1 lung pathology

Systemic pathology


NORMAL LUNG
The lungs are carry out their function, the ((exchange of gases between inspired air and the blood)). The right lung is divided into three lobes; the left lung has only two lobes,. The trachea give rise to the right and left bronchi then each of which branch to giving rise to progressively smaller airways. The right main stem bronchus is more vertical and more directly in line with the trachea than is the left. As a consequence, aspirated foreign material, such as vomitus, blood, and foreign bodies, tends to enter the right lung rather than the left.
Progressive branching of the bronchi forms bronchioles, which are distinguished from bronchi by the lack of cartilage and submucosal glands within their walls. Further branching of bronchioles leads to the terminal bronchioles, which are less than 2 mm in diameter. The part of the lung distal to the terminal bronchiole is called the acinus, (( the terminal respiratory unit)); Acini contain alveoli and are thus the site of gas exchange. The bronchioles proceed into the alveolar ducts, which immediately branch and empty into the alveolar sacs.
Microscopically, except for the vocal cords, which are covered by stratified squamous epithelium, nearly the entire respiratory tree, including the larynx, trachea, and bronchioles, is lined by pseudostratified, tall, columnar, ciliated epithelial cells, heavily admixed in the cartilaginous airways with mucus-secreting goblet cells. Numerous sub-mucosal, mucus-secreting glands are dispersed throughout the walls of the trachea and bronchi (but not the bronchioles).
The microscopic structure of the alveolar walls (or alveolar septa) consists, from blood to air, of the following
• The capillary endothelium lining the intertwining network of anastomosing capillaries.
• A basement membrane and surrounding interstitial tissue separating the endothelial cells from the alveolar lining epithelial cells.
• Alveolar epithelium, comprising a continuous layer of two principal cell types: flattened, plate-like pavement type I pneumocytes (or membranous pneumocytes) covering 95% of the alveolar surface and rounded type II pneumocytes. Type II cells are important for at least two reasons: (1) They are the source of pulmonary surfactant, contained in osmiophilic lamellar bodies seen with electron microscopy, and (2) they are the main cell type involved in the repair of alveolar epithelium after destruction of type I cells.
Alveolar macrophages, loosely attached to the epithelial cells or lying free within the alveolar spaces, derived from blood monocytes and belonging to the mononuclear phagocyte system. Often, they are filled with carbon particles and other phagocytosed materials.
Atelectasis:
Atelectasis refers either to incomplete expansion of the lungs or to the collapse of previously inflated lung substance, producing areas of relatively airless pulmonary parenchyma.


Classification:
1-Resorption atelectasis is the consequence of complete obstruction of an airway, which in time leads to resorption of the oxygen trapped in the dependent alveoli, since lung volume is diminished, the mediastinum may shift toward the atelectatic lung. Resorption atelectasis is caused principally by excessive secretions (e.g., mucous plugs) or exudates within smaller bronchi and is therefore most often found in bronchial asthma, chronic bronchitis, bronchiectasis, and postoperative states and with aspiration of foreign bodies, and neoplasms.
2-Compression atelectasis results whenever the pleural cavity is partially or completely filled by fluid exudate, tumor, blood, or air. Compressive atelectasis is most commonly encountered in patients in cardiac failure who develop pleural fluid and in patients with neoplastic effusions within the pleural cavities. With compressive atelectasis, the mediastinum shifts away from the affected lung.
3-Contraction atelectasis occurs when local or generalized fibrotic changes in the lung or pleura prevent full expansion.

BACTERIAL PNEUMONIA
Bacterial invasion of the lung parenchyma leads to exudative solidification (consolidation) of the pulmonary tissue known as bacterial pneumonia.
classification may be made according to:
1- etiologic agent (e.g., pneumococcal or staphylococcal pneumonia).
2- the nature of the host reaction (e.g., suppurative, fibrinous).
3- the gross anatomic distribution of the disease (lobular bronchopneumonia versus lobar pneumonia).
Bronchopneumonia It characterized by Patchy consolidation of the lung , this parenchymal infection usually represents an extension of a preexisting bronchitis or bronchiolitis. It is an extremely common disease that tends to occur in the more vulnerable two extremes of life--infancy and old age. In the young, there is little previous experience with pathogenic organisms, rendering these patients susceptible to organisms of even low virulence. Resistance likewise falls in the aged, particularly in those already suffering from some serious disorder. Bronchopneumonia, a common finding on postmortem examinations, frequently terminates a long course of progressive heart failure or disseminated tumor.
Lobar pneumonia is an acute bacterial infection of a large portion of a lobe or of an entire lobe. Classic lobar pneumonia is now infrequent, owing to the effectiveness with which antibiotics abort these infections and prevent the development of full-blown lobar consolidation.
These anatomic but still classic categorizations are often difficult to apply in the individual case because patterns overlap. The lobular involvement may become confluent, producing virtually total lobar consolidation; in contrast, effective antibiotic therapy for any form of pneumonia may limit involvement to a subtotal consolidation. Moreover, the same organisms may produce lobular pneumonia in one patient, whereas in the more vulnerable individual a full-blown lobar involvement develops. Most important, from the clinical standpoint, are identification of the causative agent and determination of the extent of disease.

