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THE STOMACH AND
DUODENUM
Dr. Henk Kartadinata, SpB, SpBD, FICSBagian Ilmu Bedah
Fakultas Kedokteran
Ukrida
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THE STOMACH
Embryology
arises as a spindle shaped dilatation of theforegut during 4th week of embryonic life
With later growth it undergo a rotation so that theprevious left size of the stomach becomes theanterior wall and the previous right sizebecomes to the posterior
the duodenum which was initially suspected
between dorsal and ventral mesenterica, alsorotates so that the 2nd portion of the duodenumbecomes retroperitoneal and encomprases thehand of the pancreas in its c loop
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THE STOMACH
Anatomy : The stomach can be divided into :
Fundus
Is the dorsal of the stomach to the left of and superior to the
esophagogastric junction. There is an angulation about themidline of the stomach, 5 6 cm proximal to the pylorus onthe curvature which is called the incisura angularis
Body
The area between the fundus and the line drawn from the
incisura angularis to the greater curvature of the stomach is thebody of the stomach
Antrum
The area distal to that line and proximal to the pylorus is thegastric antrum
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THE STOMACH
Anatomy :
In term of function the stomach may be divided
into :
Fundus (oxyantic gland area)
Secrets acid peptic juice
Antrum (pyloric gland area)
Secrets *a thick viscid relatively alkaline mucus
*the hormone gastrin
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THE STOMACH
Anatomy :
Lesser curvature of the stomach
The superior margin of the stomach thecardia and pylorus (12-14 cm)
Is suspended from the liver by
gastrohepatic ligament which forms thesuperior portion of the anterior wall of the
lesser omented bursa
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THE STOMACH
Anatomy :
The greater curvature
The inferior and lateral cosivax border of the
stomach
3 X as long as the lesser
From the major portion of the greater curvature
is suspended the gastrocolic ligament whichforms the lower portion of the anterior wall of the
lesser omented bursa
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THE STOMACH
Anatomy :The blood supply of the stomach
6 vessels provide the main blood supply
Left gastric artery and Right gastric artery supply the lessercurvature
Right gastroepiploic artery and left gastroepiploic artery supplythe greater curvature
Splenic artery supply the fundus by way of shore gastric
anterior Gastroduodenal artery supplies the area of the pylorus
There are 6 others arteries of secondary importance
There is arich anastomotic network and no area is served by
end arteries
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THE STOMACH
Anatomy :
The blood supply of the duodenum
Supraduodenal artery
Retroduodenal artery
Superior pancreatica duodenal artery(arises from the gastroduodenal)
Inferior pancreatica duodenal artery(arisesfrom the superior mesenteric)
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THE STOMACH
Anatomy :Nerve supply
The parasympathetic the Vagus nerves, stimulate :
Motility of the stomach Secretion of acid, pepsin and gastrin
The left as anterior Vagus nerve gives off: A hepatic branch, which also fibers to the area of the pylorus
The remaining portion innervated the anterior wall of thestomach
The posterior vagus nerve gives off : A large branch to the celicae plexus
The remaining goes to the posterior wall of the stomach
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THE STOMACH
Anatomy :
The wall of the stomach :
Composed : Mucosa
Submucosa
Muscle
Sero
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THE STOMACH
Anatomy :The wall of the stomach :
Mucosa architecture varies with the area of the stomach. Thereare several types of cells with specific function :
Parietal cell manufacture and secret HCl and gastric intrinsicfactor
Chief cells made and secret pepsinogen
Goblet cells secrets mucus
Epitheliat cells probably secrets extracellular fluid
Specialized cells within the antral gland synthesized(presumably), store and secret gastrin
Mast cells store heparin, histamine and other vasoactivesubstances within granules
Fundic argentaffin
functions unknown
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THE STOMACH
Anatomy :The wall of the stomach :
Fundic mucosa consist of deep tubular glandslined superficially with epithelial cells andcontaining in deeper portions :
Parietal cells
Chief cells
Occational argentaffin cellsThe histology of the mucosa immediately adjacentto the cardia is similar to that of the antrum
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THE STOMACH
Anatomy :
Pyloric glands consist of :
Branching tubulus lined predominanlly with
mucus cells
Mc Guigan has shown that some of these
epithelial cells, located chiefly in the middle third
of the glands react immunochemically withantigastrin antibodies and are presumably the
locus of gastrin synthesis and storage
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DUODENUM
begins at the pylorus and ends as the duodenal-jejunal junction justto the left of LII
Is divided into 4 portions : *Superior
*Descending
*Transverse
*Ascending
The majority of the first portion is occupied by the slightly dilatedduodenal bulb whose mucosa is characterized by lack of plicaecirculare
The common bile duct and the main pancreatic duct open as the
medial wall of the mid portion of the second part at the duodenalpapilla (ampulla of valve)
The superior mesenteric vessels emerge from behind the pancreas tocross over the 3rd part of the duodenum
The 4th part ascends to the duodenal jejunal flexure, which is
suspended from the posterior body wall by the ligament of Treitz
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DUODENUM
Physiology
Swallowed food enters the stomach, where it is mixedwith gastric juice and changed to a more liquid form
The viscid, pulpy chysme undergoes only a small
amount of disgetion in the stomach smoothly proteolysis Being pressed in small boluses into duodenum where it
is further mixed with bile and pancreatic juice
The mucosa of the small bowel carries out the function
of absorption of food The main function of the stomach and proximal
duodenum to alles the form of food and to supplyenzymes for its digestion
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DUODENUM
Physiology
Pepsin is active only in an acid environment, no peptic
ulceration can occur in the absence of acid.
