30: Stomach Flashcards
What might be necessary to treat a Mallory-Weiss tear that will not stop bleeding despite EGD with hemo-clips?
Gastrostomy and over-sewing of the vessel
[If EGD with hemo-clips is not successful in stopping the bleeding, gastrostomy and oversewing the vessel may be neccessary.]
[SCORE: Initial management includes volume resuscitation, gastric lavage, and nasogastric decompression. Most patients with Mallory-Weiss tears stop bleeding spontaneously either before treatment or after these early measures. Once bleeding has stopped, rebleeding is rare. Nonoperative management consisting of endoscopic electrocoagulation or injection therapy has been successfully applied to these lesions. Esophageal balloon tamponade is contraindicated because it can convert a partial thickness tear into a full-thickness esophageal laceration. In cases not amenable to endoscopic therapy, operative management consists of oversewing the laceration through an anterior longitudinal gastrotomy in the middle third of the stomach. The mortality rate in recent series has been between 5% and 10%; deaths were related to associated disease, most notably cirrhosis.]
Epigastric pain radiating to the back that abates with eating but recurs 30 minutes after is typical for what?
Gastric or duodenal ulcer
[Healthline.com: Gastric ulcer symptoms are more likely to be felt immediately after eating. Duodenal ulcers are more likely to be felt a few hours after eating.]
[Medscape: Epigastric pain is the most common symptom of both gastric and duodenal ulcers. It is characterized by a gnawing or burning sensation and occurs after meals—classically, shortly after meals with gastric ulcer and 2-3 hours afterward with duodenal ulcer. Food or antacids relieve the pain of duodenal ulcers but provide minimal relief of gastric ulcer pain.
Duodenal ulcer pain often awakens the patient at night. About 50-80% of patients with duodenal ulcers experience nightly pain, as opposed to only 30-40% of patients with gastric ulcers and 20-40% of patients with nonulcer dyspepsia (NUD). Pain typically follows a daily pattern specific to the patient. Pain with radiation to the back is suggestive of a posterior penetrating gastric ulcer complicated by pancreatitis.]
[UpToDate: Upper abdominal pain or discomfort is the most prominent symptom in patients with peptic ulcers. Approximately 80% of patients with endoscopically diagnosed ulcers have epigastric pain. Occasionally the discomfort localizes to the right or left upper quadrants of the hypochondrium. Radiation of pain to the back may occur, but back pain as the primary symptom is atypical. In untreated patients, symptoms can last a few weeks followed by symptom-free periods of weeks or months. The “classic” pain of duodenal ulcers occurs two to five hours after a meal when acid is secreted in the absence of a food buffer and at night (between about 11 PM and 2 AM) when the circadian stimulation of acid secretion is maximal.
Patients with peptic ulcers, and particularly pyloric channel ulcers, may have food-provoked symptoms due to visceral sensitization and gastroduodenal dysmotility. These symptoms include epigastric pain that worsens with eating, postprandial belching and epigastric fullness, early satiety, fatty food intolerance, nausea, and occasional vomiting.
Approximately 70% of peptic ulcers are asymptomatic. Patients with silent peptic ulcers may later present with ulcer related complications. Between 43% and 87% of patients with bleeding peptic ulcers present without antecedent dyspepsia or other heralding gastrointestinal symptoms. Older adults and individuals on nonsteroidal anti-inflammatory drugs (NSAIDs) are more likely to be asymptomatic and later present with ulcer complications.]
Should a cholecystectomy be performed during bariatric surgery (Roux-en Y approach)?
If stones are present
[UpToDate: Cholelithiasis is a common complication of any type of weight loss surgery. In the Teen-LABS study, cholecystectomy was required within three years in 8.6% of patients (9.9% for RYGB and 5.1% for sleeve gastrectomy). An additional 5% of participants required other abdominal operations, including lysis of adhesions, gastrostomy, or ventral or internal hernia repair.]
Which condition is characterized by bile reflux into the stomach, combined with histologic evidence of gastritis?
Alkaline (bile) reflux gastritis
[UpToDate: Reflux of bile into the stomach is common after operations that remove or bypass the pylorus. In most patients there are no serious clinical sequelae. However, approximately 2% of patients develop alkaline reflux gastritis, a syndrome of persistent burning epigastric pain and chronic nausea that is aggravated by meals. The diagnosis is made primarily by excluding other causes of symptoms, although endoscopy may reveal gastritis, and technetium biliary scan can demonstrate excessive reflux of bile into the stomach.]
What is the surgical treatment for chronic gastric atony causing symptoms of delayed gastric emptying (nausea, vomiting pain, early satiety)?
Near-total gastrectomy with Roux-en Y
[UpToDate: Surgery is rarely indicated in patients with gastroparesis. Indications for surgery include placement of an enterostomy tube (eg, gastrostomy, jejunostomy) that cannot be placed endoscopically and completion or subtotal gastrectomy to relieve refractory nausea and vomiting in patients with a partial gastrectomy.
Surgical pyloroplasty and gastrojejunostomy have also been performed to treat refractory gastroparesis. As an example, in one series that included 28 patients with gastroparesis, pyloroplasty was associated with an improvement in symptoms, gastric emptying, and a reduction in the need for prokinetics at three months. However, long-term studies are needed before they can be recommended.]
How do you diagnose duodenal ulcers?
Endoscopy
[UpToDate: The diagnosis of peptic ulcer disease is suspected in patients with dyspepsia, especially in the setting of nonsteroidal anti-inflammatory drug (NSAID) use or a history of Helicobacter pylori infection. While contrast imaging is not needed to diagnose peptic ulcer disease, if performed, it may be supportive of the diagnosis. The diagnosis of peptic ulcer disease is definitively established by direct visualization of the ulcer on upper endoscopy. However, the need to pursue a definitive diagnosis in patients who have undergone contrast imaging depends upon the clinical setting. In patients with benign-appearing duodenal ulcers identified on radiologic imaging and no alarm features, endoscopy is not required to establish the diagnosis. In contrast, all patients diagnosed with gastric ulceration on radiologic imaging should undergo an upper endoscopy. However, the timing of the upper endoscopy may be deferred to 12 weeks after therapy in the absence of alarm features.
On upper endoscopy, benign gastric and duodenal ulcers have smooth, regular, rounded edges, with a flat, smooth ulcer base often filled with exudate. Endoscopy is the most accurate diagnostic test for peptic ulcer disease. The sensitivity of upper endoscopy in the detection of gastroduodenal lesions is approximately 90% but varies based on the location of the ulcer and the experience of the endoscopist.]
Why is Roux-en-Y gastro-jejunostomy the best method of reconstruction following antrectomy?
Less dumping syndrome and reflux gastritis compared to Billroth I (gastro-duodenal anastamosis) and Billroth II (Gastro-jejunal anastamosis)
[UpToDate: The choice of reconstruction following antrectomy for ulcer disease or distal gastrectomy for tumor depends upon the remnant anatomy available for reconstruction, taking into consideration the complications related to the specific postgastrectomy physiology that will result. However, based upon randomized trials, Roux-en-Y reconstruction appears to be tolerated better overall and leads to a better quality of life compared with Billroth reconstruction (Billroth I or Billroth II). Whether to preferentially perform a Roux-en-Y in patients whose anatomy supports a Billroth I or Billroth II, or convert to a Roux-en-Y only if complications occur remains controversial. For patients who have not undergone vagotomy, we suggest a primary Roux-en-Y reconstruction. Patients who have had a vagotomy have an increased risk of roux stasis syndrome.
A metaanalysis of 15 randomized trials comparing at least two of the gastric reconstruction techniques (ie, Billroth I, Billroth II, or Roux-en-Y reconstruction) following gastrectomy assessed postoperative morbidity and mortality, quality of life, and the incidence of postgastrectomy syndromes. Although complication rates were similar, patients with a Roux reconstruction had fewer complaints of reflux gastritis and better quality of life. A later trial also confirmed this finding.
The longest follow-up comparing techniques was reported for a trial that has followed 75 patients treated for duodenal ulcer for 12 to 21 years. Patients were randomly assigned to Billroth II (n = 39) or Roux-en-Y (n = 36) reconstruction between 1984 and 1993. Patients who received a Roux-en-Y reconstruction had overall better clinical outcomes with a significantly lower incidence of reflux esophagitis (3% vs 33%), fewer abnormal findings on upper endoscopy of the distal esophagus and esophagogastric junction (10% vs 82%), and a lower incidence of Barrett’s esophagus (3% vs 21%). The gastric remnant was also normal in significantly more Roux-en-Y patients (100% vs 18%). There were no differences between the groups in the incidence of Helicobacter pylori infection. It is interesting to note that the Roux limb in these patients was arbitrarily chosen to be 60 cm. Although the authors were concerned about the potential for the “Roux syndrome”, it was not clinically apparent in their series.]
What are the surgical options for treating alkaline reflux gastritis?
Conversion of Billroth I or Billroth II to Roux-en Y gastrojejunostomy with afferent limb 60 cm distal to gastrojejunostomy
[UpToDate: A variety of medical therapies for alkaline gastritis have been reported, but none have proven particularly effective. Surgical therapies aim at separating the remnant stomach from duodenal content by interposing a loop of jejunum between them. Examples include Roux-en-Y reconstruction (with a 45-60 cm Roux loop), Henley loop (interposition of a 40 cm isoperistaltic jejunal loop between the gastric remnant and the duodenum), Billroth II reconstruction with Braun enteroenterostomy (positioned 45 to 60 cm from the gastrojejunal anastomosis). The reoperative procedure is chosen based upon a patient’s existing anatomy and how much remnant stomach is left.]
What is Virchow’s node?
A lymph node in the left supraclavicular fossa that takes its supply from lymph vessels in the abdominal cavity. An enlarged, hard node (referred to as Troisier’s sign) is strongly indicative of the presence of cancer in the abdomen, specifically gastric cancer, that has spread through the lymph vessels.
[UpToDate: Supraclavicular lymphadenopathy is associated with a high risk of malignancy. In two studies, malignancy was found in 34% and 50% of patients with this presentation; the risk was highest in those over the age of 40. Right supraclavicular adenopathy is associated with cancer in the mediastinum, lungs, or esophagus. Left supraclavicular adenopathy (“Virchow’s node”) suggests abdominal malignancy (eg, stomach, gallbladder, pancreas, kidneys, testicles, ovaries, or prostate).]
What are 4 symptoms of afferent-loop obstruction in patients with Billroth II or Roux-en Y?
- RUQ pain
- Steatorrhea
- Nonbilious vomiting
- Pain relieved with bilious emesis
[UpToDate: Afferent and efferent loop syndromes develop after Billroth II reconstruction with a gastrojejunostomy. They are related to mechanical obstruction of the two loops by kinking, anastomotic narrowing, adhesions, or, rarely, anastomotic ulceration.
The afferent loop refers to the duodenojejunal loop proximal to the gastrojejunal anastomosis. Most afferent loop syndromes can be prevented if the distance from the ligament of Treitz to the gastrojejunostomy is no more than 12 to 15 cm. A patient with an acute afferent loop obstruction presents with acute onset of severe abdominal pain and vomiting, which requires immediate operation to prevent bowel necrosis or duodenal blowout. Chronic afferent loop syndrome is typically associated with postprandial epigastric pain and intermittent projectile bilious vomiting which leads to resolution of the pain for a period of up to several days. In patients suspected of having afferent loop syndrome based upon symptoms (eg, intermittent projectile bilious vomiting), the detection of a distended afferent loop on abdominal computed tomography is diagnostic.]
What inhibits gastrin production?
H+ in the duodenum
[Somatostatin also inhibits the release of gastrin, along with secretin, GIP (gastroinhibitory peptide), VIP (vasoactive intestinal peptide), glucagon and calcitonin.]
[UpToDate: Gastrin is released from specialized endocrine cells (G cells) into the circulation in response to a meal. The specific components of a meal that stimulate gastrin release include protein, peptides, and amino acids. Gastrin release is profoundly influenced by the pH of the stomach; fasting and increased gastric acid in the stomach inhibit its release, whereas a high gastric pH provides a strong stimulus for its secretion. The G cells are tightly regulated by two counterbalancing hormones, gastrin-releasing peptide and somatostatin, which exert stimulatory and inhibitory effects, respectively.]
What is the surgical treatment for blind-loop syndrome following a Billroth II or a Roux-en Y?
Re-anastomosis with shorter (40-cm) afferent limb
What must be ruled out in patients with complicated ulcer disease?
Gastrinoma
[Zollinger-Ellison syndrome: Gastric acid hyper secretion, peptic ulcers, and gastrinoma]
[UpToDate: Other causes of peptic ulcer disease should be considered when H. pylori and use of NSAIDs have been excluded (eg, gastrinoma in patients with multiple simultaneous ulcers, or those in unusual locations [second portion of the duodenum and into the proximal jejunum]).
In patients with gastric ulcers without a clear etiology, we perform an upper endoscopy 12 weeks after initiating medical therapy (with biopsies of the ulcer if still present). This upper endoscopy allows for additional biopsies of the ulcer to exclude neoplastic, infiltrative, or infectious causes of ulceration.]
What is the treatment for efferent-loop obstruction in patients with Billroth II or Roux-en Y?
Balloon dilation
[Surgical option is to find the site of obstruction and relieve it]
[UpToDate: The efferent loop refers to the jejunal segment distal to the gastrojejunostomy that drains sulcus entericus away from the stomach. Obstruction of the efferent loop causes gastric outlet obstruction manifested by symptoms of epigastric pain, distension, and bilious vomiting. When diagnosed by either computed tomography or upper gastrointestinal series, surgical correction is the treatment of choice for efferent loop syndrome.]
Which type of gastric cancer has a less favorable prognosis?
Diffuse gastric cancer
[25% 5-year survival]
[UpToDate: Diffuse type cancers are highly metastatic and characterized by rapid disease progression and a poorer prognosis than intestinal cancers. Diffuse carcinomas also have a greater tendency to invade the gastric wall, sometimes extending to the lower esophagus or to the duodenum. Occasionally, a broad region of the gastric wall or even the entire stomach is extensively infiltrated, resulting in a rigid thickened stomach, termed “linitis plastica”.
Histologically, individual tumor cells are seen to invade the surrounding tissues, and there is no gland formation. When intracellular mucin is abundant, it pushes aside the nucleus of the individual cells, resulting in the so-called signet ring carcinoma. It has long been thought that signet ring histology is an independent predictor of a worse prognosis as compared to other forms of gastric cancer. However, more recent studies have begun to question this notion. Some studies suggest that signet ring histology is associated with more advanced stage of disease at presentation, and that when adjusted for stage, signet ring cancer does not portend a worse prognosis.]
Where is the vagus nerve divided in a truncal vagotomy?
Both the left and right vagal nerve trunks are divided at the level of the diaphragmatic hiatus
[This decelerates gastric emptying of solids. Proximal vagotomy divides individual fibers and does not affect emptying of solids.]
