Introduction
The lungs function to allow gaseous exchange between the inspired air and blood. The right main stem bronchus is vertical and corresponds with the trachea, and also branches to form the three lobes. Therefore, aspiration of blood, vomitus, and foreign objects usually go into the right lung. The left main stem bronchus forms 2 lobes.
Pseudostratified ciliated epithelium lines respiratory tree wall, however the trachea and bronchi contain numerous mucus-secreting goblet cells and submucosal glands. While the rest of the respiratory tree wall contain cartilages, the bronchioles lack them.
The bronchial mucosa consists of neuroendocrine cells that secrete serotonin, calcitonin, bombesin (a gastrin-releasing peptide). Terminal bronchioles with a diameter of <2mm have on their distal parts, the acinus. The acinus about round and 7mm, is made of respiratory bronchioles, alveolar ducts, and alveolar sacs.
A group of 3-5 terminal bronchioles including their acinus form the pulmonary lobule. Type I squamous pneumocytes (95% abundant) & surfactant-producing type II pneumocytes line the alveolar surface wall. The arterial supply of the lungs consists of the pulmonary and bronchial arteries.
Next, we shall focus on the disorders of the lungs.
Pulmonary hypoplasia
A congenital defective development of both lungs, resulting in reduced acini, weight and volume not proportional to body weight and gestational age. It results from factors including diaphragmatic hernia and oligohydramnios that compress the lungs and reduce their expansion.
Pulmonary edema
Accumulation of fluid in the lungs from hemodynamic disturbances or direct alveolar injury,, causing heavy, wet lungs.
Pathogenesis: congestion of the alveolar capillaries> alveolar microhemorrhages with granular pink precipitate> hemosiderin-laden macrophages (heart failure cells)or >fluid and protein leakage into the interstitium, and then into the alveoli (in alveolar injury).
Causes: left-sided heart failure; volume overload; liver disease; nephrotic syndrome; hypoalbuminemia; protein-loosing enteropathies; (in hemodynamic disturbances) or oxygen and smoke inhalation; pneumonia; septicemia; liquid aspirations; bleomycin; amphotericin B; heroin; kerosene; trauma; radiation (in alveolar injury).
Acute lung injury (ALI), Acute respiratory distress syndrome (ARDS)
These conditions result from diffuse alveolar damage, with increased pulmonary vascular permeability, endothelial and alveolar epithelial cell death. ALI causes sudden onset of hypoxemia, and diffuse pulmonary infiltrates in the absence of cardiac failure. ARDS is a severe form of acute lung injury.
Causes/predisposing factors: diffuse pulmonary infections; sepsis; head injuries; gastric aspirations; pulmonary contusions; acetylsalicylic acid; barbiturate overdose; paraquat; multiple transfusions; uremia; pancreatitis; cardiopulmonary bypass; burns.
Pathogenesis: increased vascular permeability> release of IL-8, TNF, & IL-1 by pulmonary macrophage> neutrophil activation and transmigration> neutrophils release of oxidants, proteases, PAF, leukotrienes and alveolar capillary membrane damage> alveolar flooding with loss of gaseous exchange> surfactant loss> microthrombi formation and ischemic injury> lung scarring.
Clinical manifestations: earlier dyspnea and tachypnea; increasing hypoxemia and cyanosis; diffuse bilateral lung infiltrates on chest radiogram; ventilation-perfusion mismatch and hypoxemia; respiratory acidosis.
Management: mechanical ventilation and supportive care.
Acute interstitial pneumonia
A widespread acute lung injury with a progressive clinical course, without an underlying etiology. It is uncommon and occurs at an average age of 50 years.
Clinical manifestations: respiratory failure following an illness of <3wks. duration, which may resemble an upper respiratory infection.
Chronic obstructive pulmonary disease (COPD)
A group of clinical disorders including emphysema and chronic bronchitis, with similar features of damage at the acinus and bronchus.
Causes: long-term heavy cigarette smoking; environmental pollutant and noxious exposures.
Emphysema
An irreversible enlargement of the acinus with accompanying wall damage. The types include centriacinar, panacinar, distal acinar, & irregular emphysema. Centriacinar emphysema affects the respiratory bronchioles, sparing the alveoli. It is common in the apical segment of the lungs and occurs in heavy smokers.
Panacinar emphysema affects both the respiratory bronchioles and the distal alveoli. It is common at the base and anterior margins of lungs due to α-1 antitrypsin deficiency.
Distal acinar emphysema affects the distal alveoli adjacent to the pleura and in areas pf fibrosis, scarring or atelectasis. It is common in the upper half of the lungs and a fundamental cause of spontaneous pneumothorax in young adults. Irregular emphysema affects the acinus irregularly with wall fibrosis, and is usually clinically insignificant.
Pathogenesis in serum α-1 antitrypsin levels: smoking induced-accumulation of macrophages and neutrophils in alveolar spaces> release of neutrophil elastase> elastic tissue destruction.
