NicolaeTestemitanu [601041]

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Minister of Health of the Republic Moldova
2015

Universitatea de stat de MedicinasiFarmacie
“NicolaeTestemitanu”

Diploma Thesis
Duodenal Ulcer

Head Of the Deparmtment :d.h.s.m prof univ :vladmir Hotineanu
Leader scientific :d.s.m prof univ. A.Hotineanu
Preformer :st 6”th year group 1640 Obaida Jbara

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CONTENTS :

OBJECTIVES ………………………………………………………………..5
INTRODUCTI ON AND HISTORY …………………………………… ….. 6

CHAPTER I. ANATOMY AND PHYSIOLGY OF THE DOUDENUM ….7

1.2 STRUCTURE…… ……………………………………………………….. 8
1.3 TESSELATIONS AND PATHS …………………………………………. 10
1.4 DOUDENUM VASCULARZATION …………………………… …… …10
1.5 LYMPHATIC DRAINAGE OF DOUDENUM ……………………… ….11
1.6INNERVATION OF D UODEN UM…………………………… ……….12
1.7 HISTOLGY …………………………………………………………… ….13
1.8 FIZIOLGY ……………………………………………………………….13

CHAPTER II. EPIDMIOLGY ……………………………………… .….….15

CHAPTER III .PATHOPYHSIOLGY ……………………………… ………16

3.1 GASTRIC HYPERSECRETION ………………………………… …….17
3.2 REDUCTION OF MUCOSAL RESISTENCE ……………… ..……..…20

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3.3 INFECTION WITH HELICOBACTER PYLORI ……………… ………21
3.4 ENVIORMENTAL FACTORS ……………………………… ………… 24
3.5 GENETIC FACTOR …………………………………………… ………. 25
3.6 PATHOLOGICAL ANATOMY .,……………………………………… 26

CHAPTER IV . DIAGNOSIS ………………………………………………27

CLINICAL DIAGNOSIS………… ……………………………… ……….27

4.1 LABORATORY DIAGNOSIS ……………………………………….. 28
4.2 DIFFERENTIAL DIAGNOSIS ……………………………………. …31
4.3 LOCATING RECCESS ……………………………………………….. 32
4.4 AGE OF THE PATIENT ………………………………………… .….34

CHAPTER V. TREATMENT ……………………………… …………… 35

5.1 TREATMENT IGIENODIETIC ……………………… …………….. 35
5.2 COMPLEX TREATMENT ISSUES ……………………… ….…… ..36
5.3 ANTAGONIST RECEPTOR H2 ……………………… ….………… 36
5.4 ANTICHOLINERGIC ………………………………… ….………….. 37
5.5 PROTON PUMP INHIBITOR ………………………… ….…………. 38
5.6 ANTIACIDS ………………………… ………………… ……………. 38
5.7 SACRLFATUL …………………………………………… …………. 39
5.8 ANTIMICROBIAN TREATMENT ………………………… ………. 40
5.9 SURGICAL TREATMENT ………………………………… ………. 40

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5.9.1 TRONCULAR VAGOTOMY ……………………………… ………. 42
5.9.2 SUPRASELECTIVE VAGOTOMY ……………………… .…… …..43
5.9.3 TRONCULAR VAGOTOMY ASSOCIATION ……………… ……..43
5.9.4 GASTRIC RESECTION …………………………………… ..…….…46
5.9.5 EXCLUSIVE RESECTION ………………………………… ….……..47
5.9.6 DOUDENAL ULCER POSTBULBAR TREATMENT ……… …..….48
5.9.7 GIANT DOUDENAL ULCER …………………………………… ..….48
5.9.8 MULTIPLE ENDOCRINE ULCERS …………………………… …… 49
5.9.9POSSIBILE POSTOPERATIVE COMPLICATIONS …………… …..5 0

CLINICAL CASE …………………………………………………… ..…….51
CONCLUSION ………………………………………………………………53
SUMMARY ………………………………………………………………….54
REFERNCES ………………………………………………………………… 55

