Step-Up To Medicine: Pulmonary

Front 1

What are the two classic types of COPD?

Back 1

(1) Chronic bronchitis and (2) Emphysema. The two often coexist --> pure emphysema or chronic bronchitis is RARE. COPD = 4th MCC of death

Front 2

Dx of chronic bronchitis?

Back 2

Clinical Diagnosis: Chronic cough + sputum for at least 3 months/year for at least 2 consecutive years. Excess mucus production narrows the airways; pathies often have productive cough. Inflammation and scarring in airways, enlargement in mucous glands, and smooth muscle hyperplasia lead to obstruction

Front 3

Emphysema diagnosis

Back 3

Pathologic Diagnosis: Permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls 2/2 relative increasein protease (elastase) activity, or relative deficiency of antiprotease (a1-antitrypsin) activity in the lung. Elastase is released from PMNs and macrophages and digests human lung. This is inhibited by alpha1-antitrypsin. Tobacco smoke increases the number of activated PMNs and macrophages, inhibits a1-AT, and increases oxidative stress on the lung by free radical production

Front 4

Centrilobular emphysema

Back 4

(1) MC type, seen in SMOKERS; destruction limited to respiratory bronchioles (proximal acini) with little change in distal acini. Predilection for upper lung zones

Front 5

Panlobular emphysema

Back 5

(1) Seen in patients with alpha-1 antitrypsin deficiency, destruction involves both proximal and distal acini. Predilection for lung bases

Front 6

Diagnosis of COPD

Back 6

PFTs - Obstruction as seen by (1) DECREASED FEV1 and decreased FEV1/FVC. FEV1 <70% is mild disease, <50% is severe disease; (2) Increased TLC, residual volume, and functional reserve capacity (indicating air trapping) with decreased vital capacity

Front 7

Pink Puffers (Predominant Emphysema)

Back 7

Thin 2/2 increased energy during breathing. When sitting, tend to lean forward. Barrel chest. Tachypnea with prolonged expiration through pursed lips. Accessory muscles

Front 8

Blue Bloaters (Predominant Chronic Bronchitis)

Back 8

Overweight and cyanotic 2/2 chronic hypercapnia and hypoxemia. Chronic cough and sputum production are characteristic. Signs of cor pulmnale may be present in severe or long-standing disease. Resp rate is normal or slightly increased, patient is in no apparent distress, and there is no apparent use of accessory muscles

Front 9

Treatment of COPD

Back 9

(1) SMOKING CESSATION - most important; disease progression is accelerated by continued smoking and can be greatly slowed by its cessation; (2) Inhaled beta-2 agonists [bronchodilators] provide symptomatic relief; use of long-acting agents like salmeterol for patients requiring frequent use; (3) Inhaled anticholinergics (ipratroprium); (4) Combination of albuterol+ipratroprium is more efficacious than either agent alone; (5) Inhaled corticosteroids (budesonide, fluticasone) - anti-inflammatory, may minimally slow down the decrease in FEV1 over time; however, many studies have failed to show any benefit in pulmonary function - reserved for patients whose symptoms are not controlled by bronchodilators

Front 10

What drugs are generally contraindicated during COPD or asthma exacerbations?

Back 10

Beta blockers!

Front 11

What is given during acute exacerbation of COPD?

Back 11

Steroids and antibiotics

Front 12

Use of Theophyilline in COPD

Back 12

May improve mucociliary clearance and central respiratory drive; narrow therapeutic index however and serum levels must be monitored

Front 13

Oxygen therapy in COPD

Back 13

Shown to improve survival and quality of life in patients with COPD and chronic hypoxia; some patients need continuous oxygen, whereas others may only require it during exertion or sleep. Get an ABG to determine need for oxygen. Long-standing hypoxemia may lead to pulmonary HTN and ultimately cor pulmonale. Continuous oxygen therapy for more than 18hr/day has been shown to reduce mortality in patients with these complications by controlling pulmonary HTN

Front 14

Vaccination in COPD

Back 14

(1) Influenza vaccine annually; (2) Pneumococcal vaccine q 5-6years

Front 15

Organisms MC with COPD

Back 15

(1) S. pneumoniae; (2) H. influenzae; (3) M. pneumoniae; (4) Moraxella catarrhalis; (5) Viruses. These bugs are the MCC of COPD exacerbation

Front 16

Criteria for continuous or intermittent long-term oxygen therapy in COPD

Back 16

(1) PaO2 55mmHg or O2 saturation <88% at rest or during exercise OR PaO2 55-59mmHg + polycythemia or evidence of cor pulmonale

Front 17

Steps for patients with acute COPD

Back 17

(1) CXR; (2) Beta-2 agonist and anticholinergic inhaler; (3) Systemic corticosteroids [IV solumedrol] - do not use inhaled corticosteroids in acute exacerbation; (4) Antibiotics - azithromycin or levofloxacin; (5) Supplemental oxygen to keep %sat >90% (6) Noninvasive positive-pressure ventilation with BiPAP or CPAP. Studies have shown a benefit in acute exacerbations; it may decrease the likelihood of respiratory failure requiring invasive mechanical ventilation. (7) Intubation and mechanical ventilation may be required if the above do not stabilize the patient

Front 18

Complications of COPD

Back 18

(1) Acute exacerbations - MCC is infection, noncompliance with therapy, and cardiac disease; (2) Secondary polycythemia (Hct >55% in men, >47% in women) - with compensatory response to chronic hypoxemia; (3) Pulmonary HTN and cor pulmonale - may occur in patients with severe, long-standing COPD who have chronic hypoxemia

Front 19

Asthma Triad

Back 19

(1) Airway inflammation; (2) Airway hyperresponsiveness; (3) Reversible airflow obstruction

Front 20

Extrinsic vs Intrinsic Asthma

Back 20

(1) Extrinsic [most cases]: patients are atopic, i.e., produce IgE to environmental antigens. May be associated with eczema and hay fever; Pts asthmatic at young age; (2) Intrinsic: not related to atopy or environmental triggers

Front 21

What medications can induce asthma?

Back 21

(1) Beta-blockers and (2) Aspirin

Front 22

Clinical Features of Asthma

Back 22

(1) SOB, wheezing, chest tightness, and cough; (2) Sx worse at night; (3) Wheezing is the MC finding on physical examination

Front 23

All that wheezes is NOT asthma

Back 23

(1) CHF 2/2 edema of airways and congestion of bronchial mucosa; (2) COPD - inflammed airways may be narrowed, or bronchospasm may be present; (3) Cardiomyopathies, pericardial disease can lead to edema around the bronchi; (4) Lung cancer - due to obstruction of airways (central tumor or mediastinal invasion

Front 24

Asthma Diagnosis

Back 24

(1) Requires PFTs for diagnosis - they show an obstructive pattern: decrease in expiratory flow rates, decreased FEV1 and decreased FEV1/FVC ratio <0.75; (2) Spirometry before and after bronchodilators can confirm the diagnosis by proving reversible airway obstruction. If inhalation of a bronchodilator (beta-2 agonist) results in an increase in FEV1 or FVC by at least 12%, airflow obstruction is considered reversible; (3) Peak Flow - useful measure of airflow obstruction. Normal is 450-650L/min in men and 350-500L/min in women. In the ED, peak flow is a quick method of diagnosis; (4) Bronchoprovocation test - useful when asthma is suspected by PFTs are nondiagnostic. Measures ease with which airways narrow in response to stimuli of methacholine - hyperresponsive airways develop obstruction at lower doses

Front 25

ABGs in Asthma

Back 25

(1) Hypocarbia is common. Hypoxemia may be present; (2) If PaCO2 is normal or increased, respiratory failure may ensue. Remember asthma attacks cause increased RR, therefore the PaCO2 should decrease. Increased PaCO2 is a sign of respiratory muscle fatigue or severe airway obstruction

Front 26

Treatment of Asthma

Back 26

(1) Inhaled beta-2 agonists - onset is 2-5mins, duration 4-6hrs; long-acting salmeterol good for nighttime asthma and exercise-induced asthma; (2) Inhaled corticosteroids for moderate to severe asthma [preferred over oral steroids 2/2 fewer systemic effects]; (3) Montelukast-leukotriene modifiers - less efficacious than inhaled steroids, but useful for prophylaxis of mild exercise induced asthma and for control of mild to moderate persistent disease. They may allow reductions in steroid and bronchodilator requirements; (4) Cromolyn sodium/nedocromil sodium - only for prophylaxis (e.g. before exercise)

Front 27

Treatment of severe acute asthma exacerbations

Back 27

(1) Inhaled beta-2 agonist via nebulizer or MDI. Mainstays of emergency treatment, have onset of action in minutes; (2) Corticosteroids - given IV initially, may also be given orally in equivalent doses; taper IV or oral steroids when clinical improvement is seen; (3) Theophylline and IV Magnesium are third-line agents; (4) Supplemental oxygen; (5) Antibiotics if severe exacerbation or suspicion of infection

Front 28

Side effects of inhaled corticosteroids

Back 28

OP depostion lead to sore throat, oral candidiasis (thrush) and hoarseness; using a spacer with MDIs and rinsing the mouth after use helps minimize these side effects

Front 29

Bronchiectasis

Back 29

(1) Permanent, abnormal dilation and destruction of bronchial walls. Cilia are damaged; onset usually in childhood. (2) Infection in a patient with airway obstruction or impaired defense or drainage mechanism precipitates the disease; (3) Cause is identified in fewer than half of all patients; (4) Rare today because modern antibiotics are used for respiratory infections

Front 30

Causes of bronchiectasis

Back 30

(1) Cystic Fibrosis - 50% of all cases; (2) Infection, humoral immunodeficiency (abnl lung defense), airway obstruction

Front 31

Aspirin-sensitive asthma

Back 31

Should be considered in patients with asthma and nasal polyps! Avoid aspirin or any NSAID in these patients because they may cause a severe systemic reaction

Front 32

Clinical Features of bronchiectasis

Back 32

(1) Chronic cough with large amounts of mucopurulent, foul-smelling sputum; (2) Dyspnea; (3) Hemoptysis 2/2 rupture of blood vessels near bronchial wall surfaces; usually mild and self-limited, but can be brisk and present as an emergency; (4) Recurrent or persistent pneumonia

Front 33

Treatment of bronchiectasis

Back 33

(1) Antibiotics for acute exacerbations - superimposed infections are signaled by change in quality/quantity of sputum, fever, chest pain, etc; (2) Bronchial hygiene is very important - hydration, chest physiotherapy [postural drainage, chest percussion] to help remove the mucus, inhaled bronchodilators

Front 34

Cystic Fibrosis

Back 34

Autosomal recessive condition predominantly affecting caucasians. (1) Defect in chloride channel protein causes impaired chloride and water transport, leading to excessive thick, viscous secretions in the respiratory tract, exocrine pancreas, sweat glands, intestines, and genitourinary tract; (2) Typically results in obstructive lung disease pattern with chronic pulmonary infections (PSEUDOMONAS!), pancreatic insufficiency, and other GI complications; (3) Treatment is pancreatic enzyme replacement, fat-soluble vitamin supplements, chest PT, annual influenza vaccine, and treatment of infections with antibiotics;

Front 35

Lung Cancer

Back 35

Two subgroups: (1) Small cell lung cancer [25% of lung cancers] and (2) Non-small cell lung cancer [75% of lung cancers]. Includes squamous cell carcinoma, adenocarcinoma, large cell carcinoma, and bronchoalveolar cell carcinoma. IMPT TO DISTINGUISH BTW GROUPS BECAUSE TREATMENT VARIES!

