毕业论文代写价格 Stomach And Intestines Anatomy And Physiology

Cancer

People with ulcers caused by Helicobacter pylori have 3 to 6 times the chance of developing stomach cancer later in life. There is no increased risk of developing cancer from ulcers that have other causes.

POST GASTRECTOMY SYNDROMES

Modern treatment of peptic ulcer has led to a decline in the frequency of gastrectomies and therefore, the incidence of postgastrectomy syndromes has declined to a great extent. A 10-fold reduction has occurred in elective operations for peptic ulcer disease in the last 20-30 years. The advent of histamine-2 receptor antagonists and proton pump inhibitors has accelerated the decline. Helicobacter pylori treatment and eradication in patients with peptic ulcer disease have further decreased the need for surgery. Newer gastric operations, such as proximal gastric vagotomy (which produces minimal disturbance of gastric emptying mechanisms), are associated with a much lower incidence of postgastrectomy syndromes.

Although the need for elective surgery for peptic ulcer disease has declined, the need for emergency surgery has remained the same over the last 20 years. Emergency surgery tends to be more mutilating to the stomach. This increases the incidence of more severe symptoms

The stomach serves as the receptive and storage site of ingested food. The primary functions of the stomach are to act as a reservoir, to initiate the digestive process, and to release its contents downstream into the duodenum in a controlled fashion. The capacity of the stomach in adults is approximately 1.5-2 liters, and its location in the abdomen allows for considerable distensibility. Gastric motility is regulated by the enteric nervous system, which is influenced by extrinsic innervation and by circulating hormones. Alterations in gastric anatomy after surgery or interference in its extrinsic innervation (vagotomy) may have profound effects on gastric emptying. These effects, for convenience, have been termed postgastrectomy syndromes.

Postgastrectomy syndromes include small capacity, dumping, bile gastritis, post-gastrectomy malnutrition, and afferent loop syndrome.

GASTRIC RESECTIONS

Partial gastric resection

A partial gastrectomy may be used in the treatment of ulcers that are resistant to standard therapy, ulcers that continue to recur despite aggressive treatment or ulcers that cause severe complications. Partial gastrectomy is also used as treatment for gastric malignancies restricted to the antrum. Such an operation involves removal of the gastrin-secreting antrum (up to 75% of the distal stomach). Reconstruction is performed with anastomosis of the remaining gastric segment to the duodenum, called Billroth I (BI), or to the side of the jejunum (approximately 15 centimeters distal to the ligament of treitz), called Billroth II (BII) operation. The duodenal stump is preserved in the Billroth II to allow continued flow of bile salts and pancreatic enzymes. However, because of dysynchrony of food and bile/enzyme entry, patients with a BII may still have inadequate mixing.

( Fig. 10.6). Nowadays, BI operations are rare and are used primarily for very small tumors in the antrum.

Vagotomy

BI and BII operations may or may not involve vagotomy. Furthermore, the type of vagotomy may differ. A truncal vagotomy severs the vagus on the distal esophagus. It significantly reduces acid secretion and creates gastric stasis and poor gastric emptying and is therefore combined with a drainage procedure (pyloroplasty or gastrojejunostomy). A selective vagotomy divides and severs the vagus nerve branches that supply the parietal cells while preserving those that innervate the antrum and pylorus. Thus, a drainage procedure is unnecessary, and the innervation to other organs is preserved. Unfortunately, a selective vagotomy is more technically difficult and is associated with a higher rate of ulcer recurrence.

Total gastrectomy ( TG)

Total gastrectomies are performed for gastric malignancies that affect the middle or upper part of the stomach. Total gastrectomy, by nature, involves a functional vagotomy, removing cholinergic drive and eliminating acid production.

Fig.10.6 Principles of Billroth operations

Changes after gastrectomy

Decreased acid

Decreased pepsin

Decreased Intrinsic Factor

Decreased pancreatic enzymes

Decreased mixing of food with acid, pepsin, and bile.