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OBJECTIVES / AIMS OF STUDY

– INTRODUCTION OF PUD
– REVIEW NORMAL ANATOMY AND PYHSIOLGY OF
DUODNEUM
– EPIDMIOLGY
– REVIEW OF PATHOLGICAL DUODENUM
– REVIEW OF DIAGNOSIS AND CLINICAL FEATURES
– RADIOGRAPHIC FILMS IN PATHOLGY
– THE CURRENT MANGEMENT AND TREATMENT
– REVIEW OF COMPLICATIONS
– SURGERY METHODS FOR EACH COMPLICATIONS –
INDICATIONS FOR PATIENTS
– POSTOPERATIVE SYNDROMS
– POSTOPERATIVE CARE
– CLINICAL CASE
– CON CLUSION AND SUMMARY

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Introduction and History OF PUD

Peptic ulcer has unquestionably been a disease of the twentieth century. Rare
beforethe end of the previous century, peptic ulcer became in creasingly
frequent, reaching a peak during the next 50 years and afflicting as many as 10
per cent of men. There wer e two types of peptic ulcer: gastric ulcer, which
appe ared to be due to damage to the lining of the stomach, and duodenal ulcer,
which was associated with excessive acid secretion by the stomach. Such ulcers
did not occur if t here was atrophy of the gastric mucosa, when no acid is
secreted by the stomach. Th e aetiology of peptic ulcer was fiercely debated.
Not unnaturally, in those post -Freudian days, psychosomatic
influences were for long thought to be the cause of peptic ulce r, stress being the
major culprit. The complications of peptic ulcer were an i mportant cause of
death, severe haemorrhage being common and perforation, particula rly of
duodenal ulcers, being a frequent surgical emergency. Obstruction of the
stomach by pylo ric stenosis might
also occur .

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CHAPTER I
the anatomy and phy siology of the normal duodenum
Anatomy

The duodenum is the first section of the small intestine in most higher vertebrates ,
including mammals , reptiles , and birds . In fish, the divisions of the small intestine
are not as clear, and the terms anterior intestine or proximal intes tine may be used
instead of duodenum. In mammals the duodenum may be the principal site for iron
absorption.
The duodenum precedes the jejunum and ileum and is the shortest part of the
small intestine, where most chemical digestion takes place.
In humans, the duodenum is a ho llow jointed tube about 25 –38 cm (10 –15 inches)
long connecting the stomach to the jejunum . It begins with the duodenal bulb and
ends at the suspensory muscle of duodenum . covering large vessels The
duodenum is a 25 –38 cm C -shaped structure lying adjacent to the stomach . It is
divided anatomically into four sections. Except for the first part of the duodenum,
the structure is retroperitoneal

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1.2-Structure ,:

The duodenum is a 25 –38 cm C -shaped structure lying adjacent to the stomach .
It is divided anatomically into four sections. Except for the first part of the
duodenum, the structure is retroperitoneal

-First part
The first part, or superior part, of the duodenum is a continuation from
the pylorus . It is superior to the rest of the segments, at the vertebral level of L1.
The first part of the duodenum is mobile, and connected to the liver by the
hepatoduodenal ligament of the lesseromentum . The first part of the duodenum
ends at the corner, the superior duodenal flexure .
Relations:
 Anterior
 Gallbladder
 Quadrate lobe of liver
 Posterior
 Bile duct
 Gastroduodenal artery
 Portal vein
 Inferior vena cava
 Head of pancreas
 Superior
 Neck of gallbladder
 Hepatoduodenal ligament (lesser omentum )
 Inferior
 Neck of pancreas
 Greater omentum
 Head of pancreas

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-Second part
The second part, or descending part, of the duodenum begins at the superior
duodenal flexure. It goes inferior to the lower border of vertebral body L3, before
making a sharp turn medially into the inferior duodenal flexure, the end of the
descending part.
The pancreatic duct and common bile duct enter the descending duodenum,
through the major duodenal papilla . The second part of the duodenum also
contains the minor duodenal papilla, the entrance for the accessory pancreatic
duct. The junction between the embryological foregut and midgut lies just below
the major duodenal papilla.
-Third part
The third part, or horizontal part or inferior part of the duodenum begins at
the inferior duodenal flexure and passes transversely to the left, passing in front of
the inferior vena cava , abdominal aorta and the vertebral column . The superior
mesenteric artery and vein are anterior to the third part of duodenum.
-Fourth part
The fourth part, or ascending part, of the duodenum passes upward, joining with
the jejunum at the duodenojejunal flexure . The fourth part of the duodenum is at
the vertebral level L2, and may pass directly on top of, o r slightly left to, the a orta.

