Kristen Quinn, MD, MS
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Demographic and Clinical Features Peritonitis may occur in any age group and affected person population. On bodily examination sufferers with diffuse peritoneal inflammation have abdominal tenderness and may have guarding or rebound tenderness. Bacterial peritonitis could occur in sufferers with bowel perforation, indwelling catheters, spontaneously in patients with ascites, or as a postoperative traumatic complication. Spontaneous bacterial peritonitis happens in sufferers with chronic ascites and is probably the most generally occurring type of bacterial peritonitis. The time period granulomatous peritonitis is used when granulomas type because of the inflammatory course of. Tuberculosis, histoplasmosis, and Pneumocystis pneumoniae infection can cause a granulomatous peritonitis, as can foreign material corresponding to talc and barium, meconium, bowel contents, the contents of ruptured ovarian cysts, bile, or gallstones in the peritoneal cavity. Sclerosing encapsulating peritonitis is a uncommon chronic inflammatory disorder of the peritoneum that occurs most commonly in sufferers present process continual peritoneal dialysis. It can also be idiopathic, associated with ventriculoperitoneal shunts, liver transplantation, tuberculosis, foreign material, and as a rare complication of beta-blocker therapy. Pathology Grossly, purulent materials is discovered on the peritoneal surfaces in generalized peritonitis due to bowel perforations. Granulomatous peritonitis is characterized by nodular thickening of the peritoneal surfaces. At histology the granulomata of tuberculosis characteristically have caseation with central necrosis rimmed by histiocytes and occasional lymphocytes. If the affected person has accompanying ascites, tuberculosis organisms can occasionally be cultured from the ascitic fluid. Imaging Features the imaging findings of bacterial peritonitis differ relying on the cause of the peritonitis. In bowel perforation, findings in many instances are associated to the etiology of the perforation, pneumoperitoneum, and localized abscess formation. Patients with spontaneous bacterial peritonitis usually have a big volume of ascites from continual liver disease and portal hypertension. Tuberculous peritonitis has been described as having three imaging patterns (wet, fibrotic mounted, and dry plastic), depending on the relative quantity of ascites and delicate tissue. Although tuberculous ascites characteristically has high attenuation, it could also have water attenuation. Soft tissue masses or nodules studding the peritoneal surfaces or infiltrating the omentum and mesenteries in all forms symbolize caseous nodules and fibrosis. Concomitant lymph node enlargement within the peripancreatic and periportal areas, mesenteries, or retroperitoneum may be current. The imaging features of peritoneal histoplasmosis are indistinguishable from tuberculosis. Linear calcifications could develop in the mesenteries and omenta because the disease progresses. Differential Diagnosis Loculated ascites: Ascites loculated by adhesions or inflammatory processes may simulate loculated fluid collections and abscess. Cystic or cystic-appearing metastases: Mucinous metastasis from pseudomyxoma peritonei or mucinous carcinomatosis is of low attenuation and could also be mistaken for ascites. Mucinous metastases could additionally be located within the nondependent portion of the peritoneal cavity and exhibit mass impact on intraperitoneal organs, corresponding to scalloping of their peritoneal surfaces. Management/Clinical Issues All forms of peritonitis, including spontaneous bacterial peritonitis, are sometimes tough to treat and require longterm antibiotic therapy. Ultrasound-guided paracentesis could also be required to acquire ascitic fluid for Gram stain and culture. Key Points Spontaneous bacterial peritonitis happens in sufferers with persistent ascites and is essentially the most generally occurring type of bacterial peritonitis. In tuberculous peritonitis, soft tissue masses or nodules studding the peritoneal surfaces or infiltrating the omentum and mesenteries symbolize caseation and fibrosis. Imaging options of encapsulating peritoneal sclerosis in continuous ambulatory peritoneal dialysis sufferers. Lymphangioma Definition Abdominal lymphangiomas are unusual developmental lesions of vascular origin. Lesions with giant cystic locules are often referred to as cystic hygromas, cystic lymphangiomas, or cavernous lymphangiomas. Imaging Features the majority of intra-abdominal lymphangiomas are situated within the small bowel mesentery. They may also happen in the retroperitoneum or inside intraperitoneal and retroperitoneal organs and bowel. On ultrasound the walls and inside septations of lymphangiomas are echogenic and may include detectable arterial and venous blood flow on spectral and color Doppler. Demographic and Clinical Features Lymphangiomas are mostly discovered in the pediatric inhabitants. Most lymphangiomas (95%) occur in the head and neck region and have a childhood presentation. The remaining 5% are located in the mesentery, retroperitoneum, abdominal viscera, and mediastinum. Patients with mesenteric lymphangiomas may current with stomach pain, growing stomach girth, a palpable mass, and signs and signs of bowel obstruction, or they might be asymptomatic with a cystic mesenteric mass found incidentally. Mesenteric lymphangiomas may also be part of a rare systemic dysfunction of lymphatic proliferation called lymphangiomatosis, which involves multiple anatomic websites. Fluid-filled bowel loops have an identical look to the lymphangioma but they include folds. The cystic fluid is often water attenuation and homogenous but may be heterogeneous with high-attenuation regions if hemorrhage has occurred. Evaluation of the fluid-filled constructions for bowel wall and fold patterns helps to distinguish the lymphangioma from adjoining fluid-filled bowel. The presence of protein and blood within the lymphangioma will alter the signal intensity. Differential Diagnosis Enteric duplication cyst: Its wall is composed of all layers of the gastrointestinal tract (mucosa, submucosa, and muscularis propria) and it might occur adjacent to or away from the bowel. A duplication cyst can be advised when a cyst is intimately related to the bowel. It has nonspecific imaging features and is indistinguishable from different peritoneal and mesenteric cysts. Mesothelial cyst: Rare, and is believed to represent a failure of fusion of the visceral and parietal peritoneum. Cystic or cystic-appearing metastases: Mucinous carcinoma metastases and pseudomyxoma peritonei might appear cystic due to their low attenuation. Scalloping of the margins of the intraperitoneal organs and omental nodules as properly as caking might help to distinguish these metastatic lesions from benign developmental cysts. Abscess: Typically more complex than lymphangioma with associated inflammatory change; may contain fuel.
Affected individuals usually have nonspecific clinical findings similar to chest ache, fever, dysphagia, dyspnea, or foul-smelling regurgitations. Patients with aortoesophageal fistulas may present with a "sentinel" episode of arterial hematemesis followed by a variable latent period earlier than experiencing massive hematemesis, exsanguination, and demise. These perforations usually occur as 1- to 4-cm vertically oriented linear tears on the left lateral wall of the distal esophagus close to the gastroesophageal junction. Imaging Features Most Mallory-Weiss tears (mucosal lacerations) are recognized by endoscopy. Esophageal hematomas normally seem on esophagography as solitary ovoid submucosal masses in the esophagus. Cervical esophageal perforation might seem on neck or chest radiographs as subcutaneous emphysema, retropharyngeal air, and pneumomediastinum. Single-contrast esophagogram shows a linear assortment of barium (arrows) abutting the distal esophagus as a result of a discrete mucosal laceration precipitated by recurrent retching after binge consuming in an alcoholic affected person. Single-contrast esophagogram shows focal extravasation of a water-soluble distinction agent into a small, sealed-off leak (black arrow) within the upper esophagus as a end result of tried endoscopic dilatation of a excessive esophageal stricture. Contrast agent is also seen to fill a smooth intramural collection (white arrows) paralleling the esophageal wall distal to the perforation due to an intramural dissection, producing a double-barrelled esophagus. Both the contained leak and intramural dissection healed on conservative administration. In distinction, thoracic esophageal perforation could additionally be associated with pneumomediastinum, mediastinal widening, and a pleural effusion or hydropneumothorax. Esophagography is often carried out on sufferers with suspected esophageal perforation. Some sufferers may have free leaks into the neck or mediastinum, whereas others could have small sealed-off leaks. Although barium is probably the most delicate contrast agent for detecting small leaks, it could possibly probably cause a granulomatous reaction in the mediastinum. However, water-soluble distinction agents are less radiopaque than barium and can miss a considerable share of esophageal perforations. If, due to this fact, the preliminary research with a water-soluble contrast agent exhibits no proof of perforation, it is suggested that the examination be repeated with high-density barium to detect refined leaks. In contrast, when an esophagopleural fistula is suspected, the presence and placement of the fistula may be confirmed by a water-soluble distinction research. Aortoesophageal fistulas are extraordinarily rare however are associated with a excessive mortality fee. Such fistulas could also be attributable to a ruptured aortic aneurysm, aortic dissection, contaminated aortic graft, swallowed foreign physique, or esophageal carcinoma. Patients with aortoesophageal fistulas could present with an initial episode of arterial hematemesis followed by a variable latent interval earlier than experiencing hematemesis, exsanguination, and death. Finally, when an aortoesophageal fistula is suspected, oral studies with water-soluble contrast are unlikely to present the fistula due to excessive aortic pressures. Contrast aortography can also be unsuccessful due to occlusion of the fistulous tract by thrombus. Therefore these fistulas are extraordinarily difficult to show on radiographic examinations. Single-contrast esophagogram exhibits focal extravasation of water-soluble distinction agent into a small, irregular, contained collection (arrow) at the website of perforation. This sealed-off leak healed on conservative remedy with no need for surgical restore. This patient had small-cell carcinoma of the lung with a mediastinal mass compressing the midesophagus (small black arrows). There is also focal ulceration (large black arrow) with barium filling an esophagobronchial fistula (white arrow) due to invasion of the esophagus by this mass. However, a diverticulum will have a smoother contour and rounder configuration, and distinction material is extra prone to empty from a diverticulum than from a confined perforation into the esophageal lumen. Single-contrast esophagogram reveals focal extravasation of water-soluble distinction from the left lateral wall of the midesophagus (white arrow), with distinction dispersing within the adjoining mediastinum (black arrows). Management/Clinical Issues In patients with Mallory-Weiss tears and intramural hematomas, the lesions often heal spontaneously; with conservative medical management, bleeding is subsequently Esophageal Per foration 43 self-limited. With full-thickness esophageal perforation, the treatment and prognosis depend upon the location of the harm. If untreated, perforations of the thoracic esophagus are related to a mortality rate of nearly one hundred pc because of a fulminant mediastinitis that happens in these patients. Free perforation from the thoracic esophagus subsequently necessitates early surgical intervention with surgical closure of the perforation and mediastinal drainage. In contrast, cervical esophageal perforations usually heal on conservative remedy, so these perforations (especially small or sealed-off perforations) can be treated nonoperatively. Surgical restore of esophageal-airway, esophagopleural, and aortoesophageal fistulas is normally required because of the extremely excessive mortality charges related to conservative management of these sufferers. In some circumstances, covered esophageal or bronchial stents can be placed for palliation of esophageal-airway or esophagopleural fistulas. Schatzki Ring Definition Lower esophageal rings are a standard discovering on esophagography, but solely a small percentage of patients are symptomatic. The term Schatzki ring ought to be reserved for symptomatic patients with decrease esophageal rings who present with dysphagia. Demographic and Clinical Features Patients with Schatzki rings sometimes present with episodic dysphagia for solids, which regularly recurs over a interval of years. Affected people could also be asymptomatic until a big meals bolus lodges above the ring. Because the commonest offending agent is an inadequately chewed piece of meat, this condition has been described because the steakhouse syndrome. Resolution of symptoms typically occurs when the impacted bolus is passed or regurgitated. Not occasionally, nevertheless, endoscopic elimination of the food bolus is required for sufferers with a persistent food impaction. In reality, a Schatzki ring is by far the most common reason for esophageal food impaction, accounting for about 90% of cases. Pathology Schatzki rings are virtually all the time positioned at or directly adjacent to the gastroesophageal junction. Histologically, the superior floor of the ring is lined by stratified squamous epithelium and the inferior surface by columnar epithelium. The actual pathogenesis of Schatzki rings is uncertain, however some rings are thought to develop because of scarring from reflux esophagitis. Most symptomatic sufferers have rings which might be less than 13 mm in 44 diameter, however some patients with dysphagia (depending on their consuming habits) could have rings as giant as 20 mm in diameter. Schatzki rings typically are symmetric and have a clean contour, producing a particular radiographic appearance.
Diffuse hepatic sign loss on out-of-phase (A) compared with in-phase (B) pictures is because of severe accumulation of intrahepatocellular (microscopic) fat. Notice partial fat sparing in a triangular region of the liver (arrow) immediately anterior to the best portal vein. This is a attribute location for focal fats sparing, which is attributed to anomalous nonportal venous inflow, as often occurs in this area of the liver. Common morphologic (A) patterns for focal fats accumulation and focal fats sparing include wedge-shaped, amorphous, geographic, and nodular patterns. Shown are hepatic proton-density fat-fraction maps that depict the concentration (as a percentage of proton density) and distribution of fat in the liver. The maps could additionally be depicted in grey scale (A and B) or in color (C and D) and they could also be generated using a technique that estimates proton-density fat-fraction from 0% to 50% (A and C) or from 0% to one hundred pc (B and D). Both techniques are equally fit for the aim of estimating hepatic proton-density fat fraction, which just about by no means exceeds 50%. Overlaid on each image are the proton-density fat fractions, expressed as percentages, in the corresponding portions of the liver. Focal fats accumulation and sparing, if nodular in morphology, could mimic mass lesions corresponding to metastases or major tumors. Differentiation is usually possible by cautious inspection of the photographs: focal fats accumulation/sparing causes no mass effect or vessel displacement, and normal vessels course undisturbed through areas of focal fats accumulation/sparing. Additionally, the focal fat accumulation/sparing enhances to the identical extent as background liver after administration of extracellular contrast brokers. Short-term follow-up imaging additionally may be useful: the distribution of fat accumulation/sparing may change over a brief time frame, and determination can happen after correcting the underlying metabolic abnormality or eradicating the responsible hepatic toxin. Investigational imaging primarily based strategies to diagnose steatohepatitis are in growth. Differential Diagnosis Diffuse Steatosis Hepatic fibrosis on ultrasound causes the liver to be echogenic. The liver may also have a cirrhotic morphology and the echotexture appears coarsened compared with steatosis in a noncirrhotic liver. It will not be possible to differentiate steatosis from fibrosis in a cirrhotic liver by ultrasound. These maps were acquired utilizing a way with a 0% to 50% range in 5 grownup patients; they show the next distributions: diffuse fat accumulation (A), diffuse fat accumulation with focal sparing (B), heterogeneous fat accumulation with subsegmental variation (C), focal fats accumulation in right lobe (D), and perivascular fats accumulation (E). Pitfalls Overlying adipose tissue, presence of fibrosis, and instrument settings could alter hepatic echogenicity and echotexture at ultrasound, thereby confounding the ultrasound evaluation of steatosis. Differentiation is usually possible by careful evaluation of vessels: vessels are normal in benign fat accumulation, whereas they could be distorted, irregular, or invaded in infiltrative cancer. Most scanners implement dual-echo out-of-phase and in-phase imaging as an out-of-phasein-phase design. In this design, the out-of-phase image is acquired with a shorter echo time than the in-phase image. Using this design, signal loss on the out-ofphase relative to the in-phase image unambiguously signifies the presence of fats. Signal loss on the in-phase image relative to the out-of-phase image suggests the presence of iron, because iron deposition shortens T2* and leads to progressive sign loss on images acquired at progressively longer echo instances. Some scanners implement out-of-phase and in-phase imaging utilizing an in-phaseout-of-phase design. In this design, the out-of-phase image is acquired with a longer echo time than the in-phase picture. Using this design, sign loss on the out-of-phase relative to the in-phase image could point out the presence of fat, iron, or each fat and iron. Experimental techniques are now in improvement which will permit the simultaneous assessment of liver fats and liver iron. Management/Clinical Issues Hepatic steatosis was long thought of an incidental finding of little scientific relevance. However, some sufferers with steatosis discovered at imaging could have unsuspected steatohepatitis. In addition, rising proof means that steatosis might contribute to the development of systemic insulin resistance, diabetes, and heart problems. Therefore the radiologist should embrace steatosis, if current, within the impression of the radiology report. Clinical history, laboratory exams, and generally biopsy are necessary to exclude different causes of steatosis. Therapy is often directed toward the correction of metabolic issues by weight loss and enchancment of insulin resistance (lifestyle modification). Posttransplant survival rates are much like these in patients with transplants performed for other reasons. Patterns of hepatic steatosis embody diffuse (most common), diffuse with focal fat sparing, focal fat accumulation, multinodular, subcapsular, and perivascular. No typical imaging technique can quantify hepatic fat content precisely; investigational methods to quantify fat are in improvement. Review article: epidemiology, pathogenesis and potential treatments of paediatric non-alcoholic fatty liver disease. Sirlin Definition Iron overload refers to the surplus accumulation of iron, mainly within the form of ferritin particles and hemosiderin aggregates, in the liver and other tissues. The two major etiologies of iron overload are primary hemochromatosis and secondary hemosiderosis. Primary hemochromatosis (also called hereditary hemochromatosis) is an autosomal recessive disorder in which a quantity of gene mutations result in dysregulated extra absorption of iron from the intestinal tract. Secondary hemosiderosis is a broad time period that encompasses all acquired causes of extra iron accumulation. These cases embrace multiple, frequent transfusions (typically in people with severe persistent anemias); iron-loading anemias (in which ineffective erythropoiesis stimulates physiological, or compensatory, intestinal overabsorption of iron); and persistent hepatopathy (in which preexisting chronic liver illness leads to hepatic iron overload by way of complex mechanisms). Demographic and Clinical Features Primary Hemochromatosis Primary hemochromatosis is the most common autosomal recessive genetic illness in western nations, with increased prevalence in non-Jewish Caucasians of northern European origin (1 in 220 individuals). Mutations in different genes involved in iron transport have additionally been recognized and about 6% of persons within the United States have a mutation in certainly one of these causative genes. There is a 5:1 to 7:1 male predominance with slightly earlier medical presentation in men than girls (fourth versus fifth decade) as properly as a larger (double to triple) threat of development to serious problems. Most patients are asymptomatic on the time of analysis, which often is made based on incidental laboratory or imaging findings. The medical manifestations of major hemochromatosis vary from nonspecific signs to multisystem disease. Because of preferential accumulation of iron in hepatocytes (see "Pathophysiology," further on), hepatocellular damage and liver disease might develop early and dominate the medical image. Involvement of other organs-pancreas (diabetes), myocardium (cardiomyopathy), pituitary (hypopituitarism), thyroid (hypothyroidism), joints (arthropathy), and pores and skin (hyperpigmentation), in decreasing order of severity-tends to manifest much less frequently and later. The basic triad of major hemochromatosis, consisting of cirrhosis, diabetes mellitus, and hyperpigmentation ("bronze diabetes"), is present in a minority of instances. Hepatomegaly is the commonest physical finding (90%), followed by splenomegaly (50%). Death regularly occurs because of cirrhosis (5% of the patients) and its issues.
