The normal lung is capable of receiving and distributing a large flow of air and blood to its alveoli. In emphysema, the elastic recoil of the lung decreases with loss of alveolar septa, presumably because the reduced alveolar surface area exerts a lower surface tension. Inspiration lowers alveolar pressure, allowing air to flow into the lungs; the bronchiole dilates when the pressure in the surrounding alveoli is less than that within the lumen of the bronchiole. Conversely, in expiration, the airways are compressed because the alveolar pressure surrounding the bronchiole exceeds that within the bronchiolar lumen. There is a greater tendency for airflow obstruction during expiration. In emphysema, bronchiolar obstruction due to loss of alveolar structure is irreversible.

The bronchial glands and goblet cells may be hypertrophied, producing excessive amounts of mucus, which frequently obstructs bronchiolar lumina. One aspect of therapy focuses on increasing the fluidity and mobility of mucus. Submucosal edema and cellular infiltration cause a thickening of the bronchiolar wall and narrowing of the lumen. Because vasodilatation often leads to edema, another aspect of treatment is to cause vasoconstriction by means of alpha-adrenergics. The smooth muscle may be hypertrophied in bronchitis or asthma, narrowing the lumen. Adrenergic drugs are used to smooth the muscle. COPD is usually insidious, existing in an asymptomatic unrecognized form for years prior to the appearance of noticeable dyspnea on exertion. With mild to moderate COPD, bronchiolar obstruction is found in a patchy distribution throughout the lungs. This results in uneven ventilation/perfusion ratios, which will be discussed at the end of this section. The less involved, better-ventilated lung units become insufficient to compensate for the more involved, poorly ventilated units in cases of advanced COPD or superimposed viral or bacterial infections.

Severe arterial hypoxemia is likely to increase production of erythropoietin, which stimulates the bone marrow causing erythrocytosis. This erythrocytosis may be either useful or harmful. The higher hemoglobin associated with increased O₂ capacity is good; but the increased blood volume in the presence of a failing heart is not. Increased blood viscosity causes a harmful resistance to blood flow through the lungs and coronary vessels. Early medicine utilized phlebotomies to treat hypoxia instead of O₂. This resulted in a stimulus for increased erythropoiesis causing a snowball effect.

Patients with severe bronchitis have mismatched ventilation/­perfusion. This leads to arterial hypoxemia, secondary erythrocytosis, and cor pulmonale with congestive heart failure. They are called blue bloaters due to their cyanosis and edema, or anasarca. A patient with severe emphysema may have decreased cardiac output and a relatively small heart, but as long as he/she can effectively hyperventilate and match ventilation/perfusion, he/she will not develop hypoxemia. They are called pink puffers because they maintain a near normal PaO₂ and are hyperpneic.

Auscultation

Auscultation of the lungs provides information about the airflow through the tracheobronchial tree and the presence of fluid, mucus or obstruction of the airway. Vesicular breath sounds are normally heard over the chest. They are soft and low in pitch. Bronchovesicular breath sounds are medium in intensity and pitch and heard over the large, main stem bronchi. Bronchial breath sounds are loud and high in pitch and normally heard over the trachea. One type of bronchial breath sound rarely heard is the amphoric breath sound heard over a thick walled cavity that communicates freely with a large sized bronchus. The sound resembles blowing over the top of a wine bottle. Vesicular breath sounds last longest on inspiration and when airflow to an area is diminished, they may be decreased or absent. Bronchial breath sounds are longest on expiration. Consolidation of lung tissue, as occurs in pneumonia, blocks the passage of air through the affected area and prevents the exchange of sound quality.

Remember that a patient with particularly severe asthma may have a rather quiet chest on auscultation. This is probably because airflow is so slow that it can no longer generate much sound. Breath sounds will also be absent or decreased in COPD. This is caused by lung distention and poor transmission of sound to the chest wall.

Abnormal breath sounds (adventitious or “added”) include rales, rhonchi, wheezes and pleural friction rubs. Rales are noisy murmurs caused by passage of air through liquid. Moisture causes a sound like soda fizzing, cellophane crinkling, or the sound you hear when you roll your hair between your fingers near your ears. Rales are usually heard on inspiration. Coarse rales may clear after a cough but fine rales near the bases of long fields rarely do. Rales are sometimes called “crackles.” The crackles of interstitial lung disease, such as fibrosing alveolitis, are typically heard on late inspiration as opposed to crackles from secretions.

Rhonchi are rumbling, snoring or rattling sounds caused by obstruction of a large bronchus or the collection of secretions in a large bronchus. They are most prominent on expiration. Another name for rhonchus is a “wheeze.” Snoring sounds are called sonorous rhonchi, and high-pitched musical sounds are called sibilant rhonchi. Wheezes may be audible without a stethoscope.

Pleural friction rubs occur when the pleural fluid that normally lubricates the pleura is decreased or absent. The membranes rub together causing a loud creak or a soft click that resembles a grating sound. They are heard on inspiration and expiration and are associated with pain and splinting.

Ventilation/Perfusion (V/Q) Ratio

Effective gas exchange depends on uniform distribution of function throughout the lung. Ventilation must be distributed to 300 million alveoli through 23 generations of branching airways along with blood distribution through a myriad of capillaries. Even in normal lung function, distribution is not uniform. There is a gravity-dependent gradient of pleural pressure in the upright lung of about 0.3 cm H2O pressure/cm vertical distance. The pleural pressure over a normal adult lung 30 cm in height is about 9 cm H2O more negative at the apex than at the base. Lung units near the lung apex are distended by a greater trans­pulmonary pressure and are more fully inflated than those at the base.

