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Instead bacteria genus mectizan 6 mg low cost, measurements of the clotting factors themselves are made antibiotics for acne and alcohol buy mectizan 12 mg, using sophisticated chemical procedures. Blood removed from the patient is immediately oxalated so that none of the prothrombin can change into thrombin. Then, a large excess of calcium ion and tissue factor is quickly mixed with the oxalated blood. The excess calcium nullifies the effect of the oxalate, and the tissue factor activates the prothrombin to thrombin reaction by means of the extrinsic clotting pathway. In each of these tests, excesses of calcium ions and all the other factors in addition to the one being tested are added to oxalated blood all at once. Then, the time required for coagulation is determined in the same manner as for prothrombin time. Negrier C, Shima M, Hoffman M: the central role of thrombin in bleeding disorders. The results obtained for prothrombin time may vary considerably, even in the same individual if there are differences in activity of the tissue factor and the analytical system used to perform the test. Tissue factor is olated from human tissues, such as placental tissue, and different batches may have different activity. This article is a discussion of pulmonary ventilation; the subsequent five chapters cover other respiratory functions plus the physiology of special respiratory abnormalities. When the rib cage is elevated, however, the ribs project almost directly forward, so the sternum also moves forward, away from the spine, making the anteroposterior thickness of the chest about 20% greater during maximum inspiration than during expiration. Therefore, all the muscles that elevate the chest cage are classified as muscles of inspiration, and the muscles that depress the chest cage are classified as muscles of expiration. The most important muscles that raise the rib cage are the external intercostals, but others that help are the following: (1) sternocleidomastoid muscles, which lift upward on the sternum; (2) anterior serrati, which lift many of the ribs; and (3) scaleni, which lift the first two ribs. The muscles that pull the rib cage downward during expiration are mainly the following: (1) the abdominal recti, which have the powerful effect of pulling downward on the lower ribs at the same time that they and other abdominal muscles also compress the abdominal contents upward against the diaphragm; and (2) the internal intercostals. To the left, the ribs during expiration are angled downward, and the external intercostals are elongated forward and downward. As they contract, they pull the upper ribs forward in relation to the lower ribs, which causes leverage on the ribs to raise them upward, thereby causing inspiration. The internal intercostals function in the opposite manner, functioning as expiratory muscles because they angle between the ribs in the opposite direction and cause opposite leverage. Normal quiet breathing is accomplished almost entirely by movement of the diaphragm. During inspiration, contraction of the diaphragm pulls the lower surfaces of the lungs downward. Then, during expiration, the diaphragm simply relaxes, and the elastic recoil of the lungs, chest wall, and abdominal structures compresses the lungs and expels the air. During heavy breathing, however, the elastic forces are not powerful enough to cause the necessary rapid expiration, so extra force is achieved mainly by contraction of the abdominal muscles, which pushes the abdominal contents upward against the bottom of the diaphragm, thereby compressing the lungs. The lung is an elastic structure that collapses like a balloon and expels all its air through the trachea whenever there is no force to keep it inflated. Also, there are no attachments between the lung and walls of the chest cage, except where it is suspended at its hilum from the mediastinum, the middle section of the chest cavity. Elevated rib cage Diaphragmatic contraction Abdominals contracted Volume change (liters) movement of the lungs within the cavity. Furthermore, continual suction of excess fluid into lymphatic channels maintains a slight suction between the visceral surface of the lung pleura and the parietal pleural surface of the thoracic cavity. Therefore, the lungs are held to the thoracic wall as if glued there, except that they are well lubricated and can slide freely as the chest expands and contracts. This pressure is normally a slight suction, which means a slightly negative pressure. The normal pleural pressure at the beginning of inspiration is about -5 centimeters of water (cm H2O), which is