Respiratory Flashcards
What conditions should be included in the differential diagnosis? If protein-rich exudate is found in the alveoli, what diagnosis is likely and to what condition could it lead?
Given this patient’s history, the differential diagnosis should include noncardiogenic pulmonary edema, acute pneumonitis, and acute respiratory distress syndrome. Onset of symptoms may take up to several days depending on the severity of the insult.
Protein-rich exudate in the alveoli suggests diffuse alveolar damage, which may lead to acute respiratory distress syndrome (ARDS). ARDS is a severe and potentially fatal lung disease in which acute inflammation and progressive parenchymal injury leads to hypoxemia. Typical histological presentation (Figure 14-1) involves diffuse alveolar damage and hyaline membrane formation in the alveolar walls.
What are the mechanisms of acute respiratory distress syndrome (ARDS)?
Diffuse alveolar damage involves an increase in alveolar capillary permeability because of the damage caused by an inciting agent; in this case, the inciting agent is the corrosive gas and the body’s response to it. Initial damage is due to neutrophilic substances that are toxic to tissue, oxygen-derived free radicals, and activation of the coagulation cascade. This insult leads to protein-rich exudates leaking into the lungs and the formation of an intra-alveolar hyaline membrane.
If ARDS does not resolve, what complication can arise?
If the inflammation and hyaline membrane formation do not resolve, the damaged tissue can organize, resulting in fibrosis.
How is Noncardiogenic pulmonary edema characterised?
How is Acute interstitial pneumonitis characterised?
Noncardiogenic pulmonary edema is pulmonary edema caused by injury to the lung parenchyma (such as pulmonary contusion, aspiration, or inhalation of toxic gas).
What is the most appropriate treatment for ARDS?
Oxygenation is a cornerstone of treatment and usually involves some form of mechanical ventilation in the intensive care unit. Whenever ARDS develops, the underlying cause must be treated, and patients may also need medication to treat infection, reduce inflammation, and remove fluid from the lungs.
What is the most likely diagnosis?
What other conditions should be considered in the differential diagnosis?
Asbestosis
What is the pathophysiology of Asbestosis?
The pathophysiologic process of asbestosis involves diffuse pulmonary interstitial fibrosis caused by inhaled asbestos fibers. Asbestos fibers penetrate bronchioles and lung tissue, where they are surrounded by macrophages and coated by a protein-iron complex (ferruginous bodies); Figure 14-2 shows these phagocytosed bodies. Diffuse fibrosis around the bronchioles spreads to the alveoli, causing lung tissue to become rigid and airways distorted.
What are the most likely chest x-ray findings in Asbestosis?
In cases of minor exposure, the only findings may be pleural thickening or calcified pleural plaques. In cases of extensive pulmonary fibrosis, reticular or nodular opacities will be seen throughout the lung fields, most prominently at the bases.
What is the most likely diagnosis?
Asthma exacerbation. Asthma is a form of obstructive lung disease.
What are other obstructive lung diseases other than asthma, and how do they differ from asthma? (3)
What is the pathophysiology of Asthma?
Acutely, bronchial hyperresponsiveness leads to episodic, reversible bronchoconstriction. Specifically, smooth muscle contraction in the airways leads to expiratory airflow obstruction. Chronically, airway inflammation leads to histologic changes in the bronchial tree.
What histologic findings in the lung are associated with Asthma?
Histologic examination reveals smooth muscle hypertrophy, goblet cell hyperplasia, thickening of basement membranes, and increased eosinophil recruitment (in Figure 14-3 the arrow points to plate of cartilage, and the arrowhead points to infiltrate of inflammatory cells). Dilated bronchi are filled with neutrophils and may have mucous plugs.
What are common triggers of Asthma?
Triggers of asthma exacerbation include stress, cold, exercise, dust and animal dander, mold, and viral upper respiratory tract infections.
What is the appropriate treatment for asthma?
For acute episodes, albuterol, a β2-agonist, helps relax bronchial smooth muscle and decrease airway obstruction. However, for long-term control of persistent symptoms, inhaled corticosteroids are the best treatment.
What drug was most likely given to this baby to promote lung expansion?
