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Neutralizing antibodies develop against the specific serotype that caused the infection allergy medicine for babies 6 months discount 10mg alavert fast delivery, and the titer remains stable for over a decade allergy treatment services generic 10mg alavert visa. Volunteers can be successfully infected by intranasal inoculation allergy symptoms utcroal coffing chain buy alavert 10mg on line, although replication in the lower airway has not been confirmed allergy testing elizabethtown ky discount 10 mg alavert free shipping. After 3 to 7 days of fever, a nonproductive cough may progress to dyspnea and hypoxemia in 15% of patients. The associated mortality rate is 3% to 6% (or as high as 43% to 55% when considering patients older than 60 years of age), but it is much lower in children. For the same purpose, tubes, solutions, and buffers that are used for the collection, transport, and processing of samples should be ribonuclease free. For serology, an acute sample of clotted blood is collected as early as possible during the course of the disease, and a convalescent sample is sent 2 to 3 weeks later. Ideally, at least 2 mL of blood is obtained, although in infants less will often suffice. The sample should arrive in the laboratory within 1 day and should not be frozen, as this will provoke hemolysis. Upper Respiratory Tract Specimen Samples collected during the first days of symptoms (when viral shedding is maximal) lead to higher recovery rates. Throat swabs should be collected vigorously to ensure that mucus and cellular material is obtained from the pharynx, while in older children throat gargles can be obtained. Nasal wash is shown to produce the highest viral detection rate and relatively low patient discomfort compared to swabs, aspirates, and brushings. Usually this is contained in a small sterile bottle, and, after immersion, the wooden shaft of the swab is broken level with the neck of the container, the cap is replaced, and the fluid is gently agitated. When the time interval between collection and delivery is less than 2 hours, specimens should be transferred to the laboratory at room temperature; when the time interval is 2 to 24 hours, they should be transferred on ice. They can also be used to prepare slides for immunofluorescent detection, either by rolling the swab directly on the slide or after recovery of cells by centrifugation. Although induced sputum is often contaminated by oropharyngeal components that hinder viral recovery, it is an easily obtainable sample, at least in older children, in whom the success rate is >70%. Therefore, it is often used after either filtration through 200-nm membrane filters or dilution, usually in the presence of a reducing agent such as 0. Alternatively, when the cell monolayer is permitted to grow covered by a solid (agar) medium, the foci of virus-infected cells form plaques that may be stained by specific dyes. When a suspension of erythrocytes derived from a suitable species is added to the infected cell culture, they adhere in clumps after a certain period. Rotation enhances the yield of a cultured virus, while liposomal and other agents added in the media, as well as centrifugation protocols, may increase the detection rate. However, co-culture with helper cells often leads to higher recovery rates because this technique overcomes the viral inhibitory activity of certain tissue homogenates. Cell culture can be used in two additional ways for the identification of respiratory viruses. Conversely, virus strains isolated from patients can be exposed to specific immune sera known to prevent such activities, and the final result can be assessed on the cell culture. In many cases, cell culture remains the gold standard, often achieving the highest sensitivity scores and providing an isolate for epidemiologic and typing purposes or antiviral susceptibility assays. Virus Cultures Culture of a virus from a clinical specimen confirms the presence of viable virus. Cell Culture For each respiratory virus, there are a number of cell lines that allow its replication in vitro (Table 24-2). Susceptible cell cultures may undergo degenerative processes on exposure to respiratory viruses. B, At later time points, fully developed cytopathic effect gradually leads to cellular detachment, cell debris, and separation of the cell layer. More rapid protocols that use a combination of cell culture with another detection method. With these techniques, the sample is inoculated onto the culture, and the presence of replicating virus is verified after 24 to 48 hours by the second method. The R-mix monolayers that can be used directly from cryopreserved vials are inoculated on coverslips