the amount of suction required to hold the lungs open to their resting level. During normal inspiration, expansion of the chest cage pulls outward on the lungs with greater force and creates more negative pressure to an average of about -7. To cause inward flow of air into the alveoli during inspiration, the pressure in the alveoli must fall to a value slightly below atmospheric pressure (below 0). During expiration, alveolar pressure rises to about +1 cm H2O, which forces the 0. Chapter 38 Pulmonary Ventilation Saline-filled Air-filled Lung volume change (liters) 0. This diagram shows changes in lung volume during changes in transpulmonary pressure (alveolar pressure minus pleural pressure). Compliance of the Lungs the extent to which the lungs will expand for each unit increase in transpulmonary pressure (if enough time is allowed to reach equilibrium) is called the lung compliance. The total compliance of both lungs together in the normal adult averages about 200 ml of air/cm H2O transpulmonary pressure. That is, every time the transpulmonary pressure increases by 1 cm H2O, the lung volume, after 10 to 20 seconds, will expand 200 ml. Each curve is recorded by changing the pleural pressure in small steps and allowing the lung volume to come to a steady level between successive steps. The two curves are called, respectively, the inspiratory compliance curve and the expiratory compliance curve, and the entire diagram is called the compliance diagram of the lungs. The characteristics of the compliance diagram are determined by the elastic forces of the lungs. These forces can be divided into two parts: (1) elastic forces of the lung tissue; and (2) elastic forces caused by surface tension of the fluid that lines the inside walls of the alveoli and other lung air spaces.

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This opposition to fluid reabsorption is more than counterbalanced by the colloid osmotic pressures that favor reabsorption antibiotic development generic mectizan 12 mg. The plasma colloid osmotic pressure antibiotic resistance who report 2014 cheapest mectizan, which favors reabsorption, is about 32 mm Hg, and the colloid osmotic pressure of the interstitium, which opposes reabsorption, is 15 mm Hg, causing a net colloid osmotic force of about 17 mm Hg, favoring reabsorption. Therefore, subtracting the net hydrostatic forces that oppose reabsorption (7 mm Hg) from the net colloid osmotic forces that favor reabsorption (17 mm Hg) gives a net reabsorptive force of about 10 mm Hg. This value is high, similar to that found in the glomerular capillaries, but in the opposite direction. The other factor that contributes to the high rate of fluid reabsorption in the peritubular capillaries is a large filtration coefficient (Kf) because of the high hydraulic conductivity and large surface area of the capillaries. Because the reabsorption rate is normally about 124 ml/ min and net reabsorption pressure is 10 mm Hg, Kf normally is about 12. The peritubular capillary hydrostatic pressure is influenced by the arterial pressure and resistances of the afferent and efferent arterioles as follows: 1. Increases in arterial pressure tend to raise peritubular capillary hydrostatic pressure and decrease the reabsorption rate. This effect is buffered to some extent by autoregulatory mechanisms that maintain relatively constant renal blood flow, as well as relatively constant hydrostatic pressures in the renal blood vessels. An increase in resistance of the afferent or efferent arterioles reduces peritubular capillary hydrostatic pressure and tends to increase reabsorption rate. Although constriction of the efferent arterioles increases glomerular capillary hydrostatic pressure, it lowers peritubular capillary hydrostatic pressure. The second major determinant of peritubular capillary reabsorption is the colloid osmotic pressure of the plasma in these capillaries; raising the colloid osmotic pressure increases peritubular capillary reabsorption. The colloid osmotic pressure of peritubular capillaries is determined by the following: (1) the systemic plasma colloid osmotic pressure (increasing the plasma protein concentration of systemic blood tends to raise peritubular capillary colloid osmotic pressure, thereby increasing reabsorption); and (2) the filtration fraction-the higher the filtration fraction, the greater the fraction of plasma filtered through the glomerulus and, consequently, the more concentrated the protein becomes in the plasma that remains behind. Thus, increasing the filtration fraction also tends to increase the peritubular capillary reabsorption rate. Changes in the peritubular capillary