By J. Dennis. Principia College. 2019.

Note the prolonged opacification of the left renal aureus abscess in a patient with acquired immu- cortex and the high-density focus (arrow) representing a renal 32 calculus . Contrast scan demonstrates a focal area of decreased enhancement in the interpolar region of the left kidney (arrowhead) . Multiple severe renal Devitalized renal fragments , severe compromise Catastrophic injury generally requiring surgical lacerations in contrast excretion , extensive hemorrhage , exploration and often nephrectomy . Contrast scan demonstrates a subcapsular fluid collection (straight white arrows) flattening the posterolateral contour of the left kidney . Contrast scan shows several deep lacerations of the interpolar region of the right kidney (straight arrows) associated with areas of active arterial extravasation (curved arrows) Note the anterior displacement of the duodenum (D) , pancreas (P) , and inferior vena cava (V) . Proliferation of sinus fat also occurs abnormally in association with processes causing destruction or atrophy of renal tissue, as well as with increased exogenous or endogenous steroids. This process may mimic a fat-containing neoplasm originating in the renal sinus, but there is no evidence of focal mass effect on the intrarenal collecting system. However, after contrast peripelvic cysts confined to the renal pelvis are administration, the enhanced collecting common, frequently bilateral, asymptomatic, and systems are displaced and compressed by the thought to be of lymphatic origin. A parapelvic cyst cysts originate in the medial renal parenchymal appears as a larger, single lesion with water tissue and protrude into the renal pelvis. The left renal parenchyma is markedly atrophied in associated with a large stone (arrowhead). The large amount of subcapsular hematoma (H) reflects hemorrhage complicating insertion of a nephrostomy tube for stone extraction. Hemorrhage Acute hemorrhage has a higher attenuation Generally a complication of anticoagulant therapy, than normal fluid. Urinoma Extravasation of contrast material confirms the Usually associated with ureteral obstruction sec- (see Fig 37. The enhanced calyces are stretched and attenuated but not obstructed by the cysts. Larger masses obliterate 90% are transitional cell carcinomas, with the rest the renal sinus fat and infiltrate into the sur- being of squamous cell origin. The presence of a renal stone with a large infiltrating tumor is suggestive of squamous cell carcinoma. The nephrectomy specimen showed a hemorrhagic mass due to focal invasive aspergillosis, which may be difficult to differentiate from a tumor. The renal pelvis is stretched over the tumor and Benign tumors include hemangioma, fibroma, there may be hydronephrosis. Malignant renal neoplasms include leiomyosarcoma, fibrosarcoma, liposarcoma, hemangiopericytoma, and malignant fibrous histiocytoma. Tumor of the renal A mass extending from the renal parenchyma to Renal cell carcinomas commonly extend into the parenchyma projecting invade the renal sinus produces a filling defect renal sinus. Retroperitoneal tumor Bulky retroperitoneal mass that envelops and Because the renal sinus is a medial extension of the extending into the renal surrounds the normal constituents of the renal perinephric space, any retroperitoneal tumor can sinus sinus, often with contiguous spread to the extend to the renal sinus. A characteristic feature of lymphoma are typically homogeneous with minimal is continued patency of the renal vessels despite enhancement, but considerably less than tumor encasement. A tiny amount of gas (arrowhead), due to a previously performed percutaneous nephrostomy, in seen in the renal sinus. Post-transplantation Associated with Epstein-Barr virus infection, it is a complication in 2% of solid organ recipients. In lymphoproliferative kidney transplants, it typically occurs in the renal hilum as a hypointense lesion on both T1- and T2- disorder weighted images and has minimal contrast enhancement. Metastases Although metastases to the kidney are often found at autopsy, generally in patients with widely disseminated disease, they are infrequently detected on imaging. Abscess An abscess in the perinephric region may result from a urinary tract infection or infection of a preexisting perinephric hematoma or urinoma. Lymphangiomatosis Unilocular or multilocular thin-walled perinephric cysts representing a rare benign malformation of the perinephric lymphatic system. The staghorn the right renal hilum and distorting the collecting system calculus (arrowhead) was also seen on unenhanced images. There is involvement of the perirenal space The inflammatory process extends to the perinephric space bilaterally (arrows). Diffuse nephrocalcinosis Deposition of calcium salts, primarily in the renal cortex, causes diffuse high echogenicity of this region. If the calcification is predominantly medullary, there is a reversed pattern with the medulla appearing extremely echogenic. Normal variant Corticomedullary differentiation is exaggerated in normal kidneys when there is enhanced amplification of echoes due to passage of the sound beam through a medium of low attenuation between the kidney and the transducer (eg, fluid-filled gallbladder, ascites, or cystic mass anterior to the liver). Increased renal parenchymal echogenicity correlates with the degree of interstitial (not glomerular) change and the deposition of collagen or calcium. Unlike an abscess, focal acute bacterial nephritis does not have accentuation of the far wall, does not contain shifting debris, and lacks a sharp or rounded contour. After appropriate antibiotic therapy, there is rapid resolution of the process (an abscess cavity tends to persist). Healing renal infarct Focal increase in echoes (representing parenchymal scarring) in the involved area of the cortex and medulla. Infantile polycystic kidney Generalized increase in parenchymal echoes with disease loss of corticomedullary definition (can even be diagnosed in utero by means of these criteria). Usually associated with high-level echoes in the liver representing hepatic fibrosis. The echogenicity of the renal tissue greatly exceeds that of the adjacent liver (L). Prone sonogram of the kidney (arrowheads) shows a focal loss of renal parenchyma and extension of the calyces peripherally from the renal sinus to the renal margin. Note the associated focal area of increased echogenicity due to fibrosis (arrow) in the upper pole. An effusion (E), sometimes seen with acute transplant rejection, is noted medial to the kidney (R, right. Lymphocele is the most common type of extraurinary fluid collection, seen in 1% to 15% of renal transplant patients. Generally a late complication in patients who have had a prior episode of graft rejection. Increased isotope uptake on and has relatively poorly defined borders 67Ga scintigraphy confirms the presence of an (inflammation and edema around the lesion). A large hematoma may develop because of complex mass containing echogenic and cystic graft rupture or injury to