tract

Chapter 14 Respiratory tract




COMMON CLINICAL PROBLEMS FROM RESPIRATORY TRACT DISEASE




Pathological basis of respiratory signs and symptoms







































Sign or symptom Pathological basis
Sputum




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).


Table 14.1 Major aetiological factors in respiratory disease





















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).



Table 14.2 Structure of the respiratory tree





















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.


The lungs are divided into lobes: the right lung has three lobes (upper, middle, lower); the left lung has only two lobes (upper and lower). Each lung is formed of 10 anatomically defined bronchopulmonary segments. Each segment is supplied by a segmental branches of the pulmonary artery and bronchus (the bronchovascular bundle). The veins draining adjacent segments often anastomose before they reach the hilum and run principally in the fibrous septae of the lungs.


The respiratory tree is designed to transport clean, humidified air into distal airways and alveoli, where the waste product of metabolism (CO2) is exchanged for O2.


Bronchioles branch until they form terminal bronchioles less than 2 mm in diameter. The respiratory system distal to the terminal bronchiole is called the acinus or terminal respiratory unit, where gas exchange occurs. Small airways, defined as having an internal diameter of less than 2 mm, consist of terminal and respiratory bronchioles. Respiratory bronchioles are involved with gas exchange, having alveoli in their walls. A group of three to five respiratory acini is called a lobule.


The alveoli are lined by flattened type I pneumocytes with occasional type II pneumocytes; the latter are rounded cells with surface microvilli and are believed to be the stem cell population for the alveolus. Type II cells secrete surfactant, and replicate quickly after injury to alveolar walls. Beneath the alveolar cells lie a basement membrane which is shared by the alveolar capillary epithelial cells and some interstitial matrix, including elastin fibres. The structure of the alveolar–capillary membrane permits rapid and efficient diffusion of oxygen and carbon dioxide.


The lung is encased by the visceral pleura which is a thin layer of fibroconnective tissue and elastin with overlying mesothelial cells. The lungs sit within the chest cavity surrounded by the parietal pleura, by the diaphragm, ribs and intercostal muscles, vertebral column and sternum.







PULMONARY FUNCTION TESTS


In normal quiet respiration only a relatively small proportion of the total lung capacity (TLC) is inhaled and exhaled; this is the tidal volume (TV). TLC is made up of the amount of air totally exhaled after maximum inspiration (the vital capacity or VC) and the residual volume (RV). TLC, RV, TV and VC are all easily measured in the laboratory using helium dilution techniques.


In addition to calculating volume parameters, some techniques also assess actual pulmonary function. Spiro-metry measures the amount of exhaled air per second. The maximum volume of air blown from the lungs within the first second after a previous maximum inspiration is called the forced expiratory volume (FEV1). This figure, highly reproducible in each individual, is a measure of small airway resistance. It is also dependent on the patient’s age, sex and size; for example, the small lungs of a child obviously cannot expel as much air as those of an adult. The ratio FEV1:VC compensates to a degree for the variability of lung size. It is possible to inhale more rapidly than exhale because, during inspiration, forces on the airways tend to open them further; during expiration, opposite forces tend to close the airways and thus restrict airflow. For a given lung volume, the expiratory flow rate reaches a peak (PEFR), which is again a measure of airways resistance.


An assessment of the ability of the lungs to exchange gas efficiently can be made by measuring the transfer factor for carbon monoxide (TCO). Air containing a known concentration of carbon monoxide is inhaled; the breath is held for 15 seconds and then exhaled. The amount of carbon monoxide absorbed is a measure of pulmonary gas exchange. TCO is dependent on the concentration of blood haemoglobin, which has a strong affinity for carbon monoxide. Diseases that diffusely affect the alveolar–capillary membrane (such as diffuse pulmonary fibrosis or emphysema where there is loss of alveolar surface area) will result in a low TCO.


Recently the level of nitric oxide (NO) in exhaled air has been added as a useful test; increased levels have been associated with asthma and other causes of bronchial irritation, while decreased levels have been found in cigarette smokers, patients with pulmonary hypertension and during treatment with corticosteroids.



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).


