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Tonicity determines cell volume antimicrobial questions buy genuine zentavion on line, as illustrated in the following examples antibiotic misuse quality 250mg zentavion. Na behaves as a nonpenetrating solute because it is pumped out of cells by the Na /K -ATPase at the same rate that it enters antimicrobial materials 100mg zentavion for sale. The NaCl solu- tion is also hypotonic because cells will accumulate water and swell when placed in this solution. The solution is isotonic, however, because it produces no per- manent change in cell volume. The reason is that cells shrink initially as a result of loss of water but urea is a pen- etrating solute that rapidly enters the cells. Urea entry in- creases the intracellular osmolality so water also enters FIGURE 2. Cell volume changes when a cell is urea concentration is the same inside and outside the placed in either a hypotonic or a hypertonic solution. A, In a hy- potonic solution, the reversal of the initial increase in cell volume cells. At this point, the total osmolality both inside and is known as a regulatory volume decrease. B, In a hypertonic solution, the reversal of the ini- tial decrease in cell volume is a regulatory volume increase. When cell volume increases because port systems for solute entry are activated, and water follows of extracellular hypotonicity, the response of many cells is solute into the cell. Different cells use dif- ferent regulatory volume decrease (RVD) mechanisms to move solutes out of the cell and decrease the number of creased volume triggers regulatory volume increase (RVI) particles in the cytosol, causing water to leave the cell. Because Na is sium, many RVD mechanisms involve an increased efflux of the main extracellular ion, many RVI mechanisms involve K , either by stimulating the opening of potassium chan- an influx of sodium into the cell. Other K -2Cl symport, and Na /H antiport are some of the cells activate the efflux of some amino acids, such as taurine mechanisms activated to increase the intracellular concen- or proline. The net result is a decrease in intracellular solute tration of Na and increase the cell volume toward its orig- content and a reduction of cell volume close to its original inal value (Fig. Mechanisms based on an increased Na influx are effec- When placed in a hypertonic solution, cells rapidly lose tive for only a short time because, eventually, the sodium water and their volume decreases. In many cells, a de- pump will increase its activity and reduce intracellular Na CHAPTER 2 The Plasma Membrane, Membrane Transport, and the Resting Membrane Potential 33 to its normal value. Cells that regularly encounter hyper- Passive exit + K tonic extracellular fluids have developed additional mecha- via nongated nisms for maintaining normal volume. These cells can syn- channel Active transport by thesize specific organic solutes, enabling them to increase + + Na /K -ATPase intracellular osmolality for a long time and avoiding alter- + ATP + ing the concentrations of ions they must maintain within a K 2K narrow range of values. The organic solutes are usually + small molecules that do not interfere with normal cell func- Na tion when they accumulate inside the cell. For example, cells of the medulla of the mammalian kidney can increase ++ 3 Na3 Na the level of the enzyme aldose reductase when subjected to elevated extracellular osmolality. This enzyme converts ADP glucose to an osmotically active solute, sorbitol. Synthesis of sorbitol and inositol represents different answers to the problem of in- creasing the total intracellular osmolality, allowing normal Passive entry + cell volume to be maintained in the presence of hypertonic via nongated Na extracellular fluid.

