PULMONARY DISEASES

Chapter 5 PULMONARY DISEASES



Introduction


The lungs are part of the respiratory system. As such they have a critical role in the exchange of gases—the inhalation of oxygen (O2) and expiration of carbon dioxide (CO2). Pulmonary diseases are a major cause of human morbidity and mortality as evidenced by the following clinical and epidemiologic facts:



Lung diseases can be classified according to their etiology. The relative clinical significance of various pulmonary diseases is presented graphically in Figure 5-1.





KEY WORDS



Anatomy and Physiology




Alveolus (“acinus”) Small saclike part of the lungs forming the smallest respiratory unit of the lungs. It is lined by two cell types: pulmonary pneumocytes type I, which form the air–blood interface, and pneumocytes type II, which secrete surfactant.


Bronchioli Small bronchi that lack cartilage. They are interposed between the bronchi with the alveolar ducts and alveoli and further classified as terminal or respiratory bronchioli.


Bronchus Tubular part of the airways inside the lungs arranged into a branching tree of progressively smaller and smaller ducts connecting the trachea on the proximal side and bronchioli and alveoli on the distal side. Bronchi are lined with respiratory epithelium composed of ciliated and nonciliated cylindrical cells, mucus-secreting cells, and neuroendocrine cells. Their walls contain cartilage and smooth muscle cells.


Compliance Measure of the ability of the lungs to expand in response to increased pressure by the inhaled air.


Diffusion Movement of molecules across a gradient from areas of high concentration to ones of low concentration, until equilibrium is achieved.


Elasticity Ability of a material to return to its normal shape after a force has changed its shape. The elasticity of lungs is measured as a change of pressure in response to changes of the volume of intrapulmonary air.


Larynx Part of the respiratory tract between the pharynx and the trachea, which also acts as voice-generating organ.


Mucus Gel-like substance covering the surface of mucous membranes of air spaces, such as the nose, trachea, and bronchi.


Pharynx Part of the respiratory and alimentary systems connecting the nose with the larynx and the mouth with the esophagus.


Pleura External covering of the lungs composed of a mesothelial layer and underlying connective tissue. The visceral pleura covering the lungs is continuous with the parietal pleura covering the inside of the thoracic cage. The pleural cavity is the space between the visceral and parietal pleura. Normally it contains a few milliliters of serous fluid lubricating the pleural surfaces and allowing them to glide one over another during respiration.


Pulmonary surfactant Complex semiliquid surface-tension–generating material covering the surface of the alveoli. It is essential for keeping the alveoli open during inhalation. The deficiency of surfactant is the cause of neonatal respiratory distress syndrome and hyaline membrane formation in the lungs of premature babies.


Respiration (breathing) Process that includes external and internal respiration. External respiration refers to inhalation of air into the lungs and expiration of air out of the respiratory system, as well the gas exchange between inhaled air and the blood in the lungs. Inhalation provides oxygen, and expiration allows the elimination of carbon dioxide out of the body. Internal respiration refers to cellular processes allowing the transfer of oxygen from red blood cells through the capillary wall into the tissues and intracellular utilization of oxygen.


Trachea Air-conducting tube connecting the larynx with the bronchi.


Ventilation Movement of air in and out of the lungs.


Ventilation/perfusion rate (image/image) Ratio of the overall alveolar ventilation to the overall pulmonary blood flow expressed in liters per minute, normally 0.8.



Clinical and Laboratory Findings and Procedures




Acidosis Decreased blood pH resulting from an abnormal accumulation of acids or a loss of bases from the body fluids. May be classified as respiratory or metabolic.


Alkalosis Increased blood pH resulting from an abnormal accumulation of bases or a loss of acids from body fluids. May be classified as respiratory or metabolic.


Allergy Generic term for many forms of hypersensitivity to foreign substances capable of inducing an immune response. Such substances are called allergens or immunogens.


Anoxia Condition in which the tissues do not receive oxygen. If partial, it is called hypoxia.


