Eriacta
D. Scott Lind MD, FACS
- Professor and Chief Surgical Oncology, Medical College of Georgia School of
- Medicine, Augusta, Georgia
On ultrasonography a thick-walled contracted gallbladder with gallstones may be seen erectile dysfunction quiz buy discount eriacta 100mg on line. Hepatobiliary scintigraphy is normal in 28% to 90% of patients with chronic cholecystitis erectile dysfunction see urologist order eriacta with visa, particularly in asymptomatic patients impotence from vasectomy best order for eriacta. In symptomatic patients with chronic cholecystitis there is stasis of concentrated thick bile in the diseased gallbladder erectile dysfunction caused by prostate removal eriacta 100mg lowest price, mainly in the cystic duct erectile dysfunction vacuum pump india discount 100 mg eriacta with amex, which precludes gallbladder visualization erectile dysfunction inventory of treatment satisfaction questionnaire purchase eriacta 100 mg on line. When used in conjunction with other imaging and clinical findings, the nuclear scintigraphic findings increase the overall accuracy of diagnosis of chronic cholecystitis. Clinical findings on physical examination and laboratory results are nonspecific and are not helpful in differentiating this disease from other causes. Complications include a perforated gallbladder, abscess formation, or enterobiliary fistula. Recurrent inflammation and calculi incite degeneration and necrosis of the gallbladder wall, which subsequently leads to intramural abscess formation and eventual replacement by xanthogranulomas. Chronic stages are characterized by fibrous reaction and scarring from healing of the inflammatory reaction, and the histiocytes have a granular cytoplasm containing yellow-brown ceroid pigment. Grossly there is a large or small contracted gallbladder usually associated with cholelithiasis, irregular wall thickening, and poorly demarcated nodules of varying size in the outer layers of the gallbladder wall with ulceration of the mucosal surface. The role of conventional radiography in the evaluation of xanthogranulomatous cholecystitis is limited Table 56-3). Diffuse or focal intramural lowattenuation areas are seen within the gallbladder wall. This corresponds well to the presence of an Differential Diagnosis Other causes of acute upper abdominal pain should be included in the differential diagnosis, including gastroesophageal reflux disease, acute pancreatitis, peptic ulcer disease, or irritable bowel syndrome. Because patients with porcelain gallbladder have a high incidence of gallbladder carcinoma, a prophylactic cholecystectomy is recommended. A, Axial contrast-enhanced computed tomography scan in a 64-year-old man presenting with 4 months of right upper quadrant pain and tenderness showed diffuse enhancing irregular gallbladder wall thickening and an ill-defined hypodense band at the periphery (arrow). The inflammatory lesion is seen to penetrate the serosal layer and infiltrate into the pericholecystic space with indistinct margin of the liver and gallbladder. Focal disruption of the mucosal line is also seen, although less frequently compared with gallbladder carcinoma. Extension of the inflammatory process into the liver is common and manifests as either an ill-defined hypoattenuating mass or abnormalities of parenchymal enhancement. Biliary tree obstruction is also reported and is due to the presence of choledocholithiasis or concurrent cholangiocarcinoma. Mild lymphadenopathies in the portacaval space, along the hepatoduodenal ligament, also can occur. There is low signal intensity of the wall on T1-weighted images and moderately high signal intensity on T2-weighted images. Multiple intramural hyperintense regions are seen on T2-weighted images that do not show contrast enhancement on postgadolinium T1-weighted images. Early enhancement of the hepatic parenchyma on dynamic studies is seen in the liver bed. The early enhancement is caused not only by increased cystic venous drainage but also by inflammatory changes in the adjacent hepatic parenchyma. The gallbladder wall is typically echogenic but can be sonolucent (or isoechoic) and rarely hypoechoic. The characteristic feature is the presence of oval or flat hypoechoic nodules or bands within the gallbladder wall. The soft tissue interface between the gallbladder wall and the liver is frequently maintained, but if it is lost, the differentiation from gallbladder carcinoma becomes difficult. Cholelithiasis is a well-established risk factor present in 70% to 90% of patients with gallbladder carcinoma. Porcelain gallbladder is seen in 10% to 25% of patients with gallbladder carcinoma. Other risk factors include female sex, age, postmenopausal status, cigarette smoking, chronic Salmonella typhi infection, exposure to chemicals used in rubber and metal fabricating industries, and biliary disorders such as choledochal cysts and primary sclerosing cholangitis. Lymphoma is rare and represents primary non-Hodgkin lymphoma from mucosa-associated lymphoid tissue or may be secondary to systemic disease. It is the sixth most common gastrointestinal malignancy, following cancer of the colon, pancreas, stomach, liver, and esophagus. Detection of gallbladder malignancy occurs in the late stage of the disease because of the lack of early or specific symptoms. It is three times more common in women than men and is a disease of the elderly, with a peak incidence in the eighth decade and commonly manifesting at approximately 72 years of age. Other features include jaundice, a palpable right upper quadrant mass, nausea and vomiting, anorexia, and weight loss. Five different clinical syndromes are used to describe the presentation of patients with gallbladder cancer. Laparoscopic cholecystectomy may be ineffective owing to the presence of extensive adhesions and the infiltrative nature of the disease. Thirty percent of cases are poorly differentiated, and 12% are of papillary variety; 12% are mucinous cancers, and 7% are of the adenosquamous or squamous variant. Implants of the peritoneal surfaces can lead to intra-abdominal carcinomatosis, ascites, and invasion into an adjacent hollow organ, leading to biliary-enteric fistulas. Gallbladder carcinoma spreads lymphatically to the lymph nodes around the cystic duct, common bile duct, and pancreaticoduodenal region, followed later by the para-aortic region. It occurs early in the disease course and is likely to be present in approximately 50% of the cases at the time of diagnosis. More distant sites often involved include mediastinal, bronchial, or supraclavicular lymph nodes. Rarely, calcification precipitating in mucus within the glandular tissue may also be visible Table 56-5). Diffuse gallbladder wall thickening secondary to tumor infiltration and inflammatory change is a common and late manifestation of advanced gallbladder carcinoma. Diffuse or focal gallbladder wall thickening is seen in 20% to 30% of cases of gallbladder carcinoma. The most common appearance is that of a mass replacing the gallbladder and seen in 40% to 