with the clinical sample, and 24 hours later the coverslips are removed and stained with a mixture of antisera against many respiratory viruses. If a positive signal is present, cells from a parallel coverslip can be dispersed onto a suitable chamber containing multiple coverslips that can be examined separately for the presence of individual respiratory viruses using monoclonal antibodies. Inoculation into the amniotic cavity is used mainly for the isolation of such viruses from clinical samples. Detection of Whole Viruses by Electron Microscopy this is the only method that allows direct inspection of viruses, detects pathogens that are difficult to cultivate, and is applied during epidemics of unknown etiology. Preparation of samples and negative staining techniques are fast, easy, and inexpensive processes. On the other hand, the sensitivity limit is approximately 106 viral particles/mL, which renders detection difficult after the first days of infection. Fluid Samples In a typical protocol, a 300- or 400-mesh grid is placed on a drop of sample for 5 to 15 minutes. Fluid samples should be placed on support films, made either from Collodion films (2% solution in isoamyl acetate) or from the mechanically stronger 0. The films are cast on a glass slide by experienced personnel, and grids are made by pressing the grid onto the film slide in the presence of water. A silver-gray rather than charcoalgray or gold color coincides with optimal film thickness, and additional carbon coating under vacuum facilitates spreading of the sample, which improves the results. Glow discharging under the vacuum or treatment of the grids with a suitable agent. This can be achieved with ultracentrifugation, ultrafiltration, or agar diffusion. The pseudoreplica technique is a variation whereby the drop is allowed to diffuse into the agar and then is irradiated and covered by Formvar film. Then the Formvar membrane is carefully removed and allowed to float onto a water surface. Grids are then applied on the replica membrane and picked up with the aid of filter paper. Antibodies are also used for the concentration of viruses in suspension (clumping). For aggregation, the samples can be incubated with the antiserum, centrifuged, and placed onto grids with the pseudoreplica technique; alternatively, antiserum is mixed with agar, and a grid is placed onto the gel. Virus suspension is then added and allowed to absorb, followed by removal and staining of the grid. In solid-phase immunoelectron microscopy, the film is coated with antibodies before incubation with virus suspension. Immunoprecipitation techniques are particularly helpful when picornaviruses need to be detected. Some viruses tend to clump in the absence of antiserum, reducing the specificity of this procedure. Viruses in suspension or on grids can be incubated with primary antiserum, allowed to aggregate, and after the antibody has been washed away, the preparation can be treated with a colloidal gold-labeled secondary antibody. Gold labeling has been used specifically to detect immune complexes in serum, as well as subviral particles. In a somewhat different approach, viruses are exposed to excess antibodies, resulting in extensive coating rather than aggregation of the viruses. This method allows specific identification and serotyping of viruses and can serve to assess the reactivity of convalescent serum against known viruses. On the other hand, AdV is membrane-associated and may be lost on removal of the debris with centrifugation. Because the sample area used is limited, it is wise first to stain sections with suitable stains.
National Hospital Discharge Survey data system15 dog allergy grass treatment buy 10mg alavert with mastercard,16 or the Tennessee Medicaid Database17 (approximately 1% of U allergy testing harrisonburg va alavert 10mg amex. Alveolar walls thicken allergy symptoms of rheumatoid arthritis order alavert 10 mg otc, and the alveolar space becomes occluded with exudates allergy testing symptoms buy alavert 10 mg on-line, sloughed cells, and activated macrophages. The physiology of the disease reflects an inflammatory process that interferes with gas exchange, resulting in elevation of the alveolar-arterial Po2 difference. Many cases of viral pneumonia in young children are also accompanied by inflammation of the bronchioles, and air trapping contributes to the poor level of gas exchange. Children compensate for respiratory compromise better than do adults, generally by increasing the respiratory rate. Children show a remarkable resilience when faced with respiratory compromise, even though their airways exhibit a much higher intrinsic level of resistance. The histopathologic mechanisms underlying acute