Lungs and Pleura




(1)
Department of Pathology, Sinai Hospital of Baltimore Pathology, Baltimore, MD, USA

 



Keywords
Interstitial lung diseaseGranulomasOrganizing pneumoniaBronchiAlveoliPneumoniaCarcinoidPulmonaryAllergic



Normal Histology


The lungs consist of principally four compartments: the large airways (bronchi), small airways and airspaces (bronchioles and alveoli), interstitium, and vessels. As in most organs, inflammatory processes tend to preferentially involve one or two compartments, so identifying the most affected area is key to the differential diagnosis. Normal histologic features include the following:



  • Bronchi : The bronchi are lined with ciliated or columnar epithelium with scattered goblet cells. Goblet cell metaplasia is an indication of irritation, such as in bronchitis or asthma. Squamous cell metaplasia is common in smokers. Under the epithelium you should find seromucinous (salivary-type) glands, cartilage, smooth muscle, and branches of the bronchial arteries (Figure 22.1).

    A149114_2_En_22_Fig1_HTML.jpg


    Figure 22.1.
    Normal bronchus . The bronchus is lined by ciliated columnar epithelium (1), foci of goblet cells (2), cartilage (3), and smooth muscle (4). The small arteries seen here (5) are branches of the bronchial artery, which carries oxygenated blood from the left ventricle.


  • Bronchioles : The bronchioles should have a cuboidal epithelium without goblet cells (Figure 22.2). The club (Clara) cells are secretory and reserve cells, but they are difficult to see. There is no cartilage.

    A149114_2_En_22_Fig2_HTML.jpg


    Figure 22.2.
    Bronchioles and alveoli . The small bronchiole (B) seen here is lined by a cuboidal epithelium and smooth muscle. The large adjacent arteriole (A) is a branch of the pulmonary artery. The veins or venules (V) run in septa. The alveolar walls (arrow) are normally lined with flat type I epithelium, of which only the nuclei are visible. Alveolar macrophages (arrowheads) are common.


  • Alveoli: The alveoli are the terminal air sacs and therefore have extremely thin walls (see Figure 22.2); in atelectasis, a common biopsy artifact, it is difficult to pick out the collapsed airspaces. Normally they are lined by nearly invisible flat type I epithelium. The presence of a cuboidal epithelium indicates type II hyperplasia (surfactant and reserve cells, which are normally sparse), seen in chronic inflammation or repair. Alveolar macrophages are often scattered throughout, but macrophages packing the alveoli are pathologic (see later discussion of desquamative interstitial pneumonia).


  • Vessels : The pulmonary arterioles run with bronchioles and have two elastic layers on Movat’s stain (train track appearance). The veins run in the interlobular septa and have one irregular elastic lamina. The lymphatics run with the arteries and veins in the pleura and interlobular septa.

Movat’s stain is a standard supplemental stain for non-neoplastic lung. On this pentachrome stain, you will see elastic laminae highlighted as black fibers (useful for identifying pleural involvement by tumors as well), hyaluronic acid or mucin in aqua blue, mature collagen in yellow, smooth muscle in dull red, and fibrinoid necrosis (in vessels) as bright red (Figure 22.3). This stain is very useful for identifying fibroblast foci in organizing pneumonia (discussed later) because they stand out as turquoise swirls on low power. Established interstitial fibrosis will be yellow.

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Figure 22.3.
Movat’s stain . The pulmonary arteries (A) have two elastic layers (arrowheads), while the veins (V) have one (arrow). The collagen lining the vessels is pale yellow-green in this stain.


A Brief Introduction to Non-neoplastic Lung


In non-neoplastic lung, within each of the four compartments, you are usually looking for something that does not belong. Examples of things that do not belong include heavy mononuclear cell infiltrates (lymphocytes and macrophages), neutrophils (other than in capillaries), eosinophils, granulomas, fibrosis, and fibroblast foci and substances such as amyloid, edema fluid, and asbestos. Table 22.1 lists differential diagnoses organized by what you see and in which compartment.