the vascular pedicle of the components (may be difficult to distinguish transplanted kidney. Low-attenuation tumors may be diffi- cult to distinguish from retroperitoneal fat. A 4-cm mass in the left adrenal gland (arrows) is seen posterior to the tail of the pancreas and anterior to the kidney (K). Although the adrenal glands are enlarged (arrows), their normal configuration is maintained. To make the critical distinction between adenoma and metastasis, delayed scans can be obtained to evaluate the washout of contrast material. There is a well-circumscribed left hepatic steatosis are typical findings in this disease. Large soft-tissue tumor (T) invading the Adrenal carcinoma causing adrenogenital syn- anteromedial aspect of the left kidney (K) and left crus of the drome. Bilateral adrenal metastases (arrows) in a patient senting an adrenal metastasis from oat cell carcinoma of the with colonic carcinoma. The greater than 50% washout is diagnostic of an adenoma and confirms the finding on the initial unenhanced scan. May have an clinical suspicion of a pheochromocytoma, the rest attenuation value less than that of liver or renal of the abdomen and pelvis should be examined to parenchyma and simulate a thick-walled cystic detect the approximately 10% of tumors that are lesion. The examination may be expanded to the neck and chest if the abdomen and pelvis are normal. Neuroblastoma Soft-tissue or fatty mass that often contains Computed tomography can detect calcification calcification and may have cystic components. It also can easily demonstrate hepatic, skeletal, and pulmonary metastases for accurate staging as well as assess the response to treatment and detect recurrent disease. Bilateral in 50% of cases, adrenal lym- phoma is usually associated with retroperitoneal adenopathy or other sites of metastases. Rim of calcification Most commonly a pseudocyst, which results from occurs in approximately 15% of cases. Other types of cysts include parasitic, epithelial, and endothelial (lymphangiectatic, angiomatous, and hamartomatous). Incidentally discovered right adrenal mass containing a small amount of fat (arrow). Unenhanced scan obtained two days after Note the destructive lymphomatous lesion involving the motor vehicle accident shows an enlarged right adrenal right rib (curved arrow). Scans (A) before and (B) after contrast injection show a well-circumscribed soft-tissue mass with punctate calcification (arrow in A) and peripheral nodular enhancement (arrow in B). Chemical shift imaging, which is used to detect lipid within an organ, is the most sensitive method for making the critical differentiation between adenomas and metastases. On out-of- phase images, there is signal drop-off in lipid- containing adenomas, which appear darker than on in-phase images. Conversely, adrenal metastases do not contain lipid and there is no significant signal loss on out-of-phase images. This pattern is typical for adrenal adenomas, which tend to be equal to the liver in signal intensity on all pulse sequences. The most important feature signal intensity on T2-weighted images, and differentiating metastases from adenomas is the show progressive contrast enhancement. The mass exhibits heterogeneous low signal intensity on the T1-weighted image and high signal intensity with a heterogeneous enhancement pattern and areas of necrosis (arrow in B) on the T2-weighted image. Neonatal adrenal hemorrhage may be related to the trauma of delivery, septicemia, asphyxia, or abnormal clotting factors. They may also result from degenerative necrosis and hemorrhage into an adrenal mass. Areas of hemorrhage can be differentiated from fat by comparing the appearances on non–fat saturation and fat saturation images. T2-weighted image with fat obtained 6 weeks after a motor vehicle accident shows the saturation shows a uniformly hypointense right concentric rim sign, suggestive of a subacute hematoma. Neuroblastomas arise from on T2-weighted images, with evidence of the neural crest in the adrenal medulla or along the contrast enhancement. Axial T1-weighted image shows bilateral lymphomatous deposits as areas of low signal intensity. May produce only State and Europe, it occurs most frequently in older focal bladder wall thickening or invade the men. Punctate, coarse, or linear contact of the bladder urothelium with urine calcification (5%) typically encrusts the surface containing carcinogens, predominantly from of the mass rather than lying within it. There is also a well-documented link with bladder wall and tumor are of intermediate a variety of occupational and environmental signal intensity. Most urothelial tumors are located at ideal for detection of extravesical infiltration the bladder base (80%); 60% are single and more into high-signal fat. They often are intermediate-signal tumor contrasts with the multicentric, with synchronous and metachronous high signal intensity of urine and low signal tumors of the bladder and the upper urinary tract. These sequences are best for evaluating tumor depth, differentiating tumor from fibrosis, and detecting invasion of surrounding organs and marrow metastases. Urachal carcinomas are usually located at the dome of the bladder, in or slightly off the midline. Most adenocarcinomas are aggressive lesions that demonstrate early extravesical spread. Metastases Various patterns depending on the source of Most commonly the result of direct invasion from spread. Less frequently, bladder metastases may develop from hematogenous or lymphangitic spread of cancers from the stomach, breast, or lung. A late manifestation of cancer, when bladder metastases are detected there is usually evidence of a locally invasive adjacent primary neoplasm or other signs of a distant primary tumor. Small cell/neuroendocrine Large, polypoid or nodular lesion with patchy Rare, highly aggressive tumors that are frequently tumor contrast enhancement that may have an associated with a history of cigarette smoking. Within the mass are scattered low-attenuation 51 mass that fills the pelvis and surrounds the uterus areas (arrows), which represent mucin. Non-neoplastic masses Single mass that may be exophytic or polypoid Non-neoplastic proliferation of spindle and Inflammatory and ulcerated. Intramural solid and cystic inflammatory cells with myxoid components that pseudotumor variants also occur. At times, malacoplakia may be extremely aggressive, invading the perivesical space and even causing bone destruction. Axial T2-weighted image in another patient shows a lobulated polypoid mass arising from the anterior wall of the bladder. Note the central hyperintensity (*) and low peripheral signal intensity (arrowhead). The characteristic calcification in chronic disease represents large numbers of calcified eggs within the bladder wall. Other signs of pelvic Crohn’s disease may include fibrofatty proliferation, infiltration of fat, phlegmon, and lymphadenopathy. Radiation and Focal or diffuse irregular thickening of the Severe hemorrhagic cystitis may develop after chemotherapy cystitis bladder wall in acute cystitis.

