Stomach And Intestines Anatomy And Physiology Biology


The tummy receives both sympathetic and parasympathetic excitation. The sympathetic fibres reach the tummy via celiac rete. The parasympathetic fibres reach the tummy through the left and right pneumogastric nervousnesss. The anterior pneumogastric bole, which is derived chiefly from the left pneumogastric nervus, enters the abdominal pit through the esophageal suspension in the stop. Its stomachic subdivisions are distributed on the anterio-superior surface. The posterior pneumogastric bole, which is derived chiefly from the right pneumogastric nervus, besides enters the venters through the esophageal suspension in the stop on the posterior surface of the gorge. Its stomachic subdivisions are distributed on the posterio-inferior surface of the tummy.

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Besides the extrinsic excitation described above, the tummy contains an extended enteric nervous system in the signifier of submucosal Meissner ‘s rete and Auerbach ‘s rete situated between the two beds ( round and longitudinal ) of the musculus coat. Assorted nerve cells of the enteral nervous system produce noradrenaline, acetylcholine, vasoactive enteric peptide ( VIP ) , substance P, somatostatin, or azotic oxide.

The sympathetic supply chiefly controls the blood vass and muscular coat of the tummy. Sympathetic stimulation decreases stomachic motility. Parasympathetic stimulation additions stomachic motility every bit good as the secernment of oxyntic ( parietal ) cells, main cells and G cells of the stomachic mucous membrane.

Secretory Functions of tummy

Mucosal secretory organs of the fundus and organic structure of the tummy secrete stomachic juice rich in acid and pepsinogen ( Fig 10.1 B ) . Mucosa of the pyloric parts secretes bicarbonate-rich soluble mucous secretion. The surface of the full gastric mucous membrane is lined by columnar cells that produce a gluey bicarbonate-rich mucous secretion that adheres to the cells. The cell beginning and the chief maps of the tummy are summarized in Table 10.1. .

Exocrine stomachic secernment

Hydrochloric acid

Oxyntic ( parietal cells )

Sterilizes upper GIT

Activates pepsinogen

Helps in enteric Fe soaking up

Intrinsic factor

Oxyntic ( parietal cells )

Intestinal soaking up of vitamin B 12


Chief cells

Protein digestion ( as pepsin )


Mucus cells

Pyloric secretory organs

Protection of stomachic mucous membrane


Surface epithelial cells

Protection of stomachic mucous membrane

Endocrine stomachic secernment


G cells ( in pyloric antrum )

Increased secernment of oxyntic and main cells of the tummy and of exocrine pancreatic acini


D cells ( all over stomachic mucous membrane )

Suppression of acerb secernment

Feedback control of stomachic acid ordinance

Several specialized cells in the stomachic mucous membrane contribute to the control of acerb secernment. G cells in the stomachic antrum let go of the endocrine gastrin. Gastrin acts on the enterochromaffin-like cells in the stomachic principal to let go of histamine, which stimulates parietal cells to release acid. Gastrin besides stimulates parietal cells straight and promotes growing of enterochromaffin-like and parietal cells.

Fig 10.2. Feedback control of stomachic acid. S = somatostatin releasing cell ; G = G-cell: P Parietal cell ; ECL = enterochromaffin-like cell.

Histamine H2 receptor adversaries act by barricading the consequence of histamine on parietal cells. Proton pump inhibitors act by suppressing the enzyme in parietal cells that catalyses acerb production for release into the stomachic lms. G cells, enterochromaffin-like cells, and parietal cells are all regulated by release of the repressive peptide somatostatin from somatostatin cells, which are distributed throughout the tummy. The consequence of HA pylori infection on acerb secernment depends on which portion of the tummy is most inflamed because this determines which of these cells are affected most.

Motor maps of tummy

Storage of ingested nutrient.

Empty tummy has a capacity of 50 milliliters merely. As nutrient is ingested, the stomachic capacity bit by bit increases. At the terminal of a repast, the tummy may incorporate 1000-1500 milliliter of nutrient, H2O and stomachic juice. The storage map of the tummy is chiefly served by the fundus and organic structure parts, which undergo a bit by bit increasing vagally mediated automatic receptive relaxation. That is why ; after vagotomy, the patients frequently complain of early repletion every bit good as post-prandial epigastric comprehensiveness.

Mixing, crunching and screening map

Peristaltic moving ridges go throughing down the organic structure and pyloric portion of tummy produce thorough commixture of nutrient with the stomachic juice. The nutrient is macerated into a semi-liquid chyme. The narrow pyloric sphincter Acts of the Apostless like a screen and allows atoms less than 1 millimeter in size to go forth the tummy in to the first portion of duodenum.

Regulation of stomachic voidance:

Dilatation of tummy or increased gastrin secernment increases the strength of stomachic vermiculation. On the other manus, presence of extremely acerb chyme, hyperosmolar chyme or fat-rich chyme in the duodenum decreases the strength of stomachic vermiculation. These duodenal inhibitory influences on stomachic emptying guarantee that sum of chyme incorporating acid, and nutrient atoms is ideal for the proper digestion and soaking up in the little bowel.

