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By: D. Ur-Gosh, M.B. B.A.O., M.B.B.Ch., Ph.D.

Program Director, Harvard Medical School

Without new technological advances blood pressure erratic purchase 50mg atenolol free shipping, the human growth rate has been predicted to arrhythmia strips order atenolol overnight delivery slow in the coming decades blood pressure medication that doesn't cause cough cheap atenolol 50mg fast delivery. Overcoming Density-Dependent Regulation Humans are unique in their ability to alter their environment with the conscious purpose of increasing its carrying capacity. This ability is a major factor responsible for human population growth and a way of overcoming density-dependent growth regulation. Much of this ability is related to human intelligence, society, and communication. In addition, humans use language to communicate this technology to new generations, allowing them to improve upon previous accomplishments. Humans originated in Africa, but have since migrated to nearly all inhabitable land on the Earth. Thus, it appears that the influence of infectious disease on human population growth is becoming less significant. Age Structure, Population Growth, and Economic Development the age structure of a population is an important factor in population dynamics. Age structure allows better prediction of population growth, plus the ability to associate this growth with the level of economic development in the region. Countries with rapid growth have a pyramidal shape in their age structure diagrams, showing a preponderance of younger individuals, many of whom are of reproductive age or will be soon (Figure 45. This pattern is most often observed in underdeveloped countries where individuals do not live this OpenStax book is available for free at cnx. The age structure of these populations is more conical, with an even greater percentage of middle-aged and older individuals. The rapid growth diagram narrows to a point, indicating that the number of individuals decreases rapidly with age. Stable population diagrams are rounded on the top, showing that the number of individuals per age group decreases gradually, and then increases for the older part of the population. Age structure diagrams for rapidly growing, slow growing and stable populations are shown in stages 1 through 3. In the 1970s hundreds of millions of people will starve to death in spite of any crash programs embarked upon now. Due to the fact that some couples wish to have a male heir, many Chinese couples continue to have more than one child. The policy itself, its social impacts, and the effectiveness of limiting overall population growth are controversial. At some point the food supply may run out because of the subsequent need to produce more and more food to feed our population. Another result of population growth is the endangerment of the natural environment. Many countries have attempted to reduce the human impact on climate change by reducing their emission of the greenhouse gas carbon dioxide. Furthermore, the role of human activity in causing climate change has become a hotly debated socio-political issue in some developed countries, including the United States. Thus, we enter the future with considerable uncertainty about our ability to curb human population growth and protect our environment. All populations occupying the same habitat form a community: populations inhabiting a specific area at the same time. Areas with low diversity, such as the glaciers of Antarctica, still contain a wide variety of living things, whereas the diversity of tropical rainforests is so great that it cannot be counted. Ecology is studied at the community level to understand how species interact with each other and compete for the same resources. The most often cited example of predator-prey dynamics is seen in the cycling of the lynx (predator) and the snowshoe hare (prey), using nearly 200 year-old trapping data from North American forests (Figure 45. As the hare numbers increase, there is more food available for the lynx, allowing the lynx population to increase as well. When the lynx population grows to a this OpenStax book is available for free at cnx.