What is the most likely diagnosis?
Surfactant, normally produced late in fetal life (around week 28), can be given to the baby directly. Surfactant lowers the surface tension between alveoli, helping the lung to expand. Dexamethasone can be used antenatally to aid in surfactant production; it is given to women at risk for preterm delivery to reduce the risk of respiratory distress syndrome.
What are the 5 primary types of atelectasis?
How does obstructive atelectasis differ from compressive atelectasis?
In obstructive atelectasis, the mediastinum shifts toward the atelectasis due to loss of lung volume in that area. By contrast, the mediastinum shifts away from the atelectasis with compression.
During atelectasis, to what is the patient commonly predisposed?
Atelectasis results in mucus trapping and a decrease in ventilation, thereby predisposing the patient to
infections.
What is the most likely diagnosis?
Bronchiectasis.
What radiologic findings can help diagnose Bronchiectasis?
In bronchiectasis, a “tree-in-bud” pattern is commonly seen on high-resolution CT scans. This represents the plugging of small airways with mucus and bronchiolar wall thickening.
What are the possible etiologies of bronchiectasis?
Etiologies include chronic bronchial necrotizing infections, cystic fibrosis, bronchial obstruction from granulomatous disease or neoplasms, α1-antitrypsin deficiency, impaired host defense (eg, AIDS), and airway inflammation (eg, bronchiolitis obliterans). Additionally, tuberculosis and primary ciliary dyskinesia should be evaluated.
What complications are associated with bronchiectasis? (5)
Complications of bronchiectasis include hemoptysis, hypoxemia, cor pulmonale, dyspnea, and amyloidosis.
What is the appropriate treatment for bronchiectasis?
If an infection is thought to be the cause, then antibiotics should be given. If the bronchiectasis is localized, surgery may be an option. For routine management, however, measures include postural drainage and chest percussion.
What is the most likely diagnosis?
The history of productive cough for at least 3 consecutive months over 2 consecutive years accompanied by emphysema (suggested by pursed-lip breathing) indicates chronic obstructive pulmonary disease (COPD) with features of chronic bronchitis.
What radiologic findings can help diagnose chronic bronchitis?
In patients with COPD, x-rays of the chest often reveal lung hyperinflation, flattening of the diaphragm, and decreased peripheral vascular markings.
What abnormalities would be expected on pulmonary function testing in patients with chronic bronchitis?
How would chronic bronchitis affect the patient’s arterial blood gas levels (pH, PaO2, PaCO2, and SaO2)?
The pH decreases as a result of respiratory acidosis. Although pH may be normal in a patient with chronic compensated COPD, it is low in a patient with an acute exacerbation. Arterial oxygen tension (PaO2) decreases, arterial carbon dioxide tension (PaCO2) increases, and oxygen saturation (SaO2) decreases secondary to impaired gas exchange (from destruction of alveolar septae and pulmonary capillary bed).
Why is breathing with pursed lips adaptive in COPD/chronic bronchitis?
Breathing with pursed lips maintains positive end-expiratory pressure (PEEP). PEEP prevents alveolar and small airway collapse, which is common in emphysema. Respiratory therapy often provides supplemental oxygen via a mask or nasal prongs. Positive airway pressure can be provided by continuous positive airway pressure, bilevel positive airway pressure, or intubation and ventilatory support.
What complication of chronic bronchitis is suggested by the patient’s enlarged neck veins, hepatomegaly, and edema?
Cor pulmonale. Right heart failure due to chronic pulmonary hypertension leads to systemic venous congestion, which presents with the symptoms mentioned here. This complication occurs only in patients with severe COPD who develop pulmonary hypertension.
What is the most likely diagnosis? What are the likely lung examination findings?
This patient presents with several classic findings of community-acquired pneumonia (CAP): a productive cough, fever, rigors (shaking chills), and tachypnea. His risk factors include an advanced age and a significant smoking history.
Exam findings: Decreased breath sounds, crackles, dullness to percussion, and increased tactile fremitus are probable findings and can indicate areas of consolidation (ie, areas filled with fluid).
What are the most likely causative organisms of CAP?