Small bowel: functional anatomy and physiology

The little bowel steps about, 2.5-3 centimeter in diameter and 6 metres in length during life. The ligament of Treitz demarcates duodenum from jejunum. Below the duodenum, the upper 40 % of the little bowel is called the jejunum and the staying 60 % as ileum. There is no anatomic limit between jejunum and ileum. The villi, a characteristic characteristic of little enteric mucous membrane are largest and most legion in the duodenum and jejunum, and go fewer and smaller in the ileum. The ileum ends with the ileocecal valve ( sphincter ) , which regulates the motion of chyme into the big bowel and prevents backward motion of stuff from the big bowel.

Small bowel is the site of concluding digestion and soaking up of groceries. Most of the digestive enzymes that act in the little bowel are secreted by the pancreas ( Table 10.2 ) . In add-on gall salts present in the gall ( formed in the liver ) are indispensable for proper digestion and soaking up of dietetic fats. The pancreatic and bile canals open in the 2nd portion of duodenum. As a little bolus of chyme leave the tummy, its confidant commixture with pancreatic juice and gall helps in proper digestion and soaking up. Presence of nutrient in the upper little bowel is indispensable for the release of GI endocrines such as secretin and cholecystokinin which increase the secernment of pancreas and gall. When the duodenum is bypassed ( e.g. Billroth II operation ) malabsorption normally occurs. The optimal pH for the activity of pancreatic enzymes is 6-7. Such pH is achieved by neutralisation of the extremely acidic chyme that leaves the tummy by the alkalic pancreatic and bile juices.

Table 10. 2 Principal digestive enzymes in the little bowel.















Intestinal mucous membrane









The enteric digestion of groceries consequences in production of monosaccharoses, aminic acids and fatty acids. These merchandises and assorted other constituents of nutrient such as vitamins, minerals and H2O are absorbed in specific parts of the little bowel ( Table 10. 3 ) . This cognition becomes important when a portion of the little bowel is to be resected as a intervention of some upset ( e.g. Crohn ‘s disease ) . Extensive resection of little bowel is most likely to ensue in enteric malabsorption ( short intestine or short intestine syndrome ) . Short intestine syndrome normally develops when less than 2 metres of the little bowel left after surgery.

Table 10.3. Site of soaking up of assorted groceries in the GIT.


Duodenum and jejunum





Vitamin B12


( some drugs )

Amino acids

Bile salts


Water soluble vitamins



Fat soluble vitamins


Fatty acids







Colon: Functional anatomy and physiology

Colon or the big bowel is a tubing about 6 centimeters in diameter and 1.5 metres in length. Mucus ( pH 8 ) is the main secernment of colon. Absorption of H2O and electrolytes is the main map of the big bowel. The colon contains a big figure of bacteriums which synthesize vitamin K, folic acid and a figure of other vitamins included in B composite, which are absorbed in blood circulation

Large bowel can non absorb saccharides, aminic acids or fatty acids. These merchandises reach the colon in patients with unequal digestion / soaking up of groceries in the little bowel ( maldigestive / malabsorption syndrome ) . The agitation of undigested saccharides by the colonic bacterium produces big sum of gases ( fart ) . Undigested fats are hydrolyzed by the bacteriums in to fatty acids, which can non be absorbed. Fatty acids act as thorn to the colonic mucous membrane, bring forthing diarrhoea. Undigested proteins are broken down to by the bacterial deaminases. Therefore, even in a instance with terrible maldigestion, the stools contain the debauched merchandises instead than supermolecules of saccharides, fats or proteins as such.

Infantile Hypertrophic Pyloric Stenosis

Pyloric stricture, besides known as childish hypertrophic pyloric stricture ( IHPS ) , is the most common cause of enteric obstructor in babyhood. Although less common in Asiatic population, IHPS is by no means a rareness. It is 4 times more common in male kids. Although it can happen any clip from the twenty-four hours of birth to approximately 3 to 4 months, most common presentation is between the 3rd and 6th hebdomad of age. The presenting symptoms are about ever projectile non-bilious emesis in a babe hitherto normal with no other attach toing findings of upper respiratory infection etc. The presence of an egg-shaped olive-shaped mass in the right upper quadrant country near to the epigastrium is a really of import mark.


The lesion is characterized by stomachic mercantile establishment obstructor and multiple anatomic abnormalcies of the pyloric antrum. There is marked hypertrophy and hyperplasia of the chiefly round, but besides longitudinal, musculus fibres of pylorus. The antropyloric musculus is abnormally innervated ( see below ) . In add-on, farther the luminal narrowing is caused by crowded and excess mucous membrane. The mucous membrane normally is dropsical and thickened. In advanced instances, the tummy becomes markedly dilated in response to near-complete obstructor.


Fig 10.3 The pyloric sphincter in a normal baby and in a instance of hypertrophic pyloric stricture.

Nitric oxide has been demonstrated as a major inhibitory nonadrenergic, noncholinergic neurotransmitter in the GI piece of land, doing relaxation of smooth musculus of the myenteric rete upon its release. Damage of this neural azotic oxide synthase ( nNOS ) synthesis has been implicated in IHPS, in add-on to achalasia, diabetic gastroparesis, and Hirschsprung disease.

