Anatomy of respiration system bronchioles

Anatomy of respiration system bronchioles

1. The Bronchi and Subdivisions

2. The air passageways in the lungs branch and branch again, about 23 times overall, in a pattern often called the bronchial tree. At the tips of the bronchial tree, conducting zone structures give way to respiratory zone structures. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

3. At the superior border of the fifth thoracic vertebra , the trachea divides into a right main (primary) bronchus, which goes into the right lung, and a left main (primary) bronchus, which goes into the left lung. The right main bronchus is more vertical, shorter, and wider than the left. As a result, an aspirated object is more likely to enter and lodge in the right main bronchus than the left. Like the trachea, the main bronchi contain incomplete rings of cartilage and are lined by ciliated pseudostratified columnar epithelium. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

4. The tissue composition of the walls of the main bronchi mimics that of the trachea. However, as the conducting tubes become smaller, the following structural changes occur: Support structures change. Irregular plates of cartilage replace the cartilage rings, and by the time the bronchioles are reached, the tube walls no longer contain supportive cartilage. However, the tube walls throughout the bronchial tree contain elastic fibers. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

5. Epithelium type changes . The mucosal epithelium thins as it changes from pseudostratified columnar to columnar and then to cuboidal in the terminal bronchioles. Mucusproducing cells and cilia are sparse in the bronchioles. For this reason, most airborne debris found at or below the level of the bronchioles must be removed by macrophages in the alveoli. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

6. A complete layer of circular smooth muscle in the bronchioles and the lack of supporting cartilage (which would hinder constriction) allows the bronchioles to provide substantial resistance to air passage under certain conditions (as we will describe later). Amount of smooth muscle increases. The relative amount of smooth muscle in the tube walls increases as the passageways become smaller. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

7. At the point where the trachea divides into right and left main bronchi is an internal ridge called the carina . It is formed by a posterior and somewhat inferior projection of the last tracheal cartilage. The mucous membrane of the carina is one of the most sensitive areas of the entire larynx and trachea for triggering a cough reflex. Widening and distortion of the carina is a serious sign because it usually indicates a carcinoma of the lymph nodes around the region where the trachea divides. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

8. On entering the lungs, the main bronchi divide to form smaller bronchi — the lobar (secondary) bronchi , one for each lobe of the lung. The right lung has three lobes; the left lung has two . The lobar bronchi continue to branch, forming still smaller bronchi, called segmental (tertiary) bronchi that supply the specific bronchopulmonary segments within the lobes. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

9. The segmental bronchi then divide into bronchioles. Bronchioles in turn branch repeatedly, and the smallest ones branch into even smaller tubes called terminal bronchioles. These bronchioles contain Clara cells, columnar, nonciliated cells interspersed among the epithelial cells. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

10. The terminal bronchioles represent the end of the conducting zone of the respiratory system. Because this extensive branching from the trachea through the terminal bronchioles resembles an inverted tree, it is commonly referred to collectively as the bronchial tree. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

11. Beyond the terminal bronchioles of the bronchial tree, the branches become microscopic. These branches are called the respiratory bronchioles and alveolar ducts. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

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14. The respiratory passages from the trachea to the alveolar ducts contain about 23 generations of branching; branching from the trachea into main bronchi is called first-generation branching , that from main bronchi into lobar bronchi is called second-generation branching , and so on down to the alveolar ducts. As the branching in the bronchial tree becomes more extensive, several structural changes may be noted. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

15. 1. The mucous membrane in the bronchial tree changes from ciliated pseudostratified columnar epithelium in the main bronchi, lobar bronchi, and segmental bronchi to ciliated simple columnar epithelium with some goblet cells in larger bronchioles, to mostly ciliated simple cuboidal epithelium with no goblet cells in smaller bronchioles, to mostly nonciliated simple cuboidal epithelium in terminal bronchioles. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

16. Recall that ciliated epithelium of the respiratory membrane removes inhaled particles in two ways. Mucus produced by goblet cells traps the particles and the cilia move the mucus and trapped particles toward the pharynx for removal. In regions where nonciliated simple cuboidal epithelium is present, inhaled particles are removed by macrophages. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

17. 2. Plates of cartilage gradually replace the incomplete rings of cartilage in main bronchi and finally disappear in the distal bronchioles. 3 . As the amount of cartilage decreases, the amount of smooth muscle increases. Smooth muscle encircles the lumen in spiral bands and helps maintain patency. However , because there is no supporting cartilage, muscle spasms such as those that occur during an asthma attack can close off the airways, a potentially life-threatening situation. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

18. Nerve supply During exercise, activity in the sympathetic division of the autonomic nervous system (ANS) increases and causes the adrenal medullae to release the hormones epinephrine and norepinephrine ; T hese hormones cause relaxation of smooth muscle in the bronchioles , which dilates the airways. The result is improved lung ventilation because air reaches the alveoli more quickly. The parasympathetic division of the ANS and mediators of allergic reactions such as histamine cause contraction of bronchiolar smooth muscle, resulting in constriction of distal bronchioles. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