The high pressure in the portal vein is decompressed through collateral portosystemic shunts that occur in the esophagus and the stomach . A paracentesis is a sample of the ascitic fluid obtained by needle through the anterior abdominal wall . A paracentesis is used to exclude infection , as well as to determine the etiology of the ascites if it is not clear from the history . The Gram stain is rarely positive because the density of microorganisms is so low . Although culture of the fluid is the most specific test , do not wait for the results to make a decision as to whether to give antibiotics . The presence of >250/mm3 neutrophils are the criteria to determine the presence of infection . Therefore , treat the patient with norfloxacin or ciprofloxacin daily (indefinitely) to prevent recurrence . The ascites total protein will tell you the cause of the elevated hydrostatic pressure. There is no specific therapy to reverse cirrhosis; one can only manage the complications and treat the underlying causes. That is because cirrhotics have intravascular volume depletion, producing a high aldosterone state (secondary hyperaldosteronism). Giving furosemide without spironolactone will lead to hypokalemia, which can cause encephalopathy. Encephalopathy is managed with lactulose, a nonabsorbed disaccharide that bacteria metabolize in the colon, making it more acidic. Ammonium is not absorbed very well, and that leads to an overall increased excretion of ammonia from the body. Treat with midodrine, octreotide and albumin (must give for 48 hours first to rule out pre-renal). Although vitamin K is often given because of the elevated prothrombin time, it is not effective because the liver is unable to synthesize clotting factors regardless of how much vitamin K is present. Bilirubin does not elevate until the disease is extremely far advanced (5–10 years). There is a strong association with other autoimmune diseases, such as Sjögren syndrome, rheumatoid arthritis, and scleroderma. At least 30% of patients are asymptomatic but are found to have an elevated alkaline phosphatase when measured for other reasons. Although it is more often found with ulcerative colitis, it can also occur with Crohn’s disease. Cancer of the biliary system can develop in 15% of patients from the chronic inflammation. The presentation and general lab tests are typically the same as those for primary biliary cirrhosis, except that the antimitochondrial antibody test will be negative. There is an overabsorption of iron in the duodenum, leading to iron buildup in tissue throughout the body, thus resulting in chronic hepatic inflammation and fibrosis. Transferrin saturation is the best screening test; if it is negative, diagnosis is not hemochromatosis. C282Y homozygous and C282Y/H63D are diagnostic of hemochromatosis and do need a liver biopsy for diagnosis. Phlebotomy is used to remove large amounts of iron from the body —it removes far more iron than do the chelating agents deferoxamine and deferasirox. Deferoxamine and deferasirox are used only for those who cannot undergo phlebotomy. Kayser-Fleischer rings are then found, confirming the diagnosis of Wilson disease. The most specific blood test for diagnosis is decreased ceruloplasmin but that alone is not enough. The single most specific test is liver biopsy, which will demonstrate increased copper deposition in the liver. Occasionally, hemolytic anemia is seen when copper levels go high and are toxic to the red cells. The condition is found in all ethnic groups but occurs most often in whites of European ancestry. To confirm hepatitis B: persistence of hepatitis B surface antigen >6 months (though it takes years for cirrhosis to develop) Remember, in chronic hepatitis B, the hep B surface antibody is negative. Chronic hepatitis B is treated with interferon, lamivudine, entecavir, telbivudine, or adefovir. The most commonly used is ledipasvir/sofosbuvir (trade name Harvoni), a 2-drug combination. Taken daily for 8–12 weeks, it provides cure rates of 94−99% in those infected with genotype 1 (the most common form of hepatitis C in the United States and some European countries), irrespective of the presence or absence of liver cirrhosis or prior unsuccessful treatment. It has also been evaluated for the treatment of infection with other hepatitis C genotypes and has shown promising results in genotypes 3 and 4. Patients presenting with this symptom may either have an underlying cause that is benign and requires only moderate analgesic medication or is life-threatening (e. In the evaluation of chest pain, the focus should be on excluding the more serious conditions. The healthy 26-year-old medical resident with chest pain that occurred after on-call is unlikely to have cardiovascular disease, no matter the quality or duration of chest pain. The 58-year-old man who has type 2 diabetes and dyslipidemia with chest discomfort of any type has a much higher probability for cardiac-related chest pain. Important aspects of the history include duration, quality, location, radiation, frequency, alleviating or precipitating factors (especially exercise), and associated symptoms. For both stable angina and acute coronary syndromes, the quality of chest pain is described by the patient as “tightness,” “heaviness,” or “pressure,” but symptoms resembling acute abdomen (pain in upper abdomen, nausea) are not uncommon. Nausea and vomiting are sometimes the main symptoms in inferoposterior wall ischemia (also, vagal reflexes may cause bradycardia and hypotension, presenting as dizziness or fainting). Myocardial infarction is associated with pain that lasts >20–30 minutes in duration. Response of chest pain to nitroglycerin (within a few minutes) is most consistent with transient ischemia or esophageal spasm. Chest pain that worsens with nitroglycerin sometimes occurs with gastroesophageal reflux disease. The response to nitroglycerin is not enough to confirm coronary disease as the cause of chest pain. Acute coronary syndromes in women often present without "classic" symptoms: instead, they may have dyspnea, shortness of breath, fatigue. Tachycardia and tachypnea are both nonspecific but occur in almost all cases of pulmonary embolism. Fever may suggest pneumonia or mediastinitis (esophageal rupture) as the cause of chest pain. Evidence of atherosclerosis (corneal lipid rings, narrowed retinal arteries, and pigment and hair changes in the legs) is commonly seen in patients with coronary syndromes. Inspect the chest wall for tender areas, respiratory motion, respiratory retractions, or accessory muscle use. If the tender area corresponds to the location of the patient’s pain and palpation exactly reproduces the pain, consider