[UpToDate: Truncal vagotomy is the simplest procedure to perform. Basal and stimulated acid secretions are reduced by 80% and 50%, respectively. However, truncal vagotomy sacrifices innervation to the pancreas, small intestine, proximal colon, and hepatobiliary tree, and alters gastric physiology requiring some form of gastric emptying procedure (pyloroplasty or gastroenterostomy). Highly selective vagotomy reduces basal and stimulated acid secretion by more than 75% and 50%, respectively, while minimizing the effects of vagotomy on gastric emptying. However, surgeons-in-training have less exposure to the more technically demanding procedures, like highly selective vagotomy (parietal cell vagotomy), because of the decrease in the hospitalization rate for peptic ulcer disease.]
Does central obesity have a better or worse prognosis in the general population?
Worse
[UpToDate: Both overall obesity, defined by BMI, and abdominal obesity or central obesity (assessed by measuring waist circumference, waist-to-hip ratio [WHR], or waist/height ratio), are associated with an excess risk of CVD. The WHR is infrequently used by clinicians and is not currently recommended as part of the routine obesity evaluation by the American Heart Association/American College of Cardiology/Obesity Society guideline, although it was in the previous version.
Data from the Third National Health and Nutrition Examination Survey (NHANES III) suggest that normal-weight central obesity (normal BMI with increased WHR) is associated with higher mortality than BMI-defined mortality, particularly when compared to individuals without central obesity. In a cross-sectional survey of over 15,000 individuals, men with a normal BMI (18.5 to 24.9 kg/m2) but central obesity (WHR ≥0.90) had the highest total mortality risk when compared to men without central obesity who were normal weight, overweight (25 to 29.9 kg/m2), or obese (≥30 kg/m2) (HR 1.87, 2.24, and 2.42, respectively). Normal weight women with central obesity (WHR ≥0.85) also had higher mortality risk compared to normal weight and obese women without central obesity (HR 1.48 and 1.32, respectively). A limitation of the study is that central obesity was determined by WHR only; no quantitative imaging studies of adipose tissue were performed. These data suggest that normal weight individuals with central obesity appear to have an increased mortality risk and should be targeted for lifestyle modification strategies.]
Is metastatic disease outside the area of resection a contraindication to resection of gastric cancer?
Yes
[Unless performing surgery for palliation]
[UpToDate: The only widely accepted criteria of unresectability for gastric cancer are the presence of distant metastases, invasion of a major vascular structure, such as the aorta, or disease encasement or occlusion of the hepatic artery or celiac axis/proximal splenic artery. Distal splenic artery involvement is not an indicator of unresectability; the vessel can be resected en bloc with a left upper quadrant exenteration: stomach, spleen, and distal pancreas.
The lymphatics around the stomach are rich, and the presence of locoregional lymph node metastases that are located geographically distant from the tumor (eg, celiac nodes with a primary tumor on the greater curvature of the stomach) should not necessarily be considered an indicator of unresectability. However:
- Patients who have bulky adenopathy fixed to the pancreatic head that might indicate the need for a Whipple procedure are at a high risk for occult metastatic disease. In these cases, it is probably best to consider staging laparoscopy or upfront chemotherapy rather than surgery initially. Performance of a Whipple for gastric cancer is an extremely rare occurrence.
- Lymph nodes behind or inferior to the pancreas, aorto-caval region, into the mediastinum, or in the porta hepatis are typically considered outside of the surgical field and thus evidence of unresectability. These nodes would fall into areas that would be defined as third or fourth echelon nodes in the Japanese nomenclature.
Since resection of the primary lesion also offers the most effective means of symptom palliation, exploration may also be considered in patients with known metastatic disease, if the severity of symptoms so dictates. The choice of operation for gastric cancer depends upon the location of the tumor within the stomach, the clinical stage, and the histologic type. The major surgical considerations include the extent of stomach resection (total versus partial gastrectomy) and the extent of lymph node dissection.]
What is the most common cause of leak following bariatric surgery (Roux-en Y approach)?
Ischemia
[UpToDate: The anastomotic leak remains the most dreaded technical complication of bariatric surgery, and is one of the most challenging complications of weight-loss surgery. The risk of a leak ranges from 0.8% to 6% depending on procedures chosen as well as technical and patient factors involved. As examples:
- A metaanalysis of 4888 patients who underwent laparoscopic sleeve gastrectomy revealed a leak rate of 2.4%. Body mass index (BMI) greater than 50 kg/m2 and using a bougie smaller than 40 French were the factors associated with increased leak rate.
- A retrospective analysis of 4444 patients in the longitudinal assessment of bariatric surgery (LABS) database revealed an anastomotic leak rate of 1.0% after RYGB (both open and laparoscopic). Open surgery, revision surgery, and routine drain placement were associated with an increased leak rate.
In revisional bariatric surgery, the risk of anastomotic leak approaches 35%.
Most leaks after bariatric surgery occur early, generally within the first week after surgery. Many post-sleeve-gastrectomy leaks can occur after patient discharge. Therefore, vigilant follow up during the first 30 days is recommended for that group of patients.
The clinical presentation of an anastomotic leak is subtle and requires vigilance for signs such as low-grade fevers, respiratory compromise, and/or unexplained sustained tachycardia greater than 120 bpm. These signs may also be present in the setting of pulmonary embolism.]
What is usually required to remove a trichobezoar (hairball)?
Gastrostomy and removal
[EGD generally inadequate]
[UpToDate: Therapy for gastric bezoars should be tailored to the composition of the concretion and to the underlying pathophysiologic process. In patients with pharmacobezoars, the toxicity of the underlying ingested pharmaceutical agent must be considered as decontamination may be required.
While the optimal strategy is controversial in the absence of studies comparing different modalities, for patients with mild symptoms due to bezoars, we initially attempt chemical dissolution. We use prokinetic metoclopramide as adjuvant therapy. For patients with bezoars that fail to dissolve or are resistant to chemical dissolution (trichobezoars), and patients with moderate to severe symptoms due to large bezoars, we suggest endoscopic therapy. We reserve surgery for selected patients with gastric bezoars if chemical dissolution and endoscopic fragmentation cannot be performed or fail and for patients with complications (eg, obstruction, significant bleeding).]
What are the 4 main symptoms of blind loop syndrome (small intestine bacterial overgrowth)?
- Pain
- Steatorrhea (due to bacterial deconjugation of bile)
- B12 deficiency (bacteria use it up)
- Malabsorption
[UpToDate: The majority of patients with small intestinal bacterial overgrowth (SIBO) present with nonspecific symptoms of bloating, flatulence, or abdominal discomfort, or they may be asymptomatic. Many patients diagnosed with severe SIBO have diarrhea. Although classic SIBO descriptions include steatorrhea with greasy or bulky stools, this is uncommon and occurs principally if the SIBO is caused by altered anatomy such as blind loop syndrome. Rarely, patients have weight loss due to severe diarrhea, malabsorption, or poor oral intake. Although diarrhea is a common symptom in children, they may present with chronic abdominal pain alone. Children may also have evidence of malnutrition and may fail to gain weight. Patients with hypoalbuminemia due to malabsorption may have peripheral edema on physical examination. Rarely, patients with SIBO may also present with symptoms and signs secondary to vitamin deficiencies. It is important to assess for these in subjects with severely altered anatomy causing SIBO, severe immunodeficiencies, or tropical sprue.]
What is the overall 5-year survival rate for gastric lymphomas?
50%
[UpToDate: GI diffuse large B cell lymphoma (DLBCL) includes lesions previously called “high-grade” MALT lymphoma. It can occur anywhere along the GI tract and is the most common histology for primary gastric lymphoma, representing approximately 50% of cases. Compared with patients with low-grade lymphoma, these patients tend to have more systemic symptoms, a more advanced stage at diagnosis, and a worse prognosis. In one series of 114 patients, for example, those with DLBCL had lower rates of complete remission (68% vs 92%) and five-year overall survival (46% vs 75%) when compared with those with low-grade MALT lymphoma.]
What is the effect of a truncal vagotomy on post-prandial bile flow?
Decreases post-prandial bile flow
[NCBI: The exocrine pancreatic and biliary secretion in response to vagal stimulation by insulin hypoglycemia was measured in preoperative patients with duodenal ulcer and in patients who underwent highly selective vagotomy, bilateral selective vagotomy with pyloroplasty, and truncal vagotomy with pyloroplasty. Significant stimulation of both biliary and pancreatic secretion occurred only in patients with an intact vagal nerve supply.]
What are the primary treatment modalities for gastric lymphoma?
Chemotherapy and XRT
[Surgery for complications: Only possibly indicated for stage I disease where the tumor is confined to the stomach mucosa - only partial resection is indicated]
[SCORE: When gastric lymphoma is first diagnosed by endoscopic means, evidence of systemic disease should be sought. Computed tomography of the chest and abdomen to detect lymphadenopathy, lymphangiography, bone marrow biopsy, and biopsy of enlarged peripheral lymph nodes may be appropriate. A multimodality program is used in most centers to manage primary gastric lymphomas. Gastrectomy is the first step in the therapeutic strategy. Increasing numbers of patients are treated with chemoradiation therapy alone. The risk of hemorrhage or perforation frequently alluded to in the past has probably been overstated. The risk of perforation if primary gastric lymphoma is managed with cytolytic agents and not resected approximates 5%.]
[UpToDate: Primary gastrointestinal (GI) non-Hodgkin lymphoma (NHL) is a heterogeneous group of B and T cell lymphoid malignancies. The management of these lymphomas may differ from lymphomas of lymph node origin.
For most patients with GI diffuse large B cell lymphoma (DLBCL), we recommend the use of combination chemotherapy plus immunotherapy (eg, R-CHOP) such as that used for other patients with DLBCL with or without involved-field RT rather than treatment with surgery or H pylori eradication therapy (Grade 1B).
For patients with enteropathy-associated T cell intestinal lymphoma who have a good performance status and chemotherapy sensitive disease, we suggest treatment with intensive chemotherapy followed by autologous HCT rather than chemotherapy alone.]
The Celiac trunk branches into which three arteries?
- Left Gastric Artery
- Common Hepatic Artery
- Splenic Artery
What is the effect of a proximal vagotomy on gastric emptying of solids?
No effect
[Normal emptying of solids]
[SCORE: Truncal and proximal gastric vagotomy abolish receptive relaxation. After vagotomy, an increased gastroduodenal pressure gradient occurs and correlates with accelerated liquid emptying. Emptying of solids usually is not greatly altered by proximal gastric vagotomy.]
[UpToDate: By preserving the main vagal nerve branches leading to the pylorus, this procedure preserves gastric emptying postoperatively and avoids the need for a drainage procedure such as pyloroplasty or additional anastomosis (gastrojejunostomy) in an acutely inflamed and contaminated field.]
What is the advantage of the Roux-en Y gastric bypass compared to other weight-loss procedures?
Better weight loss than just banding
[UpToDate: Roux-en-Y gastric bypass (RYGB) creates a small (less than 30 mL) proximal gastric pouch that is divided and separated from the distal stomach and anastomosed to a roux-limb of small bowel 75 to 150 cm in length. The surgery has been the most commonly performed bariatric procedure in the United States until recently, but now accounts for less than 30% of procedures in adults and adolescents.
The long-term outcomes for weight loss and comorbidity improvement are well established for RYGB, based on more than 25 years of experience with this procedure in adults. In addition, it has particularly dramatic benefits on glycemic control, which may offer some advantage for patients with type 2 diabetes. On the other hand, there are probably more risks for nutritional deficiencies compared with SG. In particular, iron sufficiency and long-term outcomes for bone health after RYGB are not well studied.]
What is the description of a type III gastric ulcer?
Pre-pyloric ulcer
[Similar to duodenal ulcer with high acid secretion]
[SCORE: Type I ulcers are not associated with acid secretion and are located on the lesser curvature of the stomach. Type II and III ulcers are associated with acid hypersecretion; the former is located on the lesser curvature in synchrony with duodenal ulcers, and the latter occurs in the prepyloric region. Type IV ulcers are found in the cardia near the gastroesophageal junction and are not associated with acid secretion. Type V ulcers are diffuse and associated with NSAID use. Initial management includes endoscopy to control bleeding, but initial biopsies are not recommended, as they may aggravate the bleeding ulcer. Should endoscopic attempts be unsuccessful, surgery may be warranted based on the location of the ulcer. Ulcers at the lesser curvature are usually best treated with wedge resection. Type II and III ulcers usually require Bilroth I reconstruction and truncal vagotomy. Ulcers near the GE junction pose a difficult challenge and may require a distal gastrectomy with Roux-en-Y reconstruction, known as the Csendes procedure.]
[UpToDate: Type III ulcers are prepyloric, although no precise anatomic definition exists. They occur in the setting of increased acid secretion and are approached in a manner similar to duodenal ulcer and type II gastric ulcer. Early surgical referral is advised for resistant ulcers or those that present with obstructive symptoms.
Curiously, highly selective vagotomy (as well as medical therapy with H2 receptor antagonists) has been associated with poor results in type III gastric ulcer, with high recurrence rates ranging from 16% to 44% reported in various series. This finding, plus the observation that these ulcers may harbor an occult gastric malignancy, makes antrectomy and vagotomy the most prudent approach.]
What is the most accurate test for H. Pylori?
Histologic examination of biopsies from the antrum
[The most accurate method for detecting H. pylori infection is with a histological examination from two sites after endoscopic biopsy, combined with either a rapid urease test or microbial culture. This is invasive, however, so the best test may actually by testing for IgG.]
[UpToDate: In patients who do not require endoscopic evaluation for evaluation of new onset dyspepsia (those under age 55 who do not have alarm symptoms), initial diagnosis of H. pylori should be made with a test for active infection (stool antigen or urea breath test). Serology, as it cannot differentiate between past or current infection and has a low positive predictive value in much of the United States, is not recommended in patients with a low pre-test probability.
Endoscopic biopsy should be reserved for patients who are undergoing a diagnostic endoscopy and are found to have an ulcer and for those who require endoscopy to follow up a gastric ulcer or for the diagnosis or follow-up of suspected MALT lymphoma. Biopsy urease testing can be performed in patients not taking antibiotics or a proton pump inhibitor when histopathology is not required.
We suggest confirmation of eradication because of the availability of accurate, relatively inexpensive, noninvasive tests (stool and breath tests) and because of increased resistance to antibiotic therapy, at least four weeks after treatment (Grade 2B).]
How is a leak diagnosed after bariatric surgery (Roux-en Y approach)?
UGI
[UpToDate: A leak may be radiographically confirmed by barium swallow or contrast computed tomography (CT). Several studies of patients undergoing upper GI series on postoperative day one show a 3% leak rate. Whether postoperative upper gastrointestinal series should be ordered routinely or selectively remains controversial. We routinely perform an upper GI series on all our patients on postoperative day one. In the rare event that a leak is present, we can address this quickly and avoid any delay.]
What is the major risk factor for development of afferent-loop obstruction in patients with Billroth II or Roux-en Y?
Long afferent limb
What is the treatment for a patient with liver failure who has an upper GI bleed that is likely from esophageal varices rather than an ulcer?