Blood flow, like ventilation, is least at the apex and increases down the lung. However, alveolar ventilation and perfusion are not evenly matched, so the gradient of perfusion is steeper than that of ventilation. The average V/Q (Ventilation-Perfusion Ratio) is 0.8.

In regions of the lung where the V/Q ratio is increased above normal, wasted ventilation occurs. This has the effect of adding a space that is ventilated but does not participate adequately in gas exchange. An extreme example can occur when perfusion is virtually eliminated, by a blood clot or following ligation of a pulmonary artery.

Ventilation of regions of the lung with high V/Q ratios is partly wasted and contributes to alveolar dead space ventilation. In decreased states, this is not uncommon. It results in hyperventilation and increased work of breathing.

When ventilation is impaired without decreased blood flow or when perfusion continues to non-ventilated regions of the lung, as in atelectasis, there is a decreased V/Q. Gas exchange is extremely impaired or absent and perfusing blood is poorly oxygenated. Hyperventilation can help hypercapnia, but not hypoxemia. The addition of poorly oxygenated blood from areas of low V/Q to normally oxygenated blood acts like a shunt. This “physiologic shunting” must be differentiated from true venous admixture produced by an “anatomic” shunt.

A shunt study can be performed by having the patient breathe 100% O₂ for 20 minutes and then obtaining arterial blood gases. True venous admixture will not be changed by breathing 100% O₂. Use extreme caution in some patients, however, making sure hypoxic drive is what is keeping them ventilated.

Clinical Features of COPD:

History & Physical Findings

Patients with COPD have at least one symptom in common: undue breathlessness on exertion. Chronic bronchitis is unusual in nonsmokers and is more common in men than in women. Cough is often worse on arising due to accumulation of secretions while sleeping. Wheezing and exercise intolerance are often present and tend to worsen during acute infections of the lower respiratory tract. The sputum may become mucopurulent or purulent. Unless the patient has a hobby or job that requires strenuous exertion, the disease may go unnoticed until quite extensive.

In general, the COPDer appears anxious and malnourished, and complains of lost appetite, use of accessory muscles, muscle atrophy, jugular engorgement, cyanosis, and digital clubbing.

The COPDer’s chest will have increased AP diameter, barrel chest, or hyper-resonant chest, with decreased breath sounds and adventitious breath sounds. Their ventilatory pattern may include paradoxical movement of the abdomen, prolonged expiratory time, active exhalation and pursed lip breathing. In advanced disease, peripheral edema may be present.

Asthmatics who show some degree of persistent airway obstruction and exertional dyspnea are classified as COPD. The accompanying cough is often paroxysmal, and wheezing is severe. Asthma can be brought on by intrinsic or extrinsic factors. An example of an intrinsic factor would be an emotional upset that brings on an attack; extrinsic factors would include specific allergens, etc. Usually by the time an emphysema patient reaches the fifth decade, dyspnea is the primary complaint. Hyperventilation may be present if the patient becomes anxious, but true orthopnea is uncommon unless heart failure is present.

The history may be helpful to distinguish other conditions like chronic pulmonary fibrosis, recurrent pulmonary thromboembolism, polycythemia vera, the diseases of hypoventilation, and myxedema. Aerophagia with gastric distension causes early satiety. Patients often complain of upper abdominal soreness, distention, and fullness, or even epigastric pain. It is important to note that 20 to 25% of emphysema patients develop ulcers at some stage of their disease.

With deteriorating blood gases, there will be gradual impairment of mental acuity, memory, and judgment, along with headache and insomnia. Patients with cor pulmonale complain of easy fatigability, and may have anterior chest pain and palpitation on exertion. With right heart failure, ankle edema appears and liver enlargement with or without ascites develops.

Clinical features of bronchiectasis principally include a chronic, loose cough with mucopurulent, foul-smelling sputum. In advanced cases, the mucus settles out into three layers: cloudy on top, clear saliva in the middle, and cloudy, purulent material on the bottom. It is frequently associated with chronic paranasal sinusitis. Hemoptysis, occasionally severe, occurs in at least a half of all cases. Advanced cases result in chronic malnutrition, sinusitis, clubbing, cor pulmonale and right heart failure. Physical signs are variable; rales may be present at times. A plain chest film may not be helpful if dilatations of air fluid levels are not present.

Often the diagnosis of the disease can be made from history alone. It is confirmed by bronchography after vigorous treatment for at least one week. A lung resection may be indicated. Iodized oil and iodine in water have been the standard contrast media for many years. Powdered tantalum appears to offer a reliable substitute without the risk of iodine sensitivity. (We will be learning more about roentgenologic features in the next section.) Bronchoscopy in bronchiectasis often reveals a deep velvety red mucosa with pus swelling up from areas of involvement. Gram stains may show fusospirochetal organisms and cultures will reveal common mouth flora and anaerobic streptococci or others. Microscopic exam of sputum may show necrotic tissue, muscle fibers and epithelial debris.

Roentgenologic Features

Correlation among symptoms, physical findings, and the appearance of chest x-rays is often poor in COPD. Films of moderately advanced disease can be read “essentially normal,” but at least they can be used to rule out other complications. In acute asthma, hyperlucency may mask emphysema, but will clear after attack. Emphysema patients will show attenuation of the peripheral pulmonary vasculature. Those with alpha-1-antitrypsin will have scarcity of vascular markings in bases, and hilar shadows present.

“By far the best ways to treat COPD are to catch it early and to stop smoking.”

