Pulmonary Path Q
Started by MudPhud20XX
A 67-year-old man with a history of congestive heart failure has been in the hospital for 2 weeks following a left cerebral infarction. He now has a sudden episode of pleuritic chest pain on the left. He had shown steady improvement up to that point, remaining afebrile. What is the most likely diagnosis?
Virchow's triad --> DVT --> PE
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so here is the clinical vignette to that question.
A 50-year-old man has had a chronic cough for the past 7 months. On physical examination his temperature is 37.8° C (100° F). He appears cachectic. His chest radiograph is shown in the image. A transbronchial biopsy shows foci of epithelioid macrophages and lymphocytes within the lung parenchyma. What is the most likely diagnosis?
correct.
Hospitalized, immobile patients are at risk for deep vein thrombosis and pulmonary embolism. Patients with preexisting heart or lung disease are at risk for pulmonary infarction with a medium-sized embolus.
A 55-year-old man has had worsening dyspnea for the past 5 years. On physical examination he is afebrile. On physical examination there is hyperresonance over all lung fields. A chest CT scan shows diminished interstitial markings. Pulmonary function studies show that his forced expiratory volume at 1 second (FEV1)is increased, his residual volume is increased, and his diffusing capacity of the lung for carbon monoxide (DLCO) is diminished. What condition is he most likely to have?
Everything about it screams emphysema except the higher FEV1. Emphysematous patients usually have a diminished FEV1, not an increased FEV1. DLCO reduction and loss of interstitial markings are likely due to the destruction of the lung parenchyma. Hyperresonance also fits the picture. Amidoinitrite?
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you are right. usually with emphysema along with other obstrucitve aireway dz, the EFV1 is decreased....
but the answer is
Emphysema is characterized by destruction with loss of lung parenchyma. There may be scarring secondarily from infection, but the pathogenesis does not involve fibrosis with increased interstitial fibrosis. Radiographic imaging studies show more air density and less tissue density, hence the hyperlucency and reduced interstitial markings. Airway obstruction leads to air trapping, hyperinflation, and prolonged FEV1 with increased residual volume. Gas molecules have a long way to go to find a capillary, so diffusing capacity is diminished.
correct.
Secondary tuberculosis is most often seen in adults from reinfection or reactivation of prior mycobacterial infection. The inflammation is granulomatous, and the granulomas are caseating and tend to cavitate when large, as shown in the x-ray. Dystrophic calcifications with long-standing tuberculous infection are common, and may be the only radiographic evidence for past tuberculosis.
I still take issue with the description of "prolonged FEV1," as FEV1 is, by definition, the air you expire in one second. The proper description would be diminished FEV1.
I'm only splitting hairs over terminology because I used to do PFTs, and very specific orders and methods of describing the information obtained are required for proper diagnosis and evaluation.
Increased FEV1 and decreased DLCO points to restrictive lung diseases since decreased FEV1 is a hallmark of obstructive lung disease.
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