Pathogenesis in smokers (from ROS): activation of macrophages and release of IL-8, TNF> neutrophil migration and accumulation in alveolar spaces> release of neutrophil elastase, cathepsin G, proteinase 3 by neutrophil> neutrophil release of ROS with resulting α-1 antitrypsin inactivation> tissue damage.
Other pathogenesis in smokers (from ROS): reduction of antioxidants (superoxide dismutase, glutathione) in lungs> tissue destruction.
Clinical manifestations: severe dyspnea; slight cough with scanty sputum; wheezing; weight loss; prolonged expiration with pursed-lip breathing; expiratory airflow limitation; overdistended lungs with barrel chest; low diffusion capacity; pink puffers; lung hyperinflation with small heart on chest X-ray.
Complications are cor pulmonale with congestion, respiratory acidosis, coma massive collapse from pneumothorax and death.
For diagnosis, spirometry is necessary. Bronchodilators, steroids, and bullectomy are important treatment options.
Chronic bronchitis
A clinical feature with persistent cough and sputum production for at least 3 months in at least 2 consecutive years, without any other identifiable cause.
Predisposing factors: inhalation of pollutants including tobacco smoke, sulfur dioxide, nitrogen dioxide, and dusts from grain, silica, and cotton.
Pathogenesis: triggering factors> release of neutrophil elastase, cathepsin, and MMP by neutrophil> submucosal gland hypertrophy with mucus hypersecretion following stimulation> marked increase in goblet cells in small bronchi and bronchioles>
excess mucus production with mucus plug formation> inflammation, fibrosis and narrowing of bronchioles> airway obstruction. Histologic features features: airway inflammation with predominantly lymphocytes, and submucosal gland hypertrophy.
Clinical manifestations: persistent cough with copious sputum; mild dyspnea non exertion; hypoxemia, hypercapnia, mild cyanosis (blue bloaters) overtime; prominent vessels with large heart on chest X-rays.
Complications are cor pulmonale, heart failure, secondary acute infections with respiratory failure and death.
Asthma
This is a partly reversible, airway hyperresponsive chronic inflammatory disorder, that causes bronchoconstriction & airflow limitation. The types include: atopic; non-atopic; occupational; drug-induced; and asthmatic bronchitis (in smokers).
Atopic asthma: A classic type I IgE-mediated hypersensitivity reaction, with evidence of allergen sensitivity on serum radioallergosorbent or skin test. Begin in childhood. Predisposing factors are: pollens, dusts, roach or animal dander, foods, history of allergic rhinitis & eczema, positive family history, class II HLA alleles.
Non-atopic asthma presents in individuals with no proof of allergen sensitivity, following skin test results that are usually negative. Predisposing factors are viral respiratory infections (parainfluenza virus, rhinovirus), ozone, sulfur dioxide, nitrogen dioxide.
Drug-induced asthma presents as urticaria and bronchoconstriction in individuals taking aspirin or other NSAIDS. Predisposing factors: history of recurrent rhinitis and nasal polyps. Aspirin inhibits cyclooxygenase pathway, sparing the lipoxygenase pathway, thereby favoring leukotrienes.
Occupational-induced asthma occurs during exposure to fumes (epoxy, resins, plastics); organic and chemical dusts (wood, cotton, platinum); gases (toluene); and other chemicals (formaldehyde and penicillin products).
Pathogenesis in atopic asthma: inhaled allergens> stimulation of TH2 cells and release of IL-4 IL-5, IL-13> IgE coats mast cells followed by degranulation> bronchoconstriction, increased mucus production, vasodilation, and vascular permeability (early phase reaction)>
eosinophil-induced inflammation, epithelial damage, and airway constriction (late phase reaction)> airway remodeling overtime.
Gross findings include occlusion of bronchi and bronchioles by Curschmann spirals (mucus plugs + shed epithelium). Other potent bronchoconstrictors: Leukotrienes C4 D4 E4 ; acetylcholine; histamine; prostaglandin D2 .
Clinical manifestations: chest tightness; wheezing; dyspnea; night or early morning cough +/- sputum; severe status asthmaticus (lasting days to wks.), cyanosis, and death.
Atelectasis
This consists of two types: neonatal and acquired atelectasis. Neonatal atelectasis is an incomplete expansion of the lungs. Acquired atelectasis is the collapse of a previously inflated lung overtime, usually in adults. Types of acquired atelectasis are: resorption, compression, and contraction atelectasis.
Resorption atelectasis results from complete obstruction of an airway by mucus plugs or exudates in smaller bronchi. Causes are chronic bronchitis, bronchial asthma, foreign body aspiration or bronchial tumors (rare). Manifests as reduced lung volume, and mediastinal shift towards atelectatic lung.
Compression atelectasis arises from the partial or complete accumulation of exudates, air, blood, or tumor in the pleural cavity. It manifests as mediastinal shift away from the affected lung. Contraction atelectasis occurs due to local or fibrotic changes within the lungs or pleura preventing complete expansion.
Leave a Reply