The Defence Mechanisms of the Lungs With Relation to Pulmonary Anatomy – Nursing Research Paper

The Defence Mechanisms of the Lungs With Relation to Pulmonary Anatomy – Nursing Research Paper
The pathway taken by air during inhalation: During inhalation, air enters the nasal cavities via the nostrils, and also into the mouth during forced

inhalation. It then passes through the nasopharynx, followed by the oropharynx. Air passes deeper into the thorax via the trachea, which then bifurcates to give the left and right primary bronchi. On entering the lungs, these become intrapulmonary bronchi, which immediately branch to give rise to the lobar (secondary) bronchi. Since the left lung is divided into two lobes, whereas the right lung is divided into three lobes, the right bronchus thus divides into three lobar bronchial branches, and the left into two bronchial branches, with each branch supplying one lobe. The left lung is further divided into eight bronchopulmonary segments, and the right lung, into ten such segments. Thus, in the right lung the lobar bronchi divide to give rise to ten segmental bronchi (tertiary bronchi), while left lobar bronchi give rise to eight segmental bronchi. The segments divide to give pulmonary lobules; each lobule is supplied by a bronchiole. Pulmonary acini are smaller units of structure that make up the lobules. Each acinus derives it air supply from a terminal bronchiole. As of yet, no gaseous exchange has occurred. Thus, the passageways mentioned above are referred to as the conducting portion of the lung. Instead, the air is conditioned. This consists of warming, moistening and removing particulate matter. Only at the 17th division of the trachea does gaseous exchange commence. It first occurs at the respiratory bronchioles that arise from each terminal bronchiole, which will in turn give off alveoli. Thus, the smallest functional unit of the lung is the respiratory bronchiole unit, which consists of a respiratory bronchiole and the alveoli it supplies. Each alveolus is confluent with a respiratory bronchiole by means of an alveolar duct and an alveolar sac.

Defence Mechanisms of the Nasal Cavities:

The vestibule communicates anteriorly with the external environment. It contains hairs that filter out the largest-sized particulate matter before it is carried in the airstream to the rest of the cavity. The next segment of the cavity, the respiratory segment, is lined by ciliated, pseudostratified columnar epithelium. It possesses a smooth medial wall called the nasal septum; however, the lateral walls are thrown into folds by the presence of three shelf-like, bony projections called turbinates or conchae. These increase the surface area as well as cause turbulence in airflow to allow more effective conditioning of inspired air. The airstream is broken into eddies, and so matter suspended in the airstream is thrown out of the stream and adheres to the mucus-covered walls of the nasal cavity. It is the goblets cells dispersed between the ciliated cells that secrete mucin. Mucin later forms the mucus that traps debris. The cilia in turn provide a coordinated sweeping motion towards the pharynx, where the mucus is swallowed.

The lamina propria of the respiratory segment has a rich vascular network that includes a complex set of capillary loops. Furthermore, the turbinates increase the total surface area; this arrangement allows the air to be warmed rapidly, so as not to compromise core body temperature. These same vessels become engorged and leaky during allergic reactions or viral infections e.g. the common cold. The lamina propria then becomes distended with fluid, resulting in marked swelling of the mucous membrane with a consequent restriction of the air passage. This makes breathing difficult.

Part of the dome of each nasal cavity, and to a lesser extent, the contiguous lateral and medial nasal walls, form the olfactory segment that contain olfactory mucosa. The main constituent of this layer is the olfactory cell. It is a bipolar ciliated neuron that possesses receptors from which the sensation of smell is derived. Over the millennia, man has evolved to dislike odours resembling that of rotting flesh, which possesses micro-organisms and viruses that are harmful not only to the pulmonary system, but to the entire body as well.

Defence Mechanisms of the Pharynx:

The sub-epithelial tissue of the posterior wall of the nasopharynx possesses diffuse lymphatic tissue. Furthermore, lymphatic nodules are concentrated in the adenoids (pharyngeal tonsils) in the roof of the pharynx, and tonsils (palatine tonsils) on either side of the pharynx. These structures are strategically located to allow the nodule cells to intercept and react with foreign antigens and then travel to regional lymph nodes, where they undergo proliferation and differentiation. Progeny of theses cells return to the lamina propria as effector B and T lymphocytes, as plasma cells, and as memory cells. Respiratory tract nodules also have large numbers of eosinophils as compared to other nodules. This is most visible in times of chronic tonsil inflammation and hypersensitivity (allergic) reactions.

Defence Mechanisms of the remainder of the conduction pathway:

The larynx shows numerous adaptations to air conduction. The luminal surface of the vocal cords of the larynx is covered with squamous epithelium. This serves to protect the inner layer of the larynx, the mucosa, from abrasion by the rapidly moving airstream. The rest of the larynx is covered by the ciliated epithelium characteristic of the respiratory system, as are the trachea, bronchi, and larger bronchioles. However, the main adaptation at this level is the presence of an epiglottis. The epiglottis is the valve-like flap of cartilage lying behind the tongue and in front of the entrance to the larynx. At rest, the epiglottis is upright and allows air to pass through the larynx and into the rest of the respiratory system. During swallowing, it folds back to cover the entrance to the larynx, preventing food and drink from entering the windpipe. If both the oesophagus and the larynx were open when a person swallowed, air could enter the stomach and food could enter the lungs. When food enters the larynx, the airways are blocked, and we start to choke. The epiglottis works with the larynx to act as a lid every time we swallow. The larynx draws upward and forward to close the windpipe. This keeps solid food and liquid out of the respiratory tract. At the end of each swallow, the epiglottis moves up again, the larynx returns to rest, and the flow of air into the windpipe continues.

