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Outcome of the unoperated adult who presents with congenitally corrected transposition of the great arteries buy cheap fluoxetine 10 mg line womens health partners st louis. Long-term outcome in congenitally corrected transposition of the great arteries: a multi-institutional study cheap 10 mg fluoxetine with amex breast cancer tattoo design. Mechanical circulatory support of systemic ventricle in adults with transposition of great arteries discount fluoxetine 10 mg with visa menstrual napkins. Early and late results of operations for defects associated with corrected transposition and other anomalies with atrioventricular discordance in a pediatric population cheap 10mg fluoxetine amex menopause forums. Long-term outcome of surgically treated patients with corrected transposition of the great arteries. Outcome of 121 patients with congenitally corrected transposition of the great arteries. Death and other events after cardiac repair in discordant atrioventricular connection. Postsurgical course of patients with congenitally corrected transposition of the great arteries. Right ventricular dysfunction in congenitally corrected transposition of the great arteries. Congenitally corrected transposition of the great arteries in the adult: functional status and complications. Intermediate-term outcome after intracardiac repair of associated cardiac defects in patients with atrioventricular and ventriculoarterial discordance. Myocardial perfusion defects and associated systemic ventricular dysfunction in congenitally corrected transposition of the great arteries. Progressive tricuspid valve disease in patients with congenitally corrected transposition of the great arteries. Congenitally corrected transposition of the great arteries: ventricular function at the time of systemic atrioventricular valve replacement predicts long- term ventricular function. Left ventricular reconditioning and anatomical correction for systemic right ventricular dysfunction. Effects of morphologic left ventricular pressure on right ventricular geometry and tricuspid valve regurgitation in patients with congenitally corrected transposition of the great arteries. Pulmonary artery banding as ‘open end’ palliation of systemic right ventricles: an interim analysis. An alternative approach to the surgical management of physiologically corrected transposition with ventricular septal defect and pulmonary stenosis or atresia. Intermediate results of the anatomic repair for congenitally corrected transposition. Palliative pulmonary artery banding versus anatomic correction for congenitally corrected transposition of the great arteries with regressed morphologic left ventricle: long-term results from a single center. Anatomic repair for congenitally corrected transposition of the great arteries: a single–institution 19-year experience. Early prophylactic pulmonary artery banding in isolated congenitally corrected transposition of the great arteries. Impact of age and duration of banding on left ventricular preparation before anatomic repair for congenitally corrected transposition of the great arteries. The morphologic left ventricle that requires training by means of pulmonary artery banding before the double-switch procedure for congenitally corrected transposition of the great arteries is at risk of late dysfunction. Physiologic versus anatomic repair of congenitally corrected transposition of the great arteries: meta-analysis of individual patient data. Health-related quality of life in patients with congenitally corrected transposition of the great arteries. Quality of life and perceived health status in adults with congenitally corrected transposition of the great arteries. Pregnancy among women with congenitally corrected transposition of great arteries. Outcome of pregnancy in patients with congenitally corrected transposition of the great arteries. Pregnancy in women with a systemic right ventricle after surgically and congenitally corrected transposition of the great arteries. Pregnancy and long-term cardiovascular outcomes in women with congenitally corrected transposition of the great arteries. There is no known racial or gender predilection, and no associated genetic defect has been identified. As with much of congenital heart disease, the physiology and treatment of these defects are derived from the embryology and morphology. With the exception of truncus arteriosus, which occurs due to failure of septation, other conotruncal defects are essentially rotational defects. The variability among the individual lesions is best understood in terms of the spectrum of development of the conal septum, which determines the