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Which of the following antihypertensive drugs is contraindicated in a hypertensive patient with a pheochromocytoma The cause is not known for certain virus living or nonliving discount 100 mg ultreon otc, but it may be related to the accumulation in the lungs of bradykinin or other inflammatory mediators virus 07092012 ultreon 100mg low price. The vasodilation caused by bradykinin antibiotics for sinus infection and sore throat buy ultreon 250 mg without prescription, histamine antimicrobial drugs antibiotics purchase generic ultreon on line, hydralazine, and acetylcholine depends in part upon nitric oxide release from the endothelium. Minoxidil activates K channels, which results in vascular smooth muscle hyperpolarization and thereby relaxation. Guanethidine does not normally cause release of catecholamines from the adrenal medulla. This action plus its ability to antagonize neuronal uptake of catecholamines could trigger a hypertensive crisis. The other drugs are good choices to lower blood pressure in a patient with pheochromocytoma: metyrosine, by decreasing synthesis; labetalol, by blocking both the - and -effects of the catecholamines; prazosin and especially phenoxybenzamine, by introducing a fairly long -blockade. The sympathetic effect on renin release is mediated by receptors, so prazosin, an -blocker would not decrease release. Nitroprusside and diazoxide are directly acting vasodilators and will promote renin release reflexively. Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Case Study Hypertensive Emergency A 50-year-old woman is seen in the emergency department complaining of a severe headache, shortness of breath, and ankle edema. Is this a hypertensive emergency, and if so what pharmacological treatment might be considered The azotemia and proteinuria are signs of renal disease and often portend deteriorating renal function. The enlarged heart and ankle edema are signs of heart failure, as is the shortness of breath. With blood pressure this high and the ominous clinical signs, this patient needs to be hospitalized and receive drug therapy to lower the blood pressure. The physician in a case such as this would likely choose intravenous therapy to get control of the blood pressure quickly. Although there are a number of choices, sodium nitroprusside should be at the top of the list. Nitroprusside has a rapid onset of action, within seconds of starting an infusion. It may benefit this patient to improve cardiac output by reducing afterload and preload. Other antihypertensives that could be considered in this situation are labetalol, a combined - and blocker, and nicardipine, a calcium channel antagonist. An advantage of these agents is that they can be administered intravenously, and once the patient is stabilized, one can switch to an oral formulation. Diuretics inhibit renal sodium transport and thereby interfere with the normal regulatory activity of the kidney. In some instances, administration of a diuretic drug is the primary treatment indicated, while in others it is one of several drugs that are used as part of a treatment regimen. In either case, an ideal diuretic would be one that caused the excretion of "extra" urine with an electrolyte composition similar to that of normal plasma. Thus, al- though diuretic therapy provides welcome relief from pulmonary congestion, ascites, edema, and hypertension, it also invites complications of organ hypoperfusion that may be accompanied by marked distortions of plasma composition. This chapter includes an overview of the features of fluid balance and renal function that are essential to understanding diuretic action, a discussion of the uses of diuretics for treating abnormalities of fluid balance, and a detailed description of the various classes of diuretics. The practitioner who is armed with the knowledge of the mechanism of action of diuretic drugs and with appropriate recognition and respect for their potential side effects can use these compounds with a high degree of efficacy and safety. The concentrations and distribution of electrolytes are not fixed, because cell membranes are permeant to ions and to water. Movement of ions and water in and out of cells is determined by the balance of thermodynamic forces, which are normally close to equilibrium. Selective changes of ion concentrations cause movement of water in or out of cells to compensate for these alterations. The loss of fluids due to illness or disease may alter intracellular and extracellular electrolyte concentrations, with attendant changes in fluid movement in or out of cells. Changes of extracellular or intracellular ion concentrations, particularly for potassium, sodium, and calcium, can have profound effects on neuronal excitability and contractility of the heart and other muscles. Glomerular Filtration Urine formation begins with the ultrafiltration of blood at the glomerulus. None of the available diuretics exerts its effects by altering the rate of glomerular filtration. Understanding the process of filtration is important to understanding the pharmacokinetics of diuretic action because most of these agents exert their inhibitory effect by blocking the entry of sodium from the urine into the cell. Therefore, these diuretics have to be present at sufficient concentrations within the tubular fluid to exert their inhibitory action on sodium transport. Most diuretics are variably bound to albumin and therefore are only partially filtered. They gain access to the tubular fluid by secretion into the proximal tubule (discussed later). In conditions of hemorrhage or liver disease resulting in hypoalbuminemia, the concentration of albumin is reduced and the fraction of bound diuretic is altered. Although this may suggest that more of the diuretic is unbound (or free) and filtered at the glomerulus, this does not occur. The decrease in Starling forces, which govern the rate of fluid filtration across the glomerular and other capillaries, now results in greater entry of fluid into the interstitial space. Most estimates of diuretic binding to albumin assume that the protein itself is not altered as part of the disease process.