EGD with variceal bands or sclerotherapy
[TIPS if this fails]
[UpToDate: For patients with small varices with red signs and/or Child B or C cirrhosis and for all patients with medium or large varices, we recommend prophylactic treatment rather than expectant management (Grade 1B). For patients with Child A cirrhosis who have small varices without red signs, we suggest expectant management with routine upper endoscopy to monitor for the development of red signs or for variceal enlargement (Grade 2C).
In patients with small varices with red signs and/or Child B or C cirrhosis, we suggest treatment with a nonselective beta blocker rather than esophageal variceal ligation (EVL) (Grade 2C). Studies have shown that treatment of patients with small varices with nonselective beta blockers reduces the likelihood of progression to large varices and decreases the probability of a first variceal hemorrhage. Data are lacking regarding the use of EVL for primary prophylaxis in patients with small varices. However, treatment with variceal ligation is a reasonable alternative if the patient does not tolerate/has a contraindication to therapy with a beta blocker, in patients with refractory ascites, or if there is variceal enlargement despite treatment with a beta blocker.
In patients with medium varices, we suggest treatment with either a nonselective beta blocker or EVL (Grade 2B). Both treatments have been shown to be effective in such patients. The choice of a nonselective beta blocker or EVL depends upon whether the patient can tolerate a nonselective beta blocker, whether a provider with expertise in EVL is available, and whether the patient is willing to accept the risks of EVL and undergo the multiple endoscopic procedures that are required.
In patients with large varices, we suggest treatment with EVL rather than a nonselective beta blocker (Grade 2C). Some data suggest EVL may be more effective than beta blockers in patients with large varices. Treatment with a nonselective beta blocker is a reasonable alternative in patients who are unwilling to accept the risks of EVL or undergo multiple endoscopic procedures for treatment or if a provider experienced in EVL is not available.
For patients being treated with nonselective beta blockers, we typically use nadolol (since it can be given once daily), starting with a dose of 40 mg per day. We then titrate the dose based upon the patient’s hemodynamic response.]
How does gastric cancer respond to chemotherapy?
Poor response
[UpToDate: The majority of patients with esophageal or gastric cancer will require palliative treatment at some point in the course of their disease. Cytotoxic chemotherapy can provide symptom palliation, improve quality of life, and prolong survival in patients with advanced esophageal or gastric cancer.
First-line chemotherapy — Goals of chemotherapy include palliation of symptoms, improvement in quality of life, and prolongation of survival. Performance status, comorbidity, patient preference, symptom burden, and histologic type are key considerations when choosing the therapeutic approach.
We prefer enrollment in a clinical trial, if available. If trials are unavailable or patients are ineligible, our general approach to first-line chemotherapy for metastatic esophagogastric cancer is presented in the algorithm.
Despite a large number of randomized trials, there is no consensus as to the best agent or regimen. In general, combination chemotherapy regimens provide higher response rates than do single agents, but this translates into only modestly longer durations of disease control and survival that are measured in weeks to a few months.
Patients with advanced gastric or esophageal adenocarcinoma who are potential candidates for trastuzumab should have their tumors assayed for the presence of HER2 overexpression utilizing tumor-specific criteria and/or gene amplification. Assaying HER2 expression on six to eight viable biopsies are ideal for evaluating HER2 status. We suggest the addition of trastuzumab to chemotherapy in patients with HER2-positive tumors (as defined by 3+ immunohistochemical [IHC] staining or fluorescence in situ hybridization [FISH] positivity), as long as they do not have a contraindication to trastuzumab (Grade 2B).
The optimal chemotherapy backbone for patients receiving trastuzumab is not established. Acceptable options include cisplatin plus fluorouracil (FU), cisplatin plus capecitabine, oxaliplatin plus leucovorin and short-term infusional FU (FOLFOX), or oxaliplatin plus capecitabine (XELOX/CAPOX).]
What is the most frequent complication of duodenal ulcers?
Bleeding
What is the first step after resuscitation (if necessary) in managing a patient with upper GI bleeding ?
Early endoscopy
[Confirms bleeding is from an ulcer etc. and can potentially treat bleeding with hemo-clips, epi injection, or cautery]
[UpToDate: Upper endoscopy is the diagnostic modality of choice for acute upper GI bleeding. Endoscopy has a high sensitivity and specificity for locating and identifying bleeding lesions in the upper GI tract. In addition, once a bleeding lesion has been identified, therapeutic endoscopy can achieve acute hemostasis and prevent recurrent bleeding in most patients. Early endoscopy (within 24 hours) is recommended for most patients with acute upper GI bleeding, though whether early endoscopy affects outcomes and resource utilization is unsettled.]
What is the most common problem patients have following vagotomy?
Diarrhea (40%)
[Caused by sustained migrating motor complex, forcing bile acids into the colon]
[UpToDate: Postoperative complications of vagotomy include ulcer recurrence due to missed or incomplete vagotomy, as well as delayed gastric emptying. Although procedures such as highly selective vagotomy were designed to prevent delayed gastric emptying, while circumventing the need for a drainage procedure, 0.5% of patients who undergo highly selective vagotomy will develop gastric retention and require the addition of a drainage procedure several months after the initial operation. Two other long-term complications of vagotomy and drainage procedures are dumping syndrome and postvagotomy diarrhea. Dumping syndrome comprises a constellation of symptoms that occur within 30 minutes of a meal, including fullness, pain, nausea, cramps, and diarrhea. Some patients describe vasomotor signs and symptoms such as diaphoresis, lightheadedness, hypotension, tachycardia, flushing, and headache. The etiology of this syndrome is thought to relate to rapid gastric emptying that may follow vagotomy and a drainage procedure, both of which allow “dumping” of hyperosmolar gastric contents into the small bowel. This triggers an influx of water into the lumen in order to maintain isotonicty, resulting in acute contraction of plasma volume and the vasomotor signs and symptoms noted above. Simultaneous release of vasoactive compounds such as serotonin and bradykinin may augment the vasomotor symptoms. Rapid gastric emptying may be demonstrated by a radionuclide gastric emptying scan in some patients with dumping syndrome, and can confirm the clinical impression. Management of dumping after vagotomy and gastric drainage procedure is aimed at lowering the sugar content of the meal, reducing the volume of liquids ingested with meals, and increasing the frequency of feeding. Reclining after a meal may help minimize the effect of gravity on rapid gastric emptying. Medications aimed at delaying gastric emptying, such as anticholinergics and sedatives, are not very useful but may be tried in cases refractory to dietary management. Surgical reconstruction of the pylorus is reserved for patients with intractable dumping and/or diarrhea, in an attempt to delay gastric emptying.
Postvagotomy diarrhea has been described in up to 30% of patients after peptic ulcer surgery, bariatric surgery, fundoplication, and esophageal resection, during which intentional or unintentional truncal vagotomy can occur. Selective vagotomy of the stomach seems to protect against diarrhea. Many patients have transient watery diarrhea for three to six months postvagotomy. In an unfortunate few, the diarrhea can be severe, chronic, and disabling. The mainstay of therapy for postvagotomy diarrhea is cholestyramine, suggesting that excess bile acids in the intestine are stimulating colonic secretion. For those few patients who do not respond to cholestyramine, reconstruction of the pylorus or interposition of a reversed jejunal segment 70-90 cm from the ligament of Treitz may provide relief of disabling diarrhea.]
Is hemorrhage associated with a higher mortality in gastric ulcers or duodenal ulcers?
Higher mortality with hemorrhage of gastric ulcers
What type of gastric cancer is seen in low-risk populations, women, and is the most common type in the USA?
Diffuse gastric cancer (linitis plastica)
[Diffuse lymphatic invasion; no glands]
[UpToDate: Like intestinal-type cancers, diffuse-type gastric carcinomas can be induced by H. pylori infection. However, there are also prominent differences between these two variants. H. pylori-associated invasive intestinal-type cancers are characterized by a defined series of preneoplastic stages which are not seen with diffuse-type cancers. From an epidemiologic standpoint, both diffuse and intestinal cancers have been decreasing in incidence in most countries, although the decline is more marked for intestinal carcinomas. Intestinal carcinomas are also more frequent in men, and they are associated with a slightly better prognosis.
Diffuse type cancers are highly metastatic and characterized by rapid disease progression and a poorer prognosis than intestinal cancers. Diffuse carcinomas also have a greater tendency to invade the gastric wall, sometimes extending to the lower esophagus or to the duodenum. Occasionally, a broad region of the gastric wall or even the entire stomach is extensively infiltrated, resulting in a rigid thickened stomach, termed “linitis plastica”.
Histologically, individual tumor cells are seen to invade the surrounding tissues, and there is no gland formation. When intracellular mucin is abundant, it pushes aside the nucleus of the individual cells, resulting in the so-called signet ring carcinoma. It has long been thought that signet ring histology is an independent predictor of a worse prognosis as compared to other forms of gastric cancer. However, more recent studies have begun to question this notion. Some studies suggest that signet ring histology is associated with more advanced stage of disease at presentation, and that when adjusted for stage, signet ring cancer does not portend a worse prognosis.]
What secretes alkaline mucus in the duodenum?
Brunner’s glands
[Wikipedia: Brunner’s glands (or duodenal glands) are compound tubular submucosal glands found in that portion of the duodenum which is above the sphincter of Oddi. The main function of these glands is to produce a mucus-rich alkaline secretion (containing bicarbonate) in order to:
- protect the duodenum from the acidic content of chyme
- provide an alkaline condition for the intestinal enzymes to be active, thus enabling absorption to take place
- lubricate the intestinal walls
They are the distinguishing feature of the duodenum, and are named for the Swiss physician who first described them, Johann Conrad Brunner.]
What percent of patients with a perforated duodenal ulcer will have free air?
80%
[UpToDate: If imaging is required, plain x-rays are typically obtained first. Careful interpretation of upright chest and abdominal films can detect diagnostic free air in many cases of perforated gastric and duodenal ulcers. The presence of free air on abdominal imaging is highly indicative of a perforated viscus, although about 10% to 20% of patients with a perforated duodenal ulcer will not have free air. If free air is found, no other diagnostic studies are necessary. Leakage of water soluble oral contrast may be useful in selected cases. Once the oral contrast is given, the patient should be rotated 360 degrees and placed on the right side to fill the antrum and duodenum with contrast. However, many perforations have already sealed spontaneously by the time of presentation, so the absence of a leak does not exclude the diagnosis of a perforated ulcer.
If there is no free air on the plain film, computed tomography (CT) or ultrasound can be useful to detect small amounts of free air or fluid. In a small proportion of cases, free fluid will be the only clue indicating perforation on imaging studies and a few percent of cases will have neither free air nor fluid. Spiral and multidetector-row CTs, especially 64 slice scanners, allow the entire abdomen to be examined on a single breath-hold and improve detection of small amounts of air and indirect findings (eg, fluid, phlegmon, abscess, wall pathology and adjacent inflammation) and can provide very useful indirect clues to pathology. Spiral CTs are undoubtedly much more sensitive than ultrasound for detecting fluid, air, or other clues to perforation. Spiral CT with oral contrast sensitively detects persisting leaks across perforated ulcers.]
What is the effect of the addition of pyloroplasty to a truncal vagotomy on gastric emptying of solids?
Accelerates gastric emptying
What is the treatment for stress gastritis?
Proton pump inhibitor
[EGD with cautery of specific bleeding point may be effective]
[UpToDate: Despite almost universal use of ulcer prophylaxis, some critically ill patients still develop stress ulcers, and a small number of them may develop clinically significant bleeding. The clinical manifestations and diagnosis of stress ulcers are discussed elsewhere.
When patients are diagnosed with bleeding stress ulcers, they should be promptly resuscitated with intravenous fluid or blood products. Any coagulopathy is corrected. A nasogastric tube should be inserted to remove gastric blood and irritants such as acid, bile, or pancreatic secretions, which may cause further injury to the gastric mucosa. An intravenous proton pump inhibitor should be administered, and broad-spectrum antibiotics should be given to septic patients. Underlying sepsis is an important cause of stress ulcers. Thus, in patients with sepsis, appropriate antibiotic coverage and source control are required for adequate ulcer healing.
Endoscopy is usually the first-line therapy for patients with bleeding stress ulcer disease, both for diagnosis and treatment. Depending upon local expertise, angiographic interventions can also stop bleeding from stress ulcers.]
Which 3 chemotherapy drugs would be used to treat gastric cancer?
- 5FU
- Doxorubicin
- Mitomycin C
[UpToDate: Despite a large number of randomized trials, there is no consensus as to the best agent or regimen. In general, combination chemotherapy regimens provide higher response rates than do single agents, but this translates into only modestly longer durations of disease control and survival that are measured in weeks to a few months.
Patients with advanced gastric or esophageal adenocarcinoma who are potential candidates for trastuzumab should have their tumors assayed for the presence of HER2 overexpression utilizing tumor-specific criteria and/or gene amplification. Assaying HER2 expression on six to eight viable biopsies are ideal for evaluating HER2 status. We suggest the addition of trastuzumab to chemotherapy in patients with HER2-positive tumors (as defined by 3+ immunohistochemical [IHC] staining or fluorescence in situ hybridization [FISH] positivity), as long as they do not have a contraindication to trastuzumab (Grade 2B).
The optimal chemotherapy backbone for patients receiving trastuzumab is not established. Acceptable options include cisplatin plus fluorouracil (FU), cisplatin plus capecitabine, oxaliplatin plus leucovorin and short-term infusional FU (FOLFOX), or oxaliplatin plus capecitabine (XELOX/CAPOX).]
If malignant, gastrointestinal stromal tumors (GISTs) are treated with which chemotherapy agent?
Imatinib
[Gleevec; Tyrosine kinase inhibitor]
[UpToDate: The standard of care for patients with a primary resectable GIST is surgery, aiming for a macroscopically complete resection with negative microscopic margins. Complete resection is possible in the majority of localized GISTs, but only approximately one-half remain recurrence-free for five or more years with surgery alone.
Small molecule tyrosine kinase inhibitors (TKIs), such as imatinib, block signaling via KIT and PDGFRA, thus halting tumor proliferation. The success of these agents in advanced disease has prompted interest in perioperative use in patients with earlier stage disease. An approach to treatment of GISTs, integrating the use of adjuvant (postoperative) and neoadjuvant (preoperative) imatinib.
Based upon data from the Scandinavian Sarcoma Group (SSG) XVIII trial, we recommend adjuvant treatment with a TKI (imatinib 400 mg daily) for a minimum of three years in patients who have a completely resected primary high-risk GIST (Grade 1A).
The optimal selection of patients who are at sufficiently high risk for recurrence to warrant adjuvant imatinib is not established. Several risk stratification tools are available, based upon tumor size, mitotic rate, location, and in some cases, the presence or absence of tumor rupture and molecular genotype. However, particularly for tools, such as nomograms, that quantify the risk of disease recurrence after complete resection as a continuous variable, it is not clear what cutoff for disease recurrence should be used to select patients for imatinib.
There is no consensus as to the indications for neoadjuvant imatinib. For patients with apparently localized tumors, we suggest initial treatment with imatinib for patients with locally advanced unresectable or borderline resectable tumors, for potentially resectable primary tumors, if a reduction in tumor size would significantly decrease the morbidity of surgical resection, and for most patients with an apparently localized rectal GIST (Grade 2C). If possible, such patients should be enrolled in a clinical trial.]