65% of cases. Wall thickening is the most diagnostically challenging pattern because it mimics the other common acute and chronic inflammatory conditions of the gallbladder. A, Axial contrast-enhanced computed tomography scan of abdomen in 78-year-old man presenting with right upper quadrant pain and weight loss shows diffuse irregular gallbladder wall thickening (arrowhead) and necrotic liver metastases (arrows). B, Axial image also shows multiple enlarged lymph nodes with heterogeneous enhancement in the perihepatic, peripancreatic, and para-aortic regions (arrows). Nodal masses around the distal common bile duct and pancreatic head may mimic pancreatic head carcinoma. Diffuse nodular wall thickening without layering is evident, and the wall shows homogeneous low signal intensity (type 4 pattern). On dynamic contrast-enhanced imaging, the outer margin of enhancement is irregular. This helps in differentiation from chronic cholecystitis, in which the outer wall of enhancement is smooth. Gadolinium-enhanced fat-suppressed T1-weighted images are useful in diagnosing tumor extent, direct invasion of surrounding organs, liver metastases, and involvement of critical vascular structures such as portal vein and hepatic artery. The diffusely thickened gallbladder wall has irregular margins and a heterogeneous echotexture. There is no role for cholescintigraphy in the evaluation of gallbladder carcinoma. Gallbladder carcinoma is differentiated from these conditions by the presence of irregular wall thickening, lymphadenopathy, hepatic metastases, and biliary obstruction. A thicker and more irregular wall is more suggestive of gallbladder cancer than chronic cholecystitis. The presence of a continuous mucosal line and of intramural hypoattenuating nodular lesions in the former helps in the diagnosis. In adenomyomatosis there is regular wall thickening with anechoic or echogenic foci in the gallbladder wall on ultrasonography, which aids in the differentiation from gallbladder carcinoma. Those in whom the tumor is confined to the gallbladder wall have a better prognosis. It is characterized by epithelial proliferation, muscular hypertrophy, and intramural diverticula (Rokitansky-Aschoff sinuses), which could be segmental or diffuse. Clinical Presentation Most patients with adenomyomatosis remain asymptomatic, and the diagnosis is usually an incidental finding on either imaging or histopathologic examination of surgical gallbladder specimens. Symptomatic patients present with reports of persistent right upper quadrant pain, and 90% have coexistent gallstones. Pathology Proliferation of the gallbladder epithelium occurs that extends downward into the crypts, into the thickened muscularis, or beyond into the outer layer of connective tissue. A Rokitansky-Aschoff sinus within the thickened muscular layer of the gallbladder is the characteristic finding of adenomyomatosis. Microscopic examination shows extension of epithelium into the mucosal invaginations of the muscle. The invaginations are lined by a single layer of tall columnar epithelial cells similar to the surface-lining epithelium. Cystic spaces within the wall may be grossly visible, and stones may be present within them. Opacification of the Rokitansky-Aschoff sinus is depicted on drip-infusion cholecystographic images, specifically in the diffuse type of adenomyomatosis, and is called the "pearl necklace" sign. Intramural fluid attenuation and nonenhancing areas suggestive of Rokitansky-Aschoff sinuses are seen within the gallbladder wall. A, Axial contrast-enhanced computed tomography scan of the abdomen in a 73-year-old man with dyspepsia shows diffuse gallbladder wall thickening, ill-defined intramural low-attenuation areas, and gallstones. B, Sagittal ultrasound image in a 67-year-old man shows wall thickening and gallstones. The characteristic feature is the presence of multiple intramural cystic spaces, some of which may contain signal void as a result of the presence of calculi. The cystic spaces are hyperintense on T2-weighted images and hypointense on T1-weighted images and are nonenhancing. It refers to a curvilinear arrangement of multiple small, rounded, high signal intensity foci representing Rokitansky-Aschoff sinuses within the thickened wall of gallbladder. This sign is highly specific for adenomyomatosis and helps in differentiation from carcinoma of the gallbladder. Diffuse gallbladder wall thickening is evident with intramural diverticula seen as anechoic spaces or as echogenic foci that may have acoustic shadows or reverberation artifacts. Intramural diverticula containing bile appear anechoic, whereas diverticula containing sludge, stones, or papillary projections appear echogenic with associated acoustic shadowing or reverberation artifact. The frond-like mucosal projections within diverticula, with their multiple interfaces of varying acoustic impedances, are the likely cause of the reverberation or "comet tail" artifacts. Hepatobiliary cholescintigraphy has no role in the routine evaluation of adenomyomatosis. However in the presence of symptoms, the manifestation is similar to that of any other gallbladder disease. The air within the wall in emphysematous cholecystitis can produce a similar artifact; however, patients with emphysematous cholecystitis are usually ill, in contrast to those with adenomyomatosis. Cholecystectomy is indicated for patients with symptomatic cases of gallbladder adenomyomatosis without cholelithiasis. Nevertheless, prophylactic laparoscopic cholecystectomy may be justified considering the uncertain nature of the disease and the difficult differentiation from malignant lesions. Radiography Conventional radiography has no role to play in the diagnostic evaluation of patients with secondary gallbladder wall thickening. Additional findings of extravascular volume overload may be seen, such as pleural or pericardial effusions, ascites, dependent subcutaneous edema, and distended inferior vena cava. Patients with congestive heart failure will demonstrate pulmonary congestion in the lung bases. Nuclear Medicine Hepatobiliary cholescintigraphy has a limited role but can be used to rule out acute cholecystitis. An extracholecystic inflammatory process such as acute hepatitis, peritonitis, acute pancreatitis, and acute pyelonephritis may cause gallbladder wall thickening. The exact pathophysiologic mechanism leading to edema of the gallbladder wall in these diverse conditions is uncertain. It has been postulated that elevated portal venous pressure, elevated systemic venous pressure, decreased intravascular osmotic pressure, or a combination of these factors could lead to gallbladder wall thickening. Liver cirrhosis, hepatitis, and congestive right heart failure are relatively frequent causes. The factors leading to the development of gallbladder wall thickening in cirrhosis include ascites, decreased systemic vascular resistance, and portal hypertension. Sagittal ultrasound image in a 68-year-old man shows diffuse regular gallbladder wall thickening and gross ascites.