Use prevalence to calculate how many in the sample do and do not actually have the disease virus protection for android ultreon 250 mg otc. For those who do not have the disease antibiotics for uti make you sleepy generic 250mg ultreon mastercard, use specificity to calculate how many will test negative for the disease (true-negatives) and how many will test positive (false-positives) infection 7th guest order generic ultreon canada. Calculate the positive predictive value by dividing the true-positives by all positive test results antibiotic resistance video pbs best order for ultreon. Calculate the negative predictive value by dividing the true-negatives by all negative results. Odds Ratio and Relative Risk Odds ratios and relative risk express how much more likely something is to occur if a certain condition is met, such as a patient being exposed to an illness or receiving a particular treatment. Relative risks and odds ratios are calculated from a chart similar to Figure 7-8 using absolute risk, which is the likelihood of an outcome over time without comparison to another group. Absolute Risk (of dying if exposed) = A / (A + B) Absolute Risk (of dying if not exposed) = C / (C + D) Attributable Risk Absolute risk (if not exposed) demonstrates that some subjects will have the outcome being studied, even when the condition is not met. To calculate how much risk is actually due to the condition being studied, use attributable risk. Relative risk is the comparison of risks between two different conditions or groups of people. For example, the relative risk of developing lung cancer for nonsmokers as compared to that for smokers is different. Relative risk is the measurement of probability of something happening in condition 1 relative to condition 2. In our example, if people are exposed to a particular pathogen, the odds of dying are 20/5 = 4. Thus, the odds of dying if one is exposed to the pathogen compared to not having been exposed are 8 times higher (4/0. Odds Ratio = (A / B) / (C / D) Studies that create a sample population based on outcome, such as case-control studies, must use odds ratios. Studies that create a sample population based on exposure or treatment, such as a controlled trial or cohort study, can use relative risk. Precision, Accuracy, and Error Precision, accuracy, and error describe the quality of measurements, such as those produced by a laboratory test. Systematic errors are errors that occur the same way every time a measurement is taken. As a result, the measurements are wrong in the same way each time and thus are not accurate, but are precise. Random error is unavoidable error that is different each time a measurement is taken. It represents the ratio between the sum of all individual observations (X) over the number of observations (n): Mean = X / n the mean, however, may not be an appropriate measure of central tendency for skewed distributions or in data sets that contain outliers. Median (middle observation) represents the 50th percentile of a distribution, or the point at which half of the observations are smaller and half are larger. The median is often a more appropriate measure of central tendency for skewed distributions or in situations with large outliers. Mode represents the most frequent value in a distribution and is commonly used for a large number of observations to identify the value that occurs most frequently. Categorical data: Variables that are not quantitative and take a value of one of several possible categories. All three are used for continuous data (ie, data that can be expressed along a numerical continuum, such as weight); the median may also be used for ordinal categorical data (eg, grades of cancer, asthma severity grades, etc). Terms that describe the curves created include: Gaussian: Also known as a "normal," or "bell-shaped," curve. Bimodal: the curve produces two "peaks" due to two separate areas of increased frequency of data in the population or data set. These curves may indicate symmetrical or asymmetrical distribution of observations. Mean > median > mode Negative skew: Asymmetrical curve with the tail to the left of the peak. There are two major types of hypotheses, differentiated by how the statement is framed: Study results support: Null hypothesis (H0): A statement that there is no difference, or association between two or more variables. H0 is tested for possible rejection under the assumption that the hypothesis is true. Alternative hypothesis (H1): A statement that there is an association between two or more variables, and contrary to the null hypothesis, the observations are the result of a real effect (Figure 7-11). Reality H1 H0 Type I Error Type I error results when one states or determines that there is an effect or difference when in reality one does not exist. Stated another way, the alternative hypothesis is accepted when in actuality the null hypothesis is correct. In other words, the null hypothesis fails to be rejected when in actuality the alternative hypothesis is correct (Figure 7-11). The power is affected by sample size and the variability or spread of the observations. Standard deviation is a statistical measurement used to describe the spread of the data around the mean within a statistical distribution (Figure 7-12). For the normal distribution, this accounts for about 68% of the set (dark red), while two standard deviations from the mean (medium and dark red) account for about 95%, and three standard deviations (light, medium, and dark red) account for about 99. The confidence interval sets boundaries within which the true population mean falls. Example: Imagine a study in which 50 people in a town have their blood pressure measured (independent samples from a population).