viral pulmonary disease in otherwise healthy children are not completely understood because lung tissue is rarely obtained for histology before mechanical ventilation or other medical interventions in previously healthy patients. It is thought that the initial infection occurs in the nasopharynx after inoculation with contaminated respiratory secretions (fomite transmission) or exposure to large-particle aerosols containing virus. The viruses that cause pneumonia all have surface fusion proteins that mediate both virus-cell fusion and cell-cell fusion in monolayer cell culture. The viruses cause cytopathic effects following infection by inducing necrosis or apoptosis of infected cells. The viral fusion peptides of these viruses cause multinucleated cell (syncytium) formation in cell monolayer cultures. It is presumed that they cause syncytia formation in vivo, but the direct evidence for this is scarce. Impaired mucociliary clearance caused by infection of ciliated cells probably contributes to progression to pneumonia. Some of the respiratory viruses cause an abortive round of infection in cultured macrophages or dendritic cells. Infection of these antigen-presenting cell types may contribute to inflammatory disease of the lung. The mechanism for spread of infection to the lower respiratory tract within days of inoculation is unknown. Virus probably spreads by microaspiration of infected secretions or by cell-to-cell spread. The rapid time course of spread in vivo suggests that aspiration of infected secretions results in direct inoculation of the lower respiratory tract. In summary, the population(s) of cells that are the primary target of respiratory virus infections in humans are probably epithelial in origin but have not been fully defined in normal hosts. These cytokine-regulated pathways appear to contribute to airway inflammation during pneumonia. Infected epithelial cells appear to initiate a cascade of events that represent components of the innate immune response. This immune cytolysis is important to disease resolution but comes at the price of inducing some level of immunopathology. The cell surface factors that facilitate homing of lymphocytes to lung tissue are under investigation. Infants show nasal flaring, grunting, and marked retractions during severe disease. Systemic toxicity is less common than with bacterial infection because respiratory viruses (other than measles virus) rarely cause viremia. In fact, most respiratory viruses appear to be limited to the most superficial cells at the lumenal surface of the airway. Of the conventional respiratory viruses, influenza virus is the one that most frequently causes high fever and toxic appearance. Physical examination reveals crackles on auscultation, generally more prominent on inspiration. Therefore, concomitant coryza is common, complicated in about one third of cases with otitis media. Nasal obstruction caused by purulent nasal secretions contributes to the respiratory distress, especially in infants. Mild to moderate dehydration is common as a result of increased respiratory and other insensible losses, and poor oral fluid intake. Lower respiratory tract illness is defined clinically as the presence of crackles, rhonchi, or wheezes on physical examination or as infiltrates on a chest radiograph. Pneumonia is an inflammation caused by infection of the lung parenchyma, comprising alveoli and interstitial tissue with possible extension to the bronchioles. Viral pneumonia during childhood is often one component of a lower respiratory illness that also affects the small and large conducting airways. Children who have an effusion or an empyema identified on chest radiograph may need a computed tomography scan to define further the scope of the problem, but these complications are rare in viral pneumonia. Radiologic findings on chest radiographs of viral pneumonia are similar to those of bronchiolitis and reactive airways disease. The usual findings on chest radiographs are hyperaeration, prominent lung markings caused by bronchial wall thickening, and focal areas of atelectasis. The findings are commonly thought to differ from the typical case of bacterial pneumonia, which usually has been thought to present as lobar consolidation. It is true that most children with focal alveolar pneumonia have laboratory evidence of a bacterial infection, especially those with lobar infiltrates. However, half of the children with solely interstitial infiltrates on chest radiograph had evidence of bacterial infection in some studies. One also cannot differentiate viral pneumonia from bronchiolitis or reactive airways disease on the basis of radiologic findings alone. Differentiation is based on non-radiologic