Administration Communication Monitoring Cost Clinical tip-Most people who find emollients ineffective are not applying them frequently enough erectile dysfunction doctors in south africa buy generic eriacta. In this case encourage them to try a cream or a lotion instead of an ointment and apply the treatment more often pomegranate juice impotence buy discount eriacta 100 mg online. However erectile dysfunction medicine name in india cheap eriacta 100mg without prescription, primary percutaneous coronary intervention (where available) has largely superseded fibrinolytics in this context erectile dysfunction foods to avoid purchase 100mg eriacta free shipping. For massive pulmonary embolism with haemodynamic instability fibrinolytic drugs reduce clot size and pulmonary artery pressures erectile dysfunction doctors in orange county buy discount eriacta 100 mg on-line, but there is no clear evidence that they improve mortality erectile dysfunction pill purchase eriacta with amex. Fibrinolytic drugs, also known as thrombolytic drugs, catalyse the conversion of plasminogen to plasmin, which acts to dissolve fibrinous clots and re-canalise occluded vessels. This allows reperfusion of affected tissue, preventing or limiting tissue infarction and cell death and improving patient outcomes. Common adverse effects include nausea and vomiting, bruising around the injection site and hypotension. Adverse effects that require treatment to be stopped include serious bleeding, allergic reaction, cardiogenic shock and cardiac arrest. Serious bleeding may require treatment with coagulation factors and antifibrinolytic drugs. Reperfusion of infarcted brain or heart tissue can lead to cerebral oedema and arrhythmias, respectively. There are many contraindications to thrombolysis, which are mostly factors that predispose to bleeding including: recent haemorrhage; recent trauma or surgery; bleeding disorders; severe hypertension; and peptic ulcers. Previous streptokinase treatment is a contraindication to repeat dosing (although other fibrinolytics can be used), as development of anti-streptokinase antibodies can block its effect. The risk of haemorrhage is increased in patients taking anticoagulants, and antiplatelet agents. Fibrinolytic drugs should be administered in a high dependency area such as the emergency department, hyperacute stroke unit or coronary care unit, by staff experienced in their use. For example, in acute stroke, explain that part of the brain is being starved of blood and oxygen due to a blocked artery, which will cause long-term damage. With or without treatment people may show some improvement, but symptoms may also get worse and one in three strokes are fatal. Although the chance of death is increased initially after receiving a clot-busting drug (due to bleeding), after the first week the chances of living independently are increased. For licensed indications, written consent is not essential but verbal consent should be obtained. Patients should be monitored in a high dependency area, with vital signs checked every 15 minutes for the first 2 hours. This should include observation for signs of bleeding, anaphylaxis and, in the case of acute stroke, neurological deterioration. Administration Communication Monitoring Cost Clinical tip-In patients with acute ischaemic stroke, likely benefits of thrombolysis diminish rapidly with time. Compared to untreated patients, the chance of being alive and independent at 6 months is increased by 10% for patients who receive thrombolysis within 3 hours of symptom onset, but by 2% if thrombolysis is performed between 3 and 6 hours. Both drugs are used for neuropathic pain; pregabalin in particular is recommended as a second-line option in painful diabetic neuropathy (after duloxetine) and as a first-line option in other painful neuropathies. It binds with voltagesensitive calcium (Ca2+) channels, where it presumably prevents inflow of Ca2+ and, in so doing, inhibits neurotransmitter release. Pregabalin is a structural analogue of gabapentin that probably has a similar mechanism of action. Gabapentin and pregabalin are generally better tolerated than other antiepileptic drugs. Their main side effects are drowsiness, dizziness and ataxia, which usually improve over the first few weeks of treatment. Both drugs depend on the kidneys for their elimination, so their doses should be reduced in renal impairment. The sedative effects of gabapentin and pregabalin may be enhanced when combined with other sedating drugs. This makes them particularly useful where combination regimens are considered necessary. The dose is then increased over subsequent days and weeks to reach a dose that strikes the optimal balance between benefits and side effects. There are no special considerations with regard to the oral administration of gabapentin and pregabalin. Explain that you are offering a medicine which you anticipate will reduce the severity of their symptoms. For this reason, you will prescribe a low dose initially, then increase this gradually (make sure they are clear on the dosing instructions). They should avoid driving or operating machines until they are confident that the symptoms have settled. There is no need to monitor serum/plasma concentrations of gabapentin or pregabalin. In spite of containing the same chemical, the brand name product is significantly more expensive; there is no reason to prefer it. At the time of writing, pregabalin is only available as an expensive branded product. Administration Communication Monitoring Cost Clinical tip-Gabapentin may cause false-positive results for detection of protein on urine dipstick testing. In this case, a sample should be sent to the laboratory for quantitative analysis. Acid is normally produced by the proton pump of the gastric parietal cell, which secretes H+ into the stomach lumen in exchange for drawing K+ into the cell. Histamine is released by local paracrine cells and binds to H2-receptors on the gastric parietal cell. However, as the proton pump can also be stimulated by other pathways, H2-blockers cannot completely suppress gastric acid production. Most common among these are bowel disturbance (diarrhoea or, less often, constipation), headache and dizziness. H2-blockers are excreted by the kidneys, so their dose should be reduced in patients with renal impairment. You will need to write a prescription if you intend for the patient to take it for more than 2 weeks. For treatment of peptic ulcer disease, repeat endoscopy may be necessary in some cases to confirm healing. Standard ranitidine tablets are inexpensive; effervescent tablets and oral solution are about ten times more expensive. This probably makes them a better choice for suppressing gastric acid production pre-operatively. The anaesthetist may prescribe a dose of ranitidine in an attempt to mitigate this. You may score brownie points if you identify such patients and prescribe ranitidine yourself. Offer ranitidine 300 mg orally, to be taken with a sip of water at least 2 hours before the start of the surgical list. Thrombin and factor Xa are key components of the final common coagulation pathway that leads to formation of a fibrin clot. By inhibiting their function, heparins and fondaparinux prevent the formation and propagation of blood clots. Low molecular weight heparins such as dalteparin and enoxaparin have a similar mechanism of action but preferentially inhibit factor Xa. Rarely, heparins may cause a dangerous syndrome characterised by low platelet count and thrombosis (heparin-induced thrombocytopenia). Anticoagulants should be used with caution in patients at increased risk of bleeding, including those with clotting disorders, severe uncontrolled hypertension, or recent surgery or trauma. Heparins should be avoided around the time of invasive procedures, particularly lumbar puncture and spinal anaesthesia. In major bleeding associated with heparin therapy, protamine can be given to reverse anticoagulation. The arm should not be used because this can cause uncomfortable and disabling bruising. Advise patients to avoid activities that may increase their risk of bleeding, such as contact sports, and to inform healthcare professionals they come into contact with that they are taking anticoagulants. If thrombocytopenia occurs, the drug must be stopped and specialist advice sought immediately. However, health economic assessments suggest they are cost effective when used appropriately. This is because warfarin inhibits the natural anticoagulant activity of proteins C and