musculoskeletal chest pain as the cause of chest pain. Abnormal heart sounds and new murmurs are commonly found in certain chest pain syndromes. Wide physiologic splitting of the second heart sound (splitting wider with inspiration) can be found in right bundle branch block or in right ventricular infarction. A new murmur may be significant: aortic regurgitation occurs in over half of patients with aortic dissection, while mitral regurgitation can occur in patients with angina or infarction and is due to papillary muscle dysfunction. Asymmetry of breath sounds may be found in patients with spontaneous pneumothorax. The extremities should be examined for pulses, edema, and signs of atherosclerotic vessel disease. Calf swelling or edema raises the odds of pulmonary embolism as the cause of chest pain. It should be done immediately after initial stabilization and taking of vital signs. Serum cardiac biomarker determinations play a vital role in the evaluation of patients who present with acute chest pain and in the diagnosis of acute myocardial infarction. Serum markers such as aspartate transaminase, lactate dehydrogenase, and lactate dehydrogenase subforms no longer are used because they lack cardiac specificity and their delayed elevation precludes early diagnosis. Because the cardiac and skeletal muscle isoforms of troponin T and I differ, they are known as the “cardiac troponins. Troponin T and I have similar sensitivity for the detection of myocardial injury, but unlike troponin I levels, troponin T may be elevated in patients with renal disease, polymyositis, or dermatomyositis. The cardiac troponins typically are measured at emergency department admission and repeated in 6–12 hours. The cardiac troponins may remain elevated up to 2 weeks after symptom onset, which makes them useful as late markers of recent acute myocardial infarction. An elevated troponin T or I is helpful for identifying patients at increased risk for death or the development of acute myocardial infarction. The troponins also can help identify low-risk patients who may be sent home with close follow-up. Progression of Cardiac Enzyme Serum Levels Chest x-ray should be obtained on patients with chest pain; it may show pneumothorax, pneumomediastinum (i. Subtle findings such as loss of lung volume or unilateral decrease in vascular markings may suggest pulmonary embolism. It typically radiates to back, and a loss of pulses or aortic insufficiency often develops. Dyspnea, tachycardia, and hypoxemia are prominent; pain is usually pleuritic, especially when pulmonary infarction develops. May be preceded by viral illness; pain is sharp, positional, pleuritic, and relieved by leaning forward. Esophageal reflux is often made worse with recumbency or after meals, may be associated with regurgitation and relieved by antacids; episodes of spasm may be brought on by cold liquids, relieved by nitroglycerin, and may closely resemble angina or infarction; diagnosis may be confirmed by upper endoscopy or esophageal manometry. Peptic ulcer disease, pancreatitis, and cholecystitis may occasionally mimic infarction; abdominal tenderness is present, with radiation to back and elevated amylase in pancreatitis; sonography can confirm cholecystitis. Onset abrupt with sharp pleuritic chest pain and dyspnea; breath sounds absent; chest x-ray confirms. Pain is sharp and increases on inspiration; friction rub or dullness may be present; other respiratory symptoms and underlying pulmonary infection usually present. Clinical Recall Which of the following is the single most important test in the management of chest pain? In nearly all cases, the reduction in blood flow is caused by coronary atherosclerotic disease. When the atherosclerotic plaque ruptures, there is superimposed thrombus formation that acutely occludes the artery; this is the most common cause of life- threatening acute coronary syndromes. As part of a systemic process that involves all arteries in the body, it is an insidious process that begins in early adulthood with fatty streaks; these lesions progress into plaques and thrombus formation in middle age. Ischemic Heart Disease The more risk factors a person has, the greater the chance that he will develop heart disease. For example, a person with total cholesterol 260 mg/dL has a greater risk than someone with total cholesterol 220 mg/dL, even though all people with total cholesterol ≥220 mg/dL are considered high risk. When other risk factors (such as high blood pressure and tobacco smoke) are present, this risk increases even more. Secondhand smoke or passive smoking increases the risk of heart disease, even for nonsmokers. The risk for myocardial infarction in those who quit smoking was reduced to that of nonsmokers within 2 years of cessation; the benefits were seen regardless of how long or how much the patient smoked. Studies have shown that loss of as little as 10–20 lb can significantly reduce the risk of cardiovascular disease. Also, women who develop myocardial ischemia at older ages have a higher mortality than men within the first few weeks of the cardiac event. Heredity: Family history is a significant independent risk factor if there is a family history of premature disease (age <55 in male relative and <65 in female relative). Several studies show that the decrease of natural estrogen as women age may contribute to a higher risk of heart disease after menopause. This may be a true association or just a secondary correlation: for example, people under stress may overeat, start smoking, or be less active than people who are not under stress. In the presence of coronary obstruction, an increase of myocardial oxygen requirements caused by exercise, tachycardia, or emotion leads to a transitory imbalance. In many circumstances, ischemia results from both an increase in oxygen demand and a reduction in supply. He has been having this on and off for 8 months, and the last episode occurred 3 days ago while he was running to the bus. This occurs during periods of increased demand for oxygen, such as exercise, or decreased supply, such as hypotension or anemia (see demand ischemia, above). Typically, patients with stable angina will have pain after a predictable amount of exertion and will have identical symptoms with each attack. For example, a profound sense of weakness and breathlessness may be an “angina equivalent. Target heart rate is 85% of predicted maximum heart rate: 85% × (220 – patient’s age). Patients who are unable to exercise or walk should be considered for chemical stress testing, such as dipyridamole (Persantine) or dobutamine stress test. In those cases patients should be evaluated by nuclear stress imaging instead of the exercise stress test.