Where does a Mallory-Weiss tear typically occur?
Lesser curvature near the GE junction
[SCORE: Mallory-Weiss syndrome involves acute upper gastrointestinal hemorrhage that occurs after retching or vomiting. These lesions account for approximately 5% to 15% of cases of patients with upper gastrointestinal bleeding. Mallory and Weiss described the presence of a laceration of the gastric cardia and postulated that violent emesis against an unrelaxed cardia was the mechanism of injury. Although the syndrome initially was associated with alcohol abuse, endoscopy has shown large numbers of patients with Mallory-Weiss syndrome without a history of alcohol abuse.]
[UpToDate: Mallory-Weiss syndrome is characterized by longitudinal mucosal lacerations (intramural dissections) in the distal esophagus and proximal stomach, which are usually associated with forceful retching. The lacerations often lead to bleeding from submucosal arteries. Since the initial description in 1929 by Mallory and Weiss in 15 alcoholic subjects, gastroesophageal tears have been a recognized cause of upper gastrointestinal hemorrhage. The prevalence of such tears among patients presenting with upper gastrointestinal bleeding is approximately 5%. Rarely, perforation can occur with repeated, protracted vomiting.]
How is afferent-loop obstruction in patients with Billroth II or Roux-en Y diagnosed?
CT scan
[UpToDate: Chronic afferent loop syndrome is typically associated with postprandial epigastric pain and intermittent projectile bilious vomiting which leads to resolution of the pain for a period of up to several days. In patients suspected of having afferent loop syndrome based upon symptoms (eg, intermittent projectile bilious vomiting), the detection of a distended afferent loop on abdominal computed tomography is diagnostic.]
What is the treatment for post-vagotomy diarrhea?
Cholestyramine, octreotide
[Surgical option: Reversed interposition jejunal graft]
[UpToDate: Postoperative complications of vagotomy include ulcer recurrence due to missed or incomplete vagotomy, as well as delayed gastric emptying. Although procedures such as highly selective vagotomy were designed to prevent delayed gastric emptying, while circumventing the need for a drainage procedure, 0.5% of patients who undergo highly selective vagotomy will develop gastric retention and require the addition of a drainage procedure several months after the initial operation. Two other long-term complications of vagotomy and drainage procedures are dumping syndrome and postvagotomy diarrhea. Dumping syndrome comprises a constellation of symptoms that occur within 30 minutes of a meal, including fullness, pain, nausea, cramps, and diarrhea. Some patients describe vasomotor signs and symptoms such as diaphoresis, lightheadedness, hypotension, tachycardia, flushing, and headache. The etiology of this syndrome is thought to relate to rapid gastric emptying that may follow vagotomy and a drainage procedure, both of which allow “dumping” of hyperosmolar gastric contents into the small bowel. This triggers an influx of water into the lumen in order to maintain isotonicty, resulting in acute contraction of plasma volume and the vasomotor signs and symptoms noted above. Simultaneous release of vasoactive compounds such as serotonin and bradykinin may augment the vasomotor symptoms. Rapid gastric emptying may be demonstrated by a radionuclide gastric emptying scan in some patients with dumping syndrome, and can confirm the clinical impression. Management of dumping after vagotomy and gastric drainage procedure is aimed at lowering the sugar content of the meal, reducing the volume of liquids ingested with meals, and increasing the frequency of feeding. Reclining after a meal may help minimize the effect of gravity on rapid gastric emptying. Medications aimed at delaying gastric emptying, such as anticholinergics and sedatives, are not very useful but may be tried in cases refractory to dietary management. Surgical reconstruction of the pylorus is reserved for patients with intractable dumping and/or diarrhea, in an attempt to delay gastric emptying.
Postvagotomy diarrhea has been described in up to 30% of patients after peptic ulcer surgery, bariatric surgery, fundoplication, and esophageal resection, during which intentional or unintentional truncal vagotomy can occur. Selective vagotomy of the stomach seems to protect against diarrhea. Many patients have transient watery diarrhea for three to six months postvagotomy. In an unfortunate few, the diarrhea can be severe, chronic, and disabling. The mainstay of therapy for postvagotomy diarrhea is cholestyramine, suggesting that excess bile acids in the intestine are stimulating colonic secretion. For those few patients who do not respond to cholestyramine, reconstruction of the pylorus or interposition of a reversed jejunal segment 70-90 cm from the ligament of Treitz may provide relief of disabling diarrhea.]
What is the standard triple therapy for helicobacter pylori?
- Bismuth salts (Pepto-Bismol)
- Amoxicillin
- Metronidazole/tetracycline
[SCORE: The observation that H. pylori infection has an important role in ulcer pathogenesis has led to the development of antimicrobial therapy for ulceration. Most successful regimens are based on omeprazole plus metronidazole in combination with amoxicillin or tetracycline. Omeprazole has been reported to increase the efficacy of antimicrobial therapy. Bismuth compounds are also effective, acting locally to achieve gastric concentrations greater than the minimum inhibitory concentration for 90% of H. pylori isolates. Metronidazole is secreted into the stomach at high concentration, and the in vivo activity of metronidazole is not diminished by gastric acidity. Triple therapy with omeprazole, metronidazole, and tetracycline or amoxicillin eradicates H. pylori in 90% of cases. Ranitidine produces no eradication.]
[Medscape: 14 days (deemed the most prudent recommendation based on a meta-analysis of 7 studies and confirmed by a large Italian randomized single-center trial).
7 days (no significant difference from 14 days based on a prospective randomized comparative trial in Nairobi).
10 days (also showed high cure rates with metronidazole 500 mg TID and high-dose esomeprazole (40 mg BID) based on a pilot study).]
[UpToDate: The regimen most commonly recommended for first line treatment of H. pylori is triple therapy with a PPI (lansoprazole 30 mg twice daily, omeprazole 20 mg twice daily, pantoprazole 40 mg twice daily, rabeprazole 20 mg twice daily, or esomeprazole 40 mg once daily), amoxicillin (1 g twice daily), and clarithromycin (500 mg twice daily) for 7 to 14 days. We suggest treatment for 14 days.
A longer duration of treatment (14 vs 7 days) may be more effective in curing infection but this remains controversial. A meta-analysis suggested that extension of PPI-based triple therapy from 7 to 14 days was associated with a 5% increase in eradication rates. Most studies included were based upon amoxicillin-based triple therapy.
Metronidazole (500 mg twice daily) can be substituted for amoxicillin in penicillin-allergic individuals. PPI-clarithromycin-metronidazole and PPI-clarithromycin-amoxicillin regimens are equivalent. Increasing the doses of PPIs has small effects on eradication rates.
An initial attempt at eradicating H. pylori fails in approximately 20% of patients. A number of studies have evaluated retreatment strategies. A systematic review estimated that eradication rates after retreatment were 70% and 76% for triple therapy and quadruple therapy, respectively. Eradication rates from studies in which two new antimicrobial agents had been added during retreatment were significantly higher than studies in which only one new antimicrobial had been added. Further studies are needed to define optimal retreatment regimens.
For patients failing an initial course of therapy, we recommend an alternate regimen (triple or quadruple therapy) using a different combination of antibiotics for 14 days.]
Gastroduodenal pain is sensed through afferent sympathetic fibers from which levels of the spinal cord?
T5-T10
What is the effect of vagotomy on gastric emptying of liquids?
Accelerates gastric emptying
[Increased liquid emptying because vagally mediated receptive relaxation is removed, resulting in increased gastric pressures]
[UpToDate: Although procedures such as highly selective vagotomy were designed to prevent delayed gastric emptying, while circumventing the need for a drainage procedure, 0.5% of patients who undergo highly selective vagotomy will develop gastric retention and require the addition of a drainage procedure several months after the initial operation. Two other long-term complications of vagotomy and drainage procedures are dumping syndrome and postvagotomy diarrhea. Dumping syndrome comprises a constellation of symptoms that occur within 30 minutes of a meal, including fullness, pain, nausea, cramps, and diarrhea. Some patients describe vasomotor signs and symptoms such as diaphoresis, lightheadedness, hypotension, tachycardia, flushing, and headache. The etiology of this syndrome is thought to relate to rapid gastric emptying that may follow vagotomy and a drainage procedure, both of which allow “dumping” of hyperosmolar gastric contents into the small bowel. This triggers an influx of water into the lumen in order to maintain isotonicty, resulting in acute contraction of plasma volume and the vasomotor signs and symptoms noted above. Simultaneous release of vasoactive compounds such as serotonin and bradykinin may augment the vasomotor symptoms. Rapid gastric emptying may be demonstrated by a radionuclide gastric emptying scan in some patients with dumping syndrome, and can confirm the clinical impression. Management of dumping after vagotomy and gastric drainage procedure is aimed at lowering the sugar content of the meal, reducing the volume of liquids ingested with meals, and increasing the frequency of feeding. Reclining after a meal may help minimize the effect of gravity on rapid gastric emptying. Medications aimed at delaying gastric emptying, such as anticholinergics and sedatives, are not very useful but may be tried in cases refractory to dietary management. Surgical reconstruction of the pylorus is reserved for patients with intractable dumping and/or diarrhea, in an attempt to delay gastric emptying.]
The right gastric artery is a branch of which artery?
Common hepatic artery
Which 2 medical conditions and 2 medications can cause delayed gastric emptying?
Medical conditions
- Diabetes
- Hypothyroidism
Medications
- Opiates
- Anticholinergics
Which stomach acid-reducing surgical procedure has the lowest rate of ulcer recurrence?
Truncal vagotomy with antrectomy
[1-2% recurrence rate and 2% mortality]
What is the normal stomach transit time?
3-4 Hours
What are 8 risk factors for gastric cancer?
- Adenomatous polyps
- Tobacco
- Previous gastric operations
- Intestinal metaplasia
- Atrophic gastritis
- Pernicious anemia
- Type A blood
- Nitrosamines
What is Blind loop syndrome?
Digested food slows or stops moving through part of the intestines, causing an overgrowth of bacteria in the intestines and problems absorbing nutrients
[Also called Small Intestinal Bacterial Overgrowth]
[UpToDate: Small intestinal bacterial overgrowth (SIBO) is a condition in which non-native bacteria and/or native bacteria are present in increased numbers resulting in excessive fermentation, inflammation, or malabsorption. It typically occurs in association with anatomical abnormalities, motility disorders, or multifactorial causes (eg, liver cirrhosis, chronic pancreatitis).]
What is the description of a type I gastric ulcer?
Lesser curve low along body of stomach
[Due to decreased mucosal protection]
[SCORE: Type I ulcers are not associated with acid secretion and are located on the lesser curvature of the stomach. Type II and III ulcers are associated with acid hypersecretion; the former is located on the lesser curvature in synchrony with duodenal ulcers, and the latter occurs in the prepyloric region. Type IV ulcers are found in the cardia near the gastroesophageal junction and are not associated with acid secretion. Type V ulcers are diffuse and associated with NSAID use. Initial management includes endoscopy to control bleeding, but initial biopsies are not recommended, as they may aggravate the bleeding ulcer. Should endoscopic attempts be unsuccessful, surgery may be warranted based on the location of the ulcer. Ulcers at the lesser curvature are usually best treated with wedge resection. Type II and III ulcers usually require Bilroth I reconstruction and truncal vagotomy. Ulcers near the GE junction pose a difficult challenge and may require a distal gastrectomy with Roux-en-Y reconstruction, known as the Csendes procedure.]
[UpToDate: Type I gastric ulcers are the most common type of gastric ulcer. These occur along the lesser curvature near the junction of fundic and antral mucosa, and occur in the setting of acid hyposecretion.
For most patients with Type I gastric ulcer, distal gastrectomy with Billroth I or Billroth II reconstruction is recommended since this approach removes the ulcer and the diseased antrum. It also treats an occult malignancy. Recurrent ulcer rates are low (0% to 5%) and excellent symptomatic relief is usually achieved. Mortality ranges from 0% to 6%.
Although type I gastric ulcer has classically been considered the consequence of inadequate gastric mucosal defense, as opposed to increased acid secretion, many advocate the addition of some form of vagotomy to the gastric resection. In a retrospective review of 349 cases of gastric ulcer at the Cleveland Clinic from 1950 to 1979, no significant differences were found in recurrence rates for gastric resection with or without vagotomy. Median follow-up was more than 11 years. This study also found comparable results for truncal vagotomy and pyloroplasty plus ulcer excision or biopsy. Thus, vagotomy is not absolutely necessary but not unreasonable for type I gastric ulcer.
Although most prefer distal gastrectomy, highly selective vagotomy has been used for type I gastric ulcer. The value of highly selective vagotomy in gastric ulcer may derive from its ability to decrease acid secretion while maintaining adequate gastric emptying and minimizing postoperative duodenogastric reflux. The procedure is performed as for duodenal ulcer, with the addition of a gastrotomy to resect or biopsy the ulcer bed. This approach has been questioned on theoretical grounds because highly selective vagotomy may promote a degree of gastric stasis and gastrin hypersecretion, two factors hypothesized to contribute to gastric ulcer pathogenesis. Despite these concerns, clinical results have been promising. In one series of 48 patients, the ulcer recurrence rate was comparable to gastrectomy at 6.5% with few adverse effects. Ulcer diameter and location may make this highly selective vagotomy difficult for some patients in whom ulcer-induced inflammation, edema, or scarring may obscure accurate dissection of the vagus nerves along the lesser curvature of the stomach.]
What are the surgical options for treating a duodenal ulcer that is refractory to medication or has some other surgical indication?
- Proximal vagotomy (10-15% ulcer recurrence, 0.1% mortality)
- Truncal vagotomy with pyloroplasty (5-10% ulcer recurrence, 1% mortality)
- Truncal vagotomy with antrectomy (1-2% ulcer recurrence, 2% mortality)
[UpToDate: Definitive acid-reducing procedures include highly selective vagotomy, truncal vagotomy with gastric drainage, and distal gastrectomy with reconstruction. The choice of procedure depends upon the clinical circumstances.
For young patients with obstructing ulcer disease who are at high risk of ulcer recurrence, we suggest performing a truncal vagotomy and antrectomy over another definitive acid-reducing procedure (Grade 2C). For older patients with obstructing ulcer disease, we suggest a drainage procedure, such as gastrojejunostomy without vagotomy (Grade 2C). Vagotomy is not performed in the absence of active ulcer disease in this group of patients, as it may exacerbate gastroparesis in a chronically obstructed stomach.
In the past, partial gastrectomy, either as an antrectomy and truncal vagotomy, or subtotal gastrectomy, was commonly used in the surgical management of duodenal ulcer disease. However, removal of the pylorus with these procedures leads to rapid emptying of liquids and solids from the stomach, and, potentially, to reflux of intestinal contents into the stomach. Given the high incidence of postgastrectomy complications, these procedures are no longer needed for the management of duodenal ulcer disease refractory to medical management.]