factors such as the age of the patient and the clinical history. The chest radiograph in newborns with viral pneumonia usually shows bilateral diffuse densities or may have a granular appearance, similar to that found in hyaline membrane disease. When infection is congenital, radiographic changes may be present at birth, whereas the radiographs of infants infected during birth may be normal initially but can progress rapidly during the first days of life. In newborns, group B streptococcus infection and hyaline membrane disease are the most common considerations. Common bacterial causes of pneumonia are Bordetella pertussis, Streptococcus pneumoniae, Haemophilus influenzae (mostly nontypable species in the era of universal immunization against type B), and Mycobacterium infections (including tuberculosis). Histoplasma capsulatum infection is relatively common in certain areas of the United States and causes an atypical pneumonia. Cryptococcus neoformans infection is also a consideration in immunocompromised patients. Many published studies have addressed the differentiation of bacterial from viral pneumonia using clinical, radiologic, and routine hematologic tests, but these methods have not been found to be sufficiently reliable in differential diagnosis. B, By 1 week of life, mechanical ventilation is discontinued and the lung fields normalize. D, By 7 weeks of life, the infant remained on a mechanical ventilator, but infiltrates and atelectasis were improving. A lobar, segmental, or rounded well-defined pneumonia affecting a single lobe is more likely to be bacterial in etiology, as are cases associated with large pleural effusions, abscess, bullae, or pneumatoceles. A bedside cold agglutinins test may be positive in the case of viral pneumonia or mycoplasmal infection, thus it is not a particularly helpful test in distinguishing etiology. There is little direct evidence in immunocompetent individuals that co-infection is characterized by a more severe clinical course than infection with a single agent. Bacterial superinfection does occur, but overt bacterial lung disease during viral pneumonia is unusual. Bacterial complication of viral pneumonia is suggested by an abrupt change in symptoms over several hours with appearance of generalized toxicity, and possibly with new radiographic findings of parenchymal consolidation or pleural effusions. Vaccine studies with a pneumococcal vaccine in a large population of children showed that a 9-valent bacterial polysaccharide vaccine prevented about one third of viral pneumonia cases, suggesting frequent interactions of bacteria and viruses that are not apparent by current methods of clinical evaluation. Viruses are identified by characteristic cytopathic effect and are confirmed by immunodetection using virus-specific antibodies and fluorescence detection. Culture techniques require a high level of expertise and generally are best performed on fresh specimens.
If steroids are to be used to help alleviate dyspnea allergy testing redmond wa alavert 10mg fast delivery, concomitant antituberculous chemotherapy is essential allergy forecast new jersey order alavert 10mg on line. Tuberculous effusions usually clear within 6 months of treatment with isoniazid allergy shots or pills cheap 10 mg alavert mastercard, rifampin allergy testing mckinney alavert 10 mg overnight delivery, and pyrazinamide. Asymptomatic noninfectious pleural exudates require only management of the underlying disorder. Improvement in the underlying systemic disease is paralleled by resolution of the accompanying pleural exudate. Pleural effusions caused by infection require specific antimicrobial treatment and certain surgical considerations. Significant early morbidity and mortality rates are associated with uncontrolled infection of the pleural space. The management of loculated parapneumonic effusions is variable and evolving with the development of new surgical modalities. The initial choice of antimicrobial agents is based on the clinical data, the bacterial epidemiology in the community, and the known pharmacologic properties of the drugs. Dosage must be adequate, and initial administration should be by the intravenous route. Infection may be polymicrobial, so more than one antimicrobial drug must be given initially. Subsequent changes in antimicrobial coverage are guided by the results of culture and sensitivity tests. A guide to antimicrobial therapy for nontuberculous bacterial pleurisy and empyema is presented in Table 70-5. Physicians always must be aware of the potential side effects of the drugs on various target organs and must be prepared to use alternative drugs, if necessary. Unlike adults, children with empyema usually do not have the