p.4
Diagnosis and Evaluation of ARDS
What should be measured if oxygen saturation falls below 90% during an asthma attack?
Arterial blood gas tensions.
p.6
Management and Treatment of COPD
What should be done if titration of oxygen therapy cannot be achieved without causing respiratory depression?
The individual’s lungs must be mechanically ventilated.
p.6
Emphysema Pathophysiology and Clinical Manifestations
Is some degree of emphysema considered normal in older adults?
Yes, some degree of emphysema is considered normal in older adults.
p.6
Emphysema Pathophysiology and Clinical Manifestations
What results from the destruction of alveolar septa and loss of elastic recoil of bronchial walls?
The destruction of alveolar septa and loss of elastic recoil of bronchial walls result in emphysema.
p.3
Asthma Pathophysiology and Risk Factors
What contributes to the thickening of airway walls in asthma?
Fibrosis and increased muscle thickness contribute to the thickening of airway walls.
p.3
Asthma Pathophysiology and Risk Factors
What role do neutrophils play in asthma?
Neutrophils contribute to the inflammatory process in asthma.
p.2
Asthma Pathophysiology and Risk Factors
What appears to create an immunologic imbalance that favors the development of allergy and asthma in some individuals?
Decreased exposure to certain infectious organisms.
p.6
Emphysema Pathophysiology and Clinical Manifestations
What does α1-antitrypsin normally inhibit?
α1-antitrypsin normally inhibits the action of many proteolytic enzymes.
p.6
Chronic Bronchitis Pathophysiology and Symptoms
What are some symptoms of chronic bronchitis and emphysema?
Symptoms include dyspnea, cough, hypoxemia, hypercapnia, and cor pulmonale.
p.3
Asthma Pathophysiology and Risk Factors
What are vasoactive mediators?
Vasoactive mediators are substances that cause vasodilation and increased capillary permeability.
p.3
Asthma Pathophysiology and Risk Factors
What is epithelial desquamation?
Epithelial desquamation is the shedding of the outer layer of the airway epithelium.
p.6
Emphysema Pathophysiology and Clinical Manifestations
What is the major mechanism of airflow limitation in emphysema?
The major mechanism of airflow limitation in emphysema is loss of elastic recoil.
p.6
Chronic Bronchitis Pathophysiology and Symptoms
What are the consequences of continuous bronchial irritation and inflammation?
Continuous bronchial irritation and inflammation can lead to chronic bronchitis, characterized by bronchial edema, hypersecretion of mucus, and bacterial colonization of airways.
p.3
Asthma Pathophysiology and Risk Factors
What damage do eosinophil products cause in asthma?
Eosinophil products, such as major basic protein and eosinophilic cationic protein, damage the respiratory epithelium.
p.8
Emphysema Pathophysiology and Clinical Manifestations
What is the most common symptom of emphysema?
Dyspnea on exertion that later progresses to marked dyspnea, even at rest, is the most common symptom of emphysema.
p.8
Emphysema Pathophysiology and Clinical Manifestations
What posture do individuals with emphysema often adopt to increase lung capacity?
Individuals with emphysema often lean forward with arms extended and braced on knees when sitting to increase lung capacity.
p.2
Asthma Pathophysiology and Risk Factors
What role does IL-8 play in asthma?
IL-8 activates neutrophils that contribute to a more exaggerated inflammatory response.
p.8
Emphysema Pathophysiology and Clinical Manifestations
What is the usual disease course of emphysema?
The disease course of emphysema is usually prolonged, with increasing dyspnea and intermittent bouts of infection that culminate in failure of the right side of the heart (cor pulmonale) and death.
p.8
Management and Treatment of COPD
What medications should be prescribed immediately for acute exacerbations of emphysema?
Oral corticosteroids and antibiotics should be prescribed immediately for acute exacerbations of emphysema.
p.2
Asthma Pathophysiology and Risk Factors
What leads to variable and uneven ventilation-perfusion relationships within different lung segments in asthma?
Increased alveolar gas pressure, decreased ventilation, and decreased perfusion.
p.6
Management and Treatment of COPD
Why must severe hypoxemia be reversed?
Severe hypoxemia must be reversed, especially if there are comorbidities that require adequate tissue oxygenation.
p.6
Emphysema Pathophysiology and Clinical Manifestations
What increases the likelihood of developing emphysema in persons with α1-antitrypsin deficiency who smoke?
Persons with α1-antitrypsin deficiency who smoke are even more likely to develop emphysema.
p.3
Asthma Pathophysiology and Risk Factors
What are chemotactic mediators?
Chemotactic mediators are substances that attract immune cells to the site of inflammation.
p.3
Asthma Pathophysiology and Risk Factors
What role does mucus secretion play in asthma?
Mucus secretion contributes to airway obstruction and impaired mucociliary function.
p.3
Asthma Pathophysiology and Risk Factors
What role do dendritic cells play in asthma?
Dendritic cells process and present antigens to Th2 cells, which produce interleukins.
p.2
Asthma Pathophysiology and Risk Factors
What factors can cause epigenetic changes that influence the function of asthma susceptibility genes?
Tobacco smoke, recurrent respiratory tract viral infections, esophageal reflux, and obesity.
p.6
Management and Treatment of COPD
What happens if the PaO2 is much more than 60 mmHg?
The stimulus to breathe decreases, PaCO2 increases, and apnea results.
p.6
Emphysema Pathophysiology and Clinical Manifestations
What is the likelihood of homozygous individuals developing lung disease?