The stomachic mercantile establishment obstructor due to the hypertrophic pylorus impairs emptying of stomachic contents into the duodenum. As a effect, all ingested nutrient and stomachic secernments can merely go out via emesis, which can be of a projectile nature. The vomited stuff does non incorporate gall because the pyloric obstructor prevents entry of duodenal contents ( incorporating gall ) into the tummy. This consequences in loss of stomachic acid ( hydrochloric acid ) , taking to metabolic alkalosis. Persistent emesis is accompanied by loss of non merely acid but besides fluids from the tummy. The ensuing hypovolaemia leads to a secondary hyperaldosteronism. The high aldosterone degrees cause the kidneys to: ( a ) avidly retain Na+ ( to rectify the intravascular volume depletion ) , and ( B ) excrete increased sums of K+ and H+ into the piss, ensuing in hypokalemia and farther exasperation of alkalosis.

Pathophysiology of peptic ulcer

It is a physiological wonder that stomachic juice can easy digest the swallowed pieces of meat but usually, it has no caustic action on the gastric mucosa itself. Several factors seem to be involved in the protection of stomachic mucous membrane from autodigestion. These factors, jointly known as stomachic mucosal barrier, include:

( a ) Mucus secreted by surface epithelial cells and mucus cervix secretory organs which forms a H2O indissoluble visco-elastic gel with hapless diffusion coefficient for H+ .

Bicarbonate secreted by surface epithelial cells into the boundary zone between the epithelial cells and the mucous secretion bed. The secernment of mucous secretion and hydrogen carbonate is believed to be mediated through prostaglandins.

Tight junctions between the next cells of stomachic surface epithelial tissue.

Rapid turnover of surface epithelial cells, and rich blood supply.

Prostaglandins. Endogenous prostaglandins stimulate secernment of stomachic mucous secretion every bit good as gastric and duodenal mucosal hydrogen carbonate. Prostaglandins besides participate in the care of stomachic mucosal blood flow and unity of mucosal barrier and advance epithelial cell reclamation in response to mucosal hurt.

Under normal conditions, a physiologic balance exists between peptic acid secernment and gastro-duodenal mucosal defence. Mucosal hurt and, therefore, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as NSAIDs, H pylori, intoxicant, coffin nail smoke, psychogenetic emphasis ( inordinate acid, and pepsin ) or Zollinger Ellison syndrome can change the mucosal defence by leting back diffusion of H ions and subsequent epithelial cell hurt.

Mechanisms of hurt differ clearly between duodenal and stomachic ulcers. Duodenal ulcer is basically an H. pylori-related disease and is caused chiefly by an addition in acerb and pepsin burden, and stomachic metaplasia in the duodenal cap. Gastric ulcer, at least in Western states, is most normally associated with NSAID consumption, although H. pylori infection might besides be present. Chronic, superficial and atrophic gastritis predominate in patients with stomachic ulcers, when even normal acid degrees can be associated with mucosal ulceration. Basically in both conditions, ulcer is associated with an instability between protective and aggressive factors, with redness being a taking cause of this instability.

Fig. 10.4. Helicobactor pylori bacteria.

Role of Helicobacter pylori

Helicobacter pylori is a Gram-negative B responsible for one of the most common infections found in worlds worldwide. H pylori beings are spiral-shaped Gram-negative bacteriums that are extremely motile because of multiple unipolar scourge. They are microaerophilic ( need less O ) and powerful manufacturers of the enzyme urease. H pylori inhabits the mucous secretion next to the stomachic mucous membrane. The most common path of H pylori infection is either oral-to-oral: caressing ( stomach contents are transmitted from oral cavity to talk ) or fecal-to-oral ( from stool to talk ) contact. Parents and siblings seem to play a primary function in transmittal

Helicobacter pylori bacteriums colonize the tummy and induces chronic gastritis. It is widely believed that in the absence of intervention, H. pylori infection-once established in its stomachic niche-persists for life. In Western states the prevalence of Helicobacter pylori infections approximately lucifers age ( i.e. , 20 % at age 20, 30 % at age 30, 80 % at age 80, etc ) . Prevalence is higher in 3rd universe states. Most persons infected by H. pylori will ne’er see clinical symptoms despite holding chronic gastritis. Approximately 10-20 % of those colonized by H. pylori will finally develop stomachic and duodenal ulcers. A larger proportion of people will acquire non-specific uncomfortableness, abdominal hurting or gastritis ( Fig. 10.5 ) . The badness of the redness is likely to underlie H. pylori-related diseases. Duodenal and tummy ulcers result when the effects of redness allow the acid and pepsin in the tummy lms to overpower the mechanisms that protect the tummy and duodenal mucous membrane from these acerb substances.

The type of ulcer that develops depends on the location of chronic gastritis, which occurs at the site of H. pylori colonisation. In those with duodenal ulcer, H. pylori colonizes the antrum. The inflammatory response to the bacterium causes devastation of somatostatin-producing D cells in the pylorus. Consequently, the G cells in the antrum secrete more of the endocrine gastrin, which travels through the blood stream to the principal. Gastrin stimulates the parietal cells in the principal to release more acid into the tummy lms. Chronically increased gastrin degrees finally cause the figure of parietal cells to besides increase, farther intensifying the sum of acid secreted. The increased acid burden amendss the duodenum, and ulceration may finally ensue.