long-term sequelae of fibrothorax or trapped lung. Management decisions revolve around strategies to promote prompt control of infection and resolution of respiratory compromise. Recent studies suggest that early introduction of videoassisted thoracoscopy (within 4 days of admission and therapy) is beneficial to reduce hospital stay and enhance resolution of the empyema. The duration of therapy for anaerobic pneumonitis requires an adjustment if the lung lesions go on to cavitate. Often 6 to 12 weeks of therapy is required before the lung lesions clear or only a small, stable residual lesion is left. If there is a mobile pleural effusion, then diagnostic thoracentesis is worthwhile. Thoracentesis is performed to relieve dyspnea during the acute stage and is repeated as required; it may be all that is necessary for free-moving effusions with pH >7. When the fluid is still mobile and is not loculated, diagnostic thoracentesis can also be therapeutic. The use of repeated thoracentesis has been supplanted by insertion of a chest drain to provide ongoing drainage of pleural effusion. The technique for thoracentesis is as previously described, with important modifications. The initial thoracentesis should be performed with a large-bore intravenous catheter. However, a large-bore needle increases the risk of Air and Liquid in the Pleural Space trauma to the chest wall and lung. The provision of appropriate sedation and analgesia is paramount to successful initial drainage of infected fluid. Consultation with anesthesia colleagues is important to ensure that appropriate analgesia, sedation, and patient monitoring are provided for the procedure. Immediate closedtube thoracostomy is indicated when examination shows frank pus in the pleural fluid, a positive Gram stain, pH <7. Application of negative pressure to the tube enhances obliteration of the empyema space and reexpansion of the lung. A thoracostomy tube has a larger bore than an intravenous catheter and, theoretically, improves drainage from the pleural space. An empyema or a parapneumonic effusion can loculate within 24 to 48 hours of the initiation of appropriate antimicrobials. Once the pleural fluid is loculated, further attempts at thoracentesis or chest tube drainage are fruitless, and the benefits of instrumenting the pleural space must be weighed carefully against the risks. If the child is responding to antimicrobial therapy, with improved appetite, increased energy level, and defervescence, then surgical intervention is not required. If there is slow resolution of symptoms, an option to enhance clearance of an empyema is the use of streptokinase or urokinase to lyse pleural adhesions and promote tube thoracostomy drainage. For children younger than 1 year of age, 10,000 units in 10 mL of normal saline is instilled through the chest tube, and for children older than 1 year of age, 40,000 units in 40 mL of normal saline is used. In some centers, the safety and tolerability of video-assisted thoracoscopic surgery has led to earlier introduction of surgery to evacuate the pleural space. With specific parenteral antimicrobial therapy and timely provision of appropriate pleural drainage, patients should recover completely from an episode of bacterial pleurisy and empyema. Symptoms usually resolve in stages, with improved energy and appetite preceding the resolution of fever. Intravenous antimicrobials should be used until the constitutional symptoms have resolved for several days. The total duration of antimicrobial administration (intravenous and oral) is at least 3 to 4 weeks. Findings on chest radiograph will resolve slowly, lagging behind clinical improvement. The clinician must take care to follow radiographic improvement in a child who is asymptomatic. Obtaining occasional chest radiographs to follow the resolution of empyema is appropriate. Residual pleural thickening will be present on chest radiographs taken even 6 months after the acute event. As long as the child is asymptomatic, infrequent imaging to follow resolution of empyema is appropriate. Noninfectious pleurisy and effusions resolve with resolution of the underlying systemic problem. Malignant pleurisy carries an extremely grave prognosis, whereas viral and Mycoplasma pleural diseases generally resolve spontaneously with time. Patients with empyema have a more prolonged and complicated hospital course and may require longer follow-up after returning home than patients with nonempyemic, free-moving pleural liquid. Parapneumonic effusions and empyema still produce significant morbidity and mortality. Most recent series report case fatality rates of 6% to 12%, with the highest rates among infants younger than 1 year of age. Prompt and adequate