Homozygous individuals have a 70% to 80% likelihood of developing lung disease.
p.3
Asthma Pathophysiology and Risk Factors
What results from allergen or irritant exposure in asthma?
Allergen or irritant exposure results in mast cell degranulation and a cascade of inflammatory events.
p.3
Asthma Pathophysiology and Risk Factors
What causes vascular congestion in asthma?
Vascular congestion is caused by increased capillary permeability and vasodilation.
p.3
Asthma Pathophysiology and Risk Factors
What do secreted mediators induce in asthma?
Secreted mediators induce active bronchospasm, edema from increased capillary permeability, and airway mucus secretion from goblet cells.
p.8
Emphysema Pathophysiology and Clinical Manifestations
What is the involvement of panacinar emphysema in the lung?
Panacinar emphysema involves the entire acinus, with damage more randomly distributed and involving the lower lobes of the lung.
p.2
Asthma Pathophysiology and Risk Factors
What initiates both an innate and an adaptive immune response in sensitized individuals during asthma?
Airway epithelial exposure to antigen.
p.2
Asthma Pathophysiology and Risk Factors
What does IL-4 stimulate in the context of asthma?
B-cell activation, proliferation, and production of antigen-specific IgE.
p.8
Diagnosis and Evaluation of ARDS
What may be indicated if pulmonary function testing is not definitive for the diagnosis of emphysema?
High-resolution CT scanning may be indicated if pulmonary function testing is not definitive for the diagnosis of emphysema.
p.2
Asthma Pathophysiology and Risk Factors
What causes a latent release of inflammatory mediators during the late asthmatic response?
Chemotactic recruitment of lymphocytes, eosinophils, and neutrophils during the acute response.
p.2
Asthma Pathophysiology and Risk Factors
What is associated with asthma in terms of T regulatory cells?
A decrease in the number or function of T regulatory (Treg) cells.
p.2
Asthma Pathophysiology and Risk Factors
What are the clinical manifestations of asthma between attacks?
Individuals are asymptomatic and pulmonary function tests are normal.
p.1
Treatment Strategies for ARDS
What alternative modalities of ventilation are being evaluated for ARDS?
Low-volume ventilation, noninvasive positive-pressure ventilation, permissive hypercapnia, prone positioning, extracorporeal gas exchange, and partial liquid ventilation.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What are frequent infectious exacerbations in chronic bronchitis complicated by?
Bronchospasm with dyspnea and productive cough.
p.6
Emphysema Pathophysiology and Clinical Manifestations
What is emphysema?
Emphysema is abnormal permanent enlargement of gas-exchange airways (acini) accompanied by destruction of alveolar walls without obvious fibrosis.
p.6
Emphysema Pathophysiology and Clinical Manifestations
What happens due to increased protease activity in the lungs?
Increased protease activity leads to the breakdown of elastin in the connective tissue of the lungs.
p.3
Asthma Pathophysiology and Risk Factors
What is autonomic dysregulation in the context of asthma?
Autonomic dysregulation refers to the imbalance in the autonomic nervous system that affects airway function.
p.3
Asthma Pathophysiology and Risk Factors
What is the increased contractile response of bronchial smooth muscle?
The increased contractile response of bronchial smooth muscle leads to bronchospasm and airway narrowing.
p.3
Asthma Pathophysiology and Risk Factors
What does IL-5 do in asthma?
IL-5 activates eosinophils.
p.8
Emphysema Pathophysiology and Clinical Manifestations
In which population does panacinar emphysema tend to occur?
Panacinar emphysema tends to occur in older adults and in those with α1-antitrypsin deficiency.
p.8
Emphysema Pathophysiology and Clinical Manifestations
What sound is heard with percussion of the chest in emphysema?
The chest has a hyperresonant sound with percussion in emphysema.
p.2
Asthma Pathophysiology and Risk Factors
What does IL-5 stimulate in asthma?
The activation, migration, and proliferation of eosinophils.
p.8
Diagnosis and Evaluation of ARDS
What do arterial blood gas measurements reveal in emphysema?
Arterial blood gas measurements reveal varying degrees of hypoxemia and/or hypercapnia in emphysema.
p.2
Asthma Pathophysiology and Risk Factors
What contributes to prolonged smooth muscle contraction in asthma?
Synthesis of leukotrienes.
p.2
Asthma Pathophysiology and Risk Factors
What does an individual experience at the beginning of an asthma attack?
Chest constriction and expiratory difficulty.
p.1
Berlin Definition of ARDS and Severity Categories
What does the new Berlin definition of ARDS provide?
Categories of severity based on hypoxemia: mild, moderate, and severe.
p.1
Acute Respiratory Distress Syndrome (ARDS) Clinical Manifestations
What eventually leads to death in ARDS?
Decreased cardiac output and hypotension.
p.5
Chronic Obstructive Pulmonary Disease (COPD) Overview
What are the systemic abnormalities associated with COPD?
Renal and hormonal abnormalities, malnutrition, muscle wasting, osteoporosis, and anemia.
p.1
Treatment Strategies for ARDS
What are some methods that have shown reductions in death rates for ARDS?
Alternative modalities of ventilation such as low-volume ventilation and prone positioning.
p.1
Obstructive Pulmonary Disease Overview
What characterizes obstructive pulmonary disease?