relative position of the two semilunar valves to the ventricles. In the normal heart, the pulmonary valve sits up on the conus, a circular tube of muscle, and is positioned anteriorly and superiorly (17). In contrast, the aortic, mitral, and tricuspid valves are all attached to the central fibrous body of the heart. The conal muscle beneath the aortic valve largely resorbs, leaving the aorta positioned inferiorly and posteriorly (Fig. In conotruncal defects, there is a spectrum between hearts in which no conus exists beneath the aorta, as seen in tetralogy of Fallot, and no conus exists under the pulmonary valve, as with transposition of the great arteries (Fig. There is a near- normal length of conus beneath the pulmonary valve and minimal conus beneath the aortic valve. Consequently, there is no aorto-mitral continuity, and the pulmonary valve is anterior and superior. In the middle is a type which has equal bilateral conus, such that the great arteries are side by side, with neither vessel tucked in posteriorly. These variations are more ambiguous both anatomically and physiologically and should be approached with an individualized management plan. In the fetus, there is a circular tube of muscle, the conus, beneath each great artery. The distribution of conal muscle is equal beneath the aorta and the pulmonary artery. In the normal heart, the pulmonary valve sits up on the conus, and is positioned anteriorly and superiorly. The conal muscle beneath the aortic valve largely resorbs, leaving the aorta positioned inferiorly and posteriorly. The more conal muscle present beneath a semilunar valve, the more that valve is pushed superiorly and anteriorly. Aorta is pushed anteriorly and superiorly, resulting in rightward positioning of the aorta relative to the pulmonary artery. However, coronary arterial anomalies are of particular importance, because they may alter considerations for surgical repair due to their effect on feasibility of conduit placement or coronary arterial transfer (23) (Fig. Likewise, associated aortic arch coarctation, hypoplasia, or interruption—also found in about 10% of patients—significantly increase the complexity of surgical repair when present (24,25).
Finally generic fluoxetine 20mg free shipping channel 9 menopause diet, the effects of changes in oxygen tension differ between the systemic and pulmonary vascular beds purchase fluoxetine 20mg online menstruation 9 days early. Pulmonary Arterial Load 20 mg fluoxetine fast delivery menstrual xex, Compliance 20mg fluoxetine premier women's health yakima, and Resistance As discussed, important components of the arterial load are the resistance and compliance of the vascular bed. Recently it has been demonstrated that, unlike in the systemic vascular bed, there is a close inverse relationship between pulmonary vascular resistance and compliance, both within the pulmonary vascular bed as a whole and even for parts of the lung. It is now recognized that while in the systemic vascular bed, the majority of the compliance is in the proximal great arteries and the resistance is more distal, together the pulmonary trunk and the proximal right and left pulmonary arteries contribute only 15% to 20% to total arterial compliance, so that a considerable proportion of the pulmonary arterial compliance resides in small vessels. As a result pulmonary vascular compliance and resistance are inseparably connected. This relationship between compliance and resistance will have a number of important consequences. First, there is a close linear relationship between systolic and diastolic pressure with mean pulmonary arterial pressure. Second, pulse pressure is usually around 100% of mean pulmonary arterial pressure compared to only 40% in the systemic circulation and third, ranges in pressures in pulmonary hypertension are relatively large, compared to those in systemic hypertension (43,44,45). Passive Regulation of Pulmonary Vascular Tone and Vessel Recruitment A mechanism within the pulmonary circulation, which is important in maintaining a low pulmonary arterial pressure in the face of increases in flow, as occurs during exercise is the ability to rapidly recruit small vessels, which may be closed under baseline conditions. As flow increases, some of these vessels may open, such that this recruitment will decrease the overall resistance to flow and maintain a low level of pulmonary arterial pressure, even in the setting of a significant increase in cardiac output. The Role of Intrathoracic Pressure Pulmonary vascular hemodynamics are modulated by changes in respiration and intrathoracic pressure through several potential mechanisms. First, respiration may alter pulmonary vascular resistance