The parietal cells concentrate hydrogen ions morethan one million times
Physiology stimulands to this : Acethycholine
Gastrin
Other potential activators : Histamine
Cholecystokinin
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DUODENUM
Physiology
Stimulation of gastric secretion :
Gastric juice is thought to be composed of Parietal component
Non parietal component
Pure parietal cell secretion contains : H+ : 150 - 170 mEq/l
Cl- : 165 170 mEg/l
K+ : 7 mEq/l
Free of Na+
Non parietal secretion, which is virtually identical withextracellular fluid : Na+ : 150 mEq/l
H+ : virtually absent
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DUODENUM
Physiology
Concentration of acid in gastric juice is dependent therefore on The rate of parietal cell secretion
Degree of admixture with non parietal secretion
There is a direct relation between the rate of gastric secretionand the blood flow to the mucosa of the stomach
It is not clear whether secretory stimulants directly influence theflow of blood to mucosa. Gastric secretion has been classifiedas : Spontaneous (on inter digestive) occurs without intentional stimulation
and may reflect a background secretion of gastrin and acethylcholine
Stimulated (on prandial) :
Cephalic phase
Gastric phase
Intestinal phase
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DUODENUM
Physiology
Cephalic phase
Stimuli presumably activate the vagal nuclei in the medulla
Impulses traverse the peripheral vagi with the release of
acetylcholine from vagal nerve ending in The gastric mucosa Direct stimulation of acid secretion by parietal cells
Release of pepsinogen by chief cells
The antral mucosa
Causes discharge of the antral hormone : gastrin, which alsoacts to stimulate the parietal cells
Stimulation of the vagus occurs with the sight as small of food
Distention of the stomach excites a vagovagal reflex that alsoresults in the release of acetylcholine in fundus and antral
mucosa
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DUODENUM
Physiology
Gatric phase
It stimulated by food in the stomach By direct contact and by distention
Gastrin : the humoral mediator of the gastric phase discovered by Edkins(1905)
Gastrin is liberated from the antral mucosa by : Acetylcholine, released by local reflexes upon antral distention
Contact with certain substances 2-carbon alcohols
Amino acids Bile salts
The vagus itself
Gastrin is acid sensitive Ph 5.5 output is diminished
Ph 1.5 further gastrin secretion is halted
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DUODENUM
Physiology
Gatric phase
The most remarkable action of gastrin is its
power to stimulate gastric acid secretion is 30 Xmore potent than histamine by weight and 500 Xmore potent on molar basis
Pure gastrin as well as its terminal tetrapeptide
is capable of eliciting, in addition a widespectrum of motor and sensory actions inmultiple target organs
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DUODENUM
Physiology
Gatric phase
Physiology actions (occurs with doses of gastrin that aresubmaximal for gastric secretion)
A strong stimulant of the secretion of water gastric intrinsic factor andelectrolyte and a weak to moderate stimulant of pepsin secretion by thestomach.