Airway obstruction that is worse with expiration.
p.1
Obstructive Pulmonary Disease Overview
What are the most common obstructive diseases?
Asthma, chronic bronchitis, and emphysema.
p.1
Asthma Pathophysiology and Risk Factors
At what ages does asthma occur?
Asthma occurs at all ages, with approximately half of all cases developing during childhood and another third before age 40.
p.4
Diagnosis and Evaluation of ARDS
What supports the diagnosis of asthma?
A history of allergies and recurrent episodes of wheezing, dyspnea and cough, or exercise intolerance.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What can hypoxemia lead to if not reversed in chronic bronchitis?
Pulmonary hypertension and eventually cor pulmonale.
p.5
Management and Treatment of COPD
When might chronic oral corticosteroids be needed in chronic bronchitis?
Late in the course of the disease, but should be considered a last resort.
p.4
Management and Treatment of COPD
What can worsen asthma in some individuals with certain genetic polymorphisms?
Long-acting beta agonists.
p.4
Chronic Obstructive Pulmonary Disease (COPD) Overview
What is the sixth leading cause of death worldwide?
Chronic obstructive pulmonary disease (COPD).
p.6
Emphysema Pathophysiology and Clinical Manifestations
What happens to individuals who have α1-antitrypsin deficiency?
Individuals who have α1-antitrypsin deficiency have an increased likelihood of developing emphysema.
p.3
Asthma Pathophysiology and Risk Factors
What is bronchial hyperresponsiveness?
Bronchial hyperresponsiveness is an increased sensitivity of the airways to various stimuli, leading to airway obstruction.
p.3
Asthma Pathophysiology and Risk Factors
What is bronchospasm?
Bronchospasm is the constriction of the bronchial smooth muscle, leading to airway narrowing.
p.3
Asthma Pathophysiology and Risk Factors
What happens when an inhaled antigen binds to mast cells covered with preformed IgE?
Mast cells degranulate and release inflammatory mediators such as histamine, bradykinins, leukotrienes, prostaglandins, platelet-activating factor, and interleukins.
p.8
Emphysema Pathophysiology and Clinical Manifestations
What physical characteristics are often observed in individuals with emphysema?
Individuals with emphysema are often thin, have tachypnea with prolonged expiration, and must use accessory muscles for ventilation.
p.8
Diagnosis and Evaluation of ARDS
How is emphysema usually diagnosed and staged?
Emphysema is usually diagnosed and staged by pulmonary function measures.
p.2
Asthma Pathophysiology and Risk Factors
What does IL-17 increase in asthma?
Neutrophilic inflammation.
p.8
Management and Treatment of COPD
What treatments may individuals with acute exacerbations of emphysema require?
Individuals with acute exacerbations of emphysema should receive oxygen and may require noninvasive positive-pressure ventilation or mechanical ventilation.
p.2
Asthma Pathophysiology and Risk Factors
What contributes to oxidative injury and chronic inflammation in asthma?
Increased synthesis of nitric oxide.
p.2
Asthma Pathophysiology and Risk Factors
What signals respiratory failure in asthma?
Respiratory acidosis, especially when left ventricular filling and cardiac output become compromised because of severe hyperinflation.
p.1
Acute Respiratory Distress Syndrome (ARDS) Clinical Manifestations
What follows hypoventilation in the progression of ARDS?
Hypercapnia, respiratory acidosis, and worsening hypoxemia.
p.5
Chronic Obstructive Pulmonary Disease (COPD) Overview
What genetic susceptibilities have been identified in relation to COPD?
Polymorphisms of genes that code for tumor necrosis factor, surfactant, proteases, antiproteases, and risks for lung cancer.
p.5
Chronic Obstructive Pulmonary Disease (COPD) Overview
What does chronic irritant exposure recruit to the lung?
Macrophages, neutrophils, and lymphocytes.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
How does tobacco smoke affect airway epithelial cells?
It directly injures airway epithelial cells.
p.1
Treatment Strategies for ARDS
What is no longer recommended for ARDS but what improves outcomes?
High-dose corticosteroid administration is no longer recommended, but low-dose therapy improves outcomes.
p.1
Obstructive Pulmonary Disease Overview
What do individuals with obstructive pulmonary disease experience?
Increased work of breathing, ventilation-perfusion mismatching, and a decreased forced expiratory volume in one second (FEV1).
p.1
Asthma Pathophysiology and Risk Factors
What is asthma?
A chronic inflammatory disorder of the bronchial mucosa that causes bronchial hyperresponsiveness, constriction of the airways, and variable airflow obstruction that is reversible.
p.1
Asthma Pathophysiology and Risk Factors
How many people in the United States have asthma?
It is estimated that 24.6 million people have asthma.
p.4
Diagnosis and Evaluation of ARDS
What does spirometry document during an induced asthma attack?
Reversible decreases in FEV1.
p.5
Management and Treatment of COPD
What may be helpful in the treatment of chronic bronchitis?
Chest physical therapy, including deep breathing and postural drainage.
p.4
Management and Treatment of COPD
What are being evaluated to personalize asthma treatment and reduce mortality?
Biomarkers and epigenetic markers.
p.4
Management and Treatment of COPD
What effects do LABAs have on asthma symptoms?
They improve symptoms and exert a long-term bronchodilatory and anti-inflammatory effect on the airways.
p.7
Emphysema Pathophysiology and Clinical Manifestations
Who is more susceptible to emphysema than those with the deficiency alone?