Table 14.3 Respiratory function tests and their diagnostic significance



























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)

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

In obstructive airways disease, RV and TLC are mildly increased due to hyperinflation of the lung while FEV1, FVC and the FEV1: VC ratio is decreased. Clearly, in conditions such as asthma, the results of pulmonary function tests will depend on the clinical state of the patient, whether in an acute attack of asthma or in remission. Restrictive diseases are those that restrict normal lung movement during respiration and are associated with reduced RV and TLC. The FEV1 and VC may be reduced but their ratio remains normal.


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.




DISEASES OF INFANCY AND CHILDHOOD


Respiratory diseases of infancy and childhood are predominantly infectious; such diseases, together with diarrhoea, are the primary cause of death in childhood in the developing world. Rarely disease may arise as a result of either developmental abnormalities or immaturity.



Developmental abnormalities


Developmental abnormalities include:
















lmmaturity


Diseases due to immaturity include:





Hyaline membrane disease or idiopathic respiratory distress syndrome





Hyaline membrane disease (HMD) is almost always seen in premature infants of birth weight less than 2.5 kg. Infants are usually of less than 36 weeks’ gestation, and the incidence of HMD rises as the gestational age decreases. The risk of developing HMD may be decreased by giving mothers oral corticosteroids prior to delivery of the baby as this appears to stimulate surfactant production in the lungs.








INFLAMMATORY DISORDERS


Rhinitis (the common cold) is caused by many different viruses, especially rhinoviruses, although respiratory syncytial virus (RSV), para-influenza viruses, coronaviruses, coxsackieviruses, echoviruses and bacteria, such as Haemophilus influenzae, may also be implicated. Rhinitis may also be caused by inhaled allergens as in ‘hay fever’ where the inflammatory reaction is mediated via type I and type III hypersensitivity reactions (Chs 9 and 10).


Nasal polyps may result from either chronic infective inflammation or chronic allergic inflammation. They consist of polypoid oedematous masses of mucosal tissue infiltrated with chronic inflammatory cells, especially plasma cells; eosinophils may be numerous if allergy is the cause.


Sinusitis is inflammation of the paranasal sinuses; it may be acute or chronic. If the drainage orifice is blocked by inflamed swollen mucosa, an abscess may follow. Cranial osteomyelitis, meningitis or cerebral abscess may then result from sinusitis by direct extension.


Wegener’s granulomatosis, a granulomatous form of vasculitis may involve the nose and upper respiratory tract and present with septal perforation or collapse of the nasal cartilages.


Otitis media is infection of the middle ear, often associated with generalised upper respiratory tract infection (URTI). The Eustachian tube may become swollen and blocked, leading to trapping of exudate in the middle ear. Eardrum perforation may ensue, followed by drainage of the effusion. More serious complications include mastoiditis, meningitis and brain abscess.



TUMOURS


Tumours of the nasal passages and sinuses are uncommon. They may be:




Haemangioma and squamous papilloma are benign lesions, the former often presenting with troublesome epistaxis (nosebleeds). Some squamous papillomas may be caused by human papillomavirus.


Juvenile angiofibromas are rare and occur exclusively in males, usually during adolescence. They are extremely vascular, and surgical removal can be difficult. These tumours contain androgen receptors, explaining the male preponderance.


Squamous cell carcinoma may be well differentiated, producing keratin, or very poorly differentiated. The latter may contain many lymphocytes and have been misnamed ‘lympho-epitheliomas’. Such tumours are most common in South-East Asia and account for 18% of all cancers in China; evidence suggests the Epstein–Barr virus is involved in the aetiology and pathogenesis of squamous cell carcinoma.


Adenocarcinoma of the nasal passages and sinuses occurs more frequently in people who have worked in woodwork and furniture industries. These tumours may present clinically up to 40 years after initial exposure.


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.






THE LUNGS






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).


Table 14.4 Classifications of pneumonia







































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.


Typical organisms include staphylococci, streptococci and Haemophilus influenzae. Patients often become septicaemic and toxic, with fever and reduced consciousness.


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:



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Jun 16, 2017 | Posted by in GENERAL SURGERY | Comments Off on tract

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