Cheyne-Stokes respiration Abnormal respiration characterized by periods of apnea and rapid breathing. Typically apnea lasts 10 to 30 seconds and is followed by a period of rapid and deepening respiratory movements, followed again by slowing down of respiration and apnea.


Cough Process resulting in the forceful expulsion of air from the respiratory tract. It may by mediated by a reflex or a voluntary expiratory effort.


Dyspnea (“shortness of breath”) Sense of difficulty with breathing.


Expectoration Process that results in removal of mucus or tracheobronchial contents during coughing and spitting.


Forced vital capacity Maximum volume of gases that can be exhaled from the lungs as fast as possible over a specified short period of time.


Functional residual capacity Volume of air that remains in the lungs after a normal expiration. It can be calculated by adding the expiratory reserve volume and the residual volume.


Hyperinflation Excessive expansion of the pulmonary air spaces that occurs due to air trapping in asthma or because of the loss of alveolar walls in emphysema.


Hyperpnea Increased depth of respiratory movements without an increased number of respirations.


Hyperventilation Increased alveolar air exchange leading to increased exhalation of carbon dioxide and hypocapnia.


Inspiratory capacity Volume of air that can be inhaled after a normal exhalation. It can be calculated by adding the tidal volume to the inspiratory reserve volume.


Intubation Passage of a tubular instrument into the air spaces, typically through the nose or the larynx. It is used to facilitate or maintain the air flow into the lungs or administer inhalational anesthetics.


Kussmaul respiration Form of abnormal breathing characterized by increased depth and rate. It is typically encountered in acidosis, especially lactic acidosis of diabetes.


Rales (“crackles”) Abnormal sounds heard over the regions of the thorax by auscultation during inspiration. These sounds result from the accumulation of fluid or exudates in the alveoli.


Shunting Process during which a stream of blood or air is diverted from its normal flow through expanded normal, newly formed or pathological passages.


Tachypnea Rapid breathing rate.



Pulmonary Diseases




Acute respiratory distress syndrome (“shock lung”) Clinical syndrome caused by numerous exogenous and endogenous insults leading to diffuse alveolar-capillary unit damage (DAD). Most often caused by shock, airborne or blood-borne infections, chemical or physical injury of the lungs, or systemic metabolic disorders.


Asthma Inflammatory disease characterized by reversible obstruction of the air passages due to bronchospasm and oversecretion of mucus.


Atelectasis Process in which the lungs become airless and the alveolar spaces collapse.


Bronchiectasis Chronic lung disease characterized by irreversible dilatation of bronchi and bronchioli caused by inflammation, obstruction, or fibrosis, or various destructive changes in the peribronchial lung parenchyma.


Bronchitis Inflammation of bronchi that may be acute or chronic. It may be caused by viral or bacterial infection or chronic irritation, as seen in smokers. Clinically it presents with cough and expectoration of mucus or mucopurulent exudate.


Chronic obstructive pulmonary disease (COPD) Chronic lung disease caused by chronic bronchitis or emphysema or both. It is most often caused by smoking. Clinically it manifests as progressive dyspnea and signs of obstructive lung disease leading to respiratory insufficiency.


Emphysema Chronic condition caused by destruction of alveolar septa and dilatation of terminal air spaces. It occurs in several pathologic forms (e.g., centriacinar or panacinar), and clinically it manifests as chronic obstructive pulmonary disease. It may be a consequence of congenital α1-antitrypsin deficiency.


Empyema Localized accumulation of pus in the pleural cavity.


Hypersensitivity pneumonitis Group of lung diseases caused by a cellular immune reaction to exogenous organic allergens inhaled into the alveoli. These diseases are often related to the workplace and are known as farmer’s lung, pigeon breeder’s lung, and air conditioner lungs, among others.


Kartagener’s syndrome Congenital ciliary dismotility disorder characterized by recurrent respiratory infections (sinusitis and bronchiectasis), situs inversus, and infertility in males (sperm immotility).


