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

AFFERENT LOOP SYNDROME (ALS) ISSUES IN GASTROENTEROLOGY, SERIES #18

Afferent loop syndrome (ALS) is a purely mechanical complication that infrequently occurs following construction of a Billroth II gastrojejunostomy. Creation of an anastomosis between the stomach and jejunum leaves a segment of small bowel, most commonly consisting of duodenum and proximal jejunum, lying upstream from the gastrojejunostomy ( Fig 10.6). This limb of intestine conducts bile, pancreatic juices, and other proximal intestinal secretions toward the gastrojejunostomy and is thus termed the afferent loop.

Passage of food and gastric secretions through the gastrojejunostomy and into the efferent loop triggers release of secretin and cholecystokinin. These enteric hormones stimulate secretion of bile, pancreatic enzymes, and pancreatic bicarbonate and water into the afferent loop. Under gastrointestinal hormonal influence, up to 1-2 L of pancreatic and biliary secretions can enter the afferent loop each day.

Symptoms associated with acute ALS are caused by increased intraluminal pressure and distension due to accumulation of enteric secretions in a completely obstructed afferent loop. ALS is one of the main causes of duodenal stump blowout in the early postoperative period and is also an etiology for postoperative obstructive jaundice, ascending cholangitis, and pancreatitis due to transmission of high pressures back to the biliopancreatic ductal system. High luminal pressures and distension increase bowel wall tension in the afferent loop and can lead to ischemia and gangrene with subsequent perforation and peritonitis.

Chronic ALS is more common. It results from prolonged stasis and pooling of secretions with partial obstruction of the afferent loop which facilitates bacterial overgrowth in the afferent loop. Bacteria deconjugate bile acids, which can lead to steatorrhea, malnutrition, and vitamin B-12 deficiency. Iron deficiency can occur because of bypassing of the duodenum.

BACTERIAL OVERGROWTH SYNDROME

Bacterial overgrowth syndrome (BOS) is a term that describes clinical manifestations that occur when the normally low number of bacteria that inhabit the stomach, duodenum, jejunum, and proximal ileum significantly increases or becomes overtaken by other pathogens.

Low concentrations of various bacteria live within or attached to its luminal surface. These bacteria are thought to be present soon after birth and through adulthood, living in symbiosis with the human host. This relationship is thought to be vital for normal digestive processes, immunity, and intestinal development.

The following defense mechanisms of the small intestine, which keep the upper intestine practically bacteria free, can be compromised in various disorders:

1. Migrating motor complexes (MMC) (or migrating myoelectric complexes) are waves of activity which sweep through the intestines in a regular cycle during fasting state. These motor complexes help trigger peristaltic waves which facilitate transportation of indigestible substances such as bone, fiber and foreign bodies from the stomach, through the small intestine past the ileocecal sphincter into the colon. The MMC originates in the stomach roughly every 75-90 minutes during the interdigestive phase (between meals) and is responsible for the rumbling experienced when hungry.

MMC also serves to transport bacteria from the small intestine to the large intestine, and to inhibit the migration of colonic bacteria into the terminal ileum. Anatomical defects can reduce peristaltic efficacy; for example, blind pouches result in a stagnant portion of the intestine, e.g. blind loop, small bowel diverticuli. Impaired motility in the small intestine is a characteristic feature of scleroderma.

2. Gastric acid reduces the bacteria populations in the proximal small intestine, particularly anaerobic bacteria. Deficiency of gastric acid after gastric resections allows the bacterial overgrowth in the small intestine.

3. The bowel mucosal integrity and mucus layer protect the gut from bacteria. This protective mechanism is disrupted in disorders such as Celiac disease, tropical sprue etc.

4. Immunoglobulin secretion and immune cells (e.g. macrophages and lymphocytes) protect the gut from bacteria.

5. Normal intestinal florae (e.g., Lactobacillus) protect the gut from bacterial overgrowth by maintaining a low pH; abnormal communications produce pathways that allow enteric bacteria to pass between the proximal and distal bowel.

In a normal person, the bacterial count in the upper small intestine is less than 103 organisms / ml aspirate. When the protective mechanisms mentioned above breakdown, the bacterial count may increase above 1010 organisms / ml aspirate. The bacteria usually found are those normally present in the colon. The overgrowth of the bacteria causes direct or indirect alteration in bile salt metabolism, and other metabolic defects. The bacteria deconjugate the bile salts leading to:

decreased concentration of bile salts, and

absorption of deconjugated bile acids in the jejunum. It further decreasing the intraluminal concentration of bile salts in the jejunum. (Bile salts are normally absorbed in the ileum).

Consequently, both intestinal digestion and absorption of fat suffers. Deconjugated bile acids directly inhibit carbohydrate transporters. The unabsorbed sugars ferment into organic acids, thereby reducing the intraluminal pH and producing osmotic diarrhea. The deconjugated bile acids also damage intestinal enterocytes and induce water secretion by the colonic mucosa. All these changes produce malabsorption syndrome (Table 10. 4). Uptake of vitamin B12 by the bacteria accounts for particularly low plasma levels of the vitamin and symptoms of pernicious anemia. In chronic ALS, iron deficiency results from deficiency of gastric acid and upper intestinal bypass.