S, and it does this before inhibiting the other clotting factors. Given intravenously, in the treatment of diabetic emergencies such as diabetic ketoacidosis and hyperglycaemic hyperosmolar syndrome, and for perioperative glycaemic control in selected diabetic patients. Alongside glucose to treat hyperkalaemia, while other measures (such as treatment of the underlying cause) are initiated. In diabetes mellitus, exogenous insulin functions similarly to endogenous insulin. It stimulates glucose uptake from the circulation into tissues, including skeletal muscle and fat, and increases use of glucose as an energy source. Insulin stimulates glycogen, lipid and protein synthesis and inhibits gluconeogenesis and ketogenesis. For the treatment of hyperkalaemia, insulin drives K+ into cells, reducing serum K+ concentrations. However, once insulin treatment is stopped, K+ leaks back out of the cells into the circulation, so this is a short-term measure while other treatment is commenced. The wide choice of insulin preparations for treatment of diabetes mellitus can be classified as: rapid acting (immediate onset, short duration): insulin aspart. Humulin I; and long acting (flat profile with regular administration): insulin glargine (Lantus), insulin detemir (Levemir). Biphasic insulin preparations contain a mixture of rapid- and intermediate-acting insulins. The main adverse effect of insulin is hypoglycaemia, which can be severe enough to lead to coma and death. In patients with renal impairment, insulin clearance is reduced, so there is an increased risk of hypoglycaemia. Although often necessary, combining insulin with other hypoglycaemic agents increases the risk of hypoglycaemia. The goal of treatment is to attain good blood glucose control without problematic hypoglycaemia. Treatment usually includes once or twice daily long-acting insulin to meet basal requirements, with intermittent rapid or short-acting insulin injected with meals to control post-prandial glucose. Example regimens: insulin glargine once daily and insulin aspart with meals and snacks; or Novomix 30 twice daily. In diabetic emergencies and peri-operative glycaemic control, 50 units of Actrapid are diluted in 50 mL of 0. In hyperkalaemia, Actrapid 10 units added to 20% glucose 100 mL and infused over 15 minutes is reasonable. It is essential that glucose is given with insulin for this indication to avoid hypoglycaemia. When starting a patient with diabetes mellitus on insulin, explain that insulin will help to control blood sugar levels and prevent complications. Advise them that lifestyle measures, including a calorie-controlled diet and regular exercise, are needed as well as insulin to improve health. Warn them of the risk of hypoglycaemia, advising them of symptoms to watch out for. Patients should measure capillary blood glucose regularly and adjust insulin dose based on results. HbA1c (glycated haemoglobin) should be measured at least annually to assess long-term glycaemic control. Prophylaxis of iron-deficiency anaemia in patients with risk factors such as poor diet, malabsorption, menorrhagia, gastrectomy, haemodialysis and infants with low birth weight. It is required for the synthesis of the haem component of haemoglobin, which gives red blood cells the ability to carry oxygen. Its absorption is increased by stomach acid and dietary acids such as ascorbic acid (vitamin C). Transferrin transports it either to be used in the bone marrow for erythropoiesis, or to be stored as ferritin in the liver, reticuloendothelial system, bone marrow, spleen and skeletal muscle. The most common adverse effect of oral iron salts is gastrointestinal upset, including nausea, epigastric pain, constipation and diarrhoea. Intravenous iron administration can cause injection site irritation and hypersensitivity reactions, including anaphylaxis. Oral iron therapy may exacerbate bowel symptoms in patients with intestinal disease, including inflammatory bowel disease, diverticular disease and intestinal strictures. Intravenous iron should be used with caution in people with an atopic predisposition due to the risk of anaphylactic reaction.
For patients who pay for prescriptions it may be cheaper to buy them over the counter statistics of erectile dysfunction in us purchase eriacta paypal. Administration Communication Monitoring Cost Clinical tip-Compound analgesics offer some advantages in terms of convenience erectile dysfunction surgery cost cheapest eriacta, and perhaps adherence erectile dysfunction in teenage buy discount eriacta. However doctor of erectile dysfunction eriacta 100 mg visa, it is often preferable to use the drugs as separate products impotence at 75 cheap 100mg eriacta overnight delivery, at least initially erectile dysfunction doctor miami order eriacta amex. Having found the optimum balance between efficacy and side effects, it may then be appropriate to switch to the equivalent compound preparation. Activation of these G protein-coupled receptors has several effects that, overall, reduce neuronal excitability and pain transmission. In the medulla, they blunt the response to hypoxia and hypercapnoea, reducing respiratory drive and breathlessness. By relieving pain, breathlessness and associated anxiety, opioids reduce sympathetic nervous system (fight or flight) activity. Thus, in myocardial infarction and acute pulmonary oedema they may reduce cardiac work and oxygen demand, as well as relieving symptoms. That said, although commonly used, the efficacy and safety of morphine in acute pulmonary oedema is not firmly established. They may cause euphoria and detachment, and in higher doses, neurological depression. They can activate the chemoreceptor trigger zone, causing nausea and vomiting, although this tends to settle with continued use. In the skin, opioids may cause histamine release, leading to itching, urticaria, vasodilatation and sweating. Continued use can lead to tolerance (a state in which the dose required to produce the same effect increases over time) and dependence. Dependence becomes apparent on cessation of the opioid, when a withdrawal reaction occurs (see Clinical tip). Most opioids rely on the liver and the kidneys for elimination, so doses should be reduced in hepatic failure and renal impairment and in the elderly. Avoid opioids in biliary colic, as they may cause spasm of the sphincter of Oddi, which may worsen pain. Then, having found the optimum dose, this is converted to a modified-release form. Prescribe immediate-release morphine at a dose of about one-sixth of the total daily regular dose. Patients may be reluctant to accept morphine, due to the stigma associated with abuse and dependence. That said, you should warn patients that the dose may need to be increased over time as they become tolerant to its effects; this is normal and should not cause alarm. Advise patients not to drive or operate heavy machinery if they feel drowsy or confused. For chronic pain, schedule a review after a couple of weeks to assess the need to step up or down the analgesic ladder and/or specialist referral. Opioid dependence is less problematic when they are taken therapeutically rather than recreationally; do not let this concern deter you from offering opioids for severe or chronic pain, especially in end-of-life care. They are metabolised in the liver to produce relatively small amounts of morphine (from codeine) or dihydromorphine (from dihydrocodeine). About 10% of Caucasians have a less active form of the key metabolising enzyme (called cytochrome P450 2D6), and these people may find codeine and dihydrocodine largely ineffective. Unlike other opioids, tramadol also affects serotonergic and adrenergic pathways, where it is thought to act as a serotonin and noradrenaline reuptake inhibitor. Common side effects of weak opioids include nausea, constipation, dizziness and drowsiness. All opioids can cause neurological and respiratory depression when taken in overdose. Tramadol may cause less constipation and respiratory depression than other opioids. Codeine and dihydrocodeine must never be given intravenously, as this can cause a severe reaction similar to anaphylaxis. Tramadol, codeine and dihydrocodeine rely on both the liver and the kidneys for their elimination. Doses should therefore be reduced in renal impairment and hepatic impairment, and also in the elderly. Tramadol lowers the seizure threshold so is best avoided in patients with epilepsy, and certainly should not be used in those with uncontrolled epilepsy. Tramadol should not be used with