By endoscopy , the whole of the interior of the stomach can be adequately in­ spected . By this endoscopy one can clearly inspect the inside of oesophagus , stomach and duode­ num . The aim of treatment for gastric ulcer is the healing of the ulcer , whereas in case of duodenal ulcer is the relief of symptoms . In doubtful cases one should even take biopsy through endoscopy to confirm that the lesion is benign . Tranquillizers at night may be helpful particularly during the period of acute exacerbation . Milk is widely used in the treatment of ulcer disease , but there are few data to support its efficacy . The medical management of upper gut ulceration varies for duodenal and gastric ulcers. If pain is not relieved within 24 hours, nasogastric aspiration and intravenous fluid therapy should be started. A careful history must be taken whether the patient is taking any ulcerogenic drug e. Once the diagnosis is confirmed as benign ulcer, current recommendation includes initial therapy with an H2-receptor blockers e. Although secretion of acid is subnormal in majority of cases, yet these drugs heal the ulcer in more than half the cases within a period of 6 to 8 weeks. H -receptor antagonist and proton pump inhibitors2 — have revolutionised the management of peptic ulceration. Most gastric ulcers and duodenal ulcers can be healed by a few weeks of treatment with these drugs provided they are taken in time and absorbed. But a few patients may be relatively refractory to conventional doses of H2-receptor antagonists. In these cases proton-pump inhibitors can be used and majority of ulcers heal within 2 weeks. Six weeks after the institution of treatment, objective evidence of healing must be obtained. Endoscopy should be performed after 6 weeks of treatment and evidence of healing should be achieved. If it is not obtained, endoscopic 4-quadrant biopsy should be taken of the ulcer and presence of H. If the latter is found amoxycillin and metronidazole alongwith bismuth tablets should be prescribed for 2 weeks. With this combination the irradication rate is around 90% but the problem is the high rate of side effects. Metronidazole resistance is an increasing problem, especially in developing countries. Nowadays commonly used combination is omeprazole 40 mg/od and amoxycillin 500 mg/qds for 14 days. It is better that a proton pump inhibitor and amoxycillin should be the first line of treatment. A combination mostly used in the present days is clarithromycin 500 mg/bd, lansoprazole 30 mg/bd and tinidazole or metronidazole 400 mg/bd. Only in case of intractable gastric ulcers which fail to respond to this medical treatment, surgery is indicated mostly in the form of Billroth 1 gastrectomy. Traditional antacids should be used, but long term use should be avoided because it may lead to metabolic alkalosis and if associated with increased intake of milk, milk-alkali syndrome may develop. Various antacids are available in the market either iri the form of liquids or tablets. Those should be prescribed to be taken after meals and at night before going to bed. Antacids mostly used are aluminium hydroxide, silicate or glycinate alongwith magnesium hydroxide, carbonate or trisilicate. These are relatively insoluble in water and are long acting if retained in the stomach. So antacids containing former tend to be laxative, whereas those containing latter may be constipating. Activated dimethicone (Simethicone) either alone or with antacid mixture acts as an antifoaming agent to reduce flatulence. Alginic acid may be combined with antacids to encourage adherence of the mixture to the mucosa. Large doses of antacids in the form of 120 ml daily of magnesium hydroxide mixture should be prescribed, because one has to consider that the aim is to buffer secreted acid. But with this high dosage of antacid there is a high incidence of diarrhoea, which may not be acceptable to all the patients. Acid secretion at the parietal cell level is mediated by histamine acting on H histamine receptors. Cimetidine tablets (200 mg) are given after each meal for thrice daily and two tablets (400 mg) are given just before going to bed. This gives maximum plasma level of cimetidine 2 hours after food which is the time of appearance of pain in duodenal ulcer. Presently Famotidine is being used, which has a longer half-life and requires fewer doses in a day. Roxatidine is also histamine H2-receptor antagonist and it is a potent and selective inhibitor of basal and stimulated gastric acid secretion. Certain drugs inhibit this proton pump and block the final and common step in gastric acid secretion. Both basal and stimulated acid secretions are inhibited irrespective of the stimulus. It is used in case of recurrent or persistent disease as it is more effective in inhibiting acid secretion. It is particularly effective in antral G-cell hyperplasia and Zollinger-Ellison syndrome. Lansoprazole is used in the dose of 30 mg once daily in the morning for 4 to 8 weeks. Only in refractory cases and Zollinger-Ellison syndrome daily dose may be increased to 60 mg for 8 to 12 weeks. Omeprazole is used in the dose of 20 mg/day for 4 to 8 weeks and in Zollinger-Ellison syndrome it is used in the dose of 60 to 100 mg in two divided doses for 8 to 12 weeks. If it is present, a course of amoxycillin and metronidazole with bismuth tablets for 2 to 3 weeks is prescribed. Combination drugs are now available containing omeprazole 20 mg, amoxycillin 750 mg and tinidazole 500 mg to get rid of H. Another combination in the form of lansoprazole 30 mg, clarithromycin 250 mg and tinidazole 400 mg or 500 mg can also be used to irradicate H. H2-receptor antagonist may be used with nocturnal dose only as maintenance therapy to prevent relapse. Prolonged therapy should be avoided, as it may mask the disease and is also expensive without any definitive advantage. In case of relapses or continuous symptoms one must be careful to reassess the diagnosis as there are various diseases which may give rise to similar symptoms as ulcer cases e. If there is no improvement by proper medical treatment given for 6 weeks, there is every reason that the medical treatment should be stopped