therapy during the acute phase should result in complete recovery. In contrast to adults, infants and children have a remarkable ability to resolve pleural thickening, with no effect on subsequent lung growth and function. A chest wall defect can be iatrogenic or from a penetrating injury from a missile or projectile. Infants and children are prone to internal injury from blunt trauma because of the greater compressibility of the chest wall. Thus, laceration or transection of major airways may accompany chest trauma, even without fractured rib fragments or obvious external injury. During assisted ventilation, sometimes the escaping air dissects along perivascular planes centripetally, to the hilum, where it ruptures into the mediastinum (pneumomediastinum) and then through the visceral pleura, into the pleural space. Alternatively, when under tension in the interstitial space, air may rupture directly through the visceral pleura, into the pleural space. When the air leak is confined to the interstitium, the condition is known as pulmonary interstitial emphysema. When under sufficient pressure, air may dissect out of the thorax, along subcutaneous tissue planes (subcutaneous emphysema), or into the peritoneal cavity (pneumoperitoneum). A large pneumomediastinum is evident from the hyperlucency overlying the thoracic vertebrae.
Blood returns via the coronary sinus allergy medicine with high blood pressure buy 10mg alavert with amex, which drains directly into the right atrium allergy symptoms numbness generic 10 mg alavert otc. Cardiac muscle is myogenic allergy shots numbness arm cheap alavert 10 mg on line, which means that it can contract on its own allergy friendly cats purchase alavert 10 mg mastercard, without needing nerve impulses. There is a complicated sequence of events at each heartbeat called the cardiac cycle. The ventricles are electrically insulated from the atria, so they do not contract at this time. The Purkinje fibres pass down through the interventricular septum as the bundle of His, which is insulated from the surrounding muscle cells, so the ventricles do not contract yet. At the base of the ventricles the Purkinje fibres spread out and initiate ventricular contraction. The ventricles therefore contract shortly after the atria, from the bottom up, squeezing blood upwards into the arteries. The semilunar valves in the arteries close as the arterial blood pushes against them, making a "dup" sound. Blood flows because of pressure differences, and it always flows from a high pressure to a low pressure, if it can. So during atrial systole the atria contract, making the atrium pressure higher than the ventricle pressure, so blood flows from the atrium to the ventricle. The valves are largely passive: they are opened by blood flowing through them the right way and are forced closed when blood tries to flow through them the wrong way. Name Atrial Systole atria contract blood enters ventricles Ventricular Systole ventricles contract blood enters arteries Diastole atria and ventricals both relax blood enters atria and ventricles Events semilunar valves open semilunar valves close 0 20 Pressure (kPa) 15 in artery 0. The two sides have identical traces except that the pressures in the right side are lower than those in the left side. The cardiac muscle itself is silent and the sounds are made by the valves closing. The first sound (lub) is due to the atrioventricular valves closing and the second (dup) is due to the semi-lunar valves closing. There are characteristic waves of electrical activity marking each phase of the cardiac cycle. Cardiac Output Cardiac Output is the amount of blood flowing through the heart each minute. This is the system that feeds the cardiac muscle cells so that they can respire and contract. Cardiac muscle works constantly throughout life and is incapable of anaerobic respiration, so it has a great demand for oxygen and glucose. There are two coronary arteries that arise directly from the aorta, and these split into numerous smaller arteries (arterioles) and then a network of capillaries, where exchange with the cardiac cells actually takes place. A blockage in a left ventricle coronary arteries coronary artery can restrict the supply of oxygen to the cardiac cells, killing them and causing a heart attack. Cholesterol and other insoluble lipids collect on the inside of a coronary artery. The plaque weakens the wall of the artery, so the pressure of blood causes a local swelling called an aneurism. If the wall is particularly weak the aneurism may burst causing blood loss and probable death. Alternatively, a mobile clot from elsewhere in the blood stream (an embolism) can become lodged in the atheroma. The clot grows until it