other drugs that lower the seizure threshold, such as serotonin-selective reuptake inhibitors and tricyclic antidepressants. A common starting prescription might be for codeine or dihydrocodeine 30 mg orally 4-hrly, or tramadol 50 mg orally 4-hrly. Whenever you prescribe an opioid for regular administration you should consider prescribing a laxative. Discuss common side effects, and if appropriate, offer a laxative to prevent constipation. Advise patients to avoid driving or operating heavy machinery if they become drowsy or confused while taking the new painkiller. Avoid using expensive branded products, such as modified-release tramadol, unless there is a clear reason to do so. This may cause a red patch to form at the injection site (which, for reasons of accessibility, is usually the lateral aspect of the thigh). Patients and clinical staff may notice this and wonder what it is and whether it has any significance. It is mediated by histamine release and, provided it is not progressive, is no cause for alarm. Its effect is to reduce the delivery of oxygen to tissues (hypoxia), forcing them to use anaerobic metabolism for energy generation. In pneumothorax, supplemental oxygen therapy has an additional benefit of reducing the fraction of nitrogen in alveolar gas. Since pleural air is composed mostly of nitrogen, this increases its rate of reabsorption. Except in pneumothorax and carbon monoxide poisoning, there is little to be gained from an abnormally high PaO2 and, indeed, there is some evidence that this may be harmful. However, this concern should not lead you to withhold oxygen in critical illness or states of severe hypoxaemia, in which oxygen may be life-saving. If exposed to high inspired oxygen concentrations, this finely balanced adaptive state may be disturbed, resulting in a rise in the blood carbon dioxide concentration. This may lead to respiratory acidosis, depressed consciousness, and worsened tissue hypoxia. This necessitates a different approach to oxygen therapy (see Prescription and Administration). Oxygen accelerates combustion and therefore presents a fire risk if it is brought into close proximity with a heat source or naked flame, including from smoking. The oxygen prescription is usually found on a dedicated section of the drug chart or a separate chart. Its key feature is the target oxygen saturation range, as measured by pulse oximetry (SpO2). For the initial delivery device, in general, prescribe a reservoir mask in critical illness and patients with SpO2 <85%; a Venturi mask (28%) for patients in chronic type 2 respiratory failure; and nasal cannulae for everyone else. Reservoir (non-rebreathing) masks have a bag (reservoir) that is continuously filled by the incoming oxygen supply. This will also specify the oxygen flow rate that, when entrained air is taken into account, produces a total gas flow rate sufficient to maintain a fixed inspired oxygen concentration. Simple facemasks are also variable performance devices; they have few advantages over nasal cannulae and are less comfortable. Explain that the facemask or nasal cannulae should generally be kept in place continuously, but may briefly be removed to allow eating and drinking. Ask them to report any discomfort, as it may be possible to improve this with a different device or the addition of humidification. Frequent SpO2 monitoring is essential in all patients receiving oxygen for acute illness. The device and/or flow rate should be adjusted as necessary to keep the SpO2 within the target range. In addition, arterial blood gas measurement is essential in patients with critical illness; those with chronic type 2 respiratory failure or at risk of hypercapnoea; and those with hypoxaemia that is unexpected, progressive, or disproportionate to their illness. Administration Communication Monitoring Cost Clinical tip-Remember that the PaO2 is only one determinant of the amount of oxygen reaching the tissues. Neglecting to correct these, if they are significantly abnormal, may render oxygen therapy worthless. Paracetamol is an antipyretic that can reduce fever and its associated symptoms. Hepatotoxicity can be prevented by treatment with the glutathione precursor acetylcysteine. There are few clinically significant interactions between paracetamol and other drugs. Paracetamol can be prescribed for regular administration or to be taken only as required, depending on the nature of the pain. Oral paracetamol is available as tablets, caplets, capsules, soluble tablets and oral suspension. Intravenous paracetamol is pre-prepared as a solution that can be infused undiluted over 15 minutes or diluted in 0. Explain that you are prescribing paracetamol with the aim of reducing or relieving pain. Where regular paracetamol is prescribed, explain the importance of taking it every 6 hours. Warn them not to exceed the recommended maximum daily dose because of the potential risk of liver poisoning. Warn them to check the label or ask the pharmacist before taking these with paracetamol. Efficacy of paracetamol in pain control can be established by enquiry about symptoms or by using a pain score. For chronic pain, schedule a review to assess the need to step up or down the analgesic ladder. Advise patients purchasing paracetamol from a shop or pharmacist to ask for the cheapest brand. Administration Communication Monitoring Cost Clinical tip-If you are writing up paracetamol on an inpatient chart, always check that it has not already been prescribed. Side chains attached to the -lactam ring can be modified to make semi-synthetic penicillins. The nature of the side chain determines the antimicrobial spectrum and other properties of the drug. Bacteria resist the actions of penicillins by making -lactamase, an enzyme which breaks the -lactam ring and prevents antimicrobial activity. Other mechanisms of resistance include limiting the intracellular concentration of penicillin (reduced bacterial permeability or increased extrusion) or changes in the target enzyme to prevent penicillin binding. Less commonly, an immediate (minutes to hours) life-threatening IgE-mediated anaphylactic reaction occurs with some or all of hypotension, bronchial and laryngeal spasm/oedema and angioedema. Central nervous system toxicity (including convulsions and coma) can occur with high doses of penicillin or where severe renal impairment delays excretion. Penicillin can generally be used safely in most clinical situations, although a dose reduction is required for patients with renal impairment. It is prescribed for the treatment of severe infections, usually at a high dose. As absorption is unpredictable and phenoxymethylpenicillin is less active than benzylpenicillin, it is not used for severe infections. If an allergy develops during treatment, give the patient written and verbal advice not to take this antibiotic in the future and make sure that the reaction is clearly documented in their medical records. Administration Communication Monitoring Cost Clinical tip-Where antibiotics are required to treat a young person with a sore throat caused by an unknown organism, make sure you choose phenoxymethylpenicillin, not amoxicillin.
Tracheobronchial invasion of the tumor erectile dysfunction treatment in singapore best 100mg eriacta, which sometimes results in fistula or airway obstruction impotence world association cheap eriacta 100 mg, is suspected if there is discrete indentation on the posterior wall or displacement of the trachea or bronchus by the tumor erectile dysfunction treatment atlanta ga purchase discount eriacta line. Metastasis Classification Metastasis to a distant organ defines the M classification erectile dysfunction caused by zoloft buy 100 mg eriacta otc. Esophageal cancer most commonly spreads to the liver (35%) but also can spread to the lungs (20%) erectile dysfunction causes mayo order eriacta 100mg on-line, bones (9%) what causes erectile dysfunction in diabetes discount eriacta 100mg, adrenal gland (5%), and, rarely, brain and peritoneum. Liver metastases appear as hypoattenuating lesions with irregular and undefined borders. Lung metastases are typically round with well-defined borders and no calcification. It is rare, but the diagnosis should be considered in patients who have risk factors such as human immunodeficiency virus infection and chronic immunosuppression. It is caused by degeneration of ganglion cells in the myenteric plexus of the esophageal body and the lower esophageal sphincter. On esophagography, it appears as a narrow esophagogastric junction