1-gastric and duodenal ulcer

8/11/2019 1-Gastric and Duodenal Ulcer

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LECTURE NR. 1

Gastric and duodenal ulcer

Elements of anatomy and physiology3011

The stomach is the most dilated part of the digestive tube, having a capacity of 1000 1500 ml in the adult. It is situated between the end of the oesophagus and the duodenum the beginning of the small intestine. It lies in the epigastric, umbilical, and left hypochondrial regions of theabdomen, and occupies a recess bounded by the upper abdominal viscera, the anterior abdominal wall and the diaphragm .

Macroscopic anatomy

The stomach has : two openings, two curvatures, two surfaces and two omenta.

1. Openings

Gastro-oesophageal unction The oesophagus communicates with the stomach via the cardiac ori.ce, which is situatedon the left of the midline at the level of T10. The intra abdominal oesophagus !antrumcardiacum" is short and conical. #fter passingthrough the diaphragm it curves sharply to

theleft, and becomes continuous with the cardiac orifice of the stomach. The right margin of the oesophagus is continuous with the lesser curvature of the stomach, while the left margin

$oins the greater curvature at an acute angle !incisura cardiaca". Gastroduodenal unction

9 The pylorus forms the gastric outlet and communicates with the duodenum. It lies to theright of the midline at the level of the upper border of %1 and may be identified on the surfaceof the stomach by a circular groove !duodeno pyloric constriction" covering the front of theorgan.

!. Cur"atures

Lesser cur"ature #Cur"atura $entriculi %inor& This e&tends from the cardiac to the pyloric orifices, thus forming the right or posterior

border of the stomach. It is a continuation of the right border of the oesophagus and lies infront of the right crus of the diaphragm. It crosses the body of %1 and ends at the pylorus. #welldemarcated notch, the incisura angularis, is seen distally although its position varies withthe state of distension of the stomach. #ttached to the lesser curvature are the two layers of the hepatogastric ligament !lesser omentum". 'etween these two layers are the left gastricartery and the right gastric branch of the hepatic artery.

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Greater cur"ature #Cur"atura $entriculi %a or& This is directed mainly forward, and is four to five times longer than the lesser curvature. Itstarts from the incisura cardiaca and arches bac(ward, upward, and to the left) thehighestpoint of the conve&ity is on a level with the si&th left costal cartilage. It then descendsdownwards and forwards, with a slight conve&ity to the left as low as the cartilage of the ninth

rib,before turning to the right, to end at the pylorus. *irectly opposite the incisura angularis of the lesser curvature, the greater curvature presents a dilatation, which is the left e&tremity of the pyloric part) this dilatation is limited on the right by a slight groove, the sulcusintermedius, which is about +.5 cm, from the duodenopyloric constriction. The portion

between the sulcus intermedius and the duodenopyloric is termed the pyloric antrum.with theduodenum. It lies to the right of the midline at the level of the upper border of %1 and may beidentified on the surface of the stomach by a circular groove !duodeno pyloric constriction".The left part of the curvature gives attachment to the gastrosplenic !lineal" ligament, while toits anterior portion are attached the two layers of the greater omentum, separated from eachother by the right and left gastroepiploic vessels.

'. (urfaces

)nterosuperior surface This surface is covered by peritoneum and lies in contact with the diaphragm, which

separates it from the base of the left lung, the pericardium, the seventhninth ribs, and theintercostal spaces of the left side. The right half lies in relation to the left and uadrate lobesof the liver together with the anterior abdominal wall. The transverse colon may lie on thefront part of thissurface when the stomach is collapsed.

*osteroinferior surface This surface is covered by peritoneum, e&cept over a small area close to the cardiac ori.ce)this area is limited by the lines of attachment of the gastrophrenic ligament, and lies inapposition with the diaphragm, and fre uently with the upper portion of the left suprarenalgland. -ther relations are to the upper part of the front of the left (idney, the anterior surfaceof the pancreas, the left colic fle&ure, and the upper layer of the transverse mesocolon. Thetransverse mesocolon separates the stomach from the duodeno$e$unal fle&ure and smallintestine. Thus the abdominal cavity is divided into supra and infra colic compartments. The anterior boundary of the lesser sac !omental bursa" is formed by this surface. This

potential space can be accessed via an opening on the free border of the lesser omentum,which contains the common hepatic artery, the common bile duct and the portal vein !theforamen of inslow".

*arts of the stomach The stomach is divided into a pyloric part and body by a plane passing through the

incisura angularis on the lesser curvature and the left limit of the opposed dilatation on thegreater curvature. The body is further subdivided into the fundus and cardia by a plane

passing hori/ontally through the cardiac orifice. *istally a plane passing from the sulcusintermedius at right angles to the long a&is of this portion further subdivides the pyloric

portion. To the right of this plane lies the pyloric antrum. #t operations, a slight groove may be seen in the serosal surface at the gastroduodenal $unction. # small, super.cial subserosalvein, lying within this groove and vertically across the front of the gut may be evident. This isthe prepyloric vein of ayo" and drains into the right gastric vein. #t operation, palpation of

this area reveals the pyloric ring between the thic( walls of the pyloric region and the thinwalls of the duodenum .