Individuals with α1-Antitrypsin deficiency.
p.7
Emphysema Pathophysiology and Clinical Manifestations
Why are bullae and blebs not effective in gas exchange?
Because they are combined with the loss of portions of the pulmonary capillary bed, leading to significant ventilation-perfusion mismatching and hypoxemia.
p.6
Emphysema Pathophysiology and Clinical Manifestations
What is primary emphysema commonly linked to?
Primary emphysema is commonly linked to an inherited deficiency of the enzyme α1-antitrypsin.
p.6
Chronic Bronchitis Pathophysiology and Symptoms
What happens due to the infiltration of inflammatory cells and release of cytokines?
The infiltration of inflammatory cells and release of cytokines lead to airway obstruction, air trapping, loss of surface area for gas exchange, and frequent exacerbations.
p.3
Asthma Pathophysiology and Risk Factors
What does immune activation involve in asthma?
Immune activation involves the production of interleukins (IL-4, IL-5, IL-8, IL-13, IL-17) and IgE.
p.3
Asthma Pathophysiology and Risk Factors
What are toxic neuropeptides?
Toxic neuropeptides are substances released during inflammation that can damage airway tissues.
p.8
Emphysema Pathophysiology and Clinical Manifestations
How much coughing and sputum production is typical in emphysema?
Little coughing and very little sputum are produced in emphysema.
p.8
Emphysema Pathophysiology and Clinical Manifestations
Why do people with emphysema often exhale through pursed lips?
People with emphysema often exhale through pursed lips to help prevent expiratory airway collapse.
p.2
Asthma Pathophysiology and Risk Factors
What are the effects of IL-13 in asthma?
IL-13 impairs mucociliary clearance, enhances fibroblast secretion, and contributes to bronchoconstriction and airway remodeling.
p.8
Management and Treatment of COPD
What is required for the management of acute exacerbations of emphysema?
Management of acute exacerbations of emphysema requires obtaining a chest radiograph, serum white blood cell count, arterial blood gas, and sputum sample.
p.2
Asthma Pathophysiology and Risk Factors
What contributes to impaired mucociliary function in asthma?
Damage to ciliated epithelial cells.
p.2
Asthma Pathophysiology and Risk Factors
What is the result of early hypoxemia without CO2 retention in asthma?
Hypoxemia further increases hyperventilation through stimulation of the respiratory center, causing PaCO2 to decrease and pH to increase (respiratory alkalosis).
p.1
Acute Respiratory Distress Syndrome (ARDS) Clinical Manifestations
What occurs after hyperventilation and respiratory alkalosis in ARDS?
Decreased tissue perfusion, metabolic acidosis, and organ dysfunction.
p.1
Diagnosis and Evaluation of ARDS
What defines ALI/ARDS?
The acute onset of bilateral infiltrates on chest radiograph, a low ratio of partial pressure of arterial oxygen to the fraction of inhaled oxygen, and the absence of clinical evidence of left atrial hypertension.
p.1
Treatment Strategies for ARDS
What are the treatment strategies for ARDS?
Early detection and management of contributing etiologies, supportive therapy to prevent progression of lung injury, and prevention of complications such as pneumonia and stress ulcer.
p.1
Treatment Strategies for ARDS
What are some new ways being investigated to prevent or treat ARDS?
Prophylactic immunotherapy, antibodies against endotoxins, antioxidants, surfactant replacement, nitric oxide inhalation, and inhibition of various inflammatory mediators.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What leads to airway obstruction in chronic bronchitis?
Thick mucus and hypertrophied bronchial smooth muscle narrow the airways.
p.1
Asthma Pathophysiology and Risk Factors
What are other risk factors for asthma?
Allergen exposure, urban residence, exposure to air pollution, tobacco smoke, and environmental factors.
p.4
Management and Treatment of COPD
When are antibiotics indicated for acute asthma?
Only if there is a documented bacterial infection.
p.5
Management and Treatment of COPD
What does teaching for chronic bronchitis include?
Nutritional counseling, respiratory hygiene, recognition of early signs of infection, and techniques that relieve dyspnea.
p.4
Management and Treatment of COPD
What offers stepwise guidelines for the diagnosis and management of chronic asthma?
The National Asthma Education and Prevention Program.
p.4
Management and Treatment of COPD
What are long-acting beta agonists (LABAs) recommended for in the treatment of asthma?
To be used in conjunction with inhaled corticosteroids as step 3 therapy for persistent asthma.
p.7
Management and Treatment of COPD
What dietary components may modulate the effects of systemic inflammation in COPD?
Increasing omega-3 fatty acids and antioxidant intake.
p.6
Emphysema Pathophysiology and Clinical Manifestations
What are some systemic effects of emphysema?
Systemic effects of emphysema include muscle weakness and weight loss.
p.3
Asthma Pathophysiology and Risk Factors
Which cells are involved in cellular infiltration during asthma?
Neutrophils, lymphocytes, and eosinophils are involved in cellular infiltration during asthma.
p.3
Asthma Pathophysiology and Risk Factors
What is the result of impaired mucociliary function?
Impaired mucociliary function leads to difficulty in clearing mucus from the airways.
p.3
Asthma Pathophysiology and Risk Factors
What does IL-4 promote in asthma?
IL-4 promotes the switching of B cells to favor immunoglobulin E (IgE) production.
p.2
Asthma Pathophysiology and Risk Factors
What increases the risk for asthma during childhood?