Lung cancer Group of malignant tumors originating from the bronchi or terminal bronchioli and pleura. Most often caused by smoking. Microscopically, lung cancer can be classified as squamous cell carcinoma, adenocarcinoma, or large- or small-cell undifferentiated carcinoma. Clinically these tumors are divided for practical purposed into two groups: small-cell carcinoma and nonsmall-cell carcinoma, including all the other microscopic variants.


Mesothelioma Malignant tumor of the pleura, often related to asbestos exposure.


Pleural effusion Accumulation of fluid in the pleural cavity. It may represent a transudate, as occurs in chronic heart failure, or generalized anasarca; or it may be an exudate, as is seen in infectious pleuritis. Tumors also cause pleural effusion (“malignant pleural effusion”).


Pleuritis Inflammation of the pleura. It may be a complication of pneumonia or it may begin as a primary infection.


Pneumoconioses Group of chronic lung diseases caused by inhalation of inorganic and organic particles, chemical fumes, and vapors. Typical entities included under this heading are coal worker’s pneumoconiosis, silicosis, asbestosis, and conditions such as farmer’s lung, bagassosis, byssinosis, and various occupational lung disease caused by vapor inhalation.


Pneumonia Inflammation of the lungs. It can be acute or chronic and involve predominantly either the alveoli (“alveolar pneumonia”) or alveolar septa (“interstitial pneumonia”). Pneumonia may be patchy (“lobular pneumonia” or “bronchopneumonia”) or diffuse (“lobar pneumonia”).


Pneumothorax Accumulation of air in the pleural cavity.


Pulmonary hypertension Increased pressure in the pulmonary circulation, typically reaching 25% of the systemic blood pressure. It may be primary, of unknown origin, or secondary, due to left heart failure and chronic lung disease or pulmonary emboli.


Restrictive lung disease Group of pathogenetically unrelated diseases characterized by reduced volume of terminal air spaces or an inability of the lungs to expand adequately during inspiration. Restrictive lung disease can be distinguished from obstructive lung disease by functional testing. This group of disease includes several forms of chronic interstitial pneumonia of unknown origin, dust-induced pneumoconioses, drug- and radiation-induced lung diseases, hypersensitivity pneumonias, and diseases of presumed immune origin such as sarcoidosis.


Sarcoidosis Systemic disease of unknown origin, characterized by the formation of noncaseating granulomas in the lungs, thoracic lymph nodes, and many other organs.


Usual interstitial pneumonia (UIP, idiopathic pulmonary fibrosis) Chronic restrictive lung disease causing irregular destruction of lung parenchyma associated with chronic alveolitis and patchy interstitial fibrosis (“honeycomb lungs”). In most instances the cause of UIP is unknown. The disease is incurable.



Normal Structure and Function



ANATOMY AND HISTOLOGY


The respiratory system is arbitrarily divided into two parts: (1) the upper respiratory system, comprising the nose, pharynx, and larynx, and (2) the lower respiratory system, comprising the tracheobronchial tree and the lungs (Fig. 5-2). In this chapter we concentrate on the lower respiratory tract, its functions, and diseases.




The respiratory tract is lined with specialized epithelia and encased by specialized support structures.


The main function of the respiratory system is to maintain external respiration. In other words, the respiratory system must enable the body to inhale and exhale air and make the exchange of gases between the blood and the air possible. Various parts of the respiratory system must thus be lined with specialized epithelia that support these functions.


The nasal and tracheobronchial mucosa. The epithelium of the nasal and tracheobronchial mucosa is pseudostratified and contains mucus-secreting and ciliated cells. The mucus-secreting cells produce mucus, which keeps the air spaces moist and also serves as a mechanical protective barrier and a receptacle for foreign particles and bacteria. The submucosa also contains larger mucous glands, which contribute mucus and fluid that covers the surface of the air spaces. Note that the epithelium of the mucosa also contains scattered neuroendocrine cells, the function of which has not been fully elucidated. Stem cells, which are important for the replacement of the more differentiated mucosal cells under both physiologic and pathologic conditions, are also scattered throughout the submucosa.