The the interstitial space can compensate for vascular volume myogenic response to elevated venous pressure may be due loss during sweating antibiotic used for mrsa zentavion 250mg otc, vomiting infection pictures generic zentavion 100 mg on-line, or diarrhea antibiotics for dogs allergies discount 500mg zentavion mastercard. As water is lost to venous pressures transmitted backward through the cap- by any of these processes, the plasma proteins are concen- illary bed to the arterioles and, perhaps, to some type of re- trated because they are not lost. THE REGULATION OF MICROVASCULAR RESISTANCE Tissue Metabolism Influences Blood Flow The vascular smooth cells around arterioles and venules re- In all organs, an increase in metabolic rate is associated with spond to a wide variety of physical and chemical stimuli, increased blood flow and extraction of oxygen to meet the altering the diameter and resistance of the microvessels. In addition, a reduction in Here we consider the various physical and chemical con- oxygen within the blood is associated with dilation of the ditions in tissues that influence the muscle cells of the mi- arterioles and increased blood flow, assuming neural re- crovasculature. The local regulation of 272 PART IV BLOOD AND CARDIOVASCULAR PHYSIOLOGY the microvasculature in response to the metabolic needs of In contrast to venules, many arterioles have a normal-to- tissues involves many different types of cellular mecha- slightly increased periarteriolar oxygen tension during nisms, one of which is linked to oxygen availability. Therefore, as long as blood flow is allowed to in- increase in metabolic rate would decrease the tissue oxygen crease substantially, it is unlikely that oxygen availability at concentration and possibly directly signal vascular muscle the arteriolar wall is a major factor in the sustained vasodi- to relax by limiting the production of ATP for the contrac- lation that occurs during increased metabolism. Only unusually low or high oxygen ten- around large venules during skeletal muscle contractions. However, either oxygen depletion in the capillary bed, possibly because venules acquire oxy- from an organ’s cells or an increased metabolic rate does gen that diffuses out of nearby arterioles. Although both cause the release of adenine nucleotides, free adenosine, periarteriolar and capillary bed tissue oxygen tensions de- Krebs cycle intermediates, and, in hypoxic conditions, lac- crease at the onset of contractions, both are restored as ar- tic acid. There is a large potential source of various mole- teriolar dilation occurs. The oxygen tension in venular cules, most of which cause vasodilation at physiological blood rapidly and dramatically decreases at the onset of concentrations, to influence the regulation of blood flow. The sustained decline in from accumulation of carbonic acid (formed from CO2 and venular blood oxygen tension probably reflects increased water) or acidic metabolites (such as lactic acid), causes va- extraction of oxygen from the blood. Endothelial Cells Can Release Chemicals That Cause Relaxation or Constriction of Arterioles An important contributor to local vascular regulation is re- leased by endothelial cells. This substance, endothelium- derived relaxing factor (EDRF), is released from all arteries, microvessels, veins, and lymphatic endothelial cells. EDRF is nitric oxide (NO), which is formed by the action of ni- tric oxide synthase on the amino acid arginine. NO causes the relaxation of vascular smooth muscle by inducing an in- crease in cyclic guanosine monophosphate (cGMP). When cGMP is increased, the smooth muscle cell extrudes cal- cium ions and decreases calcium entry into the cell, in- hibiting contraction and enzymatic processes that depend on calcium ions. Compounds such as acetylcholine, hista- mine, and adenine nucleotides (ATP, ADP) released into the interstitial space, as well as hypertonic conditions and hypoxia cause the release of NO. Adenosine causes NO re- lease from endothelial cells and directly relaxes vascular smooth muscle cells through adenosine receptors. Another important mechanism to release NO is the Arteriolar dilation and tissue oxygen ten- shear stress generated by blood moving past the endothe- FIGURE 16. Frictional forces between moving blood and the The decrease in arteriolar, capillary bed, and venous oxygen ten- stationary endothelial cells distort the endothelial cells, sions at the start of contractions reflects increased oxygen use, opening special potassium channels and causing endothe- which is not replenished by increased blood flow until the arteri- lial cell hyperpolarization. As arteriolar dilation occurs, arteriolar wall and capil- into the cell down the increased electrical gradient. The el- lary bed oxygen tensions are substantially restored, but venous evated cytosolic calcium ion concentration activates en- blood has a low oxygen tension. During recovery, oxygen ten- dothelial nitric oxide synthase to form more NO, and the sions transiently increase above resting values because blood flow remains temporarily elevated as oxygen use is rapidly lowered to blood vessels dilate. Perivascular and This mechanism is used to coordinate various sized arte- tissue PO2 in contracting rat spinotrapezius muscle. The endothelin stimulates both vas- small arteries control much more of the total vascular re- cular smooth muscle and cardiac muscle to contract more sistance than do small arterioles, the cooperation of the vigorously and induces the growth of surviving cardiac larger resistance vessels is vital to adjusting blood flow to cells.

