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When the diaphragm con- called breathing generic keflex 750 mg online, which is a largely involun- tracts order keflex 750 mg with visa, it partially descends into the abdominal cavi- tary action that moves air into (inspiration) ty trusted 750mg keflex, thus decreasing the pressure within the chest and and out of (expiration) the lungs in response drawing air into the lungs (inspiration). The intercostal muscles assist the diaphragm oxygen and carbon dioxide between the alve- in changing the volume of the thoracic cavity by ele- oli and the blood in the pulmonary capillaries vating and lowering the rib cage. Expiration: Air forced out of lungs Pectoralis minor Pectoralis minor muscles contract muscles relax Lungs expand Lungs contract Intercostal muscles contract Intercostal muscles relax Diaphragm relaxes Diaphragm contracts and moves up and flattens Figure 7-2. Connecting Body Systems–Respiratory System The main function of the respiratory system is to provide oxygen to the entire body and expel car- bon dioxide from the body. Specific functional relationships between the respiratory system and other body systems are summarized below. Blood, lymph, and immune Digestive • Tonsils, adenoids, and other immune struc- • Respiratory system provides O2 needed tures in the respiratory tract protect for digestive functions. Musculoskeletal • Respiratory system provides O2 for Female reproductive muscle contraction. Medical Word Elements This section introduces combining forms, suffixes, and prefixes related to the respiratory system. Many disorders Pulmonary Disease of the respiratory system, including bronchitis and emphysema, begin as an acute problem but Chronic obstructive pulmonary disease become chronic over time. Their damag- duce a chronic partial obstruction of the air pas- ing effects are commonly irreversible. The patient finds it difficult to breath (dys- For diagnosis, treatment, and management of pnea) especially upon exertion and usually respiratory disorders, the medical services of a spe- exhibits a chronic cough. Chronic bronchitis Excess mucus production Distended Extra mucus bronchiole Inflamed Figure 7-3. Influenza Asthma produces spasms in the bronchial pas- type A epidemics occur about every 2 to 3 years. Both viruses undergo is commonly caused by exposure to allergens or antigenic changes; consequently, new vaccines must irritants. During recovery, coughing episodes pro- is a mild flu and is not associated with epidemics. Symptoms Over time, the epithelium of the bronchial pas- include fever, chills, headache, generalized muscle sages thickens, and breathing becomes more diffi- pain (myalgia), and loss of appetite, but recovery cult. If death occurs, it is usually the result that expand the bronchi (bronchodilators) by of a secondary pneumonia caused by bacteria or relaxing their smooth muscles. Children should not do not reverse the bronchospasms, the condition use aspirin for relief of symptoms caused by virus- is referred to as status asthmaticus. Chronic bronchitis is an inflammation of the bronchi caused mainly by smoking and air pollu- Pleural Effusions tion. Bronchitis is Any abnormal fluid in the pleural cavity, the space characterized by swelling of the mucosa and a between the visceral and parietal pleura, is called a heavy, productive cough, commonly accompanied pleural effusion. Patients usually seek medical help tains only a small amount of lubricating fluid. Two initial tech- and medications that aid in the removal of mucus niques used to diagnose pleural effusion are aus- (expectorants) help to widen air passages. Auscultation is the lis- may be prescribed if the disease progresses or tening of sounds made by organs of the body using becomes chronic. Percussion is the gentle tapping the chest with the fingers and listening to the resultant Emphysema sounds to determine the position, size, or consis- Emphysema is characterized by decreased elastic- tency of the underlying structures. A transudate is a noninflammatory fluid commonly occurs with another respiratory disor- that resembles serum but with slightly less pro- der, such as asthma, tuberculosis, or chronic bron- tein. Most emphysema sufferers find it easier to breathe Both of these conditions allow serum to leak when sitting upright or standing erect (orthop- from the vascular system and collect in the pleu- nea). Various types Influenza of pleural effusions include serum (hydrothorax), Influenza (flu) is an acute infectious respiratory pus (empyema or pyothorax), and blood (hemo- viral disease. Type A is of pri- effusion, air can enter the pleural space (pneu- mary concern because it is associated with world- mothorax), resulting in a partial or complete wide epidemics (pandemics) and its causative collapse of a lung.