Kf can also influence the reabsorption rate because Kf is a measure of the permeability and surface area of the capillaries. Increases in Kf raise reabsorption, whereas decreases in Kf lower peritubular capillary reabsorption. Table 28-2 summarizes the factors that can influence the peritubular capillary reabsorption rate. Ultimately, changes in peritubular capillary the two determinants of peritubular capillary reabsorption 356 physical forces influence tubular reabsorption by changing the physical forces in the renal interstitium surrounding the tubules. This action in turn raises renal interstitial fluid hydrostatic pressure and decreases interstitial fluid colloid osmotic pressure because of dilution of the proteins in the renal interstitium. These changes then decrease the net reabsorption of fluid from the renal tubules into the interstitium, especially in the proximal tubules. Once the solutes enter the intercellular channels or renal interstitium by active transport or passive diffusion, water is drawn from the tubular lumen into the interstitium by osmosis. Furthermore, once the water and solutes are in the interstitial spaces, they can be swept up into the peritubular capillaries or diffuse back through the epithelial junctions into the tubular lumen. The so-called tight junctions between the epithelial cells of the proximal tubule are actually leaky, so considerable amounts of sodium can diffuse in both directions through these junctions. With the normal high rate of peritubular capillary reabsorption, the net movement of water and solutes is into the peritubular capillaries, with little backleak into the lumen of the tubule. The opposite is true when peritubular capillary reabsorption increases above the normal level. An initial increase in reabsorption by the peritubular capillaries tends to reduce interstitial fluid hydrostatic pressure and raise interstitial fluid colloid osmotic pressure. Both these forces favor movement of fluid and solutes out of the tubular lumen and into the interstitium; therefore, backleak of water and solutes into the tubular lumen is reduced, and net tubular reabsorption is increased. Reduced peritubular capillary reabsorption, in turn, decreases the net reabsorption of solutes and water by increasing the amounts of solutes and water that leak back into the tubular lumen through the tight junctions of the tubular epithelial cells, especially in the proximal tubule. In general, forces that increase peritubular capillary reabsorption also increase reabsorption from the renal tubules. Conversely, hemodynamic changes that inhibit peritubular capillary reabsorption also inhibit tubular reabsorption of water and solutes. A second effect of increased renal arterial pressure that raises urine output is that it decreases the percentages of the filtered loads of sodium and water that are reabsorbed by the tubules. Although the mechanisms responsible for this effect are not fully understood, they include a cascade of physical factors, as well as paracrine and hormonal effects. Increased arterial pressure causes a slight increase in peritubular capillary hydrostatic pressure, especially in the vasa recta of the renal medulla, and a subsequent increase in the renal interstitial fluid hydrostatic pressure. As discussed earlier, an increase in the renal interstitial fluid hydrostatic pressure enhances backleak of sodium into the tubular lumen, thereby reducing the net reabsorption of sodium and water and further increasing the rate of urine output when renal arterial pressure rises. A fourth factor that may contribute to pressure natriuresis is internalization of sodium transporter proteins from the apical membranes to the cytoplasm of the renal tubules, thereby reducing the amount of sodium that can be transported across the cell membranes. Likewise, when sodium intake is changed, the kidneys must adjust urinary sodium excretion appropriately without major changes in excretion of other electrolytes. Several hormones in the body provide this specificity of tubular reabsorption for different electrolytes and water. Table 28-3 summarizes some of the most important hormones for regulating tubular reabsorption, their principal sites of action on the renal tubule, and their effects on solute and water excretion. Some of these hormones are discussed in more detail in Chapters 29 and 30, but here we briefly review their renal tubular actions. A major renal tubular site of aldosterone action is on the principal cells of the cortical collecting tubule. Aldosterone also increases the sodium permeability of the luminal side of the membrane by the insertion of epithelial sodium channels.