Exposure to high levels of certain allergens.
p.2
Asthma Pathophysiology and Risk Factors
Which cells contribute to the persistent inflammation of the bronchial mucosa and hyperresponsiveness of the airways in asthma?
Macrophages, T helper 2 (Th2) lymphocytes, B lymphocytes, mast cells, neutrophils, eosinophils, and basophils.
p.8
Diagnosis and Evaluation of ARDS
What leads to a decrease in FVC and an increase in FRC, RV, and TLC in emphysema?
Airway collapse and air trapping in distal portions of the lung lead to a decrease in FVC and an increase in FRC, RV, and TLC in emphysema.
p.2
Asthma Pathophysiology and Risk Factors
What happens when the Fc portion of preformed IgE binds to receptors on the surface of mast cells in asthma?
The IgE causes the mast cells to degranulate, releasing a large number of inflammatory mediators.
p.2
Asthma Pathophysiology and Risk Factors
What do eosinophil mediators cause in asthma?
Direct tissue injury with fibroblast proliferation and airway scarring.
p.1
Acute Respiratory Distress Syndrome (ARDS) Clinical Manifestations
What are the initial clinical manifestations of ARDS?
Dyspnea and hypoxemia with poor response to oxygen supplementation.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What factors during gestation and childhood can affect pulmonary function?
Low birth weight and respiratory tract infections.
p.1
Diagnosis and Evaluation of ARDS
How is the diagnosis of ARDS made?
Based on a history of lung injury, physical examination, analysis of arterial blood gases, and chest radiographs.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
How is chronic bronchitis defined?
Hypersecretion of mucus and chronic productive cough that continues for at least 3 months of the year for at least 2 consecutive years.
p.4
Asthma Pathophysiology and Risk Factors
What are the common symptoms of an asthma attack?
Wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, and tachypnea.
p.4
Diagnosis and Evaluation of ARDS
Why should peak flow measurements be obtained during an asthma attack?
To evaluate the severity of the attack.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What happens when airways collapse early in expiration in chronic bronchitis?
Gas is trapped in the distal portions of the lung.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What is usually present in individuals with chronic bronchitis?
A productive cough ('smoker’s cough') and evidence of airway obstruction shown by spirometry.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What happens to FRC and residual volume (RV) measurements in chronic bronchitis?
They are increased as airway obstruction and air trapping become more pronounced.
p.4
Management and Treatment of COPD
What is prescribed for the mildest form of asthma (intermittent)?
Short-acting beta-agonist inhalers.
p.4
Management and Treatment of COPD
What has been shown to be an important tool in reducing asthma exacerbations?
Immunotherapy, which can now be given sublingually.
p.4
Management and Treatment of COPD
What genotype places individuals at risk for worsening bronchospasm when using LABAs?
The Arg16Arg genotype of the β-adrenergic receptor gene (ADRβ2).
p.7
Emphysema Pathophysiology and Clinical Manifestations
What characterizes emphysema?
Destruction of alveoli through the breakdown of elastin within the septa by an imbalance between proteases and antiproteases, oxidative stress, and apoptosis of lung structural cells.
p.7
Emphysema Pathophysiology and Clinical Manifestations
What are the systemic effects of chronic inflammation in emphysema?
Weight loss, muscle weakness, and increased susceptibility to comorbidities, such as infection.
p.2
Asthma Pathophysiology and Risk Factors
What do Th2 cells release during the early asthmatic response?
Numerous cytokines including IL-4, IL-5, IL-8, IL-13, IL-17, and IL-22.
p.8
Diagnosis and Evaluation of ARDS
What do radiographs show in individuals with emphysema?
Radiographs show a flattened diaphragm and overdistended lung fields in individuals with emphysema.
p.2
Asthma Pathophysiology and Risk Factors
When does the late asthmatic response begin?
4 to 8 hours after the early response.
p.2
Asthma Pathophysiology and Risk Factors
What forms plugs in the airways in asthma?
Accumulation of mucus and cellular debris.
p.2
Asthma Pathophysiology and Risk Factors
What happens with progressive obstruction of expiratory airflow in asthma?
Air trapping becomes more severe and the lungs and thorax become hyperexpanded, putting the respiratory muscles at a mechanical disadvantage.
p.1
Acute Respiratory Distress Syndrome (ARDS) Clinical Manifestations
What are the clinical manifestations of ARDS after decreased tissue perfusion?
Increased work of breathing, decreased tidal volume, and hypoventilation.
p.1
Acute Respiratory Distress Syndrome (ARDS) Clinical Manifestations
What results from decreased oxygen delivery to tissues in ARDS?
Metabolic acidosis and organ dysfunction.
p.1
Diagnosis and Evaluation of ARDS
What may the initial physical examination show in ARDS?
Fine inspiratory crackles.
p.1
Treatment Strategies for ARDS
What does traditional therapy for ARDS include?
Mechanical ventilation with PEEP and high oxygen concentrations.
p.4
Asthma Pathophysiology and Risk Factors
What symptoms are involved in severe asthma attacks?
Use of accessory muscles of respiration and wheezing heard during both inspiration and expiration.
p.4
Asthma Pathophysiology and Risk Factors
What can happen in the late asthma response?
Symptoms can be even more severe than the initial attack.
p.1
Asthma Pathophysiology and Risk Factors
What are the death rates for asthma highest for?