by altering blood pH, alveolar oxygen tension, and lung volumes. Respiratory and metabolic alkalosis cause pulmonary vasodilation, while acidosis causes vasoconstriction. As discussed later, alveolar hypoxia is thought to constrict pulmonary arterioles, diverting blood flow from poorly ventilated to well-ventilated alveoli, thereby improving the matching of ventilation to perfusion and in turn, oxygenation. Alterations in intrathoracic pressure and lung volume are also thought to directly impact pulmonary vascular resistance. In this respect, it is thought that it is the transpulmonary pressure gradient (alveolar pressure– intrapleural pressure) and the resulting change in alveolar volume that is likely to be important, rather than the intrathoracic pressure per se. The surrounding pressure for these arterioles, capillaries, and venules is the alveolar pressure. By contrast, extraalveolar vessels are located in the interstitium and are exposed to intrapleural pressure. In addition, at low lung volumes, alveolar collapse leads to hypoxic pulmonary vasoconstriction and further increases in the resistance of extraalveolar vessels. Despite a potential decrease in the resistance of alveolar vessels (as alveolar pressure falls), the net effect is a marked increase in pulmonary vascular resistance at low lung volumes. An additional influence of intrathoracic pressure on the pulmonary vessels comes from their property of being collapsible with low intravascular pressure. In the absence of cardiopulmonary disease, zone 1 conditions do not generally exist; however, they may be present in a variety of clinical scenarios. In addition to increases in Palv, zone 1 conditions may be created when cardiac output and Pa are low. Conversely, an increase in Palv may not create alveolar dead space if, for example, pulmonary venous hypertension is present as in congestive heart failure. Local Control of Pulmonary Flow by the Endothelium The recognition of the active role of the endothelium has been one of the greatest physiologic discoveries of the last 25 years. As was discussed above, it is now recognized that the endothelium produces a wide variety of mediators, which modulate the function of vascular smooth muscle, including in the pulmonary circulation. Furthermore, these mediators appear central to modulating some of the structural derangements which contribute to chronic vascular diseases such as occurs in pulmonary hypertension. As is described elsewhere in this textbook, these insights have revolutionized the management of patients with these conditions, with the introduction of orally active endothelin antagonists, phosphodiesterase inhibitors, and intravenous and inhalational prostanoids. Central Neural and Hormonal Control The pulmonary vascular bed is innervated by a relatively dense network of sympathetic nerves and expresses both pre- and postjunctional adrenergic receptors. Activity within the sympathetic nerves appears to be influenced by afferent inputs from chemoreceptors which may contribute to the changes in pulmonary vascular resistance seen during hypoxemia (46). Teleologically these differing responses make sense in that in the lung, hypoxia-mediated vasoconstriction may serve to maintain matching of ventilation and perfusion, such that flow is directed away from hypoxic regions to better-ventilated regions, while in the systemic circulation hypoxia-induced vasodilation might preserve local metabolic functions by improving O delivery in times of scarcity. It appears that it is alveolar rather than intravascular oxygen tension that is the predominant influence. Nonetheless, the precise cellular mechanisms which underlie this response are unknown and there are important deficiencies in their study in humans (48). Coupling between the Circulation and Tissue Metabolism According to Claude Bernard: “All the vital mechanisms, however varied they may be have only one object, that of preserving constant the conditions of life in the internal environment” (49). Thus, an essential function of the cardiovascular system is to generate sufficient flow of substrate, for example O , through the circulation to maintain normal tissue metabolism. We generally take the matching of systemic O2 2 consumption with adequate levels of delivery for granted in the healthy state, possibly with the exception of periods of intense exercise. There has been considerable interest, however, in the impact of inadequate oxygen delivery on metabolism during critical illness (50), for example in the setting of severe heart failure, and in the potential inability of the circulation to maintain adequate levels of systemic O delivery to match the increases in2 its consumption in