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Tanji J infection mouth purchase mectizan 6 mg free shipping, Hoshi E: Role of the lateral prefrontal cortex in executive behavioral control infection 4 weeks after hysterectomy 6 mg mectizan with amex. Tononi G, Boly M, Massimini M, Koch C: Integrated information theory: from consciousness to its physical substrate. Even the wakefulness and sleep cycle discussed in Chapter 60 is one of our most important behavioral patterns. In this articler, we deal first with the mechanisms that control activity levels in different parts of the brain. Then we discuss the causes of motivational drives, especially motivational control of the learning process and feelings of pleasure and punishment. These functions of the nervous system are performed mainly by the basal regions of the brain, which together are loosely called the limbic system, meaning the "border" system. In addition to these downward signals, this area also sends a profusion of signals in the upward direction. Most of these signals go first to the thalamus, where they excite a different set of neurons that transmit nerve signals to all regions of the cerebral cortex, as well as to multiple subcortical areas. One type is rapidly transmitted action potentials that excite the cerebrum for only a few milliseconds. These signals originate from large neuronal cell bodies that lie throughout the brain stem reticular area. Their nerve endings release the neurotransmitter acetylcholine, which serves as an excitatory agent that lasts for only a few milliseconds before it is destroyed. The second type of excitatory signal originates from large numbers of small neurons spread throughout the brain stem reticular excitatory area. Again, most of these signals pass to the thalamus, but through small, slowly conducting fibers that synapse mainly in the intralaminar nuclei of the thalamus and in the reticular nuclei over the surface of the thalamus. From here, additional small fibers are distributed throughout the cerebral cortex. The excitatory effect caused by this system of fibers can build up progressively for many seconds to a minute or more, which suggests that its signals are especially important for controlling the longer term background excitability level of the brain. In fact, severe compression of the brain stem at the juncture between the mesencephalon and cerebrum, as sometimes results from a pineal tumor, often causes the person to enter into unremitting coma lasting for the remainder of his or her life. Nerve signals in the brain stem activate the cerebrum in two ways: (1) by directly stimulating a background level of neuronal activity in wide areas of the brain and (2) by activating neurohormonal systems that release specific facilitory or inhibitory hormone-like neurotransmitters into selected areas of the brain. The central driving component of this system is an excitatory area located in the reticular substance of the pons and mesencephalon. We also discuss this area in Chapter 56 because it is the same brain stem reticular area that transmits facilitory signals downward excitatory area in the brain stem, and therefore the level of activity of the entire brain, is determined to a great extent by the number and type of sensory signals that enter the brain from the periphery. Pain signals in particular increase activity in this excitatory area and therefore strongly excite the brain to attention. The importance of sensory signals in activating the excitatory area is demonstrated by the effect of cutting the brain stem above the point where the fifth cerebral nerves enter the pons. Furthermore, signals regularly reverberate back and forth between the thalamus and the cerebral cortex, with the thalamus exciting the cortex and the cortex then re-exciting the thalamus via return fibers. Activation of these back-and-forth reverberation signals has been suggested to establish long-term memories. Whether the thalamus also functions to call forth specific memories from the cortex or to activate specific thought processes is still unclear, but the thalamus does have appropriate neuronal circuitry for these purposes. Also shown is an inhibitory area in the medulla that can inhibit or depress the activating system. In Chapter 56, we learned that this area can inhibit the reticular facilitory area of the upper brain stem and thereby decrease activity in the superior portions of the brain. One of the mechanisms for this activity is to excite serotonergic neurons, which in turn secrete the inhibitory neurohormone serotonin at crucial points in the brain; we discuss this concept in more detail later. When all these input sensory signals are gone, the level of activity in the brain excitatory area diminishes abruptly, and the brain proceeds instantly to a state of greatly reduced activity, approaching a permanent state of coma. However, when the brain stem is transected below the fifth nerves, which leaves much input of sensory signals from the facial and oral regions, the coma is averted. Increased Activity of the Excitatory Area Caused by Feedback Signals Returning From the Cerebral Cortex. This mechanism is to secrete excitatory or inhibitory neurotransmitter hormonal agents into the substance of the brain. These neurohormones often persist for minutes or hours and thereby provide long periods of control, rather than just instantaneous activation or inhibition. Norepinephrine usually functions as an excitatory hormone, whereas serotonin is usually inhibitory and dopamine is excitatory in some areas but inhibitory in others. As would be expected, these three systems have different effects on levels of excitability in different parts of the brain. The norepinephrine system spreads to virtually every area of the brain, whereas the serotonin and dopamine systems are directed much more to specific brain regions-the dopamine system mainly into the basal ganglial regions and the serotonin system more into the midline structures. Therefore, any time the cerebral cortex becomes activated by brain thought processes or by motor processes, signals are sent from the cortex to the brain stem excitatory area, which in turn sends still more excitatory signals to the cortex. This process helps to maintain the level of excitation of the cerebral cortex or even to enhance it. This is a positive feedback mechanism that allows any beginning activity in the cerebral cortex to support still more activity, thus leading to an "awake" mind.

