Carla S. Dupree, MD, PhD

• Associate Professor of Medicine
• Medical Director, University of North Carolina Hospitals Heart Center at Meadowmont
• Division of Cardiology
• Heart Failure Program
• University of North Carolina School of Medicine
• Chapel Hill, North Carolina

A postexploration T-tube cholangiogram identifies a residual stone in the intrahepatic bile ducts weight loss 500 calories a day order 60caps shuddha guggulu with visa, missed during operative exploration of the bile duct weight loss xyngular shuddha guggulu 60caps discount. A 5 weight loss pills purchase shuddha guggulu 60caps amex, the T-tube is modified by shortening the limbs to prevent proximal obstruction and distal entry into the duodenum weight loss pills 94 purchase shuddha guggulu 60 caps visa. B weight loss nyc buy discount shuddha guggulu 60caps on-line, A T-tube is modified by removing half the diameter to prevent obstruction and enable easy removal weight loss tips for women cheap shuddha guggulu american express. The choledochotomy closure is begun above, with the T-tube emerging at the lower end of the repair. It should not be attempted in the presence of a duodenal diverticulum or where there is severe periampullary inflammation. Technique Sphincteroplasty consists of the incision of the common portion of the sphincter of Oddi with partial suture of the incision margin. The papilla usually is located at the junction of the lower third with the upper two thirds of the second portion of the duodenum. If this is not the case, digital palpation can be used by running the forefinger, introduced through the duodenotomy, across the medial duodenal wall. Traction now is applied to these sutures, and incision of the sphincter is extended for a further 6 to 7 mm, with sutures placed every 2 to 3 mm (all laterally) until the entire common tract of the sphincter of Oddi is incised. Sphincteroplasty is completed when the incision is 10 to 21 mm long and forceps can be introduced easily into the common bile duct to extract stones or other foreign bodies. Anatomy the anatomic details of the extrahepatic biliary tree and adjacent hepatic arterial and portal venous structures are discussed in detail in Chapter 1, but some features warrant emphasis. The important ductal anomalies are nearly all related to the manner of confluence of the right and left hepatic ducts and of the cystic duct with the common hepatic duct. The right hepatic duct has a short extrahepatic portion, but the left hepatic duct always has a much longer extrahepatic course. The duct traverses to the left, together with the left branch of the portal vein, within a peritoneal reflection of the gastrohepatic ligament on the undersurface of the quadrate lobe. The ligamentum teres in the lower edge of the falciform ligament traverses the umbilical fissure of the liver. Elements of the portal triad are distributed to the right and left liver on a segmental basis. The ligamentum teres marks the umbilical fissure and runs to join the umbilical portion of the left branch of the portal vein. Note particularly the distribution of the left portal triad in the umbilical fissure. Preparation of a segment of the gastrointestinal tract, usually a Roux-en-Y loop of jejunum 3. Direct mucosa-to-mucosa anastomosis between these two the anastomosis may be "stented" by a transanastomotic tube. In selected cases in which the anastomosis is technically difficult and stenosis is anticipated because of recurrent malignancy or benign stricture or to provide access for subsequent interventional radiologic techniques, the Roux-en-Y loop may be developed so as to make its blind end subcutaneous. The blind end of the jejunal loop is kept deliberately long and brought to the abdominal wall. The anastomosis is splinted with a transjejunal tube, which is brought through the blind end of the jejunum and through the abdominal wall. This tube tract can be used as an avenue for subsequent interventional radiologic or choledochoscopic maneuvers. Note the clips on the jejunum and at the subcutaneous termination to guide the radiologist. In this case, the loop is used to allow transtumoral intubation and subsequent radiotherapy. A tube may be passed transjejunally (1), transhepatically (2), or as a U-tube (3). In such instances, a thoracoabdominal incision through the right seventh interspace may prove necessary (Bismuth, 1982). The duodenum frequently is found adherent to the base of the liver; the colon may be densely adherent to scar within the gallbladder fossa. Basic Anastomotic Technique A regular technique that allows anastomosis even in cases of high, difficult strictures should be developed. The opened bile duct having been prepared, a Roux-en-Y loop of jejunum 70 cm long is prepared and brought up preferably in a retrocolic fashion for anastomosis. If it is considered necessary to cross the anastomosis with a tube, the tube is inserted into the hepatic duct before beginning the anastomosis. B, Gross atrophy of the right liver and hypertrophy of the left liver leads to rotation of the hilar structures so that the portal vein comes to lie relatively more anteriorly, and the common bile duct is rotated posterolaterally (see inset). C, Cross-section of the abdomen shows how this rotation carries the hilar structures posteriorly. If more than one ductal orifice is visible at the hilus, these are approximated so that they can be treated as a single duct. If this cannot be done, the entire anterior row to all exposed ducts is inserted first so that the separated orifices can be treated as if single. Attempts to complete one anastomosis and then another are difficult or impossible. These sutures (3-0 or 4-0 polyglactin [Vicryl] or other absorbable suture material) are serially introduced starting from the left and working to the right. These maneuvers not only allow precise placement of the anterior row of sutures, which may be difficult if the posterior layer is inserted first and tied, but also facilitate precise placement of the posterior layer. Note the introduction of the absorbable suture in a mattress fashion across the ductal wall proximal to the future site of anastomosis. This displays the posterior ductal wall, and the posterior row of sutures is now placed, again from left to right. The posterior sutures are now held taut, and the jejunum is "railroaded" upward into proximity with the bile duct. Knots are all on the inside, approximating the mucosal surfaces of bile duct and jejunum accurately. This technique is particularly valuable in anastomosis of the biliary tract to the jejunum after pancreaticoduodenectomy (see Chapter 11) or as a method of anastomosis for palliative hepaticojejunostomy for nonresectable pancreatic cancer. A, Technique for end-to-side anastomosis of the bile duct below the hilus to jejunum. I, A 3-0 Vicryl suture is used, and the serosa of the jejunum is sutured to the full thickness of the bile duct. The dotted line marks the point of incision in the jejunum, which is made after the posterior layer is attached. Several interrupted sutures may be inserted before completing the anterior layer, however, so as to approximate the mucosae (inset). Hepaticojejunostomy also can be performed to the right anterior or posterior sectoral hepatic ducts. Alternatively, if access to the right or left hepatic duct at the hilus or in the umbilical fissure is technically hazardous or impossible, it is possible to approach peripheral bile ducts to perform biliary-enteric bypass procedures. These latter techniques are rarely applicable; percutaneous intubation usually is preferable. Approach to the Left Hepatic Duct At the Hilus of the Liver A tie is placed on the divided ligamentum teres so that it can be elevated and used as a tractor. The bridge of tissue (if present) connecting the left lobe of the liver to the quadrate lobe is divided with a diathermy. The structures of the left portal triad are lowered from the inferior surface of the quadrate lobe (lowering of the hilar plate). Occasionally, an overhanging mass of the lower portion of the quadrate lobe may require excision to improve exposure. If the duct cannot be adequately exposed in this way, it is possible to obtain adequate exposure by incising the liver parenchyma in the line of the gallbladder fossa. This hepatotomy (Blumgart, 1980), together with the opening of the umbilical fissure described previously, allows elevation of the entire quadrate lobe. Stay sutures are placed in the left hepatic duct, which is incised longitudinally. If it is considered necessary to cross the anastomosis with a tubal splint, this is inserted into the hepatic duct as described earlier. This is conveniently done by passing a curved director beneath it and cutting it with diathermy. The initial line of incision for an approach to the left hepatic duct by lowering of the hilar plate. The hilar plate (see Chapter 1) is lowered, and the left hepatic duct is exposed for dissection. The exposure is carried medially and to the right to expose the confluence and the right hepatic duct. A, Cholangiogram obtained after injection of contrast medium through a transjejunal tube illustrates hepaticojejunostomy Roux-en-Y by the left approach in a patient with a high benign postcholecystectomy stricture. In carcinoma of the bile duct or gallbladder, a tumor extending into the left duct from the confluence of the hepatic ducts may preclude the use of the main left duct. In any event, palliative anastomosis is best carried out at a reasonable distance from a malignant lesion. In such instances, repair can be accomplished by dissection of the left hepatic duct within the umbilical fissure (Soupault and Couinaud, 1957). Unilateral drainage of the left hepatic duct in the presence of a tumor that completely excludes the right liver and right hepatic ducts from the anastomosis effectively relieves jaundice, provided the left lobe of the liver is not atrophic (Baer et al. The liver is then held up so that its inferior surface can be seen, whereas the ligamentum teres is pulled downward and to the right. Side-to-side anastomosis to a loop of jejunum is then carried out by the techniques described earlier. The bridge of liver between the quadrate lobe and the left lobe of the liver has been divided. The peritoneum of its upper surface on the left side is incised, and the extensions passing into the liver are exposed. A, the liver is split to the left of the ligamentum teres in the umbilical fissure. A, Hilar obstruction of the biliary ductal system secondary to gallbladder carcinoma affecting branches of the segment V duct (arrows), causing complete obstruction at the confluence. The biliary ductal system was outlined by separate puncture of the right and left ductal systems using a percutaneous transhepatic approach. We now omit the placement of a transjejunal-transanastomotic splint; this is unnecessary in most cases. Excellent palliation was obtained in this patient for 20 months; tumor advanced within the liver, progressing to death. The procedure is not useful if there is left lobar atrophy and not necessary if the confluence and left hepatic duct are not involved by tumor and can be approached directly. In addition, the procedure may be difficult (1) in patients in whom longstanding obstruction has led to severe secondary biliary fibrosis, rendering the liver substance rigid and difficult to maneuver; (2) in patients with right liver atrophy and left liver hypertrophy; and (3) in patients after previous right hepatectomy. Techniques have now been developed, however, to expose the main right anterior sectoral duct for biliary enteric anastomosis. The pedicles to the right liver are exposed by delivery of the right pedicle as described for liver resection (see Chapters 2 and 3) (Launois and Jamieson, 1992). Operative Intubation of the Biliary Tract the use of stents placed at the time of operation has decreased markedly since the introduction of percutaneous transhepatic drainage methods and is likely to become obsolete. Disadvantages are that the stents protrude from the body and are a constant reminder to the patient of serious underlying disease, they can be very uncomfortable, and they inevitably lead to biliary tract infection and periodic attacks of cholangitis. In cases of malignancy it is possible for tumor cells to migrate along the tube tract and result in tumor seeding of the peritoneum or even the skin. The liver is opened as indicated, and liver tissue is cleared over a small distance and the right portal pedicles displayed. B, the relevant duct (usually the anterior sectoral duct) is opened, and anastomosis is carried out. Cholecystojejunostomy Cholecystojejunostomy is suitable for patients with malignant obstruction of the low bile duct owing to periampullary tumors. It is suitable only for patients in whom the cystic duct meets the common hepatic duct well above the tumor. The distended gallbladder is sutured using interrupted sutures or a running 3-0 Vicryl suture to the first available loop of jejunum. The posterior and anterior layers are sutured with 3-0 Vicryl to complete the cholecystojejunostomy. Choledochojejunostomy I prefer to perform this operation as an end-to-side procedure. Side-to-side hepaticojejunostomy can be performed, however, using techniques similar to those described for side-to-side choledochoduodenostomy (see below). Choledochoduodenostomy Indications the circumstances in which this operation has been effective are as follows: 1. Duodenal ulcer and acute pancreatitis also are contraindications to this procedure. In case of malignant obstruction, I prefer to do an end-to-side choledochoduodenostomy using the techniques described previously. B, the posterior layer of the anastomosis is performed with a running suture between the openings at the fundus of the gallbladder and the jejunum. After the gallbladder is removed, the common bile duct is removed through a conventional longitudinal incision following a Kocher incision (1) freeing the lateral duodenum around the common duct. In almost all instances, the incision in the duct carries into the common hepatic duct.

Early daycare is associated with an increase in airway symptoms in early childhood but is no protection against asthma or atopy at 8 years extreme weight loss 081313 cheap generic shuddha guggulu canada. Associations of wheezing phenotypes in the first 6 years of life with atopy weight loss pills you can buy under 18 order shuddha guggulu 60caps with visa, lung function and airway responsiveness in mid-childhood weight loss pills that really work buy shuddha guggulu 60caps overnight delivery. Distinguishing phenotypes of childhood wheeze and cough using latent class analysis weight loss pills that start with p buy shuddha guggulu 60 caps without a prescription. Dimensions of respiratory symptoms in preschool children: populationbased birth cohort study weight loss gnc quality shuddha guggulu 60caps. Montelukast reduces asthma exacerbations in 2- to 5-year-old children with intermittent asthma weight loss pills information order shuddha guggulu amex. Treatment of acute, episodic asthma in preschool children using intermittent high dose inhaled steroids at home. Multitrigger versus episodic wheeze in toddlers: new phenotypes or severity markers The transient value of classifying preschool wheeze into episodic viral wheeze and multiple trigger wheeze. Discriminative properties of two predictive indices for asthma diagnosis in a sample of preschoolers with recurrent wheezing. Predicting the long-term prognosis of children with symptoms suggestive of asthma at preschool age. Validation of the Asthma Predictive Index and comparison with simpler clinical prediction rules. The Asthma Predictive Index: a very useful tool for predicting asthma in young children. The Prevention of Early Asthma in Kids study: design, rationale and methods for the Childhood Asthma Research and Education network. Global strategy for the diagnosis and management of asthma in children 5 years and younger, 2009. Outcome of asthma and wheezing in the first 6 years of life: follow-up through adolescence. Age-related differences in perceived asthma control in childhood: guidelines and reality. Efficacy and safety of inhaled fluticasone propionate chlorofluorocarbon in 2- to 4-year-old patients with asthma: results of a double-blind, placebo-controlled study. Persistent wheezing in infants with an atopic tendency responds to inhaled fluticasone. Preemptive use of high-dose fluticasone for virus-induced wheezing in young children. Oral prednisolone in the acute management of children age 6 to 35 months with viral respiratory infection-induced lower airway disease: a randomized, placebo-controlled trial. A comparison between nebulized terbutaline, nebulized corticosteroid and systemic corticosteroid for acute wheezing in children up to 18 months of age. Independent parental administration of prednisone in acute asthma: a double-blind, placebo-controlled, crossover study. Parent-initiated oral corticosteroid therapy for intermittent wheezing illnesses in children. Episodic use of an inhaled corticosteroid or leukotriene receptor antagonist in preschool children with moderate-to-severe intermittent wheezing. Fluticasone or montelukast for preschool children with asthma-like symptoms: randomized controlled trial. The initial step is to ensure that the diagnosis is right, and to evaluate co-morbidities. The next step is a detailed multidisciplinary assessment, including, if possible, a home visit. More than half have ``difficult asthma', which improves if the basic management is correct; this may not be possible, but if the basics are not right, they are not candidates for potentially toxic new therapies. The remainder are termed ``severe therapy resistant' asthmatics, and an individualised treatment plan is developed after a detailed and invasive protocol of investigations, including bronchoscopy and assessment of the response to intramuscular triamcinolone. International collaborations will be essential if the mechanisms of severe therapy resistant asthma are to be understood, and evidence-based treatment delivered. Although the numbers are small compared with those with well-controlled asthma, the burden of disease is great. The exact prevalence is hard to determine but is probably,5% of all children with asthma or,0. The aim of this chapter is to review the approach to school-age children referred to specialist paediatric care because they are thought to have asthma but the prescribed treatment is not working. Preschool wheezing syndromes will be considered very briefly at the end of the chapter because there is less evidence here. The literature is fraught with loosely defined terms, such as ``difficult asthma', ``severe asthma' and many others. When evaluating both clinical and scientific studies, as always it is important to ask the correct question, which is ``to what extent have the subjects been evaluated by a specialist 22 and observed over time Of the 292 children referred for inclusion, only 55 could be randomised, because most of the rest either did not have asthma at all or were not taking their treatment. Defining problematic severe asthma this is the umbrella term used to describe the child who has been referred to the specialist because of ``asthma not responding to standard treatment' [4]. It can be criticised because such children may not have asthma at all, or may only have very mild disease once simple management steps are properly taken. Perhaps ``problematic obstructive respiratory symptoms' might have been a better term. In the developed world, problematic severe asthma comprises: wrong diagnosis (``not asthma at all'); asthma with important co-morbidities (``asthma plus. This is an important category globally but will not be discussed further in this chapter. Patterns of symptoms prompting referral Most paediatric definitions are arbitrary and not evidence based, unless otherwise stated. The symptom patterns are not mutually exclusive and are one or more of the following [6]. The definitions and most data are arbitrary and from adult studies; we define this as dramatic within-day swings in peak flow over a prolonged period of time. Again, largely defined in adult studies, but in paediatrics, a rapid onset of an acute asthma attack requiring admission to a high-dependency unit at the very least [18]. It seems likely that the pathophysiology and optimal management of these different patterns is not the same but this has yet to be proven. However, although there is some overlap, the distinction between exacerbations and baseline control is of fundamental importance and will be discussed in detail later. Unlike in adults, there is no significant sex difference in the paediatric series [20]. The pattern of severity will vary depending on the healthcare system and the availability of specialists. Prescription of multiple courses of oral steroids, admissions to hospital and ventilation in intensive care are all common [20]. In countries where there is more ready access to high-level specialists, the pattern of disease may be milder [25]. The first step is clearly a detailed history and physical examination, with simple physiological testing. Clearly there is no absolutely diagnostic test for asthma but there are four key questions, which are often glossed over. Is the child and family describing true polyphonic expiratory wheeze or are the noises less specific [26] Are there features on history and examination which suggest an alternative diagnosis Does the child have evidence of variable airflow obstruction over time and with treatment In many parts of Europe there is no word to describe polyphonic wheeze and, even where there is, there is no guarantee that it will be used correctly [26]. Ideally, a paediatrician should determine whether the child has intermittent true wheeze. Of course, wheeze may be due to many other conditions, but its absence should at least raise doubts about an asthma diagnosis. A detailed history and examination is mandatory and a history of rectal prolapse or the presence of, for example, digital clubbing point to another diagnosis. Atopy should be determined both by skin-prick tests and specific serum immunoglobulin (Ig)E measurements, since the two may not be concordant [27, 28]. If a child referred as problematic severe asthma is non-atopic, then the diagnosis should be carefully reviewed. Any physiological test may be negative in asthma but the more the paediatrician seeks and fails to find variable airflow obstruction, the less likely the diagnosis of asthma. A negative bronchial challenge in an allegedly markedly symptomatic child excludes asthma as a cause of those symptoms. Most would automatically perform a sweat test and chest radiograph, but testing should also be driven by local disease prevalence. The next two steps are an assessment of the apparent severity of asthma, and the identification of any co-morbidities. Finally, gastro-oesophageal reflux is only formally tested at the final stage of investigation. Severity is assessed in the following domains and also by considering future risk; again, all figures are arbitrarily defined. Level of current prescribed treatment: by definition, this will be at a high level if the child has been labelled ``problematic severe asthma'; level of current baseline control of asthma over at least the preceding month; and immediate past (possibly over last 6 months) burden of asthma exacerbations, including number and severity. The elephant in the room: domains of risk Severe asthma is not merely a problem because of present symptoms but also because of future risks. Many of these risks are either unquantifiable, cannot be modulated, or both, but they should be used to inform the future research agenda. The mechanism is unclear but the implication is that these children may develop fixed airflow obstruction in adult life. The best long-term follow-up of severe childhood asthma is the Melbourne cohort [33], who are now around 50 years old [20]. Clearly these children did not have access to modern therapies and cannot be compared with severe childhood asthmatics today, but these data do sound an ominous warning. Risk of harm from medications is pivotal in considering ``beyond the guidelines' therapy. Almost by definition, children with severe, therapy-resistant asthma will be exposed to potentially toxic therapies, and determining which are least harmful, given the circumstances, is an important part of therapeutic decision-making. The role of co-morbidities Asthma plus obesity this is the most easily determined co-morbidity. The relationships between asthma, nonspecific respiratory symptoms and obesity are complex. Obesity clearly leads to breathlessness which is not related to asthma [34], and evidence of reversible airway obstruction should be carefully sought before escalation of therapy in the obese. Finally, obesity is itself a proinflammatory state, and may cause steroid resistance [37]. Clearly obesity is undesirable on many grounds, but identifying the problem and achieving weight reduction are by no means the same thing! Asthma plus upper airway disease the relationship between the upper and lower airway is hotly debated but of only theoretical importance in this context. The upper airway should be examined carefully in all asthmatics seeking clues to an alternative diagnosis, and to identify morbidity which merits treatment in its own right. Upper airway symptoms may cause significant impairment in quality of life; if by treating them, asthma improves, then this is a significant bonus which should not be anticipated [38, 39]. One study suggested that obstructive sleep apnoea, which is a pro-inflammatory state, may be associated with lower airway neutrophilic inflammation [40]. Symptoms which disappear when the child is asleep are very unlikely to be due to asthma [41]. Other clues include difficulty breathing in, throat tightness, paraesthesia, cramps in the hand, and stridor or wheeze loudest over the larynx. In such cases, the aid of a skilled physiotherapist, speech therapist or clinical psychologist should be sought. Asthma plus gastro-oesophageal reflux the relationship between respiratory symptoms and reflux is complex (table 2) [42]. The evidence implicating reflux as causal in severe asthma in children is limited. If asymptomatic reflux is found, treatment is unlikely to ameliorate the symptoms of asthma. If symptomatic reflux is suspected, a therapeutic trial is reasonable, but if there is no response, a pH study is recommended before escalating therapy [43]. In our hands, treatment of reflux has rarely impacted on asthma severity in school-age children, implying it is merely a coincidental finding [44]. It is also unclear whether both severe asthma and food sensitisation reflect the underlying atopic predisposition, or food allergy is causally related to asthma [45, 46]. Since anaphylactic reactions may be particularly severe in asthmatics, aggressive management of both conditions is advisable. The next step in the protocol is a detailed multidisciplinary assessment, led by an experienced respiratory nurse. If experienced nurses are not available, other personnel should be used, including the family physician. The main message of these assessments is that professors sitting in clinic have little or no idea about what is happening at home. The nurse will typically spend a morning with the family at the hospital, visit the home by arrangement, make conTable 2. A number of via neural activity from the lower oesophagus Respiratory symptoms cause or exacerbate reflux areas are addressed, and then the the two co-exist independently results are discussed in a multiAsthma medication such as theophylline could provoke reflux disciplinary meeting. In our series, nearly 40% were not using their inhalers correctly, despite multiple previous sessions, and nearly 15% were using an inappropriate device (usually a metered-dose inhaler without a spacer) [48]. Advice about avoidance of triggers is also discussed, including allergens and detection and management of episodes of poor control or acute asthma attacks (see sections: Passive and active exposure to tobacco smoke and Allergen exposure; and [48]). The environment around the home Factors such as traffic pollution [49] and external aeroallergen exposure [50], for example, may have important effects on asthma.