and surgery is indicated. When the ulcer fails to heal after rigid medical treatment for the prescribed period, which is 2 months for gastric ulcer and 6 months for duodenal ulcer operation is required. When the patients want quick relief of their symptoms and do not want to carry on a prolonged trial of medical treatment surgery is indicated. When the history suggests that the ulcer is present for 5 years, it is unlike that the ulcer will heal without operation. When repeated pain has made the patient intolerable with frequent loss of work, surgery is indicated. When ulcer has produced obstruction in the form of hour-glass stomach or pyloric stenosis, surgery is indicated. When the ulcer is giving rise to haemorrhage in the form of haematemesis or melaena, operation is indicated. When the patient gives a history of previous perforation of ulcer, the treatment is straightway surgery. If after 6 weeks of medical treatment endoscopy does not show any sign of healing of gastric ulcer, four quadrant biopsy should be taken through endoscopy. All gastric ulcers above the age of 45 years should be considered as suspicious and endoscopic biopsy is a must. Unless a definite improvement by medical trial is achieved within one month, surgery is indicated. As the vagus nerve is responsible for the psychic phase of gastric secretion, its transection i. Vagotomy also decreases the motility of the gastric muscles, hence hampers gastric emptying. Antrum is responsible for producing gastrin — the gastric phase of gastric secretion. It must be remembered that women patients do not tolerate partial gastrectomy so well and this operation should better be avoided in their cases. Pentagastrin test is always performed to assess the gastric acid status of the individual. The operation is selected as follows :— When the maximal free acid is from 30 to 40 m. This operation involves excision of distal two-thirds of the stomach followed by anastomosis between the remnant of the stomach and duodenum. Vagotomy and Pyloroplasty, associated with frozen section biopsy of the gastric ulcer (if benign), is gradually gaining popularity. Highly selective vagotomy or proximal gastric vagotomy with excision of the ulcer is being performed in some centres. The supporters of this technique claim that it is either equal or even a better operation than Billroth I gastrectomy, as the gastric physiology is best maintained in this operation. In fact, about 5 to 7 cm of the nerves are excised so that this technique can be referred to as ‘Vagectomy’. The selective vagotomy is aimed at removal of all gastric fibres of the vagus nerves, keeping intact the hepatic and coeliac branches. The proximal gastric vagotomy or highly selective vagotomy is designed to denervate the acid secretory part of the stomach, keeping the vagal supply to the alkali secreting gastric antrum and other abdominal viscera, thus motility of the stomach is not hampered and drainage procedure will not be required. The peritoneum over the abdominal part of the oesophagus is transversely incised taking care not to damage the inferior phrenic vessels. If now, the operator passes his finger through this incision, his finger will enter the posterior mediastinum. The assistant is asked to pull the stomach down when the tense anterior trunk will be seen lying on the anterior surface of the oesophagus. About 5 to 7 cm of both these trunks are excised and remaining ends are tied with fine silk. The ligature pyloroplasty is made to avoid bleeding from the ascending oesophageal ves­ sels, which run up along with the nerves. The most important operative complication is gastric retention for which drainage operation is performed along with this operation. This operation is probably contraindicated to patients already suffering from severe diarrhoea. The reason may be a few intact vagal fi­ bres, which may be detected by Holland­ er’s insulin test and in this case reoperation should be performed to com­ plete vagotomy. One must keep in mind the possibility of Zollinger-Ellison syndrome in these cases. The hepatic branches of the anterior vagus are identified in the upper part of the lesser omentum. The dissection is started along with the anterior vagus nerve in the lesser omentum downwards to find out all the gastric branches which are ligated and divided one by one. Now for posterior selective vagotomy, an incision is made through the peritoneum at the angle of His. Right index finger is passed through the hole to reach behind the gullet and the right thumb is passed through the hole made in the lesser omentum. These two fingers will meet behind the oesophagus and will only be intervened by the so-called ‘mesentery’ in which will be lying the posterior vagal trunk. The tissues behind the posterior vagus nerve are burst through and a tube is inserted to include the gullet and the vagi. With the right index finger, the posterior trunk is pushed posteriorly and tissues in front of the finger are very minutely dissected to secure the gastric branches of the posterior vagus nerve. The last part of the oesophagus is now thoroughly exposed to clear any additional fibres, which may be left behind. The whole circumference of the cardia is examined and all residual vagal branches are divided, leaving behind a ring of bare muscles. These nerves are preserved and separated from the proximal gastric branches by passing forceps through the lesser omentum to the left of the nerve of Latarjet close to the gastric wall about 3 inches (7. It is very convenient to save the posterior nerve of Latarjet through the lesser sac, which is entered through the greater omentum at the middle part of the greater curvature. The proximal gastric branches are dissected, ligated and divided and the main nerve, which supplies the antrum and pylorus, is preserved. In this operation posterior truncal vagotomy is being performed alongwith anterior lesser curve seromyotomy. A few surgeons are performing seromyotomy in both anterior and posterior aspects of the lesser curve. The advantage of this operation is that the disturbance to the neighbouring structures is least and it can be performed by minimal access procedure also.

