By A. Yorik. American InterContinental University. 2019.
Clinical Features Biliary colic ensues when a stone obstructs the cystic duct buy discount wellbutrin sr 150 mg on-line, causing sudden distension of the gallbladder buy wellbutrin sr cheap. Its duration is seldom shorter than 15 minutes and is often sufficiently severe for many sufferers to seek medical attention and to require narcotics for relief wellbutrin sr 150mg. Although biliary-type pain can follow a large meal purchase wellbutrin sr toronto, the old adage fatty food intolerance is not specific for biliary tract disease. The patient is usually restless, and First Principles of Gastroenterology and Hepatology A. Fever and rigors are absent when they cystic duct is obstructed and there is no inflammation. Such presence of fever and rigors suggest that a stone has migrated and become lodged in the cystic duct, causing cholangitis, or that the gallbladder is acutely inflamed (acute cholelithiasis). Findings consist of mild-to-moderate right upper quadrant or epigastric tenderness. Once gallstones are complicated by an attack of biliary pain, a recurrent pattern is likely to ensue, days or weeks apart. Symptomatic gallstones have a more aggressive course than those that are asymptomatic. Although 30% of patients with one episode of biliary pain do not have further episodes, most experience a recurrent pattern that remains fairly constant. These episodes may be sporadic separated by pain-free periods lasting from days to years, during which the patient feels well and the liver biochemistry is normal. However, complications requiring surgery may arise at any time, with a frequency of 1 to 2% per year. Pain lasting more than six to 12 hours, especially if accompanied by persistent vomiting or fever, suggests another process such as cholecystitis or pancreatitis (Table 4). Diagnostic Imaging Detecting gallstones (as opposed to diagnosing clinically symptomatic gallstone disease) is by diagnostic imaging. Plain abdominal x-rays will only identify the 10-15% with high calcium content as radiopaque densities in the right upper quadrant. Ultrasonography is the most sensitive and specific method for detecting gallstones (appearing as echogenic objects that cast an acoustic shadow) or a thickened gallbladder wall (indicating inflammation). Also, if the gallbladder is fibrotic and shrunken, ultrasound may not visualize the gallbladder. Although most episodes of biliary colic resolve spontaneously, pain eventually recurs in 20-40% each year. Because of recurrent attacks of pain and these increased risks, cholecystectomy is indicated once biliary colic develops. The risk of any emergency procedure is greater then elective surgery, so this is why elective cholecystectomy is recommended. Open cholecystectomy The term open connotes the need for an incision to open the abdominal cavity for direct visualization in the course of removing the gallbladder. Open cholecystectomy is usually necessary in Mirizzis syndrome, an infrequent complication in which large gallstones compress First Principles of Gastroenterology and Hepatology A. In addition to the obvious cosmetic appeal, these smaller incisions result in less postoperative pain and shortened recovery time, allowing an early discharge from hospital (sometimes the same day as an outpatient) and return to work. The disadvantages include a somewhat higher complication rate, particularly from common duct injury and retained common duct stones, plus the potential for overuse. In 5% of cases the procedure must be converted to an open cholecystectomy because of technical problems. Laparoscopic cholecystectomy is now the standard for elective removal of the gallbladder in those with significant symptoms (e. Prophylactic cholecystectomy is not warranted in those with asymptomatic stones except for rare cases suspected of developing/ harboring carcinoma of the gallbladder (e. Chronic Calculous Cholecystitis Chronic inflammation of the gallbladder is the most common histological process, often manifest as mild fibrosis of the gallbladder wall with a round cell infiltration and an intact mucosa. Some degree of chronic inflammation inevitably accompanies gallstones, but the stones will have developed first. Even transient obstruction of the cystic duct can produce biliary colic and an element of inflammation that is chemical in origin. There is little correlation between the severity and frequency of such biliary episodes and the degree of inflammation or fibrosis. Chronic inflammation thus may follow the resolution of acute cholecystitis, evolve with recurrent episodes of biliary colic or develop insidiously. It is the presence of true biliary colic which drives the indication for cholecystectomy, not the possible presence of chronic cholecystitis. Clinical Features The clinical features are those of either biliary colic or a previous episode of acute cholecystitis that has resolved leaving the gallbladder chronically inflamed and scarred. The