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Jude Medical Aug-13 $331 Endosense is a pioneer in the ccontact force sensing Endosense catheter ablation field. The market has been growing at a torrid pace and is expected to continue to do so. The market remains a duopoly between Medtronic and Edwards Lifesciences (see Figure 8). The newer generation products seek to improve upon early-generation products on a number of areas including reduction of paravalvar leak, ease of delivery and implantation, multiple access routes, full-range of sizes to fit a patient’s anatomy, etc. Peripheral Vascular Market While coronary intervention is a mature market, peripheral vascular market is fast growing. Compared to the coronary market, peripheral vascular market is fragmented and has a range of players from large companies to small-medium companies (Table 14). But they have a number of disadvantages, including movement-related fracturing, foreign material in the vessel that could affect vessel wall, requiring dual antiplatelet therapy, etc. It is expected to grow from $80mn in this year to around $1bn near the end of this decade. With increasing prevalence of calcified and hard lesions and improving atherectomy technology, atherectomy market is expected to grow briskly. Atherectomy for coronary procedures is estimated to be ~$100mn market, growing at low-mid single digit. With some technology advantage, Cardiovascular Systems has been taking market share. Update of the Neurovascular Market Stroke is a debilitating medical condition and is poorly addressed by current therapies. According to the World Health Organization, an estimated 15 million people worldwide suffer a stroke each year. Neurovascular devices are used by neurosurgeons and neuro-interventionalists to treat stroke. According to market leader Stryker, world neurovascular market is currently around $1. Neurvascular products are broadly divided along the lines of cerebral aneurysm, ischemic stroke, and general access/balloon (see Table 18). A cerebral aneurysm is a weak spot in the wall of a blood vessel within the brain, characterized by an abnormal "ballooning" or widening of the vessel. When a brain aneurysm ruptures, the result is hemorrhagic stroke and is often fatal. Brain aneurysm treatment has been migrating from surgical clipping to endovascular coiling. According to the leader in the coil market, Terumo, in 2013, 61% brain aneurysm procedures in U. Stent-assisted coiling or balloon-assisted coiling are used for difficult cases such as wide-neck intravascular aneurysms. Flow diverter such as Pipeline™ Embolization Device from Covidien, is a notable new option for cerebral aneurysms. Instead of placing embolic material inside the aneurysm sac, a stent-like device is placed in the parental blood vessel of the aneurysm sac to divert blood away from the aneurysm. After the implantation, blood flow to the aneurysm is decreased and the aneurysm will be closed after a period. Total aneurysm market is growing at close to mid-single digit, with coils growing slower than non-coils. Of the various segments, cerebral thrombectomy is projected to have the most robust growth, driven by highly unmet medical need, strong clinical data and device innovation (see Table 19). Medical Device and Diagnostics Industry Updates Stryker is the market leader, followed by J&J, Covidien and Terumo (see Figure 11). A key trend for the neurovascular market is for players to move beyond basic access device and coils to highgrowth areas such as stents, flow diverters, thrombectomy devices (clot retrievers), liquid embolic, etc. As shown in Table 20, major neurovascular companies have been trying to flesh out their product offerings to have a total solution for stroke. First-generation device Merci Retriever from Concentric Medical (Stryker) received approval in 2004, but it has mediocre efficacy. Especially notable are the so-called Stent retriever devices such as Solitaire from Covidien and Trevo from Stryker. Both stent retrievers soundly beat Merci in various efficacy measures in robust clinical trials (see Table 21).