19. Blood supple The blood supply to the bronchi is via the left and right bronchial arteries. The veins that drain the bronchi are the right bronchial vein , which enters the azygos vein , and the left bronchial vein , which empties into the accessory hemiazygos vein or the left superior intercostal vein. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

20. AGING AND THE RESPIRATORY SYSTEM With advancing age, the airways and tissues of the respiratory tract, including the alveoli, become less elastic and more rigid; T he chest wall becomes more rigid as well. The result is a decrease in lung capacity. In fact, vital capacity (the maximum amount of air that can be exhaled after maximal inhalation) can decrease as much as 35 percent by age 70. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

21. A decrease in blood level of O2, decreased activity of alveolar macrophages, and diminished ciliary action of the epithelium lining the respiratory tract also occur . Because of all these age-related factors, older people are more susceptible to pneumonia, bronchitis, emphysema, and other pulmonary disorders. Age-related changes in the structure and functions of the lung can also contribute to an older person’s reduced ability to perform vigorous exercises, such as running. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

22. Chronic Obstructive Pulmonary Disease COPD This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

23. The chronic obstructive pulmonary diseases (COPD), exemplified best by emphysema and chronic bronchitis, are a major cause of disability and death in North America. The key physiological feature of these diseases is an irreversible decrease in the ability to force air out of the lungs. Other features they share in common: ■ More than 80% of patients have a history of smoking. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

24. Dyspnea, difficult or labored breathing often referred to as “air hunger,” gets progressively worse. Coughing and frequent pulmonary infections are common. Most COPD victims develop respiratory failure manifested as hypoventilation (insufficient ventilation in relation to metabolic needs, causing them to retain CO2), respiratory acidosis, and hypoxemia. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

25. Emphysema Emphysema is distinguished by permanent enlargement of the alveoli, accompanied by destruction of the alveolar walls. Invariably the lungs lose their elasticity. This has three important consequences: ( 1) Accessory muscles must be enlisted to breathe, and victims are perpetually exhausted because breathing requires 15–20% of their total body energy supply (as opposed to 5% in healthy individuals). ( 2) For complex reasons, the bronchioles open during inspiration but collapse during expiration, trapping huge volumes of air in the alveoli. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

26. This hyperinflation leads to development of a permanently expanded “barrel chest” and flattens the diaphragm, thus reducing ventilation efficiency. ( 3) Damage to the pulmonary capillaries as the alveolar walls disintegrate increases resistance in the pulmonary circuit, forcing the right ventricle to overwork and consequently become enlarged. In addition to smoking, hereditary factors (e.g., alpha-1 antitrypsin deficiency) cause emphysema in some patients. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

27. Chronic Bronchitis In chronic bronchitis, inhaled irritants lead to chronic production of excessive mucus. The mucosae of the lower respiratory passageways become inflamed and fibrosed . These responses obstruct the airways, severely impairing lung ventilation and gas exchange. Pulmonary infections are frequent because bacteria thrive in the stagnant pools of mucus. However , the degree of dyspnea is usually moderate compared to emphysema. As with emphysema, smoking is a major risk factor. Environmental pollution also promotes chronic bronchitis. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

28. Asthma Asthma is characterized by episodes of coughing, dyspnea, wheezing, and chest tightness—alone or in combination. A sense of panic accompanies most acute attacks. Although sometimes classed with COPD because it is an obstructive disorder, asthma is marked by acute episodes followed by symptom-free periods—that is, the obstruction is reversible . The cause of asthma has been hard to pin down. Initially it was viewed as a consequence of bronchospasms triggered by various factors such as cold air, exercise, or allergens. However , bronchoconstriction has relatively little effect on air flow through normal lungs. Researchers have found that in allergic asthma (the most common kind), active inflammation of the airways comes first. The inflammation is an immune response controlled by TH2 cells, a subset of T lymphocytes. By secreting certain interleukins, TH2 cells stimulate the production of IgE and recruit inflammatory cells (notably eosinophils ) to the site. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.

29. Once someone has allergic asthma, the inflammation persists even during symptom-free periods and makes the airways hypersensitive. (The most common triggers are in the home— the allergens from dust mites, cockroaches, cats, dogs, and fungi.) Once the airway walls are thickened with inflammatory exudate, the effect of bronchospasm is vastly magnified and can dramatically reduce air flow. About one in ten people in North America suffer from asthma—children more than adults. Over the past 20 years, the number of cases has risen dramatically, an increase which may now be plateauing. While asthma remains a major health problem, better treatment options have reduced the number of asthma-related deaths. Instead of merely treating the symptoms with fast-acting bronchodilators, we now treat the underlying inflammation using inhaled corticosteroids. Newer approaches limit airway inflammation by using antileukotrienes and antibodies against the patient’s own IgE class of antibodies. This lecture is intellectual property and it’s distribution or usage without consent of author is prohibited by low.