This reluctance has manifested in several ways bacteria have dna 250mg zentavion amex, but two of the most important are underreporting to adverse event reporting systems and chilled com- munication with patients about errors antibiotic drug classes buy 500 mg zentavion mastercard, especially preventable ones (74 treatment for uti female buy discount zentavion 250 mg line,75). Thus, in spite of malpractice law’s mission to improve quality through deterrence—indeed, perhaps because of it—litigation fears obstruct progress in patient safety. The harsh reality is that greater publicity about mistakes, disclosure to patients, and access to reported information probably would increase litigation. Such corroborative information promises reduced time and costs for initiating litigation, shifting the plaintiff attorney’s calculus in the direction of more law- suits. Proponents of malpractice litigation applaud this, citing the prevalence of uncompensated negligent injuries and reiterating the importance of litigation as a deterrent. Critics are apprehensive and attempt to ensure that reporting systems are closed to the public. They may also seek to persuade providers that honest disclosure of errors actually decreases the probability of expensive litigation. Despite anecdotal reports of such positive experiences (75,76), the notion that disclosure reduces litigation is largely unproven and somewhat implausible. TORT REFORM Each tort crisis has stimulated enthusiasm tort reform among policy- makers. For example, screening panels force an evaluation of the merits of claims before they reach court. Their goal is to encourage settlement and stop nonmeritorious claims before they turn into protracted litigation. Another type of access constraint involves shortening statutes of limi- tation (time periods within which plaintiffs are permitted to sue after discovering their injury) or enacting statutes of repose (time limits that run from the date of the allegedly negligent event rather than discovery of the injury). The second family of reforms modifies liability rules in an effort to reduce both the frequency of claims and the size of payouts. For example, eliminating joint-and-several liability means that a plaintiff may recover from multiple defendants only in proportion to their con- Chapter 16 / Health Policy Review 237 Table 1 Malpractice Reform Options Conventional tort reform Limitations on Modification access to courts of liability rules Damages reform • Statute of limitations/ • Joint and several lia- • Caps repose bility rules • Attorney fee limits • Screening panels • Informed consent • Collateral source rules • Res ipsa loquitur • Periodic payment System reform Alternative mechanisms Alternatives Relocation of legal for resolving disputes to negligence responsibility • Early offers • “No-fault” administra- • Enterprise liability • Medical courts tive system • Private contracts • Predesignated com- • Fault-based admini- pensable events strative system tribution to causing the injury. Many states have enacted legislation reversing judicial expansions of liability (77). Elimination of the doc- trine of res ipsa loquitur, new standards for expert witnesses, and the imposition of higher standards for establishing breaches of informed consent all are examples of such retrenchment. The third family of reforms directly addresses the size of awards, with caps on damages awards being by far the most prominent measure. The cap may be applied to the total damages award or only to the non- economic (pain and suffering) component. More than half of the states already cap noneconomic damages, usually at ceilings ranging from $250,000 to $700,000 (78). By making the most lucrative lawsuits worth less, damages caps also indirectly limit the contingency fee and ensure that fewer cases hold the promise of a favorable return on the attorney’s investment. An alternative for achieving the same end is to limit the return itself through direct regulation of attorney fees, which is done in approximately one-third of the states. Other tort reforms directed at reducing the size of awards include rules mandating “collateral source offsets” and “periodic payments. It is too soon to judge the impact of the most recent wave of reforms, but studies from earlier eras are informative. Regression analyses (25,79–82) controlling for the presence of multiple tort reforms in a state, along with other characteristics of states or claims, have found that damages caps significantly reduce payouts (Table 2), but their impact on premiums is less clear. In some analy- ses, shorter statutes of limitation appear to impact claim frequency and insurance premiums. Pretrial screening panels, binding arbitration, and regulation of attorney fees generally do not have significant impacts (Table 2). One study showed that insurers’ loss ratios improved after caps were adapted (82a), whereas another showed no significant effect (82b).