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At concentrations up to 2% w/w the surfactant stabilizes the suspended particles by adsorption at the drug propellant interface and in addition serves as a valve lubricant keflex 250 mg amex. Low surfactant concentrations will also avoid substantial reductions in the propellant evaporation rates from aerosolized drops buy cheap keflex 500 mg online. Density Differences in density between drug particles and the propellant will determine sedimentation rates (either sinking or floating) buy keflex 750mg overnight delivery. Deflocculation of the suspension by judicious surfactant selection may minimize the effect which can give rise to variable dosing during the life of the pressurized pack. In order to be effective, metered-dose aerosols should be triggered during the course of a deep, slow (>5 seconds) inhalation, followed by 5–10 seconds of breath holding. The breath-holding period is intended to maximize particle deposition by sedimentation and diffusion mechanisms (see Section 10. Patients can experience problems in developing an adequate inhaler technique and coordinating actuation with inspiration. Studies have shown that 50% or more adult patients have difficulty using conventional metered- dose inhalers efficiently, even after careful training. These are essentially extension tubes which effectively increase the distance between the orifice and the patient’s oropharynx. This allows for 268 deceleration of the particles and hence reduces oropharyngeal deposition. In-built flow restrictors have been introduced in attempts to control patients inhalation rate. For patient convenience, spacers and reservoirs have been’ designed as collapsible or concertina-like structures. An alternative approach to achieving patient coordination between actuation and inhalation is a breath actuated device such as the Autohaler. Conventionally, this has been achieved by micronization, although more recently spray-drying and supercritical fluid technologies have been employed. However, particles of such small sizes exhibit exceptionally high surface energies, so that: • particle aggregation readily occurs, making redispersion a difficult process; • the formulation has poor flow and entrainment properties. The most frequently employed approach to overcoming the problems associated with particle size is to use a carrier particle such as lactose. When the micronized drug is blended with a carrier of much larger size range (usually 20–100 μm), many of the drug particles become loosely associated with the lactose surface. The turbulent airflow within the device detaches the drug particles from the carrier particles within the device itself; the drug particles are then carried on the airstream into the lungs. Those carrier particles that escape from the device are largely deposited in the oropharynx of the patient. Although high levels of turbulence will facilitate stripping of the drug particles from the carrier particles within the device, this course of action will also lead to an increase in resistance of the inhaler to airflow and thus to difficulties in inhaling through the device at a flow rate which produces optimum drug delivery. One way to provide high levels of turbulence without imposing large increases in airflow resistance is the judicious use and placement of grids of varying mesh sizes. It is observations such as these which emphasize the need for parallel development of device design and powder technology. More recently ternary powder blends have been claimed to provide a higher fine particle fraction of the drug when subjected to an aerosolization process. Early dry powder inhaler devices were all unit-dose systems and depended on loading and triggering procedures. Both utilize premetered doses packed into hard gelatin capsules although different mechanisms of powder delivery are employed: • The Spinhaler contains pins for perforating the capsule, the cap of which fits into an impeller which rotates as the patient inhales through the device. The powder mass empties from the capsule body by the forces imparted by the inhaled airsteam and the drug particles subsequently enter the airways of the lung. The first device employing a multidose reservoir was the Turbuhaler, designed to deliver 200×1 mg doses of terbutaline sulphate devoid of any carrier (Figure 10. The inhaled airstream dislodges the drug from the cavities and dispersion continues in the inhalation channels which are helical to induce turbulent flow.

