Chapter 14 Respiratory tract
COMMON CLINICAL PROBLEMS FROM RESPIRATORY TRACT DISEASE
Sign or symptom | Pathological basis |
---|---|
Sputum | Excess secretion from bronchial mucous glands in, for example, asthma and chronic bronchitis Infl ammatory exudate from respiratory tract infection |
Cough | Physiological refl ex response to presence of mucus, exudate, tumour or foreign material |
Wheezing | |
Dyspnoea | Decreased oxygen in the blood from impaired alveolar gas exchange, left heart failure or anaemia |
Cyanosis | Increased non-oxygenated haemoglobin, e.g. circulatory bypassing of lungs in congenital heart diseases or impaired alveolar gas exchange |
Pleuritic pain | Irritation of the pleura due to pulmonary infl ammation, infarction or tumour |
Pleural effusion | |
Clubbing | Often accompanies carcinoma of lung and pulmonary fi brosis, as well as, less commonly, cirrhosis and chronic infl ammatory bowel disease |
Weight loss | Protein catabolic state induced by chronic infl ammatory disease (e.g. tuberculosis) or tumours |
Auscultation signs | |
Percussion signs |
Globally respiratory diseases, particularly lung infections, together with gastrointestinal infection, account for most deaths in the developing world. Respiratory disease is also a common cause of death in the industrialised nations, accounting for about 14% of deaths in each sex. Out of a global total of 55.69 million deaths in 2000, 3.86 million were due to acute lower respiratory tract infections, 1.66 million to tuberculosis, 2.94 million to HIV/AIDS, 1.21 million to lung cancer and 3.54 million to a variety of other respiratory diseases, mainly chronic obstructive pulmonary disease (2.52 million). There is also considerable morbidity due to respiratory diseases: it is estimated that, in the UK, about 40% of absence from work is the result of such diseases, approximately 85% of which are transient infections of the upper respiratory tract (Table 14.1).
Aetiological factor | Disease |
---|---|
Genetic | |
Air pollution | |
Occupation | |
Infection |
NORMAL STRUCTURE AND FUNCTION
The respiratory system extends from the nasal orifices to the periphery of the lung and the surrounding pleural cavity. From the nose to the distal bronchi, the mucosa is lined by mainly pseudostratified ciliated columnar epithelium with mucus-secreting goblet cells; this is respiratory mucosa (Fig. 14.1). A portion of the larynx is covered with stratified squamous epithelium.
Lungs
The lower respiratory tract consists of the trachea, bronchi, bronchioles, alveolar ducts and alveoli (Fig. 14.2). (Table 14.2).
Part of respiratory tract | Structure |
---|---|
Trachea | Anterior C-shaped plates of cartilage with posterior smooth muscle. Mucous glands |
Bronchi | Discontinuous foci of cartilage with smooth muscle. Mucous glands |
Bronchioles | No cartilage or submucosal mucous glands. Clara cells secreting proteinaceous fluid. Ciliated epithelium |
Alveolar duct | Flat epithelium. No glands. No cilia |
Alveoli | Type I and II pneumocytes |
The lungs develop from an outpouching of the anterior wall of the primitive foregut at about the fifth week of development. From this tube, two lateral outgrowths appear which eventually form the right and left lungs. These outgrowths are surrounded by mesenchyme from which forms the connective tissue of the respiratory tree. Thus the lungs, like the gastrointestinal tract, develop from endoderm, and developmental abnormalities such as cysts can therefore be lined by either respiratory or gastrointestinal mucosa.
Acid–base balance
Normal acid–base balance in blood is dependent on both efficient alveolar ventilation and perfusion, with consequent successful gas exchange. This leads to the normal partial pressures of O2 and CO2 in arterial blood (Pao2 and Paco2), and a normal blood pH. Various metabolic disease states lead to disturbances in acid–base balance (Fig. 14.3). If the disease becomes chronic, compensatory mechanisms by both the lungs and kidneys operate in an attempt to restore blood pH.
PULMONARY FUNCTION TESTS
Obstructive and restrictive defects
There are two major patterns of abnormal pulmonary function tests: obstructive defects (e.g. asthma) and restrictive defects (e.g. pulmonary fibrosis) (Table 14.3).
Test | Diagnostic significance |
---|---|
Peak expiratory flow rate (PEFR) | Reduced with obstructed airways or muscle weakness |
Forced expiratory volume in 1 second (FEV1) | Reduced with obstructed airways, pulmonary fibrosis or oedema, or muscle weakness |
Vital capacity (VC) | Reduced with reduction in effective lung volume (fibrosis or oedema), chest wall deformity (kyphoscoliosis), or muscle weakness |
Forced expiratory ratio (FEV1:VC) | |
Carbon monoxidetransfer (TCO) | Reduced in pulmonary fibrosis, emphysema, oedema, embolism and anaemia |
Exhaled nitric oxide (NO) | Increased in asthma, bronchiectasis and infections |
Decreased in pulmonary hypertension, cigarette smokers and after treatment with corticosteroids |
These tests are of most value in the follow-up of patients. They can also give an indication as to the possible benefits of treatment; for example, observing the improved FEV1:VC and PEFR after treatment with a bronchodilator would be a measure of the reversibility of the airways obstruction.
