Dr. Henk K-The Stomach and Duodenum

7/27/2019 Dr. Henk K-The Stomach and Duodenum

1/40

THE STOMACH AND

DUODENUM

Dr. Henk Kartadinata, SpB, SpBD, FICSBagian Ilmu Bedah

Fakultas Kedokteran

Ukrida


2/40

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


3/40

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


4/40

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


5/40

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


6/40

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


7/40

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


8/40

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)


9/40

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


10/40

THE STOMACH

Anatomy :

The wall of the stomach :

Composed : Mucosa

Submucosa

Muscle

Sero


11/40

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


12/40

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


13/40

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


14/40

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


15/40

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


16/40

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


17/40

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


18/40

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


19/40

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


20/40

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


21/40

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


22/40

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


23/40

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


24/40

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


25/40

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)


26/40

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


27/40

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.


28/40

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


29/40

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


30/40

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


31/40

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


32/40

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


33/40

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


34/40

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


35/40

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


36/40

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


37/40

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


38/40

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


Audiodigest Surgery Vo 28 No.13


39/40

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 %




40/40

Secretary effects after operation

Post .op max. acid output best diminished

by vagotomy & antrectomy

Least diminished by S.P.V., asp with

drainage



Documents

Dr. Henk K-The Stomach and Duodenum