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+. Omenta

Lesser omentum This e&tends from the inferior and posterior surfaces of the liver to the stomach and

pro&imal .0 cm of the duodenum. The free border of the lesser omentum between the portahepatis and the duodenum contains the hepatic artery, the portal vein, the common bile duct,lymph glands, lymph vessels and nerves. 'ehind this free edge is the opening into the lesser sac or epiploic foramen !of inslow". The remainder of the lesser omentum, e&tending fromthe left end of the porta hepatis to the lesser curvature, contains the right and left gastricarteries and the accompanying veins, as well as lymph glands, lymph vessels and branches of the anterior and posterior vagus nerves.

Greater omentum This is formed along the greater curvature of the stomach by the union of the peritonealcoats of the anterior and posterior gastric surfaces. -n its left it shortens into the gastrosplenicomentum, containing the short gastric branches of the splenic artery between its two layers.

-n the right it is continued for .0 cm along the lower border of the .rst part of the duodenum.2rom its origin the greater omentum hangs down in front of the intestines as a loose apron,e&tending as far as the transverse colon, where its two layers separate to enclose that part of the colon. The upper part of the greater omentum contains the greater part of the right and leftgastroepiploic arteries and their accompanying veins, lymph vessels, lymph glands, nervefilaments, fat and areolar tissue.

,lood (upply

1. )rterial (upply The coeliac artery, the artery of the foregut, supplies the stomach by its three branches. Itarises from the front of the aorta between the crura of the diaphragm and is a short wide trun(,surrounded by the coeliac lymph nodes and flan(ed by the coeliac ganglia of the sympatheticsystem. The main branches are the left gastric artery, the hepatic artery and the splenic artery .

The left gastric arteryThis runs to the left, gives off an ascending oesophageal branch, and supplies the upper

part of the stomach. 3owever, it may arise directly from the aorta !54. 6", and may provideone or both of the inferior phrenic arteries or a common trun( for the two. The left gastricartery turns downwards between the layers of the lesser omentum and runs to the right alongthe lesser curvature. 3aving divided into two parallel branches, these divide further supplyingthe anterior and posterior gastric walls. These vessels anastomose freely with arteries from thegreater curvature. #round the incisura angularis, the two main branches then anastomose withthe two branches of the right gastric artery. The hepatic artery may arise directly from the leftgastric .

The hepatic arteryThis is the second branch of the coeliac trun( and passes downwards as far as the first part

of the duodenum. #t the opening into right border of the lesser sac it turns forwards !epiploicforamen" and curves upwards between the two layers of the lesser omentum towards the portahepatis, to supply the liver. The gastroduodenal and right gastric arteries are given off as itturns into the lesser omentum. The right gastric artery passes to the left between the twolayers of the lesser omentum, and runs along the lesser curvature of the stomach before

dividing into two branches that anastomose with the branches of the left gastric artery. It alsogives off branches to the anterior and posterior gastric walls, anastomosing with branches


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from the right gastroepiploic artery. The gastroduodenal artery descends behind the first partof the duodenum, which it supplies by multiple small branches. The terminal divisions are thesuperior pancreaticoduodenal artery, supplying the second part of the duodenum and head of the pancreas, and the right gastroepiploic artery. The right gastroepiploic artery passes alongthe greater curvature of the stomach between the layers of the greater omentum and gives off

branches to the anterior and posterior gastric walls before anastomosing with the leftgastroepiploic artery.

The splenic artery This passes to the left along the upper border of the pancreas, behind the peritoneum andthe stomach, to supply the spleen. *ivision into the terminal branches close to the spleen iscalled a magistral splenic !71+ cm from the hilum", but earlier division is called adistributing splenic. *uring its course it gives off branches to the pancreas) $ust beforeentering the splenic hilum it gives off the short gastric arteries supplying the gastric forni&,and the left gastroepiploic artery. The latter passes downwards and to the right along thegreater curvature of the stomach, between the two layers of the greater omentum, toanastomose with the right gastroepiploic artery at the mid portion of the greater curvature. Itgives off branches to the anterior and posterior gastric walls, which anastomose with branchesof the gastric arteries along the lesser curvature.

!. The $enous rainageThe gastric veins are similar in position to that of the arteries along the lesser and greater

curvatures. These veins drain either directly or indirectly into the portal system .

Left gastric "einThis runs to the left along the lesser curvature, receiving the oesophageal veins below the

oesophageal hiatus in the diaphragm. It usually drains directly into the portal vein at thesuperior border of the pancreas .

Right gastric "einThis runs along the lesser curvature to the right towards the pylorus. 8osterior to the first

part of the duodenum it $oins the portal vein. It also receives the prepyloric vein whichreceives the veins from the first + cm of the duodenum.

Left gastroepiploic "ein This passes to the left along the greater curvature and with the short gastric veins drains

into the splenic vein or its tributaries. The splenic vein is $oined with tributaries from the pancreas as well as the inferior mesenteric vein) these ultimately form the portal vein with thesuperior mesenteric vein.

Right gastroepiploic "ein

This runs to the right as far as the head of the pan creas. 9sually it $oins the superior mesenteric vein and thus drains into the portal vein. 3owever, considerable variations mayoccur and the right gastroepiploic may enter the portal vein directly, or it may $oin the splenicvein. There is no gastroduodenal vein.