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On the other hand, blockade of β receptors in the bronchi will promote bronchoconstriction and may aggravate the symptoms of asthma. The β receptors in the heart mostly belong to the β1 subtype, whereas in the bronchi we mainly find β2 receptors. In this scenario, it may also be possible to improve the therapeutic index by taking advantage of agonist-specific coupling (Section 2. However, so far there are no clear-cut clinical applications of this interesting receptor behavior. In reality, drugs or other ligands may bind to several distinct receptors and possibly other kinds of binding sites as well. In order to determine whether there is a single class of binding sites or several classes with distinct affinities, one needs to measure binding data at various ligand concentrations. These data are usually obtained using a radiolabeled ligand, which allows for the facile and accurate measurement of both 32 2 Pharmacodynamics Kintr 120. All subunits bind mass action but differ in abundance and in affinthe ligand with the same affinity and change conity, occurring either alone or in combination. If there indeed is only one homogeneous population of binding sites, the graph will be a straight line. The total number of binding sites can be obtained from the x-axis intercept, and the dissociation constant from the slope. Deviations from linearity may indicate the presence of two or more classes of binding sites; however, another possible reason for deviation from linearity is a cooperative mode of ligand binding. While linear transformations like the Scatchard plot are appealing for displaying data, they have the disadvantage of introducing unequal weighting of the experimental error associated with individual data points. For quantitative analysis, it is preferable to apply nonlinear fitting methods to the untransformed underlying equation—in this case, for example, Equation 2. We further assume the three characteristic equilibrium constants (Kintr, Ki and Ka) to be the same for all subunits. Then, for both simple two–state and cooperative behavior, it is straightforward to determine the abundance of any state of conformation and ligand saturation, relative to the unbound, active state, by multiplying [L], Kintr, and Ki or Ka as many times as needed. Expressions describing the overall receptor occupancy and active fraction are then obtained by summation of terms as appropriate. This condition will be met if the rate of formation of M2 is proportional to the concentration of activated receptors, and the inactivation of M2 is a first-order process. This model is essentially the same as the one discussed by Strickland and Loeb [22], except that we here treat the receptor according to the two–state model rather than to simple mass action kinetics. A significant consequence of this change is that, at sufficiently high receptor expression levels, some basal activity will be observed even in the complete absence of agonist (which in turn might be suppressed by inverse agonists). In experimental pharmacology, however, it is also necessary to examine the function of new drugs in complex systems, for example in tissue culture or in an animal model. Even if we know that a new drug binds to a known receptor, it might also bind to other, similar receptors or even to entirely unrelated ones. In addition, the signal measured in the experiment may occur downstream of a biochemical cascade, which will cause the dose–response curves for the signal and for receptor binding to look quite different (see Section 2. A useful approach to address these problems is to measure the interaction of the new drug with a well-known drug that interacts specifically with the same receptor that we expect our new drug to bind to, yet has the opposite functional effect. One drug must be an agonist and the other one an antagonist; it is not important which one is the new drug. The experiment is carried out as follows: (1) Using incremental doses of the agonist, the signal is titrated to its half-maximal level. In each iteration, the total amounts of agonist and inhibitor added to the system are recorded. The underlying assumption of this approach is that, even though their relationship may be non-linear, the same signal intensity should still always correspond to the same level of receptor occupancy with the agonist. An experimental strategy that, like this one, achieves cancellation of systematic errors by measuring all data points at the same signal strength, is called a null method. The data points are then used to test the hypothesis that the two drugs do indeed bind to the same receptor in a competitive fashion.