Front 36

What lung cancer has the lowest association with smoking of all lung cancers?

Back 36

Adenocarcinoma of the lung has the lowest association with smoking

Front 37

Staging of lung cancers

Back 37

(1) NSCLC is staged via primary TMN; (2) SCLC is staged differently: LIMITED = confied to chest + supravlacivular nodes, but not cervical or axillary nodes; EXTENSIVE = outside of chest and supraclavicular nodes

Front 38

Squamous Cell Carcinoma of the Lung

Back 38

(1) 30% of all lung cancers; (2) Usually central in location; (3) Often show cavitation on CXR

Front 39

Adenocarcinoma of the Lung

Back 39

(1) 35% of all lung cancers therefore most common type; (2) Often peripherally located; (3) Pleural involvement in 20% of cases; (4) Less commonly associated with smoking than other types; (5) Can be associated with pulmonary scars/fibrosis

Front 40

Large cell carcinoma of the lung

Back 40

(1) Only 5-10% of all lung cancers; (2) Usually peripheral

Front 41

Small Cell Lung Cancer

Back 41

(1) 20-25% of all lung cancers; (2) Usually centrally located; (3) Tend to narrow bronchi by extrinsic compression; (4) Widespread mets are common; 50-75% have mets outside of chest by time of presentation

Front 42

SVC Syndrome

Back 42

Occurs in 5% of lung cancer patients; caused by obstruction of SVC by mediastinal tumor; most commonly occurs with SCLC. Findings = facial fullness, facial/arm edema, dilated veins over anterior chest, arms, and face; JVD

Front 43

Phrenic Nerve Palsy

Back 43

Occurs in 1% of lung cancer patients; caused by destruction of phrenic nerve by tumor as it courses through the mediastinum. Causes a hemidiaphragmatic paralysis

Front 44

Horner's Syndrome

Back 44

Due to local invasion of cervical sympathetic chain by an apical tumor. Symptoms: unilateral facial anhidrosis (no sweating), ptosis, and miosis

Front 45

Pancoast tumor

Back 45

Superior sulcus tumor - an apical tumor involving C8 and T1-T2 nerve roots, causing shoulder pain radiating down the arm. Usually squamous cell cancers. Symptoms include upper extremity weakness due to brachial plexus invasion; associated with Horner's syndrome 60% of the time

Front 46

Malignant pleural effusion

Back 46

Occurs in about 10-15% of patients with lung cancer; prognosis is very poor, equivalent to distant mets

Front 47

Metastatic disease

Back 47

Most common sites for lung cancer are brain, bone, adrenal glands, and liver

Front 48

Paraneoplastic Syndromes

Back 48

(1) SIADH: usually seen with SCLC (10% of patients); (2) Ectopic ACTH: associated with SCLC; (3) PTHrp: most common with squamous cell carcinoma; (4) Hypertrophic pulmonary osteoarthropathy: adenocarcinoma and squamous cell carcinoma - severe long bone pain may be present

Front 49

Eaton-Lambert Syndrome

Back 49

Most common in SCLC; clinical picture is similar to that of Myasthenia gravis, with proximal muscle weakness/fatigability, diminished deep tendon reflexes, paresthesias (more common in lower extremities); (6) Digitial clubbing: loss of normal angle between fingernail and nail bed 2/2 thickening of subungal soft tissue

Front 50

You see a SPN-what is next?

Back 50

Get tissue; regardless of CXR or CT findings, pathologic confirmation is required for definitive diagnosis of lung cancer. Central tumors are generally more amenable to early detection through cytologic examination of sputum

Front 51

Prognosis of lung cancer

Back 51

Extremely poor; overall 5-yr survival for lung cancer patients is 14%; 85% of patients with SCLC have extensive disease at time of presentation, and most die within 2 years.

Front 52

Treatment of NSCLC

Back 52

SURGERY is the best option; but patients with METASTATIC DISEASE outside the chest are NOT candidates for surgery; radiation therapy is an important adjunct to surgery; chemotherapy is of uncertain benefit, some studies show a modest increase in survival, more trials are underway.

Front 53

Treatment of SCLC

Back 53

Chemotherapy is the treatment of choice for both limited and extensive disease. Radiation therapy is useful in limited stage disease, but not in extensive stage disease. Surgery has a limited role because these tumors are usually nonresectable

Front 54

Mediastinal masses

Back 54

Metastatic Cancer (especially lung cancer) MCC of mediastinal mass in older patient. Most common cause according to location: (1) Anterior mediastinum: thyroid, teratoma, thymoma, terribly lymphoma; (2) Middle mediastinum: lung cancer, lymphoma, aneurysms, cysts, Morgagni hernia; (3) Posterior mediastinum: neurogenic tumors, esophageal masses, enteric cysts, aneurysms, Bochdalek's hernia

Front 55

Clinical features of mediastinal masses

Back 55

(1) Usually asymptomatic; when symptoms are present, they are due to compression or invasion of adjacent structures; (2) Cough (compression of trachea or bronchi, sometimes hemoptysis); (3) Chest pain, dyspnea; (4) Postobstructive pneumonia; (5) Dysphagia; (6) SVC syndrome; (7) Compression of nerves: Horner's syndrome [sympathetic ganglia]; Hoarseness [recurrent laryngeal nerve]; Diaphragm [phrenic nerve]

Front 56

What are the two classic types of COPD?

Back 56

(1) Chronic bronchitis and (2) Emphysema. The two often coexist --> pure emphysema or chronic bronchitis is RARE. COPD = 4th MCC of death

Front 57

What are the two classic types of COPD?

Back 57

(1) Chronic bronchitis and (2) Emphysema. The two often coexist --> pure emphysema or chronic bronchitis is RARE. COPD = 4th MCC of death

Front 58

Dx of chronic bronchitis?

Back 58

Clinical Diagnosis: Chronic cough + sputum for at least 3 months/year for at least 2 consecutive years. Excess mucus production narrows the airways; pathies often have productive cough. Inflammation and scarring in airways, enlargement in mucous glands, and smooth muscle hyperplasia lead to obstruction

Front 59

Emphysema diagnosis

Back 59

Pathologic Diagnosis: Permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls 2/2 relative increasein protease (elastase) activity, or relative deficiency of antiprotease (a1-antitrypsin) activity in the lung. Elastase is released from PMNs and macrophages and digests human lung. This is inhibited by alpha1-antitrypsin. Tobacco smoke increases the number of activated PMNs and macrophages, inhibits a1-AT, and increases oxidative stress on the lung by free radical production

Front 60

Centrilobular emphysema

Back 60

(1) MC type, seen in SMOKERS; destruction limited to respiratory bronchioles (proximal acini) with little change in distal acini. Predilection for upper lung zones

Front 61

Panlobular emphysema

Back 61

(1) Seen in patients with alpha-1 antitrypsin deficiency, destruction involves both proximal and distal acini. Predilection for lung bases

Front 62

Diagnosis of COPD

Back 62

PFTs - Obstruction as seen by (1) DECREASED FEV1 and decreased FEV1/FVC. FEV1 <70% is mild disease, <50% is severe disease; (2) Increased TLC, residual volume, and functional reserve capacity (indicating air trapping) with decreased vital capacity

Front 63

Pink Puffers (Predominant Emphysema)

Back 63

Thin 2/2 increased energy during breathing. When sitting, tend to lean forward. Barrel chest. Tachypnea with prolonged expiration through pursed lips. Accessory muscles

Front 64

Blue Bloaters (Predominant Chronic Bronchitis)

Back 64

Overweight and cyanotic 2/2 chronic hypercapnia and hypoxemia. Chronic cough and sputum production are characteristic. Signs of cor pulmnale may be present in severe or long-standing disease. Resp rate is normal or slightly increased, patient is in no apparent distress, and there is no apparent use of accessory muscles

Front 65

Treatment of COPD

Back 65

(1) SMOKING CESSATION - most important; disease progression is accelerated by continued smoking and can be greatly slowed by its cessation; (2) Inhaled beta-2 agonists [bronchodilators] provide symptomatic relief; use of long-acting agents like salmeterol for patients requiring frequent use; (3) Inhaled anticholinergics (ipratroprium); (4) Combination of albuterol+ipratroprium is more efficacious than either agent alone; (5) Inhaled corticosteroids (budesonide, fluticasone) - anti-inflammatory, may minimally slow down the decrease in FEV1 over time; however, many studies have failed to show any benefit in pulmonary function - reserved for patients whose symptoms are not controlled by bronchodilators

Front 66

What drugs are generally contraindicated during COPD or asthma exacerbations?

Back 66

Beta blockers!

Front 67

What is given during acute exacerbation of COPD?