'. Lymphatic rainage The lymphatics of the stomach can be divided into three systems:

ntramuralThis consists of three networ(s) submucosal, intermuscular and subserosal.

ntermediaryThis consists of numerous small channels between the subserosal networ( and the

e&tramural collecting systems.


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E/tramuralThis consists of four ma$or /ones of lymphatic drainage, corresponding to the arterial

supply of the stomach. 9ltimately all /ones drain into the coeliac nodes around the coeliacarterial trun( on the anterior aspect of the aorta.

The lymphatic drainage of the stomach can be divided into four /ones :

0one 1 This comprises the upper twothirds of the lesser curvature and a large part of the body of the stomach. These drain into the left gastric nodes lying along the left gastric artery. Thesenodes are $oined by lymphatics coming down from the lower part of the oesophagus, and their efferents proceed to the coeliac nodes.

0one !This is from the distal part of the lesser curvature, including the lesser curvature of the

pyloric region, to the suprapyloric nodes along the right gastric artery. ;fferent channels fromthe suprapyloric nodes drain to the hepatic and ultimately to the coeliac and aortic nodes.

0one 'This /one includes the pyloric part of the stomach as well as the right half of the greater

curvature. The lymphatics from these areas drain into the right gastroepiploic nodes in thegastrocolic ligament, lying along the right gastroepiploic vessels, and into the pyloric nodeson the anterior surface of the head of the pancreas. The direction of lymph flow is from abovedownwards, towards the pylorus and the nodes between the head of the pancreas and second

part of the duodenum. 2rom these groups, collectively called the subpyloric glands !whichalso drain the .rst part of the duodenum", efferent vessels pass along the gastroduodenal arteryto the hepatic nodes along the hepatic artery, and thence to the coeliac nodes.

0one +This comprises the left half of the greater curvature and the gastric forni&. The lymph

vessels from here pass to the left gastroepiploic nodes, lying along the left gastroepiploicartery. These drain to the pancreatico lienal nodes along the splenic artery, before terminatingin the coeliac nodes.

+. Ner"esThe autonomic nervous system consists of two components, cholinergic mostly

parasympathetic, and adrenergic mostly sympathetic nerves. 3owever, a third component of the autonomic system, which is neither cholinergic nor adrenergic, has been recognised withinthe gastrointestinal tract the peptidergic system .

*arasympathetic Ner"e (upply The anterior and posterior vagal trun(s and their branches form the parasympathetic nervesupply to the stomach. #fferent fibres are also present in the vagi .

1. )nterior "agusThis is derived mainly from the left vagus nerve but also includes .bres from the right

vagus and also some sympathetic fibres from the splanchnic nerves. It enters the abdominalcavity through the oesophageal hiatus in the diaphragm. It is usually single but may bedivided into multiple trun(s. 3aving given off several fine branches to the lower end of theoesophagus and cardiac part of the stomach, the anterior trun( brea(s up into its main

branches.%atar$et divided the nerves of the anterior vagus into two distinct functional divisions.

The first division, consisting of the direct branches, supplies the forni& and body, i.e. the

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%ucosal 2ones

The mucous membrane of the entire stomach is lined by glands that open into the gastric pits .

The gastric mucosa can be divided into three /ones, based on the predominant cell typeswithin the glands :

Cardiac 2one These glands secrete mucus*yloric 2one These glands secrete mucus. They also produce endocrine, paracrineor neurocrine regulatory peptides by virtue of the #89* cells contained in theirglands.

O/yntic 2one These glands produce nearly all the en/ymes and hydrochloric acidsecreted in the stomach as well as producing mucus.

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The secretory epithelial cells and their roles

2our ma$or types of secretory epithelial cells cover the surface of the stomach and e&tenddown into gastric pits and glands :

%ucous cells - secrete al(aline mucus that prote&ts the epithelium against shearstress and acid

*arietal cells - secrete hydrochloric acid Chief cells - secrete pepsin , a proteolytic en/yme G cells 3 secrete the hormone gastrin

*hysiology

Gastric secretions %ucus secretion

The cells of the gastric glands secrete about +500 ml of gastric $uice daily. This contains avariety of substances and gastric en/ymes, whose role is to (ill ingested bacteria, aid proteindigestion, stimulate the flow of bilary and pancreatic $uices and provide the necessary p3 for

pepsin to begin protein degradation . The most abundant epithelial cells are mucussecreting columnar cells, which cover theentire luminal surface and e&tend down into the glands as


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by the presence of gastric acid into the active protease pepsin. This is an endopeptidase that islargely responsible for the initiation of protein digestion into smaller peptides and

polypeptides. It acts at p3 1.5+.5 and above p3 5. is inactivated. It is released mainly byvagal stimulation but also by histamine gastrin secretion, alcohol, cortisol, caffeine andaceta/olamide. 8epsinogen release may also occur during periods of hypoglycaemia and

prolonged increased intracranial pressure. 4ormone secretion

The principal hormone secreted from the gastric epithelium is gastrin, a peptide that isimportant in control of acid secretion and gastric motility.