The surgical management of bile duct cysts in adults is complicated by associated hepatobiliary pathology and the added technical difficulties of repeat previous biliary surgery weight loss nutritionist generic shuddha guggulu 60caps mastercard. Initial recognition may be incidental via hepatobiliary imaging studies for unrelated processes weight loss visualization buy genuine shuddha guggulu line. Recurrent epigastric or right hypochondrial pain weight loss knoxville buy shuddha guggulu american express, abdominal tenderness weight loss 05 kg per week cost of shuddha guggulu, fever weight loss 85297 buy cheap shuddha guggulu 60 caps online, and mild jaundice are the most common symptoms weight loss pills lipodrene cheap shuddha guggulu on line. About 15% of adults with common duct cysts present with overt evidence of cirrhosis or hepatic fibrosis from chronic biliary obstruction. Pancreatitis is present in some patients who have more intense and prolonged epigastric pain and vomiting. Imaging Ultrasonography permits viewing of the adjacent liver and pancreas to define cyst extent. Ultrasound of type I cysts simply shows a hypoechoic segmental dilation of the extrahepatic bile duct. Ductal stones within the cyst also can be identified by typical echogenic features. Caroli disease is clinically recognized by multiple cysts adjacent to the major intrahepatic bile ducts on ultrasound. Endoscopic retrograde cholangiopancreatography shows the most frequent anomaly of the bile duct cyst and pancreatic duct anatomy with perpendicular fusion of the distal bile duct or cyst to the pancreatic duct and the presence of a long common channel. Direct cholangiography also provides good definition of the relationship between the distal bile duct and the pancreatic duct. Typically the bile duct cyst joins the pancreatic duct 2 to 4 cm proximal to the duodenum. Anatomic definition of the pancreaticobiliary ductal junction is crucial as a guide during operative management of bile duct cysts to avoid intraoperative damage of the pancreatic duct. Magnetic Resonance Imaging Magnetic resonance imaging cholangiography has provided equivalent or superior imaging of bile duct cysts compared with conventional cholangiography. Associated Malignancy A significant association between bile duct cysts and hepatobiliary malignancies is well established. The incidence of cholangiocarcinoma is 20 to 30 times greater than the incidence of bile duct carcinoma in the general population. Malignancies associated with bile duct cysts may arise within the cyst or elsewhere within the liver or pancreaticobiliary tract. Caroli disease (type V cysts) also has been associated with an increased incidence of carcinoma. Whether primary prophylactic excision of cysts in childhood can reduce the incidence of malignancy is unknown (Voyles et al. Percutaneous transhepatic cholangiography of a type I choledochal cyst with a polypoid intracystic cholangiocarcinoma. Percutaneous transhepatic cholangiography of a hilar cholangiocarcinoma (arrow) after excision of a type I bile duct cyst and Roux-en-Y hepaticojejunostomy. In general, all bile duct cysts should be excised and bile flow re-established by mucosa-to-mucosa biliary-enteric anastomosis. If complete excision is not feasible, partial cyst excision and Roux-en-Y cystojejunostomy to an epithelium-lined portion of the cyst remnant is preferred. Type I Cyst the treatment for type I bile duct cysts is total cystectomy and Roux-en-Y hepaticojejunostomy. Cyst excision can be accomplished by mobilizing the gallbladder and dissecting the cyst away from the hilar structures. Before division of the cyst, the distal cyst is dissected from the pancreas to identify the pancreaticobiliary ductal junction. Preoperative definition of the ductal anatomy by cholangiopancreatography is important. The distal bile duct is suture ligated just proximal to its junction with the pancreatic duct. Isolation of vascular structures, complete excision of the cyst with closure of the distal stump, and biliary-enteric reconstruction with hepaticojejunostomy with a Roux-en-Y loop. In patients with stones sequestered within the intrahepatic cysts, with refractory ductal strictures distal to the intrahepatic cysts, or with intrahepatic abscess secondary to chronic cholangitis, the abnormal hepatic segment should be resected. Adequate treatment of the extrahepatic component in these patients provides effective prophylaxis for biliary problems associated with intrahepatic cystic disease. Resection of intrahepatic cysts in cirrhotic patients is associated with an increase in morbidity and mortality and generally is contraindicated. Endoscopic retrograde cholangiopancreatography of Caroli disease and multiple saccular cysts of only the intrahepatic bile duct with intrahepatic stones. Caroli Disease Caroli disease in adults may present in a localized form limited to one hepatic lobe or segment or in a diffuse form involving the entire intrahepatic biliary tree. Most adults with Caroli disease have a unilobar fusiform dilation of the intrahepatic ducts, most commonly involving the left ductal system. In patients with Caroli disease limited to one lobe of the liver without the presence of concurrent cirrhosis or hepatic fibrosis, hepatic resection, with or without Roux-en-Y cholangiojejunostomy, remains the treatment of choice. Most patients with diffuse Caroli disease have cirrhosis, chronic recurrent cholangitis, portal hypertension with variceal bleeding, and death secondary to liver failure or carcinoma. Gallbladder cancer is an important extrahepatic biliary cancer that is often discovered incidentally. Cholangiocarcinoma occurs at the biliary confluence, in the mid-duct, or in the distal duct presenting as a periampullary tumor (see also Chapter 10). Three distinct macroscopic subtypes of cholangiocarcinoma are well described: sclerosing, nodular, and papillary (Weinbren and Mutum, 1983). Sclerosing tumors cause an annular thickening of the bile duct, often with diffuse infiltration and fibrosis of the periductal tissues. Nodular tumors are characterized by a firm, irregular nodule of tumor that projects into the lumen of the duct. Longitudinal spread along the duct wall and periductal tissues is an important pathologic feature. The papillary variant is soft and friable and may be associated with minimal transmural invasion. Biliary cancer may arise within the intrahepatic biliary tree presenting as a mass or as a biliary cyst. Generally speaking, periampullary cancer is dealt with by pancreaticoduodenectomy (see Chapter 10) and intrahepatic cholangiocarcinoma by hepatic resection (see Chapters 2 to 5). Cholangiocarcinoma involving the proximal bile ducts (hilar cholangiocarcinoma) and gallbladder cancer require biliary resection, with or without a concomitant hepatic resection. Instrumentation and previous operation significantly increase the incidence of bactibilia and the risk of postoperative infection and are associated with greater morbidity and mortality rates after surgical resection. Segmental or lobar atrophy may result from portal venous occlusion or biliary obstruction. One or both of these findings are often present in patients with hilar cholangiocarcinoma. These tumors cause a circumferential thickening of the duct wall and periductal fibrosis, which ultimately obliterates the lumen. Gross cholangiographic and microscopic appearance of a papillary cholangiocarcinoma (left, A, C, E) and a nodular-sclerosing tumor (right, B, D, F). Note the papillary tumor within the bile duct lumen (arrow in A) and the nodular-sclerosing tumor invading the hepatic parenchyma (arrow in B). Transhepatic cholangiogram of a papillary tumor (C) shows multiple filling defects that expand the duct (black arrows; the biliary drainage catheter is indicated by the white arrow). This is in contrast to the cholangiographic features of nodular-sclerosing tumors characterized by an irregular stricture that constricts the duct lumen (arrow in D); a transhepatic catheter is seen traversing the stricture. Histologic section of a papillary cholangiocarcinoma with no invasive component (asterisk in E) and an invasive nodular-sclerosing tumor associated with a desmoplastic stroma (F). The left portal vein is occluded, resulting in severe atrophy of the left liver, which is shrunken and has dilated and crowded intrahepatic ducts. Intraoperative view showing a severely atrophic left lobe of liver, which is clearly demarcated from the right liver. Abdominal discomfort, anorexia, weight loss, pruritus, and jaundice are the most common. Segmental obstruction may result in ipsilateral lobar atrophy without overt jaundice. Imaging Cholangiography shows the location of the tumor and the biliary extent of disease. The mass is in contact with the portal vein, but there is no clear invasion or venous narrowing. B, Transverse color Doppler ultrasound of the biliary confluence shows a papillary cholangiocarcinoma (m) extending into the right anterior (a) and posterior (p) sectoral ducts and the origin of the left duct (l). The tumor has occluded the right anterior sectoral branch of the portal vein, and the anterior sector appears atrophic (indicated by black lines) with crowded, dilated ducts. Similar findings are indicated in this image, in which the bile ducts appear white. Biopsy specimens of the main tumor and the intrahepatic metastases confirmed adenocarcinoma. The principal caudate lobe duct, seen joining the left hepatic duct, also is dilated (arrow). Alternative Diagnoses the most common alternative diagnoses are gallbladder carcinoma, Mirizzi syndrome. Characterization of tumor extent should take into account all available preoperative data related to local tumor, including the extent of tumor within the biliary tree, vascular involvement, lobar atrophy, and metastatic disease. This makes it possible to stage tumors preoperatively in a way that correlates with resectability and outcome. A proposed clinical staging scheme (Table 9-1) underscores the importance of considering portal vein involvement and liver atrophy in relation to the extent of ductal cancer spread. Ipsilateral involvement of vessels and bile ducts is usually amenable to resection, whereas contralateral involvement is not. A, Endoscopic retrograde cholangiography shows a characteristic large gallstone impacted in the neck of the gallbladder causing obstruction of the hepatic duct just below the biliary confluence (arrow). In most cases, the diagnosis of Mirizzi syndrome is not as clear-cut because the stone is not visualized. The major limiting factor for resection of hilar cholangiocarcinoma is related to involvement or compression of adjacent vessels and, in particular, one or other branch or the main trunk of the portal vein (Blumgart et al. Laparotomy and Exploration Staging laparoscopy may help identify some nonresectable patients before committing to a laparotomy (Jarnagin et al. The ligamentum teres is elevated, allowing thorough examination of the subhilar area. Tumor Assessment and Resection the common bile duct is first transected above the duodenum and turned upward. The liver hilus is exposed by taking down the gallbladder and lowering the hilar plate. Local Resection Local resection is now rarely performed (see below), but it may be indicated in patients who would not tolerate partial hepatectomy and is possible only if an adequate length of the hepatic ducts can be achieved beyond the tumor and there is no vascular involvement. If the tumor extends to the second-order biliary radicles unilaterally or if there is ipsilateral portal vein branch involvement, partial hepatectomy must be performed. If local bile duct excision is feasible, the left and right hepatic ducts are divided above the tumor. The common bile duct is divided immediately above the duodenum, and its lower end has been separated from the underlying portal vein and hepatic artery and elevated together with associated connective tissue and lymph nodes. A director or clamp usually can be passed beneath the liver tissue, above the pedicular structures, allowing safe division of the liver parenchyma. The bridge of liver tissue at the base of the umbilical fissure has been divided (arrows). The biliary confluence and left hepatic duct together with the tumor have been lowered from beneath the quadrate lobe. The entire extrahepatic biliary apparatus is elevated together with associated portal connective tissue and nodes to allow dissection anterior to the bifurcation of the portal vein and elevation of the tumor, which is now completely mobilized. The left hepatic duct has been divided clear of the tumor and is held on stay sutures. Its proximal end, together with the confluence of the bile ducts, common hepatic and common bile ducts, and the gallbladder, is turned upward and to the right; stay sutures are placed in the right hepatic duct, which is similarly divided with subsequent removal of the tumor. After transection of the left hepatic duct and during the retrohilar and retrotumoral dissection toward the right, one frequently encounters obstructed and dilated ducts issuing from the caudate lobe, and two right hepatic ductal orifices represent the anterior and posterior right sectoral ducts. In this instance, each duct encountered is marked individually with stay sutures for subsequent anastomosis. The exposed right and left hepatic ducts are anastomosed using a single layer of 3-0 absorbable suture to a 70-cm retrocolic Roux-en-Y loop of jejunum. If multiple ducts are exposed at the hilus, these may be approximated one to another, if possible. A sling is passed about the left branch of the portal vein, which just beyond this point is involved by a cholangiocarcinoma at the confluence of the bile ducts and extending into the left hepatic duct. Liver resection is mandatory when the lesion extends unilaterally into the right or left liver, but leaves the contralateral half of the liver free of tumor and capable of retention as a liver remnant with an intact biliary drainage and blood supply. Recent reports suggest that hepatic resection should be used in virtually all cases because tumor clearance and long-term survival have been linked directly to hepatic resection (Jarnagin et al. The lowermost hepatic veins are divided to allow palpation of the caudate lobe from behind. If the tumor involves the right duct, the left hepatic duct is secured with stay sutures, transected, and the cut duct turned upward and to the right. Similarly, if the tumor extends into the left hepatic duct, it becomes necessary to transect the right duct. It is also possible to delay transection of the ducts until the time of parenchymal division. When the ductal structures and the tumor are elevated, the relevant blood vessels are secured. In this circumstance, the procedure is similar to that described above with the exception that transection of the affected portal branch may be difficult because of the proximity of the lesion.