As the dose is increased antibiotics for sinus infection bronchitis discount 100 mg ultreon visa, the response increases until at 1 g/kg oral antibiotics for mild acne buy 250mg ultreon with mastercard, the maximum increase of 80 beats per minute occurs antibiotic resistance policy cheap ultreon 250 mg free shipping. In guinea pig e antibiotics for uti pain order ultreon master card, the maximum response is an increase in heart rate of 80 beats per minute. An estimate of the variation within the population can be indicated by calculating a statistical parameter, such as a confidence interval. To do so, one chooses a quantum of effect, for example, an increase in heart rate of 20 to 30 beats per minute above the control, or resting, rate. Doses of the drug are then plotted against the frequency with which each dose produces this amount of effect. The resulting graph has the same characteristics as the graph for the anticonvulsant activity of phenobarbital. There are many reasons for the common practice of using geometric scales, some of which will become apparent later in this book. One important reason is that in most instances significant increases in response generally occur only when doses are increased in multiples. The concept of the therapeutic index as a measure of the margin of safety has already been discussed. The responses are increases in heart rate above the rate measured before the administration of the drug. Drugs a and b are full agonists with an intrinsic activity of 1; drug c is called a partial agonist and has an intrinsic activity of 0. It is important not to equate greater potency of a drug with therapeutic superiority, since one might simply increase the dose of a less potent drug and thereby obtain an identical therapeutic response. Such factors as the severity and frequency of undesirable effects associated with each drug and their cost to the patient are more relevant factors in the choice between two similar drugs. Thus, affinity and efficacy represent kinetic constants that relate the drug, the receptor, and the response at the molecular level. Affinity is the measure of the net molecular attraction between a drug (or neurotransmitter or hormone) and its receptor. Affinity is one of the determinants of potency; efficacy contributes both to potency and to the maximum effect of the agonist. However, in contrast to intrinsic activity, no numerical value of efficacy can be calculated from the data presented. Unfortunately, the terms potency and efficacy are frequently used in a loose and misleading manner. Functional antagonism 2 Mechanisms of Drug Action 17 Chemical Antagonism Chemical antagonism involves a direct chemical interaction between the agonist and antagonist in such a way as to render the agonist pharmacologically inactive. A good example is the use of chelating agents to assist in the biological inactivation and removal from the body of toxic metals. Chelation involves a particular type of two-pronged attachment of the antagonist to a metal (the agonist). One chemical chelator, dimercaprol, is used in the treatment of toxicity from mercury, arsenic, and gold. After complexing with the dimercaprol, mercury is biologically inactive and the complex is excreted in the urine. Functional Antagonism Functional antagonism is a term used to represent the interaction of two agonists that act independently of each other but happen to cause opposite effects. Competitive Antagonism Competitive antagonism is the most frequently encountered type of drug antagonism in clinical practice. The antagonist combines with the same site on the receptor as does the agonist, but unlike the agonist, does not induce a response; that is, the antagonist has little or no efficacy. Competitive antagonists can fall into either of two subtypes, depending on the type of bond formed between the antagonist and the receptor. If the bond is a loose one, the antagonism is called equilibrium competitive or reversibly competitive. If the bond is covalent, however, the combination of the antagonist with the receptor is not readily reversible, and the antagonism is termed nonequilibrium competitive or irreversibly competitive. If the antagonism is of the equilibrium type, the antagonism increases as the concentration of the antagonist increases. Conversely, the antagonism can be overcome (surmounted) if the concentration of the agonist in the biophase (the region of the receptors) is in- creased.