Back 67

Steroids and antibiotics

Front 68

Use of Theophyilline in COPD

Back 68

May improve mucociliary clearance and central respiratory drive; narrow therapeutic index however and serum levels must be monitored

Front 69

Oxygen therapy in COPD

Back 69

Shown to improve survival and quality of life in patients with COPD and chronic hypoxia; some patients need continuous oxygen, whereas others may only require it during exertion or sleep. Get an ABG to determine need for oxygen. Long-standing hypoxemia may lead to pulmonary HTN and ultimately cor pulmonale. Continuous oxygen therapy for more than 18hr/day has been shown to reduce mortality in patients with these complications by controlling pulmonary HTN

Front 70

Vaccination in COPD

Back 70

(1) Influenza vaccine annually; (2) Pneumococcal vaccine q 5-6years

Front 71

Organisms MC with COPD

Back 71

(1) S. pneumoniae; (2) H. influenzae; (3) M. pneumoniae; (4) Moraxella catarrhalis; (5) Viruses. These bugs are the MCC of COPD exacerbation

Front 72

Criteria for continuous or intermittent long-term oxygen therapy in COPD

Back 72

(1) PaO2 55mmHg or O2 saturation <88% at rest or during exercise OR PaO2 55-59mmHg + polycythemia or evidence of cor pulmonale

Front 73

Steps for patients with acute COPD

Back 73

(1) CXR; (2) Beta-2 agonist and anticholinergic inhaler; (3) Systemic corticosteroids [IV solumedrol] - do not use inhaled corticosteroids in acute exacerbation; (4) Antibiotics - azithromycin or levofloxacin; (5) Supplemental oxygen to keep %sat >90% (6) Noninvasive positive-pressure ventilation with BiPAP or CPAP. Studies have shown a benefit in acute exacerbations; it may decrease the likelihood of respiratory failure requiring invasive mechanical ventilation. (7) Intubation and mechanical ventilation may be required if the above do not stabilize the patient

Front 74

Complications of COPD

Back 74

(1) Acute exacerbations - MCC is infection, noncompliance with therapy, and cardiac disease; (2) Secondary polycythemia (Hct >55% in men, >47% in women) - with compensatory response to chronic hypoxemia; (3) Pulmonary HTN and cor pulmonale - may occur in patients with severe, long-standing COPD who have chronic hypoxemia

Front 75

Asthma Triad

Back 75

(1) Airway inflammation; (2) Airway hyperresponsiveness; (3) Reversible airflow obstruction

Front 76

Extrinsic vs Intrinsic Asthma

Back 76

(1) Extrinsic [most cases]: patients are atopic, i.e., produce IgE to environmental antigens. May be associated with eczema and hay fever; Pts asthmatic at young age; (2) Intrinsic: not related to atopy or environmental triggers

Front 77

What medications can induce asthma?

Back 77

(1) Beta-blockers and (2) Aspirin

Front 78

Clinical Features of Asthma

Back 78

(1) SOB, wheezing, chest tightness, and cough; (2) Sx worse at night; (3) Wheezing is the MC finding on physical examination

Front 79

All that wheezes is NOT asthma

Back 79

(1) CHF 2/2 edema of airways and congestion of bronchial mucosa; (2) COPD - inflammed airways may be narrowed, or bronchospasm may be present; (3) Cardiomyopathies, pericardial disease can lead to edema around the bronchi; (4) Lung cancer - due to obstruction of airways (central tumor or mediastinal invasion

Front 80

Asthma Diagnosis

Back 80

(1) Requires PFTs for diagnosis - they show an obstructive pattern: decrease in expiratory flow rates, decreased FEV1 and decreased FEV1/FVC ratio <0.75; (2) Spirometry before and after bronchodilators can confirm the diagnosis by proving reversible airway obstruction. If inhalation of a bronchodilator (beta-2 agonist) results in an increase in FEV1 or FVC by at least 12%, airflow obstruction is considered reversible; (3) Peak Flow - useful measure of airflow obstruction. Normal is 450-650L/min in men and 350-500L/min in women. In the ED, peak flow is a quick method of diagnosis; (4) Bronchoprovocation test - useful when asthma is suspected by PFTs are nondiagnostic. Measures ease with which airways narrow in response to stimuli of methacholine - hyperresponsive airways develop obstruction at lower doses

Front 81

ABGs in Asthma

Back 81

(1) Hypocarbia is common. Hypoxemia may be present; (2) If PaCO2 is normal or increased, respiratory failure may ensue. Remember asthma attacks cause increased RR, therefore the PaCO2 should decrease. Increased PaCO2 is a sign of respiratory muscle fatigue or severe airway obstruction

Front 82

Treatment of Asthma

Back 82

(1) Inhaled beta-2 agonists - onset is 2-5mins, duration 4-6hrs; long-acting salmeterol good for nighttime asthma and exercise-induced asthma; (2) Inhaled corticosteroids for moderate to severe asthma [preferred over oral steroids 2/2 fewer systemic effects]; (3) Montelukast-leukotriene modifiers - less efficacious than inhaled steroids, but useful for prophylaxis of mild exercise induced asthma and for control of mild to moderate persistent disease. They may allow reductions in steroid and bronchodilator requirements; (4) Cromolyn sodium/nedocromil sodium - only for prophylaxis (e.g. before exercise)

Front 83

What are the two classic types of COPD?

Back 83

(1) Chronic bronchitis and (2) Emphysema. The two often coexist --> pure emphysema or chronic bronchitis is RARE. COPD = 4th MCC of death

Front 84

Dx of chronic bronchitis?

Back 84

Clinical Diagnosis: Chronic cough + sputum for at least 3 months/year for at least 2 consecutive years. Excess mucus production narrows the airways; pathies often have productive cough. Inflammation and scarring in airways, enlargement in mucous glands, and smooth muscle hyperplasia lead to obstruction

Front 85

Emphysema diagnosis

Back 85

Pathologic Diagnosis: Permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls 2/2 relative increasein protease (elastase) activity, or relative deficiency of antiprotease (a1-antitrypsin) activity in the lung. Elastase is released from PMNs and macrophages and digests human lung. This is inhibited by alpha1-antitrypsin. Tobacco smoke increases the number of activated PMNs and macrophages, inhibits a1-AT, and increases oxidative stress on the lung by free radical production

Front 86

Centrilobular emphysema

Back 86

(1) MC type, seen in SMOKERS; destruction limited to respiratory bronchioles (proximal acini) with little change in distal acini. Predilection for upper lung zones

Front 87

Panlobular emphysema

Back 87

(1) Seen in patients with alpha-1 antitrypsin deficiency, destruction involves both proximal and distal acini. Predilection for lung bases

Front 88

Diagnosis of COPD

Back 88

PFTs - Obstruction as seen by (1) DECREASED FEV1 and decreased FEV1/FVC. FEV1 <70% is mild disease, <50% is severe disease; (2) Increased TLC, residual volume, and functional reserve capacity (indicating air trapping) with decreased vital capacity

Front 89

Pink Puffers (Predominant Emphysema)

Back 89

Thin 2/2 increased energy during breathing. When sitting, tend to lean forward. Barrel chest. Tachypnea with prolonged expiration through pursed lips. Accessory muscles

Front 90

Blue Bloaters (Predominant Chronic Bronchitis)

Back 90

Overweight and cyanotic 2/2 chronic hypercapnia and hypoxemia. Chronic cough and sputum production are characteristic. Signs of cor pulmnale may be present in severe or long-standing disease. Resp rate is normal or slightly increased, patient is in no apparent distress, and there is no apparent use of accessory muscles

Front 91

Treatment of COPD

Back 91

(1) SMOKING CESSATION - most important; disease progression is accelerated by continued smoking and can be greatly slowed by its cessation; (2) Inhaled beta-2 agonists [bronchodilators] provide symptomatic relief; use of long-acting agents like salmeterol for patients requiring frequent use; (3) Inhaled anticholinergics (ipratroprium); (4) Combination of albuterol+ipratroprium is more efficacious than either agent alone; (5) Inhaled corticosteroids (budesonide, fluticasone) - anti-inflammatory, may minimally slow down the decrease in FEV1 over time; however, many studies have failed to show any benefit in pulmonary function - reserved for patients whose symptoms are not controlled by bronchodilators

Front 92

What drugs are generally contraindicated during COPD or asthma exacerbations?

Back 92

Beta blockers!

Front 93

What is given during acute exacerbation of COPD?

Back 93

Steroids and antibiotics

Front 94

Use of Theophyilline in COPD

Back 94

May improve mucociliary clearance and central respiratory drive; narrow therapeutic index however and serum levels must be monitored

Front 95

Oxygen therapy in COPD

Back 95

Shown to improve survival and quality of life in patients with COPD and chronic hypoxia; some patients need continuous oxygen, whereas others may only require it during exertion or sleep. Get an ABG to determine need for oxygen. Long-standing hypoxemia may lead to pulmonary HTN and ultimately cor pulmonale. Continuous oxygen therapy for more than 18hr/day has been shown to reduce mortality in patients with these complications by controlling pulmonary HTN

Front 96

Vaccination in COPD

Back 96

(1) Influenza vaccine annually; (2) Pneumococcal vaccine q 5-6years

Front 97

Organisms MC with COPD

Back 97

(1) S. pneumoniae; (2) H. influenzae; (3) M. pneumoniae; (4) Moraxella catarrhalis; (5) Viruses. These bugs are the MCC of COPD exacerbation

Front 98

Criteria for continuous or intermittent long-term oxygen therapy in COPD

Back 98

(1) PaO2 55mmHg or O2 saturation <88% at rest or during exercise OR PaO2 55-59mmHg + polycythemia or evidence of cor pulmonale

Front 99

Steps for patients with acute COPD

Back 99

(1) CXR; (2) Beta-2 agonist and anticholinergic inhaler; (3) Systemic corticosteroids [IV solumedrol] - do not use inhaled corticosteroids in acute exacerbation; (4) Antibiotics - azithromycin or levofloxacin; (5) Supplemental oxygen to keep %sat >90% (6) Noninvasive positive-pressure ventilation with BiPAP or CPAP. Studies have shown a benefit in acute exacerbations; it may decrease the likelihood of respiratory failure requiring invasive mechanical ventilation. (7) Intubation and mechanical ventilation may be required if the above do not stabilize the patient

Front 100

Complications of COPD

Back 100

(1) Acute exacerbations - MCC is infection, noncompliance with therapy, and cardiac disease; (2) Secondary polycythemia (Hct >55% in men, >47% in women) - with compensatory response to chronic hypoxemia; (3) Pulmonary HTN and cor pulmonale - may occur in patients with severe, long-standing COPD who have chronic hypoxemia

Front 101

Asthma Triad

Back 101

(1) Airway inflammation; (2) Airway hyperresponsiveness; (3) Reversible airflow obstruction

Front 102

Extrinsic vs Intrinsic Asthma

Back 102

(1) Extrinsic [most cases]: patients are atopic, i.e., produce IgE to environmental antigens. May be associated with eczema and hay fever; Pts asthmatic at young age; (2) Intrinsic: not related to atopy or environmental triggers

Front 103

What medications can induce asthma?