Because the nasal air spaces and the tracheobronchial tree need to be kept patent, their walls contain cartilage. Bony structures in the nasal air passages have the same protective functions. In the tracheobronchial tree the air spaces contain smooth muscle cells, which are thought to regulate the contraction or dilatation of these air spaces designed for conductance and distribution of air in the lungs.


The caliber of the air spaces diminishes gradually, and as the air duct branches their diameter decreases. Their structure also changes. Most notably, as the bronchi become smaller and smaller they contain less and less cartilage, and ultimately they transform into bronchioli, which are devoid of cartilage. Finally, the smallest air ducts, called terminal bronchioli, transform into respiratory bronchioli, which open up into alveolar sacs and alveoli.


Alveoli. These terminal parts of the respiratory system are lined with type I and type II pneumocytes. Type II pneumocytes produce surfactant, a surface-active substance that maintains alveolar patency. Type I pneumocytes are in close contact with alveolar capillaries and form with them the alveolar-capillary units, the elementary respiratory functional units of the lung.





Several cellular systems protect the lungs from airborne pathogens, allergens, and harmful particulate material.


The air inhaled through the nose or the mouth contains potentially noxious agents, including viruses, bacteria, and various organic and inorganic particles. The most important protective mechanisms (Fig. 5-5) are as follows:



Mucociliary clearance. The mucus produced by the goblet cells in the nasal mucosa or the tracheobronchial epithelium covers the entire surface of the air-conducting tubular part of the respiratory system. The bronchi also contain mucous glands. The mucus they secrete consists of glycosaminoglycans, glycoproteins, and complex carbohydrates. The mucus can bind living pathogens and other particulate matter. Bactericidal substances in the mucus, such as properdin, or immunoglobulin A, act on bacteria. Mucus also contains macrophages, which phagocytose or kill bacteria. These bacteria and other particulate matter are moved up the tracheobronchial tree through the ciliary movement of the columnar cells in the tracheobronchial epithelium. This mucociliary escalator system will, under normal circumstances, eliminate most of the particles that measure 2 to 10 μm in diameter, but particles that are smaller than 2 μm may reach the alveoli. Such particles are usually taken up by alveolar macrophages and either are expectorated or enter into the interstitial spaces and ultimately are carried by the lymph into the local lymph nodes.




Lymphatic clearance. Foreign material taken up by the alveolar macrophages is transported by the lymphatics. Although the alveoli do not contain lymphatics, well-formed lymphatic channels are recognizable at the level of alveolar ducts. The lungs have an extensive lymphatic drainage system, which extends from the alveolar ducts, along the interlobular septa, to the connective tissue surrounding the blood vessels and bronchi. The lymph from both lungs, except for the left upper lobe, drains into the right lymphatic duct; the left upper lobe drains into the thoracic duct.


Pulmonary immune response. Along the intrapulmonary lymphatics and in the mucosae of the bronchi are aggregates of nonencapsulated lymphoid tissue that form the so-called mucosa-associated lymphoid tissue (MALT). These lymphoid follicles serve as mechanical barriers but are also the main source of immune cells that protect the lungs from bacteria and foreign allergens. The immune response typically includes both T and B cells. The lungs also contain numerous resident macrophages and antigen-presenting cells such as Langerhans cells. Hence some cell-mediated immune reactions, such as those that occur in response to exposure to Mycobacterium tuberculosis or fungi, result in granuloma formation.





PHYSIOLOGY





Transfer of gases in the alveolar-capillary unit occurs by simple diffusion.