Intrinsic factor, a glycoprotein secreted by parietal cells, is necessary for intestinalabsorption of vitamin '1+. It acts by combining with the vitamin '1+ and is necessary for itsattachment to receptors in the terminal ileum. %ac( of intrinsic factor due to reduction in

parietal cell mass following gastric surgery, or the production of antibodies to the cells, called pernicious anaemia, leads to megaloblastic anaemia. Becretion of intrinsic factor occursfollowing vagal, gastrin or histamine stimulation of the parietal cells. The 5ormation and (ecretion of Gastric )cid Btimulation of the parietal cells results in acid secretion. These cells contain multipletubulovesicular structures within their cytoplasm that on stimulation move to the mucosalmembrane and fuse with it, producing a microvillous appearance that increases the surfacearea. This results in the presence of the 3@ D@ #T8ase that transports the 3@ onto the luminalsurface. This secretion is isotonic with other .uids and its p3 is E1. The 3@ is obtained from the ionisation of water, which is then actively transported intothe gastric lumen in e&change for D@ that has been recycled from the membrane. Fhlorideions are also actively transported into the gastric lumen. The resulting -3 ion is neutralised

by the carbonic acid buffer system to form a bicarbonate ion that diffuses into the interstitiumto be replaced by a further Fl ion. There is a 3F- Fl e&change mechanism within theinterstitium, but Fl also enters the cell with Aa@. The carbonic acid is replenished by thehydration of F-+, which is produced by cellular metabolism from the abundance of carbonicanhydrase within the mucosa. #fter a meal this results in the development of a negativerespiratory uotient) thus arterial F-+ is higher than venous and the gastric venous return isal(aline with a high 3F- content. Gastric hormones

GastrinThe highest density of gastrin producing C cells occurs in the distal .0 cm of the

stomach, where the concentration of gastrin is 500 times higher than in the body of thestomach. The first part of the duodenum also contains a signi.cant level of C cells. These cellsoriginate from neuroectoderm together with other cells of the #89* series .

There are two main types of gastrin, gastrin I and gastrin II, produced predominantly bythe C cells of the pyloric mucosal /one. -ther sources are the duodenal C cells, * cells in theislands of %angerhans in the pancreas, and isolated C cells in the pro&imal acid producingregion of the forni& and body of the stomach. Castrin 1 !1 amino acids" is the predominantform in the pyloric antrum, and is further subdivided into a non sulphated gastrin I and asulphated gastrin II form. There is also a


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The physiological and pharmacological effects of gastrin 6

8arietal cells to stimulate acid secretion 8epsin and intrinsic factor secretion Increased mitotic activity in the stomach and small bowel mucosa Fontraction of the lower oesophageal sphincter The release of insulin, glucagon and calcitonin 8ancreatic stimulation and bile flow Bmall bowel secretion Castric and small bowel motility to increase The gastrocolic refle&

(omatostatin

It has been identified in the central nervous system, the gastrointestinal tract and other organs, with the highest concentration being found in the pancreas. In the stomach it is foundin the pyloric and o&yntic mucosal /ones but not in the cardiac /one. ithin the pancreas it isisolated from the islet * cells.

It suppresses the release of thyroid stimulating hormone by the pituitary, the release of glucagon, insulin and e&ocrine secretions by the pancreas, the secretion of cholecysto(inin,motilin and secretin by the intestine, and the secretion of gastrin, gastric acid and pepsin bythe stomach. Bomatostatin suppresses gastric acid secretion by direct action on the parietalcells of the cardiac and o&yntic mucosal /ones. Thus by lowering the p3, it also inhibits thesecretion of gastrin through a feedbac( loop of low p3 suppressing.

$asoacti"e ntestinal *eptide #$ *&

>asoactive intestinal peptide !>I8" is a polypeptide with strong vascular effects isolatedfrom small intestine. Its actions include vasodilatation, thus lowering blood pressure,increased cardiac output, glycogenolysis and rela&ation of smooth muscle. In the stomachthere is significant inhibition of gastric secretion associated with >I8 release.

(u stance *In the stomach substance 8 is found in the o&yntic /one in a few, thin .bres only and in

fibres interconnecting in the pyloric antrum. In the duodenum substance 8 !and >I8" is present in nerve networ(s in the villi as well as in the muscularis mucosae and around bloodvessels. It has been found to cause contraction of the muscularis mucosae.

Control of Gastric )cid (ecretion

#cid secretion may be divided into two phases interprandial, when acid secretion is 15mmol h, and stimulated where acid secretion is ma&imally +0 5 mmol h. This is further subdivided into cephalic, gastric and intestinal phase. Aormal sub$ects ma&imally secrete 0.5mmol h (g body weight".

1. nterprandialJesting secretion occurs in the absence of all intestinal stimulation. 3owever, in order to

abolish all gastic acid secretions, a bilateral vagotomy !truncal" and e&cision of the pyloricantrum would be necessary .