Myringoplasty is a specific type of not remove fluid that has invaded the tympanoplasty in which the damaged mastoid air cell system medicine for uti that turns pee orange 100 mg zentavion with mastercard, however antibiotics variceal bleed order 500 mg zentavion overnight delivery, and addi- eardrum is repaired antibiotic growth promoters discount zentavion 100mg. Other types of tym- tional intervention may be necessary if the panoplasty may be performed for the sur- mastoid system is to be rendered dry. A gical repair or reconstruction of the ossicles common procedure performed during of the middle ear. Repairing or recon- myringotomy is placing ventilation- or pres- structing the conductive mechanisms of sure-equalizing tubes in the tympanic mem- the middle ear may improve or restore the brane. The pressure-equalizing tubes act as conductive component of individuals’ an artificial eustachian tube, equalizing hearing. Abnormal eustachian tube function is the most common cause Stapedectomy of middle ear problems. The ventilation tubes usually extrude on their own with- The most common surgical treatment in 3 to 18 months with few complications. The surgery due to middle ear disease is usually com- reestablishes a more normal sound path- pletely eliminated. Since the advent of antibiotics for treat- ment of mastoiditis, mastoidectomy is per- Devices and Aids for Hearing Loss formed less frequently. Mastoidectomy is a surgical procedure for removal of infect- Cochlear Implant ed mastoid air cells, which are located in the mastoid process. Because the mastoid Currently, cochlear implants are the is a portion of the acoustic system of the standard treatment for individuals with middle ear, there may be permanent severe to profound hearing loss who are hearing loss after surgery, depending on unable to have effective oral communica- the nature of the surgery. For example, tion even with the benefit of a hearing aid individuals who have had a radical mas- (Gates & Miyamoto, 2003). A cochlear toidectomy, in which other structures in implant is an auditory prosthesis. The im- addition to the mastoid cells are removed, plant is an inner ear device that helps indi- may have a greater degree of hearing loss viduals detect medium to loud environ- or permanent hearing loss. Cochlear implants trans- having a simple mastoidectomy, in late sounds into digital impulses that are which only mastoid cells are removed, fed directly to the auditory nerve, bypass- may have unaffected hearing. This elec- tronic device consists of a microphone that Tympanoplasty picks up sound; a battery-powered processor, either at ear level or typically worn on a Surgical procedures involving the mid- belt, that converts sound into digital dle ear are referred to generally as tym- impulses; and a receiver implanted into the 158 CHAPTER 5 HEARING LOSS AND DEAFNESS temporal bone that transmits digital • Severe to profound sensorineural impulses down the electrode that has been deafness surgically placed in the cochlea and that • Little or no benefit from hearing stimulates the auditory nerve directly. The processor converts able for the implant sound into digital impulses and sends it The chief predictor of success for a coch- to the receiver (the internal component, lear implant is a short duration of deafness about the size of a quarter, that is surgi- (Fischetti, 2003; Gates and Miyamoto, 2003). The receiv- though children who are prelingually deaf- er is connected to electrodes in the coch- ened may benefit from early implantation lea that receive impulses and stimulate the to facilitate speech development. Individ- auditory nerve with these digital impuls- uals receiving a cochlear implant should es, permitting perception of the digitally have realistic expectations for hearing processed information as speech. Optimal use Cochlear implants can be life-changing of cochlear implants requires a commit- for many individuals with severe to pro- ment to rehabilitation, training, and dai- found hearing loss. Although the cost of a cochlear speech reading, these individuals may be implant is typically covered by many able to engage in more effective verbal insurances, reimbursement for auditory communication because the implants en- rehabilitation, a key to successful use of able them to distinguish the beginnings implants, may be minimal or nonexistent. Implants can also and have strong ties to the Deaf commu- have a positive impact in work environ- nity may be unprepared for the social ram- ments. In addition to being able to hear ifications of a cochlear implant, since verbal communication, individuals with some individuals in the Deaf culture (dis- cochlear implants are also better able to cussed later in the chapter) are strongly hear and identify warning signals (Saxon, opposed to cochlear implants for cultural Holmes, & Spitznagel, 2001). Consequently, in some instances Although cochlear implants do not re- a cochlear implant can socially isolate store normal hearing and the sound heard individuals from other friends who are is not like an acoustic signal, individuals Deaf (Tucker, 1998).

