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Chest pain is more likely ischemic in nature when it is associated with: Exertion more than at rest Dyspnea Diaphoresis Syncope and characterized as: Substernal pressure or burning rather than pain Pressure that radiates to neck or arm Fairly reproducible with similar activity Short lived 2 to 10 minutes as opposed to hours Other important historical features include how the pain is relieved buy 130mg malegra dxt with amex erectile dysfunction kaiser. If a patient is able to continue to run and play and the pain goes away despite continuing activity order malegra dxt 130 mg on line erectile dysfunction normal testosterone, myocardial ischemia is less likely buy malegra dxt 130 mg overnight delivery erectile dysfunction treatment algorithm. A family history should screen for Marfan syndrome, other aortopathies, and for hypertrophic cardiomyopathy. A prior surgical history where the coronary arteries were manipulated or reimplanted is important in a patient with typical chest pain or ischemia. The surgical reports pertaining to the procedure and how the coronary arteries were either reimplanted or manipulated may be important to the current care of the patient and future testing that must be done. Differential Diagnosis The etiologies for nonatherosclerotic coronary artery disease and myocardial ischemia remain rare and for the most part are difficult to diagnose, require a high index of suspicion, and often involve advanced imaging studies. Most of the diagnoses are covered in other areas of this textbook and are detailed in those chapters. This group of diagnoses can be divided into those involving the coronary arteries directly and those that involve the myocardium leading to myocardial ischemia. They involve congenital anomalies of the coronary arteries and hypertrophic cardiomyopathy. Other diseases can present early in life with congestive heart failure, circulatory shock, or severe hypoxemia. 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). The latter may also have a deleterious effect on left ventricular perfusion, ultimately leading to left ventricular dysfunction (5,11). Hypertrophy can also develop in many other situations, especially in aortic stenosis and chronic systemic hypertension (7). Examination The cardiovascular examination in a patient in whom there is concern for myocardial ischemia may be completely normal. Patients with dilated cardiomyopathy and heart failure may have signs of elevated jugular venous pressure, third or fourth heart sounds, holosystolic murmur of mitral regurgitation, peripheral edema, and hepatic enlargement. Subendocardial ischemia is the common pattern for those experiencing chronic chest pain P. Biomarkers of Myocardial Injury When myocardial injury occurs, enzymes form the myocardium are released approximately 2 hours later and can be detected by various assays. After injury occurs, within 2 hours, these enzymes will rise and may continue to rise for several hours. Additionally, cardiac enzymes may be elevated with perimyocarditis due to inflammatory changes to the myocardium. The group beating is consistent with junctional tachycardia typical for digitalis toxicity. The T waves are tented consistent with hyperkalemia and must be recognized versus ischemic T waves. However, since the troponin assays are able to detect what is felt to be very small degrees of myocardial damage, in all cases; this may not be due to coronary artery disease. Myocarditis, pericardial disease, and trauma may all yield a positive troponin result. Therefore the context in which the assay is performed may be equally important to the interpretation of the result. There is increased sensitivity and specificity of the biomarkers for myocardial injury or infarction when serial assays are performed and when they are performed several hours after the onset of chest pain. If positive, there is a high likelihood of myocardial damage and appropriate therapy should be initiated if not already started based upon other data. If the initial study is negative, and there remains a high likelihood that the chest pain represents myocardial ischemia, then serial enzymes should be performed over the next 24 hours. Important in the use of cardiac biomarkers is the recommendation that patients with a very low probability for myocardial ischemia should not undergo cardiac enzyme testing because of the possibility for a false positive result leading to unnecessary testing (22,23,24). Furthermore, the indications and clinical applications of other newer echo techniques such as tissue Doppler imaging, strain and strain rate imaging, contrast and real-time three-dimensional (3-D) echocardiography to detect myocardial ischemia will need to be determined in these patients (15). It can be helpful to detect the following: hypertrophic cardiomyopathy, severe aortic stenosis, and dilated cardiomyopathy, all of them potentially associated with coronary flow abnormalities and myocardial ischemia. The main objective of stress testing for myocardial ischemia is to unmask the mismatch between myocardial oxygen demand and myocardial perfusion.