pain characteristically is a constant dull ache in the right upper quadrant or epigastrium, and sometimes also in the right shoulder or back. Flatulence, fatty food intolerance and dyspepsia occur, but are equally frequent in patients without gallstone disease. There may be local tenderness in the right upper quadrant of the abdomen but no peritoneal findings. If the gallbladder is fibrotic and shrunken, ultrasound visualization may be difficult. A nuclear medicine cholescintigraphy scan may be positive with the gallbladder failing to fill, but non-visualization is rather insensitive for chronic cholecystitis, because of frequent false positive and false negative tests. Medical management depends upon gallstone size, gallbladder function and any co-morbid conditions (e. Cholecystectomy provides definitive treatment, removing the stones and the gallbladder, and eliminating recurrences of true biliary pain. Obstruction of the cystic duct results in the gallbladder becoming distended with bile plus an inflammatory exudate or even pus. If resolution occurs, the mucosal surface heals and the wall becomes scarred, but the gallbladder may not function e. In a minority, acute cholecystitis can occur in the absence of obvious stones (acalculous cholecystitis). Although acalculous cholecystitis can occur in healthy individuals, it tends to affect elderly men who have co-existent vascular disease, debilitated individuals and even young children. Its location is usually the right upper quadrant or epigastrium, sometimes radiating to the back or the right shoulder. Pain in acute cholecystitis, unlike biliary colic, persists for more than six to 12 hours. As the gallbladder becomes inflamed, the visceral pain is replaced by parietal pain, which First Principles of Gastroenterology and Hepatology A. Abdominal examination characteristically shows tenderness in the right upper quadrant. During palpation of the right upper quadrant, a deep breath may worsen the pain and inspiration suddenly ceases (Murphys sign). An enlarged gallbladder is sometimes palpable, particularly with the first attack before fibrosis contracts it. Clinical Jaundice with mild hyperbilirubinemia (<2x normal) and elevated liver enzymes occur in about 20% of cases, even in the absence of common duct stones. Cholestasis can develop from either a concomitant bile duct stone, or a distended gallbladder that compresses the common duct (Mirizzis Syndrome). Markedly elevated bilirubin levels suggest that a stone resides in the common duct. High levels of aminotransferase or alkaline phosphatase imply a common bile duct stone. A elevated amylase or lipase indicates gallstone pancreatitis from a bile duct stone that has recently been present; but most times (80%)the stone will have already passed on its own. The clinically suspected diagnosis of acute cholecystitis is best confirmed by ultrasound, which detects the stone(s) and a thickened gallbladder wall. In doing the procedure, the radiologist may elicit marked tenderness when pressing over the gallbladder (the ultrasonographic Murphys sign). Non-visualization also can occur in chronic cholecystitis due to failure to concentrate and in cholestasis because of impaired marker secretion.
Shaffer 608 Diagnostic test Possible findings in big duct Findings in small duct disease disease Formatted: Justified purchase wellbutrin sr 150mg mastercard, Indent: Endoscopic o Abnormal (>4 features of o May be abnormal Left: 0 order 150 mg wellbutrin sr overnight delivery. As yet there are no specific medical therapies capable of reducing or reversing the pancreatic inflammation purchase cheap wellbutrin sr. Depending on the severity of the attack best wellbutrin sr 150mg, an indwelling urinary catheter and close monitoring of urinary output may be necessary. Analgesics such as meperidine should be administered Formatted: Highlight regularly during the first several days of the attack. This may alleviate the pain, decrease the patients apprehension and improve respiration, thus preventing pulmonary complications such as atelectasis. The risk of narcotic addiction is minimal during the first days; most patients settle within 72 hours. The patient is kept off oral feeding; nasogastric suctioning is maintained only if if the disease is severe and complicated by intractable vomiting and ileus. The rationale behind nasogastric suctioning is to place the pancreas at rest by removing the acidic gastric juices. Similarly, the use of acid-suppressive medications such as cimetidine has failed to show benefit in the treatment of acute pancreatitis. The use of enzyme inhibitors such as soy- bean trypsin inhibitor to prevent further damage is controversial, as is the use of prostaglandins and corticosteroids. The routine administration of antibiotics does not improve the course of mild to moderate disease. However, when the development of pancreatic abscess is suspected from an increase in fever and abdominal pain, antibiotic therapy should be instituted. The use of prophylactic antibiotics in the setting of necrotizing pancreatitis is controversial. Shaffer 609 Respiratory insufficiency may occur in up to 40% of the cases, usually in patients with severe or recurrent pancreatitis. Peritoneal lavage has been advocated in patients with severe disease, such as those with marked hypovolemia or hypotension or those who continue to deteriorate despite appropriate medical therapy. Although this technique reduces the circulatory and renal complications, it does not seem to alter the local complications. Intravenous hyperalimentation has been advocated in patients who contin- ue to have pain and whose symptoms are aggravated postprandially. Several studies have documented equally effective results with nasoenteric alimentation. If during a trial of six weeks or longer, complications develop (such as an abscess or an enlargement of phlegmon), a surgical debridement may be warranted, albeit as a last resort. Several studies have documented equally effective results with enteral alimentation. These changes include fibrosis, ductal abnormality, calcification and cellular atrophy. Repeated attacks of gallstone- related pancreatitis rarely if ever result in chronic pancreatitis. This may explain These cases may explain some of the cases of idiopathic or familial pancreatitis. Alcohol presumably causes pancreatic injury by the intraductal formation of protein plugs secondary to increased protein concentration and precipitation, with or without calcification. These plugs lead to obstruction and secondary pancreatic damage caused by autodigestion. In developed countries chronic pancreatitis occurs after a long history (6 to 17 years) of alcohol ingestion of 150 to 170 g per day. Alcoholic pancreatitis is known to occur with much less consumption of alcohol, as low as 50 g per day. The mean age of a patient with new onset of disease is around 32 years, with a male predominance. Despite heavy drinking only a small number opercentage of alcoholics develop chronic pancreatitis, suggesting other factors that potentiate the injurious side effects of alcohol, including. Potential cofactors include smoking (very high association with alcohol pancreatitis and may be independent risk factor)itis, high- protein diet with either very high or very low fat content, genetic mutations, and type of alcohol/manner of ingestion. Formatted: Indent: First line: 0", Line spacing: single Table 8: Causes of Chronic Pancreatitis Formatted: Bullets and Duct obstruction Numbering o Benign pancreatic duct obstruction Traumatic stricture Stricture after severe acute pancreatitis Duodenal wall cyst Pancreas divisum First Principles of Gastroenterology and Hepatology A. Sleisenger & Fordtrans gastrointestinal and liver disease: Pathophysiology/Diagnosis/Management 2006: page 1274. The pain is localized to the upper abdomen, with radiation to subcostal regions and to the back. When more than 90% of exocrine pancreatic function is lost, maldigestion and malabsorption ensue. This is manifested by steatorrhea (fat malabsorption) associated with diarrhea and bloating, azotorrhea (protein malabsorption) and progressive weight loss. These patients frequently present with loss of adipose tissue, judged by hanging skin folds, and more objectively by demonstrating that the skin fold at the mid-triceps is less then 8 mm in males Formatted: Highlight and less than 12 mm in females. In addition, they manifest muscle wasting and edema, indicating protein deficiency. Latent fat-soluble vitamin deficiency (vitamins A, D, E and K) in addition to deficiencies of magnesium, calcium and essential fatty acids may occur and are closely related to dysfunction of fat digestion. Endocrine insufficiency presenting as diabetes mellitus may present at the same time as exocrine insufficiency or years a few years later. One exceptional presentation is that of autoimmune pancreatitis, which, although a cause of chronic pancreatitis, can initially present as painless jaundice mimicking pancreatic cancer. The pseudocyst is usually surrounded by a non-epithelial-lined fibrous wall of granulation tissues. When a pseudocyst is present for less than six weeks, it is considered acute; after that it becomes chronic. The pseudocyst may be asymptomatic or may present as an acute exacerbation of pancreatitis, with abdominal pain, nausea, vomiting and weight loss. These pseudocysts may obstruct intra-abdominal viscera, cause pancreatic ascites, rupture into viscera or the abdominal cavity, hemorrhage or become infected. Spontaneous resolu- tion occurs in 20% of the cases within the first six weeks of the pseudocysts development. Asymptomatic patients with persistent pseudocysts should be observed and intervention may be considered if symptoms appear. The catheter may be required for up to six weeks and is frequently associated with infections. Surgical drainage is sometimes necessary for failed percutaneous drainage or for complicated pseudocysts. It presents with gradually increasing massive ascites, with high levels of amylase, abdominal pain and weight loss. Painful areas of subcutaneous fat necrosis result from the high levels of circulating pancreatic lipase. Transverse sonogram showing a cystic septated well-defined mass in the pancreatic tail. As the distal common bile duct traverses the head of the pancreas, it may be narrowed secondary to inflammation, with edema or fibrosis of the gland. Similarly, inflammation can Formatted: Font: Italic result in splenic vein thrombosis, which in extreme cases can lead to left sided portal Formatted: Indent: First line: hypertension and gastric variceal bleeding. Sleisenger & Fordtrans gastrointestinal and liver disease: Pathophysiology/Diagnosis/Management 2006: pg. The diagnosis of chronic pancreatitis is straightforward in patients with advanced pancreatic disease. This can be demonstrated by the presence of calcification seen exclusively in the ductal system on plain radiographic abdominal films, by ultrasonography or on computerized tomography. The rHowever, radiologic evidence may be seenis only seen in up to 30% of patients with chronic pancreatitis. Problems of interpretation may arise in these patients, particularly in older adults or alcoholics whose senile or fibrotic changes may be misinterpreted as a reflection of underlying chronic pancreatitis. The only pancreatic function tests that appear to accurately measure pancreatic function in chronic pancreatitis are the direct tube tests that measure the response of the pancreas to various stimuli. The commonest manifestation is a decreased bicarbonate concentration (< 50 mEq/L) and decreased volume of secretion.
The frequency of diarrhea or colitis does not appear to be related to dose or route of administration of the First Principles of Gastroenterology and Hepatology A purchase wellbutrin sr overnight. Symptoms can occur while the patient is on the antibiotic generic wellbutrin sr 150mg line, or within six weeks following its discontinuation purchase wellbutrin sr 150 mg. The diarrhea can be devastating cheap 150mg wellbutrin sr otc, with up to 30 bowel movements in a 24-hour period. The diarrhea may be associated with varying degrees of abdominal pain and low-grade fever. Depending on the severity of the diarrhea and the amount of fluid loss, hypotension, shock and even death have been reported. In many patients the problem is self-limiting and resolves spontaneously with discontinuation of the antibiotic. In recent years, a number of newly recognized and apparently more virulent strains of C. The presence of copious amounts of mucus and typical raised white pseudomembrane plaques which are not washed away are characteristic features seen on sigmoidoscopy. Colonoscopy is recommended, because the plaques may be seen in the right colon beyond the reach of the sigmoidscope, and the diagnosis would be otherwise missed. If it is certain that there is no other likely cause for the diarrhea, treatment can be undertaken while awaiting assay results, although it is usually possible to quickly obtain a sigmoidoscopy to demonstrate the pseudomembranes. If symptoms are resolving with discontinuance of the antibiotic, no further therapy may be indicated. Vancomycin is poorly absorbed and central nervous system and renal toxic effects are uncommon. The high cost of this medication limits its use, even though the eradication rate of the C. It must be stressed that the vancomycin must be given orally, and not systematically. If oral therapy cannot be used, as with severe ileus or recent surgery, parenteral metronidazole is used. Cholestyramine (Questran) binds the toxin and can provide symptomatic relief even though it will not eliminate the microorganism. In extreme cases of fulminant non- responsive disease, colectomy, may be necessary. Magnesium-Containing Antacids The osmotically-induced diarrhea produced by Mg2+ is usually mild. A change to a magnesium-free, aluminum-containing antacid is all that is required to control the diarrhea. The use of magnesium-containing antacids is a common cause of diarrhea in dyspeptic patients. Magnesium can be used to induce diarrhea by rare patient with the Mnchausen syndrome who seek medical attention for self-induced problems. Antiarrhythmic Drugs The antiarrhythmic drugs most commonly associated with diarrhea include quinidine, procainamide and disopyramide. Other Medications Colchicine, often administered for acute gout, produces diarrhea as a common side effect. The mechanism of the diarrhea is unknown, but may relate to an intestinal cytotoxic effect of colchicine. Chronic Diarrhea Mechanisms There are at least four basic mechanisms that cause chronic diarrhea, including osmotic, secretory and exudative factors, and abnormal intestinal transit (Table 12). If the diarrhea ceases when fasting, then an osmotic cause for the diarrhea is suspected. A significant osmotic gap in the stool water may be present but, under normal clinical circumstances, this