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During the 1990s purchase keflex 750mg online, however purchase keflex 250 mg without a prescription, integron cassettes (see Chapter 10) were observed to mediate rifampicin resistance in clinical isolates of purchase keflex 750mg otc, for example, Pseudomonas aerug- inosa and E. Integron-borne genes can transfer with trans- posons and with plasmids and then also horizontally between bacteria (see Chapter 10). Rifampicin resistance by ribosylation was first characterized in the nontuberculous bac- terium Mycobacterium smegmatis, which is endogenously resistant to rifampicin. The ribosylating enzyme could be speculated to have evolved as a defense against rifamycins in the microbial world of soil. A variant of arr-1 with a very similar nucleotide sequence, arr-2, has been found as an integron cassette (Chapter 10) in pathogenic clinical isolates of P. The finding of identi- cal arr-2 in both Pseudomonas and Escherichia implies the ability of the integron cassette to move between species. It could be speculated that soil-living Pseudomonas could have taken up arr-1 from mycobacteria and then transferred it to pathogenic Pseudomonas-species in which arr-1 developed into arr-2 under the selection pressure of rifampicin used clinically. The inclusion of arr-2 in an integron cassette has meant a pronounced movabil- ity between the genomes of bacteria, including transposons and plasmids, and further between different bacterial species. Isoniazid or Isonicotinic Acid Hydrazide Isoniazid (9-2) is a specific agent against tuberculosis that has been used for this purpose since 1952, when its remedial prop- erties were recognized after having been characterized as a chemical compound in 1912. It is used in several fixed combina- tions with rifampicin and with other tuberculostatic drugs, such as pyrazinamide and ethambutol (see later in the chapter). It is used to counteract the development of resistance according to the general arguments given earlier in the chapter, as well as for rifampicin resistance. To exercise its effect, it has to be activated to isonicotinic acid (9-3) in the bacterial cell. This acti- vation is effected by a mycobacteria-specific catalase-peroxidase, which normally protects the bacterial cell against peroxides by degrading them to free oxygen and water but which also seems to be able to oxidize isoniazid to its active form. Resistance against isoniazid occurs and is a threat to treat- ment, since the lowered susceptibility to one of the components of the drug combination therapy affects the total therapeutic effect and could contribute to the development of multiresis- tance (see Chapter 10). Isoniazid resistance could be caused by mutations in the katG gene expressing the catalase-peroxidase enzyme, inactivating its enzymic effect and thus preventing it from activating to its antibacterially active form any isoni- azid administered. Another form of isoniazid resistance, caused by spontaneous mutations in the gene expressing the mycolic acid–synthesizing enzyme, has been observed. This enzyme is the target of the activated form of isoniazid, and the mutations make it less susceptible to the drug. Pyrazinamide Another specifically acting tuberculostatic agent, pyrazinamide (9-4), is often used in a fixed combination with rifampicin. The exact mechanism of action for this drug is not known, but it has been shown that it must be converted enzymically inside the cell to pyrazinoic acid (9-5), which is the active antibacterial agent. The logical solution to this clinical resistance problem would then be to use pyrazinoic acid as a tuberculostatic drug. Compared to pyrazinamide, however, pyrazinoic acid is taken up very poorly in the bacterial cell. Ethambutol The ethylenediamine derivative ethambutol (9-6)isanother agent used as a component in fixed tuberculostatic drug com- binations containing, for example, rifampicin, isoniazide, and pyrazinamide. Ethambutol is a specific tuberculostatic drug which has been used for this purpose since the beginning of the 1960s. Despite many years of clinical use of ethambu- tol, its mechanism of action has not been known until relatively recently. The ethambutol-mediated interference with mycobacterial cell wall formation is regarded as being able to increase the per- meability for other antimycobacterial agents and thus contribute to that valuable clinical synergism, observed for example at the combination of ethambutol with rifampicin, which is a large molecule whose size interferes with permeability. Resistance to ethambutol has been observed, and was in many cases, but not all, shown to be caused by spontaneously occurring mutational changes in the synthesis regulation of the enzymes involved in the polymerization of arabinose. Cycloserine Cycloserine was used as a remedy against tuberculosis, but is not used much clinically nowadays because of the central ner- vous system disturbances that were sometimes experienced by patients.