Aortic coarctation

If the preceding approaches fail to heart attack song purchase generic atenolol line give a diagnosis or are not indicated for clinical reasons blood pressure 12080 buy atenolol, then one might consider the potential of a renal biopsy blood pressure medication manufacturers generic 100 mg atenolol amex. It is of limited prognostic use, and only rarely is it indicated for monitoring progression of renal disease. Table 100-6 lists the indications for renal biopsy, but it should be recognized that wide variations exist among nephrologists for indication of a renal biopsy, and therefore, it often becomes a matter of personal preference. However, each patient should be evaluated carefully to choose those patients in whom diagnostic yield is thought to be high while complication rates are minimized. In general, it is rare that a renal biopsy is indicated in chronic renal failure with small kidneys. Similarly, renal biopsy is not required to confirm diabetic nephropathy if the presentation of diabetic nephropathy is classic. However, in cases of persistent hematuria (if glomerular), proteinuria, acute renal failure, and various systemic diseases with renal failure and after renal transplant in patients with unexplained deterioration of renal function, a renal biopsy is indicated to obtain a diagnosis or to initiate or modify therapy. However, renal biopsy should not be done if the patient cannot cooperate, if he or she has bleeding abnormalities with platelets that are below 60,000/mm2 and a prothrombin time greater than 3 seconds from control, and/or if bleeding time is prolonged. Also, renal biopsy should not be done if a solitary kidney exists or before diastolic blood pressure has been brought to less than 90 mm Hg. The percutaneous approach is much more inexpensive and, when performed by a skilled nephrologist, yields adequate tissue in more than 90% of cases. Open biopsy should be reserved for uncooperative patients and those who are at risk for uncontrolled bleeding or have solitary kidneys. Clearly, in the latter case, the index of suspicion for therapeutically relevant information must be high. Adequately sized samples should be obtained for electron microscopy, immunofluorescence, and light microscopy. If minimal tissue is present, then electron microscopy should be done alone, followed by electron microscopy and immunofluorescence, and both of these should be done with light microscopy if adequate tissue is present. Although renal biopsy gives only histologic information, it nevertheless often will allow a correct clinical diagnosis that could not be made otherwise when interpreted in the context of other clinical information. Evaluating accuracy and cost-effectiveness of dipstick urinalysis and standard microscopic urinalysis to predict significant bacteriuria. Nice discussion on the indications and role of renal ultrasonography in evaluating patients who are suspected of having urinary tract obstruction and in patients with a rise in serum creatinine levels. A careful determination of sensitivities and specificities of leukocyte esterase and bacterial nitrate dipstick tests for urinary tract infections. A nice prospective analysis of the significance in fractional excretion of filtered sodium as a predictor of a prerenal versus a renal cause of azotemia. A study to examine the accuracy of the refractometer to determine the osmolarity of urine in pediatric patients. Craig Tisher the complex multicellular composition of the kidney reflects the complicated nature of its functional properties. This organ is responsible for maintaining both the volume and ionic composition of the body fluids; excreting fixed or non-volatile metabolic waste products such as creatinine, urea, and uric acid; and eliminating exogenous drugs and toxins. The kidney is a major endocrine organ, because it produces renin, erythropoietin, 1,25-dihydroxycholecalciferol, prostaglandins, and kinins; and it also serves as a target organ for many hormones. The kidney also catabolizes small-molecular-weight proteins and is responsible for a host of metabolic functions. The kidney originates from two sources: (1) the ureteral bud, which gives rise to the ureter, pelvis, calyces, and collecting ducts; and (2) the metanephric blastema, which gives rise to the glomerulus and tubules. During embryogenesis, three successive sets of excretory organs develop: the pronephros, mesonephros, and metanephros. Cellular and molecular mechanisms that underlie renal morphogenesis include cell proliferation, expression of nuclear proto-oncogenes and homeobox genes, the actions of peptide growth factors, and alterations in both cell adhesion and the composition of the extracellular matrix. The kidneys are located in the retroperitoneal space and extend from the twelfth thoracic vertebra to the third lumbar vertebra. The right organ usually is more caudad, whereas the left organ tends to be slightly larger. The cut surface of a bisected kidney reveals a darker inner region, the medulla, and a pale outer region approximately 1 cm in thickness, the cortex. The human kidney has a multipapillary configuration in which the medulla is divided into 8 to 18 striated conical masses called pyramids (Fig.