RESPIRATORY FAILURE
Respiratory failure can occur as a result of:
DISEASES OF INFANCY AND CHILDHOOD
Developmental abnormalities
Developmental abnormalities include:
TUMOURS
Tumours of the nasal passages and sinuses are uncommon. They may be:
Primary mucosal melanomas of the nose and sinuses are rare but have a very poor prognosis.
Primary extranodal lymphomas are almost always of non-Hodgkin’s type.
Plasmacytomas are tumours composed of plasma cells. They can occur as part of multiple myeloma or as isolated lesions without systemic disease.
INFLAMMATORY DISORDERS
Epiglottitis is caused by capsulated forms of Haemophilus influenzae type B. The epiglottis becomes inflamed and greatly swollen, leading to airway obstruction (Fig. 14.4). Treatment is by intubation, although, rarely, tracheostomy may be necessary; antibiotics are also given to treat the infection.
TUMOURS
Most laryngeal carcinomas arise on the vocal cords (Fig. 14.5), although they may arise above, in the pyriform fossa, or below, as upper tracheal carcinomas. The lesions ulcerate, fungate and invade locally, later causing metastases in regional lymph nodes in the neck and beyond. Symptoms are hoarseness of voice and, later, pain, haemoptysis and dysphagia. Treatment is by chemo-radiotherapy and/or resection. These patients often have widespread mucosal abnormalities throughout the respiratory tract and are at high risk of developing further cancers, especially if they continueto smoke.
THE LUNGS
RESPIRATORY INFECTIONS
The lungs have an internal surface area of approximately 500 m2 which is exposed to the external environment and potentially subjected to inhaled microbes with every breath. It is therefore not surprising that respiratory infections are relatively common, with the World Health Organization projecting such infections to continue as one of the global leading causes of death and disability. Countering the threat of pathogens are the defence mechanisms, any abnormality in which will predispose to infection. Such abnormalities include:
Pneumonia
Pneumonia is usually due to infection affecting distal airways and alveoli, with the formation of an inflammatory exudate. It may be classified according to several criteria (Table 14.4, Fig. 14.6).
Criterion | Type | Example/comment |
---|---|---|
Clinical circumstances | Primary | In an otherwise healthy person |
Secondary | With local or systemic defects in defence | |
Aetiological agent | Bacterial | Streptococcuspneumoniae,Staphylococcus aureus,Mycobacteriumtuberculosis, etc. |
Viral | Influenza, measles, etc. | |
Fungal | Cryptococcus, Candida,Aspergillus,etc. | |
Other | Pneumocystis jiroveci, Mycoplasma, aspiration, lipid, eosinophilic | |
Host reaction | According to dominant component of exudate | |
Anatomicalpattern | Most widely usedclassification before identifying aetiological agent |
Bronchopneumonia
Bronchopneumonia has a characteristic patchy distribution, centred on inflamed bronchioles and bronchi with subsequent spread to surrounding alveoli (Fig. 14.6). It occurs most commonly in old age, in infancy and in patients with debilitating diseases, such as cancer, cardiac failure, chronic renal failure or cerebrovascular accidents. Bronchopneumonia may also occur in patients with acute bronchitis, chronic obstructive airways disease or cystic fibrosis. Failure to clear respiratory secretions, such as is common in the post-operative period, also predisposes to the development of bronchopneumonia.
Affected areas of the lung tend to be basal and bilateral, and appear focally grey or grey–red at postmortem (Fig. 14.7). The inflamed lung parenchyma can be demonstrated by gently pressing on an affected area; normal lung recoils like a sponge, whereas pneumonic lung offers little resistance. Histology shows typical acute inflammation with exudation. With antibiotics and physiotherapy, the areas of inflammation most commonly resolve but may heal by organisation with scarring.
Lobar pneumonia
Pneumococcal pneumonia typically affects otherwise healthy adults between 20 and 50 years of age; however, lobar pneumonia caused by Klebsiella typically affects the elderly, diabetics or alcoholics. Symptoms include a cough, fever and production of sputum. The sputum appears purulent and may contain flecks of blood, so-called ‘rusty’ sputum. Fever can be very high (over 40°C), with rigors. Acute pleuritic chest pain on deep inspiration reflects involvement of the pleura. As the lung becomes consolidated (Fig. 14.8), the chest signs are dullness to percussion with bronchial breathing. The dullness recedes with resolution of the exudate.
The pathology of lobar pneumonia is a classic example of acute inflammation, involving four stages: