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Gastrointestinal tract

Posted by Prakash
Wednesday, September 2, 2009
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Digestive System is a series of connected organs whose purpose is to break down, or digest, the food we eat. Food is made up of large, complex molecules, which the digestive system breaks down into smaller, simple molecules that can be absorbed into the bloodstream. The simple molecules travel through the bloodstream to all of the body's cells, which use them for growth, repair, and energy.Digestion generally involves two phases: a mechanical phase and a chemical phase. In the mechanical phase, teeth or other structures physically break down large pieces of food into smaller pieces. In the chemical phase, digestive chemicals called enzymes break apart individual molecules of food to yield molecules that can be absorbed and distributed throughout the body. These enzymes are secreted (produced and released) by glands in the body.
If a human adult’s digestive tract were stretched out, it would be 6 to 9 m (20 to 30 ft) long. In humans, digestion begins in the mouth, where both mechanical and chemical digestion occur. The mouth quickly converts food into a soft, moist mass. The muscular tongue pushes the food against the teeth, which cut, chop, and grind the food. Human teeth is heterodont, thecodont, diphyodont and bunodont. Glands in the cheek linings secrete mucus, which lubricates the food, making it easier to chew and swallow. Three pairs of glands empty saliva into the mouth through ducts to moisten the food. Saliva contains the enzyme ptyalin, which begins to hydrolyze (break down) starch—a carbohydrate manufactured by green plants.

Once food has been reduced to a soft mass, it is ready to be swallowed. The tongue pushes this mass—called a bolus—to the back of the mouth and into the pharynx. This cavity between the mouth and windpipe serves as a passageway both for food on its way down the alimentary canal and for air passing into the windpipe. The epiglottis, a flap of cartilage, covers the trachea (windpipe) when a person swallows. This action of the epiglottis prevents choking by directing food from the windpipe and toward the stomach.

A. The Esophagus

The presence of food in the pharynx stimulates swallowing, which squeezes the food into the esophagus. The esophagus is a muscular tube about 25 cm (10 in) long, passes behind the trachea and heart and penetrates the diaphragm (muscular wall between the chest and abdomen) before reaching the stomach. Food advances through the alimentary canal by means of rhythmic muscle contractions (tightenings) known as peristalsis. The process begins when circular muscles in the esophagus wall contract and relax (widen) one after the other, squeezing food downward toward the stomach. Food travels the length of the esophagus in two to three seconds.

A circular muscle called the esophageal sphincter separates the esophagus and the stomach. As food is swallowed, this muscle relaxes, forming an opening through which the food can pass into the stomach. Then the muscle contracts, closing the opening to prevent food from moving back into the esophagus. The esophageal sphincter is the first of several such muscles along the alimentary canal. These muscles act as valves to regulate the passage of food and keep it from moving backward.

B. The Stomach

The stomach, located in the upper abdomen just below the diaphragm, is a saclike structure with strong, muscular walls. The stomach can expand significantly to store all the food from a meal for both mechanical and chemical processing. The stomach contracts about three times per minute, churning the food and mixing it with gastric juice. This fluid, secreted by thousands of gastric glands in the lining of the stomach, consists of water, hydrochloric acid, an enzyme called pepsin, and mucin (the main component of mucus). Hydrochloric acid creates the acidic environment that pepsin needs to begin breaking down proteins. It also kills microorganisms that may have been ingested in the food. Mucin coats the stomach, protecting it from the effects of the acid and pepsin. About four hours or less after a meal, food processed by the stomach, called chyme, begins passing a little at a time through the pyloric sphincter into the duodenum, the first portion of the small intestine.

C. The Small Intestine

Most digestion, as well as absorption of digested food, occurs in the small intestine. This narrow, twisting tube, about 2.5 cm (1 in) in diameter, fills most of the lower abdomen, extending about 6 m (20 ft) in length. Over a period of three to six hours, peristalsis moves chyme through the duodenum into the next portion of the small intestine, the jejunum, and finally into the ileum, the last section of the small intestine. During this time, the liver secretes bile into the small intestine through the bile duct. Bile breaks large fat globules into small droplets, which enzymes in the small intestine can act upon. Pancreatic juice, secreted by the pancreas, enters the small intestine through the pancreatic duct. Pancreatic juice contains enzymes that break down sugars and starches into simple sugars, fats into fatty acids and glycerol, and proteins into amino acids. Glands in the intestinal walls secrete additional enzymes that break down starches and complex sugars into nutrients that the intestine absorbs. Structures called Brunner’s glands secrete mucus to protect the intestinal walls from the acid effects of digestive juices.

The small intestine’s capacity for absorption is increased by millions of fingerlike projections called villi, which line the inner walls of the small intestine. Each villus is about 0.5 to 1.5 mm (0.02 to 0.06 in) long and covered with a single layer of cells. Even tinier fingerlike projections called microvilli cover the cell surfaces. This combination of villi and microvilli increases the surface area of the small intestine’s lining by about 150 times, multiplying its capacity for absorption. Beneath the villi’s single layer of cells are capillaries (tiny vessels) of the bloodstream and the lymphatic system. These capillaries allow nutrients produced by digestion to travel to the cells of the body. Simple sugars and amino acids pass through the capillaries to enter the bloodstream. Fatty acids and glycerol pass through to the lymphatic system.

D. The Large Intestine

A watery residue of indigestible food and digestive juices remains unabsorbed. This residue leaves the ileum of the small intestine and moves by peristalsis into the large intestine, where it spends 12 to 24 hours. The large intestine forms an inverted U over the coils of the small intestine. It starts on the lower right-hand side of the body and ends on the lower left-hand side. The large intestine is 1.5 to 1.8 m (5 to 6 ft) long and about 6 cm (2.5 in) in diameter.

The large intestine serves several important functions. It absorbs water—about 6 liters (1.6 gallons) daily—as well as dissolved salts from the residue passed on by the small intestine. In addition, bacteria in the large intestine promote the breakdown of undigested materials and make several vitamins, notably vitamin K, which the body needs for blood clotting. The large intestine moves its remaining contents toward the rectum, which makes up the final 15 to 20 cm (6 to 8 in) of the alimentary canal. The rectum stores the feces—waste material that consists largely of undigested food, digestive juices, bacteria, and mucus—until elimination. Then, muscle contractions in the walls of the rectum push the feces toward the anus. When sphincters between the rectum and anus relax, the feces pass out of the body.


V. AILMENTS OF THE DIGESTIVE SYSTEM
Infection of or damage to any part of the digestive system may affect digestion as well as other bodily functions. Common infectious agents that attack digestive organs include the mumps virus, which often infects the salivary glands; the bacterium Helicobacter pylori, which causes most stomach and duodenal ulcers; and viruses and bacteria that cause various forms of gastroenteritis, often called stomach flu or traveler’s diarrhea. Appendicitis is an inflammation of the appendix, a tube-like pouch about 9 cm (3.5 in) long that branches off the large intestine. It occurs most commonly among children and young adults. Diarrhea—frequent elimination of loose, watery feces—is a symptom of many disorders that occurs when the large intestine is irritated or inflamed. As a result, food residues move through it too quickly for it to absorb the excess water. The opposite condition, constipation, occurs when the large intestine absorbs too much water because food residues are moving slowly. As a result, the feces become hard and dry, which may make elimination difficult.

Cancerous tumors may develop in any part of the digestive system, though they most commonly occur in the large intestine, rectum, and anus. Colitis, which has various causes, is a potentially life-threatening inflammation of the large intestine. Chronic conditions that cause at least intermittent distress include irritable bowel syndrome, caused by spasms of muscles in the lower intestine, and Crohn’s disease, an inflammation of the intestines. Abnormal sensitivity to proteins called glutens can damage the lining of the small intestine and hinder absorption of nutrients, leading to malnutrition and other problems. The eating disorders anorexia nervosa and bulimia disrupt the normal functioning of the digestive system and are potentially fatal.

Diseases of Respiratory system

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The diseases and disorders of the respiratory system can affect any part of the respiratory tract and range from trivial to life-threatening. The nasal passages and pharynx, for example, are targets for the viruses that cause colds. These viruses infiltrate and destroy the cells of the nasal passage membranes. The immune system fights back by increasing blood flow to the area, bringing numerous virus-attacking white blood cells to the scene; this causes the membranes to swell, resulting in the stuffy nose associated with colds. Mucous secretions increase in response to the viral attack, creating the runny nose typical of colds. The infection can spread to the sinuses, the membrane-lined cavities in the head, as well as the lower respiratory tract and the middle ear.

The respiratory system is also subject to allergic reactions such as hay fever and asthma, brought about when the immune system is stimulated by pollen, dust, or other irritants. Hay fever is characterized by a runny nose, watery eyes, and sneezing. It usually occurs seasonally in response to abundant pollen in the air. In asthma, a person has difficulty breathing because the bronchi and bronchioles are temporarily constricted and inflamed. An asthma attack is typically mild, but can be severe enough to be life threatening.

Laryngitis, an inflammation of the larynx, is caused by a viral infection, irritants such as cigarette smoke, or by overuse of the voice. Laryngitis may cause hoarseness, or the voice may be reduced to a whisper until the inflammation subsides. Bronchitis is an inflammation of the membranes that line the bronchi or bronchioles. Bronchitis results from viral or bacterial infection or from irritating chemicals. Infections caused by bacteria or viruses can lead to pneumonia, a potentially serious condition of the lungs in which fluid and inflammation builds up in the alveoli, impeding the flow of oxygen and carbon dioxide between the capillaries and the alveoli.

Tuberculosis is the chronic or acute bacterial infection that primarily attacks the lungs, but which may also affect the kidneys, bones, lymph nodes, and brain. The disease is caused by Mycobacterium tuberculosis, a rod-shaped bacterium. Many people harbor the bacteria but have no symptoms of disease. When symptoms develop, they include coughing, chest pain, shortness of breath, loss of appetite, weight loss, fever, chills, and fatigue. Children and people with weakened immune systems are the most susceptible to TB.



A. Primary TB does not produce noticeable symptoms in its early stages, when it is not contagious. Macrophages, immune cells that detect and destroy foreign matter, ingest the TB bacteria and transport them to the lymph nodes where they may be inhibited or destroyed. If the immune cells fail to control the infection, the bacteria can multiply.

If the TB bacteria multiply, active primary tuberculosis develops. Patients with active primary TB experience such symptoms as coughing, night sweats, weight loss, and fever. A chest X ray may show shadows in the lung or fluid collection between the lung and its lining. If the immune system destroys the bacteria, the patient may experience no more than mild symptoms, such as a cough. If the bacteria are inhibited, rather than destroyed, the body’s immune cells and the bacteria form a lump known as a granuloma or tubercle. In effect, the immune cells form a wall around inactive bacteria. As long as the immune system remains strong, the TB bacteria remain walled off and inactive. The tubercles may appear as shadows in a chest X ray. If the immune system later becomes weakened, the tubercle may open, releasing the bacteria, and the infection may develop into secondary TB.


B. Secondary, or post-primary, TB, the formerly dormant bacteria multiply and destroy tissue in the lungs. They also may spread to the rest of the body via the bloodstream. Fluid or air may collect between the lungs and the lining of the lungs, while tubercles continue to develop in the lung, progressively destroying lung tissue. Coughing of blood or phlegm may occur.

Diagnosis of TB


Diagnosis of TB requires two separate methods. Tuberculin skin testing is a method of screening for exposure to TB infection. People infected with the TB bacteria develop a hypersensitivity to the bacteria even if they do not develop the disease. In the test a purified protein derived from the bacteria is injected into the skin. The skin area is inspected 48 to 72 hours later for a bump, or positive reaction. A positive reaction implies that TB infection has occurred. Skin tests are not 100 percent accurate, however, and they do not always indicate the presence of active disease.

A diagnosis of TB disease is established by identifying bacteria in sputum (material coughed up from the lungs) or other body fluids and tissues, along with an abnormal chest X ray and the presence of TB symptoms. Once TB has been diagnosed, further testing is required to determine which drugs would be most appropriate to treat the particular strain of TB bacteria.

Detecting the presence or the strain of the TB bacterium was once a time-consuming process that would often delay therapy. Today, the use of genetic engineering techniques greatly reduces the time required for diagnosis. A new technique is the polymerase chain reaction (PCR), which can rapidly duplicate a tiny amount of bacterial hereditary material from a small sample of infected sputum.

Treatment and prevention of TB

General preventive measures can be taken to reduce the spread of TB in public places. Ventilation systems lessen the chance of infection by dispersing the bacteria. Ultraviolet lighting also reduces, but does not eliminate, the threat of infection by killing TB bacteria in confined spaces. Vaccines, such as the bacillus Calmette-Guerin (BCG) vaccine, prepared from bacteria that have been weakened, are another preventive measure. The BCG vaccine is most effective in preventing childhood cases of TB.

With the advent of effective antibiotics for TB, drug therapy has become the cornerstone of treatment. Single-drug treatment often causes bacterial resistance to drugs. Therefore, all recommended therapies include multiple drugs given for at least 6 months, often for as long as 9 to 12 months. Adjustments to the treatments are made based on susceptibility of the bacterial strain. A combination of antibiotics is usually prescribed. In 1998, scientists successfully decoded the entire gene sequence, or genome, of the tuberculosis bacteria. This advance is likely to lead to the development of new methods for treatment and prevention of TB.

Pneumonia is the inflammation of one or both lungs. In people with pneumonia, air sacs in the lungs fill with fluid, preventing oxygen from reaching blood cells and nourishing the other cells of the body. Sometimes the inflammation occurs in scattered patches in the tissue around the ends of the bronchioles, the smallest air tubes in the lungs. This is known as bronchopneumonia. In other cases the inflammation is widespread and involves an entire lobe of the lung. This condition is called lobar pneumonia. In the United States about 5 million cases of pneumonia are reported each year.

Causes of Pneumonia

About 50% of pneumonia cases are caused by viruses, particularly those viruses that cause upper respiratory infections,such as the virus that cause influenza, adenoviruses, and rhinoviruses. Infection with the Streptococcus pneumoniae bacterium is the most common cause of bacterial pneumonia.Pneumococcus usually causes lobar pneumonia, attacking an entire lobe or portion of a lobe of the lung; in double pneumonia, pneumococcus attacks both lungs. Other type of pneumonia is also caused by mycoplasma. Epidemics of mycoplasma pneumonia occurs in schools and military.The most prominient symptom of mycoplasma pneumonia is a violent dry cough. Some patients experience nausea or vomiting.

Diagnosis and treatment of Pneumonia

A physician can diagnose pneumonia by tapping the chest and listening with a stethescope to the sound produced.Tapping the chest of a healthy person produces a resonant sound because of the air contained in the lungs. In a person with pneumonia, the air spaces of the lungs become filled with fluid, and tapping produces a dull, flat sound. The diagnosis of pneumonia is confirmed by taking an X-ray picture of the chest.To determine the cause of pneumonia, a physician takes a sample of the patient's sputum. Analysis of the sputum in the laboratory may identify the particular kind of microorganism causing the infection. Identification of the cause of pneumonia is important in determining treatment.


Antibiotics can cure bacterial pneumonia and speed recovery from mycoplasma pneumonia and PCP. Antibiotics rarely have an effect on pneumonia caused by viruses. However, patients with viral pneumonia often receive antibiotics to prevent bacterial pneumonia from developing during the course of their illness.Medication may be given to relieve chest pain and violent coughing, and oxygen may be administered if the patient has difficulty breathing. A vaccine is available that confers immunity against pneumococcus.


Asthma

Spasmodic asthma is characterized by contraction of the smooth muscle of the airways and, in severe attacks, by airway obstruction from mucus that has accumulated in the bronchial tree. This results in a greater or lesser degree of difficulty in breathing. One approach to classifying asthma differentiates cases that occur with an identifiable antigen, in which antigens affect tissue cells sensitized by a specific antibody, and cases that occur without an identifiable antigen or specific antibody. The former condition is known as "extrinsic" asthma and the latter as "intrinsic" asthma. Extrinsic asthma commonly manifests in childhood because the subject inherits an "atopic" characteristic: the serum contains specific antigens to pollens, mold spores, animal proteins of different kinds, and proteins from a variety of insects, particularly cockroaches and mites that occur in house dust. Exacerbation of extrinsic asthma is precipitated by contact with any of the proteins to which sensitization has occurred; airway obstruction is often worse in the early hours of the morning, for reasons not yet entirely elucidated. The other form of asthma, intrinsic, may develop at any age, and there may be no evidence of specific antigens. Persons with intrinsic asthma experience attacks of airway obstruction unrelated to seasonal changes, although it seems likely that the airway obstruction may be triggered by infections, which are assumed to be viral in many cases.


Asthma acquired as the result of occupational exposure (a special form of intrinsic asthma) is now recognized to be more common than previously suspected. Exposure to solder resin used in the electronics industry, to toluene diisocyanate (used in many processes as a solvent), to the dust of the western red cedar (in which plicatic acid is the responsible agent), and to many other substances can initiate an asthmatic state, with profound airflow obstruction developing when the subject is challenged by the agent.


It is a characteristic of all types of asthma that those with the condition may exhibit airflow obstruction when given aerosols of histamine or acetylcholine (both normally occurring smooth muscle constrictors) at much lower concentrations than provoke airflow obstruction in normal people; affected individuals may also develop airflow obstruction while breathing cold air or during exercise. These characteristics are used in the laboratory setting to study the airway status of patients. As a result of much recent work, it is thought that the diagnosis of asthma of any kind is difficult to sustain in the absence of a general increase in airway reactivity.


The acute asthmatic attack is alarming both for the sufferer and for the onlooker. There is acute difficulty in breathing, and the chest assumes a more and more inspiratory position. Despite the severe respiratory difficulty, the patient remains fully conscious. The most dangerous form of the condition is known as status asthmaticus. The bronchial spasm worsens over several hours or a day or so, the bronchi become plugged with thick mucus, and airflow is progressively more obstructed. The affected person becomes fatigued; the arterial oxygen tension falls still further, carbon dioxide accumulates in the blood (leading to drowsiness), and the acidity of the arterial blood increases to dangerous levels and may lead to cardiac arrest. Prompt treatment with intravenous corticosteroids and bronchodilators is usually sufficient to relieve the attack, but in occasional cases ventilatory assistance is required. In a few cases, death from asthma is remarkably rapid—too rapid for this complete sequence of events to have occurred, although at autopsy the lungs are overinflated. The exact mechanism of death in these cases is not completely understood.


Although the state of the airway is influenced by psychogenic factors, asthma is not correctly regarded as a disease commonly caused by psychological factors. It may interrupt normal activities and schooling to such an extent that it casts a shadow over the development of the personality. More commonly, it tends to diminish in severity with age, and people who had quite severe asthma in childhood may lead normal lives after the age of 20. It is now known that asthma attacks may be precipitated by food—in small children, possibly by milk; and some adults are extremely sensitive to sulfite compounds in food or wine. A subgroup of asthmatics are so sensitive to aspirin (acetylsalicylic acid) that ingestion of this chemical may lead to a life-threatening attack.


Changes in mortality from asthma in different countries have been closely studied, but the causes are obscure. It is clear, however, that there has been a considerable increase in the rate of hospital admissions for asthma in children and in adults up to the age of 60. Because there is now more effective treatment for asthma than was available previously, it is not clear why this should be occurring. Unless the asthma is complicated by infection (of which that by the fungus Aspergillus is common in damp climates), the chest radiograph remains normal. Asthma does not lead to the destructive lesions of emphysema (described below), although the physical appearance of the patient and the sounds of airflow obstruction in the lung may be similar in the two conditions.

Bronchitis

Acute Bronchitis: Acute bronchitis most commonly occurs as a consequence of viral infection. It may also be precipitated by acute exposure to irritant gases, such as ammonia, chlorine, or sulfur dioxide. In people with chronic bronchitis—a common condition in cigarette smokers—exacerbations of infection are common. The bronchial tree in acute bronchitis is reddened and congested, and minor blood streaking of the sputum may occur. Most cases of acute bronchitis resolve over a few days, and the mucosa repairs itself.


Bronchiolitis refers to inflammation of the small airways. Bronchiolitis probably occurs to some extent in acute viral disorders, particularly in children between the ages of one and two years, and particularly in infections with respiratory syncytial virus. In severe cases the inflammation may be severe enough to threaten life, but it normally clears spontaneously, with complete healing in all but a very small percentage of cases. In adults, acute bronchiolitis of this kind is not a well-recognized clinical syndrome, though there is little doubt that in most patients with chronic bronchitis, acute exacerbations of infection are associated with further damage to small airways. In isolated cases, an acute bronchiolitis is followed by a chronic obliterative condition, or this may develop slowly over time. This pattern of occurrence has only recently been recognized. In addition to patients acutely exposed to gases, in whom such a syndrome may follow the acute exposure, patients with rheumatoid arthritis may develop a slowly progressive obliterative bronchiolitis that may prove fatal. An obliterative bronchiolitis may appear after bone marrow replacement for leukemia and may cause shortness of breath and disability.


Exposure to oxides of nitrogen, which may occur from inhaling gas in silos, when welding in enclosed spaces such as boilers, after blasting underground, or in fires involving plastic materials, is characteristically not followed by acute symptoms. These develop some hours later, when the victim develops a short cough and progressive shortness of breath. A chest radiograph shows patchy inflammatory change, and the lesion is an acute bronchiolitis. Symptomatic recovery may mask incomplete resolution of the inflammation.


An inflammation around the small airways, known as a respiratory bronchiolitis, is believed to be the earliest change that occurs in the lung in cigarette smokers, although it does not lead to symptoms of disease at that stage. The inflammation is probably reversible if smoking is discontinued. It is not known whether those who develop this change (after possibly only a few years of smoking) are or are not at special risk of developing the long-term changes of chronic bronchitis and emphysema.
Chronic Bronchitis: The chronic cough and sputum production of chronic bronchitis were once dismissed as nothing more than "smoker's cough," without serious implications. But the striking increase in mortality from chronic bronchitis and emphysema that occurred after World War II in all Western countries indicated that the long-term consequences of chronic bronchitis could be serious. This common condition is characteristically produced by cigarette smoking. After about 15 years of smoking, a blob of mucus is coughed up in the morning, owing to an increase in size and number of mucous glands lining the large airways. The increase in mucous cells and the development of chronic bronchitis may be enhanced by breathing polluted air (particularly in areas of uncontrolled coal burning) and by a damp climate. The changes are not confined to large airways, though these produce the dominant symptom of chronic sputum production. Changes in smaller bronchioles lead to obliteration and inflammation around their walls. All of these changes together, if severe enough, can lead to disturbances in the distribution of ventilation and perfusion in the lung, causing a fall in arterial oxygen tension and a rise in carbon dioxide tension. By the time this occurs, the ventilatory ability of the patient, as measured by the velocity of a single forced expiration, is severely compromised; in a cigarette smoker, ventilatory ability has usually been declining rapidly for some years. It is not clear what determines the severity of these changes, since many people can smoke for decades without evidence of significant airway changes, while others may experience severe respiratory compromise after 15 years or less of exposure.

Pulmonary emphysema
This irreversible disease consists of destruction of alveolar walls. It occurs in two forms, centrilobular emphysema, in which the destruction begins at the centre of the lobule, and panlobular (or panacinar) emphysema, in which alveolar destruction occurs in all alveoli within the lobule simultaneously. In advanced cases of either type, this distinction can be difficult to make. Centrilobular emphysema is the form most commonly seen in cigarette smokers, and some observers believe it is confined to smokers. It is more common in the upper lobes of the lung (for unknown reasons) and probably causes abnormalities in blood gases out of proportion to the area of the lung involved by it. By the time the disease has developed, some impairment of ventilatory ability has probably occurred. Panacinar emphysema may also occur in smokers, but it is the type of emphysema characteristically found in the lower lobes of patients with a deficiency in the antiproteolytic enzyme known as alpha1-antitrypsin. Like centrilobular emphysema, panacinar emphysema causes ventilatory limitation and eventually blood gas changes. Other types of emphysema, of less importance than the two major varieties, may develop along the dividing walls of the lung (septal emphysema) or in association with scars from other lesions.


A major step forward in understanding the development of emphysema followed the identification, in Sweden, of families with an inherited deficiency of alpha1-antitrypsin, an enzyme essential for lung integrity. Members of affected families commonly developed panacinar emphysema in the lower lobes, unassociated with chronic bronchitis but leading to ventilatory impairment and disability. Intense investigation of this major clue led to the "protease-antiprotease" theory of emphysema. It is postulated that cigarette smoking either increases the concentration of protease enzymes released in the lung (probably from white blood cells), or impairs the lung's defenses against these enzymes, or both. Although many details of the essential biochemical steps at the cellular level remain to be clarified, this represents a major step forward in understanding a disease whose genesis was once ascribed to overinflation of the lung (like overdistending a bicycle tire).


Chronic bronchitis and emphysema are distinct processes. Both may follow cigarette smoking, however, and they commonly occur together, so determination of the extent of each during life is not easy. In general, significant emphysema is more likely if ventilatory impairment is constant, gas transfer in the lung (usually measured with carbon monoxide) is reduced, and the lung volumes are abnormal. The radiological technique of computerized tomography may improve the accuracy of detection of emphysema. Many people with emphysema suffer severe incapacity before the age of 60; thus, emphysema is not a disease of the elderly only. A reasonably accurate diagnosis can be made from pulmonary function tests, careful radiological examination, and a detailed history. The physical examination of the chest reveals evidence of airflow obstruction and overinflation of the lung, but the extent of lung destruction cannot be reliably gauged from these signs, and therefore laboratory tests are required.


The prime symptom of emphysema, which is always accompanied by a loss of elasticity of the lung, is shortness of breath, initially on exercise only, and associated with loss of normal ventilatory ability. The severity of this loss is a predictor of survival in this condition. But once ventilatory ability is reduced to less than half the normal value, what determines outcome is the severity of the changes in blood gases, chiefly the lowering of arterial blood oxygen tension. The chronic hypoxemia (lowered oxygen tension) is believed to lead to the development of increased blood pressure in the pulmonary circulation, which in turn leads to failure of the right ventricle of the heart. The symptom (subjective evidence perceived by the patient) of right ventricular failure is swelling of the ankles; the signs (objective evidence discovered by the examining physician) are engorgement of the neck veins and enlargement of the liver. These are portents of advanced lung disease in this condition. The hypoxemia may also lead to an increase in total hemoglobin content and in the number of circulating red blood cells, as well as to psychological depression, irritability, loss of appetite, and loss of weight. Thus the advanced syndrome of chronic obstructive lung disease may cause not only such shortness of breath that the afflicted person is unable to dress without assistance, but also numerous other symptoms.


The slight fall in ventilation that normally accompanies sleep may exacerbate the failure of lung function in chronic obstructive lung disease, leading to a further fall in arterial oxygen tension and an increase in pulmonary arterial pressure.


Unusual forms of emphysema also occur. In one form the disease appears to be unilateral, involving one lung only and causing few symptoms. Unilateral emphysema is believed to result from a severe bronchiolitis in childhood that prevented normal maturation of the lung on that side. "Congenital lobar emphysema" of infants is usually a misnomer, since there is no alveolar destruction. It is most commonly caused by overinflation of a lung lobe due to developmental malformation of cartilage in the wall of the major bronchus. Such lobes may have to be surgically removed to relieve the condition.

Lung cancer develops in individuals with a genetic predisposition to the disease who are exposed to cancer-causing agents, such as tobacco smoke, asbestos, and uranium. Cancerous tumors may start in the bronchi, bronchioles, or in the alveolar lung tissue. If lung cancer is detected before the cancer has spread to other parts of the body, treatments are more effective, and the prognosis for full recovery is good. Unfortunately, 85 percent of lung cancer cases are diagnosed after the cancer has spread, and for these cases, the prognosis is very poor.