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Multiple gene interactions generic malegra dxt 130 mg amex erectile dysfunction doctor in hyderabad, variable expressivity cheap malegra dxt 130mg overnight delivery biking causes erectile dysfunction, incomplete penetrance malegra dxt 130mg line erectile dysfunction treatment algorithm, and the influence of environmental and epigenetic factors all likely contribute to the diverse pedigrees reported in the literature (96). The suggestion from these initial case series that disease of the aortic valve and left ventricular outflow tract is both highly heritable and phenotypically diverse has subsequently been confirmed by larger genetic studies. An early analysis of familial aggregation of congenital heart disease demonstrated that first-degree relatives of probands with left ventricular outflow tract obstruction (aortic coarctation or hypoplastic left heart syndrome) were more likely to have congenital heart disease than relatives of probands with d-transposition of the great arteries (19. Statistical modeling based on pedigrees of patients with bicuspid aortic valve and hypoplastic left heart syndrome has suggested that each condition is highly heritable, with segregation patterns of both anomalies estimated to be almost entirely due to genetic factors (heritability 0. Congenital heart malformations were identified in 18% of first-degree relatives of probands with hypoplastic left heart syndrome, and the great majority (78%) of the heart disease consisted of left heart obstructive lesions. The relative risk for left ventricular outflow tract obstruction for first- degree relatives of probands in this analysis was 36. While the highly heritable nature of congenital left heart obstruction has been clearly established, the underlying molecular genetic mechanisms have not been fully elucidated. Several syndromes are known to involve aortic valve anomalies, most notably Turner syndrome, a chromosomal disorder characterized by complete or partial absence of one X chromosome in a female. A bicuspid aortic valve is present in 30% of patients with Turner syndrome, and clinically significant aortic disease (coarctation, aortic stenosis) is found in approximately 10% of affected newborns (102). Another chromosomal disorder linked to aortic valve disease is 11q terminal deletion disorder, also known as Jacobsen syndrome. More than half of patients with Jacobsen syndrome have congenital heart disease, with approximately 18% of patients having left-sided obstructive lesions (103). The critical region on 11q for left ventricular outflow tract development has not yet been identified, and the gene deletion(s) responsible for left heart obstruction in this setting are not yet known. Each of these genes is related to a syndrome known to include bicuspid aortic valve as part of its phenotype (Table 44. Supplementation with nitric oxide has been shown to prevent calcification of aortic valve interstitial cells in vitro (109), while nitric oxide deficiency is associated with bicuspid valve formation in mice (109). This suggests interaction between the two pathways in aortic valve morphogenesis (110). One intriguing potential connection between nitric oxide and aortic valve development involves the observation that mechanical factors, such as decreased flow in developing hearts, can contribute to abnormalities of the aortic valve and left ventricular outflow tract. Similarly, the unique geometry of a bicuspid aortic valve has also been shown to result in alterations in shear stress compared to a tricuspid aortic valve (115), and this is thought to contribute to the early development of calcific aortic stenosis in bicuspid valves. Subvalvar Stenosis Though often considered an acquired condition, several familial clusters of discrete subvalvar aortic stenosis have been reported, suggesting a genetic basis of disease in at least some cases. While no causative genes have been identified, inheritance patterns suggest autosomal recessive transmission may be involved in some instances. Of the ten families with inherited discrete subvalvar stenosis reported in the literature, four consisted of unaffected consanguineous parents with multiple affected children, consistent with autosomal recessive inheritance (116,117,118). The remainder of the reported pedigrees were suggestive of autosomal dominant inheritance, but limited numbers of affected individuals within the pedigrees make interpretation difficult (118). While the existence of these family clusters indicates that genetic factors play a role in the development of subvalvar stenosis in some instances, the rarity of these familial cases suggests that the heritability of subvalvar stenosis is in general far less than either valvar or supravalvar aortic disease. One additional piece of evidence suggesting some genetic influence in the development of subvalvar stenosis is the overrepresentation of bicuspid aortic valve (up to 25%) among patients with subvalvar obstruction (37). As discussed previously, bicuspid aortic valve is a highly heritable condition, with an overall prevalence of approximately 1% in the general population. The relatively high prevalence of bicuspid aortic valve among patients with subvalvar stenosis strongly suggests a genetic component in susceptibility to the disease. Given the hypothesized role for abnormal flow and shear stress in the formation of subvalvar membranes, however, it may simply be that any abnormality of the left ventricular outflow tract that provides a substrate for nonlaminar flow may result in membrane formation. Supravalvar Stenosis The molecular genetics of supravalvar aortic stenosis have been fairly well described. As discussed above, aortic disease is the most prominent manifestation of a systemic arteriopathy. Supravalvar aortic stenosis has been traditionally associated with Williams–Beuren syndrome (61,74,119), a syndrome in which the arteriopathy is accompanied by cognitive disability, distinctive “elfin facies,” hypocalcemia, small stature, and an ebullient personality (69). Identical vascular pathology is also seen in the absence of the other findings of Williams– Beuren syndrome, however, both in inherited and sporadic forms (120,121). Familial supravalvar aortic stenosis is generally inherited as an autosomal dominant trait. Williams–Beuren syndrome is now known to be caused by a microdeletion of approximately 1. Physiology The primary physiologic derangement in aortic stenosis and its subtypes is left ventricular outflow tract obstruction. While the location and mechanism of obstruction may affect disease course and treatment options, the essential pathophysiology is the same whether the stenosis is above, below, or at the level of the aortic valve. In all cases, obstruction to flow creates increased afterload for the left ventricle with a variety of downstream consequences. Assuming preserved left ventricular systolic function and cardiac output, left ventricular outflow tract obstruction results in increased left ventricular systolic pressure and wall stress. Ventricular wall stress is directly proportional to ventricular pressure, and inversely proportional to ventricular wall thickness. Myocardial hypertrophy is, therefore, initially a compensatory response, causing increased wall thickness that at least temporarily maintains constant wall stress in the face of increasing ventricular pressure. Careful hemodynamic studies have demonstrated that concentric ventricular hypertrophy in response to aortic stenosis successfully maintains wall stress within normal limits throughout the cardiac cycle despite significantly elevated ventricular systolic pressure (128), and may actually lead to decreased wall stress at rest compared to healthy controls (129). Over time, however, a persistent pressure load on the left ventricle results in pathologic ventricular remodeling with the eventual development of clinical heart failure. The mechanism by which compensatory hypertrophy progresses to heart failure is not entirely understood, but it is clear that there are gradual changes in the myocardium at the cellular level that lead to a typical sequence of hemodynamic consequences (130). As changes on the cellular level progress from myocyte hypertrophy to fibrosis and cell death, there is a progression of hemodynamic sequelae from initial mild abnormalities of diastolic function to eventual severe combined systolic and diastolic dysfunction (131,132). The first negative physiologic effect of ventricular hypertrophy is impaired ventricular relaxation (131,133), with decreased ventricular filling in early diastole. Impaired relaxation occurs independently of systolic dysfunction, and is correlated with the degree of ventricular hypertrophy (133,134,135). While significant fibrosis can be identified in patients with preserved systolic function (136), progressive fibrosis is associated with increased ventricular stiffness as well as eventual systolic dysfunction (130,137). In addition to the effects of fibrosis, myocyte death also begins to occur, likely largely through nonapoptotic cell death pathways (130). Over time, progressive cardiomyocyte loss and degradation with increased collagen replacement of myocytes results in continued deterioration of systolic and diastolic function and the eventual development of clinical heart failure. Another contributor to myocardial dysfunction in left ventricular outflow tract obstruction is the development of subendocardial ischemia.

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It would be beneficial to expand this to include a more longitudinal experience that exists throughout the training program purchase malegra dxt 130mg overnight delivery erectile dysfunction protocol reviews. Also order 130mg malegra dxt mastercard erectile dysfunction funny images, there should be improved education after fellowship training such as regional training (e cheap malegra dxt generic erectile dysfunction treatment cost in india. However, there are far too few of these specialists to currently provide care for the several hundred thousand patients who require it. These specialists could form referral networks with general adult cardiologists to allow proper and continuous care. Support Personnel In addition to physician providers, there are many other people required to ensure a successful transition and transfer process. Often, the pediatric provider may not have the time required or resources available to provide proper education and transition support. An advanced level provider (nurse practitioner or physician assistant) or nurse specialist often acts as a “transition coordinator” who is placed in charge of overseeing the entire transition process (4). This person often is involved at multiple patient visits (even sometimes scheduling visits solely related to transition) providing the patient and their family information (educational, psychosocial, and administrative) related to the transition process. Each transition program should have an established referral relationship (or directly employ) a clinical psychologist with experience in providing services to adolescents and young adults with chronic disease. All transition programs should have access to a social worker with experience in transition. These providers should have experience regarding how to smoothly transition patients from their adolescent insurance to an adult program. Moreover, they should know what social and governmental resources are available for patients with chronic healthcare needs (4,9,16,48). A similar “transition” social worker should be available to the patient after transfer of care to the adult provider as many of these “financial” transitions do not occur until well into adulthood. Barriers to Transition Even in organized healthcare systems, successful transition and transfer of care occurs less than half the time (49). This relates to the multiple barriers that exist that may belie successful transition. Several of these barriers as well as potential ways to prevent their occurrence will be discussed. The main reasons for this gap in care include the patient feeling well or not knowing that follow-up was required (5). In addition, a history of missed cardiology appointments during childhood were predictive of being lost to follow-up as a young adult (50). Solution In order to decrease the number of patients who are lost to follow-up during the transfer period, it is vital to stress to the patient and his/her family the importance of lifelong follow-up. At transfer, the pediatric provider should provide the patient with medical follow-up that includes a specific location (provider), date, and reason (4). A system should be in place for the pediatric provider to follow-up and ensure that their patient went to their first appointment with the adult cardiac provider (4,51). Problem: Communication Issues Excellent communication lies at the foundation of a successful transition and transfer—and poor communication can result in failure. A recurrent theme in the literature is the desire for better communication, especially during the transfer of care from the pediatric to the adult provider (4,5,7,13,17,25,51,52). Both providers and patients desire more thorough communication during this process. These summaries often lack the rationale for the current treatment plan and leave out key events (including adverse events, reactions or failures to previous treatments) that are vital to patient care. When the adult provider does not know these key historic events, it serves to reinforce the skepticism that many patients already carry into these relationships. Solution To improve communication, it is vital that the pediatric provider provide a thorough, written, transition note to the new adult provider (4,7,16,51,52). This note should be individualized, developed by the patient/parent/provider, and include important information regarding their diagnoses, surgical history, treatment history, and rationale for current treatment plan (8,9). For more complex patients, direct communication via telephone or an in-person discussion may further strengthen the transfer process. In some instances, the pediatric cardiologist may choose to not transfer patients if they do not feel that qualified adult providers are available (7). In addition, pediatric providers should recognize the need for transfer of care and its importance in the patient taking on responsibility for his or her healthcare needs. Problem: Loss of Insurance As mentioned previously, one of the key components to the transition process is to insure continuous insurance (or other financial) coverage (4,25). In general, over 25% of young adults in the United States lack health insurance coverage (54). Solution It is extremely important to maintain insurance coverage without a lapse throughout adolescence and into adulthood. The transition social worker should work with family during the transition process to insure plans are in place to insure continuous insurance coverage. If needed, the process to apply for government health care and/or disability should be started well in advance of these programs being required. The importance of maintaining continuous insurance coverage should be stressed to the patient and their family so this can be taken into account when making any changes or employment-related decisions (4). New guidelines and training pathways hope to provide some consistency to the current, uneven system. The prevalence of adult congenital heart disease, results from a systematic review and evidence based calculation. Congenital heart disease in the general population: changing prevalence and age distribution. Best practices in managing transition to adulthood for adolescents with congenital heart disease: the transition process and medical and psychosocial issues: a scientific statement from the American Heart Association. Transition from child-centered to adult health-care system for adolescents with chronic conditions: a position paper of the Society for Adolescent Medicine. Transition and transfer from pediatric to adult care of young adults with complex congenital heart disease. Developing a transition program from pediatric- to adult-focused cardiology care: practical considerations. Developed in Collaboration With the American Society of Echocardiography, Heart Rhythm Society, International Society for Adult Congenital Heart Disease, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Care of the adult congenital heart disease patient in the United States: a summary of the current system. Attitude toward and current practice of transfer and transition adolescents with congenital heart disease in the United States of America and Europe. The role of the pediatrician in transitioning children and adolescents with developmental disabilities and chronic illnesses from school to work to college. The emerging burden of hospital admissions of adults with congenital heart disease. American Academy of Pediatrics, American Academy of Family Physicians, American College of Physicians-American Society of Internal Medicine.

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Serial images over 20 minutes show progressive excretion and clearance of activity from the kidneys buy cheap malegra dxt 130mg online erectile dysfunction more causes risk factors. A generic malegra dxt 130 mg on line men's health erectile dysfunction pills, duced and the relative function of each kidney to be aorta cheap 130 mg malegra dxt visa erectile dysfunction pills at cvs; B, bladder; I, inferior vena cava; K, kidney. The main indications for a renogram are: • Measurement of relative renal function in each kidney – this may help the surgeon decide between nephrectomy and more conservative surgery. Note the simple cyst (C) in the left kidney, which returns a low signal on T1­ and a high signal on T2­weighted images. Urinary Tract 237 • Investigation of urinary tract obstruction, particularly pelviureteric junction obstruction. Special techniques Retrograde and antegrade pyelography The techniques of retrograde and antegrade pyelography (the term pyelography means demonstrating the pelvical­ iceal system and ureters) involve direct injection of contrast material into the pelvicaliceal system or ureters through catheters placed via cystoscopy (retrograde pyelography) or percutaneously into the kidney via the loin (antegrade pyelography). The indications are limited to those situa­ tions where the information cannot be achieved by less invasive means, e. Note that not and videourodynamics only are the arteries well shown but there is also an excellent In voiding cystourethrography, the bladder is flled with nephrogram. The renal pelvis and ureter are opacifed because of iodinated contrast medium through a catheter and flms are a previous injection of contrast. The entire process is observed fuor­ oscopically to identify vesicoureteric refux. The bladder Renal arteriography and urethra can be assessed during voiding to demonstrate Renal arteriography is performed via a catheter introduced strictures or urethral valves (see Fig. Selective injections are made into one or both tourethrography with bladder pressure measurements, renal arteries (Fig. The test is also helpful in patients with obstructive symptoms, mainly elderly men, to differentiate true obstruction from bladder instability, and in patients with a Urinary tract disorders neurogenic bladder. The imaging of The urethra is visualized during voiding cystourethrogra­ calculi