A 62-year-old man with a long history of COPD presents for routine follow-up in clinic. His symptoms are well controlled with inhaled albuterol, ipratropium, tiotropium, and fluticasone, and he has had no recent acute exacerbations.
Which of the following findings would be unlikely in this patient?
Increased pulmonary capillary wedge pressure (PCWP). This patient’s list of medications indicates that he likely has severe COPD with chronic hypoxemia. PCWP estimates left atrial pressure, which should not be elevated in this patient. One of the feared complications of severe COPD is cor pulmonale, which is the development of right heart failure from pulmonary hypertension caused by lung disease. Pulmonary hypertension is a possibility in this patient with severe disease, and the right-sided pressures (right atrium, right ventricle, pulmonary artery) might be elevated; however, the left atrial pressure (estimated by the PCWP) would be normal. (B) Chronic hypoxemia produces secondary polycythemia. Hypoxemia is sensed by the kidneys, which secrete erythropoietin that acts on hematopoietic stem cells in the bone marrow to increase production of red blood cells. (C) Patients with severe COPD often have chronic hypercapnia (respiratory acidosis) with a compensatory metabolic alkalosis due to increased bicarbonate reabsorption by the kidneys. (D) These patients will have chronic hypoxemia (low PaO2), and if the value is ≤55 mmHg, then home oxygen therapy is indicated.
A 71-year-old man complains of worsening fatigue and dyspnea on exertion. The symptoms have developed gradually over months to years, and he is now short of breath after walking short distances. He endorses night sweats and a weight loss of 10 kg over the past few months, but denies chest pain or paroxysmal nocturnal dyspnea. He is a retired textile manufacturer and has a 30 pack-year smoking history. On examination, there is some clubbing of the digits. A chest x-ray shows a mild reticulonodular pattern within the lung parenchyma and pleural plaques at the base of the lungs near the diaphragm. Pulmonary function testing shows a normal FEV1/FVC ratio and reduced total lung capacity.
What is the most common type of cancer associated with this patient’s lung disease?
Bronchogenic carcinoma. This patient has a concerning history for asbestos exposure with the development of lung cancer. Asbestos refers to a group of fibers (serpentine or amphibole) that causes lung disease years after exposure. Concerning environmental exposures include any careers with exposure to textiles, insulation, shipbuilding, and construction; in addition, exposure to someone with one of these careers is also a risk factor (e.g., wife of a shipbuilder that is exposed to asbestos from her husband’s clothing). Asbestos exposure is grouped in the category of pneumoconiosis, which are a collection of diseases caused by inhalation of various inorganic dusts.
The patient has risk factors for asbestos exposure and also has diaphragmatic pleural plaques on chest x-ray, which is virtually pathognomonic for asbestosis. Bronchogenic carcinoma is the most common lung cancer with asbestos exposure, and is dramatically increased with the synergistic effect of smoking. (B) Asbestos exposure also increases the risk of other cancers (laryngeal, biliary, etc.) but non-Hodgkin lymphoma is not one of those cancers. (C) Small cell lung cancer is not the most common type of cancer in these patients. (D) Asbestos is the only known risk factor for mesothelioma, a rare malignant disease of the pleura. However, mesothelioma is not the most common cancer in these patients, especially if there is a strong smoking history that dramatically increases the risk for bronchogenic carcinoma.
A 32-year-old man comes to the physician because of sudden onset shortness of breath. He has no medical history and was at rest when the symptoms occurred. He is 193.04 cm (6′4″) tall and weighs 74.84 kg (165 lb). There are decreased breath sounds over the right lung field with tracheal deviation to the right. He is admitted and undergoes chest imaging followed by placement of a chest tube. He is imaged again later in the day, which shows a decrease in the intrapleural volume but new fluffy opacities within the right lung.
What is the next step in management?
Observation. A complication after a large-volume thoracentesis or re-expansion of a pneumothorax is pulmonary edema, which is termed “re-expansion pulmonary edema.” There is debate over the exact mechanism, but some factors include the creation of very negative intrapleural pressures, surfactant dysfunction, and possibly direct injury to the lung during thoracentesis or chest tube placement. Most cases are mild and asymptomatic, and observation is sufficient since it is a self-limited process. In severe cases with hypoxemia, supplemental oxygen and mechanical ventilation are options for management. The other answer choices are unnecessary at this time; (A, B, C) the time course is too short for pneumonia to develop, and both heart failure and ARDS would show bilateral pulmonary edema.
A 23-year-old cross country runner with a history of asthma complains of worsening dyspnea and cough during exercise. He currently takes inhaled fluticasone and a long-acting β agonist, with inhaled albuterol used as a rescue medication. He is allergic to aspirin and penicillin. He asks about adding montelukast to his regimen.
What is the mechanism of action of this medication?
Blocks the receptor for LTC4, LTD4, and LTE4 in the leukotriene pathway. Montelukast acts as a leukotriene modifier and is a great therapy for asthma in a subset of patients, especially those with an aspirin allergy or with primarily exercise-induced asthma. (A) This is the mechanism of ipratropium, which can be used in acute asthma exacerbations but is used more commonly in COPD (both for chronic treatment and acute exacerbations). (B) Aspirin irreversibly inhibits COX-1 and COX-2. Both the cyclooxygenase pathway and the leukotriene pathway are part of the eicosanoid pathway, and they diverge from the precursor arachidonic acid. (D) Arachidonic acid is produced from membrane phospholipids via the enzyme phospholipase A2, which is inhibited by glucocorticoids. Glucocorticoids also cause lymphocyte destruction and a disruption in the adherence of neutrophils to endothelium, which is why patients that acutely start systemic steroids will have an increased white blood cell count that are predominantly neutrophils.
A 54-year-old woman presents with sudden onset shortness of breath. She denies any history of heart or lung disease, but does have a history of hypertension and chronic kidney disease. She takes hormone replacement therapy for menopausal symptoms, smokes cigarettes occasionally, does not drink alcohol, and recently returned from a trip to Hawaii. On examination, the patient is afebrile with a blood pressure of 148/94 mmHg, heart rate of 110 beats per minute, and respiratory rate of 26 breaths per minute. Her pulmonary examination is unremarkable, but she has pain, swelling, and erythema of her right lower extremity.
What is the most appropriate next step in the workup of this patient?
Ventilation–perfusion (V/Q) scan. This patient has a high likelihood of pulmonary embolism based on the following findings: tachycardia, tachypnea, clinical signs of a DVT, recent travel (and thus immobilization), and hormone replacement therapy (causing hypercoagulability). (D) The gold standard for the diagnosis of pulmonary embolism was previously pulmonary angiography; however, this procedure carries an unacceptably high morbidity and mortality and therefore is rarely performed. (C) CT angiography is the preferred method of diagnosis in patients with a likely diagnosis of pulmonary embolism; however, chronic renal failure is a contraindication to this procedure due to the use of contrast material that can be damaging to the kidneys (contrast-induced nephropathy). In these patients, a V/Q scan is the most appropriate next step and identifies areas of mismatched ventilation and perfusion. Although there is good sensitivity with this procedure, the specificity is poor; however, if there is a high likelihood of pulmonary embolism, the specificity improves dramatically. (A) D-dimers have a high sensitivity and are used with a low pretest probability of pulmonary embolism to rule out the diagnosis. A positive test must be followed up with further tests given the low specificity of a positive D-dimers result. (E) A Doppler ultrasound of the lower extremities has limited usefulness. If a DVT is diagnosed, then it is treated the same way as pulmonary embolism; however, if there is no DVT on imaging, this does not rule out a pulmonary embolism.
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