!. (timulated secretion

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The cephalic phaseThe cephalic phase is initiated by seeing, smelling and anticipating food. These

influences act on the limbic system and hypothalamus and these nuclei stimulate the dorsal

motor nucleus of the vagus. This stimulus is transmitted thought the vagus nerve to the entericnervous system, resulting in release of acetylcholine in the vicinity of C cells and parietalcells. 'inding of acetylcholine to its receptor on C cells induces secretion of the hormonegastrin, which, in concert with acetylcholine and histamine, stimulates parietal cells to secretesmall amounts of acid. #dditionally, a low level of gastric motility is induced.1 The release of acetylcholine and bombesin !gastrin releasing peptide" initiates gastrinrelease from the C cells. The gastrin passes via the portal circulation to stimulate the parietalcells. It potentiates the effect of vagal stimulation, thus resulting in increased acid secretion.The parietal cells also have 3+ receptors !histamine" stimulated by the release of histaminefrom mast cells close to the parietal cells. The histamine sensitises the parietal cell to theaction of gastrin and acetylcholine. The 3+ receptor bloc(ers !cimetidine and ranitidine" acton these receptors, thus reducing acid secretion.

The gastric phase7 hen food enters the stomach several additional factors come into play, foremostamong them being distension and mucosal irritation. *istension e&cites stretch receptors andirritation activates chemoreceptors in the mucosa. These events are sensed by entericneurones, which secrete additional acetylcholine, further stimulating both C cells and parietalcells. Castrin from the C cells feeds bac( to the parietal cells, stimulating it even further,mediated by vagovagal refle&es through the dorsal motor nucleus. #dditionally, activation of the enteric nervous system and release of gastrin cause vigorous smooth muscle contractions.The net result is that secretory and motor functions of the stomach are fully turned on acid

and pepsinogen are secreted, pepsinogen is converted into pepsin and vigorous grinding andmi&ing contractions ta(e place. 3owever, acid secretion may be inhibited during the gastric phase by local mechanisms. If the antral p3 falls to 11.5, inhibition of gastrin release occurs.This is mediated by two mechanisms the effect of luminal acid on the microvilli of the Ccell and the stimulation of somatostatin from * cells in the antrum, which acts inhibitsdirectly on the C cells and parietal cells by a local paracrine effect.

The intestinal phaseThis phase of gastric function is dominated by the small intestine sending inhibitory

signals to the stomach to slow secretion and motility. Two types of signals are used: nervousand endocrine. *istension of the small intestine, as well as chemical and osmotic irritation of the mucosa, is transduced into gastric inhibitory impulses in the enteric nervous system this

nervous pathway is called the enterogastric re.e&. 2at and carbohydrate in the chyme cause therelease of CI8 !gastric inhibiting peptide", which inhibits gastrin secretion. Becondly, enterichormones such as cholecysto(inin and secretin are released from cells in the small intestineand contribute to suppression of gastric activity. Castrin also causes the release of calcitoninfrom the F cells of the thyroid gland, which inhibits further release of gastrin via a feedbac( loop.

Ethiopathogeny of peptic ulcer

The pathophysiology of peptic ulcers, whether gastric or duodenal, is multifactorial.

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9lcers develop depending on the balance of in$urious factors and host defense mechanisms.;nvironmental stressors are numerous. #cid secretion is involved in the final common

pathway of ulcer formation.

In regards to duodenal ulceration, mucosal e&posure of acid is a necessary component of

their pathogenesis. In general, patients with duodenal ulcers have an increased capacity for acid secretion. a&imal acid output in normal patients is usually around +0 m; hour but

patients with duodenal ulcers may e&ceed 0 m; hr. #dditionally, patients with duodenalulcer have increased basal acid outputs with normal basal gastrin levels.

The role that acid secretion plays with the formation of gastric ulcers is less clear.3ypersecretion of acid is not associated with all subtypes of gastric ulcers. Castric acid does,however, play a role in the chain of events that leads to ulceration.

5actors 7hich are associated 7ith the de"elopment of peptic ulcers6

4elico acter pylori is a spiral bacterium which specifically coloni/es gastric mucosa.

It is able to survive in a near neutral p3 through the production of urease. 3. pylori infectionhas been correlated with the formation of peptic ulcers. Beveral lines of evidence lin( 3.

pylori to peptic ulceration:;radication of 3. pylori, without the suppression of acid, leads to ulcer healing rates that

are similar to those of acid suppression therapy alone)Jelapse of duodenal ulceration after antimicrobial treatment is preceded by reinfection

of gastric mucosa. The prevalence of 3. pylori in patients with duodenal ulceration is near 1006. 8atientswith gastric ulcers have a prevalence of 3. pylori in the range of 40 H06.Fomparatively,3elicobacter coloni/es appro&imately +06 of those without peptic ulcer disease.

etection of 4elico acter pylori Three tests areavailable to assess the presence of 3. pylori: endoscopic biopsy, the breath test,and ;%IB# antibody testing.

;ndoscopic 'iopsy ucosal biopsy specimens can be e&amined histologically for the presence of bacterium andgastritis. The best use of the biopsy specimen is to perform a ureasetest, in which the specimen is placed in a solution of urea containing a p3 indicator. If ureaseis present, ammonia is generated from the urea, causing the solution to turn more al(ali. Theurease test is highly specific and sensitive. # biopsy specimen can also be cultured to grow the

bacterium. hile highly specific, culture has very low sensitivity. 'reath Test 9rea labeled with either 1 F or 1 F is administered with a meal. If 3.

pylori infection is present, its urease will cleave the labeled urea, releasing labeled bicarbonate that is then converted into labeled e&pired F-+. The great value of this test is thatit can be used serially to assess the efficacy of 3. pylori eradication therapy.

