A. The right lung consists of three lobes (upper, middle, and lower) separated by a horizontal fissure and an oblique fissure.

1. The right upper lobe lies in a superior and anterior position.

2. The right middle lobe lies in an anterior position between costal cartilages 4 and 6.

3. The right lower lobe lies in an inferior and posterior position.

4. The horizontal fissure runs at the level of costal cartilage 4 and meets the oblique fissure at the midaxillary line.

5. The diaphragmatic surface consists of the middle and lower lobes.

B. The left lung consists of two lobes (upper and lower) separated by an oblique fissure.

1. The left upper lobe lies in a superior and anterior position and contains the cardiac notch, where the left ventricle and pericardial sac abut the lung. The lingula, which is the embryologic counterpart to the right middle lobe, lies just beneath the cardiac notch.

2. The left lower lobe lies in an inferior and posterior position.

3. The diaphragmatic surface consists of the lower lobe.

Figure 4-5. (/\) Posteroanterior radiograph showing primary tuberculosis. Note the consolidation (P) in the right lower lobe of the lung. Secondary, or reactivation, tuberculosis usually is located in the apex (S). (B) Posteroanterior radiograph of miliary tuberculosis. Note the many small consolidations scattered throughout both lungs. (C) Gross specimen of the cut surface of the lung showing bronchopneumonia. Note the patchy consolidations throughout the lung (multilobar), surrounding the bronchi. A large area of consolidation also is seen in the basal portion of the lower lobe because of gravitational pooling of bacteria. (D) Gross specimen of the lung showing lobar pneumonia. Note that the entire lower lobe (X) is uniformly consolidated. The upper and lower lobes appear different because the lower lobe is in the late consolidation, or "gray hepatization," stage, in which the lung has a typical gray-brown, dry surface. (E) Posteroanterior radiograph showing cystic fibrosis. Note the hyperinflation of both lungs and the reduced size of the heart as a result of pulmonary compression. Both lungs show cyst formation and atelectasis (collapse of alveoli). (F) Gross specimen of the cut surface of the lung showing a pulmonary infarction. Note the hemorrhagic pulmonary infarct (Pf) within the lower lobe. A pulmonary infarct typically appears wedge-shaped. (A adapted and Band Ereprinted with permission from Freundlich IM, Bragg DG: A Radiologic Approach to Diseases of the Chest, 2nd ed. Baltimore, Williams & Wilkins, 1997, pp 309, 470, 471; C reprinted with permission from Bhushan V, Le T, Amin C: First Aid for the USMLE Step 1. Stamford, CT, Appleton & Lange, 1999; D and F adapted with permission from Cotran RS, Kumor V, Robbins SL: Robbins' Pathologic Basis of Disease, 5th ed. Philadelphia, WB Saunders, 1994, pp 686, 697.)

C. Bronchopulmonary segment

1. The bronchopulmonary segment contains a segmental bronchus, a branch of the pulmonary artery, and a branch of the bronchial artery. These structures run together through the central part of the segment.

2. The bronchopulmonary segment contains tributaries of the pulmonary vein that are found at the periphery between two adjacent bronchopulmonary segments. These veins form surgical landmarks during segmental resection of the lung.

D. Clinical considerations (Figure 4-5)

1. Primary tuberculosis a. Primary tuberculosis is caused by Mycobacterium tuberculosis (acid fast).

b. The lung is the usual location of the initial infection.

c. The initial focus is the Ghon complex, which consists of parenchymal or sub-pleural lesions near a fissure and enlarged caseous lymph nodes.

d. Most patients remain asymptomatic with the initial infection. The infection may be reactivated years later if the immune system is compromised (e.g., advanced age, poor nutrition, AIDS).

2. Secondary tuberculosis. Most cases represent reactivation (versus reinfection) of a primary tuberculosis infection. Because M. tuberculosis is a strict aerobe, reactivation usually occurs within the apex of the lung. Secondary tuberculosis begins as a small focus of consolidation, usually less than 3 cm in diameter.

3. Miliary tuberculosis is caused by dissemination by lymphatics or blood. The dissemination sometimes is confined to the lungs, with multiple nodules (areas of consolidation) scattered throughout both lungs. However, the dissemination usually spreads widely to other organs.

4. Bronchopneumonia is caused by infection with Streptococcus pneumoniae, Staphylococcus species, H. influenzae, Pseudomonas species, and coliform bacilli. It is characterized by patchy consolidation of the lung, which often is multilobar, bilateral, and basal because of gravitational pooling of bacteria.

5. Lobar pneumonia usually is caused by acute infection with S. pneumoniae. Klebsiella and type II pneumococcus infections may occur in elderly persons, alcoholics, and diabetics. It is characterized by consolidation of an entire lobe or a large part of an entire lobe. The inflammatory response has four stages:

a. The initial stage is characterized by acute congestion, intraalveolar fluid, few neutrophils, and many bacteria.

b. Early consolidation, or "red hepatization," lasts 2—4 days and is characterized by consolidation with infiltration of neutrophils and fibrin within the alveoli. The lung is red as a result of extravasated red blood cells. In addition, it is firm and airless, with a liver-like consistency.

c. Late consolidation, or "gray hepatization," lasts 4-8 days and is characterized by large amounts of fibrin with decreasing numbers of red and white blood cells. The lung has a gray-brown, dry surface.

d. Resolution begins after 8 days.

6. Cystic fibrosis a. Cystic fibrosis is characterized by the production of abnormally thick mucus by epithelial cells that line the respiratory and gastrointestinal tracts. Clinically, this mucus causes obstruction of airways and recurrent bacterial infections (e.g., Staphylococcus aureus, Pseudomonas aeruginosa).

b. Cystic fibrosis is caused by autosomal recessive mutations of the CF gene, which is located on the long arm of chromosome 7 (q7). The CF gene encodes for a protein called CFTR (cystic fibrosis transporter). This protein functions as a CI" ion channel.

c. In the neonate, cystic fibrosis causes meconium ileus (i.e., obstruction of the bowel). In childhood, cystic fibrosis causes steatorrhea (fatty stool) or obstruction of the bowel. Cor pulmonale (right-sided heart failure) usually develops as a result of pulmonary hypertension.

7. Pulmonary embolism is the occlusion of a pulmonary artery by an embolic blood clot that originates from a deep vein thrombosis in the leg or pelvic area.

a. A large embolus may occlude the main pulmonary artery or lodge at the bifurcation as a "saddle embolus." It may cause sudden death, with symptoms easily confused with those of myocardial infarction (e.g., chest pain, severe dyspnea, shock, increased serum lactate dehydrogenase levels). A small embolus may occlude smaller peripheral branches of the pulmonary artery. A pulmonary embolism may cause a pulmonary infarction. This wedge-shaped infarction usually occurs in the lower lobes of the lungs.

b. Risk factors for pulmonary embolism include: obesity, cancer, pregnancy, use of oral contraceptives, hypercoagulability, multiple bone fractures, burns, and a history of deep vein thrombosis (a typical clinical scenario involves a postsurgical, bedridden patient who has sudden shortness of breath).

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