What is the effect of a truncal vagotomy on gastrin-producing G cells?
Causes G cell hyperplasia
[UpToDate: Vagotomy is a procedure that transects or removes a portion of the vagus nerves or branches of the vagus nerves to decrease gastric acid secretion. Vagotomy eliminates direct cholinergic stimulation of acid secretion and renders the acid-producing parietal cells less responsive to histamine and gastrin. Vagotomy also abolishes the vagal stimulus for release of antral gastrin.]
[NCBI: The basal and food-stimulated gastrin secretion after selective proximal vagotomy, selective gastric vagotomy and truncular vagotomy was found to be elevated. Hypergastrinemia increased as gastric secretion was inhibited, thus attesting to the role of acid formation inhibition in the origin of the postvagotomy increase in the hormonal secretion. However the values of the intragastral pH being equal, the blood gastrin level was higher after vagotomy as compared to that seen in unoperated peptic ulcer patients. After vagotomy coupled with antrumectomy gastrin secretion remained at the level seen in the unoperated patients, indirect evidence for increased function of extraantral G cells. Inhibition of gastric secretion is no single cause of the postvagotomy hypergastrinemia, since the latter was essentially increased in the early postoperative times and in the presence of the vagotomy-induced disorders. It is concluded that increased secretion of gastrin after vagotomy secures trophic and compensatory-adaptation processes.]
By what mechanism does gastrin cause H+ release from parietal cells of the stomach?
It activates phospholipase
[PIP -> DAG + IP3 -> Increased Ca -> Increased Ca-Calmodulin activates phosphorylase kinase -> Increased H+ release]
[Wikipedia: Parietal cells secrete acid in response gastrin, stimulating CCK2 receptors (least significant contribution, but also causes histamine secretion by local ECL cells)
Activation of histamine through H2 receptor causes increases intracellular cAMP level while Ach through M3 receptor and gastrin through CCK2 receptor increases intracellular calcium level. These receptors are present on basolateral side of membrane.
Gastrin primarily induces acid-secretion indirectly, increasing histamine synthesis in ECL cells,which in turn signal parietal cells via histamine release/H2 stimulation. Gastrin itself has no effect on the maximum histamine-stimulated gastric acid secretion.
The effect of histamine, acetylcholine and gastrin is synergistic, that is, effect of two simultaneously is more than additive of effect of the two individually. It helps in non-linear increase of secretion with stimuli physiologically.]
What is the treatment for a perforated duodenal ulcer?
Graham patch (place omentum over the perforation) + acid-reducing surgery if ulceration occurred despite the patient being on a PPI
[UpToDate: Perforated duodenal ulcers can generally be treated by closure with a piece of omentum (Graham patch) or, for perforated ulcers close to the pylorus, by truncal vagotomy with pyloroplasty (incorporating the perforation). Both approaches are simple and expedient, and the results have generally been good.
Simple patch closure of the perforation should be considered in the setting of ongoing shock, delayed presentation, significant medical comorbidities, or significant peritoneal contamination. Patch closure may also be appropriate for patients who have never been treated for peptic ulcer disease and who are candidates for proton pump inhibitors and antibiotic therapy for H. pylori. NSAID-related perforation can generally be treated with simple closure, as the drug can almost always be discontinued.]
40% of gastric cancers occur where?
Antrum
[UpToDate: More than 90% of stomach cancers are adenocarcinomas. In 1930, most cases originated in the distal stomach (gastric body and antrum). Since then, the incidence of distal gastric carcinoma has declined dramatically, while the incidence of adenocarcinoma of the esophagogastric junction (EGJ) and proximal stomach has increased at a rate exceeding that of any other cancer. The increasing incidence has paralleled the rise in incidence of esophageal adenocarcinoma. The term “EGJ tumor” reflects the frequent difficulty in separating the primary location of distal esophageal and proximal gastric cancers; their natural history, response to therapy, and overall prognosis appears to be similar.]
What are some methods of palliation for obstruction caused by gastric cancer?
Proximal lesions can be stented
Distal lesions can be bypassed with gastrojejunostomy
[If fails, consider palliative gastrectomy for obstruction or bleeding]
[UpToDate: For palliation of obstructive symptoms, endoscopic placement of a stent provides a less invasive alternative to surgery for symptom palliation and may possibly be more effective in symptom relief. Published experience with enteral stenting for gastroduodenal obstruction is derived mostly from case series and small comparative trials. The available data suggest that enteral stenting has a similar success rate as surgical palliation (with approximately 90% of patients improving clinically) but is associated with less morbidity, procedure-related mortality, and cost. Furthermore, stenting may achieve a better quality of life compared with other forms of palliation (such as non-oral feeding through a jejunostomy tube), although they have not been directly compared in controlled trials.
In a review of two randomized trials of endoscopic stenting versus palliative gastrojejunostomy, six comparative studies, and 36 retrospective series, there were no statistically significant differences between the two procedures in terms of efficacy or complications. However, stenting was associated with a trend toward shorter hospital stay, a higher clinical success rate, and a faster relief of obstructive symptoms. Patients who received stents did require reintervention more frequently than did surgically-treated patients.
Palliative gastrojejunostomy for gastric outlet obstruction associated with unresectable advanced gastric cancer can improve food intake. Multiple case reports and small studies report successful palliation of malignant gastric outlet obstruction using minimally invasive laparoscopic gastrojejunostomy. A small retrospective comparison of patients who had palliative laparoscopic (n = 10) versus open (n = 10) gastrojejunostomy showed a similar mean surgery time but less intraoperative blood loss (23 vs 142 mL) and a shorter length of stay (8 vs 124 days) for the laparoscopically-treated group. However, the differences were not statistically significant, likely because of the small sample size.
In current practice, palliative gastrojejunostomy for patients with metastatic gastric cancer is reserved for cases where less invasive methods, such as palliative RT with or without chemotherapy and endoscopic procedures, such as ablation, stenting, or J-tube placement to establish a route for enteral nutrition, cannot be used.]
What are some methods of palliation for bleeding caused by gastric cancer?
XRT
[If fails, consider palliative gastrectomy for obstruction or bleeding]
[UpToDate: External beam RT has a well-defined role in the control of pain, bleeding, or obstruction in patients with localized but unresectable gastric cancer. A retrospective review of 115 patients with gastric cancer treated with palliative RT (ranging from 8 Gy single fraction to 40 Gy in 16 fractions) revealed that control of bleeding, dysphagia/obstruction, and pain was achieved in 81%, 53%, and 46% of patients, respectively, at one month. Treatment was well tolerated, with only three (2.6%) with grade 3 toxicity (nausea, vomiting, and anorexia, respectively). Palliation lasted the duration of most patients’ lives. There was no difference in response between low (≤39 Gy) and high (>39) biologically effective dose regimens, although there was a trend toward poorer local control with doses ≤39 Gy.
Three other studies evaluating palliative chemoradiotherapy have also demonstrated durable palliation of dysphagia, as well as pain and bleeding.
There are no controlled studies that directly compare RT or chemoradiotherapy with endoscopic or surgical techniques for symptomatic palliation. However, responses to RT are not as immediate as with stenting or surgical palliation. Furthermore, while control of bleeding may be possible with low RT doses that are not associated with significant side effects, doses above 40 Gy (which may be associated with significant adverse effects) are often required for palliation of obstruction.]
What type of gastric cancer is increased in high-risk populations, older men, Japan, but is rare in the USA?
Intestinal-type gastric cancer
[UpToDate: There are two distinct types of gastric adenocarcinoma, intestinal (well-differentiated) and diffuse (undifferentiated), which have distinct morphologic appearance, epidemiology, pathogenesis, and genetic profiles. The morphologic differences are attributable to intercellular adhesion molecules, which are well preserved in intestinal-type tumors and defective in diffuse carcinomas. In intestinal tumors, the tumor cells adhere to each other, and tend to arrange themselves in tubular or glandular formations, similar to adenocarcinomas arising elsewhere in the intestinal tract (hence their designation as intestinal-type). In contrast, a lack of adhesion molecules in diffuse carcinomas allows the individual tumor cells to grow and invade neighboring structures without the formation of tubules or glands.
The intestinal type of gastric adenocarcinoma is most common in high-risk populations, more likely to be sporadic than inherited, and related to environmental factors such as diet, cigarette smoking and alcohol use. It is also the type that has decreased most markedly over the past several decades. In low-risk populations, the frequency of intestinal-type gastric adenocarcinomas more closely approximates the incidence of diffuse-type tumors.]
What are the surgical options for treating dumping syndrome?
Conversion of Billroth I or Billroth II to Roux-en Y gastrojejunostomy, operations to increase gastric reservoir (jejunal pouch) or increase emptying time (reversed jejunal loop)
[Surgical treatment of dumping syndrome is rarely needed]
[UpToDate: For post-bariatric surgery patients, the rare patients with intractable dumping symptoms who fail dietary and medical therapy may require reoperation. In patients who had a distal gastrectomy, conversion from a loop gastrojejunostomy to a Roux-en-Y reconstruction is the procedure of choice. This operation slows gastric emptying by impaired motility of the Roux loop. Thus, a gastric remnant of no more than 25% should be left to avoid postoperative Roux stasis syndrome. In patients who had a prior loop gastrojejunostomy without gastrectomy, simple takedown of the gastrojejunostomy usually resolves dumping syndrome, provided that normal antropyloric and duodenal functions are maintained.
What are 6 of the disadvantages of Roux-en Y gastric bypass?
- Risk of marginal ulcers
- Leak
- Necrosis
- B12 deficiency (intrinsic factor needs acidic environment to bind B12
- Iron-deficiency anemia (bypasses duodenum where Fe is absorbed)
- Gallstones (from rapid weight loss)
[UpToDate: Roux-en-Y gastric bypass complications are diverse and include gastric remnant distension, stomal stenosis, marginal ulcer formation, cholelithiasis, ventral hernias, internal hernias, hypoglycemia, dumping, metabolic and nutritional derangements and weight regain. Some complications are seen during the early postoperative periods while others may present weeks to months following the surgery.]
Why is an antrectomy helpful in treating ulcer disease?
Gastrin-producing G cells are located in the antrum
[UpToDate: The vast majority of gastrin is produced in endocrine cells of the gastric antrum. Much smaller amounts of gastrin are produced in other regions of the gastrointestinal tract including the nonantral stomach, duodenum, jejunum, ileum, and pancreas. Gastrin has also been found outside of the gastrointestinal tract including the brain, adrenal glands, respiratory tract, and reproductive organs, although its biological role in these sites is unknown.]
What is the treatment for an early leak (not contaminated) following bariatric surgery (Roux-en Y approach)?
Re-operation
[UpToDate: If a leak is suspected clinically, emergent surgical exploration should be performed, even if the imaging is negative, given the rapid progression to sepsis in the severely obese patient with comorbidities. A negative exploration that does not reveal a leak should not be considered a complication but rather evidence of good surgical judgment. Multiple studies have shown that re-exploration is safe when compared with missing or delaying the treatment of a leak. In experienced hands, surgical exploration and management of a leak is often feasible via a laparoscopic approach.]
What is the failure rate for bariatric surgery (Roux-en Y approach)?
10%
[Due to high-carbohydrate snacking]
[UpToDate: Both sleeve gastrectomy (SG) and roux-en-Y gastric bypass (RYGB) in adolescents lead to clinically important decreases in weight and body mass index (BMI) in the majority of patients in the short to intermediate term (one to three years postoperatively). Information about long-term outcomes (longer than three years) is more limited, but the weight loss appears to be sustained, though attrition over time could bias findings. Adjustable gastric band (AGB) is a less popular choice for adolescents in the United States, possibly due to lack of US Food and Drug Administration (FDA) approval for adolescents and the relatively better weight loss from SG and RYBG.
The best data on outcomes of weight loss surgery in adolescents come from a prospective study of 242 adolescents with severe obesity who predominantly underwent SG or RYGB at five centers in the United States with special expertise in bariatric surgery for this age group (Teen-LABS study). The mean age of the participants was 17±1.6 years, and one-third were between 13 and 15 years of age. Among 67 participants undergoing SG, BMI decreased from 50 kg/m2 at baseline to 37 kg/m2 (a 26% reduction) three years postoperatively. Among 161 participants undergoing RYGB, BMI decreased from 54 kg/m2 at baseline to 39 kg/m2 (a 28% reduction) three years postoperatively. At three years, weight regain to above baseline occurred in only 4% of participants with SG and 2% of those with RYGB.
Previous studies reporting outcomes of weight loss surgery in adolescents have utilized a retrospective design and report short- to intermediate-term outcomes (outcomes measured from 1 to 6.3 years after surgery). A few studies have reported small numbers of patients 10 or more years after their procedure. In most of these long-term studies, a substantial number of subjects were lost to follow-up, which could bias findings.
Despite these limitations, these studies confirm that clinically significant and durable weight loss can be achieved in most patients by either SG or RYGB, while AGB is probably somewhat less effective, with slower and less weight loss. As an example, a meta-analysis of 37 studies reported substantial weight loss with any of these procedures. Mean BMI loss was 16.6 kg/m2 for RYGB, 14.1 kg/m2 for SG, and 11.6 kg/m2 for AGB; these differences were not statistically significant, and comparison of outcomes was limited by lack of randomization among the procedures and different lengths of follow-up.
Of note, the nadir postoperative BMI tends to be lower in patients with less severe obesity preoperatively as compared with those with more severe obesity, although the percent BMI change is similar. In a large series of patients from a single center undergoing RYGB, the mean nadir postoperative BMI was 31, 38, and 47 kg/m2 for patients with starting BMIs between 40 to 54, 55 to 65, and >65 kg/m2, respectively.
It is not clear to what degree weight loss will be sustained in adolescents and whether comorbid conditions will recur if significant weight is regained in long-term follow-up. Two studies with 4 to 10 years of follow-up suggest that 10% to 15% of patients regain significant weight after RYGB procedures. Specific predictors of weight regain after surgical weight loss procedures are unknown for adults and adolescents. There is still insufficient information to directly compare the long-term weight loss outcomes of SG with those for RYGB or AGB in adolescents.]
What should be done if a patient with a prior jejunoileal bypass is encountered?
Correct these patients and perform Roux-en Y gastric bypass
[UpToDate: Jejunoileal bypass (JIB) is a purely malabsorptive procedure popular in the 1960s and 1970s. The procedure produces significant weight loss by creating a surgical short bowel syndrome.
JIB is no longer used today because of a 50% morbidity rate and 10% mortality rate. Patients who previously underwent JIB should be followed carefully for signs of complications, particularly a deterioration in liver function. Studies have shown a high long-term complication rate, with a 21% rate of cirrhosis after fifteen years.]
What is the surgical treatment for intestinal-type gastric cancer?