Chronic radiation harm to the pharynx is characterised by vascular harm with mucosal atrophy and fibrosis of muscle and submucosal tissue. Paresis of the constrictor muscles could result in poor clearance from the hypopharynx with overflow aspiration. Carcinomas of the bottom of the tongue: analysis utilizing double-contrast radiography of the pharynx. Pharyngography after head and neck irradiation: differentiation of postirradiation edema from recurrent tumor. Demographic and Clinical Features Primary achalasia sometimes occurs in young or middle-aged adults who present with long-standing dysphagia that slowly progresses over a interval of years. Affected particular person are usually able to keep their weight by modifying their diets, even in advanced disease. In contrast, secondary achalasia is most incessantly attributable to malignant tumors involving the gastroesophageal junction; therefore affected sufferers tend to be elderly people (over 60 years of age) who current with a latest onset of dysphagia (less than 6 months) and weight reduction. Pathology Primary achalasia is an idiopathic condition resulting from the degeneration of ganglion cells in the distal esophagus and at the gastroesophageal junction. In distinction, secondary achalasia is an acquired condition brought on by malignant tumor in North America and by Chagas illness in South America. Many sufferers with secondary achalasia have tumor that directly infiltrates the gastroesophageal junction, destroying the ganglion cells in this region. In North America, as many as 75% of sufferers with secondary achalasia are found to have a carcinoma of the cardia or fundus as the trigger of this situation. Carcinoma of the lung, breast, and pancreas and different malignant tumors also can metastasize to the gastroesophageal junction, causing secondary achalasia. Other sufferers might develop secondary achalasia because of tumor involving the vagus nerve, dorsal motor nucleus of the vagus nerve, or mind stem. Still other sufferers have tumors that secrete a vasoactive substance, producing a paraneoplastic syndrome that mimics achalasia. Barium research typically reveal a standing column of barium in the thoracic esophagus with markedly delayed emptying into the abdomen. Some sufferers with achalasia have related nonperistaltic contractions of varying severity in the esophagus, a situation often known as vigorous achalasia. In secondary achalasia, nevertheless, the esophagus is much less dilated due to rapid development of illness. The narrowed distal esophagus can also be uneven, nodular, or ulcerated due to underlying tumor on this region. In sufferers with secondary achalasia caused by primary carcinoma of the cardia, barium research might reveal other signs of malignant tumor, with an ulcerated, polypoid, or infiltrating lesion within the cardia and fundus. In sufferers with markedly delayed emptying of barium from the esophagus, the abdomen paradoxically could empty extra quickly than it fills, limiting analysis of the cardia and fundus. In such cases, the affected person can be requested to sip further barium in a recumbent, left-side-down place to facilitate radiologic evaluation of the proximal stomach. This patient has a longer section of narrowing and greater angulation than is often seen in main achalasia. There can additionally be marked narrowing and irregularity of the proximal stomach as a end result of encasement by an advanced scirrhous carcinoma invading the distal esophagus (arrow), producing an achalasia-like look. Differential Diagnosis Peptic stricture: A tapered peptic stricture within the distal esophagus could resemble achalasia however main peristalsis is preserved, and peptic strictures are almost at all times related to hiatal hernias. Extrinsic compression by an ectatic or aneurysmal descending thoracic aorta: this indentation may cause tapered narrowing of the distal esophagus, however the dilated aorta will displace the distal esophagus and is often calcified and esophageal peristalsis is preserved. This patient has a massively dilated esophagus with a tortuous distal configuration (also known as a sigmoid esophagus) and appreciable retained debris. Also note tapered narrowing of the distal esophagus just above the gastroesophageal junction (arrow). In such cases, nonetheless, the distal esophagus opens normally and primary peristalsis is regular on inclined right-anterior oblique Esophageal Motilit y Disorders 13 radiographs. Rarely, sufferers with end-stage achalasia might require an esophagogastrectomy and gastric pull-through for amelioration of symptoms. In distinction, patients with secondary achalasia require a tumor workup for diagnosis and staging of the underlying malignant tumor answerable for their condition. Diffuse Esophageal Spasm Definition Diffuse esophageal spasm is an uncommon esophageal motility disorder characterized by intermittent weakening or absence of main peristalsis with simultaneous, repetitive nonperistaltic contractions in the esophagus. Demographic and Clinical Features Diffuse esophageal spasm is a disease of the elderly; most patients with this condition are over 60 years of age. Affected individuals usually present with substernal chest pain, dysphagia, or each. The chest ache is thought to be brought on by multiple repetitive nonperistaltic contractions of reasonable to marked depth. This situation typically includes the sleek muscle portion of the esophagus at or under the level of the aortic arch. In some sufferers, the esophageal wall could turn into markedly thickened owing to hypertrophy and thickening of the muscularis propria. It has subsequently been postulated that the latter sufferers have a transitional form of diffuse esophageal spasm that will progress over time to traditional achalasia. Imaging Features Diffuse esophageal spasm seems on esophagography by intermittently weakened or absent major esophageal peristalsis related to multiple repetitive nonperistaltic contractions of various intensity. Therefore the absence of a corkscrew esophagus on barium studies by no means excludes this diagnosis. In sufferers with achalasia, however, primary peristalsis is absent on all swallows, whereas in sufferers with diffuse esophaeal spasm, primary peristalsis is present on Further Reading 1. Diagnosis of major versus secondary achalasia: reassessment of clinical and radiographic criteria. Differential Diagnosis Presbyesophagus: A form of esophageal dysmotility associated with aging. These sufferers are often asymptomatic, whereas sufferers with diffuse esophageal spasm current with chest pain, dysphagia, or both. Incomplete opening of the sphincter is seen as a tapered, beak-like narrowing identical to that in patients with achalasia. However, other typical radiologic and manometric options of diffuse esophageal spasm allow differentiation from true achalasia. Management/Clinical Issues When sufferers with diffuse esophageal spasm present with chest ache because of a number of severe nonperistaltic contractions within the esophagus, therapy with calcium channel blockers or different brokers has generally been really helpful to lower esophageal spasm, although such therapy has had limited success. Severe, close to lumen-obliterating nonperistaltic contractions in the decrease third of the thoracic esophagus produce a corkscrew look. Real-time intermittent absence of major peristalsis within the thoracic esophagus was additionally observed in this patient with typical radiographic findings of diffuse esophageal spasm. Mild-to-moderate nonperistaltic contractions within the decrease third of the thoracic esophagus point out diffuse esophageal spasm. Relationship between diffuse esophageal spasm and decrease esophageal sphincter dysfunction on barium research and manometry in 14 patients. Scleroderma: Appears on barium studies as absent primary peristalsis in the portion of the thoracic esophagus lined by smooth muscle (below the aortic arch); it is due to easy muscle atrophy and fibrosis.
The affected bile ducts are diffusely thickened by an enormous lymphoplasmacytic infiltration intermingled with a storiform fibrosis. Imaging Findings Transabdominal ultrasound has restricted value for the diagnosis of IgG4-related sclerosing cholangitis. Cholangiography sometimes demonstrates prestenotic dilatation with long steady strictures usually isolated to the distal bile ducts. Patients with major sclerosing cholangitis are typically younger (30 to 40 years of age) and fewer symptomatic than those with IgG4-related illness. Multifocal intrahepatic duct involvement with short segmental strictures and a beaded, pruned-tree, diverticulum-like appearance is suggestive of primary sclerosing cholangitis. Solitary lesions with irregular margins, eccentric wall thickening, invisible bile duct lumen within the concerned phase, extra outstanding wall thickening (more than three mm), contrast enhancement on the arterial- and portal-phase images, and an abrupt transition between the traditional and involved bile duct might counsel a possible cholangiocarcinoma. It is important to concentrate on IgG4-related sclerosing cholangitis and to make an accurate diagnosis, since this condition exhibits a good response to steroids. Other organ involvement of IgG4-related illness can happen synchronously or metachronously. Imaging options: Long segmental, symmetric, circumferential thickening of the bile duct wall, incessantly with prestenotic dilatation and distinction enhancement on the delayed-phase photographs. An endoscopic retrograde cholangiogram shows a beaded look of the intrahepatic ducts (arrows) owing to alternating areas of biliary stricturing and delicate dilatation. Intrahepatic bile duct involvement is much less widespread than in typical primary sclerosing cholangitis. Such bile duct wall thickening can mimic the looks of main sclerosing cholangitis or cholangiocarcinoma. The wall of the gallbladder is also thickened and reflects IgG4-related cholecystitis (arrowheads). Clinical variations between main sclerosing cholangitis and sclerosing cholangitis with autoimmune pancreatitis. IgG4-related sclerosing illness: autoimmune pancreatitis and extrapancreatic manifestations. Demographics and Clinical Features Neuroendocrine neoplasms may develop in just about any organ, but main biliary neuroendocrine neoplasm comprises less than 1% of all neuroendocrine neoplasms. The frequent bile duct is the most common anatomic website, followed by the hilar bile duct, the cystic duct, and the frequent hepatic duct. Management/Clinical Issues Patients with biliary neuroendocrine neoplasms show extremely variable medical outcomes based on the histopathologic subtype. Since surgical procedure provides the only potential remedy, aggressive surgical remedy is generally advocated in patients with resectable biliary neuroendocrine neoplasms. Intraductal Papillary Neoplasm of the Bile Duct Definition Intraductal papillary neoplasm of the bile duct is characterized by dilated bile ducts distended by a papillary or villous biliary neoplasm overlaying delicate fibrovascular stalks. Demographics and Clinical Features Clinical symptoms include recurrent upper stomach pain, fever, chills, and jaundice, which are associated to obstruction of the bile duct by tumor or to the presence of extreme mucin. Intraductal papillary neoplasms of the bile duct have been reported more incessantly in East Asian international locations and will have an affiliation with intrahepatic stones or liver fluke infestation. Pathology Intraductal papillary neoplasms grow slowly and tend to unfold along the mucosal surface. Synchronous and metachronous intraductal papillary neoplasms can develop in the intrahepatic and extrahepatic bile ducts. According to degree of mobile and nuclear atypia, intraductal papillary neoplasms of the bile duct are categorised as low, intermediate, or high grade. Intraductal papillary neoplasms could be associated with invasive carcinoma and can be categorized as an intraductal growth type of cholangiocarcinoma. Intraductal papillary neoplasms with cystic luminal dilatation can have a similar appearance to biliary cystadenomas however can be distinguished histologically with the standards of luminal communication with the bile duct and absence of ovarian stroma at histopathology. Carcinoid of the extra-hepatic bile duct: a case report with long-term follow-up and review of literature. High-grade neuroendocrine carcinomas of the gallbladder and bile duct: report of four cases with pathological correlation. Non-functioning well-differentiated neuroendocrine tumor of the extrahepatic bile duct: an unusual suspect Further Reading Imaging Findings Imaging features of intraductal papillary neoplasms of the bile duct differ by tumor dimension, the amount of mucin produced by tumors, the places of tumors (large duct versus peribiliary gland), and the diploma of bile duct obstruction. When tumors are very small or unfold alongside the mucosal floor, it can be difficult to determine them on imaging studies. Anatomic variation of the bile duct can also be famous: the right posterior segmental bile duct drains into the frequent hepatic duct separately from proper anterior segmental bile duct. Bile duct resection confirmed biliary intraductal papillary neoplasms related to invasive carcinoma. Dilated peripheral intrahepatic bile ducts could rupture into the peritoneal area, leading to localized mucin collections or even pseudomyxoma peritonei. Differential Diagnosis Recurrent pyogenic cholangitis related to hepatolithiasis. Lack of distinction enhancement of nodular filling defects in the bile duct helps to differentiate stones of recurrent pyogenic cholangitis from intraductal papillary neoplasms of the bile duct. However, it must be noted that recurrent pyogenic cholangitis increases the incidence of intraductal papillary neoplasm. Normalcaliber bile ducts upstream of the cystic mass and large dimension of the mass counsel a biliary cystadenoma. The neoplasm on this case was in a roundabout way visualized by imaging however the analysis was suggested by the presence of enormous quantities of mucin. Although a radiopaque stone (arrowheads) is seen in the dilated bile duct, no enhancing papillary tumors are recognized. A geometric filling defect in the distal bile duct (arrowhead) suggests choledocholithiasis. Right hepatectomy and bile duct resection confirmed the analysis of a mucin-secreting intraductal papillary neoplasm related to invasive carcinoma. Benign tumors and tumor-like lesions of the gallbladder and extrahepatic bile ducts: radiologic-pathologic correlation. Mucin-producing bile duct tumors: radiological-pathological correlation and diagnostic technique. Intraductal papillary neoplasm of the bile duct: a biliary equivalent to intraductal papillary mucinous neoplasm of the pancreas Imaging Findings the radiologic discovering of a liver tumor associated with bile duct dilatation ought to increase concerns for possible cholangiocarcinoma, particularly within the elderly affected person with no history of other malignancy. Cholangiocarcinoma Definition Cholangiocarcinomas are malignant tumors arising from the epithelial cells of the bile ducts. They carry an exceedingly poor prognosis because most are regionally advanced at diagnosis and reply poorly to chemoradiation. Demographic and Clinical Features Cholangiocarcinoma typically occurs in aged and predominantly male sufferers, with the peak prevalence through the seventh decade. Cholangiocarcinoma is the second most typical primary hepatobiliary cancer after hepatocellular carcinoma, with the highest prevalence in Southeast Asia.