Increased prominence of the basal vascular markings is often seen in patients with severe chronic bronchitis or bronchiectasis, with or without emphysema. In patients with pulmonary hypertension and right ventricular enlargement, classically there is prominence of the main pulmonary artery segment, bulging of the anterior cardiac contour into the retrosternal space, and enlargement of the right and left pulmonary artery shadows. In combined right and left ventricular failure, the transverse diameter of the heart is widened, and the basal vascular markings show increased prominence. Comparison with x-rays previously taken may show progressive flattening of the diaphragm, increased radiolucency of the lung fields, increased size of bullous areas, and increased heart size.

The best radiologic criteria for the presence of emphysema is a flattened diaphragm, as seen in lateral view, and an increased depth of the retrosternal space of more than 3 cm between the anterior wall of the origin of the ascending aorta and the sternum. Fluoroscopy in COPD may be helpful because radiolucency of the lung bases tend to persist during forced expiration, in contrast to the increased density seen in normal subjects. Expiratory films should be obtained four or five seconds after the command to exhale is given, to allow time for the full effects of airway obstruction to be registered. CT Scans and modern MRI’s have replaced most need for older lung laminagrams to demonstrate size and location of bullae. Lung photoscans following intravenous injection of macroaggregated particles of serum albumin tagged with iodine are helpful in demonstrating areas of non-perfused or under-perfused areas. Occasionally, Xenon scans are used for this purpose. Pulmonary arteriograms may be indicated to rule out embolism.

EKG Aspects

The electrocardiogram is often normal in early or moderate emphysema. One of the most frequent changes in COPD is a shift of the P wave axis toward the right, often greater than +80 degrees in the frontal plane. Observing the P wave in a VL easily assesses this; it is isoelectric at the +60 degree axis and becomes increasingly negative as its axis moves further to the right, greater than +60 degrees. The P waves frequently are symmetrically peaked in leads II, III, and a VF; and when their height is 2.5 mm or more they are classified as “P pulmonale.”

The QRS complexes often show low voltage in both the limb leads and the precordial leads, especially leads V5- 6. The mean QRS axis is displaced posteriorly and superiorly and shifted toward the left (clockwise rotation). The frontal electrical axis is often vertical, frequently more than +70 degrees. Superior rotation of the electrical vector manifested by a late R wave in a VR ABG gives rise to a SI, SII, SIII pattern with an indeterminate mean axis. With more severe rotation, axes greater than -30 degrees (left axis deviation) may be seen.

When right ventricular hypertrophy develops as a result of increased pulmonary vascular resistance and pulmonary hypertension, the QRS vector shift anteriorly and to the right. R waves then appear in the right precordial leads. Complete right bundle branch block is occasionally observed.

The QRS abnormalities may sometimes simulate those of myocardial infarction, particularly of the inferior portion of the heart. The presence of abnormal pulmonale-type P Ò26 waves suggests that emphysema is the sole cause of the EKG abnormality.

“Chronic obstructive pulmonary disease (COPD) is characterised by poorly reversible airflow obstruction and an abnormal inflammatory response in the lungs.  The latter represents the innate and adaptive immune responses to long term exposure to noxious particles and gases, particularly cigarette smoke. People with COPD are at increased risk of developing heart disease, lung cancer and a variety of other conditions especially if its due to smoking.  Inflammation is present in the lungs, particularly the small airways, of all people who smoke. This normal protective response to the inhaled toxins is amplified in COPD, leading to tissue destruction, impairment of the defence mechanisms that limit such destruction, and disruption of the repair mechanisms. In general, the inflammatory and structural changes in the airways increase with disease severity and persist even after smoking cessation.”

National Library of Medicine NIH

Etiology

By far the most common etiological cause of COPD remains smoking. Even after the client quits smoking, the disease process continues to worsen. Air pollution and occupation also play an important role in COPD. Smog and second-hand smoke contribute to worsening of the disease.

Occupational exposure to irritating fumes and dusts may aggravate COPD. Silicosis and other pneumonoconioses may bring about lung fibrosis and focal emphysema. Exposure to certain vegetable dusts, such as cotton fiber, molds and fungi in grain dust, may increase airway resistance and sometimes produce permanent respiratory impairment. Exposures to irritating gases, such as chlorine and oxides of nitrogen and sulfur, produce pulmonary edema, bronchiolitis and at times permanent parenchymal damage.

Repeated bronchopulmonary infections can also intensify the existing pathological changes, playing a role in destruction of lung parenchyma and the progression of COPD.

Heredity or biological factors can determine the reactions of pulmonary tissue to noxious agents. For example, a genetic familial form of emphysema involves a deficiency of the major normal serum alpha-1 globulin (alpha-1 antitrypsin). A single autosomal recessive gene transmits this deficiency. The homozygotes may develop severe panlobular emphysema (PLE) early in adult life. The heterozygotes appear to be predisposed to the development of centrilobular emphysema related to cigarette smoking. The other better-known cause of chronic lung disease is mucoviscidosis or cystic fibrosis, which produces thickened secretions via the endocrine system and throughout the body.

Aging by itself is not a primary cause of COPD, but some degree of panlobular emphysema is commonly discovered on histopathologic examination. Age related dorsal kyphosis with the barrel-shaped thorax has often been called senile emphysema, even though there is little destruction of interalveolar septa. The morphologic changes consist of dilated air spaces and pores of Kohn.

Pathogenesis

The pathogenesis of COPD is not fully understood despite attempts to correlate the morphologic appearance of lungs at necropsy to the clinical measurements of functioning during life. Chronic bronchitis and centrilobular emphysema do seem to develop after prolonged exposure to cigarette smoke and/or other air pollutants. Whatever the causes, bronchiolar obstruction by itself does not result in focal atelectasis, provided there is collateral ventilation from adjacent pulmonary parenchyma via the pores of Kohn.