The transition of O2 from air into the blood and CO2 from blood to the air occurs through diffusion across the alveolar lining and the basement membranes of the alveolar capillaries (Fig. 5-7). This process is governed by Fick’s law as stated here:





image




Fick’s law indicates that the diffusion of gases is directly proportional to the surface area of the alveoli and inversely proportional to the thickness of the tissue that prevents diffusion. In practice this diffusion rate is determined by measuring the inhalation efficiency of CO, a gas that has high solubility in blood and can be readily measured after inhalation in both the alveolar spaces and the blood.





Oxygen pressure in inspired dry air is higher than in the humidified air in the trachea or the alveoli or the oxygenated arterial blood leaving the lungs.


Assuming that the air contains 21% O2, at sea level the oxygen pressure in dry inhaled air is 160 mm Hg (760 × 0.21 = 160). This air is humidified during its passage through the nose and trachea, which brings down the oxygen pressure to 150 mm Hg (see Fig. 5-7). As the air passes into the alveoli, the oxygen pressure drops to 100 mm Hg. This is in part due to the fact that oxygen diffuses rather rapidly into the blood and is also diluted with CO2 diffusing from the venous blood into the alveoli.


Theoretically the oxygen pressure in the alveoli should be the same as that in the pulmonary artery branches. However, the arterial oxygen pressure is lower than that in the alveoli, and thus the ventilation/perfusion ratio (image/image) is normally 0.8. This defect results from the admixture of venous bronchial blood entering the pulmonary veins and a small amount of pulmonary venous blood that bypasses the alveoli through a physiologic right-to-left shunt and is not oxygenated. Approximately 2% of the normal cardiac output bypasses the alveoli. image/image ratio is reduced in many lung diseases.





Breathing is an involuntary action that is under the control of the respiratory center in the brainstem.


Breathing is a vital function that is tightly controlled by the central nervous system, which receives impulses from the periphery and then sends efferent signals to the periphery (Fig. 5-8). The key anatomic foci of the respiratory control sensory and effector system are as follows:




Respiratory centers. Respiration is controlled by three centers in the brainstem: the medullary respiratory center, the apneustic center, and the pneumotaxic center. Automatic respiratory movements are under the control of the inspiratory center in the dorsal medulla, which receives the stimulatory impulses from the peripheral sensors, mostly through the glossopharyngeal and vagus nerves. Efferent signals are sent to the diaphragm through the phrenic nerve. The expiratory center located in the ventral medulla is dormant because expiration is normally a passive process. It becomes activated, however, during exercise. The inspiratory center also receives positive stimuli from the apneustic center in the lower pons. This center prolongs the inspiratory gaps (“apneusis”) by prolonging the contraction of the diaphragm. The pneumotaxic center in the upper pons inhibits respiration by reducing the tidal volume, but it does not affect the rhythmicity of breathing.


Cerebral cortex. Respiration can be controlled to a certain extent by voluntarily cortical stimuli. Hyperventilation can be induced relatively easily, but once the arterial partial pressure of carbon dioxide (Paæ{2) falls below a critical level, the person loses consciousness and automatic respirations resume. Hypoventilation can also be induced but it does not last long because the reduction of the arterial partial pressure of oxygen (Pa{2) and increased Paæ{2 are strong stimuli for the resumption of respiration.


Chemoreceptors. Chemoreceptors can be classified as central or peripheral.





Mechanoreceptors. Receptors responding to stretch in the smooth muscles of the bronchi activate the Hering-Breuer reflex, which slows down respiration by prolonging the expiratory time. Stretch receptors found in the skeletal muscles and joints may also increase the respiratory rate.


Irritant receptors in the mucosa of the bronchi react to chemical stimuli and particles, causing bronchoconstriction, which also increases the rate of respiration. Irritant receptors are important for initiating coughing, which can, however, also be triggered by the stimuli reaching the mechanoreceptors. Likewise, the irritant receptors in the nose are important for the initiation of sneezing. Irritant receptors are linked to C type nerve fibers, which also transmit pain.



The volume of air entering and leaving the lungs during inspiration and expiration can be measured objectively under controlled circumstances.