Stimulates the secretion of water and electrolytes by the pancreas, liverand Brunmors glands
Inhibit the absorption of water and electrolytes from the ilium
Stimulates secretion of enzymes by the pancreas Causes contraction of the stomach muscle of the lower esophageal
sphincter and stomach
Inhibit contraction of the sphincter of odds
Increase gastric mucosal blood flow
Stimulate incorporation of amino acid into protein in gastric mucosa
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DUODENUM
Physiology
Gatric phase
Large doses of gastrin Have a trophic effect on gastric mucosa
Stimulate the release of insulin Stimulate the smooth muscle of the gut
Gastrin appears to be synthesized and stored by specializedcell lying chief by within the middle third of the thickness of theantral mucosa
Gastrin is released from cells in the pyloric glands and iscarried by the blood to effector sites in various organs of the gut
Gastrin and two other gut hormones : Cholecystokinin andsecretin act on the some target organs
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DUODENUM
Physiology
Gatric phase
Because of this structure similarity, Cholecysokinin andgastrin probably act on the same receptor site
Secretin blocks the action of gastrin on the parietal cellsand seems also to block the release of gastrin.
Calcium acts to stimulate gastric secretion byy releasinggastrin and gastrin stimulates the release of calcitonin
Serum gastrin concentrations are higher in patient withgastric ulcer than in patients with duodenal ulcer
In achlorhydria the serum gastrin levels are to be quitehigh
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DUODENUM
Physiology
Gatric phase
Conditions of gastric hypersecretion associated with
hypergastrinemia : Zollinger and silison Syndrome (1955)
Massive gastric hypersecretion
Peptic ulceration
Pancreatic cell tumor (non cell)
Diarrhea and malabsorption
The secretagogus liberated by the pancreatic tumor
was found to resemble gastrin (Gregory cs)
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DUODENUM
Physiology
Gatric phase
Treatment: total gastretomy may completely relieve thesymptoms of the disease, although profound hypergastrinemia
may persist When antral tissue has been sequesterd with the duodenum
following gastric resection This permanently sequestered alkaline environment, this antral mucosa
secrets gastrin without consequent exposure to acid feedback
Gastrin is released rapidly and is capable of effecting brinkgastric secretion within 15 minutes after stimulation
The biologic halftime of gastrin is 2 - 10 min
Catabolic system for gastrin in the kidney, possibly in the liver
and fundic mucosa
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DUODENUM
Physiology
Intestinal phase
Can be stimulated by Installation of food, particularly protein or acid into the proximal jejunum
Distention of jejunum
The agent responsible for the stimulation of intestinal phasesecretion is unknown, although some have suggested that thesecretagogus may be an intestinal analog of gastrin
shunting of portal blood results is profound acid hypersecretion,which is thought to be due to an unmarking of the intestinalphase stimulant that is ordinarily inactivated by the liver. Thissuggest that normally the stimulant is nearly completelydestroyed on hepatic hansit.
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Inhibit of gastric secretion
Decrease in vagas activity caused by removal of cephalicstimotestion
The secretion of acids itself ..
To block further release of gastrin To bring atant active duodenal suppression of gastric secretion
Gastric secretion is inhibited by the presence of acid fat orhypertonic solution in the duodenum
This is caused by a humoral agent : interogastrone Acidification of the duodenum
Inhibits gastric secretion
Releases secretin
Secretin is known to inhibit gastrin stimulated gastric secretion
Secretion has been proposed as the enterogastron from the duodenum
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Inhibit of gastric secretion Acid installed into :
The duodenum : inhibits gastric secretin
The jejunum : stimulates grotic secretion
The ilium : no effect
Eat is an effective inhibitor of gastric secretion.. instilled at any level of the small intestine
Hypertonic solution of sugar, salt and pepton
inhibit gastric secretion, apparently bystimulating a duodenum osmo receptor whichreleases a humoral inhibitor
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Peptic Ulcer
Peptic ulcer may occur wherever mucosa is bathed by fundicsecretion
Acute ulcer are commonly shallow and multiple, where aschronic ulcer are apt to be single, deep and
Pathogenesis : Is not weel under stood
Duodenal ulcer tend to be associated with hypersecretion ofacid bit not are duodenal ulcers hypersecrete
Gastric ulcers and the ulceration associated with acute mucosalinjury are not associated with the hypersecretion of acid
The presence of acid is necessary to ulcers to occur.
