Archive by category 'Tip of the Day'
April 23rd, 2007
Peptic Ulcer Disease – Part 8
Type 2 gastric ulcers are found in the body of the stomach in association with a duodenal ulcer. They comprise about 25% of peptic ulcers and are associated with acid hypersecretion. The surgical treatment (if the ulcer is too big for a simple wedge resection) for this type of ulcer that has not responded to medical treatment is antrectomy (removal of the stomach that contains the ulcer) with truncal vagotomy and either a Billroth 1 or Billroth 2 reconstruction.
Copyright 2007 InsideSurgery.com
April 12th, 2007
Peptic Ulcer Disease – Part 7
Peptic ulcers can either be duodenal ulcers or gastric (stomach) ulcers. There are four types of gastric ulcers. Type 1 gastric ulcers occur on the lesser curvature of the stomach where the inner oblique muscle of the stomach is absent. This point is usually at or close to the incisura and is marked by the junction of the antral and parietal mucosa. Type 1 gastric ulcers usually have normal acid secretion.
There are several options for surgical resection of this ulcer if it is refractory (does not respond to) medical treatment. The most definitive is a Billroth I resection. Some surgeons feel it is not necessary to do a truncal vagotomy (cutting the vagus nerve as it enters the abdominal cavity on either side of the esophagus) as it does not confer added benefit. The recurrence rate with this procedure is around 3%.
A second surgical option is to perform a wedge resection of the ulcer with a parietal cell vagotomy (i.e., highly selective vagotomy) that spars the vagus nerve running to the antrum and pylorus of the stomach. This procedure is associated with a higher recurrence rate and can be technically difficult to perform.
Copyright 2007 InsideSurgery.com
April 11th, 2007
Peptic Ulcer Disease – Part 6
Duodenal ulcers usually occur in the first part of the duodenum and have a minimal risk of malignancy as compared to gastric (stomach) ulcers. Although they are usually biopsied on EGD, excision of these ulcers if uncomplicated (i.e., not associated with bleeding, obstruction, or perforation) is not performed. Biopsy will often show gastric metaplasia. These ulcers are associated with acid hypersecretion.
Copyright 2007 InsideSurgery.com
April 10th, 2007
Peptic Ulcer Disease – Part 5
One rare cause of peptic and gastric ulcers is Zollinger-Ellison syndrome, which usually results from an islet tumor in the pancreas. This condition should be suspected in patients with recurrent ulcers after adequate treatment, the presence of multiple ulcers, ulcers that have produced complications such as bleeding and obstruction, and ulcers in unusual locations such as the second and third parts of the duodenum. The best screening test for Zollinger-Ellison syndrome is a fasting serum gastrin level.
Copyright 2007 InsideSurgery.com
April 8th, 2007
Peptic Ulcer Disease – Part 4
There are several tests used to diagnose peptic ulcer disease and to differentiate this condition from other causes. Typically the first imaging test a patient with a complaint of epigastric (the area on the abdominal wall just below the sternum) or right upper quadrant pain receives is an ultrasound of the upper abdomen. This is a quick, cheap, noninvasive test that will pick up the signs of cholecystitis (inflammation of the gallbladder). These signs include cholelithiasis (presence of gallstones in the gallbladder), gallbladder sludge (self-explanatory), pericholecystic fluid (fluid around the gallbladder), gallbladder wall thickening, choledocholithiasis (gallstones in the common bile duct), and dilated common and hepatic bile ducts.
If the ultrasound is negative, the next test usually obtained is a computed tomography (CT scan) with intravenous and oral contrast. This test is good at picking up intraabdominal masses that might be causing pain but is not particularly good at picking up ulcer disease.
If the ultrasound and CT scan are negative, the patient is usually offered esophagogastroduodenoscopy (EGD). This is both more sensitive and specific than contrast examination (Upper GI test) and provides for direct visualization of the stomach and duodenum through placement of a lighted, flexible scope through the mouth and into the stomach. During EGD tissue biopsies are always obtained to check for the presence of H. pylori and to rule out the presence of malignancy in gastric ulcers.
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Copyright 2007 InsideSurgery.com
April 7th, 2007
Peptic Ulcer Disease – Part 3
Infection with the bacterium Helicobacter pylori is associated with 90% of duodenal ulcers and 75% of gastric ulcers. There are several methods used to diagnose the presence of H. pylori. Blood can be tested for for the serum immunoglobulin for H. pylori, although the test can be positive in previous H pylori infections that have been adequately treated.
The labeled urea breath test is a noninvasive test that will show eradication of the bacterium. The cod liver oil (CLO) test is the test used on tissue obtained from endoscopy and biopsy of the ulcer. This is a rapid urease test that produces relatively rapid results and is inexpensive to perform once the tissue has been biopsied.
Copyright 2007 InsideSurgery.com
April 1st, 2007
Peptic Ulcer Disease – Part 2
There are several conditions that are risk factors for the development of peptic ulcer disease (PUD). These include cigarette smoking and the use of nonsteroidal antiinflammatory drugs. It is not clear if significant alcohol intake contributes to ulcerogenesis. Diet and caffeine intake do not appear to be important.
Symptoms of peptic ulcer disease include burning or or chronic, intermittent gnawing epigastric pain (abdominal pain just below the sternum). If the ulcer is in the duodenum ingestion of food sometimes will alleviate the discomfort. if the ulcer is in the stomach (gastric) ingestion of food may worsen the symptoms.
The differential diagnosis of peptic ulcer disease includes reflux esophagitis (GERD), pancreatitis (inflammation of the pancreas), acute cholecystitis, and gastric (stomach) cancer.
Copyright 2007 Insidesurgery.com
March 31st, 2007
Peptic Ulcer Disease – Part 1
Peptic ulcer disease (PUD) is the formation of ulcers the lining and wall of the stomach and duodenum. The understanding and treatment of PUD has changed considerably in the last two decades. Previously the etiology of these conditions was thought to be one of acid hypersecretion of the stomach and the mainstay of treatment was surgery, with often radical resections (removal of tissue) being performed.
It is now known that the bacterium Helicobacter pylori plays a causative role in the development of most peptic ulcers. With the development of easy-to-take antibiotic regimens and the use of proton pump inhibitors (e.g., esmeprazole) and H2 blockers (e.g., ranitidine), the need for surgery to treat PUD is quite low and usually reserved for the complications of neglected peptic ulcer disease (perforation, bleeding, gastric outlet obstruction).
Copyright 2007 InsideSurgery.com
January 14th, 2007
Cellcept (Mycophenolate Mofetil) – Part 3
Cellcept can be used in both adults and children. It can be administered either orally (by mouth) or intravenously (by vein). It is given twice a day and the dose is usually adjusted frequently in the beginning of treatment with the aim of a stable dosing regimen. Generally the dose for cardiac (heart) and hepatic (liver) transplants is higher than that for renal (kidney) transplants.
Generally, Cellcept is not as well tolerated in elderly patients as in younger patients. The elderly are at a higher risk of developing liver, kidney, and heart problems. They are also at risk of developing infections, gastrointestinal bleeding (bleeding from the bowel), and pulmonary edema (fluid overload of the lungs causing breathing difficulty).
Cellcept is not removed by hemodialysis or peritoneal dialysis and supplemental dosing for patients receiving it while on dialysis is not necessary.
Copyright 2007 Insidesurgery.com
January 13th, 2007
Cellcept (Mycophenolate Mofetil) – Part 2
The active chemical compound in Cellcept is mycophenolic acid (MPA). MPA is a very strong inhibitor (stops the action) of the molecule inosine monophosphate dehydrogenase (IMPDH). This inhibition is reversible in the sense that when Cellcept is discontinued the IMPDH molecule again functions. Blocking the function of IMPDH blocks the formation of T- and B-cell lymphocytes, which are two cell types that figure prominently in the body rejecting organs.