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In persons with serious airway obstruction bacteria 5 letters purchase mectizan 6 mg, as often occurs with acute asthma infection eyelid 6 mg mectizan with amex, this value can decrease to less than 20%. However, this term is usually used to describe a complex obstructive and destructive process of the lungs caused by many years of smoking. Chronic infection, caused by inhaling smoke or other substances that irritate the bronchi and bronchioles. The chronic infection seriously deranges the normal protective mechanisms of the airways, including partial paralysis of the cilia of the respiratory epithelium, an effect caused by nicotine. Also, stimulation of excess mucus secretion occurs, which further exacerbates the condition. There is also inhibition of the alveolar macrophages, so they become less effective in combating infection. The infection, excess mucus, and inflammatory edema of the bronchiolar epithelium together cause chronic obstruction of many of the smaller airways. The obstruction of the airways makes it especially difficult to expire, thus causing entrapment of air in the alveoli and overstretching them. This effect, combined with the lung infection, causes marked destruction of as much as 50% to 80% of the alveolar walls. The physiological effects of chronic emphysema are variable, depending on the severity of the disease and the relative degrees of bronchiolar obstruction versus lung parenchymal destruction. The bronchiolar obstruction increases airway resistance and results in greatly increased work of breathing. It is especially difficult for the person to move air through the bronchioles during expiration because the compressive force on the outside of the lung not only compresses the alveoli but also compresses the bronchioles, which further increases their resistance during expiration. The marked loss of alveolar walls greatly decreases the diffusing capacity of the lung. Now, study the difference between the two records for (1) normal lungs and (2) partial airway obstruction. There is, however, a major difference in the amounts of air that these persons can expire each second, especially during the first second. Recordings during the forced vital capacity maneuver in a healthy person (A) and in a person with partial airway obstruction (B). The obstructive process is frequently much worse in some parts of the lungs than in other parts, so some portions of the lungs are well ventilated, whereas other portions are poorly ventilated. Loss of large portions of the alveolar walls also decreases the number of pulmonary capillaries through which blood can pass. As a result, the pulmonary vascular resistance often increases markedly, causing pulmonary hypertension, which in turn overloads the right side of the heart and frequently causes right-sided heart failure. Both hypoxia and hypercapnia develop because of hypoventilation of many alveoli plus loss of alveolar walls. The net result of all these effects is severe, prolonged, devastating air hunger that can last for years until the hypoxia and hypercapnia cause death-a high penalty to pay for smoking. A common type of pneumonia is bacterial pneumonia, caused most frequently by pneumococci. This disease begins with infection in the alveoli; the pulmonary membrane becomes inflamed and highly porous so that fluid and even red and white blood cells leak out of the blood into the alveoli. Thus, the infected alveoli become progressively filled with fluid and cells, and the infection spreads by extension of bacteria or virus from alveolus to alveolus. Eventually, large areas of the lungs, sometimes whole lobes or even a whole lung, become "consolidated," which means that they are filled with fluid and cellular debris. In persons with pneumonia, the gas exchange functions of the lungs decline in different stages of the disease. In early stages, the pneumonia process might well be localized to only one lung, with alveolar ventilation being reduced while blood flow through the lung continues normally. Contrast of the emphysematous lung (top) with the normal lung (bottom) showing extensive alveolar destruction in emphysema. Emphysema 544 Chapter 43 Respiratory Insufficiency-Pathophysiology, Diagnosis, Oxygen Therapy ventilation-perfusion