If the duct or the mouth of the sebaceous gland becomes blocked , the gland becomes distended with its own secretion and forms a sebaceous cyst . The characteristic feature here is — that the cysts are multiple and when well formed they feel solid . There is no sebaceous gland in the palm or sole , so sebaceous cyst is never seen in these areas . The surface is smooth and there is a bluish or blackish spot or punctum which indicates the blocked opening of the duct . Due to presence of sebum there may be indentation due to pressure with finger tip . If the cyst is a big one , fluctuation test may be positive otherwise it is difficult to perform . Note that punctum cannot structures and it can be be seen which is a common finding of a sebaceous cyst of the scalp . If the cyst is infected, preliminary antibiotic treatment should be given and the excision is only possible when the infection has subsided. It must be remembered that the whole of the cyst wall must be removed, otherwise recurrence is inevitable. Such dissection method is particularly applicable when the cyst was infected previously since this will make the cyst wall well defined and thick. The cyst wall is then held with a pair of dissecting forceps and the cyst is carefully avulsed out. If the infection subsides, excision of the cyst should be carried out as mentioned above. If infection does not subside with antibiotic treatment, it should be incised and the pus and semiliquid foetid material are expelled. When the sebaceous cyst of the scalp ulcerated, excessive granulation tissue forms resembling fungating epithelioma. The most important two processes which play part are abnormal reproduction and abnormal differentiation. A few definitions should be clearly understood in respect of tumours — Metaplasia. Examples of squamous metaplasia are that simple columnar epithelium of gallbladder in chronic cholecystitis especially if accompanied by stones may be converted to squamous epithelium which is a precancerous condition. Similarly transitional epithelium of renal pelvis and bladder in chronic infection particularly with presence of stones may be converted to squamous epithelium. Columnar metaplasia is relatively uncommon and is sometimes seen in cervical erosion when squamous epithelium of ectocervix is replaced by a simple columnar epithelium. The alternative term dysplasia may also be used for such an abnormal development of tissue. Dyscrasia literally means a bad mixture and is now used only by haematologists to describe any blood disorder of uncertain aetiology. Teratomatous dermoid is one type of these tumours which may be seen in the ovary, testis, superior mediastinum, retroperitoneum and in the presacral area. The excessive accumulation of cells produces an expanding lesion which causes atrophy of the surrounding tissues which form a capsule around such tumour. The arrangement of the cells closely resembles that of the parent tissue — well differentiated. In nutshell the characteristics of benign tumours are — (i) These tumours are well circumscribed and possess capsules. The tumour edge is therefore ill-defined in contrast to the well-defined encapsulated margin of benign tumours. The characteristic features of malignant tumours are — (i) Invasiveness as mentioned earlier. This type of tumour is characterized by failure of cells to differentiate normally. A comparison of the main features of benign and malignant tumours are given below:— Benign Malignant 1. Malignant tumours show more tendency tendency towards haemorrhage and towards haemorrhage and ulceration due ulceration. The microscopic changes represent an early morphological indication that a carcinoma or any malignant tumour is beginning to develop. Examples of this condition is mostly seen in the epithelium particularly in the stratified squamous epithelium of the skin, mouth and cervix. It is often said that these tumours are probably show growing and that is why remain dormant for a considerable period of time until they are provoked by trauma or intercurrent illness or a change in hormonal balance e. This incidence falls to 70% between the ages of 80 to 90 years and 25% in patients of 50 to 60 years. These lesions are latent, many presumably remain so until death occurs from another cause. Cigarette smoking is often held responsible for cancer of the lung, but it has got nothing to do with malignant melanoma or cancer of the breast. The various agents which may be responsible for cancers in the body are described below. Sir Percival Pott observed that cancer of the skin is more common in men who worked with tar and suggested it to be the causal agent. A hydrocarbon benzpyrene was isolated from tar and showed that it had a high degree of carcinogenic activity. It was considered that 1:2: 5:6- dibenzanthracene is the main component which is responsible to cause cancer. To be more precise 1:2- benzanthracene has practically no carcinogenic effect, but the attachment of a new benzene ring in the 5 : 6 position gives it great carcinogenic power. It was found that cholanthrene and methyl cholanthrene are among the most powerful carcinogenic agents known. Both methyl cholanthrene and benzpyrene contain 1:2- benzanthracene ring system, though this ring is almost completely lacking in carcinogenic activity. The carcinogenic property of azocompounds first came to light as a result of investigation into the action of scarlet red, an azodye as a stimulant of wound healing. This acts at a distance and only on the liver, the main organ of metabolism in the body. However its carcinogenic action on the liver is manifested only when there is deficiency in riboflavin. Another well known example is the aniline dye cancer of the urinary bladder, in which the carcinogen is beta naphthylamine. This tumour not only occurs in aniline dye workers, but also can be readily induced in the dog. Oestrogen does not act on the skin, but it acts on the mammary epithelium which is normally under the influence of ovarian stimulation. Though it is said that when the supply is constant and prolonged cancer may result, yet it seems that oestrogens require co-operation of one or more additional agencies. In the prostate there seems to be little doubt that an endocrine dysfunction