It has been proposed that airway obstruction at times may result in a check-valve mechanism leading to overdistension and rupture of alveolar septa, especially if the latter are inflamed and exposed to high positive pressure (i.e. barotrauma). This concept of pathogenesis of emphysema is entirely speculative. Airflow obstruction alone does not necessarily result in tissue destruction. Moreover, both centrilobular and panlobular emphysema may exist in lungs of asymptomatic individuals. It has been reported that up to 30% of lung tissue can be destroyed by emphysema without resulting in demonstrable airflow obstruction. Normally, radial traction forces of the attached alveolar septa support the bronchiolar walls. With loss of alveolar surface in emphysema, there is a decrease in surface tension, resulting in expiratory airway collapse. Additional investigative work continues in an effort to link disease states to pathogenesis.

Control of Ventilation

A brief description of respiratory control mechanisms will help the you with COPD or family members or the nurse better understand how the progression of COPD results in pathophysiologic changes. The respiratory centers impart rhythmicity to breathing. The sensory-motor mechanisms provide fine regulation of respiratory muscle tension and the chemical or humoral regulation that maintains normal arterial blood gases. This will help the nurse to understand why hypercapnia (increased PaCO₂) results in the COPDers’ extreme reliance on the hypoxic drive.

The reticular formation of the medulla oblongata constitutes the medullar control center responsible for respiratory rhythmicity. The mechanism whereby rhythmicity is established is not clear, but it may be the end result of the interaction of two oscillating circuits, one for inspiration and one for expiration, which inhibit each other. Although medullar centers are inherently rhythmic, medullar breathing without pontine influence is not well coordinated; therefore, pontine as well as medullar centers participate in producing normal respiratory rhythm.

In the pons, a neural mechanism has been identified as the pneumotaxic center. Stimulation of this center leads to an increase in respiratory frequency with an inspiratory shift, whereas ablation of the center leads to a slowing of respiration. The pneumotaxic center has no intrinsic rhythmicity but appears to serve by modulation of the tonic activity of the apneustic center. The latter is located in the middle and caudal pons. Stimulation of the apneustic center results in respiratory arrest in the maximal inspiratory position, or apneusis.

Respiratory muscles, like other skeletal muscles, possess muscle spindles, which, by sensing length, form a part of a reflex loop that assures that the muscle contraction is appropriate to the anticipated respiratory load and required effort. This servo-­mechanism facilitates fine regulation of respiratory movements and may stabilize the normal respiration in spite of changes in mechanical loading. Breathing is automatic when the respiratory load is constant or when changes in load are subconsciously anticipated. Thus, because it is anticipated, we are not consciously aware of the increase in expiratory resistance during phonation. Under such circumstances the increase in effort is not sensed because it is appropriate to the expected load.

It has been suggested that signals from respiratory muscle and joint mechano-receptors are integrated to produce a sensation that may reach consciousness when there is this “length tension appropriateness.”

Humoral regulation of the medullar centers is mediated by chemosensitive areas in the medulla and through peripheral chemoreceptors. Peripheral chemoreceptors are primarily responsible for the hypoxic drive. These receptors are highly vascular structures located at the carotid bifurcation and arch of the aorta. A diminution of oxygen supply results in anaerobic metabolism in cells of these carotid and aortic bodies. The resulting locally produced metabolites stimulate receptor nerve endings and, through signals conveyed to medullar control centers, lead to increased ventilation. The extremely high blood flow of the chemoreceptors and their almost immeasurable arterial-venous difference make them sensitive to reduced arterial oxygen tension (PaO₂) but not to a reduction in oxygen content alone. However, a decrease in blood flow to these chemoreceptor organs, by permitting accumulation of metabolites, results in their stimulation and an increase in ventilation. Very high PaCO₂ minimizes receptor stimulation regardless of blood flow.

A decrease in arterial pH also stimulates these peripheral chemoreceptors. The stimulation resulting from an increase in arterial carbon dioxide tension (PaCO₂) is probably secondary to the increase in pH. The effect of pH has been attributed to dilatation of arteriovenous anastomoses in the periphery of the chemoreceptor bodies, with resulting reduction in blood flow to the chemosensitive cells. However, the effect of carbon dioxide and pH on respiration is mediated only to a limited extent by peripheral chemoreceptors. Denervation of these receptor organs abolishes the hypoxic drive to respiration but has little effect on the influence on ventilation of carbon dioxide or pH.

Changes in PaCO₂ have a profound effect on central chemoreceptors located in the medulla. These are primarily responsible for mediating the hypercapnic respiratory drive. The precise location and characteristics of these central chemoreceptor sites nor their neural connections with the medullar respiratory control centers have been established. The chemosensitive areas appear to be directly responsive to hydrogen ions rather than to carbon dioxide.

Central chemoreceptors are sensitive to changes in pH, and through this mechanism they appear to be specifically responsive to PaCO₂. Hydrogen ions themselves do not readily traverse the blood-brain barrier. Under normal circumstances, CO₂ plays the primary role in chemical control of ventilation while PaO₂ and extracellular pH have lesser roles. Normal subjects increase their ventilation more than two-fold while breathing 5% CO₂ gas mixture.

Chronic elevation of PaCO₂ (hypercapnia) is found in patients having COPD. The respiratory response to CO₂ is markedly diminished in these clients and they become markedly sensitive to their diminished PaO₂ (hypoxemia). An exuberant use of oxygen for hours may have dire consequences by removing the dominant respiratory stimulus in these clients.  If a patient has Emphysema whose brain is use to high carbon diozide levels in their blood secondary to bad breathing and getting low 02 blood levels in their body so their brain gets use to being messaged to tell the patient to breath on low levels of carbon dioxide blood levels when reaching the brain.  If this emphysema pt is given high doses of O2 for hours it turns the brain off making it think it doesn’t need to send messages to the person to breath.  A normal person with no emphysema COPD is use to breathing due to hypoxia but a emphysema is use to breathing when they have hypocapnia.  That is why when a emphysema pt who is no respiratory arrest is given 2L or less daily.  When is distress high 02 levels temporarily unlikely to hurt the pt, since the high 02 is given for a short period.

“Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that causes obstructed airflow from the lungs. Symptoms include breathing difficulty, cough, mucus (sputum) production and wheezing. It’s typically caused by long-term exposure to irritating gases or particulate matter, most often from cigarette smoke. People with COPD are at increased risk of developing heart disease, lung cancer and a variety of other conditions.

Emphysema and chronic bronchitis are the two most common conditions that contribute to COPD. These two conditions usually occur together and can vary in severity among individuals with COPD.

Chronic bronchitis is inflammation of the lining of the bronchial tubes, which carry air to and from the air sacs (alveoli) of the lungs. It’s characterized by daily cough and mucus (sputum) production.

Emphysema is a condition in which the alveoli at the end of the smallest air passages (bronchioles) of the lungs are destroyed as a result of damaging exposure to cigarette smoke and other irritating gases and particulate matter.

Although COPD is a progressive disease that gets worse over time, COPD is treatable.”

MAYO CLINIC

   Usually due to smoking

This is Healthy Lung Month covering COPD.

What is Chronic Obstructive Pulmonary Disease (COPD)?

Chronic obstructive pulmonary disease (COPD) is a term that applies to patients with chronic bronchitis, bronchiectasis, emphysema and, to a certain extent, asthma. A brief review of normal functional anatomy will provide a background for the discussion of pathology.

The airway down to the bronchioles normally is lined with ciliated pseudo-stratified columnar cells and goblet cells. Mucus derives from mucus glands that are freely distributed in the walls of the trachea and bronchi. The cilia sweep mucus and minor debris toward the upper airway. Low humidity, anesthesia gases, cigarette smoking and other chemical irritants paralyze the action of these cilia. The mucociliary action starts again after a matter of time. This is why people awaken to “smokers cough.”

“Chronic obstructive pulmonary disease (COPD) is a term that applies to patients with chronic bronchitis, bronchiectasis, emphysema and, to a certain extent, asthma.”

Bronchi run in septal connective tissue, but bronchioles are suspended in lung parenchyma by alveolar elastic tissue. The elastic tissue extends throughout alveolar walls, air passages, and vessels, connecting them in a delicate web. Bronchiolar epithelium is ciliated, single-layered and columnar or cuboidal. Beyond the bronchioles the epithelium is flat and lined with a film of phospholipid (surfactant), which lowers surface tension and thereby helps to keep these air spaces from collapsing. Remember that the phospholipid develops during later gestation in utero. This is the reason why premature infant’s lungs cannot stay inflated without the addition of surfactant therapy. Macrophages are found in alveolar lining. Smooth muscles surround the walls of all bronchi, bronchioles, and alveolar ducts and when stimulated they shorten and narrow the passages. Cartilage lends rigidity and lies in regular horse-shaped rings in the tracheal wall. Cartilage is absent in bronchi less than 1 mm in diameter.

The terminal bronchiole is lined with columnar epithelium and is the last purely conducting airway. An acinus includes a terminal bronchiole and its distal structures. Five to ten acini together constitute a secondary lobule, which is generally 1 to 2 cm in diameter and is partly surrounded by grossly visible fibrous septa. Passages distal to the terminal bronchiole include an average of three but as many as nine generations of respiratory bronchioles lined with both columnar and alveolar epithelium. Each of the last respiratory bronchioles gives rise to about six alveolar ducts, each of these to one or two alveolar sacs, and finally each of the sacs to perhaps seventy-five alveoli. Alveolar pores (pores of Kohn) may connect alveoli in adjacent lobules.

Two different circulations supply the lungs. The pulmonary arteries and veins are involved in gas exchange. The pulmonary arteries branch with the bronchi, dividing into capillaries at the level of the respiratory bronchiole, and supplying these as well as the alveolar ducts and alveoli. In the periphery of the lung, the pulmonary veins lie in the interlobular septa rather than accompanying the arteries and airways. The bronchial arteries are small and arise mostly from the aorta. They accompany the bronchi to supply their walls. In some cases of COPD, like bronchiectasis, extensive anastomoses develop between the pulmonary and bronchial circulations. This can allow major shunting and recirculation of blood, therefore contributing to cardiac overload and failure. Lymphatics run chiefly in bronchial walls and as a fine network in the pleural membrane. The lumina of the capillaries in the alveolar walls are separated from the alveolar lining surfaces by the alveolar-capillary membrane, consisting of thin endothelial and epithelial cells and a minute but expansile interstitial space. This interface between air and blood, only 2 microns in thickness, is the only place where gases may be exchanged effectively.

Disease Specific Review

Chronic Bronchitis

Chronic bronchitis is a clinical disorder characterized by excessive mucus secretion in the bronchi. It was traditionally defined by chronic or recurrent productive cough lasting for a minimum of three months per year and for at least two consecutive years, in which all other causes for the cough have been eliminated. Today’s definition remains more simplistic to include a productive cough progressing over a period of time and lasting longer and longer. Sometimes, chronic bronchitis is broken down into three types: simple, mucopurulent or obstructive. The pathologic changes consist of inflammation, primarily mononuclear, infiltrate in the bronchial wall, hypertrophy and hyperplasia of the mucus-secreting bronchial glands and mucosal goblet cells, metaplasia of bronchial and bronchiolar epithelium, and loss of cilia. Eventually, there may be distortion and scarring of the bronchial wall.