Subtotal gastrectomy
[10cm margins required]
[SCORE: In gastric cancer, microscopic involvement of the resection margin by tumor cells is associated with a poor prognosis. Unlike colon cancer, gastric cancer frequently has extensive intramural spread. Results of retrospective studies suggest that a line of resection 6 cm from the tumor mass is necessary to ensure a low rate of anastomotic recurrence. The value of extended lymphadenectomy in the management of gastric adenocarcinoma is controversial. The largest favorable experience has been reported in Japan, where retrospective studies have shown improvement of approximately 10%, stage for stage, for patients with advanced disease. The benefits of extensive lymphadenectomy have not been confirmed in western countries. Histologically positive lymph nodes are frequently present in the splenic hilum and along the splenic artery, and routine splenectomy has been practiced in some centers. Prophylactic splenectomy has not been found to improve outcome for similarly staged patients. Resection of adjacent organs may be needed for local control if direct invasion has occurred. In this circumstance, operative morbidity is increased, and long-term survival is rare.]
[UpToDate: Gastrectomy is the most widely used approach for therapy of invasive gastric cancer, although superficial cancers can sometimes be treated endoscopically. Total gastrectomy, which removes the entire stomach, is usually performed for lesions in the proximal (upper third) of the stomach, while partial gastrectomy (distal gastrectomy, subtotal gastrectomy) with resection of adjacent lymph nodes appears to be sufficient for lesions in the distal (lower two-thirds) of the stomach. Patients with large midgastric lesions or infiltrative disease (eg, linitis plastica) may require total gastrectomy. In most series, quality of life after partial gastrectomy is superior to that after a total gastrectomy, at least in the short term. Data on quality of life in long-term survivors of total gastrectomy, particularly those with a jejunal reservoir reconstruction, are limited.
For patients without suspected lymph node involvement who meet the standard or expanded criteria for endoscopic resection, we suggest endoscopic resection rather than gastrectomy, provided that there is local expertise in the endoscopic resection techniques (Grade 2C). It is imperative that a thorough evaluation for involved lymph nodes be performed prior to therapy to determine if endoscopic resection is an appropriate treatment option. This is often done with endoscopic ultrasound.
Endoscopic resection is associated with less treatment-related morbidity than gastrectomy and the available data suggest similar outcomes for appropriately selected patients with EGC when the procedure is performed by individuals experienced in endoscopic resection. Such expertise is less common in the United States compared with Asia. However, comparisons of endoscopic resection with gastrectomy are limited by the lack of trials directly comparing the two approaches.]
Where do peptic ulcers most commonly occur?
Most commonly on the anterior aspect of the 1st part of the duodenum
[More common in men]
[UpToDate: Ulcer incidence increases with age for both DUs and GUs, but DUs emerge two decades earlier than GUs, particularly in males. The incidence of bleeding from PUD is 13-fold higher in individuals > 70 years as compared with those < 40 years. The incidence of uncomplicated PUD reached a plateau with age, whereas for complicated PUD incidence increased exponentially with age.]
Mucosa-associated lymphoid tissue lymphoma (MALT lymphoma) is associated with what?
H. Pylori infection
[It usually regresses after treatment of H. Pylori infection]
[UpToDate: An overwhelming body of evidence has shown that the development of MALT lymphomas (also called MALTomas) is due to the clonal expansion of B cells that accompanies chronic gastritis in the presence of Helicobacter pylori. H pylori-induced gastritis first leads to the accumulation of CD4+ lymphocytes and mature B cells in the gastric lamina propria. Antigens derived from H pylori drive the activation of T cells, B cell proliferation, and lymphoid follicle formation, which if persistent can evolve into a monoclonal lymphoma.
Therapy directed at the H pylori infection results in regression of most early lesions and has become the treatment of choice for most patients. Most patients (>90%) with gastric MALT lymphoma are H pylori positive.]
The right gastroepiploic artery is a branch of which artery?
Gastroduodenal artery
What do Parietal cells of the stomach produce?
H+ and intrinsic factor
[Wikipedia: Parietal cells (also known as oxyntic or delomorphous cells), are the epithelial cells that secrete hydrochloric acid (HCl) and intrinsic factor. These cells are located in the gastric glands found in the lining of the fundus and in the body of the stomach. They contain an extensive secretory network (called canaliculi) from which the HCl is secreted by active transport into the stomach. The enzyme hydrogen potassium ATPase (H+/K+ ATPase) is unique to the parietal cells and transports the H+ against a concentration gradient of about 3 million to 1, which is the steepest ion gradient formed in the human body. Parietal cells are primarily regulated via histamine, acetylcholine and gastrin signaling from both central and local modulators.]
What is the treatment for blind-loop syndrome?
Tetracycline and flagyl, metoclopramide to improve motility
[UpToDate: The mainstay of treatment of small intestinal bacterial overgrowth (SIBO) is antibiotic therapy. If present, the underlying cause/disease should be treated. Dietary manipulation and surgical therapy may also be helpful.
The underlying cause of SIBO may be small intestinal stasis due to anatomic abnormalities (eg, diverticulosis, surgical blind loops or strictures), abnormal small intestinal motility (eg, drug-induced dysmotility, diabetes), abnormal communication between the proximal and distal intestine (eg, fistula), or may be multifactorial in etiology (eg, hypochlorhydria, chronic pancreatitis, associated with irritable bowel syndrome).
Nonsurgical conditions associated with intestinal stasis should be corrected when possible. This includes the elimination or substitution of drugs known to decrease intestinal motility (eg, narcotics, benzodiazepines).
In cases of sluggish motility, such as chronic intestinal pseudo-obstruction, methods to enhance motility can be attempted. Prokinetic agents including metoclopramide, domperidone, cisapride, erythromycin, and tegaserod may have benefit but large studies are lacking. Prokinetics may be a useful adjunct for SIBO in patients who do not respond to or are intolerant of antibiotics, provided that they have documented dysmotility. A short two-week trial of erythromycin (30 to 50 mg/kg, maximum 2 grams daily) is sufficient to identify any beneficial effects.
Octreotide induces phase III of the migrating motor complex that causes a propagating peristaltic wave through the small intestine. A pilot study in five patients with intestinal scleroderma and SIBO found improved symptoms and reduced breath hydrogen excretion after the administration of low doses of octreotide (50 micrograms). However, additional studies are needed to confirm these findings.]
What is the surgical treatment for diffuse gastric cancer?
Total gastrectomy
[Because of diffuse nature of linitis plastica]
[SCORE: In gastric cancer, microscopic involvement of the resection margin by tumor cells is associated with a poor prognosis. Unlike colon cancer, gastric cancer frequently has extensive intramural spread. Results of retrospective studies suggest that a line of resection 6 cm from the tumor mass is necessary to ensure a low rate of anastomotic recurrence. The value of extended lymphadenectomy in the management of gastric adenocarcinoma is controversial. The largest favorable experience has been reported in Japan, where retrospective studies have shown improvement of approximately 10%, stage for stage, for patients with advanced disease. The benefits of extensive lymphadenectomy have not been confirmed in western countries. Histologically positive lymph nodes are frequently present in the splenic hilum and along the splenic artery, and routine splenectomy has been practiced in some centers. Prophylactic splenectomy has not been found to improve outcome for similarly staged patients. Resection of adjacent organs may be needed for local control if direct invasion has occurred. In this circumstance, operative morbidity is increased, and long-term survival is rare.]
[UpToDate: In about 5% of primary gastric cancers, a broad region of the gastric wall or even the entire stomach is extensively infiltrated by malignancy, resulting in a rigid thickened stomach, termed linitis plastica. The prevalence may be higher in younger individuals. Although most commonly due to poorly-differentiated (diffuse-type) infiltrating gastric cancers, this pattern can, in rare circumstances, represent metastatic spread from lobular cancer of the breast.
Linitis plastica has an extremely poor prognosis, and this is attributed to the potential for early spread and advanced stage at diagnosis, as well as the frequent presence of microscopic disease at the surgical margins because of its diffuse nature. In one report, one-half of all patients had metastatic disease (mainly within the peritoneal cavity) at diagnosis. Nodal involvement is frequent, and extensive surgery may be required for complete excision. Many surgeons consider the presence of linitis plastica to be a contraindication to potentially curative resection. However, others report that long-term survival in selected patients who undergo optimal resection (negative margins guided by intraoperative frozen section analysis and a D2/D3 lymphadenectomy) is comparable to that of optimally resected patients without linitis plastica. In our view, all of these patients should undergo some form of preoperative therapy and diagnostic laparoscopy prior to resection to identify the subset of patients who might benefit from resection.]
Where is the vagus nerve divided in a proximal vagotomy?
Vagal fibers that supply the gastric fundus are divided, but branches to the antropyloric region of the stomach are not transected and the hepatic and celiac divisions of the vagus nerve remain intact.
What is the most common location for Mucosa-associated lymphoid tissue lymphoma (MALT lymphoma)?
Stomach
[UpToDate: The clinical presentation of extranodal MALT lymphoma (MZL) differs depending upon the tissue involved. Patients can present with symptoms of peptic ulcer disease, abdominal pain, sicca/Sjögren’s syndrome, or with a slow growing mass at the site of involvement. The majority present with localized stage I or II extranodal disease, involving glandular epithelial tissues of various sites.
The stomach is the most frequent site of involvement, but this tumor can involve the lung, thyroid, breast, synovium, lacrimal and salivary glands, orbit, dura, skin, and soft tissues.
These lymphomas disseminate to other MALT sites, lymph nodes, or marrow in about 30% of cases. It had been thought that this was often a late event. However, increasing evidence suggests that disease may often be disseminated at diagnosis.
- A review of 158 patients found disseminated disease in 54 (34%) at diagnosis; 17 of these patients had multiple involved mucosal sites.
- In another series of 36 patients presenting with nongastrointestinal MALT lymphoma (eg, salivary gland, ocular adnexa, lung, oral cavity), 12 (33%) were found to have gastric involvement at the time of initial workup.
Results of these and similar studies suggest that routine evaluation of the stomach should be a part of the initial staging workup, and at relapse, of most non-GI MALT lymphomas.]
What is the treatment for a late leak (weeks out from surgery, likely contained) following bariatric surgery (Roux-en Y approach)?
Percutaneous drain, antibiotics
[UpToDate: Percutaneous drainage of a contained fluid collection may be an option in patients who are stable. Surgical therapies for persistent gastric leak are technically difficult and often unsuccessful. New approaches using minimally invasive endoscopic repair techniques appear safe and effective in some patients. These include use of glue or placement of covered stents across the leak, or place of clips to close the opening.]
What is the most common type of gastric volvulus?
Organoaxial volvulus
[Stomach rotates around an axis that connects the gastroesophageal junction and the pylorus. The antrum rotates in opposite direction to the fundus of the stomach]
[UpToDate: Organoaxial rotation refers to rotation of the stomach along its long axis through a line that connects the gastroesophageal junction and the pylorus. The antrum rotates anterosuperiorly and the fundus rotates posteroinferiorly. The greater curvature of the stomach comes to rest superior to the lesser curvature of the stomach in an inverted position (upside-down stomach). Organoaxial volvulus is the most common type of abnormal rotation, occurring in 60% of cases of gastric volvulus, and is associated with secondary etiologies (eg, paraesophageal hernias, diaphragmatic hernia, and diaphragmatic eventration). Strangulation of the stomach is more common with this type of volvulus, occurring in up to 30% of cases.]
Which 2 modulators directly phosphorylate the H+/K+ ATPase, leading to increased H+ secretion and K+ absorption at the parietal cell membrane?
- Phosporylase kinase
- Protein kinase A
[UpToDate: Parietal cell activation involves an increase in cytoplasmic calcium or generation of cyclic AMP, followed by activation of a cAMP-dependent protein kinase cascade that triggers translocation of proton pump containing membranes to the apical surface.]
What do G cells in the antrum of the stomach produce?
Gastrin
[UpToDate: Gastrin is the major hormonal regulator of gastric acid secretion [1]. Its discovery at the turn of the century was based upon its profound effect on meal-stimulated acid secretion, making it one of the first hormones to be described. The study of gastrin accelerated with the isolation and characterization of the peptide in 1964 after which it was found to promote growth of the gastric antrum and have a proliferative effect, which has implicated it as having a possible role in cancer. The cloning and characterization of the gastrin receptor in 1992 has provided a valuable tool in the study of gastrointestinal hormones.]
What is the description of a type V gastric ulcer?
Ulcer associated with NSAIDs
[SCORE: Type I ulcers are not associated with acid secretion and are located on the lesser curvature of the stomach. Type II and III ulcers are associated with acid hypersecretion; the former is located on the lesser curvature in synchrony with duodenal ulcers, and the latter occurs in the prepyloric region. Type IV ulcers are found in the cardia near the gastroesophageal junction and are not associated with acid secretion. Type V ulcers are diffuse and associated with NSAID use. Initial management includes endoscopy to control bleeding, but initial biopsies are not recommended, as they may aggravate the bleeding ulcer. Should endoscopic attempts be unsuccessful, surgery may be warranted based on the location of the ulcer. Ulcers at the lesser curvature are usually best treated with wedge resection. Type II and III ulcers usually require Bilroth I reconstruction and truncal vagotomy. Ulcers near the GE junction pose a difficult challenge and may require a distal gastrectomy with Roux-en-Y reconstruction, known as the Csendes procedure.]
What is the treatment for gastric volvulus?
Reduction and Nissen
[UpToDate: For patients diagnosed with acute gastric distention due to gastric volvulus, we suggest initial gastric decompression by placing a nasogastric tube rather than endoscopic decompression (Grade 2C). This is initially attempted at the bedside, but, if unsuccessful, may require endoscopic assistance. In addition to nasogastric decompression, initial management includes fluid resuscitation and correction of electrolyte abnormalities.
Most patients who present with symptoms due to gastric volvulus will require some form of repair. The goals of repair are restoring the stomach back to a more normal anatomic position, repairing any associated anatomic abnormalities, and preventing future stomach rotation. These goals can be accomplished with endoscopic or surgical (open or laparoscopic) techniques. However, endoscopic repair does not address anatomic abnormalities, and thus, is less optimal for patients with secondary volvulus.
- For symptomatic patients with secondary gastric volvulus and good surgical anesthetic risk, we suggest surgical repair of the anatomic defect (eg, paraesophageal hernia), rather than gastric fixation alone (Grade 2C). Surgical repair appears to reduce the risk of future recurrence. For patients with significant medical comorbidities, not repairing the anatomic defect is an acceptable alternative, provided de-rotation and gastric fixation can be accomplished (laparoscopic or endoscopic).
- For symptomatic patients with primary gastric volvulus (acute or chronic), we suggest gastric fixation (laparoscopic or percutaneous endoscopic gastrostomy [PEG] tubes) to anchor the stomach into position to minimize recurrence rather than conservative therapy (Grade 2C).]
What is the surgical treatment for a small gastric remnant causing early satiety?
Jejunal pouch construction
[Small gastric remnant is the goal of gastric bypass]
[UpToDate: The optimal method of reconstruction after total gastrectomy would provide for a functional reservoir, preserve duodenal and jejunal continuity, and minimize postgastrectomy functional disturbance. No one reconstruction technique fulfills all these criteria; however, pouch reconstruction appears to have better functional outcomes and improved quality of life compared with other types of reconstruction. We prefer to use a Hunt-Lawrence type pouch with a Roux-en-Y jejuno-jejunal anastomosis.
