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The director should begin to take an inventory of what supplies are on hand to contend with such an emergency 30gm v-gel otc herbals information, such as food buy discount v-gel 30 gm on-line herbals in the philippines, water discount diovan, and medical supplies. In addition, the director should also begin to formulate a plan concerning how those supplies will be delivered quickly and, if it is possible, how to position some of those resources in depots close to where the hurricane may strike the coast. The director will need manpower to move the supplies and vehicles to carry the supplies to key locations. In addi- tion, the director will need temporary shelters for personnel as well as mobile generators and refrigeration units to store food and medicine that may be needed in case of an emergency. Interacting with state and local ofcials that are in the possible strike area of the hurricane is critical to determine what resources may be needed by those communi- ties. In addition, the director will need to communicate with other federal department heads to coordinate eforts on getting supplies where they will be needed the most. Stage 2 of the Disaster On September 21, the governor of one state activated 1,200 National Guardsmen, 1,100 state guardsmen, and state game wardens to contend with the impending crisis. In addition, the governor of that state reversed the fow of trafc, making the interstate highways one direction—only out of the major port city of that state for Case Studies: Disasters from Natural Causes—Hurricanes ◾ 57 evacuation purposes (Hays, 2005). You are receiving some good news that patients from certain major hospitals and some shut-ins have already been transferred to cities out of reach of the hurricane (Easton, 2005). However, you are now aware that trafc has been gridlocked for one state in particular and that evacuation is not occurring as fast as you would like. In addition, much of the nation’s oil refnery production centers are vulnerable (Townsend, 2005). The director should attempt to provide fueling points for vehicles that are along the evacuation route as well as food and water to the drivers. The director should contact the state emergency response coordinator and see if there are any alternative ways that trafc can be rerouted or phased into certain highways to temporarily alleviate the trafc jams. If at all possible, as much oil and chemicals as possible should be removed prior to the hurricane strikes to avoid chemical and hazardous material situations. The director should stay in close contact with other federal agency directors as well as state and local government of- cials in order to coordinate efective disaster response relief eforts. Stage 3 of the Disaster On September 24 the hurricane makes landfall between two neighboring states (Hurricane Headquarters, 2007). As the hurricane hits the coastline, three com- munities in one state are completely obliterated, with another six communities suf- fering heavy damage (Struck and Milbank, 2005). Two million people are now without electricity (Diamond, 2005), and the estimate for property damage stands at $10 billion (National Weather Service, 2007).

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Other diseases can present early in life with congestive heart failure purchase v-gel cheap himalaya herbals wiki, circulatory shock order v-gel canada zigma herbals, or severe hypoxemia discount 5mg altace amex. All these factors can compromise coronary circulation and lead to myocardial ischemia. Congenital Anomalies of the Coronary Arteries The entire blood flow to the myocardium comes from two main coronary arteries that arise from the right and left aortic sinuses of Valsalva. Although there are normal variations of the coronary anatomy, a comprehensive discussion of this topic is beyond the scope of this chapter, which will focus only on the clinically significant anomalies. The most common anomaly, accounting for about one-third of all major coronary arterial anomalies, is origin of the left circumflex coronary artery from the right main coronary artery. Less common, the origin of the left coronary artery from the right sinus of Valsalva is of greater significance, and is associated with sudden death in children during or just after vigorous exercise (9). A single coronary artery may be observed in 5% to 20% of major coronary anomalies. When the coronary arteries (either right or left) have their origins in inappropriate sinus, the mechanism of ischemia and death involves an increase in myocardial oxygen demand during exercise that, in turn, causes increases in systolic blood pressure and aortic root distension. If part of the anomalous artery runs within (intramural course) or adjacent to the aortic wall, it may be stretched, compressed, or both, leading to insufficient coronary blood flow. Other rare coronary anomalies include coronary atresia, stenosis or atresia of a coronary ostium, all coronary arteries from pulmonary artery, left anterior descending coronary artery from pulmonary artery, left circumflex coronary artery from the pulmonary artery or branches, right coronary artery from pulmonary artery, myocardial bridges, etc. The left ventricle vessels then dilate to reduce their resistance and increase flow, but this is often not enough to prevent ischemia with compromise of left ventricular function especially in concert with the physiologic drop in pulmonary vascular resistance. This leads to congestive heart failure that can be worsened by mitral regurgitation. With time, the collaterals between the right and left coronary artery enlarge until the collateral flow tends to reverse in the left coronary and ultimately into the pulmonary artery. This anomaly is usually isolated but can be associated with patent ductus arteriosus, ventricular septal defect, tetralogy of Fallot, or coarctation of the aorta (7,9). Tetralogy of Fallot In this disease, a hypertrophied right ventricle is always present, with a high oxygen demand to overcome the outflow tract obstruction and provide pulmonary blood flow. In face of severe cyanosis and hemodynamic impairment, the oxygen supply may not balance the high requirements of the right ventricle, leading to myocardial ischemia (7). Severe aortic regurgitation can lead to the same deleterious consequences with diastolic pressures. In patients with hypoplastic left heart syndrome, the ascending aorta receives retrograde poorly oxygenated blood that originated from a patent ductus arteriosus. Therefore, these patients are particularly sensitive to hypotension, severe hypoxemia, imbalances between pulmonary and systemic blood flows, and a claudicating ductus arteriosus (7). Once ventricular dilation and hypertrophy settle in, the blood supply through a normal right coronary artery can become insufficient to meet the increased metabolic demands of the systemic right ventricle leading to further ventricular dysfunction (5,10).