Table 22.1.
Differential diagnoses in non-neoplastic lung , by compartment.


















































































































Infiltrate

Large and small airways

Alveoli

Interstitium/septa

Vessels

Lymphocytes and mononuclear cells

Atypical/viral pneumonia

Atypical/viral pneumonia

CHP
 

DAD

CHP

CHP

LCH (histiocytes)

Respiratory bronchiolitis (macrophages)

Desquamative interstitial pneumonia (macrophages)

LIP

NSIP

Systemic CTD

UIP

Neutrophils

Bronchopneumonia

Bronchopneumonia
 
Wegener’s granulomatosis

Bronchocentric granulomatosis

Eosinophils

ABPA

Chronic eosinophilic pneumonia

Chronic eosinophilic pneumonia

Churg–Strauss syndrome

Asthma

Bronchocentric granulomatosis

Churg–Strauss syndrome

LCH

Chronic eosinophilic pneumonia

Loeffler syndrome

Granulomas

TB and fungus

TB and fungus

CHP (poorly formed)

Churg–Strauss syndrome

Bronchocentric granulomatosis

Sarcoidosis

Invasive aspergillosis

Rheumatoid nodules

Sarcoidosis

Wegener’s granulomatosis

Fibrosis and fibroblast foci

Organizing pneumonia

Organizing pneumonia

DAD (late or organizing)

Pulmonary hypertension

Constrictive bronchiolitis

DIP

Pneumoconioses

Sarcoidosis

Systemic CTD

UIP and NSIP

Other substances (mucus, exudates, etc.)

Asthma

Early DAD (HM)

Lymphangioleiomyomatosis (smooth muscle)

Amyloidosis

Chronic bronchitis

Goodpasture’s syndrome (heme)

DAD (fibrin thrombi)

Pulmonary alveolar proteinosis (exudate)

Pneumoconioses (refractile material)

Pneumocystis pneumonia (foamy material)


ABPA allergic bronchopulmonary aspergillosis, CHP chronic hypersensitivity pneumonitis, CIP chronic interstitial pneumonia, CTD connective tissue disease, DAD diffuse alveolar damage, HM hyaline membranes, LCH Langerhans cell histiocytosis, LIP lymphocytic interstitial pneumonia, NSIP nonspecific interstitial pneumonia, TB tuberculosis, UIP usual interstitial pneumonia


Response to Injury in the Lung


Part of what makes the non-neoplastic lung so challenging is that there are a finite number of histologic patterns of injury, and each pattern can be caused by up to dozens of etiologies. In addition, a single etiology can cause more than one pattern. For this reason, you can only get so far on histology alone, and after that you need a pretty strong grasp of the clinical differential, radiology, and history. What follows is largely a discussion of patterns rather than the clinical nomenclature. Note that most of these are not diagnoses that can be made on a core or transbronchial biopsy; they require the larger context of a wedge biopsy.

It is useful to think of the three phases of injury response in the lung: acute, subacute, and chronic. Acute injury, which may be from infection, trauma, toxins, drugs, or a transfusion reaction, manifests as diffuse alveolar damage (DAD) . This pattern correlates with the clinical entity acute respiratory distress syndrome (ARDS) . Idiopathic DAD, when no known precipitating factor can be identified, is called acute interstitial pneumonia (AIP) . The histologic picture is a nonspecific indication of injury and includes interstitial edema and hemorrhage , hyaline membrane formation, type II hyperplasia, fibrin thrombi, and fibrin extravasation into alveolar spaces (Figure 22.4). There should be a uniform and diffuse appearance throughout the field of view (although it may be patchy grossly). Acute bronchopneumonia , on the other hand, is the accumulation of neutrophils in the alveolar spaces, on top of the nonspecific findings of acute injury.
Jan 30, 2018 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Lungs and Pleura
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