;%IB# #ntibody Test 3. pylori infection leads to the development of antibodies thatcan be detected in the blood. The ;%IB# antibody test is not as useful as the breath test tomonitor response to 3. pylori eradication because antibody titers in the blood decrease slowly.

Cigarette smo8ing has been associated with peptic ulcer disease in so far as itimpairs healing, decreases the effectiveness of therapy, increases recurrence rates, andincreases the li(elihood of complications.

Ethanol also has in$urious effects on gastroduodenal mucosa.

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N() use has also shown ulcerogenic effects. 9lcer formation is promoted throughthe systemic effects of cycloo&ygenase inhibition and a direct to&ic effect on mucosal cells.The use of AB#I*B is more strongly associated with gastric ulcers.

)ltered host defense mechanisms play a role in the pathogenesis of peptic ulcer formation. Burface epithelial cells produce bicarbonate and mucus. The generation of thesesubstances allows for the creation of a p3 gradient at the luminal interface such that there is anear neutral environment at the mucosal surface. #dditionally, prostaglandins 8C;+ and 8CI+have a protective effect on the mucosa through inhibition of acid secretion by the parietal cell.8atients with peptic ulcer disease have been shown to have decreased bicarbonate secretionand decreased production of mucosal prostaglandins.

%otility disorders can also promote ulcerogenesis presumably through a mechanismof impaired clearance of no&ious substances.

Clinical and paraclinical diagnosis

Clinical presentationThe characteristic ulcer symptom is a


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The diagnosis of peptic ulcer disease is best verified by upper endoscopy.;sophagogastroduodenoscopy is greater than K56 sensitive and near 1006 specific inidentifying peptic ulcers of both the duodenum and stomach.

There are several endoscopic features, additionally, of gastric ulcers that can help todistinguish between peptic ulceration and malignant ulceration.

'enign ulcers typically appear as round lesions with slightly raised, smooth borders.The surrounding mucosal folds are symmetric and taper evenly toward the edge of the ulcer. In addition, benign ulcers often have a smooth base covered with a fibrouslayer. #lthough these characteristics may suggest a benign ulcer the only way to trulydistinguish is with multiple biopsies at the ulcer edge.

alignancy must be ruled out with biopsy upon the discovery of a gastric ulcer.

,arium meal The use of the barium meal to diagnose peptic ulcer has declined withadvances in fiberoptic endoscopy. # gastric ulcer usually shows as a niche along the lesser curvature, with the barium e&tending outward beyond the stomach. In contrast, the floor of anulcer crater that is malignant does not e&tend outside the lesser curvature !Farlan?s sign".Jadiating mucosal folds from the ulcer may be apparent when seen en face. In duodenalulcers, a barium filled crater and deformity of the duodenal cap are typical signs. The

presence of stenosis or gastric outlet obstruction can also be assessed.

(u types of gastric ulcers6

Type ulcers occur along the lesser curvature, in the body of the stomach, $ust abovethe incisura angularis. These ulcers account for about 0 506 of gastric ulcers and as such arethe most common type of gastric ulcer. Castric acid output is within the normal range.Burgical therapy consists of a distal gastrectomy with gastro$e$unostomy. >agotomy is notnecessary since these ulcers are not associated with acid hypersecretion. In fact, the additionof a vagotomy does not decrease the ulcer recurrence rate, which is about 6.

Type ulcers also occur along the lesser curvature, in the body of the stomach, andagain are found $ust above the incisura. These ulcers, however, are associated with thesimultaneous presence of a duodenal ulcer. They account for about +56 of gastric ulcers.Type II ulcers are associated with gastric acid hypersecretion. Burgical therapy generallyconsists of a truncal vagotomy with either antrectomy or pyloroplasty.

Type ulcers are prepyloric ulcers. They account for about +56 of gastric ulcers.These ulcers are also associated with gastric acid hypersecretion. Burgical therapy consists of

truncal vagotomy with either antrectomy or pyloroplasty. 8arietal cell vagotomy is associatedwith higher rates of ulcer recurrence when used for the treatment of type III ulcers.

Type $ ulcers occur high on the lesser curvature, near the C; $unction. Theyaccount for less than 106 of gastric ulcers. Type I> ulcers are associated with normal levelsof gastric acid secretion. Burgical therapy is more complicated than with the other types of gastric ulcers and depends on the pro&imity of the ulcer to the C; $unction.;sophagogastrectomy may be necessary for ulcers too close to the distal esophagus to allowfor preservation of the C; $unction.

*ositi"e and differential diagnosis

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The diagnosis of gastric or duodenal ulcer is probable when the patient is a young or adultman, who smo(es and has a stressing $ob and who has a sudden digestive haemorrhage, in astate of perfect health or with associated dispeptic problems.

*ifferential diagnosis : ;&tragastric lesion :

1. ;pigastric hernia+. *iafragmatic hernia

. Fholecystitis

. 8ancreatitis5. #ppendicitis4. # disease of transverse colon.