In contrast, stomachic ulcers are frequently associated with normal or decreased stomachic acid production, proposing that the mechanisms that protect the stomachic mucous membrane are faulty. In these patients H. pylori can besides colonise the principal of the tummy, where the acid-secreting parietal cells are located. However, chronic redness induced by the bacterium causes farther decrease of acerb production, and finally wasting of the tummy liner. Gastric wasting may take to stomachic ulcer and increases the hazard for tummy malignant neoplastic disease.

H pylori infection and its association with stomachic malignance have been good described in several epidemiologic surveies. However, the class of patterned advance from redness to malignant neoplastic disease remains ill-defined. One theoretical account describes the stepwise patterned advance of H pylori infection to hypochlorhydria, chronic gastritis, atrophic gastritis, enteric metaplasia, and stomachic malignant neoplastic disease. Increased production of the cytokine interleukin -1I? has been linked to an increased hazard of hypochlorhydria and stomachic malignant neoplastic disease in septic topics.

Fig.10.5. Consequences of H pylori infection.

Complications of peptic ulcers


Bleeding: Mild to severe bleeding is the most common complication of peptic ulcer disease. It may happen even when the ulcer hurting is non terrible. Symptoms include haematemesis ( fresh blood or “ java land ” stuff ) ; transition of bloody stools or black tarry stools ( melaena ) ; and failing, faint, thirst, and sudating caused by blood loss. However, little sums of blood in the stool may non be noticeable but, if relentless, can still take to anemia


A peptic ulcer may perforate the wall of the tummy. If adhesions prevent escape into the peritoneal pit, free incursion is avoided and confined perforation occurs. Ulcers on the front surface of the duodenum, or less normally the tummy, can travel through the wall, making an gap to the free infinite in the abdominal pit. Perforation frequently leads to catastrophic effects. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of tummy or enteric content into the abdominal pit. Perforation at the anterior surface of the tummy leads to acute peritoneal inflammation, ab initio chemical and subsequently bacterial peritoneal inflammation. The first mark is frequently sudden intense abdominal hurting. Posterior wall perforation leads to pancreatitis ; hurting in this state of affairs frequently radiates to the dorsum.


An ulcer may perforate the muscular wall of the tummy or duodenum and go on into an next organ, such as the liver or pancreas.

Gastric mercantile establishment obstructor: Gastric mercantile establishment obstructor is the 3rd most frequent complication of peptic ulcer disease after shed blooding and perforation. It can happen during the acute stage of the disease or in chronic disease. Gastric mercantile establishment obstructor has traditionally been considered synonymous with pyloric stricture as a consequence of peptic ulcer disease in grownups.

Obstruction may be caused by marking, cramp, or redness from an ulcer. Symptoms include perennial, large-volume emesis, happening more often at the terminal of the twenty-four hours and frequently every bit late as 6 H after the last repast. Loss of appetency with relentless bloating or comprehensiveness after eating besides suggests stomachic mercantile establishment obstructor. Prolonged purging may do weight loss, desiccation, and alkalosis.


Peoples with ulcers caused by Helicobacter pylori have 3 to 6 times the opportunity of developing tummy malignant neoplastic disease later in life. There is no increased hazard of developing malignant neoplastic disease from ulcers that have other causes.


Modern intervention of peptic ulcer has led to a diminution in the frequence of gastrectomies and hence, the incidence of postgastrectomy syndromes has declined to a great extent. A 10-fold decrease has occurred in elected operations for peptic ulcer disease in the last 20-30 old ages. The coming of histamine-2 receptor adversaries and proton pump inhibitors has accelerated the diminution. Helicobacter pylori intervention and obliteration in patients with peptic ulcer disease have further decreased the demand for surgery. Newer stomachic operations, such as proximal stomachic vagotomy ( which produces minimum perturbation of stomachic emptying mechanisms ) , are associated with a much lower incidence of postgastrectomy syndromes.

Although the demand for elected surgery for peptic ulcer disease has declined, the demand for exigency surgery has remained the same over the last 20 old ages. Emergency surgery tends to be more mutilating to the tummy. This increases the incidence of more terrible symptoms

The tummy serves as the receptive and storage site of ingested nutrient. The primary maps of the tummy are to move as a reservoir, to originate the digestive procedure, and to let go of its contents downstream into the duodenum in a controlled manner. The capacity of the tummy in grownups is about 1.5-2 litres, and its location in the venters allows for considerable distensibility. Gastric motility is regulated by the enteral nervous system, which is influenced by extrinsic excitation and by go arounding endocrines. Changes in stomachic anatomy after surgery or intervention in its extrinsic excitation ( vagotomy ) may hold profound effects on stomachic voidance. These effects, for convenience, have been termed postgastrectomy syndromes.