ratio. The blood passing through the aerated lung becomes 97% saturated with O2, whereas that passing through the unaerated lung is about 60% saturated. Therefore, the average saturation of the blood pumped by the left heart into the aorta is only about 78%, which is far below normal. Common causes of atelectasis are (1) total obstruction of the airway and (2) lack of surfactant in the fluids lining the alveoli. The airway obstruction type of atelectasis usually results from the following: (1) blockage of many small bronchi with mucus; or (2) obstruction of a major bronchus by a large mucous plug or some solid object, such as a tumor. The air entrapped beyond the block is absorbed within minutes to hours by the blood flowing in the pulmonary capillaries. If the lung tissue is pliable enough, this will lead simply to collapse of the alveoli. However, if the lung is rigid because of fibrotic tissue and cannot collapse, absorption of air from the alveoli creates very negative pressures within the alveoli, which pull fluid out of the pulmonary capillaries into the alveoli, thus causing the alveoli to fill completely with edema fluid. This process almost always is the effect that occurs when an entire lung becomes atelectatic, a condition called massive collapse of the lung. Collapse of the lung tissue Pulmonary arterial blood 60% saturated with O2 not only occludes the alveoli but also almost always increases the resistance to blood flow through the pulmonary vessels of the collapsed lung. This resistance increase occurs partially because of the lung collapse, which compresses and folds the vessels as the volume of the lung decreases. In addition, hypoxia in the collapsed alveoli causes additional vasoconstriction, as explained in Chapter 39. Because of the vascular constriction, blood flow through the atelectatic lung is greatly reduced.

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Normal H+ Concentration and pH of Body Fluids and Changes That Occur in Acidosis and Alkalosis antibiotic bomb generic mectizan 3 mg visa. The blood H+ concentration is normally maintained within tight limits around a normal value of about 0 antimicrobial overview mectizan 3 mg buy amex. Normal variations are only about 3 to 5 nEq/L but, under extreme conditions, the H+ concentration can vary from as low as 10 nEq/L to as high as 160 nEq/L without resulting in death. Because H+ concentration normally is low, and because these small numbers are cumbersome, it is customary to express H+ concentration on a logarithm scale using pH units. The H+ concentration in these cells is about 4 million times greater than the hydrogen concentration in blood, with a pH of 0. In the remainder of this chapter, we discuss the regulation of extracellular fluid H+ concentration. When there is a change in H+ concentration, the buffer systems of the body fluids react within seconds to minimize these changes. Buffer systems do not eliminate H+ from or add H+ to the body but only keep them tied up until balance can be re-established. These first two lines of defense keep the H+ concentration from changing too much until the more slowly responding third line of defense, the kidneys, can eliminate the excess acid or base from the body. Although the kidneys are relatively slow to respond compared with the other defenses, over a period of hours to several days, they are by far the most powerful of the acid­base regulatory systems. The lower limit of pH at which a person can live more than a few hours is about 6. Depending on the type of cells, the pH of intracellular fluid has been estimated to range between 6. Hypoxia of the tissues and poor blood flow to the tissues can cause acid accumulation and decreased intracellular pH. The terms acidosis and alkalosis describe the processes that lead to acidemia and alkalemia, respectively. As discussed later, the kidneys play a major role in correcting abnormalities of extracellular fluid H+ concentration by excreting acids or bases at variable rates. The general form of the buffering reaction is as follows: Buffer + H+ H Buffer H+ Concentration of Body Fluids pH H+ Concentration (mEq/L) In this example, a free H+ combines with the buffer to form a weak acid (H buffer) that can either remain as an unassociated molecule or dissociate