Castritis 3iatus hernia *uodenal diverticulum *uodenal stasis Castric cancer

%edical treatment

4! receptor antagonists competitively bind histamine receptors on the surface of thegastric parietal cell. Beveral different 3+ bloc(ers are clinically available. 3owever, there isno significant difference among these different 3+ bloc(ers in regards to their efficacy inhealing ulcers. #bout 06 of patients are ulcer free after wee(s of treatment. 9p to K06 of

patients will be ulcer free at the end of H wee(s of treatment. *roton pump inhi itors bind to membrane bound 3@ D@ #T8ase on parietal cells

and in doing so bloc( the intraluminal secretion of hydrogen ion. *irect comparisons betweenomepra/ole and 3+ bloc(ers have demonstrated that omepra/ole is superior in regards to painrelief and ulcer healing. #bout H06 of patients are ulcer free after + wee(s of treatment. 9p toK56 are ulcer free at the end of wee(s of treatment.

(ucralfate is activated at a p3 of E .5 and polymeri/es to form an insoluble gel which binds to proteins on in$ured mucosa. In doing so it forms a barrier between in$ured mucosa

and luminal acid to prevent further acid induced in$ury. Bucralfate also binds free bile saltsand pepsin, reducing their ability to cause mucosal damage. #dditionally, it stimulatesmucosal production of mucus, bicarbonate, and prostaglandins. #s it does not influence acidsecretion, sucralfate does not promote bacterial overgrowth within the stomach. #cidreducing therapy with proton pump inhibitors or 3+ receptor antagonists raise intraluminalgastric p3 and conse uently decrease the efficacy of sucralfate when these medications areused in combination. Bucralfate displays ulcer healing efficacy similar to that of 3+ bloc(ers.

)ntacids wor( by neutrali/ing gastric acid. They have ulcer healing efficacycomparable to 3+ bloc(ers. 3owever, effective treatment with antacids re uires fre uent dailydosing which negatively influences patient compliance. The antimicrobial treatment of 3elicobacter pylori is an important component of thetreatment of peptic ulceration. #s previously mentioned, 3. pylori is associated with duodenalulceration in nearly 1006 of cases and with gastric ulceration in about 406 of cases.

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3elicobacter infection should be considered when patients e&perience ulcer recurrence onmaintenance medical therapy or when peptic ulcers fail to heal. ultiple medical regimense&ist consisting of some combination of clarithromycin, metronida/ole, bismuth, and or tetracycline. Triple therapy is becoming more popular with use of a 88I and two antibiotics!i.e., omepra/ole, clarithromycin and metrinida/ole". Jegardless of the e&act regimen used, a

10 1 day course leads to eradication of 3. pylori in appro&imately K06 of cases.

(urgical treatment

There are three basic operations for uncomplicated peptic ulceration: parietal cellvagotomy, truncal vagotomy with pyloroplasty, and truncal vagotomy with antrectomy. iththe advent of 3+ receptor antagonists and, more recently, proton pump inhibitors the surgicaltreatment of peptic ulcer disease has become less common.

Burgical treatment is indicated when ulcers fail to heal after months of appropriate

medical therapy or when ulcers recur on maintenance therapy. Burgery is also indicated whenmalignancy cannot be e&cluded and when complications of disease occur. Fomplications of peptic ulcer disease include perforation, hemorrhage, and obstruction. *arietal cell "agotomy selectively inhibits vagal stimulation of parietal cells andsmooth muscle cells of the gastric fundus. It spares the vagal enervation to the antrum,

pylorus, small bowel, biliary tract, and pancreas. #cid secretion is diminished by theinterruption of vagal stimuli to parietal cells. Bpecifically, basal acid secretion is decreased byabout H06 and ma&imal acid secretion is decreased by about 06. There is some rebounding of both basal and ma&imal acid secretion over time butneither rebound to preoperative levels. >agal denervation of the gastric fundus inhibitsreceptive rela&ation of the fundus. #s a result, gastric emptying of li uids is increased. #s the

antrum and pylorus are spared, there is no effect on the emptying of solids. Truncal "agotomy has similar efficacy in regards to the reduction of acid secretion. #swith parietal cell vagotomy, truncal vagotomy decreases receptive rela&ation of the gastricfundus increasing the emptying of li uids. Truncal vagotomy additionally inhibits antral and

pyloric motility which results in poor emptying of solids. 8yloroplasty is included toovercome the effect of diminished gastric emptying. It effectively provides a wider gastricoutflow tract so that the emptying of solids is increased. )ntrectomy removes the bul( of gastrin producing cells and effectively reduces basalgastrin levels by 506 and postprandial gastrin levels by 4 6. Jeconstruction of the upper CItract is via gastroduodenostomy !'illroth I" or loop gastro$e$unostomy !'illroth II". Truncal"agotomy and antrectomy results in the reduction of basal and ma&imal acid secretion byabout H56. Inhibited fundic receptive rela&ation again results in the increased emptying of li uids. The emptying of solids is decreased. 'oth forms of reconstruction are similar inregards to operative mortality, morbidity, and rates of recurrence.