the patient with, for example severe sepsis (51). Conversely, in nature, the hibernating animal is able to tolerate extreme reductions in cardiac output and systemic O delivery for months on end, because of a2 dramatic reduction in O requirements (2 52). The systemic delivery of O can be calculated from the product of2 the O content of the arterial blood and the cardiac output. The systemic O consumption is in turn calculated2 2 from the product of the arteriovenous O content difference and the cardiac output. Clearly circulatory physiology2 is central to maintaining the relationship between systemic O delivery and consumption. From first principles this ability to maintain a constant level of O consumption in the face of a reduction in delivery reflects2 potentially two phenomena; the first is the ability of some organs to increase their O extraction, in the face of2 reduced flow and the second, the ability of other organs to maintain flow locally, in the face of a global reduction in cardiac output (autoregulation). Nonetheless, if O delivery falls below a “critical” level, this is accompanied by2 a concomitant fall in consumption, as the ability of these essential homeostatic mechanisms is overwhelmed. The Relationship between Systemic O Delivery and Consumption after Cardiac Surgery2 The changes in systemic O consumption and delivery in the adult, early after cardiac surgery have been well2 described. Typically, O delivery is reduced, reflecting a diminished cardiac output, while paradoxically O2 2 consumption may be elevated, secondary to an elevation in temperature and possibly a systemic inflammatory response. In a study of children during the early hours after cardiac surgery, it was observed that the initial O2 consumption was unrelated to either the duration of cardiopulmonary bypass or to the duration of aortic cross- clamping. During subsequent hours, changes in O consumption closely followed changes in core temperature. Given the pivotal role of metabolism in the preservation of tissue function, one might expect that changes in the balance between systemic O consumption and delivery might provide a predictor of outcome after pediatric2 cardiac surgery.
Note common pulmonary trunk originating from posterolateral aspect of truncal root and bifurcating into right and left pulmonary arteries purchase fluoxetine 10mg line menopause excessive bleeding. Rarely trusted 20mg fluoxetine breast cancer 6s jordans, the patient with truncus arteriosus with associated interruption at the aortic arch or single pulmonary artery will need angiography to delineate aortic arch anatomy or the anatomy of the pulmonary arterial tree precisely discount fluoxetine 10 mg with mastercard womens health danbury ct. Patients with truncus arteriosus are at risk of having pulmonary vascular obstructive disease develop at an early age purchase fluoxetine 10mg with mastercard menstruation 19th century, and this has driven the major impetus for early surgical correction (10). Even more uncommonly in this era, a patient with truncus arteriosus presents beyond early infancy for consideration of surgical correction, and cardiac catheterization may be necessary to assess the status of the pulmonary vascular bed (22). Although direct measurement of pulmonary resistance is not possible, the calculated indirect value, obtained by dividing the mean driving pressure across the pulmonary bed (in mm Hg) by the total pulmonary flow index (in liters per minute per square meter), provides a reliable estimation of the status of the pulmonary arterioles. Patients with truncus arteriosus who have two pulmonary arteries and a pulmonary arteriolar resistance >8 units 2 m are at higher operative risk than patients with resistances below that level (20,22). Among the group with 2 resistances >8 units m , late deaths were due to progression of pulmonary vascular obstructive disease with secondary severe pulmonary hypertension and right ventricular failure. Among the survivors of operation in the 2 group with preoperative resistance <8 units m , no late deaths occurred secondary to progressive pulmonary hypertension. Fortunately, the trend toward early corrective surgery has reduced the number of patients who are inoperable because of pulmonary vascular obstructive disease. Our current policy is not to offer corrective surgery to patients with truncus arteriosus who have two pulmonary arteries and whose pulmonary arteriolar resistance is 2 >8 units m. The exceptions are children younger than 2 years of age whose resistance decreases to <8 units 2 m , when 100% oxygen is breathed or after administration of a pharmacologic vasodilator such as inhaled nitric oxide. In such young