1.3-Tessellation and paths:

The duodenal motility is subdivided into four parts: upper,
downward, horizontal and ascending.

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The first portion extends from the pylorus to the knee or higher flexura and is in its turn,
formed from an area proximal and intraperitoneal, furniture, more called the
duodenal bulb and a distal fixed area.

1.4-Duodenum Vascularization

The duodenum receives arterial blood from two different sources. The transition
between these sources is important as it demarcates the foregut from the midgut.
Proximal to the 2nd part of the duodenum (approximately at the major duodenal
papilla – where t he bile duct enters) the arterial supply is from the gastroduodenal
artery and its branch the superiorpancreaticoduodenal artery . Distal to this point
(the midgut) the arterial supply is from the superior mesenteric artery (SMA), and
its branch the inferior pancreaticoduodenal artery supplies the 3rd and 4th
sections. The superior and inferior pancreaticoduodenal arteries (from the
gastroduodenal artery and SMA respectively) form an anastomotic loop between
the celiac trunk and the SMA; so there is potential for collateral circulation here.

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The venous drainage of the duodenum follows the arteries. Ultimately these veins
drain into the portal system , either directly or indirectly through
the splenic or superior mesenteric vein .

1.5-Lymphatic drainage the duodenum

The lymphatic vessels follow the arteries in a retrograde fashion. The anterior
lymphatic vessels drain into the pancreatoduodenal lymph nodes located along the
superior and inferior pancreatoduodenal arterie s and then into the pyloric lymph
nodes (along the gastroduodenal artery). The posterior lymphatic vessels pass
posterior to the head of the pancreas and drain into the superior mesenteric lymph
nodes. Efferent lymphatic vessels from the duodenal lymph nod es ultimately pass
into the celiac lymph nodes.

1.6-Inervation Of the Doudenum

Extrinsic Inervation of the duodenum is made up of nerve fibers belonging to
thethe sympathetic and parasympathetic systems originating from celiac is,
mezenteric
liver and above.

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Inervation is operated by the parasympathetic vagus nerve sends fibers
toduodenum in his trunk before. It should be noted that besides the fibers
related, parasympathicus, from the duodenum come via efferent fibers and
vagus
Federico, who transmit information from receptors, osmoreceptors pH
(etc.)
duodenali.
Preganglio n sympathetic fibers arising from the thoracic segments of
the spinal cord Synapse in ganglia are located in the above mentioned is
withpostganglion fibers that end up going along with the blood vessels
isintramural.
Intrinsic Inervaț tion is made up of mi senteric is located between Auerbach
circular muscle layer and the longitudinal and submucous Plexus
Meisner.
Intrinsic Inervation far from being a mere extension of the parasympathetic
system so
as it was considered in the past, it consists of a large number of motor neurons,
sensitive and integrative playing a central role in the motility of the duodenum.

1.7 Histolgy

Under microscopy , the duodenum has a villous mucosa. This is distinct from the
mucosa of the pylorus , which directly joins to the duodenum. Like other structures
of the gastrointestinal tract , the duodenum has
a mucosa , submucosa , muscularisexterna , and adventitia . Glands line the

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duodenum, known as Brunner's glands , which secrete mucus and bicarbonate in
order to neu tralise stomach acids. These are distinct glands not found in the ileum
or jejunum, the other parts of the small intestine

1.8-Fiziolo gy

The main functions of the duodenum are to (1) alk -alinize acidic chyme, thereby
protecting its mucosa and facilitating digestion, (2) absorb calcium and iron, (3)
further the breakdown of food products, and (4) exert neuroendocrine control of
upper GI motility and secretion.
Alkalinization and Duodenal Mucosal Defense
Duodenal luminal pH can fluctuate rapidly between pH 2 and 7 as secreted
bicarbonate and gastric acid mix. Therefore, prevention of mucosal damage