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Inhaled aminoglycosides have been done in adults, pregnant women, and sides may also have a role in patients with persistently children for a variety of indications, including serious positive sputum despite therapy. Streptomycin is useful infections, pelvic inflammatory disease, abdominal sepin the initial therapy of severe or disseminated tubercusis, cystic fibrosis, and the empirical treatment of neulosis, which is most common in immunocompromised tropenic patients with fever. Special high-dose formulations of gentamAminoglycosides cause nephrotoxicity, and the relative icin are necessary for treating bacterial ophthalmic kertoxicity of the various aminoglycosides can be correatitis. Gentamicin is not active against viral conjunctivitis, lated with the number of constituent amine groups that although it may prevent a secondary bacterial infection. Although their polycationic humor, usually requires both vitreous aspiration and instructure prevents their entry into most cells, aminoglytravitreal instillation of gentamicin and cefazolin. Passage of the aminoglycosides across the apical membrane occurs Spectinomycin (Trobicin), an aminocyclitol antibiotic via a saturable process of adsorption of polycationic chemically related to the aminoglycosides, is occasionaminoglycoside molecules to the proximal renal tubular ally used to treat uncomplicated gonococcal urethritis lumen’s anionic brush border and subsequent endocyin patients who are allergic to -lactam. This leads to lysosomal distension, rupture, and release of acid hydrolases and the aminoglycoside into the cytosol. Gentamicin accumulation in mitoSingle daily doses of aminoglycosides are at least as efchondria displaces Ca, leading to mitochondrial defective as and no more toxic than multiple daily doses. The necrotic cellular debris Some studies suggest that single daily dosing may actuthen sloughs off and is passed in the urine, leaving a deally be less nephrotoxic than more frequent dosing. The development of Since aminoglycoside uptake across the brush border of toxicity depends upon the duration of aminoglycoside proximal renal cortical tubular cells is saturable, giving therapy and the mean trough blood plasma drug cona single large dose should result in less renal accumulacentration. Nephrotoxicity is more likely in aminoglytion; this has now been shown in patients receiving a coside-treated patients with gram-negative bacillary single bolus injection of gentamicin compared with bacteremia than in those with staphylococcal bacthose administered a continuous 24-hour intravenous teremia. One clinical trial recently demonstrated that vere in patients with extrahepatic biliary obstruction, ototoxicity was also reduced when single daily dosing hepatitis, or cirrhosis. The severity of aminoglycoside nephrotoxicity is adthe magnitude of the rapid-killing effect and the duditive with that of vancomycin, polymixin, gallium, ration of the postantibiotic effect of the aminoglycosides furosemide, enflurane, cisplatin, and cephalosporins. Verapamil and Ca can lessen of aminoglycoside-induced ototoxicity is worsened the nephrotoxicity, but the latter may also inhibit the by the coadministration of vancomycin, furosemide, antibacterial effect of the aminoglycosides. Ca may lessen the acid is a promising new agent that lessens aminoglycoototoxic effect. This is usually clinically centration gradient between blood and the otolymph; significant only in patients with myasthenia gravis, this process is saturable. Sustained high concentrations hypocalcemia, or hypermagnesemia or when the aminoin otolymph first destroy hair cells that are sensitive to glycoside is given shortly after the use of a neuromuscuhigh-frequency sounds. Many antibiotics appear to have as their mechanism (B) Aminoglycosides cause an increased metaboof action the capacity to inhibit bacterial cell wall lism of acetylcholine. Many antibiotics are not useful in treating infechibit significant metabolism in the patient. The most tions in the central nervous system because they do likely reason is that not readily penetrate the blood-brain barrier. Which (A) Their chemical structure is unique and not one of the following agents does get into the brain prone to chemical reactions commonly seen in drug in reasonable concentrations? The aminoglycosides appear to act by binding to (A) the combination provides for a much greater various sites on bacterial 30S ribosomal subunits spectrum of activity. The selection of agents to treat brain infections of the aminoglycoside antibiotics. Patients with myasthenia gravis may exhibit greater aminoglycoside and -lactam antibiotic are admintoxicity to aminoglycosides than do patients without istered concurrently is well documented. The most likely explanation is sons for the synergistic response are not well docu(A) Aminoglycosides have muscarinic blocking mented but may be related to the actions of the properties. Aminoglycosides can cause neuromuscular juncpresses premature stop mutations in patients with tion blockade by the mechanism of displacing Ca cystic fibrosis. Am J Respir Crit Care Med from the neuromuscular junction and thus leading 2001;163:1683–1692. This is of clinical significance only in amikacin in children with community-acquired bacpatients with myasthenia gravis, hypocalcemia, and terial meningitis. Clinical response to are poorly metabolized, and nearly all of an intraaminoglycosides: Importance of the ratio of peak venous dose can be recovered in the urine.