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


Partial stomachic resection

A partial gastrectomy may be used in the intervention of ulcers that are immune to standard therapy, ulcers that continue to repeat despite aggressive intervention or ulcers that cause terrible complications. Partial gastrectomy is besides used as intervention for stomachic malignances restricted to the antrum. Such an operation involves remotion of the gastrin-secreting antrum ( up to 75 % of the distal tummy ) . Reconstruction is performed with inosculation of the staying stomachic section to the duodenum, called Billroth I ( BI ) , or to the side of the jejunum ( about 15 centimetres distal to the ligament of treitz ) , called Billroth II ( BII ) operation. The duodenal stump is preserved in the Billroth II to let continued flow of bile salts and pancreatic enzymes. However, because of dysynchrony of nutrient and bile/enzyme entry, patients with a BII may still hold unequal commixture.

( Fig. 10.6 ) . Nowadays, BI operations are rare and are used chiefly for really little tumours in the antrum.


BI and BII operations may or may non affect vagotomy. Furthermore, the type of vagotomy may differ. A truncal vagotomy severs the pneumogastric on the distal gorge. It significantly reduces acerb secernment and creates stomachic stasis and hapless stomachic voidance and is hence combined with a drainage process ( pyloroplasty or gastrojejunostomy ) . A selective vagotomy divides and severs the pneumogastric nervus subdivisions that supply the parietal cells while continuing those that innervate the antrum and pylorus. Therefore, a drainage process is unneeded, and the excitation to other variety meats is preserved. Unfortunately, a selective vagotomy is more technically hard and is associated with a higher rate of ulcer return.

Entire gastrectomy ( TG )

Entire gastrectomies are performed for stomachic malignances that affect the center or upper portion of the tummy. Entire gastrectomy, by nature, involves a functional vagotomy, taking cholinergic thrust and extinguishing acerb production.

Fig.10.6 Principles of Billroth operations

Changes after gastrectomy

Decreased acid

Decreased pepsin

Decreased Intrinsic Factor

Decreased pancreatic enzymes

Decreased commixture of nutrient with acid, pepsin, and gall.

Decreased soaking up of proteins, Ca, vitamin D & A ; B, Fe, fat

Rapid soaking up of glucose.

Increased enteric motility

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

1. Dumping Syndrome


Postprandially, the map of the tummy is to hive away nutrient and to let the initial chemical digestion by acid and peptidases before reassigning nutrient to the stomachic antrum. In the antrum, powerful peristaltic contractions pulverize the solids, cut downing the atom size to 1-2 millimeter. Once solids have been reduced to the desired size, they are able to go through through the pylorus. An integral pylorus prevents the transition of larger atoms into the duodenum. Gastric voidance is controlled by fundic tone, antropyloric mechanisms, and duodenal feedback. Gastric surgery alters these mechanisms in several ways.

Gastric resection can cut down the fundic reservoir, thereby cut downing the tummy ‘s capacity to suit a big repast. Similarly, vagotomy bounds receptive relaxation of the tummy. An operation in which the pylorus is removed, bypassed, or destroyed increases the rate of stomachic emptying. Duodenal feedback suppression of stomachic voidance is lost after a beltway process, such as gastrojejunostomy. Accelerated stomachic voidance of tummy is a characteristic characteristic and a critical measure in the pathogenesis of dumping syndrome. Gastric mucosal map is altered by surgery, and acid and enzymatic secernments are decreased. Besides, hormonal secernments that sustain the stomachic stage of digestion are affected adversely. All these factors interplay in the pathophysiology of dumping syndrome.

The construct of pathophysiology of dumping syndrome discussed above is supported by the fact that a alteration of dietetic wonts normally bring partial or even complete alleviation in most of the patients. Peoples who have gastric dumping syndrome are advised to eat several little repasts ( e.g. six little repasts instead than the usual three big repasts ) a twenty-four hours. The nutrient should be low in saccharides, avoiding simple sugars. The patient is advised to imbibe liquids between repasts, non with them. Fiber-rich nutrient besides helps since it delays stomachic voidance and cut down insulin extremums.

Incidence and badness of symptoms in dumping syndrome are related straight to the extent of stomachic surgery. An estimated 25-50 % of all patients who have undergone stomachic surgery have some symptoms of dumping. However, merely 1-5 % patients are reported to hold terrible disenabling symptoms.

A Dumping syndrome manifestations

Early dumping: When symptoms of dumping syndrome occur during a repast or 30-60 min postprandial: they may include:



Abdominal hurting, spasms


Dizziness, dizziness

Bloating, burping


Heart palpitations, rapid bosom rate

Late dumping: When marks and symptoms develop subsequently, normally one to three hours after eating: they may include:


Weakness, weariness

Dizziness, dizziness


Feelingss of anxiousness, jitteriness

Palpitation, tachycardia


Mental confusion



Early on dumping

Symptoms of early dumping syndrome ( 30-60 min postprandial ) are believed to ensue from accelerated stomachic voidance of hyperosmolar chyme into the little intestine. This leads to fluid displacements from the intravascular compartment into the intestine lms, ensuing in rapid little intestine dilatation and an addition in the frequence of intestine contractions. Experimentally, rapid instillment of liquid repasts into the little intestine has been shown to bring on dumping symptoms in healthy persons. Bowel dilatation may be responsible for GI symptoms, such as crampy abdominal hurting, bloating, and diarrhoea. Intravascular volume contraction due to osmotic fluid displacements is possibly responsible for vasomotor symptoms, such as tachycardia and dizziness.