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requires a coordinated defense via regulated premucosal, mucosal, and
submucosal components. These components include mucus and bicarbonate
(HCO3−) secretion, intracellular buffering, neuronal activation, and increased
blood flow.
After duodenal luminal acidification, a number of compounds stimulate
bicarbonate secretion from the liver, pancreas, and duodenum including secretin,
vagally produced acety lcholine, vasoactive intestinal polypeptide (VIP), pituitary
adenylate cyclase -activating polypeptide (PACAP)

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CHAPTER II

Epidemiolgy
Ulcerative disease is a major public health issue and affects
10-12% of the patients treated in the hospital, to which is added the patients
treated on an outpatient basis.
However it is found in the last two decades a continuous decrease in morbidity
and the number of days of hospitalization for ulcers, which reflect the
evolution of the situation
scientific data regarding etiopathogenesis and treatment of the disease.
Thus, duodenal ulcer
tends to become increasingly more a medical disease due to the purchase of
modern ,
the ulcer therapy and surgery became a solution only for the complications of
this disease .
Duodenal Ulcer occurs more frequently in adult age, with a maximum of
7frequency between 30 and 50 years. The disease prevails in males, in the report
between 6/1 and 4/1 after various statistics. Also the ulcer duodenum prevails over
the gastric location 4/1. Duodenal ulcer is more common in people with stressful
living conditions. A role in the occurrence and hereditary factor: hereditary
predisposition is manifested in the increased number of parietal cells and increased
gastric secretion.

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CHAPTER III
Pathophysiology
Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the
muscularis mucosa. The epithelial cells of the stomach and duodenum secrete
mucus in response to irritation of the epithelial lining and as a result of cholinergic
stimulation. The superficial portion of the gastric and duodenal mucosa exists in
the form of a gel la yer, which is impermeable to acid and pepsin. Other gastric and
duodenal cells secrete bicarbonate, which aids in buffering acid that lies near the
mucosa. Prostaglandins of the E type (PGE) have an important protective role,
because PGE increases the prod uction of both bicarbonate and the mucous layer.
In the event of acid and pepsin entering the epithelial cells, additional mechanisms
are in place to reduce injury. Within the epithelial cells, ion pumps in the
basolateral cell membrane help to regulate in tracellular pH by removing excess
hydrogen ions. Through the process of restitution, healthy cells migrate to the site
of injury. Mucosal blood flow removes acid that diffuses through the injured
mucosa and provides bicarbonate to the surface epithelial ce lls.
Under normal conditions, a physiologic balance exists between gastric acid
secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic
ulcer occur when the balance between the aggressive factors and the defensive
mechanisms is disru pted. Aggressive factors, such as NSAIDs, H pylori infection,
alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing
back diffusion of hydrogen ions and subsequent epithelial cell injury. The
defensive mechanisms include tight int ercellular junctions, mucus, mucosal blood
flow, cellular restitution, and epithelial renewal.
The gram -negative spirochete H pylori was first linked to gastritis in 1983. Since
then, further study of H pylori has revealed that it is a major part of the tr iad,
which includes acid and pepsin, that contributes to primary peptic ulcer disease.

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The unique microbiologic characteristics of this organism, such as urease
production, allows it to alkalinize its microenvironment and survive for years in
the hostile a cidic environment of the stomach, where it causes mucosal
inflammation and, in some individuals, worsens the severity of peptic ulcer
disease.
When H pylori colonizes the gastric mucosa, inflammation usually results. The
causal association between H pylori gastritis and duodenal ulceration is now well
established in the adult and pediatric literature. In patients infected with H
pylori, high levels of gastrin and pepsinogen and reduced levels of somatostatin
have been measured. In infected patients, exposure of the duodenum to acid is
increased. Virulence factors produced by H pylori, including urease, catalase,
vacuolatingcytotoxin, and lipopolysaccharide, are well described .