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Cellular uptake and lysosomal targeting are mediated by mannose6-phosphate receptors on the target cells. For expression of the enzyme, cell cultures have been genetically engineered so as to maximize the number of mannose-6-phosphate residues incorporated into the enzyme molecule during posttranslational modification [207]. Gaucher disease the enzyme defect in Gaucher disease concerns glucocerebrosidase, which cleaves the glucose headgroup from glucocerebroside, a sphingolipid that occurs in cell membranes (Figure 10. Only a small fraction of the surplus organ mass consists of accumulated lipid; the pathogenetic mechanism that leads to the additional organ enlargement is not exactly understood. Since macrophages originate in the bone marrow, transplantation of bone marrow is an effective and established therapeutic option, and gene therapy of bone marrow stem cells an experimental one. Enzyme therapy again requires uptake of the enzyme molecules into the phagolysosomes. Macrophages have multiple classes of cell surface receptors that trigger endocytosis. One class are lectins, which bind to the cell surface oligosaccharides of microbes and initiate their ingestion. To facilitate this interaction, the enzyme is partially deglycosylated so as to expose the mannose residues contained within its native glycosyl moiety (see Figure 10. In addition to enzyme therapy, Gaucher patients are being treated with inhibitors of glucocerebroside synthesis such as miglustat (Figure 10. A: Lysosomal β-glucosidase or glucocerebrosidase cleaves the glucose moiety from glucocerebroside (glucosylceramide), a membrane lipid. C: Plasma clearance of native β-glucosidase, and of a partially deglycosylated enzyme in which all sugar moieties distal of the mannose residues were removed. The rate of disappearance from the plasma reflects uptake by macrophages via mannose receptors. D: Structure of miglustat, an inhibitor of glucocerebroside synthesis that is used in the treatment of Gaucher disease. Serendipitously, miglustat was also found to inhibit spermatogenesis in mice, raising hopes for a new approach for male contraception. Monosodium urate is poorly soluble, and at elevated levels it forms crystals in connective tissues, particularly within joints. Urate crystals trigger inflammation by a recently elucidated mechanism [210], which leads to the characteristic gouty arthritis. While inflammation occurs acutely and intermittently, the underlying deposition of urate crystals is a long-term process. It is subject to glomerular filtration and to both reuptake and active secretion by tubular epithelial cells. The reaction carried out by adenosine deaminase is shown in red, and the two successive reactions catalyzed by xanthine oxidase are shown in blue. Typically, when present in the lumen of the tubule, they will compete with urate reuptake; this is the mode of action of uricosuric drugs such as benzbromarone or probenecid. On the other hand, when present inside the tubular epithelial cells, they may become substrates for exchange and therefore increase the rate of urate reuptake, as is the case with the metabolites of pyrazinamide (see Figure 10. The sugar moieties are utilized, while the pyrimidine and purine bases are mostly degraded and excreted. Gout is promoted by food and beverages that are rich in nucleic acids or nucleosides, such as, for example, meat and beer. Accordingly, dietary restrictions placed on such foods are a cornerstone of therapy. Fructose has been linked to increased uric acid production both statistically [212] and experimentally [213, 214]. Fructokinase, the first enzyme in fructose degradation, produces fructose-1-phosphate more rapidly than it is utilized. The transiently sequestered phosphate will eventually be brought back into circulation by the degradation of fructose-1-phosphate, which starts with aldolase B. The severe liver cell damage characteristic of this disease is again due to phosphate sequestration, which, however, is much more pronounced in this case. While heterozygous carriers of the enzyme defect don’t suffer acute liver damage, they still have an increased likelihood to develop gout in response to a diet rich in fructose or sucrose.

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For example, drugs that block adrenergic receptors or activate cholinergic ones will both lower the heart rate, but the maximal strength of that effect will likely differ. Two drugs that act on the same receptor may also differ in efficacy if one is a full agonist and the other a partial agonist. Both potency and efficacy of a drug may be affected by the existence of spare receptors if the observed effect is indirectly related to receptor occupancy, as discussed in Section 2. With partial agonists, a larger number of occupied receptors may compensate for partial receptor activation and therefore increase not only the potency but also the efficacy, possibly to the same level attained by a full receptor agonist. In some cases, toxicity arises simply as an extension of the beneficial or therapeutic effect. As an example, consider warfarin, an