patients, surgery may still be offered if the parents are willing to accept a higher surgical risk because it is possible that increased resistances may result from arteriolar or medial smooth muscle hypertrophy and vasoconstriction rather than advanced intimal occlusive disease. These changes potentially may be reversible, and such patients can be treated with pulmonary vasodilator therapy after surgical repair is undertaken. Different criteria must be used to assess the feasibility of operation in patients with unilateral absence of pulmonary artery (34). Severe pulmonary vascular disease is particularly likely to develop at an early age in patients with a single pulmonary artery (22,35). To achieve good surgical results in this subgroup, corrective surgery should be performed in the neonatal period. Even in patients who survive corrective operation, pulmonary vascular disease tends to progress postoperatively more often than it does in patients with corrected truncus arteriosus who have two pulmonary arteries (35). This difference may be related to the fact that the entire cardiac output must still pass through one lung so that the rate of flow through each arteriole remains approximately double. This may be a potential stimulus for the progression of pulmonary vascular changes. Differential Diagnosis In infants with truncus arteriosus and increased pulmonary blood flow, the differential diagnosis includes the other congenital cardiac conditions that cause early heart failure and are associated with either mild or no cyanosis. Such malformations include ventricular septal defect, patent ductus arteriosus, aorticopulmonary window, pulmonary atresia with ventricular septal defect, and patent ductus arteriosus, or large collateral arteries, double-outlet right ventricle, univentricular heart, and total anomalous pulmonary venous connection. In truncus arteriosus with decreased pulmonary flow, other conditions to be considered include pulmonary atresia, tricuspid atresia, tetralogy of Fallot, univentricular heart with pulmonary stenosis, and double-outlet right ventricle with pulmonary stenosis. Although certain physical findings, chest radiographic evidence, and electrocardiographic features may suggest the increased likelihood of a particular lesion, echocardiography is necessary to establish the diagnosis definitively. A: Anterior sagittal oblique image demonstrating the truncal root with origin of the left pulmonary artery depicted by arrow, leftward and superiorly, and continuation of the right aortic arch (Ao). B: Slightly more posterior angulated view showing origin of the right pulmonary artery (double arrow) and continuation of the left pulmonary artery (single arrow). Natural History Although patients with truncus arteriosus occasionally survive to adulthood without surgery, the natural history of this condition is generally dismal. In patients who survived the first 4 years, death may occur from heart failure, but more frequently it results from the complications of hypertensive pulmonary vascular disease and infective endocarditis. Once severe pulmonary vascular disease is present (38), deterioration often is rapid, with severe morbidity and death frequently occurring in late childhood or early adolescence. This dismal natural history was the main factor that gave rise to the approach of early surgical repair that is now advocated for these patients. A: Anteroposterior view with the proximal leftward origin of the left pulmonary artery (single white arrow) and continuation of the right aortic arch (Ao). B: Lateral view shows the posterior/inferior origin of the right pulmonary artery (double dark arrows) and leftward/superior origin of the left pulmonary artery (single dark arrow). Treatment The diagnosis of truncus arteriosus, itself, is an indication for operation. Medical stabilization is performed in the intensive care unit, and operation with complete repair is preferred in the first weeks of life. Delay in operation results in chronic ischemia of the hypertrophied ventricle, which is perfused by desaturated blood at a low diastolic perfusion pressure caused by runoff through the pulmonary arteries, and, when present, “aortic” insufficiency. This hazard of ventricular dysfunction may explain, in part, the observation that repair of truncus at 6 to 12 months of age is associated with mortality twice that for repair between 6 weeks and 6 months of age (10). Pulmonary vascular obstructive disease also can develop early, which provides additional impetus for correction in the first few months of life. Pulmonary vascular obstructive disease, no doubt, also is partly responsible for the P. Although pulmonary artery banding may provide