Factors involved in the pathogenesis of peptic ulceration
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Enzymatic digestion of mucous membrane
Attack Defense
Acid peptic digestion (Ph < 4) Dilution (non parietal secretion)
Drugs :
-Salicylates
-Steroids
-NSAID
Neutralization (HCO3 from bile
and pancreas)
Trauma Mucus barrier
Ischemia Rich blood supply
H.PYLORI
STRES
ROKOK
Cellular resistance
Emptying
Pathogenesis
Peptic Ulcer
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Pathogenesis :
Peptic ulcer are caused by pepsin which is inactiveabove a pH of 5.4 6 and has an optimum pH of around1.5-2.5 acid peptic digestion is certainly the most potent
agent attacking the mucosa. Emptying of the acid gastrin chyone into the crucible of
the duodenal bulb where it is neutralized by HCO3from bile and pancreatic juice is certainly one of themost important defences.
The mean based and maximal acid output of duodenalulcur patient is 1 -2 X as great as that of controlepatients
Peptic Ulcer
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Pathogenesis :
Cox : the stomachs of patient with duodenal ulcer have almosttwice the numbers of parietal cells as do normal stomachs.
Baron : there may be a treshold of acid secretory response to
the augomented histamins test, bellow which duodenal ulcerdoes not occur : 15 mEq / hour for males
18 mEq / hour for females
The etiology of hypersecretion is unknow, possibly duo to : Genetically larger mass of parietal cells
Increased sensitivity of the stimulatory mechanism
Responsive of inhibitory feed back mechanism
Failure of inhibitory feed back mechanism
Peptic Ulcer
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Pathogenesis :
If duodenal ulcer seem to be caused by an increased inthe caused by deficiencies is the mucosa defensesmechanism
Gastric ulcers invariable occurs in areas of gastritis Bile regurgitation may influence the development of
ulcers not only by damage to the gastric mucosa but alsoby direct release of gastrin.
Cigarette smoking may be a causative factor in pepticulcerations
Peptic Ulcer
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Pathogenesis : Intra gastric titration
Duodenal ulcer patients vs normal individuals
ulcer patients had higer based acid secretions and
higher response to amino acid meal at pH 7.0, 5.5, 4.0,2.5
acid secretion of both groups greater inhibited at pH 1.5
ulcer patients showed greater gastrin response to aminoacid meal at all level tested.
Gastrin cells and parietal cells appears to have differentsusceptibility to low pH levels.
Acid suppression of parietal cells output not totallydependent upon removal of gastrin stimulation.
Peptic Ulcer
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Recurrent dyspepsia after gastric operation Pain similar to that of original ulcer
Cause : Peptic ulceration
Mimicking disease
Iatrogenic disease produced by operation
Endoscopy best method of making diagnosis
If pH not lowered to below 3.5 after gastric surgeryunlikely that patient has true peptic recurrence
Duodenal ulcer respond to adequate dose of H2 blocker(Cimetidine)
Avoid reoperation to recurrent ulcer, heal ulcer withcimetiidin before reoperating: Do vagotomy + antrectomy
Roux-en y anastomosis advocated
Peptic Ulcer
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Peptic Problems and the Surgeon
Audiodigest Surgery Vo 28 No.13Goal of all medical and surgical ulur therapy : Achieve intraluminal pH > 5
surgically reducing number of gastric parietalcells
Historical survey of operations for duodenal ulcers: Gastro-enterostomy
Distal gastric resection BI or BII
Vagotomy & gastrojejunostomy
Vagotomy & pyloroplasty
Vagotomy & distalgastrric resection orantrectomy
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Subtotal gastrectomy:
mortality : low
ulcer recurrence; low
visick rating scale : goodTruncal vagotomy + drainage
Mortality : 1% or less
Ulcer recurrence 3-10%
Prevalence of diarrhea increased
General clinical rating : good to excellent
Peptic Problems and the Surgeon
Audiodigest Surgery Vo 28 No.13
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Truncal vagotomy & antrectomy
Ulcer recurrence rate lowest of all procedures
Clinical rating : good to excellent
Prevalence of diarrhea 1-30%
Selective gastric vagotomy & drainages
Little or on clinical advantage over tuncal vagotomy
Selective proximal vagotomy (user, without drainage)
Proximal .and distal denervation
dumping and diarrhea eliminated
mortality very low
ulcer recurrence 10-12 %
Peptic Problems and the Surgeon
Audiodigest Surgery Vo 28 No.13
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Secretary effects after operation
Post .op max. acid output best diminished
by vagotomy & antrectomy
Least diminished by S.P.V., asp with
drainage
Peptic Problems and the Surgeon
Audiodigest Surgery Vo 28 No.13
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