Decreased absorption of proteins, calcium, vitamin D & B, Fe, fat

Rapid absorption of glucose.

Increased intestinal motility

Creation of a “blind loop” i.e. afferent loop.

1. Dumping Syndrome

Pathophysiology

Postprandially, the function of the stomach is to store food and to allow the initial chemical digestion by acid and proteases before transferring food to the gastric antrum. In the antrum, powerful peristaltic contractions pulverize the solids, reducing the particle size to 1-2 mm. Once solids have been reduced to the desired size, they are able to pass through the pylorus. An intact pylorus prevents the passage of larger particles into the duodenum. Gastric emptying is controlled by fundic tone, antropyloric mechanisms, and duodenal feedback. Gastric surgery alters these mechanisms in several ways.

Gastric resection can reduce the fundic reservoir, thereby reducing the stomach’s capacity to accommodate a large meal. Similarly, vagotomy limits receptive relaxation of the stomach. An operation in which the pylorus is removed, bypassed, or destroyed increases the rate of gastric emptying. Duodenal feedback inhibition of gastric emptying is lost after a bypass procedure, such as gastrojejunostomy. Accelerated gastric emptying of stomach is a characteristic feature and a critical step in the pathogenesis of dumping syndrome. Gastric mucosal function is altered by surgery, and acid and enzymatic secretions are decreased. Also, hormonal secretions that sustain the gastric phase of digestion are affected adversely. All these factors interplay in the pathophysiology of dumping syndrome.

The concept of pathophysiology of dumping syndrome discussed above is supported by the fact that a change of dietary habits usually bring partial or even complete relief in most of the patients. People who have gastric dumping syndrome are advised to eat several small meals (e.g. six small meals rather than the usual three large meals) a day. The food should be low in carbohydrates, avoiding simple sugars. The patient is advised to drink liquids between meals, not with them. Fiber-rich food also helps since it delays gastric emptying and reduce insulin peaks.

Incidence and severity of symptoms in dumping syndrome are related directly to the extent of gastric surgery. An estimated 25-50% of all patients who have undergone gastric surgery have some symptoms of dumping. However, only 1-5% patients are reported to have severe disabling symptoms.

Early dumping

Symptoms of early dumping syndrome (30-60 min postprandial) are believed to result from accelerated gastric emptying of hyperosmolar chyme into the small bowel. This leads to fluid shifts from the intravascular compartment into the bowel lumen, resulting in rapid small bowel distention and an increase in the frequency of bowel contractions. Experimentally, rapid instillation of liquid meals into the small bowel has been shown to induce dumping symptoms in healthy individuals. Bowel distention may be responsible for GI symptoms, such as crampy abdominal pain, bloating, and diarrhea. Intravascular volume contraction due to osmotic fluid shifts is perhaps responsible for vasomotor symptoms, such as tachycardia and lightheadedness.

Postprandial release of gut hormones, such as enteroglucagon, peptide YY, pancreatic polypeptide, vasoactive intestinal polypeptide, glucagon-like peptide-1 (GLP-1), and neurotensin, is higher in patients with dumping syndrome compared to asymptomatic patients after gastric surgery. Some or all of these peptides are likely to participate in the pathogenesis of dumping syndrome. One of the effects of these hormones is the retardation of proximal GI motility and the inhibition of secretion. This function is called the ileal brake. Some authors have suggested that the accelerated release of these hormones is an attempt to activate the ileal brake, thereby delaying proximal transit time in response to rapid delivery of food to the distal small bowel.