palliation for young patients with truncus arteriosus, there are well-documented risks and potential complications of banding for this condition. In addition, successful banding has not guaranteed that these patients will be good candidates for later correction (39). During the past 15 years, improved surgical techniques and postoperative care have made correction of truncus arteriosus during infancy possible at an operative risk less than that previously reported for banding. Surgical Correction Successful definitive surgical correction in a patient with truncus arteriosus was first accomplished by McGoon et al. Cryopreserved homograft tissue continues to be the conduit of choice for repair of this defect in early infancy (41). The early and late results experienced by the initial 92 patients who had correction at the Mayo Clinic were reported in 1977 (20). Although overall hospital mortality was 25%, the operative mortality decreased to 9% in the 33 patients operated on during the last 2. Since that time, an operative mortality of 5% was achieved in patients without severe associated abnormalities who subsequently have undergone correction of truncus arteriosus. At this time, the importance of complete repair in early infancy to prevent the development of pulmonary vascular obstructive disease was also emphasized. During the last three decades, there has been great progress in the surgical management of infants (42). In the current era, excellent results have been obtained with corrective operation during infancy (42,43,44,45,46,47,48). However, combined repair of truncus and interrupted aortic arch carries a higher risk of mortality and increased need for intervention postoperatively. In patients who undergo successful correction during early infancy, the small right ventricular to pulmonary artery conduit eventually must be replaced with a larger one, but reoperation for conduit replacement alone carries a low risk (49,50,51,52).
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In addition discount 10 mg fluoxetine fast delivery menstrual cycle phases, the Pittsburgh variant results in bleeding disorder because the Pittsburgh variant acts a potent inhibitor (gain of function) of the thrombin- fibrinogen reaction purchase fluoxetine 20mg with visa womens health recipe finder. First purchase 20 mg fluoxetine with amex breast cancer volleyball shirts, a gene is a hereditary factor that interacts with the environ- ment to produce a trait cheap 10 mg fluoxetine with visa menstruation kidney pain. Fourth, a poly- morphism is the occurrence of two or more alleles at a specific locus in frequencies greater than can be explained by mutations alone (a polymorphism does not cause a genetic disease). Silent mutations may accumulate in the genome where they are called single nucleotide polymorphisms. A polymorphism results in the maternal chromatid having an extra repeat sequence (no. During Meiosis I when crossover occurs, the cleavage and rejoining of sister chromatids occurs at Maternal Paternal different positions on the maternal chro- mosome usually within a region of tan- dem repeats. A polymorphism results in one sister maternal chromatid having two repeat sequences (no. A deletion polymorphism occurs due to forward slip- ● Figure 8-13 Replication Slippage. Chapter 9 Proto-Oncogenes, Oncogenes, and Tumor-Suppressor Genes I Proto-Oncogenes and Oncogenes A. A proto-oncogene is a normal gene that encodes a protein involved in stimulation of the cell cycle. Because the cell cycle can be regulated at many different points, proto-oncogenes fall into many different classes (i. An oncogene is a mutated proto-oncogene that encodes for an oncoprotein in- volved in the hyperstimulation of the cell cycle leading to oncogenesis. This is because the mutations cause an increased activity of the oncoprotein (either a hyperactive oncoprotein or increased amounts of normal protein), not a loss of activity of the oncoprotein. Instead, most human cancers are caused by the alteration of proto-oncogenes so that oncogenes are formed producing an oncoprotein. A single mutant allele is suffi- cient to change the phenotype of a cell from normal to cancerous (i. This results in a hyperactive oncoprotein that hyperstimulates the cell cycle leading to oncogenesis. Note: proto-oncogenes only require a mutation in one allele for the cell to become oncogenic, whereas tumor-suppressor genes require a mutation in both alleles for the cell to become oncogenic. A translocation results from breakage and exchange of segments between chromosomes. This may result in the formation of an oncogene (also called a fusion gene or chimeric gene) which encodes for an oncoprotein (also called