The bioavailability of MPA is higher with use of mycophenolate mofetil (80% – 94%) as compared with enteric coated mycophenolate sodium (70%). MPA is highly bound by the blood protein albumin (97% – 99%). It is metabolised to a molecule MPA-glucoronide (MPAG) in the body by uridine diphosphate gluconosyltransferases (UGTs). Although MPAG builds up to levels 20 times that of MPA it is not pharmacologically active in the body.
Copyright 2007 Insidesurgery.com
January 12th, 2007
Cellcept (Mycophenolate Mofetil) – Part 1
Mycophenolate is an immunosuppressant drug that is sold under the brand names of Cellcept and Myfortic. It is approved for use by the FDA to suppress the immune system in patients who have received kidney, heart, or liver transplants. There are several diseases that is prescribed for that are considered “off-label.” These conditions include vasculitis, minimal change disease, linear IgA disease, and myasthenia gravis.
Mycophenolate is classified as an antimetabolite immunosuppression drug. There are two compounds commercially availabe that contain mycophenolate – mycophenolate mofetil and enteric-coated mycophenolate sodium. Both of these compounds are hydrolysed (broken down) by the liver, wall of the gut, and blood cells to mycophenolic acid, which is the active compound.
Copyright 2007 Insidesurgery.com
January 11th, 2007
Cirrhosis and Variceal Bleeding – Part 5
It is important to note that octreotide used in treating variceal bleeding has effects on other hormones such as insulin, vasoactive intestinal peptide, and growth hormone. Side effects of octreotide include nausea, diarrhea, vomiting, constipation, stomach upset, gas, bloating, dizziness, headache, lightheadedness, fatigue, flushing, and dry mouth. Pain and irritation have been reported at the injection site.
Copyright 2007 Insidesurgery.com
January 10th, 2007
Cirrhosis and Variceal Bleeding – Part 4
Endoscopic therapy (placing a scope down the esophagus) is a mainstay of invasive treatment for bleeding varices. There are two therapeutic options available with endoscopy – sclerotherapy and ligation (”tying off” the vein). Octreotide in combination with sclerotherapy has been shown to be superior to sclerotherapy alone in that it decreases the incidence of early rebleeding. a similar effect is observed when octreotide is used in combination with variceal ligation.
In addition, octreotide reduces the bleeding and aids in better visualization of the varices during endoscopy when used prior to the procedure. Most hepatologists (liver specialists) recommend continuing it for at least 24 to 48 hours after endoscopy to reduce the risk of rebleeding.
Copyright 2007 Insidesurgery.com
January 9th, 2007
Cirrhosis and Variceal Bleeding – Part 3
Octreotide is a drug used to treat bleeding varices. It is a long-acting synthetic analogue (similar chemical structure) of somatostatin. An intravenous injection of 50-mcgs/hour has been shown to cause significant decrease in portal pressure. The effect of a single-dose of octreotide on reducing portal pressure is effective but short-lived (the half-life is three hours in patients with liver disease), thus requiring a continuous administration.
Copyright 2007 Insidesurgery.com
January 8th, 2007
Cirrhosis and Variceal Bleeding – Part 2
Various treatments have been used over the years for treating varices (enlarged veins). Previously, vasopression and terlipressin, which directly constrict the mesenteric arterioles and reduce the portal venous flow, were used in medical management of bleeding varices. However, these drugs are falling out of favor somewhat due to their ischemic effects on the heart, brain, bowel, and limbs.
Currently, more commonly used drugs in the medical management of variceal bleeds include somatostatin and octreotide. These drugs inhibit the release of vasodilator hormones such as glucagon and indirectly cause splanchnic vasocontriction (contriction of the blood vessels in the bowel).
Copyright 2007 Insidesurgery.com
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