Back 103

(1) Beta-blockers and (2) Aspirin

Front 104

Clinical Features of Asthma

Back 104

(1) SOB, wheezing, chest tightness, and cough; (2) Sx worse at night; (3) Wheezing is the MC finding on physical examination

Front 105

All that wheezes is NOT asthma

Back 105

(1) CHF 2/2 edema of airways and congestion of bronchial mucosa; (2) COPD - inflammed airways may be narrowed, or bronchospasm may be present; (3) Cardiomyopathies, pericardial disease can lead to edema around the bronchi; (4) Lung cancer - due to obstruction of airways (central tumor or mediastinal invasion

Front 106

Asthma Diagnosis

Back 106

(1) Requires PFTs for diagnosis - they show an obstructive pattern: decrease in expiratory flow rates, decreased FEV1 and decreased FEV1/FVC ratio <0.75; (2) Spirometry before and after bronchodilators can confirm the diagnosis by proving reversible airway obstruction. If inhalation of a bronchodilator (beta-2 agonist) results in an increase in FEV1 or FVC by at least 12%, airflow obstruction is considered reversible; (3) Peak Flow - useful measure of airflow obstruction. Normal is 450-650L/min in men and 350-500L/min in women. In the ED, peak flow is a quick method of diagnosis; (4) Bronchoprovocation test - useful when asthma is suspected by PFTs are nondiagnostic. Measures ease with which airways narrow in response to stimuli of methacholine - hyperresponsive airways develop obstruction at lower doses

Front 107

ABGs in Asthma

Back 107

(1) Hypocarbia is common. Hypoxemia may be present; (2) If PaCO2 is normal or increased, respiratory failure may ensue. Remember asthma attacks cause increased RR, therefore the PaCO2 should decrease. Increased PaCO2 is a sign of respiratory muscle fatigue or severe airway obstruction

Front 108

Treatment of Asthma

Back 108

(1) Inhaled beta-2 agonists - onset is 2-5mins, duration 4-6hrs; long-acting salmeterol good for nighttime asthma and exercise-induced asthma; (2) Inhaled corticosteroids for moderate to severe asthma [preferred over oral steroids 2/2 fewer systemic effects]; (3) Montelukast-leukotriene modifiers - less efficacious than inhaled steroids, but useful for prophylaxis of mild exercise induced asthma and for control of mild to moderate persistent disease. They may allow reductions in steroid and bronchodilator requirements; (4) Cromolyn sodium/nedocromil sodium - only for prophylaxis (e.g. before exercise)

Front 109

What are the two classic types of COPD?

Back 109

(1) Chronic bronchitis and (2) Emphysema. The two often coexist --> pure emphysema or chronic bronchitis is RARE. COPD = 4th MCC of death

Front 110

Dx of chronic bronchitis?

Back 110

Clinical Diagnosis: Chronic cough + sputum for at least 3 months/year for at least 2 consecutive years. Excess mucus production narrows the airways; pathies often have productive cough. Inflammation and scarring in airways, enlargement in mucous glands, and smooth muscle hyperplasia lead to obstruction

Front 111

Emphysema diagnosis

Back 111

Pathologic Diagnosis: Permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls 2/2 relative increasein protease (elastase) activity, or relative deficiency of antiprotease (a1-antitrypsin) activity in the lung. Elastase is released from PMNs and macrophages and digests human lung. This is inhibited by alpha1-antitrypsin. Tobacco smoke increases the number of activated PMNs and macrophages, inhibits a1-AT, and increases oxidative stress on the lung by free radical production

Front 112

Centrilobular emphysema

Back 112

(1) MC type, seen in SMOKERS; destruction limited to respiratory bronchioles (proximal acini) with little change in distal acini. Predilection for upper lung zones

Front 113

Panlobular emphysema

Back 113

(1) Seen in patients with alpha-1 antitrypsin deficiency, destruction involves both proximal and distal acini. Predilection for lung bases

Front 114

Diagnosis of COPD

Back 114

PFTs - Obstruction as seen by (1) DECREASED FEV1 and decreased FEV1/FVC. FEV1 <70% is mild disease, <50% is severe disease; (2) Increased TLC, residual volume, and functional reserve capacity (indicating air trapping) with decreased vital capacity

Front 115

Pink Puffers (Predominant Emphysema)

Back 115

Thin 2/2 increased energy during breathing. When sitting, tend to lean forward. Barrel chest. Tachypnea with prolonged expiration through pursed lips. Accessory muscles

Front 116

Blue Bloaters (Predominant Chronic Bronchitis)

Back 116

Overweight and cyanotic 2/2 chronic hypercapnia and hypoxemia. Chronic cough and sputum production are characteristic. Signs of cor pulmnale may be present in severe or long-standing disease. Resp rate is normal or slightly increased, patient is in no apparent distress, and there is no apparent use of accessory muscles

Front 117

Treatment of COPD

Back 117

(1) SMOKING CESSATION - most important; disease progression is accelerated by continued smoking and can be greatly slowed by its cessation; (2) Inhaled beta-2 agonists [bronchodilators] provide symptomatic relief; use of long-acting agents like salmeterol for patients requiring frequent use; (3) Inhaled anticholinergics (ipratroprium); (4) Combination of albuterol+ipratroprium is more efficacious than either agent alone; (5) Inhaled corticosteroids (budesonide, fluticasone) - anti-inflammatory, may minimally slow down the decrease in FEV1 over time; however, many studies have failed to show any benefit in pulmonary function - reserved for patients whose symptoms are not controlled by bronchodilators

Front 118

What drugs are generally contraindicated during COPD or asthma exacerbations?

Back 118

Beta blockers!

Front 119

What is given during acute exacerbation of COPD?

Back 119

Steroids and antibiotics

Front 120

Use of Theophyilline in COPD

Back 120

May improve mucociliary clearance and central respiratory drive; narrow therapeutic index however and serum levels must be monitored

Front 121

Oxygen therapy in COPD

Back 121

Shown to improve survival and quality of life in patients with COPD and chronic hypoxia; some patients need continuous oxygen, whereas others may only require it during exertion or sleep. Get an ABG to determine need for oxygen. Long-standing hypoxemia may lead to pulmonary HTN and ultimately cor pulmonale. Continuous oxygen therapy for more than 18hr/day has been shown to reduce mortality in patients with these complications by controlling pulmonary HTN

Front 122

Vaccination in COPD

Back 122

(1) Influenza vaccine annually; (2) Pneumococcal vaccine q 5-6years

Front 123

Organisms MC with COPD

Back 123

(1) S. pneumoniae; (2) H. influenzae; (3) M. pneumoniae; (4) Moraxella catarrhalis; (5) Viruses. These bugs are the MCC of COPD exacerbation

Front 124

Criteria for continuous or intermittent long-term oxygen therapy in COPD

Back 124

(1) PaO2 55mmHg or O2 saturation <88% at rest or during exercise OR PaO2 55-59mmHg + polycythemia or evidence of cor pulmonale

Front 125

Steps for patients with acute COPD

Back 125

(1) CXR; (2) Beta-2 agonist and anticholinergic inhaler; (3) Systemic corticosteroids [IV solumedrol] - do not use inhaled corticosteroids in acute exacerbation; (4) Antibiotics - azithromycin or levofloxacin; (5) Supplemental oxygen to keep %sat >90% (6) Noninvasive positive-pressure ventilation with BiPAP or CPAP. Studies have shown a benefit in acute exacerbations; it may decrease the likelihood of respiratory failure requiring invasive mechanical ventilation. (7) Intubation and mechanical ventilation may be required if the above do not stabilize the patient

Front 126

Complications of COPD

Back 126

(1) Acute exacerbations - MCC is infection, noncompliance with therapy, and cardiac disease; (2) Secondary polycythemia (Hct >55% in men, >47% in women) - with compensatory response to chronic hypoxemia; (3) Pulmonary HTN and cor pulmonale - may occur in patients with severe, long-standing COPD who have chronic hypoxemia

Front 127

Asthma Triad

Back 127

(1) Airway inflammation; (2) Airway hyperresponsiveness; (3) Reversible airflow obstruction

Front 128

Extrinsic vs Intrinsic Asthma

Back 128

(1) Extrinsic [most cases]: patients are atopic, i.e., produce IgE to environmental antigens. May be associated with eczema and hay fever; Pts asthmatic at young age; (2) Intrinsic: not related to atopy or environmental triggers

Front 129

What medications can induce asthma?

Back 129

(1) Beta-blockers and (2) Aspirin

Front 130

Clinical Features of Asthma

Back 130

(1) SOB, wheezing, chest tightness, and cough; (2) Sx worse at night; (3) Wheezing is the MC finding on physical examination

Front 131

All that wheezes is NOT asthma

Back 131

(1) CHF 2/2 edema of airways and congestion of bronchial mucosa; (2) COPD - inflammed airways may be narrowed, or bronchospasm may be present; (3) Cardiomyopathies, pericardial disease can lead to edema around the bronchi; (4) Lung cancer - due to obstruction of airways (central tumor or mediastinal invasion

Front 132

Asthma Diagnosis

Back 132

(1) Requires PFTs for diagnosis - they show an obstructive pattern: decrease in expiratory flow rates, decreased FEV1 and decreased FEV1/FVC ratio <0.75; (2) Spirometry before and after bronchodilators can confirm the diagnosis by proving reversible airway obstruction. If inhalation of a bronchodilator (beta-2 agonist) results in an increase in FEV1 or FVC by at least 12%, airflow obstruction is considered reversible; (3) Peak Flow - useful measure of airflow obstruction. Normal is 450-650L/min in men and 350-500L/min in women. In the ED, peak flow is a quick method of diagnosis; (4) Bronchoprovocation test - useful when asthma is suspected by PFTs are nondiagnostic. Measures ease with which airways narrow in response to stimuli of methacholine - hyperresponsive airways develop obstruction at lower doses

Front 133

ABGs in Asthma

Back 133

(1) Hypocarbia is common. Hypoxemia may be present; (2) If PaCO2 is normal or increased, respiratory failure may ensue. Remember asthma attacks cause increased RR, therefore the PaCO2 should decrease. Increased PaCO2 is a sign of respiratory muscle fatigue or severe airway obstruction