The clinical uses of these drugs are associated with their potent vasoconstrictor action bacteria reproduce by binary fission discount ultreon 100mg on line. They are used to restore or maintain blood pressure during spinal anesthesia and certain other hypotensive states antibiotic resistance conference order 100mg ultreon mastercard. The reflex bradycardia induced by their rapid intravenous injection has been used to terminate attacks of paroxysmal atrial tachycardia infection 3 weeks after surgery discount ultreon 250 mg visa. The latter effects are primarily due to its indirect actions and depend largely on the release of norepinephrine antibiotic heartburn cheap ultreon 250 mg without a prescription. However, ephedrine may cause some direct receptor stimulation, particularly in its bronchodilating effects. Unlike epinephrine or norepinephrine, however, ephedrine is effective when administered orally. Ephedrine should not be used in patients with cardiac disease, hypertension, or hyperthyroidism. Pharmacological Actions Ephedrine increases systolic and diastolic blood pressure; heart rate is generally not increased. Ephedrine produces bronchial smooth muscle relaxation of prolonged duration when administered orally. Clinical Uses Ephedrine is useful in relieving bronchoconstriction and mucosal congestion associated with bronchial asthma, asthmatic bronchitis, chronic bronchitis, and bronchial spasms. It is often used prophylactically to prevent asthmatic attacks and is used as a nasal decongestant, as a mydriatic, and in certain allergic disorders. Although its bronchodilator action is weaker than that of isoproterenol, its oral effectiveness and prolonged duration of action make it valuable in the treatment of these conditions. Because of their oral effectiveness and greater bronchiolar selectivity, terbutaline and albuterol are replacing ephedrine for bronchodilation. Tachycardia, premature systoles, Amphetamine Amphetamine is an indirectly acting adrenomimetic amine that depends for its action on the release of norepinephrine from noradrenergic nerves. Both systolic and diastolic blood pressures are increased by oral dosing with amphetamine. It has been used in the treatment of obesity because of its anorexic effect, although tolerance to this effect develops rapidly. Amphetamine is no longer recommended for these uses because of its potential for abuse. Amphetamine is useful in certain cases of narcolepsy or minimal brain dysfunction. Epinephrine given in small therapeutic doses (A) Increases systolic blood pressure through 2 receptor stimulation in the left ventricle (B) Decreases heart rate reflexively. When phenylephrine is administered by slow infusion of the therapeutic dose, which is the most likely effect illustrated in the following table: increase ; decrease ; no change (0) Phentolamine blocks -adrenoceptors, allowing parasympathetic nerves innervating the sphincter muscle to take over. This leads to a less opposed contraction of the sphincter muscle induced by transmitter acetylcholine and a constriction of the pupil or miosis. The depressor effect of small doses is due to greater sensitivity to epinephrine of vasodilator 2-adrenoceptors than of constrictor -adrenoceptors and a dominant action on 2-adrenoceptors of vessels in skeletal muscle. The compensatory baroreceptor reflexes do not appreciably antagonize the direct cardiac actions. Amphetamine is an indirectly acting adrenomimetic amine that depends on the release of norepinephrine from noradrenergic nerves for its action. Thus, its effect depends on neuronal uptake (blocked by cocaine) to displace norepinephrine from the vesicles and the availability of norepinephrine (depleted by reserpine). The major cardiovascular response to this drug is a rise in blood pressure associated with reflex bradycardia. Molecular biological approaches to unravel adenylyl cyclase signaling and function. He has a family history of cardiovascular disease, having lost both his father and grandfather before either reached age 60. He has recently noticed decreased energy, especially during exercise, and had symptoms (difficulty in breathing, chest pain) that took him to the emergency department. The examining physician thought the best treatment would be short-term therapy with a directly acting inotropic agent, especially one that would not markedly increase an already elevated heart rate. Based on a knowledge of the distribution of cardiovascular autonomic receptors, which of the following agents- epinephrine, norepinephrine, amphetamine, or dobutamine-would be a logical choice to use in this initial short-term treatment Dobutamine augments ventricular contractility and thus enhances cardiac output, especially stroke volume, in patients with depressed cardiac function. It does this by stimulating -adrenoceptors in the heart while producing relatively little increase in chronotropic activity or any significant elevation in systemic blood pressure since it lacks -adrenoceptor stimulating effects. Agents that inhibit responses mediated by adrenoceptor activation are known as adrenoceptor antagonists, adrenergic antagonists, or adrenergic blocking agents. Norepinephrine is released from the varicosities of the postganglionic sympathetic nerves during neural activity and interacts with the adrenoceptors of the effector organ, producing the characteristic response of the effector. This occurs because norepinephrine has an affinity for the receptors and possesses intrinsic activity; that is, it has the capacity to activate the receptors. Circulating catecholamines and other directly acting adrenomimetic drugs also interact with these receptors. The antagonists, however, have only limited or no capacity to activate the receptors; that is, they have little or negligible intrinsic activity. The blocking drugs compete with adrenomimetic substances for access to the receptors. Thus, these agents reduce the effects produced by both sympathetic nerve stimulation and by exogenously administered adrenomimetics. Because agonist and antagonist have an affinity for the same receptors, the two substances compete for binding to the receptors.
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