Gram stain of the sputum in a patient with suspected CAP reveals gram-positive cocci in pairs and short chains. Additional testing reveals that the organism is optochin sensitive and the Quellung reaction is positive. What is the causative organism?
S pneumoniae is a gram-positive, encapsulated organism, hence the positive Quellung reaction, which is performed by adding anticapsular antisera that cause the capsule to swell. The organism is also catalase negative, α-hemolytic (partial hemolysis; the blood turns greenish), and optochin sensitive (which differentiates it from Streptococcus viridans, which is also α-hemolytic).
What are the appropriate treatments for S pneumoniae CAP?
Penicillin V and amoxicillin are rarely used in clinical practice because resistance with these drugs is an increasing problem. The typical treatment is either a macrolide in combination with a cephalosporin or fluoroquinolone monotherapy.
What factors would indicate hospitalization for a patient with community acquired pneumonia?
Factors that increase the need for hospitalization include age older than 65 years, altered mental status, underlying chronic illness, elevated blood pressure, elevated temperature, and abnormally high kidney function tests (ie, creatinine and blood urea nitrogen).
How many segments of lung will be resected if the entire right lower lobe is removed?
There are five segments in the right lower lobe (Figure 14-8): Medial, Anterior, Lateral, Posterior, and Superior (mnemonic: MALPS).
Which vessels supply arterial and venous branches to the lungs, and what paths do the branches follow to supply each lung segment?
The lung alveoli are supplied by branches of the pulmonary artery and vein. The bronchial tree also receives its arterial supply from the bronchial arteries (from the aorta) and venous drainage from bronchial veins that feed into the azygos and accessory hemiazygos veins. Pulmonary and bronchial arteries follow the airways into the periphery. Pulmonary veins course in the septa between adjacent lung segments.
When entering the thoracic cavity through an intercostal space, the surgeon preserves the intercostal nerves and vessels. What is the anatomic relationship between the intercostal nerves and vessels and the ribs?
The intercostal nerves and vessels lie in the costal groove inferior to each rib. They are positioned between the innermost intercostal and internal intercostal muscles for the length of those muscles.
During development, the pulmonary arteries arise from which aortic arch?
The sixth aortic arch produces the pulmonary arteries as well as to the ductus arteriosus.
What genetically transmitted condition does this patient likely have?
The patient likely has cystic fibrosis (CF), which is caused by loss-of-function mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) protein, a chloride channel found in all exocrine tissues. As a result of these mutations, secretions in the lung, intestine, pancreas, and reproductive tract are extremely viscous.
What is the probable etiology of the patient’s current symptoms?
The lungs in patients with CF are colonized at an early age with various bacteria not normally found in the lung. Therefore, patients suffer from repeated pulmonary bacterial infections (Staphylococcus aureus, Haemophilus influenzae, and Pseudomonas aeruginosa are the most common organisms), which increase production of viscous secretions. These increased secretions lead to increased cough and pulmonary obstruction, which can result in acute respiratory distress.
What is the most likely diagnosis?
What is the pathophysiology of Emphysema?
Destruction of alveolar walls results in enlargement of air spaces. Compared with a normal lung (Figure 14-9A), the lung in emphysema (Figure 14-9B) shows destruction of lung parenchyma and marked dilatation of terminal air spaces. Destruction of lung parenchyma also decreases elastic recoil, which increases airway collapsibility, causing expiratory obstruction. As a result, patients with emphysema often find it easier to exhale through pursed lips (which maintains a high end-expiratory pressure, thereby stenting the alveoli open)—hence the term “pink puffers.” Because of chronic hyperinflation, lungs are expanded close to total lung capacity with little inspiratory reserve, and diaphragms are flattened to a point of significant mechanical disadvantage.
What is the most likely diagnosis?
What is the likely source of this infection?
What additional microorganisms can cause this presentation?
What is the main virulence factor of H influenzae?
The polysaccharide capsule is the major virulence factor of H influenzae, which has both encapsulated and nonencapsulated strains. The nonencapsulated forms are limited to local infections such as otitis media in children and mild respiratory infection in adults (Table 14-1). The encapsulated strains are significantly more virulent and can cause disseminated diseases such as meningitis, epiglottitis, and septic arthritis. There are six capsular types of H influenzae, designated a through f. The b-type capsule accounts for approximately 95% of serious H influenzae infections in children.