Adult females, black persons, and adults older than 65.
p.4
Management and Treatment of COPD
What provides information necessary to determine whether hospitalization is necessary during an asthma attack?
Careful monitoring of gas exchange and airway obstruction in response to therapy.
p.5
Management and Treatment of COPD
What will individuals with severe hypoxemia require in chronic bronchitis?
Continuous oxygen therapy.
p.4
Management and Treatment of COPD
What has been found to be helpful in selected individuals with asthma?
Monoclonal antibodies to IgE (omalizumab).
p.4
Chronic Obstructive Pulmonary Disease (COPD) Overview
How has mortality in women from COPD changed compared to men?
Mortality in women has increased more than twice as much as in men.
p.7
Emphysema Pathophysiology and Clinical Manifestations
What contributes to the loss of alveolar cells and reduced surface area for gas exchange in emphysema?
Cellular apoptosis and early cellular senescence.
p.7
Emphysema Pathophysiology and Clinical Manifestations
What are the two types of emphysema based on the site of involvement?
Centriacinar (centrilobular) and panacinar (panlobular).
p.7
Management and Treatment of COPD
Why is malnutrition a major concern in individuals with COPD?
Because they have increased work of breathing and energy expenditure, decreased energy intake, and impaired oxygenation.
p.7
Management and Treatment of COPD
How can the medical nutrition therapy goal be accomplished in COPD?
Through high-energy foods, oral nutritional support, frequent snacking, soft foods and beverages, assistance with shopping, and meal preparation.
p.8
Emphysema Pathophysiology and Clinical Manifestations
What change occurs in the anteroposterior diameter of the chest in emphysema?
The anteroposterior diameter of the chest is increased (barrel chest) in emphysema.
p.8
Diagnosis and Evaluation of ARDS
What do pulmonary function tests indicate in COPD?
Pulmonary function tests in COPD indicate obstruction to gas flow during expiration with a marked decrease in FEV1.
p.2
Asthma Pathophysiology and Risk Factors
What does IL-22 stimulate in asthma?
Airway epithelial cells, which play an important role in stimulating further innate and adaptive immune responses.
p.8
Management and Treatment of COPD
How should inhaled bronchodilators be administered in emphysema?
Inhaled bronchodilators should be administered by either inhaler or nebulizer in emphysema.
p.2
Asthma Pathophysiology and Risk Factors
What can untreated inflammation lead to in asthma?
Long-term airway damage that is irreversible, known as airway remodeling.
p.2
Asthma Pathophysiology and Risk Factors
What are the clinical symptoms during partial remission of asthma?
No clinical symptoms are present, but pulmonary function tests are abnormal.
p.1
Acute Respiratory Distress Syndrome (ARDS) Clinical Manifestations
What are the final clinical manifestations of ARDS?
Decreased cardiac output, hypotension, and death.
p.1
Acute Respiratory Distress Syndrome (ARDS) Clinical Manifestations
What leads to respiratory failure in ARDS?
Worsening hypoxemia and hypercapnia.
p.5
Chronic Obstructive Pulmonary Disease (COPD) Overview
What are the clinical phenotypes of COPD?
Chronic bronchitis and emphysema.
p.1
Diagnosis and Evaluation of ARDS
What appears on chest radiographs over the first 24 to 48 hours after injury in ARDS?
Interstitial and alveolar infiltrates.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What does continual bronchial inflammation cause?
Bronchial edema and increases the size and number of mucous glands and goblet cells in the airway epithelium.
p.4
Asthma Pathophysiology and Risk Factors
What is pulsus paradoxus?
A decrease in systolic blood pressure during inspiration of more than 10 mmHg.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What does airway obstruction eventually lead to in chronic bronchitis?
Ventilation-perfusion mismatch with hypoxemia.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What are the common symptoms of chronic bronchitis?
Decreased exercise tolerance, wheezing, and shortness of breath.
p.4
Asthma Pathophysiology and Risk Factors
When does asthma become life-threatening?
If treatment does not reverse the process quickly.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What do FVC and FEV1 values indicate in chronic bronchitis?
They become markedly reduced.
p.4
Diagnosis and Evaluation of ARDS
What are expected early in the course of an acute asthma attack?
Hypoxemia and respiratory alkalosis.
p.5
Diagnosis and Evaluation of ARDS
How is chronic bronchitis diagnosed?
Based on history of symptoms, physical examination, chest radiograph, pulmonary function tests, and blood gas analyses.
p.4
Management and Treatment of COPD
What begins the management of asthma?
Avoidance of allergens and irritants.
p.5
Management and Treatment of COPD
How should oxygen be administered to individuals with severe hypoxemia and CO2 retention in chronic bronchitis?
With care, as chronic elevation of PaCO2 diminishes the sensitivity of central chemoreceptors.
p.4
Chronic Obstructive Pulmonary Disease (COPD) Overview
How is chronic obstructive pulmonary disease (COPD) defined?
A preventable and treatable disease with significant extrapulmonary effects that contribute to severity, characterized by airflow limitation that is not fully reversible.
p.4
Management and Treatment of COPD
Why has the safety of LABAs been questioned?
Because of the increased mortality in some populations using these drugs.
p.7
Emphysema Pathophysiology and Clinical Manifestations
What is suggested in nonsmokers and individuals who develop emphysema before age 40 years?
α1-Antitrypsin deficiency.
p.7
Emphysema Pathophysiology and Clinical Manifestations
Why does expiration become difficult in emphysema?