Normal breathing occurs in a cycle that includes four phases: rest, inspiration, a rest phase, and expiration. By measuring the volume of air entering the lungs during inspiration and leaving it during expiration the critical aspects of respiratory capacity can be defined as illustrated in Figure 5-9. By convention these static lung volumes are defined as follows:



image Tidal volume (VT)—the amount of air entering and leaving the lung with each breath in a person who is breathing normally. In adults it measures approximately 500 mL.


image Functional residual capacity (FRC)—the amount of air remaining in the lungs after expiration in a person who is breathing normally. FRC cannot be measured by routine spirometry, but can be measured by the helium dilution method, the nitrogen washout technique, or whole-body plethysmography.


image Expiratory reserve volume (ERV)—the amount of air that can be exhaled from the lungs by forceful expiration.


image Residual volume (RV)—the amount of air remaining in the lungs after forceful expiration. RV is calculated by subtracting ERV from FRC (RV = FRC − ERV). In young adults it accounts for 20% of the total lung capacity. It increases by 1% per year and in older individuals it accounts for more than 60% of the total lung capacity.


image Inspiratory reserve volume (IRV)—the amount of air that can be forcefully inhaled in addition to the VT.


image Inspiratory capacity (IC)—the amount of air that can be inhaled into the lungs in addition to the air accounting for the FRC (IC = VT + IRV).


image Vital capacity (VC)—the amount of air expelled from the lungs during forceful expiration.


image Total lung capacity (TLC)—the total amount of air inside the lungs and the bronchial tree after maximal inspiration.


image Forced vital capacity (FVC)—the amount of air that can be expelled from the lungs if a person is told to exhale as fast as possible. Normally FVC does not differ from VC. However, FVC can be prolonged due to air trapping that occurs in persons who have emphysema.


image Forced expiratory volume (FEV1)—the amount of air that can be expired in 1 second following maximal inspiration. FEV1 in healthy young adults is normally 80% of the forced vital capacity (FEV1/FVC = 0.8), but with aging FEV1 is reduced to 65% to 70%. FEV1/FVC is effort-dependent and is influenced by increased expiratory effort. In obstructive lung diseases FEV1 is reduced (FEV1/FVC < 70%). In restrictive lung diseases, both FEV1 and FVC are reduced (FEV1/FVC > 70%).


image Forced expiratory flow rate (FEF25–75%)—the rate of air flow over the middle (25% to 75%) half of the FVC. It is also called maximal midexpiratory flow rate and is considered to be the most sensitive parameter for identifying early obstruction. It reflects the status of small airways and it is effort-independent.






Clinical and Laboratory Evaluation of Pulmonary Diseases


The evaluation of patients who may have lung diseases includes a complete history and physical examination, with special emphasis on symptoms that may be related to respiratory problems. In addition chest radiographs, laboratory test data, and acid–base balance must be reviewed. Spirometry and testing of respiratory function may be indicated. Bronchoscopy, thoracentesis, and fine-needle or tissue biopsy are required in certain conditions.




SIGNS AND SYMPTOMS OF LUNG DISEASES


The most important signs and symptoms of lung diseases are as follows:




Dyspnea is a sensation of breathlessness out of proportion to the level of physical activity.


Dyspnea, also known as shortness of breath, is a subjective sensation of difficult breathing. The patients describe it as strained breathing or simply state that they are “short of breath.” As stated by a famous pulmonary physician, “Dyspnea is not tachypnea, hyperpnea, or hyperventilation but difficult labored and uncomfortable breathing.”


Elemental sensations include tightness in the chest, excessive ventilation, excessive frequency, and trouble breathing. These sensations have an objective aspect based on the integration of physiologic sensory impulses reaching the respiratory centers of the brainstem and a subjective aspect depending on the cortical perception of the efficiency of respiration. The objective impulses from central and peripheral chemoreceptors responding to blood oxygen levels, CO2 content, and pH, and mechanoreceptors in the pulmonary parenchyma, airways, and respiratory muscles, can be measured. The subjective perception is, however, less quantifiable and varies from one person to another.