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Management of Refractory Peripheral Edema Several strategies should be considered in the management of patients with refractory edema arteria nutrients ulnae cheap atenolol 100 mg without a prescription. Non-steroidal anti-inflammatory drugs blood pressure chart youth atenolol 100 mg lowest price, which can decrease the efficacy and increase the risk of diuretics heart attack right arm buy atenolol with visa, should be withdrawn. If the patient fails to respond to the intravenous administration of large doses of furosemide, the physician may add a second diuretic with a different renal tubular site of action. A combination of two diuretics can produce a dramatic increase in urine output, but such a regimen is commonly accompanied by striking (and occasionally life-threatening) degrees of hypokalemia. If a combination of intravenous furosemide and oral metolazone proves ineffective, these diuretics should be co-administered with drugs that increase renal blood flow. Finally, if the edema becomes refractory to all pharmacologic interventions, hemofiltration or peritoneal dialysis may be useful in restoring fluid balance in selected patients. Regardless of the severity of fluid retention, every effort should be made to achieve dry weight, even if achievement of this goal requires a prolonged hospitalization. Patients discharged prematurely with residual edema due to an inadequate diuresis are commonly readmitted to the hospital for refractory edema within several weeks. In contrast, patients who achieve dry weight frequently become responsive to conventional treatments for heart failure and have a lower risk of recurrent hospitalization. Pulmonary Congestion (Acute Pulmonary Edema) One of the most common clinical presentations of advanced left ventricular failure is the syndrome of pulmonary congestion. These patients complain of dyspnea at rest and have pulmonary rales on physical examination. Pulmonary congestion may be the first evidence of heart failure in patients without a history of cardiac disease; it may appear in patients who are already hospitalized for an acute cardiac disorder. If severe, abrupt, and accompanied by clinical evidence of sympathetic overactivity (tachycardia, diaphoresis and vasoconstriction), the syndrome is designated as acute pulmonary edema. Acute pulmonary edema may also be triggered by non-cardiac disorders, including direct injury to the alveolar-capillary membrane, high-altitude stress, catastrophes of the central nervous system, narcotic overdose, or pulmonary embolism. Regardless of its cause, pulmonary edema reflects the transudation of fluid into the alveolar space and arises from an imbalance in the factors that regulate the transport of fluid from the pulmonary microcirculation to the interstitial space of the lung. When the cause of the syndrome is cardiac, pulmonary edema results from the rapid onset of intense peripheral vasoconstriction that leads to a marked increase in pulmonary venous pressures. The profound constriction of systemic arteries and veins causes a sudden and dramatic redistribution of blood from peripheral reservoirs to the pulmonary circuit, causing the pulmonary capillary hydrostatic pressure in the lung to exceed the capillary colloid osmotic pressure. However, the transudation of fluid into the alveoli cannot occur if pulmonary blood flow is impaired; thus, patients with an elevated pulmonary vascular resistance or depressed right ventricular function rarely develop acute pulmonary edema. Management of Pulmonary Edema Several general measures are advisable for most patients with pulmonary congestion. Every effort should be made to identify an underlying precipitating factor, because its correction is often critical to the success of treatment. Patients usually feel most comfortable resting in bed in the upright position with the legs dependent. Special attention should be devoted to maintaining adequate oxygenation, which can be achieved by increasing the concentration of 225 inspired oxygen or (if necessary) by endotracheal intubation and mechanical ventilation. Given the importance of peripheral vasoconstriction in the pathogenesis of pulmonary edema, pharmacologic dilation of peripheral vessels represents the critical element in any successful approach to management. This goal can be achieved with the use of (1) morphine; (2) loop diuretic drugs. Because of the need for rapid and reliable treatment, these interventions are generally administered intravenously. Morphine remains the most effective single agent for the treatment of acute cardiogenic pulmonary edema. The drug acts specifically to antagonize the peripheral vasoconstrictor effects of the sympathetic nervous system; the resultant vasodilatation leads to an immediate and dramatic decline in pulmonary arterial and venous pressures, leading directly to symptomatic improvement. The magnitude of venodilation produced by the drug in the limbs is insufficient to explain its effects on pulmonary flow and pressures; instead, morphine appears to act primarily to increase the pooling of blood in the splanchnic circulation.