3.1-Gastric Hypersecretion

Gastric acid secretion is largely control by cholinergic, histaminergic and
peptidinergic(especially gastrin) pathways[. Disorders in a number of these
pathways can lead to gastric acid hypersecretion including ones, which primarily
mediate the hypersecret ion by causing hypergastrinemia, causing
hyperhistaminemia or by an unknown etiology. While these disorders may have
different etiologies, they frequently share similar clinical features [i.e., peptic ulcer

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disease (PUD), gastroesophageal reflux disease (G ERD)] due to the effects of the
acid hypersecretion on the esophagus, stomach and the duodenum. In some cases
where the hypersecretion is severe, the PUD/GERD may be refractory and severe
enough to lead to compilations such as PUD penetration, perforation, and bleeding
or esophageal strictures. The most severe disease is seen in patients with
Zollinger -Ellison syndrome (ZES), where gastric acid hypersecretion is frequently
>5 times the upper limit of normal .In addition to PUD/GERD the acid
hypersecretion c an result in diarrhea and malabsorption of nutrients, particularly
vitamin B 12 and iron

Currently the gastric acid hypersecretion mediated by these different disorders can
all be treated by gastric antisecretory agents. Of these the most effective and
generally used are proton pump inhibitors (PPIs) because of the their long duration
of action allowing once a day dosing. Histamine H 2 receptor antagonists are also
effective but because of their lower potency and s horter durations of action, more
frequent dosing is required and in some cases such as ZES, higher doses are
needed in some patients than used in routine peptic ulcer disease.
At present gastric acid secretory rates are only measured in a few centers and
therefore these disorders are frequently not suspected or diagnosed by measuring
the gastric secretion. Nevertheless, it is important to recognize these disorders,
because a number have specific other aspects of their treatment, rather than just
chronic tre atment with gastric antisecretory agents, that are needed or if
undertaken may lead to cure of the disorder (i.e., H. pylori ). Of these disorders the
most severe gastric acid hypersecretion is seen in patients with ZES , therefore it
is essential this disor der be diagnosed, the acid hypersecretion appropriately

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treated both short -term and long -term, and that treatment also be directed against
the gastrinoma, itself .
In this paper, advances in the diagnosis and treatment of the disorders listed
in will be b riefly reviewed. This review will concentrate on recent studies,
primarily within the last 3 –4 years, and will not attempt to cover all areas if there
is not a recent specific study. There are a number of recent reviews dealing with
these general aspects i ncluding reviews on ZES ,mastocytosisand H. pylori and
acid secretion. There have been no recent articles on acid secretion and renal
failure, antral G short bowel syndrome, basophilic granulocytic leukemia, head
injuries, stress related acid hypersecretio n, or hypertrophy
hypersecretorygastropathy, and a reader interested in these disorders is referred to
older literature dealing with these areas.
Of these gastric acid hypersecretorydisorders , the disorder which has been the
most dealt with in studies ove r the last few years, is various aspects of ZES. The
areas covered by these studies will be dealt with first .

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3.2-Reduction of mucosal resistance

Mucosal defense‖ is a term used to describe the various factors and components
that permit the mucosa to remain intact despite its frequent exposure to substances
with a wide range of temperature, pH, and osmolarity, as well as to substances
with detergent or cytotoxic actions, and bacterial products capable of causing local
and systemic inflammatory reactions . It is important to realize that the gastric
mucosa is not impervious to damage by these agents. The use of the term gastric
mucosal barrier has oft en been misconstrued to suggest that this tissue is
impenetrable. It was coined by Charles Code to explain the relatively small
amount of hydrochloric acid that ―back -diffuses‖ into the mucosa. In fact, mucosal
injury occurs regularly, but does not lead to clinically significant disruption of the
function or even the ―barrier‖ properties of the tissue. The reasons for this include
the fact that there are several ―layers‖ to mucosal defense, with secondary
components becoming more important when more superfi cial components are
breached, and because of a very rapid process of repair when damage to the
epithelium occurs . Moreover, the various components of mucosal defense can be
modulated by a number of endogenous substances, including prostaglandins. The
net result is that the systemic circulation is protected from invasion by microbes,
microbial products, and other toxins. On the other hand, there are certain
circumstances in which mucosal defense is impaired, such as after administration
of NSAIDs, thereby r endering the mucosa more susceptible to injury