Front 134

Treatment of Asthma

Back 134

(1) Inhaled beta-2 agonists - onset is 2-5mins, duration 4-6hrs; long-acting salmeterol good for nighttime asthma and exercise-induced asthma; (2) Inhaled corticosteroids for moderate to severe asthma [preferred over oral steroids 2/2 fewer systemic effects]; (3) Montelukast-leukotriene modifiers - less efficacious than inhaled steroids, but useful for prophylaxis of mild exercise induced asthma and for control of mild to moderate persistent disease. They may allow reductions in steroid and bronchodilator requirements; (4) Cromolyn sodium/nedocromil sodium - only for prophylaxis (e.g. before exercise)

Front 135

Treatment of severe acute asthma exacerbations

Back 135

(1) Inhaled beta-2 agonist via nebulizer or MDI. Mainstays of emergency treatment, have onset of action in minutes; (2) Corticosteroids - given IV initially, may also be given orally in equivalent doses; taper IV or oral steroids when clinical improvement is seen; (3) Theophylline and IV Magnesium are third-line agents; (4) Supplemental oxygen; (5) Antibiotics if severe exacerbation or suspicion of infection

Front 136

Side effects of inhaled corticosteroids

Back 136

OP depostion lead to sore throat, oral candidiasis (thrush) and hoarseness; using a spacer with MDIs and rinsing the mouth after use helps minimize these side effects

Front 137

Bronchiectasis

Back 137

(1) Permanent, abnormal dilation and destruction of bronchial walls. Cilia are damaged; onset usually in childhood. (2) Infection in a patient with airway obstruction or impaired defense or drainage mechanism precipitates the disease; (3) Cause is identified in fewer than half of all patients; (4) Rare today because modern antibiotics are used for respiratory infections

Front 138

Causes of bronchiectasis

Back 138

(1) Cystic Fibrosis - 50% of all cases; (2) Infection, humoral immunodeficiency (abnl lung defense), airway obstruction

Front 139

Aspirin-sensitive asthma

Back 139

Should be considered in patients with asthma and nasal polyps! Avoid aspirin or any NSAID in these patients because they may cause a severe systemic reaction

Front 140

Clinical Features of bronchiectasis

Back 140

(1) Chronic cough with large amounts of mucopurulent, foul-smelling sputum; (2) Dyspnea; (3) Hemoptysis 2/2 rupture of blood vessels near bronchial wall surfaces; usually mild and self-limited, but can be brisk and present as an emergency; (4) Recurrent or persistent pneumonia

Front 141

Treatment of bronchiectasis

Back 141

(1) Antibiotics for acute exacerbations - superimposed infections are signaled by change in quality/quantity of sputum, fever, chest pain, etc; (2) Bronchial hygiene is very important - hydration, chest physiotherapy [postural drainage, chest percussion] to help remove the mucus, inhaled bronchodilators

Front 142

Cystic Fibrosis

Back 142

Autosomal recessive condition predominantly affecting caucasians. (1) Defect in chloride channel protein causes impaired chloride and water transport, leading to excessive thick, viscous secretions in the respiratory tract, exocrine pancreas, sweat glands, intestines, and genitourinary tract; (2) Typically results in obstructive lung disease pattern with chronic pulmonary infections (PSEUDOMONAS!), pancreatic insufficiency, and other GI complications; (3) Treatment is pancreatic enzyme replacement, fat-soluble vitamin supplements, chest PT, annual influenza vaccine, and treatment of infections with antibiotics;

Front 143

Lung Cancer

Back 143

Two subgroups: (1) Small cell lung cancer [25% of lung cancers] and (2) Non-small cell lung cancer [75% of lung cancers]. Includes squamous cell carcinoma, adenocarcinoma, large cell carcinoma, and bronchoalveolar cell carcinoma. IMPT TO DISTINGUISH BTW GROUPS BECAUSE TREATMENT VARIES!

Front 144

What lung cancer has the lowest association with smoking of all lung cancers?

Back 144

Adenocarcinoma of the lung has the lowest association with smoking

Front 145

Staging of lung cancers

Back 145

(1) NSCLC is staged via primary TMN; (2) SCLC is staged differently: LIMITED = confied to chest + supravlacivular nodes, but not cervical or axillary nodes; EXTENSIVE = outside of chest and supraclavicular nodes

Front 146

Squamous Cell Carcinoma of the Lung

Back 146

(1) 30% of all lung cancers; (2) Usually central in location; (3) Often show cavitation on CXR

Front 147

Adenocarcinoma of the Lung

Back 147

(1) 35% of all lung cancers therefore most common type; (2) Often peripherally located; (3) Pleural involvement in 20% of cases; (4) Less commonly associated with smoking than other types; (5) Can be associated with pulmonary scars/fibrosis

Front 148

Large cell carcinoma of the lung

Back 148

(1) Only 5-10% of all lung cancers; (2) Usually peripheral

Front 149

Small Cell Lung Cancer

Back 149

(1) 20-25% of all lung cancers; (2) Usually centrally located; (3) Tend to narrow bronchi by extrinsic compression; (4) Widespread mets are common; 50-75% have mets outside of chest by time of presentation

Front 150

SVC Syndrome

Back 150

Occurs in 5% of lung cancer patients; caused by obstruction of SVC by mediastinal tumor; most commonly occurs with SCLC. Findings = facial fullness, facial/arm edema, dilated veins over anterior chest, arms, and face; JVD

Front 151

Phrenic Nerve Palsy

Back 151

Occurs in 1% of lung cancer patients; caused by destruction of phrenic nerve by tumor as it courses through the mediastinum. Causes a hemidiaphragmatic paralysis

Front 152

Horner's Syndrome

Back 152

Due to local invasion of cervical sympathetic chain by an apical tumor. Symptoms: unilateral facial anhidrosis (no sweating), ptosis, and miosis

Front 153

Pancoast tumor

Back 153

Superior sulcus tumor - an apical tumor involving C8 and T1-T2 nerve roots, causing shoulder pain radiating down the arm. Usually squamous cell cancers. Symptoms include upper extremity weakness due to brachial plexus invasion; associated with Horner's syndrome 60% of the time

Front 154

Malignant pleural effusion

Back 154

Occurs in about 10-15% of patients with lung cancer; prognosis is very poor, equivalent to distant mets

Front 155

Metastatic disease

Back 155

Most common sites for lung cancer are brain, bone, adrenal glands, and liver

Front 156

Paraneoplastic Syndromes

Back 156

(1) SIADH: usually seen with SCLC (10% of patients); (2) Ectopic ACTH: associated with SCLC; (3) PTHrp: most common with squamous cell carcinoma; (4) Hypertrophic pulmonary osteoarthropathy: adenocarcinoma and squamous cell carcinoma - severe long bone pain may be present

Front 157

Eaton-Lambert Syndrome

Back 157

Most common in SCLC; clinical picture is similar to that of Myasthenia gravis, with proximal muscle weakness/fatigability, diminished deep tendon reflexes, paresthesias (more common in lower extremities); (6) Digitial clubbing: loss of normal angle between fingernail and nail bed 2/2 thickening of subungal soft tissue

Front 158

You see a SPN-what is next?

Back 158

Get tissue; regardless of CXR or CT findings, pathologic confirmation is required for definitive diagnosis of lung cancer. Central tumors are generally more amenable to early detection through cytologic examination of sputum

Front 159

Prognosis of lung cancer

Back 159

Extremely poor; overall 5-yr survival for lung cancer patients is 14%; 85% of patients with SCLC have extensive disease at time of presentation, and most die within 2 years.

Front 160

Treatment of NSCLC

Back 160

SURGERY is the best option; but patients with METASTATIC DISEASE outside the chest are NOT candidates for surgery; radiation therapy is an important adjunct to surgery; chemotherapy is of uncertain benefit, some studies show a modest increase in survival, more trials are underway.

Front 161

Treatment of SCLC

Back 161

Chemotherapy is the treatment of choice for both limited and extensive disease. Radiation therapy is useful in limited stage disease, but not in extensive stage disease. Surgery has a limited role because these tumors are usually nonresectable

Front 162

Mediastinal masses

Back 162

Metastatic Cancer (especially lung cancer) MCC of mediastinal mass in older patient. Most common cause according to location: (1) Anterior mediastinum: thyroid, teratoma, thymoma, terribly lymphoma; (2) Middle mediastinum: lung cancer, lymphoma, aneurysms, cysts, Morgagni hernia; (3) Posterior mediastinum: neurogenic tumors, esophageal masses, enteric cysts, aneurysms, Bochdalek's hernia

Front 163

Clinical features of mediastinal masses

Back 163

(1) Usually asymptomatic; when symptoms are present, they are due to compression or invasion of adjacent structures; (2) Cough (compression of trachea or bronchi, sometimes hemoptysis); (3) Chest pain, dyspnea; (4) Postobstructive pneumonia; (5) Dysphagia; (6) SVC syndrome; (7) Compression of nerves: Horner's syndrome [sympathetic ganglia]; Hoarseness [recurrent laryngeal nerve]; Diaphragm [phrenic nerve]

Front 164

Diagnosis of Mediastinal Mass

Back 164

Chest CT is test of choice when discovered incidentally on CXR performed for another reason

Front 165

Pleural Effusion

Back 165

Caused by either (1) increased drainage of fluid into pleural space, (2) increased production of fluid by cells in the pleural space, or (3) decreased drainage of fluid from the pleural space

Front 166

Transudative effusions

Back 166

Due to either (1) Elevated capillary pressure in visceral or parenteral pleura (e.g. CHF) or (2) Decreased plasma oncotic pressure (e.g. hypoalbuminemia). CAUSES: CHF, cirrhosis, pulmonary embolism, nephrotic syndrome, peritoneal dialysis, hypoalbuminemia, atelectasis

Front 167

Exudative effusions

Back 167

Caused by either (1) Increased permeability of pleural surfaces or (2) Decreased lymphatic flow from pleural surface because of damage to pleural membranes or vasculature. CAUSES: bacterial pneumonia, TB, malignancy, metastatic disease, viral infection, PE, collagen vascular disease

Front 168

Light's Criteria for transudate vs exudate

Back 168

Exudates have at least one of these true: (1) Protein (pleural)/protein (serum) >0.5; (2) LDH (pleural)/LDH (serum) >0.6; (3) LDH >2/3 upper limit of normal serum LDH

Front 169

Causes of pleural effusion

Back 169

(1) CHF is MCC; (2) Pneumonia (bacterial); (3) Malignancies (lung 36%, breast 25%, lymphoma 10%); (4) Pulmonary embolus; (5) Viral diseases; (6) Cirrhosis + ascites

Front 170

CXR findings with pleural effusion

Back 170

(1) Blunting of costophrenic angle; (2) About 250ml of pleural fluid must accumulate before an effusion can be detected; (3) Lateral decubitus films: more reliable than PA and lateral CXRs for detecting small pleural effusions; can also determine whether fluid is free flowing or loculated. A CT is more reliable than CXR for detecting effusions

Front 171

Thoracentesis

Back 171

Useful if etiology is not obvious. Provides a diagnosis in 75% of patients, and even when it is not diagnostic, provides important clinical information. Therapeutic - provides relief of large effusions; Pneumothorax is a complication seen in 10-15% of thoracenteses, but it requires a chest tube in <5% of cases; Do NOT perform a thoracentesis if effusion is <1cm thick on lateral decubitus CXR.