The neurons that innervate the pancreas also release unique transmitters that include peptides and amines ez 60 weight loss pills purchase 60 caps shuddha guggulu. The distribution of pancreatic mass is 85% exocrine weight loss pills 74 order shuddha guggulu 60caps without prescription, 2% endocrine weight loss jackson tn order shuddha guggulu 60 caps overnight delivery, 10% extracellular matrix weight loss zachary la shuddha guggulu 60 caps with amex, and 4% blood vessels and ducts weight loss pills at cvs buy shuddha guggulu toronto. The exocrine cells are clustered in acini (lobules) divided by connective tissue and connected to a duct that drains into the pancreatic duct and into the duodenum weight loss pills uk 2015 discount 60 caps shuddha guggulu. Small clusters of endocrine cells-islets of Langerhans-are embedded within the acini. The colorless, bicarbonate-rich, and protein-rich pancreatic juice plays key roles in duodenal alkalinization and food digestion. The acinar cells secrete the enzymes required for the digestion of the three main food types: amylase for carbohydrate (starch) digestion, proteases. The acinar cells are pyramidal in shape with the apices facing the lumen of the acinus, where the enzyme-containing zymogen granules fuse with the apical cell membrane for release. Acinar cells, unlike the endocrine cells of the pancreas, are not specialized and produce all three types of pancreatic enzymes from the same cell type. Amylase is secreted in its active form and hydrolyzes starch and glycogen to the simple sugars of dextrins and maltose; maltose is then metabolized to glucose by intestinal maltase. The proteolytic enzymes are secreted as proenzymes and must be activated in the duodenum. Phospholipase B cleaves the fatty acid off lysolecithin to form glycerol phosphatidylcholine. Centroacinar cells and pancreatic duct cells secrete electrolytes, bicarbonate, and water into the pancreatic juice. The cephalic phase-in response to the smell, sight, and taste of food-accounts for 10% of meal-stimulated pancreatic secretion and is mediated by peripherally released acetylcholine. The gastric phase-in response to gastric distension from food-accounts for 10% of meal-stimulated pancreatic secretion. Secretin then stimulates increased production of centroacinar cell bicarbonate to buffer the acidic chyme. Cholecystokinin is also released in response to protein and fat in the proximal small intestine, and it enhances the centroacinar cell response to secretin. The exocrine (acinar) cells are clustered in acini, divided by connective tissue, and connected to a duct that drains into the pancreatic duct and into the duodenum. The -cells are columnar in shape and are located primarily in islets in the body and tail of the pancreas. Insulin also facilitates glucose transport into cells and stimulates protein synthesis. As with insulin, cholinergic and -adrenergic sympathetic innervation stimulate glucagon release, and -adrenergic sympathetic innervation inhibits glucagon secretion. Thus, measurement of serum C-peptide concentration serves as a measure of -cell secretory capacity. Insulin is released in a pulsatile and rhythmic background pattern throughout the day and serves to suppress hepatic glucose production and mediates glucose disposal by adipose tissue. Superimposed on the background secretion of insulin is the meal-induced insulin release. The second phase is a slower onset and longer sustained release because of the production of new insulin. Defects in any of these steps in insulin secretion can lead to hyperglycemia and diabetes mellitus. Approximately 80% of insulin is cleared by the hepatic cell surface insulin receptors with the first pass through the liver. The number of insulin receptors expressed on the cell membrane can be modulated by diet, body type, exercise, insulin, and other hormones. Obesity and high serum insulin concentrations downregulate the number of insulin receptors. Cell membranes are impermeable to hydrophilic molecules such as glucose and require a carrier system to transport glucose across the lipid bilayer cell membrane. In adipose tissue, insulin inhibits lipolysis by promoting dephosphorylation of hormone-sensitive (intracellular) lipase. The decreased breakdown of adipocyte triglycerides to fatty acids and glycerol leads to decreased substrate for ketogenesis. Insulin also promotes hepatic synthesis of triglycerides, very low-density lipoprotein, and proteins. Glycolysis can function either aerobically or anaerobically, depending on the availability of oxygen and the electron transport chain. At this stage, the hexose molecule is cleaved by aldolase into two 3-carbon compounds: glyceraldehyde 3-phosphate and dihydroxyacetone phosphate. For example, in protein catabolism, proteins are broken down by proteases into their constituent amino acids. From one molecule of glucose, glycolysis (see Plate 5-6) provides two molecules of pyruvate. Citrate synthase catalyzes the initial reaction between acetylCoA and oxaloacetate. Fumarase catalyzes the addition of water across the double bond of fumarate to form malate. Thiamine (vitamin B1) serves as the coenzyme for decarboxylation of the -ketoglutarate dehydrogenase step. Catalyzed by glucokinase in the liver and hexokinase in the muscle, glucose is phosphorylated to glucose 6-phosphate. This cleaving starts at the terminal glucosyl residues until 4 glucose residues remain on either side of a 16 linkage, at which point glucan transferase transfers a trisaccharide unit from one branch to the other to expose the 16 linkage. Debranching enzyme can then hydrolyze the 16 linkage, and further phosphorylase actions proceed to completely convert the glycogen chain to glucose 1-phosphate. The glucose 6-phosphate molecules have three possible fates: (1) transformation to glucose 1-phosphate by phosphoglucomutase and proceeding to glycogenesis; (2) hydrolyzation by glucose 6phosphatase in the liver and kidney to produce glucose for release into the bloodstream; or (3) proceeding on to the glycolysis or the pentose phosphate (pentose shunt) pathways. Glucose continues to be added to the glycogen chains as long as glucose and insulin are supplied. Insulin deprivation can result from surgical removal (pancreatectomy) or autoimmune destruction of -cells (type 1 diabetes mellitus); both lead to absence or severe curtailment of insulin production and release. Cell membranes are impermeable to hydrophilic molecules such as glucose and require a carrier system. In insulin-sensitive tissues, metabolic adjustments occur as a consequence of the curtailed glucose supply. The nonprotein nitrogen excreted in the urine rises and a negative nitrogen balance results. The severity of the metabolic acidosis depends on the rate and duration of ketoacid production. The outcomes of severe insulin deprivation include negative nitrogen balance, weight loss, ketosis, and acidosis. These are the hallmarks of the most severe state of metabolic decompensation characteristic of insulin deprivation in individuals with no endogenous source of insulin. In addition, acidosis affects the contractile responses of the small blood vessels throughout the body that, when coupled with osmotic diuresis-induced volume loss, results in hypotension and vascular collapse. Thus, diabetic coma and death-the fate of all those with type 1 diabetes mellitus before the advent of insulin replacement therapy-are the end result of uncompensated and untreated insulin deprivation. However, with absolute insulin deficiency, metabolic decompensation can intervene rapidly over 24 hours. Insulin should be administered intravenously to avoid slow absorption from hypoperfused subcutaneous tissues. With volume repletion, resolving acidosis, and improving blood glucose concentrations, an underlying potassium deficit usually becomes evident and should be replaced when the serum potassium concentration decreases below 5. There are three general types of diabetes: type 1, type 2 (see Plate 5-12), and gestational (see Plate 5-19). Type 1 diabetes mellitus affects less than 10% of all patients diagnosed with diabetes. Type 1 diabetes mellitus is the result of pancreatic -cell destruction; in more than 95% of the cases, it has an autoimmune basis caused by an apparent selected loss of immune tolerance. Immune-mediated type 1 diabetes is most common in northern Europe, where the approximate annual incidence is 30 per 100,000 persons. Environmental factors (infectious or toxic environmental insult) have a major role in disease development; only 50% of identical twins of type 1 diabetic patients develop diabetes. The autoimmune destruction of -cells progresses over months and years, during which time affected individuals are euglycemic and asymptomatic (termed the latent period). At the time of clinical presentation, a chronic inflammatory infiltrate of the islets is present (insulitis). The hyperosmolar state may also cause blurred vision caused by osmolar impact on lens and retina. As insulin