Asthma

Asthma is a disease characterized by increased responsiveness of the trachea and bronchi to various stimuli (intrinsic or extrinsic), causing difficulty in breathing due to narrowing airways. The narrowing is dynamic and changes in degree. It occurs either spontaneously or because of therapy. The basic defect appears to be an altered state of the host, which periodically produces a hyperirritable contraction of smooth muscle and hypersecretion of bronchial mucus. This mucus is abnormally sticky and therefore obstructive. In some instances, the illness seems related to an altered immunologic state.

Histological changes of asthma include an increase in the size and number of the mucosal goblet cells and submucosal mucus glands. There is marked thickening of the bronchial basement membrane and hypertrophy of bronchial and bronchiolar smooth muscle tissue. A submucosal infiltration of mononuclear inflammatory cells, eosinophils and plugs of mucus blocks small airways. Patients who have had asthma for many years may develop cor pulmonale and emphysema.

Emphysema

Pulmonary emphysema is described in clinical, radiological and physiologic terms, but the condition is best defined morphologically. It is an enlargement of the air spaces distal to the terminal non-respiratory bronchiole, with destruction of alveolar walls.

Although the normal lung has about 35,000 terminal bronchioles and their total internal cross-sectional area is at least 40 times as great as that of the lobar bronchi, the bronchioles are more delicate and vulnerable. Bronchioles may be obstructed partially or completely, temporarily or permanently, by thickening of their walls, by collapse due to loss of elasticity of the surrounding parenchyma, or by influx of exudate. In advanced emphysema, the lungs are large, pale, and relatively bloodless. They do not readily collapse. They many contain many superficial blebs or bullae, which occasionally are huge. The right ventricle of the heart is often enlarged (cor pulmonale), reflecting pulmonary arterial hypertension. Right ventricular enlargement is found in about 40% of autopsies of patients with severe emphysema. The distal air spaces are distended and disrupted, thus excessively confluent and reduced in number. There may be marked decrease in the number and size of the smaller vascular channels. The decrease in alveolar-capillary membrane surface area may be critical. Death may result from infection that obliterates the small bronchi and bronchioles. There is often organized pneumonia or scarring of the lung parenchyma due to previous infections.

Classification of emphysema relies on descriptive morphology, requiring the study of inflated lungs. The two principal types are centrilobular and panlobular emphysema. The two types may coexist in the same lung or lobe.

Centrilobular emphysema (CLE) or centriacinar emphysema affects respiratory bronchioles selectively. Fenestrations develop in the walls, enlarge, become confluent, and tend to form a single space as the walls disintegrate. There is often bronchiolitis with narrowing of lumina. The more distal parenchyma (alveolar ducts and sacs and alveoli) is initially preserved, then similarly destroyed as fenestrations develop and progress.

The disease commonly affects the upper portions of the lung more severely, but it tends to be unevenly distributed. The walls of the emphysematous spaces may be deeply pigmented. This discoloration may represent failure of clearance mechanisms to remove dust particles, or perhaps the pigment plays an active role in lung destruction. CLE is much more prevalent in males than in females. It is usually associated with chronic bronchitis and is seldom found in nonsmokers.

Panlobular emphysema (PLE) or panacinar emphysema is a nearly uniform enlargement and destruction of the alveoli in the pulmonary acinus. As the disease progresses, there is gradual loss of all components of the acinus until only a few strands of tissue, which are usually blood vessels, remain. PLE is usually diffuse, but is more severe in the lower lung areas. It is often found to some degree in older people, who do not have chronic bronchitis or clinical impairment of lung function. The term senile emphysema was formerly applied to this condition. PLE occurs as commonly in women and men, but is less frequent than CLE. It is a characteristic finding in those with homozygous deficiency of serum alpha-1 antitrypsin. It has also been found that certain populations of IV Ritalin abusers show PLE.

Bullae are common in both CLE and PLE, but may exist in the absence of either. Air-filled spaces in the visceral pleura are commonly termed blebs, and those in the parenchyma greater than 1 cm in diameter are called bullae. A valve mechanism in the bronchial communication of a bulla permits air trapping and enlargement of the air space. This scenario may compress the surrounding normal lung. Blebs may rupture into the pleural cavity causing a pneumothorax, and through a valve mechanism in the bronchopleural fistula a tension pneumothorax may develop.

Paracicatricial emphysema occurring adjacent to pulmonary scars represents another type of localized emphysema. When the air spaces distal to terminal bronchioles are increased beyond the normal size but do not show destructive changes of the alveolar walls, the condition is called pulmonary overinflation. This condition may be obstructive, because of air trapping beyond an incomplete bronchial obstruction due to a foreign body or a neoplasm. Many lung lobules may be simultaneously affected as a result of many check-valve obstructions, as in bronchial asthma. Pulmonary overinflation may also be nonobstructive, less properly called “compensatory emphysema”, when associated with atelectasis or resection of other areas of the lung.

Bronchiectasis

Bronchiectasis means irreversible dilation and distortion of the bronchi and bronchioles. Saccular bronchiectasis is the classic advanced form characterized by irregular dilatations and narrowing. The term cystic is used when the dilatations are especially large and numerous. Cystic bronchiectasis can be further classified as fusiform or varicose.

Tubular bronchiectasis is simply the absence of normal bronchial tapering and is usually a manifestation of severe chronic bronchitis rather than of true bronchial wall destruction.

Repeated or prolonged episodes of pneumonitis, inhaled foreign objects or neoplasms have been known to cause bronchiectasis. When the bronchiectatic process involves most or all of the bronchial tree, whether in one or both lungs, it is believed to be genetic or developmental in origin.