Front 172

What should fluid be sent for from a thoracentesis?

Back 172

(1) CBC, diff, protein, LDH, pH, glucose, gram stain, and cytology; (2) REMEMBER THE 4 C's! Chemistry [glucose, protein], Cytology, Cell count [CBC with diff] and Culture

Front 173

Associated with pleural fluid amylase?

Back 173

Esophageal rupture, pancreatitis, or malignancy

Front 174

Milky opalescent fluid on thoracentesis

Back 174

Chylothorax (lymph in pleural space)

Front 175

Frankly purulent fluid on thoracentesis

Back 175

Empyema (pus in pleural space)

Front 176

Bloody effusion

Back 176

Associated with malignancy

Front 177

Exudative effusions that are primarily lymphocytic

Back 177

Associated with TB

Front 178

Thoracentesis with pH <7.2

Back 178

Parapneumonic effusion of empyema

Front 179

If pleural fluid glucose is <60, what disease needs to be ruled out?

Back 179

Rheumatoid arthritis; may also be 2/2 TB, esophageal rupture, malignancy, or lupus

Front 180

Treatment of transudative effusion

Back 180

(1) Diuretics and sodium restriction; (2) Therapeutic thoracentesis - only if massive effusion is causing dyspnea

Front 181

Treatment of exudative effusion

Back 181

(1) Treat underlying disease

Front 182

Parapneumonic effusions [Pleural effusion in presence of pneumonia]

Back 182

(1) If uncomplicated, treat with antibiotics alone; (2) Otherwise, chest tube drainage, intrapleural injection of thrombolytic agent may accelerate drainage, and surgical lysis of adhesions may be needed

Front 183

Empyema

Back 183

Complicated parapneumonic effusion, which means the leural effusion is INFECTED; exudative pleural effusions, if left untreated, can lead to empyema [pus within pleural space]. Most cases are a complication of bacterial pneumonia, but other foci of infection can also spread to the pleural space (mediastinitis, abscess)

Front 184

Treatment of Empyema

Back 184

Aggressive drainage of the pleura (Via thoracentesis) and antibiotic therapy; the infection is very difficult to eradicate, and recurrence is common, requiring repeated drainage. If empyema is severe and persistent, a rib resection and open drainage may be necessary

Front 185

Pneumothorax

Back 185

Defined as air in the normally airless pleural space; There are two major categories: spontaneous and traumatic pneumothoraces

Front 186

Traumatic pneumothorax

Back 186

Often iatrogenic: always obtain a CXR after the following procedues: (1) thoracentesis; (2) Transthoracic needle aspiration; (3) Central line placement

Front 187

Spontaneous pneumothorax occurs w/o any trauma

Back 187

(1) Primary (simple) pnuemothorax - occurs without any underlying disease -i.e., in 'healthy' individuals; (2) Caused by spontaneous rupture of subpleural blebs (air-filled sacs on the lung) at the apex of lungs - escape of air from the lung into pleural space causes lung to collapse. Spontaneous pneumothorax has a high rate of recurrence - 50% in 2 years. More common in tall, young, lean men. There patients have sufficent pulmonary reserve, so severe respiratory distress does not occur in most cases

Front 188

Secondary (complicated) pneumothorax

Back 188

Occurs as a complication of underlying lung disease, most commonly COPD; other underlying conditions include asthma, interstitial lung disease (ILD), neoplasms, CF, and tuberculosis (TB). Is more life-threatening because of lack of pulmonary reserve in these patients

Front 189

What is the treatment of spontaneous pneumothorax?

Back 189

Supplemental oxygen; it hastens the resorption of air in the pleural space! Sometimes a small chest tube with a one-way valve may benefit patients. NOTE if pneumothorax is larger and/or patient is symptomatic, administer supplemental oxygen and perform a chest tube insertion to allow air to be released and lung to re-expand.

Front 190

Clinical Symptoms of Pneumothorax

Back 190

(1) Ipsilateral chest pain, usually sudden in onset; (2) Dyspnea; (3) Cough. Physical signs include decreased breath sounds on affected side, hyperresonance over chest, decreased or absent tactile fremitus on affected side, and mediastinal shift towards side of pneumothorax

Front 191

Tension pneumothorax

Back 191

(1) Accumulation of air within pleural space such that tissues surrounding the opening into the pleural cavity act as valves, allowing air to enter but not to escape; (2) The accumulation of air under (positive) pressure in the pleural space collapses the ipsilateral lung and SHIFTS THE MEDIASTINUM AWAY FROM THE SIDE OF THE TENSION PNEUMOTHORAX

Front 192

Causes of tension pneumothorax

Back 192

(1) Mechanical ventilation with associated barotrauma; (2) CPR; (3) Trauma

Front 193

Clinical features of tension pneumothorax

Back 193

(1) Hypotension- cardiac filling is impaired 2/2 compression of great veins; (2) Distended neck veins; (3) Shift of trachea away from side on pneumothorax on CXR; (4) Decreased breath sounds on affected side; (5) Hyperresonance to percussion on side of tension pneumothorax

Front 194

What should you do if a tension pneumo is suspected?

Back 194

DO NOT get a CXR; immediately decompress pleural space via largebore needle or chest tube!

Front 195

Treatment of tension pneumothorax

Back 195

(1) Must be treated as a medical EMERGENCY! - if the tension in the pleural space is not relived, pt will die 2/2 hemodynamic compromise (inadequate CO or hypoxemia); (2) Immediately perform chest decompression with a large-bore needle (in 2nd or 3rd intercostal space of midclavicular line) followed by chest tube placement

Front 196

Malignant Mesothelioma

Back 196

(1) Most cases are 2/2 asbestos exposure; (2) Dyspnea, weight loss, and cough are common findings; (3) Bloody effusion is common; (4) Prognosis is dismal (Few months). NOTE: not all mesotheliomas are malignant; benign mesotheliomas have excellent prognoses (and are unrelated to asbestos exposure)

Front 197

Interstitial Lung Disease

Back 197

Inflammatory process involving the alveolar wall (resilting in widespread fibroelastic proliferation and collagen deposition) that can lead to irreversible fibrosis, distortion of lung architecture, and impaired gas exchange; Prognosis is very variable, and depends on diagnosis; Many patients have environmental or occupational lung disease.

Front 198

Environmental Lung Disease

Back 198

(1) Coal Worker's pneumoconiosis; (2) Silicosis; (3) Asbestosis; (4) Berylliosis

Front 199

ILD associated with granulomas

Back 199

(1) Sarcoidosis - other organs in addition to lungs involved; (2) Histiocytosis X; (3) Wegener's granulomatosis; (4) Churg-Strauss syndrome

Front 200

Alveolar filling disease

Back 200

(1) Goodpasture's syndrome; (2) Idiopathic pulmonary hemosiderosis; (3) Alveolar proteinosis

Front 201

Drug-induced ILD

Back 201

(1) Amiodarone; (2) Nitrofurantoin; (3) Bleomycin; (4) Phenytoin; (5) Illicit drugs; (6) Gold; (7) Penicillamine

Front 202

Signs and Symptoms of ILD

Back 202

(1) Dyspnea (at first with exertion, later at rest); (2) Cough (nonproductive); (3) Fatigue; (4) Other symptoms may be present secodnary to another condition (such as a mixed connective tissue disorder); (5) Rales at bases are common; (6) Digital clubbing is common (esp. w/ idiopathic pulmonary fibrosis); (7) Signs of pulmonary HTN and cyanosis in advanced disease

Front 203

What is honeycomb lung?

Back 203

Scarred and shrunken lung and is an end-stage finding with poor prognosis. Air spaces are dilated, and there are fibrous scars in the interstitium. It can arise from many different types of ILD

Front 204

Diagnosis of ILD

Back 204

(1) Nonspecific CXR findings, with diffuse changes such as reticular, reticulonodular, ground glass, or honeycombing noted; (2) High-res CT shows extent of fibrosis better than other imaging modalities; (3) PFTs show a restrictive pattern with FEV1/FVC increased. All lung volumes are low. Both FEV1 and FVC are low, but the matter more so. There is also low DLco. (4) Oxygen desaturation with exercise; (5) BAL is controversial; (6) Tissue biopsy often required in patients with ILD via bronchoscopy with transbronchial biopsy, open lung biopsy, or video-assisted thoracoscopic lung biopsy; (7) Urinalysis if there are signs of glomerular injury [For Goodpasture's syndrome and Wegener's granulomatosis]

Front 205

Sarcoidosis

Back 205

Chronic, systemic granulomatous disease characterized by NON-CASEATING GRANULOMAS, often involving multiple organ systems. Lungs are almost always involved; (1) Occurs MC in blacks, esp. women. 75% of cases when individual is <40yrs; good prognosis in majority of pts

Front 206

Clinical features of Sarcoidosis

Back 206

(1) Constituational Symptoms: malaise, fever, anorexia, weight loss; (2) Lungs: dry cough, dyspnea; (3) Skin: ERYTHEMA NODOSUM, plaques, nodules, maculopapular eruptions; (4) Eyes: ANTERIOR UVEITIS in 75%; (5) Heart: arrhythmias, conduction disturbances such as heart block; (6) MSK: arthralgias, arthritis, bone lesions; (7) NEURO: cranial nerve VII involvement --> Bell's palsy; optic nerve dysfunction, papilledema, peripheal neuopathy

Front 207

Diagnosis of Sarcoidosis

Back 207

(1) CXR: Bilateral HILAR adnopathy is hallmark but not specific; (2) Skin anergy; (3) ACE ELEVATED in 50-80% of patients; (5) Hypercalciuria and hypercalcemia are common; (6) Definitive diagnosis requires transbronchial biopsy with NONCASEATING GRANULOMAS; (7) PFTs show decreased lung volumes, decreased DLco, and decreased FEV1/FVC