indirect inhibitor of the posttranslational γ-glutamyl carboxylation and concomitant activation of several blood coagulation factors (see Section 10. While warfarin helps to prevent thrombosis and stroke when used in low amounts, an excessive drug effect will be highly dangerous, leading to events such as spontaneous hemorrhage into the brain. Therefore, warfarin is very clearly an exception from the rule stated above that we typically want to achieve receptor saturation. Generally speaking, toxicity as an extension of therapeutic action is usually associated with a small therapeutic index, which is simply the ratio of the toxic concentration of the drug in the blood plasma over the therapeutic concentration: [Drug] toxic Therapeutic index = (2. Such variations may easily cause the plasma concentration to either exceed the toxicity threshold, or drop below the minimum amount required for the therapeutic effect. To avoid this, the concentration or the functional effect of a drug with a small therapeutic index must be monitored. Accordingly, in our example, patients receiving warfarin treatment must have their blood clotting activity measured at regular, frequent intervals. The challenge then will be to find drugs that will selectively act on the receptor responsible for the therapeutic effect. The blockade of β-adrenergic receptors in the heart is used in the treatment of hypertension and of heart disease. Using the assumptions that (1) all data points were acquired at the same level of receptor saturation with agonist, and (2) the inhibitor acts indeed by competition, we can write, for the first data point (inhibitor concentration [I]0 = 0, agonist concentration [A]0) and any other data point (inhibitor concentration [I], agonist concentration [A]I) [A]0 [A]I Y = = (2. The Schild plot yields the expected straight line, and the unknown drug is the inhibitor. The Schild plot yields the expected straight line, and the unknown drug is the agonist. We then still can assume that it binds to the same receptor as the known antagonist; however, we will not know its binding constant. Then, we have to conclude that the two drugs do not bind competitively and may interact with different receptors. The concentrations of each of the two drugs is independently varied, and the strength of the observable effect is measured. Chapter 3 Pharmacokinetics Whatever the actual mechanism of action of a drug may be, we will always want to know: Will the drug actually reach its site of action, and if so, for how long will it stay there? While it might seem merely a distraction to someone chiefly interested in biochemical mechanisms of drug action, pharmacokinetics is a crucial and often limiting factor in any form of pharmacotherapy, and it will be wise for anyone aspiring to develop novel therapeutic approaches to take it into consideration right from the beginning. A drug’s site of action may be a single anatomical location, such as a single organ, a localized infection, or a solid tumor. On the other hand, it may also be diffusely distributed throughout the entire body. This is the case, for example, in diabetes—insulin is required in all kinds of tissues—or in a systemic infection. If the site of action is confined, it may be possible to apply the drug topically, that is, directly and exclusively to this site. This will minimize any unnecessary exposure of organs that are not afflicted by the disease. Topical application also permits the use of drugs that would be too toxic for systemic application, such as iodine-based antiseptics, which can be used in the treatment of skin infections. The more common case, however, is that the drug must be applied systemically, because the site of action is either diffuse or inaccessible.

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Drew recruits through his small private practice, question at hand while minimizing risks and he will receive $1,000 to help defray the costs of maximizing benefits to subjects. Drew should quarterly blood draws and the additional consider whether subjects will be selected fairly, and paperwork required by the study. Drew’s should consider the quality of the ethical and computer system to enable better patient tracking. Drew could really use the protocol raises ethical issues that have not been financial support but wonders what benefits this addressed. Is it simply a me-too or whether the payment offered is commensurate with copycat drug, designed primarily to make money the time, effort, and actual expenditures to enroll for the drug company? Drew finds the financial incentives especially troubling, since it is debatable whether tempting and knows the risk to patients is low. Drew faces many ethical questions in physicians not accept gifts over $100 in value even if deciding whether or not to participate in the drug they offer benefit to patients, so Dr. Drew should trial for hypertension sponsored by the Modern not accept the computer system even if its absence Pharmaceutical Company. Drew feels that the study is valuable, of the role of physician, with the attendant duty to well designed, and meets ethical standards, before protect patients from