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Does the presence of gynecomastia differentiate between hypogonadotropic hypogonadism and hypergonadotropic hypogonadism during adolescence? Although gynecomastia is considered as a typical feature of hypergo- nadotropic hypogonadism (particularly Klinefelter’s syndrome) purchase v-gel australia herbs like kratom, 30–40% of patients with hypogonadotropic hypogonadism can also have gynecomastia order v-gel 30gm otc herbals medicine. However buy bystolic uk, detection of low-grade mosa- icism in a male without any phenotypic features does not merit a diagnosis of Klinefelter’s syndrome. The prevalence of congenital malformations (skeletal and cardiac anomalies), learning disabilities, and mental retardation are more in patients with higher-grade chromosomal aneu- ploidies. How to differentiate between hypogonadotropic hypogonadism and hypergo- nadotropic hypogonadism? The presence of anosmia, synkinesia, midline defects, skeletal anomalies, cryptorchidism, micropenis, small soft testes, and eunuchoidal proportions points to the diagnosis of hypogonadotropic hypogonadism (idiopathic), 7 Delayed Puberty 243 whereas long-leggedness, small frm testes, gynecomastia, learning disabilities, and moderate degree of spontaneous virilization suggest the diagnosis of hyper- gonadotropic hypogonadism (Klinefelter’s syndrome). The clinical features which suggest a diagnosis of Klinefelter’s syndrome in early childhood include long-leggedness, docile behavior, developmental delay in speech, and learning disabilities. How to explain the variability in phenotypic manifestations in patients with Klinefelter’s syndrome? However, it has been shown that testicular degenerative process is rela- tively slower in these subjects. Skewed inactivation of X chromosome was also considered as a cause for variability in phenotypic manifestations; how- ever, this hypothesis has been refuted in recent studies. In addition, patients with mosaic Klinefelter’s syndrome may also have variable phenotypic mani- festations (Fig. The degenerative process continues during childhood and accelerates during ado- lescence. Seminiferous Sertoli Serum tubules cells Germ cells Leydig cells testosterone Fetus Normal Normal Reduced Normal – Mini- Normal Normal Reduced Normal Reduced puberty Childhood Normal Normal Reduced – – Puberty Hyalinization Reduced Reduced Pseudohypertrophy Initially and fbrosis normal, later decline Adulthood Hyalinization Reduced Reduced/ Pseudohypertrophy Reduced and fbrosis absent 69. The onset of puberty is nor- mal in most patients with Klinefelter’s syndrome, but majority have incomplete development of pubertal events. However, the rise in serum testos- terone is accompanied with accelerated hyalinization and fbrosis of seminifer- ous tubules and degeneration of Sertoli cells. The cause for accelerated testicular damage during puberty is not clear; however, elevated levels of gonadotropins, increased intratesticular estradiol levels, and alteration in intratesticular testos- terone/estradiol ratio have been implicated. Patients with Klinefelter’s syndrome are at high risk for the development of breast cancer, lung cancer, mediastinal germ cell tumors, and non-Hodgkin’s lymphoma. The risk for breast cancer is increased by 50-fold, while that of mediastinal germ cell tumors is 500-fold. Although the exact mechanism for increased cancer risk is not clear, the most likely explanation is overdosage of genes present in X chromosome which are not lyonized. In addition, abnormal estradiol/testosterone ratio may also contribute to the development of breast cancer.