Options for restoration of gastrointestinal continuity include a straight esophagojejunal anastomosis, looped esophagojejunal anastomosis, jejunal interposition, colon interposition, and jejunal pouch construction, which can be brought behind the colon (Hunt) or in front of the colon (Rodino). A meta-analysis pooled the outcomes of four randomized trials that followed patients for up to 15 months after total gastrectomy. Patients who had a gastric pouch reconstruction had a significantly decreased incidence of dumping syndrome (10.3% vs 19.6%), and improved quality of life compared with patients who did not undergo pouch reconstruction. Pouch reconstruction, regardless of type, did not increase morbidity or mortality, the length of the operation, or length of hospital stay. In one of these trials, patients with pouch reconstruction regained preoperative quality of life within two years of their gastrectomy, compared with five years for those without pouch reconstruction.
Small intestinal reconstruction techniques that preserve propulsion initiated by the duodenal pacemaker maintain antegrade flow of duodenal contents into jejunum, thereby preventing retrograde and mixed propulsion. This may be best accomplished using roux-en-Y reconstruction. A trial of 60 patients found that patients who received duodenal continuity and pouch reconstruction after total gastrectomy had higher body weight and better physiologic regulation of gastrointestinal hormones than those who underwent other reconstructions that did not preserve passage of contents through the duodenum. This study, however, did not report on perioperative complications associated with the different reconstruction techniques.]
Which 3 molecules stimulate H+ release from parietal cells of the stomach?
- Acetylcholine (vagus nerve input)
- Gastrin (from G cells of antrum)
- Histamine (from mast cells)
[Wikipedia: Parietal cells secrete acid in response to three types of stimuli:
- Histamine, stimulates H2 histamine receptors (most significant contribution).
- Acetylcholine, from parasympathetic activity via the vagus nerve and enteric nervous system, stimulating M3 receptors.
- Gastrin, stimulating CCK2 receptors (least significant contribution, but also causes histamine secretion by local ECL cells)
Activation of histamine through H2 receptor causes increases intracellular cAMP level while Ach through M3 receptor and gastrin through CCK2 receptor increases intracellular calcium level. These receptors are present on basolateral side of membrane.
Increased cAMP level results in increased protein kinase A. Protein kinase A phosphorylates proteins involved in the transport of H+/K+ ATPase from the cytoplasm to the cell membrane. This causes resorption of K+ ions and secretion of H+ ions. The pH of the secreted fluid can fall by 0.8.
Gastrin primarily induces acid-secretion indirectly, increasing histamine synthesis in ECL cells,which in turn signal parietal cells via histamine release/H2 stimulation. Gastrin itself has no effect on the maximum histamine-stimulated gastric acid secretion.
The effect of histamine, acetylcholine and gastrin is synergistic, that is, effect of two simultaneously is more than additive of effect of the two individually. It helps in non-linear increase of secretion with stimuli physiologically.]
Blood supply to the pylorus is carried by which vessel(s)?
Gastroduodenal artery
What kind of stomach ulcer is caused by a vascular malformation?
Dieulafoy’s ulcer
[UpToDate: A Dieulafoy’s lesion is a dilated aberrant submucosal vessel that erodes the overlying epithelium in the absence of a primary ulcer. The submucosal artery does not undergo normal branching within the wall of the stomach. As a result, the caliber of the artery is in the range of 1-3 mm, approximately 10x the normal caliber of mucosal capillaries. Dieulafoy’s lesions are usually located in the proximal stomach along the lesser curvature, near the esophagogastric junction (typically within 5 cm), although they have been found in all areas of the GI tract, including the esophagus, duodenum, and colon.
The etiology of Dieulafoy’s lesion is unknown. Additionally, events triggering bleeding are not well understood. Patients who bleed from Dieulafoy’s lesions are typically men with comorbidities including cardiovascular disease, hypertension, chronic kidney disease, diabetes, or alcohol abuse. The use of NSAIDS is also common among patients with Dieulafoy’s lesions; one theory is that NSAIDS incite bleeding by causing mucosal atrophy and ischemic injury. Bleeding episodes are often self-limited, although bleeding is usually recurrent and can be profuse.]
What is the treatment for adenomatous gastric polyps?
Endoscopic resection
[UpToDate: Given the increased risk of gastric cancer, all gastric adenomas should be resected. This can usually be accomplished endoscopically, but on occasion surgery may be required for lesions that contain invasive carcinoma or in patients with multiple adenomas.
Because of the association of gastric dysplasia with synchronous gastric carcinomas, the remainder of the stomach must be examined carefully. In addition, as adenomatous polyps are associated with atrophic gastritis, the normal-appearing antral and corpus mucosa should be sampled to assess the stage of gastritis and, thus, cancer risk. All patients should be tested for active H. pylori infection and, if present, the infection should be treated.
We perform an upper endoscopy for surveillance one year after initial resection of adenomatous gastric polyps to assess recurrence at the prior excision site, new or previously missed polyps, confirm eradication of H. pylori, and/or detect an early carcinoma.
In individuals at high risk for gastric cancer (eg, migrants from areas with high gastric cancer incidence, family history of gastric cancer, OLGA stage 3 or 4 with moderate diffuse or severe atrophy in the corpus or antrum usually accompanied by extensive intestinal metaplasia, patients with FAP), surveillance is continued indefinitely.]
What are the 3 biggest risk factors for rebleeding at the time of an EGD?
- Spurting blood vessel (60% chance of rebleed)
- Visible blood vessel (40% chance of rebleed)
- Diffuse oozing (30% chance of rebleed)
What is the effect of a truncal vagotomy on gastric emptying of solids?
Decelerates gastric emptying of solids
[Proximal vagotomy divides individual fibers and does not affect emptying of solids.]
Gastrointestinal stromal tumors (GISTs) are considered malignant if they meet one of which two criteria?
- Greater than 5cm in size
- Greater than 5 mitoses / 50 HPF
[UpToDate: The clinical behavior of GISTs is highly variable. Criteria for identifying those tumors most likely to display malignant behavior (recur and/or metastasize) have been sought, analyzed, and disputed for years.
Tumor characteristics on CT or endoscopic ultrasound (EUS) may not only suggest the diagnosis of a GIST but may also, to some extent, correlate with recurrence risk. Tumors that are larger than 5 cm, lobulated, enhance heterogeneously, and have mesenteric fat infiltration, ulceration, regional lymphadenopathy, or an exophytic growth pattern on CT are more likely to metastasize. In contrast, GISTs with less metastatic potential tend to enhance in a homogeneous pattern and often show an endoluminal growth pattern.
From a histologic standpoint, as a group, GISTs tend to have bland morphologic features, although this morphology does not predict benign behavior. With prolonged follow-up, it appears that almost any GIST presenting with clinical symptoms or signs leading to treatment has the potential to behave in a malignant fashion. It is now widely accepted that the terms “benign” or “malignant” should not be applied to GIST, since these terms are not clinically useful for patient management. Since all GISTs are now regarded as potentially malignant, consensus classifications focus on stratifying lesions (clinicopathobiologic risk categorization) according to the relative risk of recurrence and metastasis.
Tumor size and mitotic rate formed the foundation for the NIH 2002 consensus approach to GIST risk stratification. One of the tenets of this risk stratification schema is that virtually all GISTs (especially those larger than 1 cm) have malignant potential, a concept supported by three large retrospective studies from the Armed Forces Institute of Pathology (AFIP).]
Adenomatous gastric polyps have what percent risk of cancer?
15%
[UpToDate:It is estimated that 8% to 59% of adenomas are associated with synchronous gastric carcinomas. The presence of invasive carcinoma in an adenoma correlates with increasing size, villous contour, and the degree of dysplasia. The risk of malignancy is lower in flat adenomas. High-grade dysplasia has been identified in close proximity to a high proportion (40% to 100%) of early gastric cancers.
Dysplasia is a precursor of invasive adenocarcinoma. Patients with high-grade dysplasia have a higher risk of progression as compared with patients with low-grade dysplasia. A nationwide cohort study in the Netherlands evaluated the progression of dysplasia to frank gastric cancer in 165 patients with high-grade dysplasia and 270 patients with low-grade dysplasia. Gastric cancer was diagnosed within 1, 5, and 10 years from the initial diagnosis in 25%, 30%, and 33% of patients with high-grade dysplasia and 2%, 3%, and 4% with low-grade dysplasia, respectively.]
After bariatric surgery (Roux-en Y approach), when should a UGI be performed?
Post-op day #2
[UpToDate: There is no consensus as to whether imaging should be performed routinely, or selectively following bariatric surgery. Before initiating a diet, most bariatric surgeons who obtain imaging following bariatric procedures that involve an anastomosis or stapling get an upper gastrointestinal series (UGI) series on POD #1. The advantage of this approach is that any leak, if present, can be addressed quickly. However, some surgeons only perform postoperative imaging selectively, based upon the patient’s clinical progress.
A systematic review evaluated the sensitivity and specificity of UGI from data obtained from 19 studies involving 10,139 patients. UGI had an overall sensitivity of 54% and a specificity of 100% for detecting anastomotic leak within 2 days of bariatric surgery. The threshold used to distinguish between positive and negative test results varied between institutions. Given the moderate sensitivity, the authors of this study suggested that treating marginal radiological evidence of leakage as presumptively positive maximizes the clinical utility of UGI. Although a majority of articles show that UGI series are better for identifying leak following bariatric surgery, a later study found better sensitivity and specificity with abdominal computed tomography (CT) compared with UGI (100% vs 95%). Irrespective of imaging modality chosen, any clinical suspicion of leak warrants investigation.
When bariatric surgery patients present with complaints of heartburn, nausea or vomiting, abdominal pain, or weight loss failure, imaging studies should be obtained to ensure prompt diagnosis of infection, obstruction, ischemia, or mechanical or technical failures of an operation. Radiologic examination of severely obese patients can be technically difficult because of patient size, resulting in suboptimal imaging.
Radiologic evaluation and endoscopy are complementary studies, and endoscopy is often necessary for diagnostic certainty in bariatric patients with postoperative complications. Usually, imaging is performed first and then a decision about proceeding to endoscopy is made based upon the imaging findings and the patient’s symptoms.]
Blood supply to the lesser curvature of the stomach is carried by which vessel(s)?
Right and left gastrics
Which cell type secretes intrinsic factor?
Parietal cells of the stomach
[Wikipedia: Parietal cells (also known as oxyntic or delomorphous cells), are the epithelial cells that secrete hydrochloric acid (HCl) and intrinsic factor. These cells are located in the gastric glands found in the lining of the fundus and in the body of the stomach. They contain an extensive secretory network (called canaliculi) from which the HCl is secreted by active transport into the stomach. The enzyme hydrogen potassium ATPase (H+/K+ ATPase) is unique to the parietal cells and transports the H+ against a concentration gradient of about 3 million to 1, which is the steepest ion gradient formed in the human body. Parietal cells are primarily regulated via histamine, acetylcholine and gastrin signaling from both central and local modulators.]
What is the description of a type IV gastric ulcer?
Lesser curve high along cardia of stomach
[Due to decreased mucosal protection]
[SCORE: Type I ulcers are not associated with acid secretion and are located on the lesser curvature of the stomach. Type II and III ulcers are associated with acid hypersecretion; the former is located on the lesser curvature in synchrony with duodenal ulcers, and the latter occurs in the prepyloric region. Type IV ulcers are found in the cardia near the gastroesophageal junction and are not associated with acid secretion. Type V ulcers are diffuse and associated with NSAID use. Initial management includes endoscopy to control bleeding, but initial biopsies are not recommended, as they may aggravate the bleeding ulcer. Should endoscopic attempts be unsuccessful, surgery may be warranted based on the location of the ulcer. Ulcers at the lesser curvature are usually best treated with wedge resection. Type II and III ulcers usually require Bilroth I reconstruction and truncal vagotomy. Ulcers near the GE junction pose a difficult challenge and may require a distal gastrectomy with Roux-en-Y reconstruction, known as the Csendes procedure.]
[UpToDate: Type IV gastric ulcer is distinguished by its anatomic location high along the lesser curvature, close to the gastroesophageal junction. Antral mucosa may extend to within 1 to 2 cm of the gastroesophageal junction; thus, type IV ulcers may represent a subset of type I gastric ulcers.
Type IV ulcers are associated with gastric acid hyposecretion and present early with dysphagia and reflux. Large ulcer diameter, the degree of surrounding inflammation, and proximity to the gastroesophageal junction render operative management difficult and potentially dangerous. If the integrity of the distal esophagus can be assured, subtotal gastric resection (including the ulcer bed) is considered optimal therapy. Typically, an attempt is made to preserve a margin of unaffected stomach to facilitate the anastomosis. Alternatives include the Pauchet procedure, which is a distal gastrectomy extended along the lesser curvature to include the ulcer, or the Kelly-Madlener procedure, in which distal gastrectomy is performed but the ulcer is left in place to avoid compromise of the gastroesophageal junction. Although there is no consensus in the literature, many surgeons feel more comfortable performing an esophageal anastomosis knowing that the ulcer is removed. When most of the stomach is removed, a roux-en-y reconstruction if often performed.]
The left gastroepiploic artery and the short gastric artery are branches of which artery?
Splenic Artery
What is the initial treatment for post-gastrectomy duodenal stump blow-out?
Place lateral duodenostomy tube and drains
[UpToDate: The most feared anastomotic complication following partial gastrectomy is a breakdown of the duodenal stump closure, or duodenal stump leak, following a Billroth II or Roux-en-Y type of procedure. The most important goal of treatment of duodenal stump leak is control of sepsis and drainage of the surgical bed. In addition to carrying out the routine surgical management of an anastomotic leak, the surgeon may decide to insert a tube duodenostomy, if feasible, depending upon the extent of inflammation.]
What is the treatment of a Mallory-Weiss tear?
EGD with hemo-clips
[SCORE: Initial management includes volume resuscitation, gastric lavage, and nasogastric decompression. Most patients with Mallory-Weiss tears stop bleeding spontaneously either before treatment or after these early measures. Once bleeding has stopped, rebleeding is rare. Nonoperative management consisting of endoscopic electrocoagulation or injection therapy has been successfully applied to these lesions. Esophageal balloon tamponade is contraindicated because it can convert a partial thickness tear into a full-thickness esophageal laceration. In cases not amenable to endoscopic therapy, operative management consists of oversewing the laceration through an anterior longitudinal gastrotomy in the middle third of the stomach. The mortality rate in recent series has been between 5% and 10%; deaths were related to associated disease, most notably cirrhosis.]
[UpToDate: Although 40-70% of patients with bleeding Mallory-Weiss tears require blood transfusions, most tears heal spontaneously. A classification scheme has been proposed to identify patients at risk for recurrent bleeding and mortality and those patients requiring only brief hospitalization. Portal hypertension and coagulopathy were identified as the major risk factors for rebleeding. Rebleeding usually occurred within 24 hours and most often in patients with a coagulopathy. Clinical features that indicated a severe bleed were those of hematochezia and hemodynamic instability.