Front 208

Treatment of Sarcoid

Back 208

(1) Most cases resolve or significantly improve spontaneously in 2 years and do not require treatment; (2) Systemic corticosteroids are the treatment of choice. The indications for treatment of unclear, however pts who are symptomatic or have active lung disease, pulmonary function deterioration, conduction disturbances, or severe skin/eye involvement should be treated. (3) Methotrexate may be used in patients with progressive disease refractory to corticosteroids

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Histiocytosis X

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Chronic Interstitial Pneumonia caused by abnormal proliferation of histiocytes (related to Langerhans cells of the skin). Most patients (90%) are cigarette smokers! (1) Variants include eosinophilic granuloma [localized to bone or lung] and two systemic forms: Letterer-Siwe Disease and Hand-Schuller-Christian syndrome; (2) Common findings include dyspnea and nonproductive cough. Other possible manifestations are spontaneous pneumothorax, lytic bone lesions, and diabetes insipidus; (3) CXR has honeycomb appearance, CT shows cystic lesions; (4) Prognosis and course are highly variable; Corticosteroids are sometimes effective. Lung transplantation may be necessary

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Wegener's Granulomatosis

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(1) Characterized by necrotizing granulomatous vasculitis that affects the vessels of the LUNGS, KIDNEYS, UPPER AIRWAYS, and sometimes other organs. (2) Manifestations of the disease include upper and lower respiratory infections, glomerulonephritis, and pulmonary nodules; (3) The gold standard for diagnosis is tissue biopsy, but if the patient tests positive for c-ANCA, the likelihood of having this condition is high; (4) Rx: Immunosuppresants and glucocorticoids

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Churg-Strauss Syndrome

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(1) Granulomatous vasculitis seen in PATIENTS WITH ASTHMA! Typically presents with pulmonary infiltrates, rash, and eosinophilia; (2) DIAGNOSIS: significant blood eosinophilia, positive p-ANCA; (3) Rx: systemic glucocorticoids

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What is a pneumoconiosis?

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Accumulation of dust in the lungs, and the tissue reaction to its presence.

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Coal Worker's Pneumoconiosis

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(1) Most have simple coal worker's pneumoconiosis, which usually causes no significant respiratory disability; (2) Some patients may develop complicated pneumoconiosis, which is characterized by fibrosis (restrictive lung disease); (3) CAUSES: inhalation of coal dust, which contains carbon and silica

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Asbestosis

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(1) Characterized by diffuse interstitial fibrosis of lung 2/2 inhalation of asbestos fibers; predilection for LOWER LOBES; (2) Develops 15-20+ years after exposure; (3) Increased risk of bronchogenic carcinoma (smoking is synergistic) and malignant mesothelioma; (4) Symptoms and physical findings are nonspecific, Dx made on clinical findings and history of exposure to asbestos; (5) CXR shows hazy infiltrates with bilateral linear opacities

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Silicosis

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(1) Localized and NODULAR peribronchial fibrosis (upper lobes more common); (2) Can be acute [massive exposure leading to rapid onset and death], or chronic (symptoms years after exposure - up to 15 years or longer!); (3) Associated with increased risk of TB; (4) Sources include MINING, STONE CUTTING, and GLASS MANUFACTURING; (4) Exertional dyspnea is main symptom, cough with sputum is also seen; (5) Restrictive pulmonary function abnormalities; (6) Treatment involves removal from exposure to silica

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Classical CXR findings in environmental lung disease

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Asbestosis = 'pleural plaques'; Silicosis = 'egg shell' calcifications

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Berylliosis

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(1) Like silicosis, has acute and chronic forms; (2) Acute disease is a diffuse pneumonitis caused by massive expsoure to beryllium; (3) Chronic disease is very similar to sarcoidosis: granulomas, skin lesions, and hypercalcemia may be present; (5) Beryllium lymphocyte proliferation test is a useful diagnostic test; (6) Give glucocorticoid therapy for both acute and chronic berylliosis

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Hypersensitivity pneumonitis (extrinsic allergic alveolitis)

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(1) Inhalation of an antigenic agent to the alveolar level induces an immune-mediated pneumonitis. Chronic exposure may lead to restrictive lung disease; (2) Variety of organic dusts and chemicals have been implicated; (3) Presence of serum IgG and IgA to the inhaled antigen is a hallmark finding, although many may have these Ab without developing disease; (4) Acute form has flu-like symptoms (fever, chills, cough, dyspnea). CXR during acute phase shows pulmonary infiltrates. The chronic form is more insidious and more difficult to diagnose. Treatment involves removal of offending agent and sometimes glucocorticoids

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Some causes of hypersensitivity pneumonitis

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(1) Farmer's lung* (moldy hay); (2) Bird-breeder's lung (avian droppings); (3) Air-conditioner lung*; (4) Mushroom worker's lung* (compost); (5) Caused by spores of thermophilic actinomycetes

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Eosinophilic pneumonia

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(1) Fever and peripheral eosinophilia are features; (2) Eosinophilic pneumonia may be acute or chronic; (3) CXR shows peripheral pulmonary infiltrates; (4) Treatment with glucocorticoids is usually very effective, but relapses may occur

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Goodpasture's Syndrome

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(1) Autoimmune disease caused by IgG antibodies directed against glomerular and alveolar basement membranes (type II hypersensitivity reaction) that results in hemorrhagic pneumonitis and glomerulonephritis; (2) Ultimately, renal failure is a complication of proliferative glomerulonephritis! (3) Usually presents with hemoptysis and dyspnea; (4) Diagnosis is made by tissue biopsy and serolgoic evidence of anti-GBM antibodies. Prognosis is poor, treat with plasmapheresis, cyclophosphamide, and corticosteroids

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Pulmonary Alveolar Proteinosis

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(1) Rare condition caused by accumulation of surfactant-like protein and phospholipids in the alveoli. Usually presents with dry cough, dyspnea, hypoxia, and rales. (2) CXR typically has GROUND GLASS APPEARANCE WITH BILATERAL ALVEOLAR INFILTRATES THAT RESEMBLE A BAT SHAPE; lung biopsy req'd for diagnosis. (3) Lung lavage is mainstay of treatment, but G-CSF is new therapy...patients are at increased risk of infection; do not treat with steroids

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Idiopathic pulmonary fibrosis

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(1) Unknown etiology, more common in men, smokers. (2) Presents with gradual onset of progressive dyspnea, nonproductive cough; (3) Devastating and unrelenting disease, variable prognosis but mean survival is only 3-7 years after first diagnosis. (4) Diagnosis: CXR = ground glass or honeycombed appearance, but may also be normal. Definitive diagnosis requires open lung biopsy. TREATMENT: no effective treatment is available; most patients >70% do not improve with therapy and experience progressive and gradual respiratory failure. Supplemental O2, Corticosteroids without/with Cytoxan, and lung transplant are the only available options

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Cryptogenic Organic Pneumonitis (COP)

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(1) Inflammatory lung disease with similar clinical and radiographic features to infectious pnuemonia; (2) Associated with many entities [viral, meds, CVDs] but most cases are idiopathic. Features: cough, dyspnea, flu-like symptoms; bilateral patchy infiltrates on CXR; (3) Antibiotics NOT effective; (4) Spontaneous recovery may occur, but corticosteroids are used most commonly (>60% of pts recover); (5) Relapse may occur after cessation of steroids (requiring resumption of steroids)

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Radiation pneumonitis

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(1) Interstitial pulmonary inflammation - occurs in 5-15% of patients who undergo thoracic irradiation for lung cancer, breast cancer, lymphoma, or thymoma. Mortality and morbidity are related to the irradiated lung volume, dose, patient status, and concurrent chemotherapy; (2) Acute form occurs 1-6mo after irradiation; chronic form develops 1-2 years later - characterized by alveolar thickening and pulmonary fibrosis. Features: low-grade fever, cough, chest fullness, dyspnea, pleuritic chest pain, hemoptysis, acute respiratory distress; CXR is usually normal, therefore CT SCAN IS BEST STUDY. (1) Diffuse infiltrates (hallmark) and ground glass density, patchy/homogenous consolidation, pleural/pericardial effusions. TREATMENT: corticosteroids

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Definition of Hypoxia

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PaO2 <60mmHg and PaCO2 >50mmHg

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Hypoxemic respiratory failure vs Hypercarbic (ventilatory) failure

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Hypoxemic respiratory failure is Low PaO2 and PaCO2 is low or normal. Causes include disease of lung itself (ARDS, pneumonia, pulmonary edema). Hypercarbic (ventilatory) respiratory failure is due to a failure of alveolar ventilation and may be caused by decrease in minute ventilation or increase in physiologic dead space leading to CO2 retention. Often caused by underlying lung idsease (COPD, asthma, CF, severe bronchitis) or patients with neuromuscular disease/CNS depression, etc

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How do you measure ventilation?

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Ventilation is measured by PaCO2. To decrease PacO2, one must either increase the RR or Tidal volume

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How do you measure oxygenation?

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Oxygenation is measured by O2 sats and PaO2. To decrease PaO2 in the ventilated patient, one must either decreased FiO2 or decrease PEEP.

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V/Q mismatch

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Typically leads to hypoxia without hypercapnia; in fact, PacO2 levels are often low or normal. Most common mechanism of hypoxemia (esp in chronic lung disorders), responsive to supplemental O2!

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Intrapulmonary shunting

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Little or no ventilation in perfused areas (due to collapsed or fluid-filled alveoli); venous blood is shunted into arterial circulation without being oxygenated; Causes of shunts include atelectasis or fluid building 2/2 PNA of pulmonary edema, direct R to L intracardiac blood flow; HYPOXIA DUE TO A SHUNT IS NOT RESPONSIVE TO SUPPLEMENTAL OXYGEN

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When is the A-a gradient normal?