Respiratory Distress Syndrome (RDS) is the name for a cluster of symptoms that indicate severe malfunctioning of the lungs. In infants, RDS is termed Infant Respiratory Distress Syndrome (IRDS). Commonly found in premature infants, IRDS results when the alveoli fail to fully expand during inhalation. Expansion of the alveoli requires a chemical called surfactant, but in many premature infants, the alveoli are not developed enough to produce this vital substance. IRDS is treated by administering air and surfactant through a breathing tube until the alveoli begin producing surfactant on their own. Adult Respiratory Distress Syndrome (ARDS) results when lungs are severely injured, for example, in an automobile accident, by poisonous gases, or as a response to inflammation in the lungs. ARDS is a life-threatening condition with a survival rate of about 50 percent.

Respiratory system

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Respiratory System is responsible to deliver oxygen to the circulatory system for transport to all body cells. Oxygen is essential for cells, which use this vital substance to liberate the energy needed for cellular activities. In addition to supplying oxygen, the respiratory system aids in removing of carbon dioxide, preventing the lethal buildup of this waste product in body tissues. Day-in and day-out, without the prompt of conscious thought, the respiratory system carries out its life-sustaining activities. If the respiratory system’s tasks are interrupted for more than a few minutes, serious, irreversible damage to tissues occurs, followed by the failure of all body systems, and ultimately, death.

While the intake of oxygen and removal of carbon dioxide are the primary functions of the respiratory system, it plays other important roles in the body. The respiratory system helps regulate the balance of acid and base in tissues, a process crucial for the normal functioning of cells. It protects the body against disease-causing organisms and toxic substances inhaled with air. The respiratory system also houses the cells that detect smell, and assists in the production of sounds for speech.

The respiratory and circulatory systems work together to deliver oxygen to cells and remove carbon dioxide in a two-phase process called respiration. The first phase of respiration begins with breathing in, or inhalation. Inhalation brings air from outside the body into the lungs. Oxygen in the air moves from the lungs through blood vessels to the heart, which pumps the oxygen-rich blood to all parts of the body. Oxygen then moves from the bloodstream into cells, which completes the first phase of respiration. In the cells, oxygen is used in a separate energy-producing process called cellular respiration, which produces carbon dioxide as a byproduct. The second phase of respiration begins with the movement of carbon dioxide from the cells to the bloodstream. The bloodstream carries carbon dioxide to the heart, which pumps the carbon dioxide-laden blood to the lungs. In the lungs, breathing out, or exhalation, removes carbon dioxide from the body, thus completing the respiration cycle.

NASAL PASSAGE
The flow of air from outside of the body to the lungs begins with the nose, which is divided into the left and right nasal passages. The nasal passages are lined with a membrane composed primarily of one layer of flat, closely packed cells called epithelial cells. Each epithelial cell is densely fringed with thousands of microscopic cilia, fingerlike extensions of the cells. Interspersed among the epithelial cells are goblet cells, specialized cells that produce mucus, a sticky, thick, moist fluid that coats the epithelial cells and the cilia. Numerous tiny blood vessels called capillaries lie just under the mucous membrane, near the surface of the nasal passages. While transporting air to the pharynx, the nasal passages play two critical roles: they filter the air to remove potentially disease-causing particles; and they moisten and warm the air to protect the structures in the respiratory system.

Filtering prevents airborne bacteria, viruses, other potentially disease-causing substances from entering the lungs, where they may cause infection. Filtering also eliminates smog and dust particles, which may clog the narrow air passages in the smallest bronchioles. Coarse hairs found just inside the nostrils of the nose trap airborne particles as they are inhaled. The particles drop down onto the mucous membrane lining the nasal passages. The cilia embedded in the mucous membrane wave constantly, creating a current of mucus that propels the particles out of the nose or downward to the pharynx. In the pharynx, the mucus is swallowed and passed to the stomach, where the particles are destroyed by stomach acid. If more particles are in the nasal passages than the cilia can handle, the particles build up on the mucus and irritate the membrane beneath it. This irritation triggers a reflex that produces a sneeze to get rid of the polluted air.

The nasal passages also moisten and warm air to prevent it from damaging the delicate membranes of the lung. The mucous membranes of the nasal passages release water vapor, which moistens the air as it passes over the membranes. As air moves over the extensive capillaries in the nasal passages, it is warmed by the blood in the capillaries. If the nose is blocked or “stuffy” due to a cold or allergies, a person is forced to breathe through the mouth. This can be potentially harmful to the respiratory system membranes, since the mouth does not filter, warm, or moisten air.

In addition to their role in the respiratory system, the nasal passages house cells called olfactory receptors, which are involved in the sense of smell. When chemicals enter the nasal passages, they contact the olfactory receptors. This triggers the receptors to send a signal to the brain, which creates the perception of smell.

PHARYNX
Air leaves the nasal passages and flows to the pharynx, a short, funnel-shaped tube about 13 cm (5 in) long that transports air to the larynx. Like the nasal passages, the pharynx is lined with a protective mucous membrane and ciliated cells that remove impurities from the air. In addition to serving as an air passage, the pharynx houses the tonsils, lymphatic tissues that contain white blood cells. The white blood cells attack any disease-causing organisms that escape the hairs, cilia, and mucus of the nasal passages and pharynx. The tonsils are strategically located to prevent these organisms from moving further into the body. One tonsil, called the adenoids, is found high in the rear wall of the pharynx. A pair of tonsils, the palatine tonsils, is located at the back of the pharynx on either side of the tongue. Another pair, the lingual tonsils, is found deep in the pharynx at the base of the tongue. In their battles with disease-causing organisms, the tonsils sometimes become swollen with infection. When the adenoids are swollen, they block the flow of air from the nasal passages to the pharynx, and a person must breathe through the mouth.

LARYNX
Air moves from the pharynx to the larynx, a structure about 5 cm (2 in) long located approximately in the middle of the neck. Several layers of cartilage, a tough and flexible tissue, comprise most of the larynx. A protrusion in the cartilage called the Adam’s apple sometimes enlarges in males during puberty, creating a prominent bulge visible on the neck.