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This hemoglobin is filtered by the kidneys, reabsorbed by the proximal convoluted tubules, and deposited within the renal cortex as ferritin and hemosiderin. Hepatic iron overload could happen in patients with continual liver disease in the absence of transfusions or anemia. The extra iron accumulates primarily in the liver, affecting both hepatocytes and Kupffer cells, with comparatively little involvement of different organs. While modest in diploma, the hepatic iron overload appears to play a synergistic position within the improvement and development of hepatic fibrosis. However, it might be used to assess issues of cirrhosis in those that have progressed to end-stage liver disease. For example, steatosis and edema might reduce hepatic attenuation, while copper, glycogen, and some drugs. Despite identified severe hepatic iron deposition secondary to transfusional hemosiderosis, transverse ultrasound pictures of the liver at the ranges of the venous confluence (A) and left portal vein (B) show no abnormality. Notice that the spleen is markedly hypointense on all photographs, indicating concomitant splenic iron overload. Involvement of spleen along with liver is characteristic of transfusional iron overload. Unequivocal signal loss between the first and second echoes on a dual-echo acquisition indicates brief T2* decay and suggests the presence of excess tissue iron. Iron also shortens T1 relaxation and, in precept, might trigger iron-overloaded tissues to seem hyperintense on T1-weighted pictures. These quantitative strategies acquire spin-echo or gradient-echo pictures by way of the liver at a quantity of completely different echo occasions. Using an applicable mathematical model, the T2 (spin-echo images) or T2* (gradient-echo images) signal decay time constants, which then are calculated from the source images pixel by pixel to generate T2 or T2* parametric maps. Alternatively, the corresponding R2 or R2* sign decay rates can be calculated from the supply photographs to generate R2 or R2* parametric maps. Iron-overloaded liver has rapid R2 and R2* and hence seems shiny on these maps. These calibration curves is most likely not relevant, nevertheless, if an incorrect acquisition or postprocessing method is used. Patterns of Iron Overload Detected at Imaging Organ involvement displays the etiology. Primary hemochromatosis is characterised by preferential involvement of the liver, pancreas, and coronary heart and sparing of the extrahepatic reticuloendothelial organs (spleen, bone marrow). To calculate T2* or R2* maps, gradient-echo photographs are acquired with progressively longer echo times (A to E). The signal decay time fixed (T2*, normally in units of milliseconds) or the signal decay rate fixed (R2*, usually in models of s -1) are then calculated pixel by pixel to generate T2* (F) or R2* (G) maps. T2* and R2* are mathematical reciprocals; therefore low T2* and high R2* both connote iron overload. T2* and R2* maps are helpful for depicting the relative amount and distribution of iron all through the liver. Disorders of Iron Overload 321 reticuloendothelial organs (spleen, bone marrow) along with the liver, pancreas, and coronary heart. Patients with secondary hemosiderosis due to iron-loading anemias, however, may manifest a primary hemochromatosis pattern. In patients with hemolytic anemias, iron deposition within the renal cortex may be observed. In sufferers with persistent hepatopathy, the iron overload is often confined to the liver. Lobar/segmental, heterogeneous, or patchy distributions of hepatic iron overload are distinctly less frequent. In sufferers with cirrhosis, the iron may accumulate selectively in some nodules (siderotic nodules) in contrast with others. In an iron overloaded cirrhotic liver, a solid nodule with proportionately lower iron content than background liver is suspicious for hepatocellular carcinoma. Using this design, signal loss on the second echo compared with the first echo signifies T2* shortening and suggests iron overload, as discussed earlier, whereas sign loss on the first echo indicates fat-water sign cancellation and suggests hepatic steatosis. Management/Clinical Issues the goals of management of iron overload problems are to take away the excess iron and forestall development to irreversible tissue damage. Patients with major hemochromatosis are treated with regular phlebotomy while those with transfusion-related secondary hemosiderosis are handled with iron chelators. In hepatic iron overload associated with viral hepatitis, iron-chelating therapy is under investigation. Liver transplantation is reserved for patients with decompensated cirrhosis or hepatocellular carcinoma. Primary hemochromatosis results in preferential accumulation of iron in hepatocytes and should progress to end-stage liver disease. Patients with cirrhosis secondary to primary hemochromatosis are at risk for hepatocellular carcinoma. Secondary hemosiderosis is a broad term that encompasses all acquired causes of extra iron accumulation. The key mechanism of iron overload typically of secondary hemosiderosis is a quantity of blood transfusions; involvement of extrahepatic organs dominates the scientific manifestations; liver disease tends to be much less common and less severe than in major hemochromatosis. Primary hemochromatosis normally spares the spleen and bone marrow; secondary hemosiderosis usually impacts the spleen and bone marrow. In a affected person with diffuse iron overload and cirrhosis, a solid nodule with disproportionately lower iron content material than background liver is suspicious for hepatocellular carcinoma. Quantification of hepatic iron deposition in patients with liver illness: comparability of chemical shift imaging with single-echo T2*-weighted imaging. Sirlin Definition Cirrhosis is the continual response to repeated episodes of hepatocellular harm, characterized by in depth fibrosis, nodular regeneration, architectural distortion, and altered hepatic hemodynamics. Cirrhosis is the 4th leading cause of death in adults between the ages of 25 to 64. Virtually any chronic insult to the liver, if sufficiently severe and lengthy standing, could end in cirrhosis. Although cirrhosis is usually asymptomatic initially, issues may develop as cirrhosis progresses. These embrace portal hypertension (ascites, splenomegaly, esophageal varices, and hemorrhoids), coagulopathy, renal failure (hepatorenal syndrome), spontaneous bacterial peritonitis, and hepatic encephalopathy. Other laboratory findings widespread in cirrhosis include elevated complete bilirubin, abnormal prothrombin time and worldwide normalized ratio, hypoalbuminemia, and thrombocytopenia. The most common causes of liver-related death in individuals with cirrhosis are progressive liver failure, issues from portal hypertension, and the event of hepatocellular carcinoma. Pathophysiology and Pathology the fundamental pathogenic mechanism of cirrhosis is that of "injury and repair. Fibrosis (the deposition of collagen and different macromolecules in the perisinusoidal and sinusoidal spaces) causes elevated resistance to move via the hepatic microcirculation and induces portal hypertension. Portal hypertension may result in extrahepatic varices, ascites, and hypersplenism. Portosystemic shunts are commonly encountered in or around the decrease esophagus, paraumbilical veins, left gastric vein, and splenic vein.