Late dumping

Late dumping occurs 1-3 hours after a meal. The pathogenesis is thought to be related to the early development of hyperinsulinemic (reactive) hypoglycemia. Rapid delivery of a meal to the small intestine results in an initial high concentration of carbohydrates in the proximal small bowel and rapid absorption of glucose. This is countered by a hyperinsulinemic response. The high insulin levels are responsible for the subsequent hypoglycemia. Experimentally it is has been shown that intra-jejunal glucose induces a higher insulin release than intravenous infusion of glucose, even when serum glucose levels are the same in both experiments. Two hormones are thought to play a pivotal role. These are gastric inhibitory peptide (GIP) also known as glucose-dependent insulinotropic peptide and glucagon like peptide -1(GLP-1). In human studies, an increase in GLP-1 response has been noted after an oral glucose challenge. An increased GLP-1 response has been noted in patients after total gastrectomy, esophageal resection, and partial gastrectomy. Furthermore, a positive correlation has been found between the rise in plasma GLP-1 and insulin release. Exaggerated GLP-1 response likely plays an important role in the hyperinsulinemia and hypoglycemia in patients with late dumping. The reason why some patients remain asymptomatic after gastric surgery, while others develop severe symptoms, remains elusive.

2. Bile gastritis

Bile reflux gastritis can be a disabling post- partial-gastrectomy condition characterized by abdominal pain, bilious vomiting, and weight loss. The syndrome appears to be caused by free enterogastric reflux of bile and other proximal small bowel constituents. The effects of bile salts on gastric mucosa appear to be similar to the effects of nonsteroidal anti-inflammatory drugs. Both will break down the gastric mucosal barrier thereby increasing the risk of inflammation, ulcer development and associated symptoms of pain and bleeding. The same effects have been shown in animal models using bile as the irritant. With mucosal barrier disruption there is a back diffusion of hydrogen ions and the subsequent destruction of the mucosal cell.

There is a wide range of presentation in patients with bile gastritis. Most commonly it is asymptomatic and is a coincidental finding on endoscopy. The other extreme is the development of severe nausea, bilious vomiting, abdominal pain, and anorexia and weight loss. It is most commonly seen in patients with a Bilroth II operation. This procedure allows bile to pass the anastomosis with increased chance of reflux into the stomach.

3. Post-gastrectomy malnutrition

Weight loss

Diarrhea

Steatorrhea

Gross malabsorption syndrome

Anemia – either iron deficiency or megaloblastic

Vitamin B deficiency

Metabolic bone disease

Post-gastrectomy malnutrition results from nutritional intolerance and deficiencies. Combination of fat maldigestion and lactose intolerance is most likely responsible for acute post-operative weight loss, the most frequent complication of gastrectomized patients. Nutrient deficiencies develop months to years after gastric resections and can result in deleterious clinical consequences. Anemia and bone disease are the most common manifestations of the nutritional deficiency seen in these patients.

Protein malnutrition may result from several frequently associated pathogenic factors. Insufficient protein intake is reported in most of the cases. The consequences of such an inadequate diet are aggravated in patients who are alcoholic or of a poor socio-economic status. Another important cause of protein malnutrition is malabsorption of ingested proteins due to a deficient pancreatic secretion.

The gastric stump empties itself early and the gastric content moves rapidly through the upper digestive tract, reaching the jejunum and ileum sooner than the pancreatic enzymes. Other factors may contribute to a post-gastrectomy malnutrition. Bacterial invasion of the small intestine resulting from achlorhydria and stasis in the afferent loop accounts sometimes for steatorrhea. Primary malabsorption due to an atrophy of the intestinal villi is sometimes responsible for malnutrition in a gastrectomized patient.

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Weight loss

. Weight loss usually follows gastric resection with reported loss ranging from 10%-30% of preoperative weight. This loss has been attributed to inadequate dietary intake, malabsorption, rapid intestinal transit time or bacterial overgrowth. More likely, it is a combination of all these factors. Nevertheless, weight gain after surgery is possible. Frequent nutrition follow-up in the early postoperative period is the key to preventing a decline in nutritional status. Indeed, several reports confirm that in the absence of nutrition follow-up, patients become progressively malnourished. Too often, gastrectomized patients are discharged without adequate instruction on what and how much to eat. It is therefore essential for clinicians to provide nutrition intervention and follow-up until patients demonstrate the ability to maintain or gain weight, as the case necessitates.