a fusion protein or chimeric protein). This results in a hyperactive oncoprotein that hyperstimulates the cell cycle leading to oncogenesis. These extra copies are found as either small paired chromatin bodies separated from the chromosomes or as insertions within normal chromosomes. This results in increased amounts of normal protein that hyperstimulates the cell cycle leading to oncogenesis. A translocation results from breakage and exchange of segments between chromosomes. This may result in the formation of an oncogene by placing a gene in a transcriptionally active re- gion. Burkitt lymphoma t(8;14)(q24;q32) is caused by a reciprocal translocation between band q24 on chromosome 8 and band q32 on chromosome 14. This results in increased amounts of normal protein that hyperstimulates the cell cycle leading to oncogenesis. The G protein is attached to the cytoplasmic face of the cell membrane by a lipid called far- nesyl isoprenoid. A tumor-suppressor gene is a normal gene that encodes a protein involved in suppression of the cell cycle. Many human cancers are caused by loss- of-function mutations of tumor-suppressor genes. Note: tumor-suppressor genes require a mutation in both alleles for a cell to become oncogenic, whereas, proto-oncogenes only require a mutation in one allele for a cell to become oncogenic. These genes encode for proteins that either regulate the transition of cells through the checkpoints (“gates”) of the cell cycle or promote apoptosis. Loss-of-function mutations in gate- keeper tumor-suppressor genes lead to oncogenesis. Loss-of-function mutations in caretaker tumor-suppressor genes lead to oncogenesis. This has become known as Knudson’s two-hit hypothesis and serves as a model for cancers involving tumor-suppressor genes. How can cancer due to tumor-suppressor genes be autosomal dominant when both copies of the gene must be inactivated for tumor formation to occur? The inher- ited deleterious allele is in fact transmitted in an autosomal dominant manner and most heterozygotes do develop cancer. However, while the predisposition for can- cer is inherited in an autosomal dominant manner, changes at the cellular level require the loss of both alleles, which is a recessive mechanism. Clinical features: a malignant tumor of the retina develops in children 5 years of age; whitish mass in the pupillary area behind the lens (leukokoria; the cat’s eye; white eye reflex) and strabismus. The bottom photograph of a surgical specimen shows an eye that is almost completely filled a cream-colored intraocular retinoblastoma. The binding of p21 to the Cdk2-cyclin D and Cdk2-cyclin E inhibits their action and causes downstream stoppage at the G1 checkpoint. Clinical features include multiple neural tumors (called neurofibromas that are widely dispersed over the body and reveal proliferation of all elements of a periph- eral nerve including neurites, fibroblasts, and Schwann cells of neural crest ori- gin), numerous pigmented skin lesions (called café au lait spots) probably associ- ated with melanocytes of neural crest origin, axillary and inguinal freckling, scoliosis, vertebral dysplasia, and pigmented iris hamartomas (called Lisch nodules). Clinical features include colorectal adenomatous polyps appear at 7–35 years of age inevitably leading to colon cancer; thousands of polyps can be observed in the colon; gastric polyps may be present; and patients are often advised to undergo prophylactic colectomy early in life to avert colon cancer. Note the convoluted, irregular arrangement of the intestinal glands with the basement membrane intact. The bot- tom photograph shows the colon that contains thousands of adenomatous polyps. Clinical features include early onset of breast cancer, bilateral breast cancer, fam- ily history of breast or ovarian cancer consistent with autosomal dominant inheri- tance, and a family history of male breast. The mammogram shows a malignant mass that has the following characteristics: shape is irregular with many lobulations; margins are irregular or spiculated; den- sity is medium-high; breast architecture may be distorted; and calcifications (not shows) are small, irregular, variable, and found within ducts (called ductal casts). Mitosis is the process by which a cell with the diploid number of chromosomes, which in humans is 46, passes on the diploid number of chromosomes to daughter cells. The term “diploid” is classically used to refer to a cell containing 46 chro- mosomes. The term “haploid” is classically used to refer to a cell containing 23 chromo- somes. The process ensures that the diploid number of 46 chromosomes is maintained in the cells.
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