causing urinary obstruction is described below. For full visualization of the male urethra, however, an Most urinary calculi are calcifed and show varying ascending urethrogram with contrast medium injection via density on x­ray examinations. The fed but some, particularly bladder stones, may be usual indications for the examination are the identifcation laminated. Only pure uric acid and xanthine stones are of urethral strictures and to demonstrate extravasation radiolucent on plain radiography, but they can be identifed from the urethra or bladder neck following trauma. Renal stones are not visible on the right and are very poorly visualized on the left. Filling defects are seen in the right lower calix and pelvis and in the left upper pole calices (arrows). Small renal calculi are often round or oval; the larger ones frequently assume the shape of the pelvicaliceal system and are known as staghorn calculi (Fig. Plain flm examination of the urinary tract is more sensi­ tive than ultrasound for detecting opaque renal and uret­ eric calculi. Stones in the ureters may be partly obscured where they overlie the ver­ tebral transverse processes or the sacrum. Most renal calculi of more than 5 mm in size are readily seen at ultrasound, but smaller calculi may be missed, par­ ticularly if they are located within the renal sinus, where they may be obscured by echoes from the surrounding fat. Stones, regardless of their composition, produce intense echoes and cast acoustic shadows (Fig. Staghorn calculi, flling the caliceal system, cast very large acoustic shadows, which may even mask an associated hydroneph­ Fig. Stones in the ureters cannot be excluded on ultra­ (vertical arrows) appear as bright echoes. Stones in the bladder, or in bladder diverticula, are well demonstrated on anatomical localization of stones prior to treatment in most ultrasound. If a stone is obstructing a ureter, Computed tomography without intravenous contrast the dilated ureter can usually be followed down to the level medium is exquisitely sensitive for the detection of calculi. Multiple stones were demonstrated (arrows), allowing accurate planning of his Fig. The patient also has kidney stones in the left pelvicaliceal system (short arrows). In these cases, the use of intravenous contrast tubules in which small calculi can form) in the presence of media and delayed phase imaging can be very helpful to normal calcium metabolism. Urinary tract obstruction Nephrocalcinosis The principal feature of obstruction is dilatation of the Nephrocalcinosis is the term used to describe focal or pelvicaliceal system and ureter. Diffuse nephrocalcinosis may be associated with the depends on the chronicity, with more marked dilatation following: seen more often in longstanding obstruction. The obstructed • Hypercalcaemia and/or hypercalciuria, notably hyper­ collecting system is dilated down to the level of the obstruct­ parathyroidism and renal tubular acidosis. Ultrasound and uro­ sible to determine the cause of urinary tract obstruction at graphic examination play major roles when evaluating ultrasound examination. Radionuclide studies show typical changes, but are rarely the primary imaging procedures. Plain flms may demonstrate graphically as a multiloculate fuid collection in the central the calculus responsible for the obstruction. However, as echo complex, caused by pooling of urine within the dis­ parts of the ureter overlie the transverse processes of the tended pelvis and calices (Fig. As the distension vertebrae and the wings of the sacrum, the calculus may be becomes more severe, the dilated calices can resemble mul­ impossible to see on plain flm. Following injection of intra­ tiple renal cysts, but dilated calices, unlike cysts, show con­ venous contrast medium, a flm of the renal tract is taken tinuity with the renal pelvis (Fig. If the urogram is normal, obstruction, thinning of the cortex due to atrophy will be with contrast seen in normal, undistended ureters bilater­ seen. If one of the ureters is obstructed, then a but overlying bowel often obscures dilatation of the mid dense nephrogram will be seen and opacifcation of the and distal ureter. If the obstruction is at the level of the pelvicaliceal system and ureter on the obstructed side takes vesicoureteric junction, the distal ureter can usually be much longer. In time, the collecting system and the level or a stone at the vesicoureteric junction), it is often not pos­ of obstruction can usually be demonstrated (Fig. The left kidney shows a very dense nephrogram which is characteristic of acute ureteric obstruction. Computed tomography is now widely used to evaluate urinary tract obstruction (Fig. Chronic obstruction Calculi are by far the commonest cause of obstruction of by tumour, either within the renal collecting system or by the urinary tract. The imaging techniques are described an external tumour causing compression, may be visual­ above. A sloughed papilla in papillary necrosis is a rare 244 Chapter 8 P P P P (b) (a) U Fig.