is not measured. Examples include diarrhea after ingesting milk (and resulting from lactase deficiency), taking drugs such as magnesium- containing antacids, or the excessive use of artificial sweeteners (eg. If the patients diarrhea persists when fasting (such as may occur at nighttime when the diarrhea awakens the person from sleep), a secretory diarrhea is likely. Secretory diarrhea usually arises from infection or inflammation associated with toxigenic and invasive bacteria. Secretory diarrhea may also result from the spillage of excess bile acids into the colon (choleretic enteropathy) or from the cathartic effect of hydroxy fatty acids arising from the colonic bacterial action on malabsorbed fat (or fermented carbohydrate substrates). Very rarely, secretory diarrhea can arise from a tumor producing an intestinal secretagogue (e. Scleroderma leads to bacterial overgrowth and steatorrhea (as can the rapid transit in hyperthyroidism). The mechanism of diarrhea in these conditions relates to a combination of bacterial overgrowth, bile salt wastage and disorders of motility (slow or rapid intestinal transit). Osmotic Diarrhea Retention of solute molecules within the bowel lumen generates osmotic forces that retard the normal absorption of water and even act to draw water from the circulation into the intestinal lumen (Table 13). Practical examples and may include poorly absorbed carbohydrates, or poorly absorbed divalent ions (e. Since the pores through which ions are absorbed are highly charged, these polyvalent ions tend to be absorbed slowly. Thus, they accumulate within the intestinal lumen, raise the osmolality, and diarrhea results. Shaffer 223 Some carbohydrates are poorly absorbed by everybody; for example, was developed to be a nonhydrolyzable, nonabsorbable disaccharide that would act as a cathartic. This common condition normally develops after weaning in the majority of African-, Caribbean- or Asian-Canadians, and also occurs in about a third of persons with southern European ancestry. Since carbohydrates are not inert in the colon, their metabolism leads to further osmotic forces. Osmotic diarrhea should stop when the patient stops ingesting the poorly absorbed solute. As the extent of carbohydrate malabsorption increases, more short-chain fatty acids are formed than can be reabsorbed. This results in diarrhea due to the presence of osmotically active short-chain fatty acids. The stool pH consequently begins to fall, which further decreases colonic salvage. In persons with osmotically-induced dirrhea, there will be a detectable positive osmotic + + gap that is, stool osmolality minus stool Na plus stool K times 2 (multiplied by 2 to account for anions) is greater than 50, the size of the osmotic gap being approximately equivalent to the concentration of poorly absorbed solutes in fecal water. Secretory Diarrhea The small intestine normally secretes as well as absorbs fluid and electrolytes. Normally the secretion rate is lower than the absorption rate, and the net effect is absorption of fluid. For clinical purposes, it is best to consider inhibition of ion absorption and stimulation of ion secretion together (Table 14). Shaffer 225 Secretion is also stimulated experimentally by paracrine hormones, luminal factors (e. Diarrhea secondary to prostaglandin-stimulated intestinal secretion is a common side effect of orally administered prostaglandin analogues (misoprostil). The intestinal distention that occurs with obstruction or ileus also produces a local secretory state in the bowel proximal to the obstruction. The mechanism may be related to changes in permeability (as tight junctions are stretched and broken) and perhaps direct neural stimulation of secretory mechanisms. With more extensive resections (>100 cm) there will be both steatorrhea and bile salt wastage, and treatment must be focused on the steatorrhea as long as the loss of electolytes and water doesnt lead to severe depletion, in which case intravenous fluid replacement may be necessary. These forms of small intestinal motility control the rate at which material travels along the intestine, and hence arrives at the anus. Gastrointestinal motor activity also determines the time and degree of contact between food, the digestive enzymes, and the absorptive epithelium. Accelerated transit of material through the gut produces diarrhea by limiting the time available for digestion and absorption. It extends over a 4 cm length of distal small intestine, and produces a high pressure zone of about 20 mm/Hg. Distention of the ileum results in a decrease in the ileocecal sphincter pressure, whereas distention of the colon results in an increased pressure in this area. The ileocecal valve slows down intestinal transit (ileal break), and also prevents backwash or regurgitation of contents from the colon. Surgical removal of the ileocecal valve results in rapid intestinal transit as well as the potential for bacterial overgrowth from colonic fecal backwash.