Postprandial release of intestine endocrines, such as enteroglucagon, peptide YY, pancreatic polypeptide, vasoactive enteric polypeptide, glucagon-like peptide-1 ( GLP-1 ) , and neurotensin, is higher in patients with dumping syndrome compared to symptomless patients after stomachic surgery. Some or all of these peptides are likely to take part in the pathogenesis of dumping syndrome. One of the effects of these endocrines is the deceleration of proximal GI motility and the suppression of secernment. This map is called the ileal brake. Some writers have suggested that the accelerated release of these endocrines is an effort to trip the ileal brake, thereby detaining proximal theodolite clip in response to rapid bringing of nutrient to the distal little intestine.

Late dumping

Late dumping occurs 1-3 hours after a repast. The pathogenesis is thought to be related to the early development of hyperinsulinemic ( reactive ) hypoglycaemia. Rapid bringing of a repast to the little bowel consequences in an initial high concentration of saccharides in the proximal little intestine and rapid soaking up of glucose. This is countered by a hyperinsulinemic response. The high insulin degrees are responsible for the subsequent hypoglycaemia. Experimentally it is has been shown that intra-jejunal glucose induces a higher insulin release than endovenous extract of glucose, even when serum glucose degrees are the same in both experiments. Two endocrines are thought to play a polar function. These are stomachic repressive peptide ( GIP ) besides known as glucose-dependent insulinotropic peptide and glucagon like peptide -1 ( GLP-1 ) . In human surveies, an addition in GLP-1 response has been noted after an unwritten glucose challenge. An increased GLP-1 response has been noted in patients after entire gastrectomy, esophageal resection, and partial gastrectomy. Furthermore, a positive correlativity has been found between the rise in plasma GLP-1 and insulin release. Exaggerated GLP-1 response likely plays an of import function in the hyperinsulinemia and hypoglycaemia in patients with late dumping. The ground why some patients remain symptomless after stomachic surgery, while others develop terrible symptoms, remains elusive.

2. Bile gastritis

Bile reflux gastritis can be a crippling post- partial-gastrectomy status characterized by abdominal hurting, biliary emesis, and weight loss. The syndrome appears to be caused by free enterogastric reflux of gall and other proximal little intestine components. The effects of gall salts on stomachic mucous membrane appear to be similar to the effects of nonsteroidal anti-inflammatory drugs. Both will interrupt down the stomachic mucosal barrier thereby increasing the hazard of redness, ulcer development and associated symptoms of hurting and hemorrhage. The same effects have been shown in animate being theoretical accounts utilizing gall as the thorn. With mucosal barrier break there is a back diffusion of H ions and the subsequent devastation of the mucosal cell.

There is a broad scope of presentation in patients with bile gastritis. Most commonly it is symptomless and is a coinciding determination on endoscopy. The other extreme is the development of terrible sickness, biliary emesis, abdominal hurting, and anorexia and weight loss. It is most normally seen in patients with a Bilroth II operation. This process allows gall to go through the inosculation with increased opportunity of reflux into the tummy.

3. Post-gastrectomy malnutrition

Weight loss



Gross malabsorption syndrome

Anemia – either iron lack or megaloblastic

Vitamin B lack

Metabolic bone disease

Post-gastrectomy malnutrition consequences from nutritionary intolerance and lacks. 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 lacks develop months to old ages after stomachic resections and can ensue in hurtful clinical effects. Anemia and bone disease are the most common manifestations of the nutritionary lack seen in these patients.

Protein malnutrition may ensue from several often associated infective factors. Insufficient protein consumption is reported in most of the instances. The effects of such an unequal diet are aggravated in patients who are alcoholic or of a hapless socio-economic position. Another of import cause of protein malnutrition is malabsorption of ingested proteins due to a lacking pancreatic secernment.

The stomachic stump empties itself early and the stomachic content moves quickly through the upper digestive piece of land, making the jejunum and ileum Oklahoman than the pancreatic enzymes. Other factors may lend to a post-gastrectomy malnutrition. Bacterial invasion of the little bowel ensuing from achlorhydria and stasis in the sensory nerve cringle histories sometimes for steatorrhea. Primary malabsorption due to an wasting of the enteric villi is sometimes responsible for malnutrition in a gastrectomized patient.


Weight loss

. Weight loss normally follows stomachic resection with reported loss runing from 10 % -30 % of preoperative weight. This loss has been attributed to inadequate dietetic consumption, malabsorption, rapid enteric theodolite clip or bacterial giantism. More likely, it is a combination of all these factors. Nevertheless, weight addition after surgery is possible. Frequent nutrition followup in the early postoperative period is the key to forestalling a diminution in nutritionary position. Indeed, several studies confirm that in the absence of nutrition followup, patients become increasingly malnourished. Too frequently, gastrectomized patients are discharged without equal direction on what and how much to eat. It is hence indispensable for clinicians to supply nutrition intercession and follow-up until patients demonstrate the ability to keep or derive weight, as the instance necessitates.