Owing to ulceration, patients most often present with gastrointestinal bleeding (hematemesis, melena, guaiac-positive stool, iron-deficiency anemia). Other symptoms might include belly ache, dysphagia, nausea, vomiting, weight reduction, and a palpable belly mass. Lesions in between these two categories are thought of indeterminate with uncertain malignant potential. Mitotic exercise, cellular atypia, and nuclear pleomorphism might differ throughout a lesion. The discovery of gastric ulcers and the differential prognosis between benignancy and malignancy. Malignancy is determined by the biologic conduct of the lesion, tumor measurement, mitotic rate, invasion of adjoining organs, and distant metastases. There could additionally be large areas of cavitation with contrast materials extending into a big delicate tissue mass. The solely indication of a gastric origin of the tumor may be a central dimple or spicule at the web site of attachment of a pedicle to the mass. Central low density signifies necrosis, cystic degeneration and/or hemorrhage, and peripheral enhancement is seen within viable tumor. It could additionally be difficult to decide the gastric origin of a mass with a bulky extragastric extent. In common larger, lobulated, submucosal lots with necrosis or ulceration usually tend to be malignant. Additional pictures (not shown) demonstrated that the lesion was separate from the spleen, pancreas, and left kidney. Any seen involvement of the gastric wall ought to help to distinguish the gastric origin. Management/Clinical Issues Accurate analysis of malignancy could also be difficult with out resection. Endoscopic biopsy could also be unfavorable until the overlying mucosa is ulcerated or a deep biopsy is obtained. Tumors less than 5 cm in size are most often curable, however many of these lesions is in all probability not malignant. The finest predictors of malignancy on imaging embody lesion size (greater than 5 cm), cavitation, exogastric growth, invasion of adjoining structures, and metastatic illness. Computed tomography imaging of gastrointestinal stromal tumors with pathologic correlation. Gastric Lymphoma Definition Gastric lymphoma is a neoplasm that may contain the stomach primarily or secondarily; it accounts for 3% to 5% of malignant gastric tumors. Demographic and Clinical Features Gastric lymphoma is extra widespread in males than in girls, with patients most frequently diagnosed between 50 and 60 years of age. Patients might present with stomach pain, bleeding, nausea, vomiting, anorexia, weight loss, or a palpable epigastric mass. Symptoms are sometimes similar to those of much more widespread benign circumstances corresponding to gastritis and peptic ulcer disease. Gastric lymphoma has a much better prognosis than gastric adenocarcinoma, with 5-year survival of 50% to 60%. The abdomen is the most frequent site of gastrointestinal involvement with lymphoma, accounting for 50& to 70% of all main gastrointestinal lymphomas and 25% of extranodal lymphomas. More than 50% of sufferers have main gastric lymphoma with disease confined to the abdomen and regional nodes. Secondary lymphoma occurs with gastric involvement within the setting of generalized lymphoma. Over a time period, this lymphoid tissue could degenerate right into a low-grade lymphoma. At prognosis, main gastric lymphoma is usually confined to the stomach and regional nodes, however it could spread throughout the pylorus to contain the duodenum. Important prognostic indicators on the time of diagnosis include depth of gastric wall invasion and the presence or absence of nodal illness. Lymphoma could be broadly disseminated, involving extra-abdominal nodes, peritoneum, mesentery, omentum, liver, spleen, lungs, and/or brain. Despite in depth involvement, luminal diameter and distensibility are maintained. Advanced gastric lymphoma may seem as huge lesions, more than 10 cm in size at prognosis. Infiltrative lymphoma has thickened, lobulated folds both focally or diffusely with tumor infiltration within the submucosa. Despite extensive lymphomatous infiltration, distensibility of the gastric lumen is usually maintained. Rarely, infiltrative gastric lymphoma could have a linitis plastic appearance much like that of main scirrhous gastric carcinoma, with luminal narrowing, nodularity, and effaced folds. Ulcerative lymphoma appears as one or more ulcerative masses, with irregular ulcer craters and surrounding thickened folds due (A) to lymphomatous infiltration. Nodular lymphoma is seen as multiple submucosal nodules ranging in dimension from a quantity of millimeters to several centimeters. Gastric lymphoma could spread proximally into the esophagus with thickened irregular folds and luminal narrowing in up to 10% of patients. Gastric adenocarcinoma spreads across the pylorus much less usually than lymphoma, so that the presence of gastric and duodenal involvement may favor lymphoma over adenocarcinoma. The gastric contour may be preserved but the normal mural stratification pattern is lost, often with homogeneous soft tissue density within the gastric wall. The imaging findings overlap with adenocarcinoma; nonetheless, gastric wall thickening tends to be more pronounced with lymphoma than with adenocarcinoma. In addition, most patients with lymphoma have related cumbersome lymphadenopathy, which may prolong inferiorly beneath the renal hila. Lymphoid hyperplasia with multiple tiny, welldefined nodules having discrete borders. Other findings of hypoprotienemia, similar to ascities, gallbladder and small bowel wall thickening, and anasarca may be current. Common Mimic Infiltrative lymphoma can produce a linitis plastica look similar to that of scirrhous gastric carcinoma. Key Points Gastric lymphoma may be primary or secondary, is less frequent than adenocarcinoma, and has many overlapping imaging options with adenocarcinoma. Gastric mucosa-associated lymphoid tissue lymphoma: spectrum of findings at double contrast gastrointestinal examination with pathologic correlation. Primary gastrointestinal lymphoma: spectrum of imaging findings with pathologic correlation. Double-contrast upper gastrointestinal radiography: a sample approach for illness of the stomach.