Mucoviscidosis, Kartagener’s syndrome (bronchiectasis with dextrocardia and paranasal sinusitis), and agammaglobulinemia are all examples of inherited or developmental diseases associated with bronchiectasis. The term pseudobronchiectasis is applied to cylindrical bronchial widening, which may complicate a pneumonitis but which disappears after a few months. Bronchiectasis is true saccular bronchiectasis but without cough or expectoration. It is located especially in the upper lobes where good dependent drainage is available. A proximal form of bronchiectasis (with normal distal airways) complicates aspergillus mucus plugging.

Advanced bronchiectasis is often accompanied by anastomoses between the bronchial and pulmonary vessels. These cause right-to-left shunts, with resulting hypoxemia, pulmonary hypertension and cor pulmonale.

Keeping a healthy lung prevents emphysema.  So for starters don’t smoke and exercise; which includes don’t be exposed to smoke frequently!

“Regarding newly diagnosed diabetics 1.5 million people will be diagnosed with DM this year. $237 billion is spent each year on direct medical costs and another $90 billion on reduced productivity. Some people can manage it with healthy eating and exercise, or with oral medications, while others may also need to use insulin.  Sometimes one medication will be enough, but in other cases, your doctor may prescribe a combination of medications.  It’s common for your medication needs to change over time. And that’s a good thing. The most important thing is to get to feeling your best.”

American Diabetes Association (https://diabetes.org/)

“Research shows that people with prediabetes or type 2 diabetes have a higher risk of getting Alzheimer’s disease and other types of dementia later in life.

WEB MD (https://www.webmd.com/)

If You Have Diabetes, Your Risk of Alzheimer’s Increases Dramatically

Diabetes is linked to a 65 percent increased risk of developing Alzheimer’s, which may be due, in part, because insulin resistance and/or diabetes appear to accelerate the development of plaque in your brain, which is a hallmark of Alzheimer’s. Separate research has found that impaired insulin response was associated with a 30 percent higher risk of Alzheimer’s disease, and overall dementia and cognitive risks were associated with high fasting serum insulin, insulin resistance, impaired insulin secretion and glucose intolerance.

A drop in insulin production in your brain may contribute to the degeneration of your brain cells, mainly by depriving them of glucose, and studies have found that people with lower levels of insulin and insulin receptors in their brain often have Alzheimer’s disease (people with type 2 diabetes often wind up with low levels of insulin in their brains as well). As explained in New Scientist, which highlighted this latest research:

What’s more, it encourages the process through which neurons change shape, make new connections and strengthen others. And it is important for the function and growth of blood vessels, which supply the brain with oxygen and glucose.

As a result, reducing the level of insulin in the brain can immediately impair cognition. Spatial memory, in particular, seems to suffer when you block insulin uptake in the hippocampus… Conversely, a boost of insulin seems to improve its functioning.

When people frequently gorge on fatty, sugary food, their insulin spikes repeatedly until it sticks at a high level. Muscle, liver and fat cells then stop responding to the hormone, meaning they don’t mop up glucose and fat in the blood. As a result, the pancreas desperately works overtime to make more insulin to control the glucose – and levels of the two molecules skyrocket.

The pancreas can’t keep up with the demand indefinitely, however, and as time passes people with type 2 diabetes often end up with abnormally low levels of insulin.”

Alzheimer’s Might be “Brain Diabetes”

BBA – Molecular Basis of Disease, Accepted manuscript. doi:10.1016/j.bbadis.2016.04.017

It’s becoming increasingly clear that the same pathological process that leads to insulin resistance and type 2 diabetes may also hold true for your brain. As you over-indulge on sugar and grains, your brain becomes overwhelmed by the consistently high levels of insulin and eventually shuts down its insulin signaling, leading to impairments in your thinking and memory abilities, and eventually causing permanent brain damage.

Regularly consuming more than 25 grams of fructose per day will dramatically increase your risk of dementia and Alzheimer’s disease. Consuming too much fructose will inevitably wreak havoc on your body’s ability to regulate proper insulin levels.

Although fructose is relatively “low glycemic” on the front end, it reduces the affinity for insulin for its receptor leading to chronic insulin resistance and elevated blood sugar on the back end. So, while you may not notice a steep increase in blood sugar immediately following fructose consumption, it is likely changing your entire endocrine system’s ability to function properly behind the scenes.

Additionally, fructose has other modes of neurotoxicity, including causing damage to the circulatory system upon which the health of your nervous system depends, as well as profoundly changing your brain’s craving mechanism, often resulting in excessive hunger and subsequent consumption of additional empty carbohydrate-based calories.

In one study from UCLA, researchers found that rats fed a fructose-rich and omega-3 fat deficient diet (similar to what is consumed by many Americans) developed both insulin resistance and impaired brain function in just six weeks.

Plus, when your liver is busy processing fructose (which your liver turns into fat), it severely hampers its ability to make cholesterol ^{, an essential building block of your brain crucial to its health. This is yet another important facet that explains how and why excessive fructose consumption is so detrimental to your health.  Decreasing fructose intake is one of the most important moves you can take in decreasing the risk of Alzheimer’s disease in your lifetime.}

“It’s important to keep your blood sugar levels in your target range as much as possible to help prevent or delay long-term, serious health problems, such as heart disease, vision loss, and kidney disease. Staying in your target range of blood glucose (Before a meal glucose in the blood should range the following: 80 to 130 mg/dL. Two hours after the start of a meal: Less than 180 mg/dL.).  Keeping the glucose in therapeutic range can also help improve your energy and mood.”

Center for Disease Control and Prevention (CDC)

Find answers to common questions about blood sugar for people with diabetes

Here is a fast review of Part I and Part II:

Diabetes occurs when the pancreas, a gland behind the stomach, does not produce enough of the hormone insulin, or the body cannot use insulin properly. Insulin helps carry sugar from the bloodstream into the cells. Once inside the cells, sugar is converted into energy for immediate use or stored for the future. That energy fuels many of our bodily functions.