As discussed in Chapter 4, dyspnea can be classified as cardiac or noncardiac, acute or chronic. The most important causes of dyspnea are listed in Table 5-2.


Table 5-2 Causes of Dyspnea

















































TYPE OF DYSPNEA PATHOGENESIS CLINICAL CONDITIONS
Pulmonary dyspnea Obstruction of airways
Alveolar filling
Interstitial lung disease
Pulmonary artery obstruction
Pleural disease
Cardiac dyspnea Left heart failure Myocardial infarction
Pericardial disease Pericardial tamponade
Endocardial defect Chronic endocarditis
Other forms of dyspnea Loss of RBC/Hb/O2 transport
Hypoperfusion of lungs Multiple organ failure (shock)
Psychogenic Anxiety, panic attack
Neuromuscular diseases Myopathy/muscular dystrophy
Thoracic deformities Kyphoscoliosis

RBC/Hb/O2, red blood cell/hemoglobin/oxygen.


Patients can usually grade their dyspnea as mild, moderate, or severe, and whether it is related to physical activity or also occurs at rest. The precipitating cause can often be identified.


Patients also can describe the time of onset and the duration of shortness of breath. The timing of dyspnea provides important diagnostic clues, as listed in Table 5-3.


Table 5-3 Classification of Dyspnea by Type of Onset



















ARDS, acute respiratory distress syndrome; COPD, chronic obstructive pulmonary disease.


Data from Warrell DA, Cox TM, Firth JD (eds): Oxford Textbook of Medicine, 4th ed. Oxford, Oxford University Press, 2003.



Cough involves a reflex that can be triggered by a wide variety of stimuli.


Cough is a defense mechanism based on a reflex, which can be initiated by chemical or mechanical irritants or by voluntary action. The irritants, such as chemicals or foreign bodies reaching the larynx or the lower respiratory tract mucosa, act on mechanoreceptors and nociceptors. These receptors are connected to C type nerve fibers that serve as the conduit for pain impulses, leading them into the medulla oblongata through the vagus nerve. In the medulla the impulses trigger the efferent reaction that has three phases:





Cough may be clinically classified as acute, lasting a few days or a week or two, or chronic if it last more than 3 weeks. It may be accompanied by bleeding or sputum production (productive cough). Some irritants that cause cough may also cause bronchospasm, and in such cases cough is associated with wheezing (e.g., in asthma). Cough may be the only complaint, but often it is just one of the symptoms of a complex disease such as asthma or bronchopneumonia. The most important causes of cough are listed in Table 5-4.


Table 5-4 Causes of Cough



















ACE, angiotensin-converting enzyme; COPD, chronic obstructive pulmonary disease; GERD, gastroesophageal reflux disease.





Hemoptysis may present as mild, in the form of blood-stained sputum, or massive and life-threatening.


Hemoptysis is defined as expectoration of blood from the respiratory tract. Most often it originates from the bronchial arterial circulation, but it may have other sources as well. Remember that the bronchial arteries are part of the greater arterial system, and the blood in these arteries circulates under much higher pressure than the blood in the pulmonary venous or arterial circulation, which are low-pressure systems. Hence, if these vessels rupture, the bleeding occurs under much higher pressure than if it stemmed from pulmonary arteries and veins. However, if the pressure inside the pulmonary circulation rises, as in pulmonary hypertension, bleeding may occur from other vessels as well. Tumors may cause bleeding by eroding into any blood vessel. Autoimmune diseases, such as Wegener’s granulomatosis or Goodpasture’s syndrome, may cause vascular lesions, leading to a rupture of various blood vessels from small capillaries to larger arteries and veins. The most important causes of hemoptysis are listed in Table 5-5.


Table 5-5 Sources and Causes of Hemoptysis










SITE LESION/CAUSE DISEASES
Bronchi

Oct 29, 2016 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on PULMONARY DISEASES
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