harm, and recognize that the enrolling any patient Dr. Having whether that patient is doing well on current established the priority of Dr. Enrollment is most easily justifiable for a provide good patient care and protect patients from patient who is not doing well on standard therapy harm, Dr. These issues, although generated will change the course of patient care or complex, must be considered and resolved before otherwise provide a valuable scientific benefit, over Dr. Drew can determine the ethical justifiability of and above profit for the pharmaceutical company. Wonderlin 81 General Organization and 99 Functions of the Ner vous System William W. The first neuron in this sequence is called the somatic nervous system can function on a reflex basis, preganglionic neuron. The second neuron, whose cell voluntary control of skeletal muscle is of primary imbody is within the ganglion, travels to the visceral effecportance. In contrast, in the autonomic nervous system tor cell; it is called the postganglionic neuron. For example, when the body is exthe preganglionic neurons of the sympathetic nervous posed to cold, heat loss is minimized by vasoconstricsystem have their cell bodies in the thoracic and lumbar tion of blood vessels in the skin and by the curling up of regions of the spinal cord, termed the thoracolumbar dithe body. The preganglionic neurons of the parasympaby an increase in skeletal muscle tone and shivering and thetic division have their cell bodies in the brainstem and by an increase in metabolism owing in part to secretion in the sacral region of the spinal cord, termed the cranof epinephrine. The cranial part of the parasympathetic In general terms, the function of the autonomic nervous system innervates structures in the head, neck, nervous system is to maintain the constancy of the inthorax, and abdomen. A few sympathetic ganglia lie near sion of the parasympathetic nervous system innervates the organs innervated. In contrast, the parasymLocation of the Autonomic Ganglia pathetic ganglia lie very close to or actually within the organs innervated by the parasympathetic postganthe sympathetic ganglia consist of two chains of 22 segglionic neurons. The preganglionic fibers leave the spinal cord in Ratio of Preganglionic to Postganglionic adjacent ventral roots and enter neighboring ganglia, Neurons where they make synaptic connections with postganglionic neurons. Some preganglionic fibers pass through A single sympathetic preganglionic fiber branches a the vertebral ganglia without making synaptic connecnumber of times after entering a ganglion and makes tions and travel by way of splanchnic nerves to paired synaptic connection with a number of postganglionic prevertebral ganglia in front of the vertebral column, neurons. Furthermore, some branches of this preganwhere they make synaptic connections with postganglionic fiber may ascend or descend to adjacent verteglionic neurons. In addition, some sympathetic preganbral ganglia and terminate on an additional number of glionic fibers pass through the splanchnic nerves into postganglionic neurons in these ganglia as well. Postganglionic fibers are generally long, signed to produce widespread physiological activity. The since they arise in vertebral ganglia and must travel to sympathetic nervous system prepares the body for the innervated effector cells. Neurons that release acetylcholine are the ganglia are near or are embedded in the organs incalled cholinergic neurons. The parasympathetic nervous sysNeurons that release this substance are called adrenertem is involved with the accumulation, storage, and gic or noradrenergic neurons. The sympathetic When the sympathetic integrative centers in the postganglionic neurons that innervate the sweat glands brain are activated (by anger, stress, or emergency), the and some of the blood vessels in skeletal muscle are body’s resources are mobilized for combat or for flight. There is increased Drugs that mimic the actions of acetylcholine are blood flow (vasodilation) through skeletal muscle and termed cholinomimetic, and those that mimic epinephdecreased blood flow (vasoconstriction) through the rine and/or norepinephrine are adrenomimetic.

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Breast fullness and of the diuretics themselves may be a factor in diuretic subcutaneous swelling or puffiness are the most comresistance. These patients may thus, when present in relatively high concentrations, be vulnerable to ototoxicity or other adverse effects if may produce some expansion of the extracellular fluid larger amounts of the diuretic are employed. Excessive premenstrual edema freCompensatory proximal tubular sodium absorption quently responds well to thiazide therapy. Recent expemay contribute to or be responsible for the resistance rience has diminished enthusiasm for use of any diuretto loop diuretics. Since the edema of pregnancy is used as an alternative approach to treating diuretic resistance once it has been verified that satisfactory Na frequently well tolerated, concerns of compromised uteroplacental perfusion, possible ineffectiveness of direstriction is being followed and that