deficiency becomes nearly complete, the signs and symptoms of diabetic ketoacidosis predominate (see Plate 5-10). Individuals with plasma glucose concentrations at or above 140 mg/dL, but not over 200 mg/dL, 2 hours after a 75-g oral glucose load are considered to have impaired glucose tolerance. There are three general types of diabetes-type 1 (see Plate 5-11), type 2, and gestational (see Plate 5-19). Unlike type 1 diabetes, in which the individual has an absolute insulin deficiency, individuals with type 2 diabetes have a relative insulin deficiency in part because of a resistance to insulin action. Most patients with type 2 diabetes are obese and are diagnosed after the age of 30 years. Insulin resistance in patients with type 2 diabetes is related to polygenic factors, abdominal visceral obesity, sedentary lifestyle, and aging. Approximately 40% of patients with type 2 diabetes have a least one parent with the disorder. Although many genetic factors are yet to be discovered, several common genetic polymorphisms increase the risk for type 2 diabetes. The combination of abdominal obesity, hyperglycemia, hyperinsulinemia, dyslipidemia, and hypertension has been referred to as the metabolic syndrome (see Plate 7-15). Excess production of the four insulin counterregulatory hormones can also cause diabetes. The hyperglycemia in patients with these endocrinopathies typically is cured by effective treatment of the underlying disorder. These individuals are usually not obese and are diagnosed with diabetes in late childhood or as young adults. Vision loss is caused by retinal hemorrhage, macular edema, retinal detachment, or neovascular glaucoma. Nearly all patients with type 1 diabetes and more than 50% of patients with type 2 diabetes develop some degree of retinopathy within 20 years of their diagnosis. For example, retinal blood flow does not change in normal individuals unless the mean arterial blood pressure is raised more than 40%. Hyperglycemia impairs this autoregulation, and retinal blood flow increases lead to increased shear stress, vascular leakage, and extracellular fluid accumulation. Microthrombosis and occlusion of retinal capillaries lead to retinal ischemia and capillary leakage. These growth factors promote the development of new blood vessels (neovascularization) in an attempt to revascularize ischemic retina. The two major forms of diabetic retinopathy are nonproliferative and proliferative. The intraluminal proliferation of cells results in vascular occlusion and rupture, resulting in the appearance of flame-shaped (occur in inner retina closer to the vitreous) and dot-and-blot hemorrhages (occur deeper in the retina) proximal to the occlusion and intraretinal infarcts (cotton-wool patches) distal to the occlusion. Intravenously administered fluorescein dye (fluorescein angiography) can assess areas of capillary under perfusion and leakage from sites of neovascularization. Macular edema is the most common cause of vision loss from diabetes and can be diagnosed by stereoscopic fundus examination or fluorescein angiography. It is termed clinically significant macular edema when the thickening in the macular region is of sufficient extent and location to threaten central visual function. However, as the vitreous gradually pulls away and detaches from the retina, the new vessels extend into the vitreous cavity. These aberrant vessels are fragile and at high risk for rupture with resultant vitreous hemorrhage. The neovascularization process can also lead to a fibrovascular proliferation that can distort the retina and predispose to retinal detachment. In addition, if hypertension is present, treatment should be targeted for average blood pressure less than 130/80 mm Hg. Administering approximately 1200 to 1800 laser burns (in grid that targets peripheral retinal tissue and avoids large vessels and the optic disc) per eye over two to three sessions decreases the risk of severe vision loss by 50%. Focal laser photocoagulation is the optimal treatment for clinically significant macular edema. Laser treatment is directed at microaneurysms and the Fibrovascular proliferation on optic disc and on vessels Interaction between hematogenous iron and vitreous accelerates shrinkage and traction Vitreoretinal traction Vitreous hemorrhage Fibrovascular proliferation and vitreous contraction cause traction retinal detachment Vitreous contraction Traction retinal detachment microvascular lesions around hard exudates, avoiding the fovea region. Vitreal contraction also predisposes to traction retinal detachment, which leads to vision loss when the fovea or the macula is involved.

Visceral involvement is not prominent weight loss 3 months buy 60 caps shuddha guggulu otc, but excess sulfatides are found in the liver weight loss pills yahoo answers purchase shuddha guggulu 60 caps with mastercard, kidney weight loss pills sold at walmart proven 60caps shuddha guggulu, and spleen weight loss pills phen phen purchase 60 caps shuddha guggulu overnight delivery. Electromyography shows decreased nerve conduction velocities weight loss pills from mexico buy shuddha guggulu 60 caps without a prescription, and cerebrospinal fluid examination shows increased protein concentration weight loss 80 20 rule shuddha guggulu 60 caps discount. Similar to other acidic polysaccharides, certain dyes may be used to detect the sulfatides by the metachromasia they produce. The gene that encodes -galactosidase A is located on the X chromosome, and the disease is inherited in an X-linked recessive manner. In individuals with Fabry disease, Gb3 accumulates in the vascular endothelium, glomeruli, and distal renal tubules. The diagnosis can be confirmed by documenting low leukocyte -galactosidase A activity. Although the cause is unknown, anorexia nervosa is associated with cultural, biologic, and psychologic risk factors. The signs and symptoms of anorexia nervosa usually begin in middle to late adolescence; the disorder rarely develops after age 40 years. Enlargement of the salivary glands is common and associated with starvation and then binge eating and emesis. A diet of predominantly yellow and orange vegetables, which have a high -carotene content, results in a yellow tint to the skin, especially evident on the palms. The severe weight loss in individuals with anorexia nervosa affects most of the endocrine glands. Waist circumferences more than 80 cm in Asian women and more than 90 cm in Asian men are consistent with abdominal obesity. Key pieces of the history include age at onset of weight gain, body weight at different life stages, current and past dietary patterns, exercise habits, details on previous weight loss efforts, current and past medications, patient motivation to lose weight, and history of smoking cessation. Medications that can contribute to weight gain include corticosteroids, antipsychotics, antidepressants, antiepileptics, thiazolidinediones, and insulin. The physical examination should include blood pressure measurement, waist circumference, and an assessment of potential secondary forms of obesity. Thus, the goal of treatment is to improve current obesity-related comorbid conditions and to decrease the risk of developing additional comorbidities in the future. Treatment options include dietary interventions, lifestyle modification, pharmacotherapy, and surgery (see Plate 7-26). This degree of weight loss improves quality of life and cures or improves obesity-related comorbidities (diabetes mellitus, obstructive sleep apnea, hypertension, hyperlipidemia, fatty liver). Contraindications for bariatric surgery include patients with binge eating disorders, drug or alcohol abuse, major depression or psychosis, other medical diagnoses associated with prohibitive anesthetic risks, or predicted inability to comply with postoperative nutritional requirements. Bariatric surgery needs to be a component of a larger management program that includes nutritional and behavioral followup. With restrictive procedures, the absorptive function of the small intestine is intact. Gastric stapling (vertical banded gastroplasty) is an example of a restrictive surgical procedure in which the upper part of the stomach is partitioned by a vertical staple line with a tight outlet (stoma) that is wrapped by a band or prosthetic mesh. However, because of limited long-term efficacy and need for revisions (because of stomal stenosis, staple line disruption, band erosion, or pouch dilatation), the gastric stapling procedure has been replaced with laparoscopic adjustable gastric banding. A silicone band is placed at the gastric cardia near the gastroesophageal junction to limit food intake. The diameter of the band can be adjusted by injecting or removing saline from a reservoir that is implanted under the skin. Sleeve gastrectomy appears to have an advantage over other restrictive procedures because of better appetite control related to removing the major source of ghrelin. There is a proximal biliopancreatic limb that transports the