Electi"e surgical procedures for duodenal ulcer8

*ro/imal Gastric $agotomy It is generally agreed that pro&imal gastric vagotomy!8C>"Lalso (nown as highly selective vagotomy !3B>" or parietal cell vagotomy !8F>"L is the elective surgical treatment of choice for duodenal ulcer because it has the lowestoperative mortality !E0.16" and few, if any, side effects. The long term se uelae of

vagotomy and gastrectomy !e.g., dumping syndrome, diarrhea, anemia, weight loss, and soon" are not seen with 8C>. -n the other hand, the operation must be performed meticulously

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by well trained surgeons. 8C> can be done via laparotomy or laparoscopically. Theadvantage of the laparoscopic approach is that visibility is improved by magnification, and

both hospital stay and postoperative pain are significantly reduced. hether the operation isdone is limited. 'efore embar(ing on pyloroplasty, the surgeon should carefully inspectthe first part of the duodenum. If there is an associated inflammatory mass or very severedistortion from strictures, the preferred drainage procedure is gastro$e$unostomy rather than

pyloroplasty. In this way, the surgeon avoids the problem of a difficult pyloroplasty or duodenal stump closure.

(electi"e Total Gastric $agotomy Belective total gastric vagotomy divides the vagaltrun(s below the origin of the hepatic branches !anterior vagus" and celiac branches !posterior vagus". This procedure is now only of historic importance. %i(e truncal vagotomy, it re uiresa drainage procedure because the entire stomach is vagally denervated. 3ence, it has the same

potential to cause dumping syndrome. 9nli(e truncal vagotomy, however, it preserves thee&tragastric fibers that supply the liver, biliary tree, pancreas, and small intestine.Fonse uently, the incidence of postvagotomy diarrhea is significantly lower after selectivetotal gastric vagotomy than after truncal vagotomy.

Truncal $agotomy and )ntrectomy 2rom the acid reducing perspective and that of postoperative recurrence of ulcer, truncal vagotomy and antrectomy comprise the superior procedure for duodenal ulcer. It removes both the vagal !cholinergic" and gastrin drive of acidsecretion. The problem with the operation is that it creates the potential for the side effects of

both vagotomy and gastrectomy. 2or this reason, it should be used rarely to treatuncomplicated duodenal ulcer.Relati"e %erits of Operati"e *rocedures

orldwide, 8C> is the elective operation of choice for duodenal ulcer. It has thelowest operative mortality rate and is not associated with the undesirable side effects seenwith other procedures !e.g., dumping syndrome, diarrhea". 9nfortunately, patients treated with8C> have a higher recurrence rate) now that elective surgery for duodenal ulcer is rare, fewsurgeons are appropriately trained to perform 8C>. 3ence, truncal vagotomy and drainage!T>", a simpler operation to do, has retained popularity, particularly in the 9nited Btates. Ithas a low operative mortality, and the incidence of ulcer recurrence is H6 to 106. Belective total vagotomy is the most appropriate type of vagotomy to be combinedwith antrectomy because it preserves hepatic, biliary, pancreatic, and intestinal vagalinnervation. It also reduces the incidence of postoperative diarrhea. Aone of these operations are as effective as vagotomy and antrectomy !> M #" in

preventing ulcer recurrence. 9nfortunately, the low ulcer recurrence rate of E0.56 comes atthe e&pense of long term complications from both vagotomy and gastrectomy.

Electi"e surgical procedures for gastric ulcer

hile vagotomy is the cornerstone of elective surgery for duodenal ulcer, gastricresection is often more appropriate to treat patients with gastric ulcer. Two reasons supportthis philosophy.

2irst, unli(e duodenal ulcer,where increased or inappropriate acid secretion is invariablya factor, gastric ulcer appears to be associated more with reduced mucosal defense. Becond,although a duodenal ulcer is nearly always benign, a gastric ulcer can be malignant. Jesection

provides the best chance for the diagnosis and cure of gastric ulcer.Types of Gastric Ulcer Three types of gastric ulcer have been described :

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1. Type , the most common type of gastric ulcer, occurs at the lesser curvature and istypically found in the transitional mucosa between the body of the stomach and the antrum.+. Type is a gastric ulcer that coe&ists with a duodenal ulcer.

. Type is a prepyloric or pyloric channel ulcer that seems to be associated with gastricacid hypersecretion.

Choice of Operation The operation of choice differs for these three types of gastric ulcer.

The best surgical procedure for Type I ulcer is conservative distal gastrectomy, which canoften be limited to antrectomy. # gastroduodenal anastomosis is associated with fewer longterm complications, and so is preferred over a gastro$e$unal anastomosis. 8atients with Type II gastric ulcers are also best treated with conservative distalgastrectomy and gastroduodenal anastomosis. Bome surgeons add truncal vagotomy to this

procedure because gastric acid hypersecretion is fre uently seen with this type of ulcer.#ny benefits of truncal vagotomy may be outweighed by the long term se uelae of postvagotomydiarrhea. # large clinical e&perience is now documented to indicate that 8C> as the onlyoperation is inappropriate in this setting because ulcer recurrence in patients approaches 06. 8atients with Type III gastric ulcers are more definitively treated with vagotomy andantrectomy. Ideally, a selective gastric vagotomy should be done to preserve e&tragastric vagalinnervation and minimi/e the incidence of postvagotomy diarrhea.

Types of Electi"e *eptic Ulcer (urgery

Abbreviations : 'I, 'ilroth I gastrectomy) 8C>, pro&imal gastric vagotomy)T>, truncal vagotomy) > M #, vagotomy and antrectomy .

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1H


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1K


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1-gastric and duodenal ulcer

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