Because the loss of elastic recoil reduces the volume of air that can be expired passively, causing air to be trapped in the lungs.
p.7
Chronic Obstructive Pulmonary Disease (COPD) Overview
What causes air trapping and hyperinflation on expiration in COPD?
Mucous plugs and narrowed airways.
p.7
Chronic Bronchitis Pathophysiology and Symptoms
Is prolonged expiration always present in chronic bronchitis?
Yes, it is always present.
p.2
Asthma Pathophysiology and Risk Factors
What happens during the early asthmatic response?
Antigen exposure to the bronchial mucosa activates dendritic cells to present the antigen to CD4+ T cells, which differentiate into Th2 cells.
p.8
Diagnosis and Evaluation of ARDS
Why is diffusing capacity decreased in emphysema?
Diffusing capacity is decreased in emphysema because of the destruction of the alveolocapillary membranes.
p.2
Asthma Pathophysiology and Risk Factors
What do the inflammatory mediators released by mast cells cause in asthma?
Vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction (bronchospasm), and tenacious mucus secretion.
p.2
Asthma Pathophysiology and Risk Factors
What contributes to increased bronchial hyperresponsiveness in asthma?
Release of toxic neuropeptides.
p.2
Asthma Pathophysiology and Risk Factors
What triggers hyperventilation in asthma?
Lung receptors responding to increased lung volume and obstruction.
p.1
Berlin Definition of ARDS and Severity Categories
What are the severity categories of ARDS according to the Berlin definition?
Mild (200 mmHg < PaO2/FIO2 ≤ 300 mmHg), moderate (100 mmHg < PaO2/FIO2 ≤ 200 mmHg), and severe (PaO2/FIO2 ≤ 100 mmHg).
p.5
Chronic Obstructive Pulmonary Disease (COPD) Overview
Where do the pathologic changes of COPD occur?
In large central airways, small peripheral airways, and the lung parenchyma.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What results from inspired irritants in chronic bronchitis?
Airway inflammation with infiltration of neutrophils, macrophages, and lymphocytes into the bronchial wall.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What increases susceptibility to pulmonary infection in chronic bronchitis?
Compromised lung defense mechanisms.
p.1
Obstructive Pulmonary Disease Overview
What is required to expire a given volume of air in obstructive pulmonary disease?
More force (use of accessory muscles of expiration) or more time.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What does air trapping in chronic bronchitis lead to?
Expansion of the thorax, putting respiratory muscles at a mechanical disadvantage.
p.4
Asthma Pathophysiology and Risk Factors
What are ominous signs of impending death during an asthma attack?
A silent chest (no audible air movement) and a PaCO2 greater than 70 mmHg.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What does marked hypoxemia lead to in chronic bronchitis?
Polycythemia (overproduction of erythrocytes) and cyanosis.
p.4
Diagnosis and Evaluation of ARDS
What signals the need for mechanical ventilation during an asthma attack?
The development of hypercapnia with respiratory acidosis.
p.5
Management and Treatment of COPD
What medications are prescribed to reduce dyspnea and control cough in chronic bronchitis?
Bronchodilators (long-acting inhaled anticholinergics or long-acting inhaled beta agonists) and expectorants.
p.4
Management and Treatment of COPD
What is essential for all categories of persistent asthma?
Anti-inflammatory medications, with inhaled corticosteroids being the mainstay of therapy.
p.4
Chronic Obstructive Pulmonary Disease (COPD) Overview
What are the risk factors for COPD?
Tobacco smoke, occupational dusts and chemicals, indoor air pollution from biomass fuel, outdoor air pollution, and any factor that affects lung growth.
p.7
Emphysema Pathophysiology and Clinical Manifestations
What does alveolar destruction produce within the lung parenchyma?
Large air spaces (bullae) and air spaces adjacent to pleurae (blebs).
p.7
Emphysema Pathophysiology and Clinical Manifestations
Where does septal destruction occur in centriacinar emphysema?
In the respiratory bronchioles and alveolar ducts, usually in the upper lobes of the lung.
p.7
Management and Treatment of COPD
What is the medical nutrition therapy goal for individuals with COPD?
To maintain an acceptable and stable weight.
p.1
Acute Respiratory Distress Syndrome (ARDS) Clinical Manifestations
What follows dyspnea and hypoxemia in the progression of ARDS?
Hyperventilation and respiratory alkalosis.
p.5
Chronic Obstructive Pulmonary Disease (COPD) Overview
What results from an inherited mutation in the α1-antitrypsin gene?
Development of COPD (emphysema) at an early age, even in nonsmokers.
p.1
Diagnosis and Evaluation of ARDS
What serum biomarkers are being studied in ARDS?
TNF, brain natriuretic peptide (BNP), IL-6 and IL-8, and surfactant proteins.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
Why can't thick, tenacious mucus be cleared in chronic bronchitis?
Because of impaired ciliary function.
p.4
Diagnosis and Evaluation of ARDS
What are the usual findings in blood gas alterations during an asthma attack?
Hypoxemia with an associated respiratory alkalosis.
p.4
Asthma Pathophysiology and Risk Factors
What happens if status asthmaticus continues?
Hypoxemia worsens, expiratory flows decrease further, and effective ventilation decreases.
p.4
Diagnosis and Evaluation of ARDS
What does the evaluation of an acute asthma attack require?