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When hypoventilation is the cause of hypoxia. It is increased in most other causes

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ARDS

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ARDS is a diffuse inflammatory process (not necessarily infectious) involving both lungs - PMN activation in the systemic or pulmonary circulations is the primary mechanism. ARDS is not a primary disease,but rather a disorder that arises 2/2 other conditions that cause a widespread inflammatory process. It is a clinical diangosis

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Pathophysiology of ARDS

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Massive intrapulmonary shunting of blood is a key pathophysiologic event in ARDS - severe hypoxemia with no significant improvement on 100% oxygen! Shunting is 2/2 widespread atelectasis, collapse of alveoli, and surfact dysfunction. NOTE: the effects of the increase in pulmonary fluid are identical to those seen in cardiogenic pulmonary edema, but the CAUSE is different: an increase in alveolar capillary permeability causes ARDS, whereas congestive hydrostatic forces cause cardiogenic pulmonary edema, but the CAUSE is different: an increase in alveolar capillary permeability causes ARDS, whereas congestive hydrostatic forces cause cardiogenic pulmonary edema

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Causes of ARDS

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(1) Sepsis is the MC risk factor - can be 2/2 variety of infections (pneumonia, urosepsis, wound infections); (2) Aspiration of gastric contents; (3) Severe trauma, fractures (e.g. femur, pelvis), acute pancreatitis, multiple or massive transfusions, near-drowning; (4) Drug overdose, toxic inhalation; (5) Intracranial HTN; (6) cardiopulmonary bypass

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Classical Clinical Criteria for diagnosing ARDS

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(1) Hypoxemia refractory to oxygen therapy: ratio of PaO2/FiO2 < 200; (3) Bilateral diffuse pulmonary infiltrates on CXR; (4) No evidence of CHF: PCWP <18mmHg

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What does PCWP measure?

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PCWP reflects left heart filling pressures and is an indirect marker of intravascular volume status. PCWP is the MOST USEFUL PARAMETER IN DIFFERENTIATING ARDS FROM CARDIOGENIC PULMONARY EDEMA. If PCWP is low <18mmHg, ARDS is more likely, wherea if PCWP is high >18mmHg, then cardiogenic pulmonary edema is more likely

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Treatment of ARDS

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(1) Oxygenation - try to keep O2 saturation >90%; (2) Mechanical ventilation with PEEP is usually required; this serves to increase lung volume by opening collapsed alveoli and decrease shunting; (3) Fluid management: volume overload should be avoided. A low-normal intravascular volume is preferred; the goal should be a PCWP of 12-15 mmHg. Vasopressors may be needed to maintain BP. On the other hand, patients with sepsis have high fluid requirements, so determining the appropriate fluid management may be difficult; (4) Treat the UNDERLYING CONDITION - e.g. infection, and don't forget patient's nutritional needs - tube feedings preferred over parenteral nutrition

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Definition of Pulmonary Hypertension

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Mean Pulmonary Arterial Pressure greater than 25mmHg at rest or 30mmHg during exercise

Front 240

Signs of PAH

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(1) loud pulmonic component of second heart sound P2 nd subtle lift of sternum (sign of RV dilatation). These may be the ONLY findings, yet patient may have severe disease! When RV failure occurs, the corresponding signs of JVD, hepatomegaly, ascites, and peripheral edema occur

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Primary Pulmonary Hypertension

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Defined as pulmonary HTN in absence of diseases of the heart or lung; it is a diagnosis of exclusion. An abnl increase in pulmonary arteriolar resistance leads to thickening of pulmonary arteriolar walls. This worsens the pulmonary HTN, in turn causing further wall thickening and leading to a vicious cycle! Cause is unknown; affects young-middle aged women most often. Poor prognosis, and mean survival is 2-3yrs from diagnosis. Disease often unreversible by the time Pt seeks medical attention

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Treatment of Primary Pulmonary HTN

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(1) Treatment with vasodilators such as IV prostacyclins (epoprostenol) and CCBs can lower pulmonary vascular resistance; (2) OAT with warfarin is generally rec'd due to venous stasis, physical inactivity, and increased risk of microvascular thrombosis; (3) Lung transplantation may be an option in qualified patients

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Cor pulmonale

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Right ventricular hypertrophy with eventual RV failure resulting from Pulmonary HTN secondary to PULMONARY DISEASE. The definition does not encompass any of the causes of pulmonary HTN due to left-sided heart disease (such as mitral stenosis or L to R shunts). Cor pulmonale is best thought of as the right-sided counterpart to left ventricular heart disease due to systemic HTN!

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Death due to cor pulmonale

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Many COPD patients die of right ventricular failure 2/2 chronic pulmonary HTN. Many deaths due to PE result from acute pulmonary HTN and RV failure

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Causes of cor pulmonale

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(1) MC 2/2 COPD; (2) Other causes include PE, ILD ,asthma, sleep apnea, and pneumoconioses

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Clinical features of cor pulmnale

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(1) Decrease in exercise tolerance; (2) Cyanosis and clubbing; (3) Signs of RV failure: hepatomegaly, edema, JVD; (4) Parasterna life; (5) Polycythemia if COPD is cause of cor pulmonale

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Diagnosis of cor pulmonale

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Enlargement of RA, RV, and pulmonary arteries; right-axis deviation, P pulmonale (Peaked P waves), right ventricular hypertrophy. Echo shows RV dilatation, but normal LV size and function; useful in excluding LV dysfunction

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Treatment of cor pulmonale

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(1) Treat underlying pulmonary disorder; (2) Be careful with diuretics - patients may be preload dependent! (3) Apply continuous long-term oxygen therapy if patientis hypoxic; (4) Administer digoxin only if there is coexistent LV failure; (5) A variety of vasodilators have been studied; Viagra?

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Pulmonary Embolism (PE)

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(1) PE occurs when a thrombus in another region of the body embolizes to the pulmonary vascular tree via the RV and pulmonary artery. Blood flow distal to the embolus is obstructred; (2) Consider PE and DVT as a continuum of one clinicalentity (venous thromboembolism) diagnosing either PE or DVT is an indication for treatment

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Other sources of emboli to the lungs

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(1) Fat embolism from long bone fractures; (2) Amniotic fluid embolism (during or after delivery); (3) Air embolism (trauma to thorax, indwelling venous/arterial lines); (4) Septic embolism (IVDU); (5) Schistosomiasis

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What should you think if a patient with long bone fracture develops dyspnea, mental status change, and petechiae?

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FAT EMBOLSIM! Respiratory failure and death can ensue rapidly

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Lower Extremity DVT

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Most PE arise from thromboses in the deep veins of the lower extremities above the knee (ileofemoral DVT). PE can also arise from the deep veins of the pelvis. Although calf vein thrombi have a low incidence of embolizing to the lungs, in many patients, these thrombi progress into the proximal veins, increasing the incidence of PE

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Pathophysiology of PE

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(1) Emboli block a portion of pulmonary vasculature, leading to increased pulmonary vascular resistance, pulmonary artery pressure, and RV pressure. If it is severe (large blockage), acute cor pulmonale may result; (2) Blood flow decreases in some areas of the lung. Dead space is created in areas of the lung in which there is ventilation but no perfusion. The resulting hypoxemia and hypercarbia drive respiratory effort, which leads to tachypnea. If the size of the dead space is large (Large PE), clinical signs of SOB, tachypnea are more overt

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Course and prognosis of PE

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(1) Most often, PE is silent. Recurrences are common, which can lead to development of chronic pulmonary HTN and chronic cor pulmonale; (2) When PE is undiagnosed, mortality approaches 30%. A significant number of cases are undiagnosed (as many as 50%)! (3) When PE is diagnosed, mortality is 50% in the first 60 minutes. Of those who survive the initial event, approximately 30% of patients will die of a recurrent PE if left untreated

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What complications are common in patients with PE who survive the initial event?

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(1) Recurrent PE; (2) Pulmonary HTN - seen in up to 2/3 of patients

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D-dimer assay for PE diagnosis

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D-Dimer is a specific fibrin degradation production; levels can be elevated in patients with PE and DVT. D-Dimer assay is a fairly sensitive test (90-98%). If results are normal and clinical suspicion is low, PE is very unlikely. Specificity is low - meaning that D-dimer results may also be elevated in MI, CHF, pneumonia, and the post-operative state

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Treatment of PE

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(1) O2 to correct hypoxia; (2) Acute anticoagulation with heparin or LMWH to prevent another PE; start immediately on a basis of clinical suspicion - DO NOT WAIT for studies to confirm PE if clinical suspicion is high! (3) Give one bolus, followed by continuous infusion for 5-10 days, the goal is an aPTT of 1.5-2.5x control. (4) Oral warfarin for long-term treatment - can start with heparin on day 1. Therapeutic INR is 2-3; continue for 3-6 months or more, depending on risk factors. Some patients at significant risk for recurrent PE (malignancy, hypercoagulable sates, etc) may be considered for lifelong OAT

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How does Heparin work?

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Heparin works by promoting the action of Antithrombin III. Contraindications to heparin include active bleeding, uncontrolled HTN, recent stroke, or heparin-induced thrombocytopenia

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What is LMWH better than Heparin?

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Better bioavailability and lower complication rates than unfractioned heparin. It has been shown to be at least as effective or more effective than unfractionated heparin

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When should thrombolysis be considered in a patient with a PE?

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(1) Patients with massive PE who are hemodynamically stable or (2) Patients with evidence of right heart failure (thrombolysis can reverse this)

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IVC filter in PE

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(1) Use has become more common; indications include: [a] contraindication to anticoagulation in a patient with documented DVT or PE; [b] A complication of current anticoagulant; [c] failure of adequate anticoagulation as reflected by recurrent DVT or PE; [d] a patient with low pulmonary reserve who is at high risk of death from PE

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Therapeutic INR

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Usually between 2-3. Notable exceptions are prosthetic mechanical heart valves, prophylaxis of recurrent MI, and treatment of antiphospholipid antibody syndrome, for which 2.5 to 3.5 is rec'd

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What should you do in a patient with PE that cannot take OAT 2/2 contraindication?

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Get an IVC filter!

Front 264

Aspiration PNA

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Right lung is most often involved 2/2 anatomy (right main bronchus follows a more straight path down), particularly the lower segments of the right upper lobe and the upper segments of the right lower lobe

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Predisposing factors of aspiration PNA

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(1) reduced LOC 2/2 seizures, strokes, sedating drugs; (2) alcoholism; (3) extubation with impaired pharyngeal or laryngeal function; (4) excessive vomiting, ileus; (5) tube feeding, tracheostomy tubes; (6) anesthesia/surgery; (7) neuromuscular diseases; (8) esophageal disorders (achalasia, GERD, cancer)

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Treatment of aspiration PNA

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(1) antibiotics [penicillin G or clindamycin]; the bugs are often mixed (aerobic-anaerobic); (2) aspiration can lead to lung abscess if untreated. Poor oral hygiene predisposes to such infections. Foul-smelling sputum often indicates anaerobic infection