Pathogenesis.
The normal lung is free from bacteria. A number of potent defense mechanisms clear or destroy any bacteria inhaled with air or fortuitously deposited in the airway passages as follows :
Nasal clearance: Particles, including aerosolized droplets carrying microorganisms deposited near the front of the airway on the nonciliated epithelium, are normally removed by sneezing and blowing, whereas those deposited posteriorly are swept over the mucus-lined ciliated epithelium to the nasopharynx, where they are swallowed.
Tracheobronchial clearance: This is accomplished by mucociliary action: The beating motion of cilia moves a film of mucus continuously from the lung toward the oropharynx; particles deposited on this film are eventually either swallowed or expectorated.
Alveolar clearance: Bacteria or solid particles deposited in the alveoli are phagocytosed by alveolar macrophages. A particle is either digested or carried to the ciliated bronchioles. From here, the macrophage is propelled to the oropharynx and then swallowed. Alternatively the particle-laden macrophage may move through the interstitial space and either reenter the bronchioles or enter lymphatic capillaries. If the particle load is heavy and macrophage transport to the surface and alveolar pathways is overwhelmed, some particles may eventually reach the regional lymph nodes and, via the bloodstream, be carried elsewhere in the body.
Pneumonia can result whenever these defense mechanisms are impaired or whenever the resistance of the host in general is lowered. Factors that affect resistance in general include chronic diseases, immunologic deficiency, treatment with immunosuppressive agents, leukopenia, and unusually virulent infections.

The clearing mechanisms can be interfered with by many factors, such as the following:
1-Loss or suppression of the cough reflex, as a result of coma, anesthesia, neuromuscular disorders, drugs, or chest pain (this may lead to aspiration of gastric contents).
2-Injury to the mucociliary apparatus, by either impairment of ciliary function or destruction of ciliated epithelium, owing to cigarette smoke, inhalation of hot or corrosive gases, viral diseases, or genetic disturbances (e.g., the immotile cilia syndrome)
3-Interference with the phagocytic or bactericidal action of alveolar macrophages, by alcohol, tobacco smoke, anoxia, or oxygen intoxication
4-Pulmonary congestion and edema
5-Accumulation of secretions in conditions such as cystic fibrosis and bronchial obstruction.


Etiology.
For bronchopneumonia, the common agents are staphylococci, streptococci, pneumococci, Haemophilus influenzae, and Pseudomonas aeruginosa. In the case of lobar pneumonia, 90 to 95% are caused by pneumococci ( Streptococcus pneumoniae).
MORPHOLOGY.
Four stages of the inflammatory response have classically been described: congestion, red hepatization, gray hepatization, and resolution.
In the first stage of congestion, the lung is heavy, boggy, and red. It is characterized by vascular engorgement, intra-alveolar fluid with few neutrophils.
The stage of red hepatization that follows is characterized by massive confluent exudation with red cells (congestion) and neutrophils and fibrin filling the alveolar spaces. On gross examination, the lobe now appears red, firm, and airless with a liver-like consistency, so the term hepatization.
The stage of gray hepatization follows with progressive disintegration of red cells and the persistence of fibrino-suppurative exudates, giving the gross appearance of a grayish brown, dry surface.
In the final stage of resolution, the consolidated exudates within the alveolar spaces undergoes progressive enzymatic digestion to produce a granular, and debris that is resorbed, ingested by macrophages, or coughed up.
Foci of bronchopneumonia are consolidated areas of acute suppurative inflammation. The consolidation may be patchy through one lobe but is more often multi-lobar and frequently bilateral and basal because of the tendency of secretions
Histologically the reaction usually comprises a suppurative, neutrophil-rich exudates that fills the bronchi, bronchioles, and adjacent alveolar spaces .