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The prognosis for more severe toxic gas exposures varies with duration and extent of exposure blood pressure good buy atenolol with visa. Because improvement after the initial exposure may be temporary arrhythmia recognition posters purchase generic atenolol on line, close observation for 48 hours after the exposure is advisable heart attack follow me discount atenolol online american express. Oxygen is toxic to the lungs when used in high concentrations for prolonged periods. This toxicity occurs clinically in patients in intensive care units who are on mechanical ventilators. The toxic effects of hyperoxia are believed to result from excessive generation of superoxide, an unstable free radical produced by the single electron reduction of oxygen. Superoxide is produced as a normal by-product of oxidative metabolism and scavenged by the protective enzymes, the superoxide dismutases, that catalyze its dismutation to hydrogen peroxide (Fig. If it is not scavenged enzymatically, superoxide anion can donate an electron to hydrogen peroxide in the presence of transition metals. Hydroxyl radical is highly reactive and can initiate lipid peroxidation and oxidize protein and nucleic acids. In the adult, the major sites of oxygen injury are the alveolar epithelium and the capillary endothelium. Advanced injury destroys the capillary bed with resultant interstitial and alveolar edema, hypoxemia, and sometimes death. Oxygen toxicity usually occurs in acutely ill patients who are receiving oxygen in high concentrations and mechanical ventilation for lung injuries that obscure the onset of pulmonary toxicity. Lung compliance progressively falls; the alveolar-arterial oxygen gradient gradually widens, and increasing concentrations of oxygen are needed to maintain adequate oxygenation of arterial blood. A dry, hacking cough and substernal pain may occur after 6 to 12 hours of breathing pure oxygen. The flow of tracheal mucus decreases after short exposures to excess oxygen, probably reflecting functional injury of airway epithelium. These patients are therefore more susceptible to mucus impaction and to infection caused by failure to clear inhaled pathogens adequately. The only proven therapy is to prevent the insult by judicious use of high oxygen concentrations. The physician often faces a dilemma in that increasing concentrations of oxygen are needed to save the patient immediately but can eventually kill the patient. Alternative methods to enhance arterial oxygen content should be used whenever possible; these methods include a number of maneuvers based on strategies related to mechanical support of ventilation (see Chapter 93) and transfusion of packed red cells to maintain the hematocrit near 30%. Cardiac output should be maintained and accompanied by measures to decrease the tissue oxygen demand by reducing fever or agitation. Little or no injury occurs in normal animals or human volunteers breathing oxygen concentrations of 40 to 50% for prolonged periods. When oxygen (O2) is reduced incompletely, toxic oxygen species are formed such as singlet oxygen (1 O2), superoxide anion (O- 2), and hydrogen peroxide (H2 O2). Quenchers react with reactive oxygen species or with oxidized cellular molecules to prevent further oxidation. A rational therapy is to use only enough oxygen to provide adequate arterial blood saturation. Corticosteroids have no benefit and may actually worsen the lung injury caused by hyperoxia. If the patient survives oxygen toxicity, some residual damage to the lung parenchyma may remain, with septal fibrosis replacing areas where the pulmonary capillary bed was destroyed by the hyperoxia. Ionizing radiation produces oxidant lung injury related to the degree of the radiation exposure. The clinical occurrence of radiation pneumonitis is determined by the total radiation dose, the number of fractions, and the duration of time over which the radiation is given. Chemotherapeutic drugs that produce oxidant-based lung toxicity, such as bleomycin, may potentiate lung injury from radiation. A total lung dose of less than 2000 cGy generally is not associated with severe radiation pneumonitis, whereas a total dose in excess of 4000 cGy, even if distributed over as many as 30 fractions, has virtually a 100% risk of radiation pneumonitis. The alveolar walls become infiltrated with mononuclear inflammatory cells and fibroblasts. Alveolar fibrosis and capillary sclerosis are its predominant histologic features. If large volumes of lung have been irradiated, or if high radiation doses have been given over short periods, the patient can develop dyspnea, tachypnea, and fever.

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