Fat maldigestion

Surveies looking at fat malabsorption after PG and TG have demonstrated inordinate faecal fat elimination. The etiology of fat malabsorption appears to be multifactorial. First, the stomachic stump empties itself early and the stomachic content moves quickly through the upper digestive piece of land, making the jejunum and ileum Oklahoman than the pancreatic enzymes. Second, decreased theodolite clip prevents sufficient commixture of nutrient with digestive enzymes and gall salts, particularly in TG or BII patients. Third, decreased enzyme production reduces the ratio of enzymes to nutrient. One survey mensurating exocrine pancreatic map in TG patients found that all patients had terrible exocrine pancreatic inadequacy three months after surgery. Finally, due to loss of the antrum, and therefore its screening map, larger than normal nutrient atoms empty into the jejunum, doing enzyme onslaught more hard. Qualitative or quantitative faecal fat appraisal is utile in the diagnosing of fat maldigestion

Lactose intolerance

Lactase, the enzyme required for lactose soaking up, is found chiefly on villi in the jejunum. Most gastrectomized patients have an integral jejunum, hence lactose intolerance, in these patients, is deemed “ functional. ” Patients complaining of abdominal cramping or hurting, bloating, diarrhoea, flatulency and dilatation after ingestion of milk sugar may make good to diminish or avoid it. Tolerance to lactose is typically dose-dependent and may better over clip. Many patients may be able to digest smaller sums of lactose incorporating nutrients throughout the twenty-four hours. Lactase enzymes are available for patients who wish to go on devouring dairy merchandises.

Although diet therapy may be good in handling nutritionary intolerances, it is of import to minimise diet limitations. Otiose limitations may do defeat to the patient and can farther worsen weight loss.


Nutritional anaemias ensuing from Fe lack, vitamin B12, or vitamin Bc are common in gastrectomized patients. Consequences of anaemia can be terrible. Therefore baseline haemoglobin appraisal and periodic monitoring is of import. Anemia frequently presents as a late complication of stomachic resection, puting patients with a distant history of the surgery at an even greater hazard.

Microcytic Anemia

Iron lack is the most common anaemia following stomachic resection.

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

Changes in digestion and soaking up of dietetic Fe are thought to be responsible for Fe lack in TG and PG patients. Duodenum, the primary site for Fe soaking up, is bypassed ( except with BI ) and decreased stomachic sourness impairs the transition of ferrous Fe to the more absorbable ferric signifier. Reduced Fe consumption may besides play a function.

Megaloblastic and baneful anaemia

Megaloblastic anaemia may be the consequence of either vitamin B12 or folate lack. B12 lack may ensue in PG and TG patients for legion grounds. Normally, intrinsic factor is complexed to B12 and facilitates its soaking up by the terminal ileum. Decrease in intrinsic factor and decreased stomachic sourness in gastrectomized patients impairs cleavage of protein edge B12. Bacterial giantism and decreased consumption of B12 rich nutrients may besides lend to a lack province. Folate lack may develop after stomachic surgery but is non good reported. Causes of folate lack are likely multifactorial including malabsorption ( the first site of folate soaking up is the duodenum ) .

Metabolic Bone Disease

Metabolic bone disease, such as osteoporosis, and osteomalacia, is normally reported in gastrectomy patients taking to a greater hazard of bone breaks. A low bone mineral denseness ( BMD ) has been reported in 27 % to 44 % of gastrectomized patients. The etiology of bone disease in gastrectomized patients is unsure but appears to be a combination of reduced consumption of Ca, vitamin D and lactose-containing nutrients, coupled with altered soaking up and metamorphosis of vitamin D. Vitamin D lack may ensue from reduced consumption instead than malabsorption. A important addition in 25-OHD degrees have been recorded when TG and PG patients were supplemented with 400 IU of vitamin D per twenty-four hours.


Afferent loop syndrome ( ALS ) is a strictly mechanical complication that infrequently occurs following building of a Billroth II gastrojejunostomy. Creation of an inosculation between the tummy and jejunum leaves a section of little intestine, most normally dwelling of duodenum and proximal jejunum, lying upstream from the gastrojejunostomy ( Fig 10.6 ) . This limb of intestine behaviors gall, pancreatic juices, and other proximal enteric secernments toward the gastrojejunostomy and is therefore termed the sensory nerve cringle.

Passage of nutrient and stomachic secernments through the gastrojejunostomy and into the motorial cringle triggers release of secretin and cholecystokinin. These enteral endocrines stimulate secernment of gall, pancreatic enzymes, and pancreatic hydrogen carbonate and H2O into the afferent cringle. Under GI hormonal influence, up to 1-2 L of pancreatic and bilious secernments can come in the sensory nerve loop each twenty-four hours.

Symptoms associated with acute ALS are caused by increased intraluminal force per unit area and distention due to accretion of enteral secernments in a wholly obstructed sensory nerve cringle. ALS is one of the chief causes of duodenal stump runaway in the early postoperative period and is besides an etiology for postoperative clogging icterus, go uping cholangitis, and pancreatitis due to transmittal of high force per unit areas back to the biliopancreatic ductal system. High luminal force per unit areas and distention addition intestine wall tenseness in the sensory nerve cringle and can take to ischemia and necrose with subsequent perforation and peritoneal inflammation.