While the primary role of the larynx is to transport air to the trachea, it also serves other functions. It plays a primary role in producing sound; it prevents food and fluid from entering the air passage to cause choking; and its mucous membranes and cilia-bearing cells help filter air. The cilia in the larynx waft airborne particles up toward the pharynx to be swallowed.

Food and fluids from the pharynx usually are prevented from entering the larynx by the epiglottis, a thin leaf like tissue. The “stem” of the leaf attaches to the front and top of the larynx. When a person is breathing, the epiglottis is held in a vertical position, like an open trap door. When a person swallows, however, a reflex causes the larynx and the epiglottis to move toward each other, forming a protective seal, and food and fluids are routed to the esophagus. If a person is eating or drinking too rapidly, or laughs while swallowing, the swallowing reflex may not work, and food or fluid can enter the larynx. Food, fluid, or other substances in the larynx initiate a cough reflex as the body attempts to clear the larynx of the obstruction. If the cough reflex does not work, a person can choke, a life-threatening situation. The Heimlich maneuver is a technique used to clear a blocked larynx (see First Aid). A surgical procedure called a tracheotomy is used to bypass the larynx and get air to the trachea in extreme cases of choking.

TRECHEA, BRONCHI AND BRONCHIOLES
Air passes from the larynx into the trachea, a tube about 12 to 15 cm (about 5 to 6 in) long located just below the larynx. The trachea is formed of 15 to 20 C-shaped rings of cartilage. The sturdy cartilage rings hold the trachea open, enabling air to pass freely at all times. The open part of the C-shaped cartilage lies at the back of the trachea, and the ends of the “C” are connected by muscle tissue.

The base of the trachea is located a little below where the neck meets the trunk of the body. Here the trachea branches into two tubes, the left and right bronchi, which deliver air to the left and right lungs, respectively. Within the lungs, the bronchi branch into smaller tubes called bronchioles. The trachea, bronchi, and the first few bronchioles contribute to the cleansing function of the respiratory system, for they, too, are lined with mucous membranes and ciliated cells that move mucus upward to the pharynx.

ALVEOLI
The bronchioles divide many more times in the lungs to create an impressive tree with smaller and smaller branches, some no larger than 0.5 mm (0.02 in) in diameter. These branches dead-end into tiny air sacs called alveoli. The alveoli deliver oxygen to the circulatory system and remove carbon dioxide. Interspersed among the alveoli are numerous macrophages, large white blood cells that patrol the alveoli and remove foreign substances that have not been filtered out earlier. The macrophages are the last line of defense of the respiratory system; their presence helps ensure that the alveoli are protected from infection so that they can carry out their vital role.

The alveoli number about 150 million per lung and comprise most of the lung tissue. Alveoli resemble tiny, collapsed balloons with thin elastic walls that expand as air flows into them and collapse when the air is exhaled. Alveoli are arranged in grapelike clusters, and each cluster is surrounded by a dense hairnet of tiny, thin-walled capillaries. The alveoli and capillaries are arranged in such a way that air in the wall of the alveoli is only about 0.1 to 0.2 microns from the blood in the capillary. Since the concentration of oxygen is much higher in the alveoli than in the capillaries, the oxygen diffuses from the alveoli to the capillaries. The oxygen flows through the capillaries to larger vessels, which carry the oxygenated blood to the heart, where it is pumped to the rest of the body.

Carbon dioxide that has been dumped into the bloodstream as a waste product from cells throughout the body flows through the bloodstream to the heart, and then to the alveolar capillaries. The concentration of carbon dioxide in the capillaries is much higher than in the alveoli, causing carbon dioxide to diffuse into the alveoli. Exhalation forces the carbon dioxide back through the respiratory passages and then to the outside of the body.

REGULATION
The flow of air in and out of the lungs is controlled by the nervous system, which ensures that humans breathe in a regular pattern and at a regular rate. Breathing is carried out day and night by an unconscious process. It begins with a cluster of nerve cells in the brain stem called the respiratory center. These cells send simultaneous signals to the diaphragm and rib muscles, the muscles involved in inhalation. The diaphragm is a large, dome-shaped muscle that lies just under the lungs. When the diaphragm is stimulated by a nervous impulse, it flattens. The downward movement of the diaphragm expands the volume of the cavity that contains the lungs, the thoracic cavity. When the rib muscles are stimulated, they also contract, pulling the rib cage up and out like the handle of a pail. This movement also expands the thoracic cavity. The increased volume of the thoracic cavity causes air to rush into the lungs. The nervous stimulation is brief, and when it ceases, the diaphragm and rib muscles relax and exhalation occurs. Under normal conditions, the respiratory center emits signals 12 to 20 times a minute, causing a person to take 12 to 20 breaths a minute. Newborns breathe at a faster rate, about 30 to 50 breaths a minute.

The rhythm set by the respiratory center can be altered by conscious control. The breathing pattern changes when a person sings or whistles, for example. A person also can alter the breathing pattern by holding the breath. The cerebral cortex, the part of the brain involved in thinking, can send signals to the diaphragm and rib muscles that temporarily override the signals from the respiratory center. The ability to hold one’s breathe has survival value. If a person encounters noxious fumes, for example, it is possible to avoid inhaling the fumes.

A person cannot hold the breath indefinitely, however. If exhalation does not occur, carbon dioxide accumulates in the blood, which, in turn, causes the blood to become more acidic. Increased acidity interferes with the action of enzymes, the specialized proteins that participate in virtually all biochemical reaction in the body. To prevent the blood from becoming too acidic, the blood is monitored by special receptors called chemoreceptors, located in the brainstem and in the blood vessels of the neck. If acid builds up in the blood, the chemoreceptors send nervous signals to the respiratory center, which overrides the signals from the cerebral cortex and causes a person to exhale and then resume breathing. These exhalations expel the carbon dioxide and bring the blood acid level back to normal.