Rapid assessment of arterial blood gases and expiratory flow rates, and a search for underlying triggers.
p.1
Asthma Pathophysiology and Risk Factors
What do specific gene expressions in asthma impart?
Associated phenotypes such as inflammation, sensitization to allergens, airway fibroblasts, airway remodeling, and responsiveness to asthma therapies.
p.5
Management and Treatment of COPD
What is the best treatment for chronic bronchitis?
Prevention, because pathologic changes are not reversible.
p.4
Management and Treatment of COPD
Why is extensive education important for individuals with asthma?
Because they tend to underestimate the severity of their asthma.
p.5
Management and Treatment of COPD
What role do peripheral chemoreceptors take over in chronic bronchitis?
They become the primary stimulus for breathing, sensitive to changes in PaO2.
p.4
Chronic Obstructive Pulmonary Disease (COPD) Overview
What is the third leading cause of death in the United States?
Chronic obstructive pulmonary disease (COPD).
p.4
Management and Treatment of COPD
What is one explanation for the increased mortality in some individuals using LABAs?
Those individuals were using LABAs instead of (rather than in conjunction with) inhaled corticosteroids, masking ongoing inflammation and airway damage.
p.7
Emphysema Pathophysiology and Clinical Manifestations
What are known contributing factors to secondary emphysema besides cigarette smoke?
Air pollution, occupational exposures, and childhood respiratory tract infections.
p.7
Emphysema Pathophysiology and Clinical Manifestations
What results from the increased work of breathing in emphysema?
Many individuals will develop hypoventilation and hypercapnia late in the course of the disease.
p.7
Chronic Obstructive Pulmonary Disease (COPD) Overview
What results in the collapse of the airways and prevents normal expiratory airflow in COPD?
Decreased elastic recoil of the bronchial walls.
p.7
Emphysema Pathophysiology and Clinical Manifestations
Is prolonged expiration always present in emphysema?
Yes, it is always present.
p.4
Asthma Pathophysiology and Risk Factors
What is considered severe bronchospasm or status asthmaticus?
If bronchospasm is not reversed by usual measures.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What happens as chronic bronchitis progresses?
Copious amounts of sputum are produced, accompanied by frequent pulmonary infections.
p.5
Chronic Bronchitis Pathophysiology and Symptoms
What does airway obstruction result in chronic bronchitis?
Decreased alveolar ventilation and increased PaCO2.
p.4
Management and Treatment of COPD
What is required for the management of an acute asthma attack?
Immediate administration of oxygen and inhaled beta-agonist bronchodilators.
p.5
Management and Treatment of COPD
What is required during acute exacerbations of chronic bronchitis?
Treatment with antibiotics and corticosteroids, and possibly mechanical ventilation.
p.4
Management and Treatment of COPD
What can be used to control persistent bronchospasm in more severe asthma?
Long-acting beta agonists.
p.4
Chronic Obstructive Pulmonary Disease (COPD) Overview
What characterizes the pulmonary component of COPD?
Airflow limitation that is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.
p.4
Management and Treatment of COPD
What is recommended once asthma is controlled by combination therapy with LABAs?
LABAs should be withdrawn.
p.7
Emphysema Pathophysiology and Clinical Manifestations
What is the major cause of secondary emphysema?
The inhalation of cigarette smoke.
p.7
Emphysema Pathophysiology and Clinical Manifestations
What does air trapping cause in the chest?
Hyperexpansion of the chest, which puts the muscles of respiration at a mechanical disadvantage.
p.7
Chronic Obstructive Pulmonary Disease (COPD) Overview
What happens during inspiration in COPD?
The airways are pulled open, allowing gas to flow past the obstruction.
p.7
Management and Treatment of COPD
What is similar to the disproportionate muscle wasting seen in COPD?
Muscle wasting seen in other chronic diseases, such as cancer, heart failure, and AIDS.
p.7
Management and Treatment of COPD
What supplementation is indicated to improve bone health in COPD?
Vitamin D and calcium supplementation.
p.7
Emphysema Pathophysiology and Clinical Manifestations
What percentage of smokers are especially susceptible to developing significant lung damage if they continue to smoke?
Approximately 15% to 20%.
p.7
Emphysema Pathophysiology and Clinical Manifestations
What can persistent inflammation in the airways result in?
Hyperreactivity of the bronchi with bronchoconstriction, which may be partially reversible with bronchodilators.
p.7
Management and Treatment of COPD
What may impair appetite and contribute to hypermetabolism in COPD?
Systemic inflammatory mediators.
p.7
Emphysema Pathophysiology and Clinical Manifestations
What remains intact in centriacinar emphysema?
The alveolar sac (alveoli distal to the respiratory bronchiole).
p.7
Emphysema Pathophysiology and Clinical Manifestations
When does a productive cough occur in emphysema?
Late in the course with infection.
p.7
Management and Treatment of COPD
What dietary adjustments may improve carbon dioxide balance in COPD?
Reducing the amount of carbohydrates while providing adequate protein and lipids.
p.7
Management and Treatment of COPD
What are the adverse effects of malnutrition in COPD?
It adversely affects exercise tolerance, limits surfactant production, reduces cell-mediated immune responses, decreases protein synthesis, and increases morbidity and mortality.
p.7
Management and Treatment of COPD
Why should serum phosphate levels be monitored in COPD?
To prevent hypophosphatemia, which can contribute to muscle weakness.