Pylori and Peptic Ulcer Disease fifty nine Benign ulcers on the lesser curvature typically seem as clean, round, or ovoid craters that project past the contour of the adjoining gastric wall. Occasionally, inflammation surrounding the crater seems mass-like, seen in profile as smooth masses projecting into the lumen on either side of the crater (ulcer mound). Ulcers on the dependent or posterior gastric wall fill with barium in the supine place, revealing the characteristic ulcer crater. Shallow ulcers of the posterior wall could seem as ring shadows as a result of barium coating the rim of an unfilled crater. Flow method can be used to fill the crater with barium and distinguish an ulcer from a polypoid abnormality. Edema and spasm associated with antral ulcers may cause severe narrowing and deformity of the distal abdomen. Anterior wall ulcers on the nondependent floor of the antrum or body may seem as ring shadows with barium coating the rim of an unfilled crater. Benign gastric ulcers normally respond properly to therapy with antisecretory brokers. With therapeutic, the crater decreases in measurement and may change shape, taking on a more linear appearance on follow-up studies. Healing ulcers may end up in outstanding transverse folds, deformity, and tapered luminal narrowing. Asymmetric scarring can flatten and shorten the lesser or larger curvature and create an eccentric pylorus. Severe scarring in the antral-pyloric region might seem as a brief section of narrowing with wall thickening. Differential Diagnosis Malignant ulcer: Projects into a soft tissue mass and never beyond the anticipated gastric contour. Findings suggesting underlying malignancy embrace nodularity of the ulcer crater, eccentric crater within a mass, irregularity, clubbing, or amputation of radiating folds. Ulcerated submucosal mass similar to a gastrointestinal stromal tumor: Edema surrounding a benign ulcer can seem mass-like, simulating an ulcerative neoplasm. Scirrhous carcinoma: Distal gastric ulcers with massive edema, scarring, deformity, and luminal narrowing could also be troublesome to distinguish from malignancy. Common Variants And Mimics Variants Ulcers of the Greater Curvature Ulcers on the high greater curvature should be considered malignant till confirmed otherwise. Benign ulcers of the higher curvature may have suspicious features requiring endoscopy, as they could appear intraluminal as a result of pronounced spasm and retraction of the adjacent gastric wall. Erosions Erosions are focal areas of mucosal necrosis confined to the epithelium or lamina propria without extending by way of the muscularis mucosae into the submucosa. Erosions are often located in the gastric antrum and tend to happen along thickened folds. Calcifications and other densities overlying the abdomen may be mistaken for ulcers (see-though phenomenon). These potential ulcer mimics ought to all be easily distinguished from true ulcers at fluoroscopy and by obtaining photographs in different projections. Management/Clinical Issues Treatment for gastric ulcers relies upon upon the underlying cause. H2-receptor antagonist and proton pump inhibitors may be used to diminish gastric acid and accelerate ulcer healing. Key Points Gastric ulcers are now less frequent than duodenal ulcers however are more doubtless to bleed. Ulcers on the excessive higher curvature should be thought-about malignant until confirmed otherwise. Detection of gastric ulcer: comparability of single- and double-contrast examination. Double-contrast higher gastrointestinal radiology: a sample strategy for ailments of the stomach. Atrophic Gastritis Definition Atrophic gastritis is characterized by loss of gastric mucosal glands with intestinal metaplasia. It could occur as a consequence of an autoimmune course of with pernicious anemia or on a multifactorial basis, most often in association with Helicobacter pylori (H. B12 alternative remedy could also be initiated earlier than irreversible neurologic symptoms develop. Pathology As above, there are two kinds of atrophic gastritis (A and B) with differing histologic, immunologic, and secretory features. Type A is related to pernicious anemia and is manifest by mucosal glandular atrophy and an inflammatory reaction confined to the gastric body and fundus with relative sparing of the antrum. This is thought to be a consequence of an immune response directed at parietal cells. Lack of intrinsic factor leads to vitamin B12 malabsorption, which might cause pernicious anemia. Decreased acid manufacturing permits for the overproduction of gastrin as well as the looks of microcarcinoid tumors and neuroendocrine hyperplasia. There are patchy areas of chronic inflammation, glandular atrophy, and intestinal metaplasia replacing lost gastric glands. Metaplasia is the change of 1 epithelial cell sort to another, and intestinal metaplasia is believed to be sixty one Demographic and Clinical Features There are two kinds of atrophic gastritis, A and B. Type A is associated with pernicious anemia-a megaloblastic anemia caused by diminished intrinsic issue with subsequent vitamin B12 malabsorption. Pernicious anemia affects the aged, and 90% of sufferers with pernicious anemia have atrophic gastritis. This kind of atrophic gastritis is assumed to happen via an autoimmune mechanism and is most incessantly seen in northern Europe and Scandinavia. Type B atrophic gastritis is more common than kind A and is thought to be multifactorial and/or environmental in etiology. This is most prevalent in China and Japan and less usually seen in Europe, the United States, and concrete parts of South America. Other associated components may include gastric reflux of bile acids or ingestion of alcohol, salts, or nitrates. Patients with recognized atrophic gastritis and occult gastrointestinal bleeding ought to endure analysis for a possible superimposed gastric carcinoma. These patients have an increased risk of gastric carcinoma, up to three times higher than the final inhabitants; up to 10% of sufferers with atrophic gastritis and H. Patients with pernicious anemia could current with neurologic symptoms from vitamin B12 deficiency. If identified early, vitamin sixty two Gastrointestinal Imaging a precursor to gastric cancer, accounting for an elevated risk of gastric most cancers in sufferers with atrophic gastritis. With the single-contrast approach, atrophic gastritis in pernicious anemia classically seems as a tubular, narrowed stomach with a parallel look of the lesser and greater curvatures.
References
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