the drug is being uretics in preeclampsia, and the risk of adverse effects adequately absorbed. Administration of a carbonic anhydrase inhibitor may be sufficient to enhance Na deof diuretics on the baby. Alternatively, thiazide newborns) have led to diminished routine use of these diuretics may be combined with the loop diuretic to agents in pregnancy. The thiazidelike diuretic metolazone, which has some proximal tubule effects unrelated to carbonic anhydrase, apResistance to Diuretic Administration pears to be the most effective of the thiazide and Since the effectiveness of many diuretics ultimately dethiazidelike drugs in this regard. Therefore, one cause of therapeutic failure or apparent patient refracExcessively vigorous diuresis may lead to intravascular toriness to diuretics could be the patient’s continued indehydration before removal of edema fluid from the gestion of large quantities of NaC1. This is especially Some of the older diuretic drugs were self-limiting; dangerous if the patient has significant liver or kidney that is, prolonged administration resulted in a gradual disease. This problem was cortrolyte derangement has been achieved, the effect sought rected through the use of intermittent diuretic therapy. Drug Such a program of several days of diuresis followed by dosage, frequency of administration, and Na intake several days of drug withdrawal delayed refractoriness should be adjusted to achieve homeostasis. Solution Manufacturer Since the 1950s, diuretic therapy has changed draNormosol-R Abbott matically. Either because of Polysal Cutter toxicity or lack of efficacy, these agents are rarely if Lactated Ringer’s (Several) ever used. Most of these solutions contain electrolytes in the following mEq range: sodium (130–150), potassium (4–12), chloride (98–109), bicarbonate (50–55), calcium (3–5), and magnesium (0–3). The beneficial effect of the sustained (A) Na reduction of blood pressure is due to reduced vascu(B) K lar resistance. Extracellular volume remains modestly (C) Ca and Mg reduced and cardiac output returns to pretreatment (D) Uric acid levels. Which of the following drugs is an appropriate iniand is associated with an increased risk of ventricular tial antihypertensive therapy in an otherwise fibrillation and malignant arrhythmias. However, the degree to (B) Triamterene which individual patients are affected varies, though (C) Hydrochlorothiazide chronic administration of even small doses causes (D) Aldactone some K depletion. One is competition of the thiazide class of pulmonary edema, there is often symptomatic relief diuretics, which are weak organic acids, with uric acid within 5 minutes of starting treatment. Serum concentrations of (A) A rapid diuretic effect uric acid are further elevated by the reduced extracel(B) An increase in venous capacitance lular volume. Diuretic-induced hyperuricemia may (C) A direct effect on myocardial contractility cause acute gouty attacks. The use of diuretics in congestive heart failacid excretion decreases as a consequence of comure. Clinical complications of diuretic therof a thiazide diuretic for monotherapy has been recapy. Diuretic drugs and the treatment of Detection, Evaluation and treatment of High Blood edema: From clinic to bench and back again. Diuretics in cardiovascular However, thiazide diuretics are a more conservative therapy: the new clinicopharmacological bases that and approved approach for the initial treatment of matter. Metolazone would be expected to be very effective, particularly in combination with a loop diuretic. Case Study Furosemide Resistance A 26-year-old woman with nephrotic syn(C) Sequestration of furosemide by intraluminal alAdrome comes to your office because of worsbumin thereby reducing its inhibition of the ening edema.

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Perhaps resumption of bacterial riminimum inhibitory concentration against the isolated bosomal function requires the time-consuming synthepathogen is a useful indicator of the adequacy of aminosis of new ribosomes after their disruption by aminoglyglycoside dosing. The postantibiotic effect explains why Both the rate and extent of gastrointestinal absorpaminoglycosides can be given in single daily doses detion of individual aminoglycosides are generally quite spite their short half-life. For example, more than 95% of an oral dose of Penetration of aminoglycosides through the outer neomycin is excreted unchanged in the feces. The sysbacterial membrane occurs both by outer membrane temic bioavailability of the aminoglycosides is low disruption and by diffusion through outer membrane across other membranes as well. Penetration through the inner bacterial memicin is poorly absorbed from a topical ophthalmic brane occurs in two phases. The first requires that the preparation, and there is little systemic absorption of eicytosol have a negative electron potential and therefore ther inhaled tobramycin or aminoglycosides instilled be inhibited by the presence of a low pH. Neomycin bioavailability phase depends on aerobic bacterial metabolism and across intact skin is also low, although absorption across therefore will be inhibited