with a dilated esophagus, which is called the "bird-beak" appearance. Regarding association with malignancy, the risk for esophageal cancer (especially squamous cell carcinoma) is substantially increased in patients with long-standing achalasia. When patients who have a long history of achalasia show rapid worsening of symptoms, the possibility of esophageal cancer should be considered. Esophageal Varices Esophageal varices are typically caused by portal hypertension and obstruction of the superior vena cava. Portal hypertension increases portal venous pressure, which leads to hepatofugal venous flow through the coronary vein into a plexus of dilated esophageal and periesophageal veins. Obstruction of superior vena cava results in reversal of flow into the cervical and upper thoracic esophagus via the superior intercostal vein, inferior thyroid vein, and other mediastinal collateral vessels. The diagnosis of esophageal varices is important because variceal rupture and bleeding are sometimes fatal. It is also important to check the portal venous system, superior vena cava, and surrounding collateral vessels if esophageal varices are discovered. Esophageal Perforation Esophageal perforation or rupture can result in a mediastinal infection, which may be fatal. Dilated veins are appreciated in the esophageal wall (A) secondary to portal hypertension from liver cirrhosis (B). A, Extravasation of contrast material and fluid collections (arrow) resulting from perforation. Perforation of the cervical esophagus typically causes cervical subcutaneous emphysema or a superior mediastinal fluid collection. Vagli P, Solito B, Neri E, et al: Giant fibrovascular polyp of the esophagus-imaging techniques for proper treatment planning: report of two cases. Kato H, Kuwano H, Nakajima M, et al: Comparison between positron emission tomography and computed tomography in the use of the assessment of esophageal carcinoma. Flamen P, Lerut A, Van Cutsem E, et al: Utility of positron emission tomography for the staging of patients with potentially operable esophageal carcinoma. Kloppel G: Classification and pathology of gastroenteropancreatic neuroendocrine neoplasms. Spot views of the esophagus are taken at the beginning (anteroposterior and right anterior oblique positions) while barium is being swallowed (if clinically indicated), and then the patient is asked to lie down on the left side (thus preventing the barium reaching the distal duodenum too quickly and obscuring views of the greater curvature and antrum of the stomach). The patient then is asked to lie slightly on the right so that the barium is against the gastroesophageal junction to check for reflux while screening. If reflux is not elicited, the patient may be asked to cough, swallow water, or tip the head down while being observed fluoroscopically and spot films are taken. Duodenum Views Duodenal loop: the patient lies prone on the compression pad to prevent barium flooding into the duodenum (additional views of the anterior wall of the duodenal loop can be taken in the right anterior oblique position). Single-Contrast Examination A single-contrast examination can emphasize mucosal relief, compression, and barium filling. This includes spot views of the barium-filled stomach with the patient recumbent: prone, left posterior oblique, right lateral, and right anterior oblique. The anterior gastric wall is better seen on the singlecontrast study than the double-contrast examination. Compression views require compression of the stomach, which is moderately distended with a small amount of barium to spread on the rugal folds. Overdistention makes it impossible to penetrate the barium radiographically, and the amount of barium used can be controlled by patient rotation or tilting the table. The views seen vary according to patient body habitus, and compression can be performed only below the rib cage; hence, often only the distal stomach can be identified. The compression view often demonstrates ulcers and masses, although small flat lesions can be missed and wall rigidity may occur from scarring or infiltration. The stomach has two surfaces: anterosuperior and posteroinferior, bounded by two borders, the lesser and greater curvatures, respectively. This hollow organ is completely covered by peritoneum, which passes as a double layer from the lesser curve (as the lesser omentum) and from the greater curve (as the greater omentum). The outer serosal layer consists of layers of connective tissue continuous with the peritoneum. The muscularis externa consists of three layers: the inner oblique layer (thicker at the antrum to perform forceful contractions); a middle circular layer that is thickest at the pylorus, forming a pyloric sphincter; and an outer longitudinal layer. The stomach is lined by columnar cells (for acid protection), unlike the esophagus, which is lined with squamous cells. The first (superior) portion extends from the pylorus to the neck of the gallbladder and consists primarily of the duodenal bulb. Posteromedially at the junction of the upper two thirds and the lower third of the duodenum lies the opening of the duodenal papilla or ampulla of Vater (opening of the bile and pancreatic ducts). This is an important landmark when distinguishing malrotation of the small intestine in children. The first part of the duodenum is the only part that is intraperitoneal, whereas the rest are retroperitoneal structures, again an important point for localizing a pathologic process. Helicobacter is a gram-negative bacteria that is recognized as an important cause of 70% of peptic ulcer disease and 95% of duodenal ulcers in the United States. Other causes of infectious gastritis include tuberculosis, histoplasmosis, and syphilis. Often they are common on the posterior wall of the stomach and least common on the fundus. Primarily, the signs include pooling of barium within the ulcer crater (on the dependent wall). If the ulcer is on the nondependent wall, the barium coats the "rim," causing a ring-like effect. Often a small mound of edema is seen surrounding the crater, causing a circular filling defect. The folds radiating from this should be smooth and symmetric with normal areae gastricae, suggesting benignity. A healed ulcer is identified when folds converge to the site of the ulcer, whereas incomplete healing, irregularity of the folds, residual mass, or loss of mucosal pattern suggests malignancy. When examined in profile with compression, the ulcer has a semicircular (meniscoid) configuration. The combination of this characteristic type of barium-filled ulcer and a radiolucent shadow of the elevated ridge of neoplastic tissue surrounding it is called the Carman-Kirklin complex. It is always convex toward the lumen, in contrast to the "crescent sign" of a benign gastric ulcer in which the inner margin is concave toward the lumen. Nodularity, clubbing, and amputation of normal radiating folds also suggest a malignant lesion. Note the marked narrowing of the body and antrum of the stomach as a result of lymphatic infiltration (arrows). The tumor invades the gastric wall, resulting in a desmoplastic reaction that leads to diffuse thickening and fixation of the stomach wall. On a double-contrast study they appear as a fine reticular pattern surrounded by barium-filled grooves. Hyperplastic polyps are the most common causes of discrete gastric filling defects, accounting for up to 90% of all gastric polyps. Most hyperplastic polyps appear as sharply defined, round or oval filling defects measuring less than 1 cm. An adenomatous polyp is a true neoplasm; it shows a tendency to malignant transformation and is therefore vital to identify. Characteristic features include size greater than 1 cm, lobulated or pedunculated shape, and a variation in size over time. Other lesions that can present as filling defects include lymphoma, carcinoid tumor, and metastases. Cysts arising from the kidney, spleen, and pancreas can produce these appearances. Maintenance of normal wall layering may distinguish benign and malignant conditions. Giant gastric ulcers are almost always greater than 3 cm and benign but have a higher rate of complications. It gives the appearance of "pseudo thickening," which can often be mistaken for tumor infiltration. Pseudotumor at the gastroesophageal junction in patients with hiatal hernia or apparent thickening resulting from underdistention of the stomach needs to be excluded. It is essential to ensure aggressive gastric and gastroesophageal junction distention with water or air contrast. Often, the mucosal wall may enhance avidly during the arterial phase of scanning because of hyperemia, causing a three-layered wall appearance suggesting possible malignant change. It may help to identify secondary signs such as stranding at the gastroesophageal junction or around the stomach, celiac axis lymphadenopathy, and metastasis to other organs such as the liver. It has been proved that in a well-distended stomach, a wall thickness of more than 1 cm that is focal, eccentric, and enhancing after intravenous contrast administration has a sensitivity of 100% and a specificity of 98% in detecting a malignant or potentially malignant lesion, warranting further investigation by upper gastrointestinal study with barium contrast or endoscopy. Blurring of the serosal surfaces, fat stranding, and peritoneal deposits are often seen. Nodal involvement is likely if the nodes are heterogeneous or enhance markedly after administration of a contrast agent. There may be transgastric spread, occasionally with direct invasion of adjacent structures (namely, liver, spleen, pancreas, transverse colon); hematogenous spread to liver, lung, adrenal glands, kidneys, bones and brain; or diffuse intraperitoneal spread. Leiomyosarcoma Leiomyosarcoma is an uncommon tumor, accounting for 1% of gastric lesions. However, it is the second most common type of polypoid lesion in the stomach after hyperplastic polyps. It is a smooth muscle tumor arising from the muscularis propria, and growth is often exophytic and exogastric or dumbbell shaped. Leiomyosarcoma is often heterogeneous with areas of low attenuation suggestive of necrosis and with primarily exophytic growth. The most common primary tumors metastasizing to the stomach are breast cancer, malignant melanoma, and lung cancer. Hematogenous spread to the stomach may manifest as submucosal masses that may appear nonspecific. Splenic vein thrombosis often manifests as gastric varices without esophageal varices. Computed Tomography of the Duodenum It is important to identify and recognize the pancreaticoduodenal groove because multiple disease processes may affect this region. For example, inflammatory processes such as pancreatitis can affect the surrounding peripancreatic fat and the second, third, and fourth parts of the duodenum, resulting in an associated duodenitis. Duodenal tumors, too, can be aggressive, such as leiomyosarcoma (although this tumor accounts for only 10% of duodenal tumors). Most patients with peptic ulcers can be investigated endoscopically; however, the upper gastrointestinal study with barium contrast is excellent at demonstrating duodenal ulcers. Giant duodenal ulcers are defined as a benign ulcer crater of more than 2 cm in diameter and have a tendency to bleed. The release of the pancreatic enzymes causes reactive edema of the duodenum, the extent of which may be severe enough to cause gastric outlet obstruction. Disruption of the intramural vasculature by the digestive pancreatic enzyme elastase can result in intramural hematoma. Severe cholecystitis can result in inflammation of the duodenum, and, if this is of long standing, it can result in a gallstone eroding through the gallbladder wall into the duodenum, eventually causing gallstone ileus. However, occasionally a diverticulum can be lined by aberrant pancreatic, gastric, or other functioning mucosa and can be the site of ulceration or perforation. Aberrant insertion of the common bile duct into a duodenal diverticulum may cause cholangitis or pancreatitis. However, the features of duodenal diverticulitis are similar to those seen in the colon, with wall thickening and retroperitoneal fat stranding. Note the duodenal wall thickening (arrow), fat stranding, and extensive inflammatory change. Presentation of these tumors can vary and include obstruction or the appearance of peptic ulcer disease. Secondary Involvement the most common tumors involving the duodenum include gastric carcinoma and lymphoma; in both cases, duodenal involvement is typically secondary to direct spread across the pylorus.
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Primary lymphangiectasia manifests with protein-losing enteropathy drugs for erectile dysfunction philippines cheap 100 mg eriacta, ascites best erectile dysfunction pills side effects buy cheap eriacta 100mg line, pleural effusions can you get erectile dysfunction pills over the counter 100 mg eriacta amex, and asymmetric edema of the extremities erectile dysfunction and stress purchase generic eriacta online. The main findings are reduced serum concentrations of albumin best erectile dysfunction pills over the counter purchase eriacta on line amex, and gamma globulins (IgA erectile dysfunction in young age order 100mg eriacta visa, IgG, and IgM). Malabsorption, hypoalbuminemia, and lymphocytopenia can be seen secondary to development of lymphoenteric fistulas. A, Small bowel follow-through shows thickened folds in the proximal jejunum (arrow) and fold effacement (arrowhead) and luminal narrowing in the ileum segments. B, Axial computed tomography image demonstrates the wall thickening involving the ileal segments with a mural stratification pattern and increased enhancement of the mucosa (arrows). In addition to nonspecific changes in barium studies, including mild fold thickening, dilatation, and increased fluid, enteroclysis can show a micronodular surface pattern produced by dilatation of the lacteals in the villi in patients with lymphangiectasia. This sign may be seen in patients with intestinal lymphangiectasia as well as another colitis or enteritis. The differential diagnosis list is long and includes inflammatory bowel disease, infectious enteritis, neoplasms, and connective tissue diseases. Common radiographic findings of these diseases are bowel wall thickening and micronodularity. Treatment of small intestine amyloidosis is supportive until the development of rare complications such as bleeding, ischemia, or obstruction. In secondary amyloidosis, treatment of the underlying cause (neoplasm or chronic infection) is the main focus. Depending on the seriousness of the disease, treatment also may include fluid and electrolyte replacement, iron, folate, vitamin D, calcium, and magnesium. Treatment of intestinal lymphangiectasia first starts with the treatment of the underlying cause, which can be inflammation or neoplasm. Supportive therapy includes a low-fat diet rich in medium-chain triglycerides and diuretics. Surgical Treatment Surgery is usually not indicated in the treatment of the diseases discussed in this section. There are lesions of congenital origin that may remain asymptomatic until adulthood. These include heterotopic pancreas, heterotopic gastric mucosa, duplication cysts, and myoepithelial hamartoma. Carcinoid, which can be benign or malignant, is probably the most common of the small bowel tumors, constituting 25% to 40% of the small bowel neoplasms. Excluding the malignant neuroendocrine tumors, benign tumors of neural origin are rare. Other rare tumors include hemangiomas, lymphangiomas, hyperplastic polyps, inflammatory fibroid polyps, and hamartomatous polyps associated with Peutz-Jeghers syndrome. Most benign tumors are clinically silent and may be discovered incidentally; however, large or soft lesions may act as a lead point for an intussusception and cause bowel obstruction. This can occur in up to one third of benign tumors and cause symptoms such as early satiety, nausea, vomiting, constipation, abdominal distention, and a palpable mass. Large tumors may erode the overlying mucosa and cause bleeding (melena, gastrointestinal hemorrhage, pain, and, rarely, perforation). In fact, bleeding as a manifesting sign is reported in almost 40% of benign small bowel tumors. For patients with symptoms, diagnosis is usually made in 6 to 12 months from the onset of symptoms. Peutz-Jeghers Syndrome this autosomal dominant syndrome that occurs equally in men and women of all races and is usually diagnosed in the teens or early 20s with frequently a known family history. The hamartomatous intestinal polyps can cause acute intestinal obstruction secondary to intussusception in approximately 40% of patients. Other manifestations include abdominal pain, gastrointestinal bleeding, and prolapse of a rectal polyp. Less common clinical findings include precocious puberty, gynecomastia in males when associated with a Sertoli cell testicular tumor, and irregular menses in females as a result of hyperestrogenism from a sex cord tumor). Approximately