Cough, Sneeze and Gag Reflexes:

The function of both the cough reflex and the sneeze reflex is to dislodge foreign matter or irritating material from respiratory passages. The bronchi and the trachea contain sensory receptors that are sensitive to foreign particles and irritating substances. It is also thought that the upper gastrointestinal tract possesses cough receptors. The cough reflex is initiated with the sensory receptors detect these substances and initiate action potentials that pass along the afferent vagus nerves to the medulla oblongata, where a poorly defined cough centre is located. The movements resulting in a cough occur as follows: about 2.5 litres of air are inspired. The epiglottis closes, and the vestibular folds and vocal cords close tightly to trap the inspired air in the lung as a result of stimulation by efferent neurons. The abdominal muscles contract to force the abdominal contents up against the diaphragm, and the muscles of expiration contract forcefully. As a consequence, the immense pressures are developed in the lungs that may reach up to 100 mm Hg. The vestibular folds, the vocal cords, and the epiglottis then open suddenly, causing air to rush out of the lungs at a high velocity, carrying foreign particles with it.

The sneeze reflex is similar to the cough reflex, but it differs in several ways. The source of irritation that initiates the sneeze reflex is in the nasal passages instead of in the trachea and bronchi, and the action potentials are conducted along the afferent trigeminal nerves to a different centre in the medulla. During the sneeze reflex the uvula and the soft palate are depressed so the air is directed primarily through the nasal passages, although a considerable amount passes through the oral cavity. The rapidly flowing air dislodges particulate matter from the nasal passages and propels it a considerable distance from the nose.

The gag reflex is important for removing foreign bodies from the pharynx and oral cavity. The normal gag reflex is a mass contraction of both sides of the posterior oral and pharyngeal musculature. The contractions of the pharyngeal musculature on the same side as the site of stimulus is called the direct response, while the contractions of the other side are called the consensual response.

Defence mechanisms of the Alveoli:

The alveoli possess numerous macrophages that pass with ease between alveolar cells. They are unusual in that they function in both the connective tissue of the septum and in the air spaces of the alveoli. In the air spaces, they are referred to as dust cells, because they scavenge the surface to remove inhaled particulate matter. They also phagocytise erythrocytes that may enter the alveoli in heart failure. Some engorged macrophages pass up the bronchial tree in the mucus and are disposed of by swallowing or expectoration when they reach the pharynx. Other macrophages return to or remain in the septal connective tissue, where, filled with accumulated phagocytised material, they may stay for much of an individual’s life. Finally, they phagocytose infectious microbes such as tubercle bacilli. These bacilli are not digested by the macrophage, so other infections or conditions that damage alveolar macrophages can cause the release of tubercle bacilli and recurrent tuberculosis.

Diseases of the pulmonary system:

Smoking greatly reduces the effectiveness of pulmonary defence. First, smoking reduces coughing in response to smoke, which is why they can smoke without continuously coughing, and second, smoking effects the rate at which the lungs’ cilia beat. In acute (short term) cases of exposure to smoke, cilia are paralysed temporarily. In the long run, the cilia will be destroyed permenantly. Furthermore, smoke contains irritants, namely tar, that stimuklates mucus secretion in the larger bronchioles by goblet cells. The resultant stagnation produced at that point in long-term smokers means that the lungs are very susceptible to recurrent infection, particularly pneumonia. To eliminate the mucus, such people develop smoker’s cough, which is so violent it can tear parts of the respiratory vessels and burst numerous alveoli. Blod will often be present in the sputum, and the damaged tissue is replaced by scar tissue. The resulting emphysema is further complicated by the fact that alveolar macrophages secrete proteases and elastases that digest the elastin surrounding alveolar sacs and allow these cells to reach rapidlt to the sites of infection. The reduction in compiance is dueto the fact that alveolar air cannot be replaced as efficiently as before without the recoil provided by elastic tissue.

Asthma is an inflammatory disease of the airways characterised by wheezing, swelling, excess fluid build-up and mucus plug formation. The major step in the inflammatory process is exposure to these allergens or triggers. In the first exposure to the harmless allergen, specific B-lymphocytes recognises an antigen of the allergen, and so it divides rapidly by clonal expansion to produce plasma cells and memory cells. The plasma cells, in turn, produce IgE immunoglobulins. Mast cells and basophils in the lungs have special IgE receptor sites on their surfaces to which the IgE molecules attach. These cells are now sensitised to that allergen. On the next exposure to the allergen, the attached IgE antibody comes in contact with the allergen it was designed specifically to recognize, and, and the mast cells begin to degranulate. The released chemicals attract memory cells. Secretion of more IgE by the proliferating memory cells stimulates the release of several inflammatory-response mediators. These chemicals include histamine, leukotrienes, and prostaglandins. They are what cause the symptoms of an allergic reaction. They can stimulate the production of excess amounts of mucus and fluid in the airway, which plug the airway, and also bind to specific receptors on the smooth muscles of the bronchioles, causing severe bronchoconstriction.

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