Fat maldigestion

Studies looking at fat malabsorption after PG and TG have demonstrated excessive fecal fat excretion. The etiology of fat malabsorption appears to be multifactorial. First, the gastric stump empties itself early and the gastric content moves rapidly through the upper digestive tract, reaching the jejunum and ileum sooner than the pancreatic enzymes. Second, decreased transit time prevents sufficient mixing of food with digestive enzymes and bile salts, especially in TG or BII patients. Third, decreased enzyme production reduces the ratio of enzymes to food. One study measuring exocrine pancreatic function in TG patients found that all patients had severe exocrine pancreatic insufficiency three months after surgery. Finally, due to loss of the antrum, and hence its sieving function, larger than normal food particles empty into the jejunum, making enzyme attack more difficult. Qualitative or quantitative fecal fat estimation is useful in the diagnosis of fat maldigestion

Lactose intolerance

Lactase, the enzyme required for lactose absorption, is found primarily on villi in the jejunum. Most gastrectomized patients have an intact jejunum, therefore lactose intolerance, in these patients, is deemed “functional.” Patients complaining of abdominal cramping or pain, bloating, diarrhea, flatulence and distention after consumption of lactose may do well to decrease or avoid it. Tolerance to lactose is typically dose-dependent and may improve over time. Many patients may be able to tolerate smaller amounts of lactose containing foods throughout the day. Lactase enzymes are available for patients who wish to continue consuming dairy products.

Although diet therapy may be beneficial in treating nutritional intolerances, it is important to minimize diet restrictions. Superfluous restrictions may cause frustration to the patient and can further aggravate weight loss.

Anemia

Nutritional anemias resulting from iron deficiency, vitamin B12, or folate are common in gastrectomized patients. Consequences of anemia can be severe. Therefore baseline hemoglobin estimation and periodic monitoring is important. Anemia often presents as a late complication of gastric resection, placing patients with a distant history of the surgery at an even greater risk.

Microcytic Anemia

Iron deficiency is the most common anemia following gastric resection.

The reported incidence varies from 5% to 62% of patients with BII.

Alterations in digestion and absorption of dietary iron are thought to be responsible for iron deficiency in TG and PG patients. Duodenum, the primary site for iron absorption, is bypassed (except with BI) and reduced gastric acidity impairs the conversion of ferric iron to the more absorbable ferrous form. Reduced iron intake may also play a role.

Megaloblastic and pernicious anemia

Megaloblastic anemia may be the result of either vitamin B12 or folate deficiency. B12 deficiency may result in PG and TG patients for numerous reasons. Normally, intrinsic factor is complexed to B12 and facilitates its absorption by the terminal ileum. Reduction in intrinsic factor and reduced gastric acidity in gastrectomized patients impairs cleavage of protein bound B12. Bacterial overgrowth and reduced intake of B12 rich foods may also contribute to a deficiency state. Folate deficiency may develop after gastric surgery but is not well reported. Causes of folate deficiency are likely multifactorial including malabsorption (the first site of folate absorption is the duodenum).

Metabolic Bone Disease

Metabolic bone disease, such as osteoporosis, and osteomalacia, is commonly reported in gastrectomy patients leading to a greater risk of bone fractures. A low bone mineral density (BMD) has been reported in 27% to 44% of gastrectomized patients. The etiology of bone disease in gastrectomized patients is uncertain but appears to be a combination of decreased intake of calcium, vitamin D and lactose-containing foods, coupled with altered absorption and metabolism of vitamin D. Vitamin D deficiency may result from decreased intake rather than malabsorption. A significant increase in 25-OHD levels have been recorded when TG and PG patients were supplemented with 400 IU of vitamin D per day.