Complications of pneumonia include
1) tissue destruction and necrosis, causing abscess formation.
2) spread of infection to the pleural cavity, causing the intrapleural suppurative known as empyema
3) bacteremic dissemination to the heart valves, pericardium, brain, kidneys, spleen, or joints, causing metastatic abscesses, endocarditis, meningitis, or suppurative arthritis.
Clinical Course.
The major symptoms of pneumonia are malaise, fever, and cough productive of sputum. When fibrinosuppurative pleuritis is present, it is accompanied by pleuritic pain and pleural friction rub. The characteristic radiologic appearance of lobar pneumonia is that of a radiopaque, usually well-circumscribed lobe, whereas bronchopneumonia shows focal opacities.
The clinical picture is dramatically modified by the administration of antibiotics. Treated patients may be relatively a febrile with few clinical signs 48 to 72 hours after the initiation of antibiotics. The identification of the organism and the determination of its antibiotic sensitivity are the keystones to appropriate therapy. Fewer than 10% of patients with pneumonia severe enough to merit hospitalization now succumb, and in most such instances, death may be attributed either to a complication, such as empyema, meningitis, endocarditis, or pericarditis, or to some predisposing influence, such as debility or chronic alcoholism

CHRONIC BRONCHITIS:
Is defined clinically as present in any patient who has persistent cough with sputum production for at least 3 months in at least 2 consecutive years.
In simple chronic bronchitis, patients have a productive cough but no physiologic evidence of airflow obstruction.
some individuals may demonstrate hyper-reactive airways with intermittent bronchospasm and wheezing. This condition is called chronic asthmatic bronchitis.
Pathogenesis.
Two sets of factors are important in the genesis of chronic bronchitis:
(1) chronic irritation by inhaled substances.
(2) microbiologic infections.
Both sexes and all ages may be affected, but chronic bronchitis is most frequent in middle-aged men. Cigarette smoking remains the paramount influence. Chronic bronchitis is 4 to 10 times more common in heavy smokers regardless of age, sex, occupation, and place of dwelling.
The hallmark and earliest feature of chronic bronchitis is hypersecretion of mucus in the large airways, and it is associated with hypertrophy of the submucosal glands in the trachea and bronchi. As chronic bronchitis persists, there is also a marked increase in goblet cells of small airways, small bronchi and bronchioles leading to excessive mucus production that contributes to airway obstruction. It is thought that both the submucosal gland hypertrophy and the increase in goblet cells are caused by tobacco smoke or other pollutants.

Histologic studies of the small airways in young smokers disclose:
(1) goblet cell metaplasia with mucous plugging of the lumen.
(2) clustering of pigmented alveolar macrophages.
(3) inflammatory infiltration.
(4) fibrosis of the bronchiolar wall.
The role of infection appears to be secondary. It is not responsible for the initiation of chronic bronchitis but is probably significant in maintaining it and may be critical in producing acute exacerbations.
Cigarette smoke predisposes to infection in more than one way: It interferes with ciliary action of the respiratory epithelium, may cause direct damage to airway epithelium, and inhibits the ability of bronchial and alveolar leukocytes to clear bacteria. Viral infections can also cause exacerbations of chronic bronchitis.


MORPHOLOGY.
Grossly, there may be hyperemia, swelling, of the mucous membranes, frequently accompanied by excessive mucinous to mucopurulent secretions layering the epithelial surfaces. Sometimes, heavy casts of secretions and pus fill the bronchi and bronchioles.
The characteristic histologic feature of chronic bronchitis is enlargement of the mucus-secreting glands of the trachea and bronchi. Although the numbers of goblet cells increase slightly, the major increase is in the size of the mucous glands. the bronchial epithelium may exhibit squamous metaplasia and dysplasia. There is marked narrowing of bronchioles caused by goblet cell metaplasia, mucous plugging, inflammation, and fibrosis. In the most severe cases, there may be obliteration of lumens ( bronchiolitis obliterans).
Clinical Features.
The important clinical finding in of chronic bronchitis is a persistent cough productive of copious sputum. For many years, no other respiratory functional impairment is present, but eventually dyspnea on exertion develops. With the passage of time, and usually with continued smoking, other elements of COPD may appear, including hypercapnia, hypoxemia, and mild cyanosis. Differentiation of pure chronic bronchitis from that associated with emphysema can be made in the classic case, but, as mentioned, many patients with COPD have both conditions. Long-standing severe chronic bronchitis commonly leads to cor pulmonale with cardiac failure. Death may also result from further impairment of respiratory function incident to acute intercurrent bacterial infections.