2. Reduce risk of future exacerbations * Achieve these goals by following pharmacologic and non-pharmacologic managements * |
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Pharmacologic management should be guided by: |
1. Severity of symptoms 2. Risk of exacerbations 3. Patient response 4. Patient ability to use various delivery devices |
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Pharmacologic management for Stable COPD |
1. Bronchodilators 2. Inhaled corticosteroids 3. Phosphodiesterase 4 inhibitors (roflumilast) 4. Vaccines 5. Mucolytics 6. O2 therapy 7. Antibiotics |
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Group A: Pharmacologic management |
1. SABA PRN 2. If not responding, try alternative class of bronchodilators |
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Group B: Pharmacologic management |
1. Add LABA or LAMA 2. Use LABA and LAMA if symptoms persist |
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Group C: pharmacologic management |
1. Add LAMA short acting bronchodilator 2. Add LABA or add LABA and ICS for further exacerbations |
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Group D: pharmacologic management |
1. Add LAMA and LABA to short acting bronchodilators 2. Add ICS if further exacerbations 3. Add Roflumilast if having further exacerbations |
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O2 therapy |
Target sats: > or equal to 90% Indications: - PaO2 is at < or equal to 55 mmHg with sat < 88% -PaO2 55-65 mmHg with evidence of: 1. Right heart failure 2. Polycythemia |
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Non-pharmacologic Management |
1. Lung reduction 2. Lung transplant 3. Pulmonary rehab (group B) 4. Smoking cessation |
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Setting for pulmonary rehab |
1. Hospital 2. Home 3. Outpatient rehab |
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Pulmonary rehab incorporate: |
1. Psychological support 2. Nutritional guidance 3. Oxygen therapy 4. Education 5. Exercise |
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Benefits and goals of rehab |
1. Decrease severity of dyspnea 2. Improve diaphragmatic breathing 3. Decrease resting heart rate 4. Decrease hospitalization |
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Pulmonary rehab program structure |
- minimum length: 6 weeks - strength training - endurance training - patient education |
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Pulmonary Rehab Techniques |
1. Pursed lip breathing 2. Diaphragmatic breathing 3. Cough control techniques |
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COPD exacerbation |
Acute worsening of respiratory symptoms that results in additional therapy |
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Mild COPD exacerbation |
Treated with SA bronchodilators |
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Moderate COPD exacerbation |
Treated with SA / antibiotics/ oral corticosteroids |
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Severe COPD exacerbation |
- Requires hospitalization or ER visit - May be associated with acute respiratory failure |
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COPD exacerbations negatively impact: |
- Health status - Rates of hospitalization - Readmissions - Disease progression |
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COPD exacerbation symptoms |
1. Increased airway inflammation 2. Increased mucous production 3. Marked gas trapping 4. Increased coughing and wheezing |
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COPD exacerbation: No respiratory failure clinical manifestation |
- RR - 22-30 bpm - Accessory muscle use: NO - Mental state: NO changes - Signs of improvement on low O2 24-35% - NO CO2 increase - Hemodynamic: Stable |
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Acute respiratory failure Non-life threatening clinical manifestation |
- RR > 30 bpm - Accessory muscle use: YES - Mental state: NO changes - Decreased O2 on 24-35% - Increased CO2 from baseline - pH < 7.35 - Hemodynamic: Stable |
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Acute Respiratory Failure - Life threatening |
- RR > 30 bpm - Accessory muscle use: YES - Changes in Mental Status - Decreased O2 on > 40% - Hemodynamic: Unstable |
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No Respiratory Failure -- Treatment |
Pharmacologic / Non-pharmacologic therapy
Low flow O2 |
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Acute Resp Failure Non-life threatening -- Treatment |
Pharmacologic / Non-pharmacologic therapy NIV |
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Acute Resp Failure - Life threatening -- Treatment |
Invasive Ventilation Transfer to ICU |
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Treatment/testing for COPD exacerbation without Acute respiratory failure |
1. Chest X-ray 2. ABG 3. Sputum culture 4. CBC 5. Diuretics/fluid management |
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Invasive Ventilation Indications |
1. Failure of NIV 2. Changes in MS 3. Hemodynamic instability 4. Severe hypoxemia 5. Cardiac or respiratory arrest |
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Mechanical Ventilation settings |
1. Long expiratory time, larger Vt and lower RR's 2. Oxygenate 3. Normalize pH and not the PCO2 |
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Management as pt improves from exacerbation |
1. NIV (wean to VM or NC) 2. Invasive Vent (extubate to bipap if necessary) 3. O2 therapy (wean to RA or evaluate for home O2) 4. Airway clearance therapy 5. Management of comorbidities |
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Treatments used in palliative end of life care for COPD patients |
1. Opiates 2. Oxygen 3. Fan blowing air on face 4. Nutritional supplements |
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Medicare's All Cause Readmission Program |
Hospitals will be penalized for readmissions for any cause within a 30 day period. This is to improve care and lower cost and prevent a "revolving-room" syndrome. |
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What disease processes does all cause readmission program affect? |
1. Heart Failure 2. Pneumonia 3. COPD |
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What's causing the readmissions? |
1. Inadequate quality of care in hospital 2. Lack of coordination of post discharge care |
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Lower the rate of readmission by: |
- Clarify patient discharge instruction - Coordinate eith primary care physicians - Provision of home health care services |
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Chronic Bronchitis -- Blue Bloaters |
Excessive mucus production with chronic or recurrent cough on most days for 2-3 months of the year for at least 2 successive years. |
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Etiology (causes) |
1. Cigarrette smoking 2. Atmosphere pollutants 3. Repeated bacterial or viral infections |
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Epidemiology |
- More common in males - Middle aged (incidence increases with age) |
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Pathophysiology (structural changes) |
1. Enlargement of mucous glands 2. Loss of cilia 3. Bronchoconstriction 4. Mucosal edema 5. Air trapping and hyperinflation |
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Emphysema -- Pink Puffers |
Abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis |
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Centrilobular Etiology |
Most Common (affect resp bronchioles) - Smoking and chronic bronchitis - Frequent resp infections - Occupational dust and chemicals - Air pollution |
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Panlobular Etiology |
Less Common (affect entire acinus) - Alpha 1 anti-trypsin deficiency |
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Centrilobular Pathophysiology |
Respiratory bronchiole walls are enlarged, run together, and then destroyed. |
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Panlobular Pathophysiology |
Weakening, enlargement, and destruction of the acinus including: - Respiratory bronchioles - Alveolar ducts - Alveolar sacs - Alveoli |
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Treatment for Panlobular emphysema |
Augmentation therapy: - Infusing alpha-1 antitrypsin protein - Weekly infusion -- Lifelong - Not a cure |
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Comparison of Emphysema and Chronic Bronchitis |
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