half of the patients die in their 50s from cancer of the gastrointestinal tract or elsewhere (see section on Pathology). The valvulae conniventes or small bowel folds are deeper and more prominent in the jejunum. In the ileum, the folds are more shallow, farther apart, and more effaceable with distention or compression. Small bowel adenomas are neoplastic growths from the mucosa that may be histologically tubular (most common), villous, or mixed tubulovillous with varying degrees of differentiation. A, Spot film from enteroclysis shows a lobulated polypoid mass projecting into the contrast-filled lumen (arrow). The surface features are well outlined by the graded compression of the loop, showing a frondlike appearance that corresponds well to the surgical specimen (B). A, Spot film from small bowel follow-through demonstrates a large intraluminal polypoid mass (arrow) in the duodenum. B, Coronal computed tomography image shows a large, well-defined, homogeneous, soft tissue mass (arrows) in the region of the duodenum. Double-contrast radiograph shows a large, well-defined, compressible, polypoid mass (arrow) in the duodenum. There is a variable amount of fibrous tissue in some lipomas; thus there is a spectrum from pure lipoma to fibrolipoma and fibroma. Neural tumors originate in the submucosa, are usually solitary, and are varied in histologic category. Most are gangliocytic paragangliomas found in neurofibromatosis type 1 and, when present, are most commonly found in the duodenum, often near the ampulla of Vater. These account for 5% to 10% of small bowel tumors and are submucosal lesions that come in three main types: capillary, cavernous (most common), and mixed. When left untreated, the hemangiomas may develop phleboliths in veinlike channels and may undergo fibrosis. When not fibrotic, the gross appearance will be red and/or blue, suggesting the vascular nature of the lesions. However, when fibrosed, the lesion will be white and mimic other small bowel masses, in which case, if seen by endoscopy, it could be confused for a malignant mucosal lesion. Stromal tumors are composed of nests of spindle-shaped cells usually located between the muscularis propria and muscularis mucosa. Coronal computed tomography enterography image shows an enhancing small mass (arrow) within a mid-jejunal segment. Malignant features are assessed by judging the number of mitotic cells per high-power field. They are often silent clinically and therefore can be large at the time of diagnosis. The most common polyposis syndrome to involve the small intestine is Peutz-Jeghers syndrome. The disease is characterized by hamartomatous polyps with smooth muscle radiating within the polyp (in distinction from the hamartomas of Cronkite-Canada syndrome, which are characterized by cystic dilatation of glands). The polyps nearly always involve the small intestine, but fewer polyps are commonly found in the stomach or colon. Mucocutaneous melanotic macules are seen on the hands, face, and lips that involve buccal and sometimes anal mucosa. The hamartomas have no malignant potential, but sometimes a few adenomas or carcinomas may occur in the gastrointestinal tract (or elsewhere, including the esophagus, stomach, small intestine, colon, pancreas, lung, breast, uterus, and ovary). Congenital pancreatic tissue is known by several names: pancreatic rests, ectopic pancreas, accessory pancreas, and aberrant pancreas. Approximately 75% are located in the upper gastrointestinal tract, in which case they can become symptomatic. More commonly, it is an incidental finding on endoscopy or upper gastrointestinal series in an infant or child. Small 2- to 5-mm submucosal nodule(s) are typically found on the greater curvature of the antrum or first portion of the duodenum, characterized by central umbilication. This characteristic central umbilication is thought to be an aborted form of a pancreatic duct. Brunner glands are mucosal and submucosal alkaline-secreting glands, most commonly found in the first and proximal second parts of the duodenum. When multiple, they will produce a cobblestone pattern that should be distinguished from polyps, lymphoid hyperplasia, carcinoid, or metastases. They constitute 5% of all duodenal masses and are important to differentiate from other duodenal lesions. The association of gynecologic complaints and gastrointestinal symptoms in a premenopausal woman should raise the suspicion for endometriosis. These are rare benign submucosal lesions that occur in the small intestine and are of unknown cause, although some familial cases have been reported. Approximately 70% are pedunculated and therefore may act as a lead point for intussusception, causing pain, but other presentations, including bleeding, weight loss, diarrhea, or anemia, are reported. Heterotopic gastric mucosa can occur in a variety of locations, including the esophagus, duodenum, and colon or within a Meckel diverticulum, the gallbladder, and elsewhere. The abnormality often can be seen to be contiguous with the pyloric channel, extending to involve the duodenal bulb for a variable distance. Nodular lymphoid hyperplasia can be a normal variant, particularly in the terminal ileum in children. Spot film from a dedicated small bowel follow-through shows multifocal sites of angulation and tenting consistent with adhesions. At least three distinct sites of eccentric nodular luminal deformity (arrows) were present, each with a crenulated concave mural margin. This can be helpful in characterizing vascular lesions such as hemangiomas or varices, which will have a blue or reddish color or characteristic shape. If the lesions are large or cause intussusception, plain radiography may show dilated small bowel with a partial small bowel obstruction. Sometimes, complete mechanical obstruction may be present secondary to an intussusception. Rarely, bowel gas may outline polyps or masses that project intraluminally, but this is more likely to be a retrospective observation than a prospective diagnostic feature. When the polyp contour is outlined by gas or on barium studies, the submucosal lesions have a smooth surface with acute angles except for lesions that are ulcerated. The adenomas have features of a mucosal lesion, irregular surface (especially for villous tumors), and acute angles. Small filling defects of various sizes are shown on a double-contrast radiograph of the duodenal bulb. Multiple small, nodular filling defects are evenly distributed through several loops of small bowel. Most masses are hypodense and show some enhancement on portal venous phase imaging. Except in children, ultrasonography is usually not performed in the evaluation of the small bowel. In patients who present with signs of brisk gastrointestinal bleeding, a tagged red blood cell scan can help identify the site of bleeding. Barium studies show small bowel polyps that are too numerous to count and some gastric and colonic polyps. Typically, some segments of the small bowel are spared but short segments with carpeting of polyps can be seen. Ultrasonography can have a potential role for surveillance of the testes for males with the syndrome, surveillance of the pancreas for tumors, and surveillance of the ovaries for tumors. Patients known to have Peutz-Jeghers syndrome should undergo surveillance for malignancy of the gastrointestinal tract, breasts, and testes. Imaging is used for initial diagnosis and for the evaluation of complications Table 27-5). In an adult with no prior surgery and no evidence of a primary malignancy, infection, or ischemia, a small bowel tumor should be included in the differential diagnosis. For patients with a gastrointestinal hemorrhage, the differential diagnosis is also vast. Angiography can be done to detect bleeding sites or embolize active bleeding sites. Patients with anemia and active gastrointestinal bleeding are referred for diagnostic and therapeutic triage. Large tumors causing symptoms that might also be malignant may be evaluated for elective resection. Myoepithelial hamartoma occurs in the stomach or duodenum; Brunner gland polyps are in the first or second portion of the duodenum; inflammatory fibroid polyps occur in the terminal ileum (as can solitary carcinoid); and gangliocytic paragangliomas are found near the ampulla of Vater. Fleckenstein P, Pedersen G: the value of the duodenal intubation method (Sellink modification) for the radiological visualization of the small bowel. Parente F, Greco S, Molteni M, et al: Imaging inflammatory bowel disease using bowel ultrasound.