is an aetiologic factor. The serum acid phosphatase and urinary 17-ketosteroid levels are elevated which are indicators of androgen secretion as well. The remarkable beneficial effects of castration and administration of oestrogen on prostatic cancers also signify this. The early workers in the X-ray department suffered radiation dermatitis followed by cancer of the skin of the hand after many years. Osteosarcoma has been reported in bones subjected to radiation for bone cyst and giant-cell tumour. Cancer of the thyroid has also developed long time after irradiation of the neck for some other reason. Later on in 1936 Bittner found that when new bom mice of a high mammary cancer strain were fostered by mothers of a low cancer strain, the tumour incidence was greatly reduced. On the other hand new bom mice of a low strain when fostered by mothers of a high strain showed an increased incidence of breast cancer. A match may start a fire, but the material must be inflammable; a little damp or high breeze may extinguish the flame. The various factors which probably help carcinogens to form cancers are — (i) Heredity. It cannot be denied that injury may cause cell destruction followed by regeneration and this may serve as a promoter where an initiating carcinogen has already produced a condition of latent cancer. It has been noticed that those people with a high incidence of cancer in the liver, the diet is very low in vitamine. At the end it must be confessed that though very little is known about this subject yet it deserves mention. Cancer of the liver is a rare disease in most countries, though it is very common in Java and South Africa. Whereas carcinoma of stomach is so common in Japan, but carcinoma of breast is not so frequent there. Infiltration into the surrounding tissues is a salient feature of all malignant tumours. The invading cells come across various natural passages, which then afford an easy route for the malignant cells for further spread. The most important structures involved in this way are the lymphatics and blood vessels. If these cells survive and multiply, a distinct mass of tumour is produced at this distant site. This means that the microscopic extent of a malignant tumour is more than its microscopic extent. The cancer cells are free because of greatly reduced adhesiveness, which in turn seems to be due to deficiency of calcium in the cell membrane. The cells of benign tumours are incapable of movement as they are firmly adherent to one another by cell adhesiveness. It has been suggested that invasiveness of cancer cells is due to hyaluronidase which these cells produce. Hyaluronidase breaks down resistance of the viscid ground substance which contains hyaluronic acid. The invading cancer cells tend to follow natural clefts or tissue planes and gradually move in the line of least resistance. Dense fascial sheaths may form barriers which confine malignant cells for sometimes. This is a well known fact in case of osteosarcoma where periosteum resists cancer cells to invade surrounding soft tissues for quite sometime. Carcinoma cells readily enter lymphatics and pass through lymphatics by either permeation or embolism. The tumour cells grow progressively within the lumen of the lymphatics as a solid cord. Sometimes the central area of the malignant cord may undergo necrosis and even disappear, while the advancing ends proliferate. Eventually the cord of cells reaches the draining lymph nodes by blocking the main ducts, the lymph is diverted to adjacent channels and in this way there may be retrograde deviation of tumour cells. Through this lymphatic permeation, the entire skin of the chest wall may be a sheet of confluent carcinoma, producing cancer-en-cuirasse. The cancer cells stimulate perilymphatic fibrosis, but this does not stop advancement of lymphatic permeation. In malignant melanoma black spots are seen along the track of lymphatics which are nothing but intermediate deposits left by lymphatic permeation in its way from the primary growth towards the regional lymph nodes. Such lymphatic permeation is seen to advance through the peribroncheal and periarterial lymphatics in bronchogenic carcinoma and through the perineural lymphatics in carcinoma of the prostate. The regional and distant lymph nodes are early involved by the process of lymphatic embolism. In case of lymph nodes, the metastases are at first confined to the subcapsular space. Direct spread from node to node is not seen usually as the capsule of the lymph node is not penetrated till late stage. All the lymph from the abdominal organs reach the thoracic duct, which finally opens into the left jugular vein. Moreover, familiar involvement of the supraclavicular lymph nodes is due to tumour emboli lodging behind the valves near the termination of the duct, thus blocking the duct. Sometimes the entire length of the thoracic duct is filled with tumour, the obstruction leading to chylothorax and chylous ascites. Though less importance is given to the posterior or dorsal spinal lymph path by which tumour cells may pass up or down for considerable distances, this may explain the upward passage of tumour cells from the prostate and downward passage of cancer cells from the breast. At this site the emboli become impacted, proliferate and develop into secondary tumour. It is difficult to assess how much blood spread is due to primary venous invasion and how much is secondary to lymphatic involvement. In case of sarcoma, there is no doubt that invasion is primarily venous, as lymphatic spread is quite uncommon. In case of carcinomata blood spread occurs sometime after lymphatic involvement and it is quite possible that much of the blood stream invasion is secondary to lymphatic spread. Four groups of veins may be invaded : (i) The systemic veins are frequently invaded by sarcoma as also by carcinoma. In case of the latter there is a tendency for the tumour to grow as a solid column along the lumen of the vein. Similarly the testicular tumours, particularly the teratomas, distend the spermatic vein by tumour permeation. Thus the tumour cells reach the left side of the heart from where they are distributed to the systemic circulation.

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