secretions from the pancreas, liver, and gastric remnant. Biliopancreatic diversion includes a partial gastrectomy and gastroileostomy with a long segment of Roux limb. Biliopancreatic diversion is associated with high rates of stomal ulceration, anemia, protein malnutrition, and diarrhea. In addition, neoplasms may arise in the adrenal glands, duodenum (gastrinoma), lung (carcinoid tumor), thymus gland (carcinoid tumor), and esophagus (leiomyoma). Recurrent hypercalcemia may require reoperation or percutaneous ethanol injection. Thus, normalization of the serum calcium concentration is important in the management of patients with this syndrome. The dermal and subcutaneous lesions are benign and should be removed only if symptomatic. When an endocrine cell lacks menin tumor suppressor function, it begins the process of proliferation and neoplasia. Some clinicians recommend a prophylactic thyroidectomy by age 5 years, but others suggest thyroidectomy by age 10 years. Genetic information can also be useful to assess the risk of developing pheochromocytoma. In contrast, it is unlikely that pheochromocytoma will develop in patients with mutations in codon 768 or in those with the mutation p. They may be asymptomatic or cause mass-effect symptoms because of pressure on adjacent structures or hemorrhage. However, surgery or stereotactic radiotherapy (or both) is typically reserved for rapidly growing or symptomatic lesions. Early tumor detection and selective resec- Brain Endolymphatic sac tumor Mastoid cells Cerebellum Paragangliomas can be mediastinal, abdominal, or pelvic Renal cell carcinomas are commonly multicentric and bilateral Pancreatic serous cystadenomas are typically asymptomatic Endolymphatic sac tumor Hemangioblastoma of cerebellum Pancreatic neuroendocrine tumors are frequently nonfunctional and may be malignant Hemangioblastomas of spinal cord Broad ligament Uterus Pheochromocytomas, when present, are frequently multicentric and bilateral Epididymal cyst Testicle Cystadenoma Papillary cystadenoma of broad ligament (female) and epididymal cysts (male) are benign and frequently bilateral tion with renal-sparing surgery or ablative therapies is the optimal management strategy. Retinal angiomas develop in the retina and within the optic nerve and may be multifocal and bilateral. Laser photocoagulation and cryotherapy are very effective treatments for angiomas that do not involve the optic nerve. The neuroendocrine tumors of the pancreas are similar to those found in multiple endocrine neoplasia type 1, and they are frequently nonfunctional; however, they may cause symptoms related to hormone hypersecretion. The epididymal cysts (frequently bilateral) in men and the papillary cystadenomas in the broad ligament in women are benign and usually asymptomatic. Papillary cystadenomas of the endolymphatic sac are vascular lesions arising within the posterior temporal bone, and affected patients may present with tinnitus, hearing loss, and vertigo. The four types of neurofibromas are cutaneous, subcutaneous, nodular plexiform, and diffuse plexiform. Cutaneous neurofibromas-the most common type- are soft and fleshy tumors that arise from the peripheral nerve sheath and start to appear during adolescence and increase in size and number with age. Patients may have just a few or may have hundreds, with the trunk being the most common location. Hypoparathyroidism or chronic mucocutaneous candidiasis are usually the first manifestations that typically appear during infancy or childhood and are followed shortly thereafter (average age, 15 years) by primary adrenal insufficiency. Initially, the alopecia may be spotty before progressing to complete loss of hair (including the eyebrows). However, the clinical presentation can be variable, probably because of environmental and genetic factors. In patients with chronic untreated hypoparathyroidism, careful examination of the eye with a slit lamp shows spiculated opacities in the posterior subcapsular area of the lens, which may progress to cataract formation and blindness. If it began before age 6 years, dental hypoplasia, with poor dental root formation, is usually present. The inheritance pattern can be autosomal recessive, autosomal dominant, or polygenic. Seventy-five percent of carcinoid tumors are in the gastrointestinal tract (most commonly in the small intestine with lower frequencies in the rectum and the stomach), and 25% are bronchopulmonary carcinoids. However, some genetic conditions, such as multiple endocrine neoplasia type 1, predispose to carcinoid tumors. When metastatic, these tumors spread primarily to the regional lymph nodes, liver, bone, and the brain. Chromogranin A is secreted together with hormones and amines; all three secretory products can be used as tumor markers. Neuroendocrine cells often contain somatostatin and other peptide receptors on the cell surface, a finding that may used diagnostically with somatostatin receptor scintigraphy or therapeutically with somatostatin analogues. Most patients with the carcinoid syndrome presentation have liver metastases, so that the usual hepatic degradation of amines and peptides is bypassed. The diarrhea is attributable to hyperperistalsis caused by a variety of factors, including serotonin, tachykinins, histamine, kallikrein, and prostaglandins. The hypersecretion of tachykinins and bradykinins is the most probable cause of bronchoconstriction. The selection of imaging tests and the order in which they are preformed depend on the clinical presentation and the clinical suspicion for pulmonary or gastrointestinal location. Lymphocytic infundibulo-neurohypophysitis and infundibulopanhypophysitis regarded as lymphocytic hypophysitis variant. Endocrine manifestations of the rapid-onset obesity with hypoventilation, hypothalamic, autonomic dysregulation, and neural tumor syndrome in childhood. Predicting impairment of central vision from dimensions of the optic chiasm in patients with pituitary adenoma. Relation of plasma oxytocin and prolactin concentrations to milk production in mothers of preterm infants: influence of stress. Criteria for early detection of temporal hemianopia in asymptomatic pituitary tumor. Guidelines for the treatment of growth hormone excess and growth hormone deficiency in adults. How should a nonfunctioning pituitary macroadenoma be monitored after debulking surgery Pituitary apoplexy: retrospective review of 30 patients-is surgical intervention always necessary Macroprolactinaemia: prevalence and aetiologies in a large group of hospital workers. Role of transcription factors in midline central nervous system and pituitary defects. Gamma Knife surgery for adrenocorticotropic hormone-producing pituitary adenomas after bilateral adrenalectomy. Laboratory diagnosis of multiple pituitary hormone deficiencies: issues with testing of the growth and thyroid axes. Predictors of diabetes insipidus after transsphenoidal surgery: a review of 881 patients. Proton stereotactic radiotherapy for persistent adrenocorticotropin-producing adenomas. Update on epidemiology, etiology, and diagnosis of adult growth hormone deficiency. Secondary deterioration of visual field during cabergoline treatment for macroprolactinoma. Features at diagnosis of 324 patients with acromegaly did not change from 1981 to 2006; acromegaly remains underrecognized and under-diagnosed. Interrelationships between ovarian and pituitary hormones in ovulatory menstrual cycles across reproductive age. Incomplete deficiency of hypothalamic hormones in hypothalamic hypopituitarism associated with an old traumatic brain injury. Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society Clinical Practice Guideline. Follicular thyroid carcinoma in an iodine-replete endemic goiter region: a prospectively collected, retrospectively analyzed clinical trial. Incidental papillary carcinoma in patients treated surgically for benign thyroid diseases. Impact of proto-oncogene mutation detection in cytological specimens from thyroid nodules improves the diagnostic accuracy of cytology. A pathologic rereview of follicular thyroid neoplasms: the impact of changing the threshold for the diagnosis of the follicular variant of papillary thyroid carcinoma. Problems and controversies in the histopathology of thyroid carcinomas of follicular cell origin. The long term outcome of papillary thyroid carcinoma patients without primary central lymph node dissection: expected improvement of routine dissection. Assessment of the incremental value of recombinant thyrotropin stimulation before 2-[18F]-Fluoro-2-deoxyD-glucose positron emission tomography/computed tomography imaging to localize residual differentiated thyroid cancer. Thyroid-stimulating hormone-receptor antibody and thyroid hormone concentrations in smokers vs nonsmokers with Graves disease treated with carbimazole. The utility of radioiodine uptake and thyroid scintigraphy in the diagnosis and management of hyperthyroidism.

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