Finally keflex 250 mg online, the last new buy keflex 750mg low cost, selectively acting antibacterial agent buy 250mg keflex mastercard, linezolid, is described, together with its effect on bacterial protein synthesis by means of an earlier unknown mechanism. It was isolated from Streptomyces venezuelae in 1947 and was intro- duced in clinical medicine in the 1950s. The effect of chloramphenicol, which Antibiotics and Antibiotics Resistance, First Edition. Experiments with radioactively labeled chlo- ramphenicol have shown its exclusive binding to the larger, 50S subunit of the bacterial ribosome (70S), one molecule per 50S particle. It does not bind at all to mammalian 80S ribosomes, which explaines its selective action on bacteria. As noted ear- lier, the Swedberg unit defines the movement of the particle in the gravitational field of an ultracentrifuge. Simple experiments explain the reversible bacteriostatic effect of chloramphenicol, in that the drug can easily be removed from a bacterial culture, by centrifugation or filtration, allowing the bacterial ribosomes to resume their normal function. This has been an important tool in earlier investigations of the interplay between protein synthe- sis and the formation of other macromolecules in the bacterial cell, by allowing the temporary inhibition of protein synthesis. Specifically, chloramphenicol binds to several peptides of the 50S particle, including L15, L18, and L27 (L for large, the larger sub- unit of the 70S bacterial ribosome). These observations do not, however, allow a complete understanding of protein synthesis inhibition by chloramphenicol, the details of which remain to be explained. In the liquor cerebrospinalis it reaches concentrations that are 30 to 50% of those in the blood serum, which means that this drug can be used efficiently for the treatment of meningitis. Clinical Side Effects Chloramphenicol ought to be a much appreciated antibiotic for the systemic treatment of bacterial infections—but it is not. This is because of a feared side effect, blood dyscrasias, which occur in two forms, one dose related and reversible, the other dose independent, appearing late in the treatment and mediating an irreversible and fatal aplastic anemia. The latter side effect has a low incidence, about one in 200,000 cases treated, but still has led to a very limited use of this drug in clinical praxis. It has been speculated that the known inhibition of mitocondrial protein synthesis in mammalian cells by chloramphenicol could play a role, but this is not consistent with the very low incidence of this side effect. In later years the sensitivity to chloramphenicol and the appearance of aplastic anemia have been shown to have a hereditary component, which has not been defined further. In severe infectious diseases such as meningitis and typhoid fever, when the risk of the disease and the risk of side effects are in the balance, chloramphenicol is a very valuable antibacterial agent. Bacterial Resistance to Chloramphenicol Resistance to chloramphenicol occurs in two forms. One is easily observed in the laboratory by growing experimental bacteria at incrementally increasing concentrations of chloramphenicol. The clinically most important form of resistance is of another type, how- ever, mediated by an enzymatic inactivation of chloramphenicol by the acetylation of its two hydroxyl groups (see 7-1). This acetylation is effected by foreign genes expressing chloram- phenicol acetyl transferases by transferring an acetyl group from acetyl coenzymeA to the outer of the two hydroxyl groups in the chloramphenicol molecule. The outer hydroxyl group is again acetylated by an acetyl transferase to give a final product, diacetyl chloramphenicol. The two acetyl groups pre- vent the binding of chloramphenicol to the bacterial ribosome, invalidating its antibacterial effect. Chloramphenicol acetylating enzymes can be observed in both gram-negative and gram-positive bacteria, and their corre- sponding genes are located chromosomally or borne on plasmids. In the latter case they are likely to be transferable horizon- tally (see Chapter 10). One chloramphenicol acetyl transferase common among gram-negative enterobacteria is borne on a trans- poson, Tn9. The chloramphenicol acetyl transferases transferring between pathogens and mediating clinical resistance probably have their origins among chloramphenicol-producing soil organ- isms, where they protect the producing organism against its own product. Resistance against chloramphenicol was among the first horizontally transferred resistance properties discovered in a clinical context, observed in the early 1950s in Japan during epidemics of bacterial dysentery. It could be seen that patients excreting antibiotic-susceptible Shigella bacteria at the beginning of the infection, later and after antibiotic treatment excreted multiply-resistant bacteria carrying resistance to chlorampheni- col, streptomycin, tetracycline, and sulfonamides, despite the fact that they had been treated with only one of these agents.

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