Since diffusion across the plasma ported solute on one side of the membrane and releases it membrane usually implies that the diffusing solute enters at the other side bacteria from water order line zentavion. Although the details of this transport the lipid bilayer to cross it infection breastfeeding purchase 100mg zentavion amex, the solute’s solubility in a lipid mechanism are unknown infection in the blood order zentavion 250 mg, it is hypothesized that the bind- solvent (e. Because there are limited numbers of these carri- A substance’s solubility in oil compared with its solu- ers in any cell membrane, increasing the concentration of bility in water is its partition coefficient. Lipophilic sub- the solute initially uses the existing “spare” carriers to trans- stances that mix well with the lipids in the plasma mem- port the solute at a higher rate than by simple diffusion. As brane have high partition coefficients and, as a result, the concentration of the solute increases further and more high permeability coefficients; they tend to cross the solute molecules bind to carriers, the transport system plasma membrane easily. Hydrophilic substances, such as eventually reaches saturation, when all the carriers are in- ions and sugars, do not interact well with the lipid com- volved in translocating molecules of solute. At this point, ponent of the membrane, have low partition coefficients additional increases in solute concentration do not increase and low permeability coefficients, and diffuse across the the rate of solute transport (see Fig. The types of carrier-mediated transport mechanisms For solutes that diffuse across the lipid part of the plasma considered here can transport a solute along its concentra- membrane, the relationship between the rate of movement tion gradient only, as in simple diffusion. Net movement Simple diffusion Carrier-mediated transport 10 10 Vmax 5 5 1 3 1 2 3 Solute concentration (mmol/L) Solute concentration (mmol/L) outside cell outside cell FIGURE 2. Once all are occupied by solute, further increases in extracellular concentration have no ef- fect on the rate of transport. B, Bound solute readily dissociates from the carrier because of plasma membrane. In this example, solute transport into the cell the low intracellular concentration of solute. The release of solute is driven by the high solute concentration outside compared to may allow the carrier to revert to its original conformation (A) to inside. A, Binding of extracellular solute to the carrier, a mem- begin the cycle again. The throcyte GLUT 1 has an affinity for D-glucose that is about transport systems function until the solute concentrations 2,000-fold greater than the affinity for L-glucose. However, equilibrium is attained much tegral membrane protein that contains 12 membrane-span- faster than with simple diffusion. Equilibrating carrier-mediated transport systems have Equilibrating carrier-mediated transport, like simple several characteristics: diffusion, does not have directional preferences. It func- • They allow the transport of polar (hydrophilic) mole- tions equally well in bringing its specific solutes into or cules at rates much higher than expected from the parti- out of the cell, depending on the concentration gradient. Net movement by equilibrating carrier-mediated trans- • They eventually reach saturation at high substrate con- port ceases once the concentrations inside and outside the centration. AE1 is folded into at least 12 trans- • They show competitive inhibition by molecules with membrane -helices and normally permits the one-for- similar chemical structure. For example, carrier-medi- one exchange of Cl and HCO3 ions across the plasma ated transport of D-glucose occurs at a slower rate when membrane. The direction of ion movement is dependent molecules of D-galactose also are present. This is be- only on the concentration gradients of the transported cause galactose, structurally similar to glucose, competes ions. AE1 has an important role in transporting CO2 from with glucose for the available glucose carrier proteins. The erythrocytes in systemic A specific example of this type of carrier-mediated trans- capillaries pick up CO2 from tissues and convert it to port is the movement of glucose from the blood to the in- HCO3 , which exits the cells via AE1.

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