by low oxygen tension. The damaged skin can be significant: nephrotoxicity can oclatter two observations are of considerable clinical relecur in burn patients treated with topical neomycin. Administration binding to plasma and tissue proteins, the distribution of -lactam antibiotics will reverse the negative effects of the aminoglycosides corresponds to that of the extraof both low pH and low oxygen tension on the ability of cellular fluid. Gentamicin fails to reach intraocular fluid or cereconstant over the past 2 decades. Of the three recogbrospinal fluid in significant concentrations after intranized mechanisms of resistance that occur in aerobic venous injection, although it may reach bactericidal gram-negative bacteria, plasmid-mediated expression levels in cerebrospinal fluid in patients with meningeal of enzymes that acetylate, adenylate, or phosphorylate inflammation, such as occurs in meningitis. Ring one is rect intrathecal injection of gentamicin may still be rethe primary target of these enzymes. Nearly all of an gram-negative bacilli to exhibit resistance to gentaintravenous dose is cleared by the kidneys and can be micin. Aminoglycoside clearance is aptamicin may be susceptible to amikacin or tobramycin. Orally administered neomycin is Infections sometimes used to suppress the facultative flora of the Gentamicin is the aminoglycoside antibiotic most comgut in patients with hepatic encephalopathy. It is unmonly used to treat serious infections due to gramclear how this improves coma, but one theory is that it negative aerobic bacilli, such as Escherichia coli and Klebreduces systemic absorption of the bacterial metabosiella pneumoniae, and Proteus, Serratia, Acinetobacter, lites that allegedly cause hepatic encephalopathy. Gentamicin also has Although more than 95% of an oral dose of neomycin significant activity against Staphylococcus aureus. The is excreted unchanged in the stool of normal subjects, aminoglycosides are often used in combination with the bioavailability of neomycin may be much higher in lactams in the initial empirical therapy of sepsis and of patients with an abnormal gastrointestinal mucosa. The combination Neomycin is often combined with other antibiotics, is used both to ensure adequate antibiotic coverage in such as polymyxin B and bacitracin, and applied as an these seriously ill patients and to exploit the synergistic ointment to prevent any infection of minor skin abraantibiotic activity that -lactams and aminoglycosides sions, burns, and cuts. These drugs should not, however, be injected simultaneously, since the -lactams can Cystic Fibrosis chemically inactivate the aminoglycosides. Single daily dosing inhalation of large doses of tobramycin decreased the may be of particular importance in patients with pneucolonization by this organism 100-fold and significantly monia, since this regimen can increase the peak conimproved pulmonary function. Acute salpingitis (pelvic inflammatory disease) due Endocarditis to Neisseria gonorrhoeae, Chlamydia trachomatis, or A combination of gentamicin and ampicillin is recomboth is often complicated by superinfection with grammended as prophylaxis of endocarditis prior to surgery negative bacilli and anaerobes. A combination of genor instrumentation of the gastrointestinal or genitouritamicin, clindamycin, and doxycycline has been shown nary tracts for patients at high risk for endocarditis. Gentamicin or streptomycin useful in patients with an intraabdominal infection or will act synergistically with penicillin for the treatment an abscess secondary to penetrating trauma, diverticuliof enterococcal endocarditis. These infections are often polymicroMeningitis bial, including gram-negative bacilli and anaerobes. Definitive treatment of these conditions may also rethe degree of penetration of the aminoglycosides into quire surgical or other intervention to drain the abscess. However, aminoglycosides treatment of serious infections should be guided both are best combined with the -lactams or other antibiby assessment of the antibiotic sensitivities of the speotics in the treatment of meningitis. Single daily dosing In response to the increasing prevalence of mycobactewith amikacin results in higher drug concentrations in rial resistance to standard antibiotic chemotherapy, the the bronchial secretions of patients with pneumonia. Amikacin levels in bronchia secretions of 10 pneumonia patients with respiratory support treated once daily versus twice daily. You the patient complains that he can’t hear as well immediately arrange to check renal function and now as he could prior to his recent hospitalization.

References:

  • https://www.med.navy.mil/sites/nmcphc/Documents/policy-and-instruction/oem-prevention-and-treatment-of-heat-and-cold-stress-injuries.pdf
  • https://bnssgccg-media.ams3.cdn.digitaloceanspaces.com/attachments/09_20150213_governing_body_report_cprg_policies.pdf
  • https://austinpublishinggroup.com/dermatology/download.php?file=fulltext/ajd-v3-id1044.pdf
  • https://vtechworks.lib.vt.edu/bitstream/handle/10919/28568/ALODISSERTATION.pdf?sequence=2&isAllowed=y
  • http://www.scielo.br/pdf/abd/v79n3/v79n3a10.pdf