What is the most likely diagnosis?
The pleural thickening (indicated by the arrows in Figure 14-10) in addition to a history of exposure to asbestos makes the diagnosis of malignant mesothelioma of high concern. Benign pleural plaques could also present similarly. As the malignant mesothelioma progresses, the lung is surrounded and compressed by a thick layer of tumor. Although mesotheliomas are rare, an exposure history greatly increases the risk. Common features of the disease include dyspnea, chest pain, and pleural effusions.
What is the most likely diagnosis?
A pleural effusion consists of fluid accumulation in the pleural space (between the visceral pleura and the parietal pleura) of the lung. Normally, the pleural space is only a potential space, with a small amount of fluid.
How are pleural effusions classified?
What is the most likely diagnosis?
Mycoplasma pneumoniae, which causes primary atypical pneumonia (“walking pneumonia”), is the most common cause of pneumonia in teenagers (Table 14-2). This organism is the smallest free-living bacterium. It has no cell wall and its membrane is the only bacterial membrane containing cholesterol.
What is the most likely diagnosis? What other conditions should be included in the differential diagnosis?
This is a case of pulmonary embolism (also known as pulmonary thrombo- embolism, or PTE).
What test remains the gold standard for diagnosing PE?
Pulmonary angiography remains the most specific test available for definitively diagnosing PTE. However, because of the invasiveness of angiography, CT of the chest with thin cuts is the most frequently used diagnostic test. A ventilation-perfusion lung scan is still often used. A lung scan showing normal perfusion virtually excludes PTE. An x-ray of the chest can show signs of PTE including Hampton hump (a wedge-shaped indicator of infarction in a region served by an occluded vessel) and Westermark sign (oligemia distal to a PTE) but neither sign is specific and additional imaging is necessary to confirm the diagnosis.
Plasma D-dimer levels have a negative predictive value in cases of low clinical suspicion but are elevated in more than 90% of patients with PTE. This assay is nonspecific and levels may also be elevated in conditions such as myocardial infarction or sepsis. The current strategy for diagnosing PTE and deep venous thrombosis is shown in Figure 14-12.
What is the most likely cause of these symptoms? What is the most likely diagnosis?
The patient has respiratory acidosis (pH < 7.4 and PCO2 > 40 mm Hg) with compensatory metabolic alkalosis. Respiratory acidosis can be caused by COPD, airway obstruction, and hypoventilation.
The patient has a chronic respiratory acidosis, as indicated by the large compensatory increase in bicarbonate to correct for an elevated PCO2. It is most likely due to her underlying COPD since a patient with a more acute process would not be able to compensate as robustly.
In Figure 14-13, which area corresponds to respiratory acidosis, respiratory alkalo- sis, metabolic acidosis, and metabolic alkalosis?
Letter A in Figure 14-13 re- fers to respiratory acidosis, and letter B refers to meta- bolic acidosis. Letter C re- fers to respiratory alkalosis, and letter D refers to meta- bolic alkalosis.
What is the anion gap, and what factors can increase the anion gap in this condition?
What is ILD and what are the common causes?
What is the most likely cause of ILD in this patient?
Sarcoidosis is the most likely cause. This diagnosis is supported by the patient’s race, the presence of noncaseating granulomas (discrete collections of tissue macrophages termed histiocytes often organized into multinucleated giant cells without central necrosis), and the bilateral hilar lymphadenopathy on x-ray of the chest.
What is this most likely diagnosis?
Small cell lung carcinoma is strongly suggested by the central, hilar nature of the lung mass; a significant weight loss; and a serum sodium of 119 mEq/L, as a result of syndrome of inappropriate antidiuretic hormone (SIADH) as part of the paraneoplastic process.
What is the most likely diagnosis?
Pneumothorax—more specifically, secondary spontaneous pneumothorax. Whereas primary spontaneous pneumothorax occurs in the absence of underlying lung disease, secondary spontaneous pneumothorax occurs in the setting of chronic lung parenchymal disruption.