completely blocks the artery, forming a coronary thrombosis. The thrombosis prevents oxygen reaching the cardiac cells "downstream" of the blockage, so they cannot respire and so die. This death of myocytes is a myocardial infarction, more commonly known as a heart attack. The severity of the heart attack depends on how far along the coronary artery the thrombosis is. If only a small part of one ventricle is killed then the patient will recover, but a thrombosis early in the coronary artery will always be fatal. Cholesterol in the blood comes from the diet and from the liver, where it is synthesised. High blood pressure increases the risk of an aneurism and stimulates thickening of artery wall, increasing the risk of thrombosis. Both blood pressure and fat metabolism are affected by genes, so genes undoubtedly affect the chance of a coronary thrombosis. High levels of saturated fat increase the amount of cholesterol carried in the blood and so increase the risk of atherosclerosis. Smokers are between two and six times more likely to suffer from coronary heart disease than non-smokers. The carbon monoxide and nicotine in cigarette smoke both cause an increase in blood pressure. The lining wall of the alimentary canal appears different in different parts of the gut, reflecting their different roles, but always has these four basic layers: capillaries Lumen (space) lacteal epithelium Mucosa Submucosa Muscle Serosa blood vessels lymph vessel circular longitudinal microvilli (brush border) villus gland in mucosa gland in submucosa duct to external gland. These epithelial cells contain microvilli, membrane proteins for facilitated diffusion and active transport, mitochondria, and membrane-bound enzymes. Epithelial cells are constantly worn away by friction with food moving through the gut, so are constantly being replaced. It can be subdivided into circular muscle (which squeezes the gut when it contracts) and longitudinal muscle (which shortens the gut when it contracts). The combination of these two muscles allows food to be pushed along the gut by peristalsis. The teeth and tongue physically break up the food into small pieces with a larger surface area, and form it into a ball or bolus. The salivary glands secrete saliva, which contains water to dissolve soluble substances, mucus for lubrication, lysozymes to kill bacteria and salivary amylase to digest starch. The food bolus is swallowed by an involuntary reflex action through the pharynx (the back of the mouth). During swallowing the trachea is blocked off by the epiglottis to stop food entering the lungs. This is a simple tube through the thorax, which connects the mouth to the rest of the gut. There is a epithelium, no villi, a few glands secreting mucus, and a thick layer of circular and longitudinal muscle to propel the food by peristalsis. Peristalsis is a wave of circular muscle contraction, which passes down the gut and is completely involuntary. The oesophagus is a soft tube that can be closed, unlike the trachea, which is a hard tube, held open by rings of cartilage. Food circular muscle circular muscle contracted relaxed + + longitudinal muscle longitudinal muscle relaxed contracted circular muscle circular muscle relaxed contracted + + longitudinal muscle longitudinal muscle contracted relaxed 3. This chime is gradually released in to the small intestine by a sphincter, a region of thick circular muscle that acts as a valve. The mucosa of the stomach wall has no villi, but does have numerous gastric pits (104 cm-2) leading to gastric glands in the mucosa layer. These glands secrete gastric juice, which contains: hydrochloric acid (pH 1) to kill bacteria (the acid does not help digestion, in fact it hinders it by denaturing most enzymes); mucus to lubricate the food and to line the epithelium to protect it from the acid; and some protease enzymes. Although this is short, almost all the digestion takes place here, due to two secretions: pancreatic juice and bile. Pancreatic juice is secreted by the pancreas into the duodenum through the pancreatic duct. Bile is secreted by the liver, stored in the gall bladder, and released into the duodenum through the bile duct. The mucosa of the duodenum has few villi, since there is no absorption, but the submucosa contains glands secreting mucus and sodium hydrogen carbonate. There are numerous glands in the mucosa and submucosa secreting enzymes, mucus and sodium hydrogen carbonate. It is over 6m long; the mucosa has large circular folds, villi and the epithelial cells have microvilli. Microvilli can only be seen clearly with an electron microscope, and appear as a fuzzy brush border under the light microscope.
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