A person can exert some degree of control over the amount of air inhaled, with some limitations. To prevent the lungs from bursting from overinflation, specialized cells in the lungs called stretch receptors measure the volume of air in the lungs. When the volume reaches an unsafe threshold, the stretch receptors send signals to the respiratory center, which shuts down the muscles of inhalation and halts the intake of air.

CELLEULAR RESPIRATION
The first stage of glucose catabolism is glycolysis. A glucose molecule breaks to give two molecules of pyruvic acid in a series of ten reactions. It is the common process for aerobic as well as anaerobic respiration. Glycolysis is also called EMP pathway in honour of its discoverers.

The second stage of cellular respiration, the three-stage process by which living cells break down organic fuel molecules in the presence of oxygen to harvest the energy they need to grow and divide. This metabolic process occurs in most plants, animals, fungi, and many bacteria. In all organisms except bacteria the TCA cycle is carried out in the matrix of intracellular structures called mitochondria.
The TCA cycle plays a central role in the breakdown, or catabolism, of organic fuel molecules—i.e., glucose and some other sugars, fatty acids, and some amino acids. Before these rather large molecules can enter the TCA cycle they must be degraded into a two-carbon compound called acetyl coenzyme A (acetyl CoA). Once fed into the TCA cycle, acetyl CoA is converted into carbon dioxide and energy.

The TCA cycle consists of eight steps catalyzed by eight different enzymes. The cycle is initiated (1) when acetyl CoA reacts with the compound oxaloacetate to form citrate and to release coenzyme A (CoA-SH). Then, in a succession of reactions, (2) citrate is rearranged to form isocitrate; (3) isocitrate loses a molecule of carbon dioxide and then undergoes oxidation to form alpha-ketoglutarate; (4) alpha-ketoglutarate loses a molecule of carbon dioxide and is oxidized to form succinyl CoA; (5) succinyl CoA is enzymatically converted to succinate; (6) succinate is oxidized to fumarate; (7) fumarate is hydrated to produce malate; and, to end the cycle, (8) malate is oxidized to oxaloacetate. Each complete turn of the cycle results in the regeneration of oxaloacetate and the formation of two molecules of carbon dioxide.
Energy is produced in a number of steps in this cycle of reactions. In step 5, one molecule of adenosine triphosphate (ATP), the molecule that powers most cellular functions, is produced. Most of the energy obtained from the TCA cycle, however, is captured by the compounds nicotinamide adenine dinucleotide (NAD+) and flavin adenine dinucleotide (FAD) and converted later to ATP. Energy transfers occur through the relay of electrons from one substance to another, a process carried out through the chemical reactions known as oxidation and reduction, or redox reactions. (Oxidation involves the loss of electrons from a substance and reduction the addition of electrons.) For each turn of the TCA cycle, three molecules of NAD+ are reduced to NADH and one molecule of FAD is reduced to FADH2. These molecules then transfer their energy to the electron transport chain, a pathway that is part of the third stage of cellular respiration. The electron transport chain in turn releases energy so that it can be converted to ATP through the process of oxidative phosphorylation.


HAZARDS
The respiratory system can be damaged by a variety of chemicals found in the environment, ranging from automobile fumes and industrial smoke to household cleaning products. Cigarette smoke, however, poses a particularly serious threat to the respiratory system because of the tar and other substances that enter the lungs. After a person smokes just one cigarette, for example, tar temporarily paralyzes the cilia of the upper and lower respiratory tracts. The tar also temporarily immobilizes the macrophages in the alveoli of the lungs. With the filtering and cleansing functions inactivated, the air passages and lungs are exposed not only to the irritating effects of tar but also to airborne bacteria, viruses, and other particles. These, along with the tar, settle in the mucous layers of the lungs. The paralyzed cilia recover after about one hour, but repeated smoking eventually kills them. Repeated smoking also causes mucus to build up in the lungs and block the smaller air passages. The blockage triggers a cough reflex—the familiar “smoker’s cough”—the lung’s effort to clear the airways. In addition, tobacco smoke contains over 40 chemicals known to cause cancer. Smoking is responsible for almost 90 percent of lung cancer cases among men, and more than 70 percent among women.

Workers in occupations that produce impurities released into the air are at high risk for respiratory illnesses. Sandblasters, stone cutters, quarry workers, miners, construction workers, people who install brake lining or insulation, people who work in shipyards or on farms, and people who pick cotton are among those at risk. In the United States, the Occupational Safety and Health Administration (OSHA) issues regulations that protect workers—requiring air masks with filters for certain jobs, for example. The Environmental Protection Agency (EPA) monitors and regulates the amount of pollutants released into the air. Despite these efforts, respiratory illnesses remain higher among workers who have significant exposure to air pollutants (see Environmental and Occupational Diseases).

Normal, everyday exposure to air pollution from cars and industrial emissions in the city also weakens the respiratory system of city-dwellers. Even if a person does not smoke, the city air gradually changes pink, healthy lung tissue to tissue darkened with particles of smog, dust, and other pollutants, making the lungs more vulnerable to infection. While outdoor pollutants pose threats to the respiratory system, a far greater threat is created by indoor air pollution. In homes and offices, a variety of substances, including cleaning compounds, air fresheners, synthetic carpets and furniture, and certain construction materials, can emit hazardous gases, which become highly concentrated in unventilated rooms. Individuals at greatest risk are those who spend most of their time indoors, children, the elderly, and people with a history of respiratory illnesses. Like outdoor air pollutants, indoor air pollutants weaken the lungs and invite infection. The long-term effects of air pollution are difficult to measure, but may include cancer and other serious diseases.

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