back to the buffer and H+. When the H+ concentration increases, the reaction is forced to the right, and more H+ binds to the buffer, as long as buffer is available. Conversely, when the H+ concentration decreases, the reaction shifts toward the left, and H+ is released from the buffer. The importance of the body fluid buffers can be quickly realized if one considers the low concentration of H+ in the body fluids and the relatively large amounts 404 Chapter 31 Acid­Base Regulation of acids produced by the body each day. About 80 milliequivalents of H+ is ingested or produced each day by metabolism, whereas the H+ concentration of the body fluids normally is only about 0. Without buffering, the daily production and ingestion of acids would cause lethal changes in the body fluid H+ concentration. The action of acid­base buffers can perhaps best be explained by considering the buffer system that is quantitatively the most important in the extracellular fluid-the bicarbonate buffer system. Acidosis caused by an increase in Pco2 is called respiratory acidosis, whereas alkalosis caused by a decrease in Pco2 is termed respiratory alkalosis. When the concentrations of these two components are equal, the right-hand portion of Equation 8 becomes the log of 1, which is equal to 0. Therefore, when the two components of the buffer system are equal, the pH of the solution is the same as the pK (6. Buffer Power Determined by Amount and Relative Concentrations of Buffer Components. As discussed earlier, it is customary to express the H+ concentration in pH units rather than in actual concentrations. An increase in Pco2 causes the pH to decrease, shifting the acid­base balance toward acidosis. The Henderson-Hasselbalch equation, in addition to defining the determinants of normal pH regulation and acid­base balance in the extracellular fluid, provides insight into the physiological control of the acid and base composition of the extracellular fluid. This phenomenon means that the change in pH for any given amount of acid or base added to the system is least when the pH is near the pK of the system. The absolute concentration of the buffers is also an important factor in determining the buffer power of a system. With low concentrations of the buffers, only a small amount of acid or base added to the solution changes the pH considerably. For this reason, this system operates on the portion of the buffering curve where the slope is low, and the buffering power is poor. Despite these characteristics, the bicarbonate buffer system is the most powerful extracellular buffer in the body. However, its concentration in the extracellular fluid is low, at only about 8% of the concentration of the bicarbonate buffer. Therefore, the total buffering power of the phosphate system in the extracellular fluid is much less than that of the bicarbonate buffering system. In contrast to its minor role as an extracellular buffer, the phosphate buffer is especially important in the tubular fluids of the kidneys for two reasons: (1) phosphate usually becomes greatly concentrated in the tubules, thereby increasing the buffering power of the phosphate system; and (2) the tubular fluid usually has a considerably lower pH than the extracellular fluid, bringing the operating range of the buffer closer to the pK (6. The phosphate buffer system is also important in buffering intracellular fluid because the concentration of phosphate in this fluid is many times higher than in the extracellular fluid. Also, the pH of intracellular fluid is lower than that of extracellular fluid and, therefore, is usually closer to the pK of the phosphate buffer system compared with the extracellular fluid.

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• Johnson TM 2nd, Kincade JE, Bernard SL, et al: Self-care practices used by older men and women to manage urinary incontinence: results from the national follow-up survey on self-care and aging, J Am Geriatr Soc 48:894n902, 2000.
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• Goldhirsch A, Winer EP, Coates AS, et al. Personalizing the treatment of women with early breast cancer: highlights of the St Gallen International Expert Consensus on the Primary Therapy of Early Breast Cancer 2013.
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