Endoscopic therapy is the first-line treatment for actively bleeding lacerations. Several hemostatic methods have been used to control bleeding. The results obtained with any modality depend upon technique, experience, and practice.]
What is the best method of reconstruction following antrectomy?
Roux-en-Y gastro-jejunostomy
[UpToDate: The choice of reconstruction following antrectomy for ulcer disease or distal gastrectomy for tumor depends upon the remnant anatomy available for reconstruction, taking into consideration the complications related to the specific postgastrectomy physiology that will result. However, based upon randomized trials, Roux-en-Y reconstruction appears to be tolerated better overall and leads to a better quality of life compared with Billroth reconstruction (Billroth I or Billroth II). Whether to preferentially perform a Roux-en-Y in patients whose anatomy supports a Billroth I or Billroth II, or convert to a Roux-en-Y only if complications occur remains controversial. For patients who have not undergone vagotomy, we suggest a primary Roux-en-Y reconstruction. Patients who have had a vagotomy have an increased risk of roux stasis syndrome.
A metaanalysis of 15 randomized trials comparing at least two of the gastric reconstruction techniques (ie, Billroth I, Billroth II, or Roux-en-Y reconstruction) following gastrectomy assessed postoperative morbidity and mortality, quality of life, and the incidence of postgastrectomy syndromes. Although complication rates were similar, patients with a Roux reconstruction had fewer complaints of reflux gastritis and better quality of life. A later trial also confirmed this finding.
The longest follow-up comparing techniques was reported for a trial that has followed 75 patients treated for duodenal ulcer for 12 to 21 years. Patients were randomly assigned to Billroth II (n = 39) or Roux-en-Y (n = 36) reconstruction between 1984 and 1993. Patients who received a Roux-en-Y reconstruction had overall better clinical outcomes with a significantly lower incidence of reflux esophagitis (3% vs 33%), fewer abnormal findings on upper endoscopy of the distal esophagus and esophagogastric junction (10% vs 82%), and a lower incidence of Barrett’s esophagus (3% vs 21%). The gastric remnant was also normal in significantly more Roux-en-Y patients (100% vs 18%). There were no differences between the groups in the incidence of Helicobacter pylori infection. It is interesting to note that the Roux limb in these patients was arbitrarily chosen to be 60 cm. Although the authors were concerned about the potential for the “Roux syndrome”, it was not clinically apparent in their series.]
What do Chief cells of the stomach produce?
Pepsinogen
[1st enzyme in proteolysis]
By what mechanism does histamine cause H+ release from parietal cells of the stomach?
It activates adenylate cyclase
[Adenylate cyclase -> cAMP -> activates protein kinase A -> Increased H+ release]
[Wikipedia: Parietal cells secrete acid in response to histamine stimulating H2 histamine receptors (most significant contribution).
Activation of histamine through H2 receptor causes increases intracellular cAMP level while Ach through M3 receptor and gastrin through CCK2 receptor increases intracellular calcium level. These receptors are present on basolateral side of membrane.
Increased cAMP level results in increased protein kinase A. Protein kinase A phosphorylates proteins involved in the transport of H+/K+ ATPase from the cytoplasm to the cell membrane. This causes resorption of K+ ions and secretion of H+ ions. The pH of the secreted fluid can fall by 0.8.
Gastrin primarily induces acid-secretion indirectly, increasing histamine synthesis in ECL cells,which in turn signal parietal cells via histamine release/H2 stimulation. Gastrin itself has no effect on the maximum histamine-stimulated gastric acid secretion.
The effect of histamine, acetylcholine and gastrin is synergistic, that is, effect of two simultaneously is more than additive of effect of the two individually. It helps in non-linear increase of secretion with stimuli physiologically.]
Which 4 molecules inhibit H+ release from parietal cells of the stomach?
- Somatostatin
- Prostaglandins (PGE1)
- Secretin
- CCK
What is the description of a type II gastric ulcer?
2 ulcers (lesser curve and duodenal)
[Similar to duodenal ulcer with high acid secretion]
[SCORE: Type I ulcers are not associated with acid secretion and are located on the lesser curvature of the stomach. Type II and III ulcers are associated with acid hypersecretion; the former is located on the lesser curvature in synchrony with duodenal ulcers, and the latter occurs in the prepyloric region. Type IV ulcers are found in the cardia near the gastroesophageal junction and are not associated with acid secretion. Type V ulcers are diffuse and associated with NSAID use. Initial management includes endoscopy to control bleeding, but initial biopsies are not recommended, as they may aggravate the bleeding ulcer. Should endoscopic attempts be unsuccessful, surgery may be warranted based on the location of the ulcer. Ulcers at the lesser curvature are usually best treated with wedge resection. Type II and III ulcers usually require Bilroth I reconstruction and truncal vagotomy. Ulcers near the GE junction pose a difficult challenge and may require a distal gastrectomy with Roux-en-Y reconstruction, known as the Csendes procedure.]
[UpToDate: Type II gastric ulcers occur synchronously with scarring or ulceration in the duodenum or pyloric channel. They tend to be large, deep ulcers, with poorly defined margins. They frequently occur in younger men and are associated with increased acid secretion.
For type II gastric ulcer, antrectomy and vagotomy are the preferred approaches.]
By what mechanism does acetylcholine cause H+ release from parietal cells of the stomach?
It activates phospholipase
[PIP -> DAG + IP3 -> Increased Ca -> Increased Ca-Calmodulin activates phosphorylase kinase -> Increased H+ release]
[Wikipedia: Parietal cells secrete acid in response to acetylcholine, from parasympathetic activity via the vagus nerve and enteric nervous system, stimulating M3 receptors. Ach through M3 receptor increases intracellular calcium level.]
What is the initial treatment for chronic gastric atony causing symptoms of delayed gastric emptying (nausea, vomiting pain, early satiety)?
Metoclopramide, prokinetics
[UpToDate: Initial management of gastroparesis consists of dietary modification, optimization of glycemic control and hydration, and in patients with continued symptoms, pharmacologic therapy with prokinetic and antiemetics.
We suggest that patients consume small, frequent meals that are low in fat and contain only soluble fiber (Grade 2C). In patients who cannot tolerate solids, meals can be homogenized and liquid meals supplemented with vitamins.
In patients who fail to respond to dietary modification, we start pharmacologic treatment with prokinetics to increase the rate of gastric emptying. We use liquid formulations in order to facilitate absorption, if available, and administer prokinetics 10 to 15 minutes before meals, with an additional dose before bedtime in patients with continued symptoms.
We recommend initial pharmacologic treatment with metoclopramide (Grade 1A). In patients who fail to respond to metoclopramide, we suggest a trial of domperidone and subsequently oral erythromycin (Grade 2B).
In patients with nausea and vomiting that fail to respond to metoclopramide, domperidone, and erythromycin, we suggest cisapride if available (Grade 2B).]
Blood supply to the greater curvature of the stomach is carried by which vessel(s)?
Right and left gastroepiploics, short gastrics
What causes blind-loop syndrome (Small Intestinal Bacterial Overgrowth) in patients with Billroth II or Roux-en Y?
Poor motility
[Bacterial overgrowth (E. Coli, GNRs) occurs from stasis in afferent limb]
[UpToDate: The classic mechanism for cleansing the small bowel of debris and preventing SIBO is the migrating motor complex (MMC) and in particular, phase III of the MMC. A lack of interdigestive phase III activity is seen in irritable bowel syndrome, narcotic use, intestinal pseudo-obstruction, and diabetes. Small bowel motility may be affected in patients with acute or chronic radiation enteritis. More extreme motility disorders, such as scleroderma, can progress to include neuropathy and even myopathy of the gut, which further reduce flow, leading to SIBO.
Anatomic abnormalities can lead to SIBO by causing stasis. Anatomic disorders associated with SIBO include adhesions from previous surgery; strictures due to radiation, inflammatory bowel disease, or tumors of the small bowel; small intestinal diverticulosis; blind intestinal loops; reversed segments; and gastric bypass for the treatment of obesity.]
What is/are the non-surgical treatment(s) for alkaline (bile) reflux gastritis?
Proton pump inhibitor, cholestyramine, metoclopramide
[UpToDate: Definitive treatment of symptomatic chronic bile acid reflux gastropathy is surgery to divert bile from refluxing into the stomach (usually a Roux-en-Y revision), which has been associated with improvement in symptoms in 50% to 90% of patients in several reports. Improvement is less likely in patients with delayed gastric emptying.
A number of medical treatments have been evaluated in small clinical trials with variable success:
- Ursodeoxycholic acid significantly decreased pain and almost abolished nausea and vomiting, but did not improve histology in a small placebo-controlled crossover trial involving 12 patients. The rationale for its use was based upon the hypothesis that changing the composition of bile acids could have a favorable effect on gastric mucosa and symptoms.
- Sucralfate improved histologic features but not symptoms in a controlled trial involving 23 patients.
- Prostaglandin E2 was ineffective in improving endoscopic features or symptoms in a double-blind crossover trial.
- Cholestyramine combined with alginates (to improve contact time in the gastric remnant) was ineffective on symptoms or histology in a placebo controlled trial that included 32 patients.]
What is the effect of somatostatin on the cells of the stomach?
Inhibits gastrin and H+ release
[UpToDate: The physiological effects of somatostatin are largely inhibitory. In the peripheral organs, somatostatin decreases endocrine and exocrine secretion and blood flow, reduces gastrointestinal motility and gallbladder contraction, and inhibits secretion of most gastrointestinal hormones. Somatostatin also inhibits neurotransmission in the brain, but depending on the neural pathways affected, somatostatin in the central nervous system may stimulate endocrine secretion. For example, somatostatin inhibits ghrelin release from X/A-like cells of the gastric mucosa, but in the brain, somatostatin receptor activation increases plasma ghrelin levels.]
What is the treatment for afferent-loop obstruction in patients with Billroth II or Roux-en Y?
Re-anastomosis with shorter (40cm) afferent limb to relieve obstruction
[Balloon dilation may be possible]
[UpToDate: Surgical revision of the gastrojejunostomy or conversion to a Roux-en-Y anastomosis is necessary to treat this problem. Alternatively, a Braun’s enteroenterostomy between the afferent and efferent loops may also decompress the afferent loop.]
What do D cells of the stomach (mostly in the antrum) produce?
Somatostatin
[Somatostatin is produced by delta cells in the pyloric antrum, the duodenum and the pancreatic islets.]
[UpToDate: Somatostatin holds an interesting place in gastrointestinal endocrinology. Originally discovered as an inhibitor of growth hormone release, it is now known to inhibit a variety of gastrointestinal processes. Somatostatin is produced by paracrine cells that are scattered throughout the gastrointestinal tract and inhibits gastrointestinal endocrine secretion. Somatostatin is also found in various locations in the nervous system and exerts neural control over many physiological functions. Given this vast array of effects, it is not surprising that somatostatin has been the subject of intensive investigation. The development of synthetic analogues has led to treatment of clinical disorders such as acromegaly, hormone-secreting tumors of the gastrointestinal tract, and portal hypertensive bleeding.]
How do gastrointestinal stromal tumors (GISTs) appear on ultrasound?
Hypoechoic with smooth edges
[UpToDate: EUS is the most accurate method for distinguishing leiomyomas from other submucosal lesions. Leiomyomas arise from the fourth hypoechoic layer (the muscularis propria), distinguishing them from more superficial lesions. Specific sonographic features may also distinguish a leiomyoma from other submucosal lesions, such as a lipoma or esophagogastric varices, and from other neoplasms such as lymphomas, carcinoids, cysts, pancreatic rests, and polyps. In one series, EUS correctly diagnosed 48 of 50 submucosal mass lesions confirmed by pathology or angiography.
EUS also may be helpful for distinguishing a leiomyoma from a leiomyosarcoma. Tumors that disrupt the normal tissue planes, contain cystic spaces, and are associated with enlarged lymph nodes are more likely to be malignant. Benign tumors are more likely to have regular margins, a tumor size ≤30 mm, and a homogeneous echo pattern. In one report, the combined presence of two out of three EUS features (irregular extraluminal margins, cystic spaces, and lymph nodes with a malignant pattern) had a positive predictive value of 100% for a malignant or borderline GIST. However, sonographic characteristics alone are usually insufficient proof that a tumor is benign. Serial examinations may be helpful in such cases.
The combined use of cytologic analysis and immunohistochemistry for KIT mutations may permit the diagnosis of some of these lesions by EUS-guided fine-needle aspiration (FNA). In a study of 65 patients undergoing EUS-FNA for an upper gastrointestinal tract submucosal lesion, among the 28 lesions with a definitive pathologic diagnosis, the sensitivity of EUS-FNA for diagnosis of GIST was 82% and the specificity was 100%.]
Marginal ulcers develop in what percent of patients following bariatric surgery (Roux-en Y approach)?
10%
[Treatment is a PPI]
[UpToDate: Marginal ulcers have been reported in 0.6% to 16% of patients. Marginal ulcers occur near the gastrojejunostomy and result from acid injuring the jejunum, or they can be associated with a gastrogastric fistula.
Causes of marginal ulcers include:
- Poor tissue perfusion due to tension or ischemia at the anastomosis
- Presence of foreign material, such as staples or nonabsorbable suture
- Excess acid exposure in the gastric pouch due to gastrogastric fistulas
- Nonsteroidal anti-inflammatory drug use
- Helicobacter pylori infection
- Smoking
Patients with marginal ulcers present with nausea, pain, bleeding and/or perforation. The diagnosis of a marginal ulcer is established by upper endoscopy.
Initial medical treatment consisting of gastric acid suppression, with or without the addition of sucralfate, is successful in the majority of patients (95%). Nonsteroidal antiinflammatory drugs should be discontinued and patients should be encouraged to stop smoking.
The prevalence of H. pylori infection in patients undergoing weight-loss surgery is high, and a significant proportion of them have postoperative foregut symptoms. Observational studies have shown that patients with H. pylori colonization have a higher incidence of marginal ulcer formation. Furthermore, in one study, preoperative testing and treatment of H. pylori significantly reduced the incidence of postoperative marginal ulcers (2.4% vs 6.8% in unscreened patients).
Surgical treatment for marginal ulcers is indicated if persistent pain or recurrent bleeding occurs, despite maximal medical management. Medical management is usually successful and surgical intervention is rarely needed, but, when required, revision of the gastrojejunostomy with truncal vagotomy should be performed if the patient is hemodynamically stable. Management of a perforated ulcer is described elsewhere.]
What binds B12 (cobalamin), forming a complex that is reabsorbed in the terminal ileum?
Intrinsic factor
[UpToDate: Animal products provide the only dietary source of cobalamin (B12) for humans. In the presence of acid and pepsin, B12 is liberated from binding to protein and binds to B12-binding proteins in saliva and gastric juice. B12 is freed from R proteins by pancreatic proteases in the duodenum, binds specifically to gastric-derived intrinsic factor, and is absorbed in the terminal ileum via a specific receptor
What is the surgical treatment for gastric ulcer that is best for complications?
Truncal vagotomy and antrectomy
[Ulcer should be included in resection or separate resection of the ulcer should be performed due to high risk of gastric cancer in ulcer]