The body produces glucose from the foods you eat. The liver also releases sugar when you are not eating. The pancreas produces the hormone insulin, which allows glucose from the bloodstream to enter the body’s cells where it is used for energy. In type 2 diabetes, too little insulin is produced, or the body cannot use insulin properly, or both. This results in a build-up of glucose in the blood.

People with diabetes are at risk of developing signs and symptoms of hyperglycemia to serious health problems (complications).

HOW we can decrease the risk of complications and decrease the chance of diabetes worsening = KEEP IT UNDER CONTROL = PRACTICING VERY GOOD MANAGEMENT IN CARING FOR YOUR DIABETES. 

This is how you can reach this goal:

-Controlling your blood glucose, blood pressure, and cholesterol can make a huge difference in staying healthy. Talk with your doctor about what your goals should be and how to reach them but make sure you are given information on paper or write down what it is you have discussed in the doctor’s office based on your care for diabetes and what to do. Usually diabetic information on paper is available and given to you.

To reach controlling your glucose and treatment for Diabetes:

-Your healthy eating plan that you and your doctor with a dietician have discussed.

-Overweight? Than diet down to your therapeutic weight range for your height after discussed with by you with your doctor.

-Be physically active for 30 to 60 minutes most days but if this is new get your doctor to clear this activity for you with what kind of activity you are allowed and not allowed.

-Take your medicines as directed and keep taking them even after you’ve reached your goals; or you will be at high risk of ending up the way you were earlier=Diabetes badly controlled with running into the problems you had earlier.It’s very important to take your diabetes medications as recommended by your doctor. Left untreated, diabetes can lead to serious, even life-threatening complications.

-If you smoke=QUIT.

-Check your skin daily in particular the FEET and LOWER LEGS to check for redness, swelling to blisters, sores and sore toenails

-Ask your doctor if you should be taking aspirin to prevent a heart attack or stroke by making the blood less thick to thinner making it easier for the heart to pump and less stress to the organ.

The key is to controlling your DIABETES is to be living a healthy life! This consists of diet, exercise or activity and healthy habits learned and practiced routinely in your life that will help prevent or assist in treating diabetic disease. The better we treat ourselves regarding health the higher the odds we will live a longer and healthier life. There is not just one food to eat or one type of exercise to do or one healthy habit to practice in order to keep you healthy, there’s choices. To be a part learn what healthier habits or changes you want for a healthier way of living; learn how to eat out of the 4 food groups to prevent Diabetes or eating out of the 4 food groups that are following your diabetic diet as ordered by your MD. It allows you to make all the decisions in what you want to do regarding what to eat (diet). Now with diet you must include exercise/activity, and what healthy habits you want to add in your life that are not so healthy; you know what that is and if not read a book on how to get heathier-including how to prevent diabetes where the library and book stores have many options for you. Provide yourself with the information and healthy foods in your diet, if you decide you want it. You make all the choices.

The ending line of all problems resulting from Diabetes is due to the thick high glucose blood in the blood stream filtering throughout the different organs in our body causing from peripheral neuropathy to necrotic skin to amputations for LE’s usually or same effect elsewhere causing macular degeneration to blindness or increase of cancers, heart disease, Diabetes Alzheimer’s and we could go on about the effects of diabetes.  Get it now its control your blood glucose keeping it in therapeutic range  decreasing the odds of developing these conditions or the severity of these conditions.

If you don’t have diabetes than take the steps to prevent being diagnosed with it later in life.  WHAT are those steps? Eat Right (Healthy), Keep your weight in therapeutic range, Exercise the body balancing it with rest, decrease stress, and take care of yourself.  BUT if there is heredity in the family, especially your nuclear family, when you see your primary care doctor every 6 months or yearly have your glucose checked to see if it is high or not.  Simply get a BMP or CMP blood test that looks at blood electrolyte levels that includes glucose.  If its high the next step is getting the doctor to check your hemoglobin A1C another blood test done with no eating for 12 hrs prior to see what your real glucose level is prior to your first meal in the morning (done on a empty stomach).  For if you eat prior to the test it won’t accurate on your true glucose level.  2 Easy blood tests.

It is all up to you!

Wouldn’t you want less disease/illness for yourself, for your family, others significant to you and even throughout the nation including our future generations. Wouldn’t it be great to see Diabetes decrease in America for future years and giving us an ending result of higher probability that we would overall a healthier country with less diseases. If that included Diabetes decreased significantly what an impact it would play in decreasing other diseases, that occurred due to the diabetes alone  (That would decrease cardiac disease, renal disease, blurred vision, neuropathy, I could go on).  Besides how much it would decrease in this country to take care of patients with diabetes.

I’m not a diabetic but eating overall healthy and in my diet range (barely) but there and trying to increase my activity. Do yourself and maybe others a favor by making yourself and America a healthier country for less Diabetes and the diseases it can cause from cardiac to vision to renal to brain, etc…

Again its all up to you!

–REFERENCES for Part I, Part II & III this week on diabetes:

1.)  Center for Disease (CDC) – “National Diabetes Fact Sheet”

2.)  NYS Dept. of Health –Diabetes

3.)  Diabetic Neuropathy.org “All about diabetic neuropathy and nerve damage caused by Diabetes.”

4.)  NIDDK “National Institute of Diabetes and Digestive and Kidney Diseases.

5.)  National Diabetes Information Clearinghouse (NIDC) – U.S. Department of Health and Human Services.       “Preventing Diabetes Problems: What you need to know”