Chronic ALS is more common. It consequences from drawn-out stasis and pooling of secernments with partial obstructor of the sensory nerve cringle which facilitates bacterial giantism in the sensory nerve cringle. Bacteria deconjugate gall acids, which can take to steatorrhea, malnutrition, and vitamin B-12 lack. Iron lack can happen because of bypassing of the duodenum.


Bacterial giantism syndrome ( BOS ) is a term that describes clinical manifestations that occur when the usually low figure of bacteriums that inhabit the tummy, duodenum, jejunum, and proximal ileum significantly increases or becomes overtaken by other pathogens.

Low concentrations of assorted bacteriums live within or attached to its luminal surface. These bacteriums are thought to be present shortly after birth and through maturity, populating in mutualism with the human host. This relationship is thought to be critical for normal digestive procedures, unsusceptibility, and enteric development.

The undermentioned defence mechanisms of the little bowel, which keep the upper bowel practically bacteria free, can be compromised in assorted upsets:

1. Migrating motor composites ( MMC ) ( or migrating myoelectric composites ) are moving ridges of activity which sweep through the bowels in a regular rhythm during fasting province. These motor composites help trip peristaltic moving ridges which facilitate transit of indigestible substances such as bone, fibre and foreign organic structures from the tummy, through the little bowel past the ileocecal sphincter into the colon. The MMC originates in the tummy approximately every 75-90 proceedingss during the interdigestive stage ( between repasts ) and is responsible for the rumble experienced when hungry.

MMC besides serves to transport bacteriums from the little bowel to the big bowel, and to suppress the migration of colonic bacteriums into the terminal ileum. Anatomic defects can cut down peristaltic efficaciousness ; for illustration, blind pouches result in a dead part of the bowel, e.g. blind cringle, little intestine diverticuli. Impaired motility in the little bowel is a characteristic characteristic of dermatosclerosis.

2. Gastric acid reduces the bacterium populations in the proximal little bowel, peculiarly anaerobiotic bacteriums. Lack of stomachic acid after stomachic resections allows the bacterial giantism in the little bowel.

3. The intestine mucosal unity and mucous secretion bed protect the intestine from bacterium. This protective mechanism is disrupted in upsets such as Celiac disease, tropical psilosis etc.

4. Immunoglobulin secernment and immune cells ( e.g. macrophages and lymph cells ) protect the intestine from bacteriums.

5. Normal enteric vegetation ( e.g. , Lactobacillus ) protect the intestine from bacterial giantism by keeping a low pH ; unnatural communications produce tracts that allow enteral bacteriums to go through between the proximal and distal intestine.

In a normal individual, the bacterial count in the upper little bowel is less than 103 beings / ml aspirate. When the protective mechanisms mentioned above dislocation, the bacterial count may increase above 1010 beings / ml aspirate. The bacteriums normally found are those normally present in the colon. The giantism of the bacterium causes direct or indirect change in bile salt metamorphosis, and other metabolic defects. The bacterium deconjugate the gall salts taking to:

reduced concentration of gall salts, and

soaking up of deconjugated bile acids in the jejunum. It further diminishing the intraluminal concentration of gall salts in the jejunum. ( Bile salts are usually absorbed in the ileum ) .

Consequently, both enteric digestion and soaking up of fat suffers. Deconjugated bile acids straight inhibit carbohydrate transporters. The unabsorbed sugars agitation into organic acids, thereby cut downing the intraluminal pH and bring forthing osmotic diarrhoea. The deconjugated gall acids besides damage enteric enterocytes and bring on H2O secernment by the colonic mucous membrane. All these alterations produce malabsorption syndrome ( Table 10. 4 ) . Uptake of vitamin B12 by the bacterium histories for peculiarly low plasma degrees of the vitamin and symptoms of baneful anaemia. In chronic ALS, Fe lack consequences from lack of stomachic acid and upper enteric beltway.

Table 10. 4. Pathophysiological mechanisms of assorted characteristics of malabsorption syndrome.

Organ system

Clinical characteristics

Pathophysiological mechanisms


Generalized failing

Hypotension, amenorrhoea, decreased libido

Loss of Calories and vitamins due to malabsorption of nutrient, anorexia

Fluid and electrolyte loss and protein-caloric depletion taking to secondary hypopituitarism.

G I tract



Abdominal hurting

Glossitis, perleche, stomatitis

Malabsorption in little bowel taking to greater solute and H2O burden on the colon ; annoyance of colon by fatty acids

Bacterial agitation of unabsorbed saccharides in the colon.

Distention or redness of bowl

Lack of vitamins and Fe.



Shed blooding

Impaired soaking up of Fe, folic acid and vitamin B12.

Vitamin K malabsorption


Bone strivings

Vitamin D malabsorption, osteomalacia

Protein depletion osteoporosis

Nervous system

Tetany Paresthesias



Peripheral neuropathy


Vitamin A lack

Vitamins B1and B12deficiency.

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Stomach And Intestines Anatomy And Physiology Biology. (2017, Jul 07). Retrieved from