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3.3-Infection with Helicobacter pylori

Helicobacter pylori (/ˌhɛlɪkɵˈbæktər paɪˈlɔəraɪ/), previously
named Campylobacter pylori , is a Gram –
negative , microaerophilic bacterium found in the stomach , and may be present in
other parts of the body, such as the eye.[1][2][3] It was identified in 1982 by
Australian scientists Barry Marshall and Robin Warren with further resear ch led
by British scientist Stewart Goodwin, who found that it was present in patients
with chronic gastritis and gastric ulcers , conditions not previously believed to have
a microbial cause. It is also linked to the development of duodenal ulcers
and stomach cancer . However, over 80% of individuals infected with the
bacterium are asymptomatic and it may play an important role in the natural
stomach ecology.[4]
More than 50% of the world's population harbor H. pylori in their
upper gastrointestinal tract . Infection is more prevalent in developing countries,
and incidence is decreasing in Western countries. H. pylori' s helical shape (from
which the generic name is derived) is thought to have evolved to penetrate
the mucoid lining of the stomach
H. pylori is a helix -shaped (classified as a curved rod, not spirochaete ) Gram –
negative bacterium about 3 μm long with a diameter of about 0.5 μm. It
is microaerophilic ; that is, it requires oxygen , but at lower concentration than is
found in the atmosphere . It contains a hydrogenase which can be used to obtain
energy by oxidizing molecular hydrogen (H2) produced by intestinal bacteria .[15] It
produces oxidase , catalase , and urease . It is capable of forming biofilms[16] and can
convert from spiral to a possibly viable but nonculturable coccoid form,[17] both
likely to favor its survival and be factors in the epidemiology of the bacterium.

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H. pylori possesses five major outer membrane protein families.[11] The largest
family includes known and putative adhesins . The other four families are porins ,
iron transporters, flagellum -associated pr oteins, and proteins of unknown function.
Like other typical Gram -negative bacteria, the outer membrane of H.
pylori consists of phospholipids and lipopolysaccharide (LPS). The O antigen of
LPS may be fucosylated and mimic Lewis blood group antigens found on the
gastric epithelium.[11] The outer membrane also contains cholesterol glucosides,
which are found in few other bacteria. H. pylori has four to six
lophotrichous flagella ; all gastric and enterohepatic Helicobacter species are highly
motile owing to flagella. The characteristic sheathed flagellar filaments
ofHelicobacter are composed of two copolymeri zed flagellins, FlaA and FlaB.
H. pylori harms the stomach and duodenal linings by several mechanisms. The
ammonia produced to regulate pH is toxic to epithelial cells, as are biochemicals
produced by H. pylori such as proteases , vacuolatingcytotoxin A (VacA) [this
damages epithelial cells, disrupts tight junctions and causes apoptosis], and
certain phospholipases .
Cytotoxin associated gene CagA can also cause inflammation and is potentially a
carcinogen.
Colonization of the stomach by H. pylori can result in chronic gastritis , an
inflammation of the stomach lining, at the site of infection. Helicobacter cysteine –
rich proteins (Hcp), particularly HcpA (hp0211), are known to trigger an immune
response, ca using inflammation. Chronic gastritis is likely to underlie H. pylori –
related diseases.
Ulcers in the stomach and duodenum result when the consequences of
inflammation allow stomach acid and the digestive enzyme pepsin to overwhelm
the mechanisms that protect the stomach and duodenal mucous membranes . The
location of colonization of H. pylori , which affects the loca tion of the ulcer,
depends on the acidity of the stomach.[36]In people producing large amounts of

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acid, H. pylori colonizes near the pyloric antrum (exit to the duodenum) to avoid
the acid -secreting parietal cells at the fundus (near the entrance to the
stomach).[11] In people producing normal or reduce d amounts of acid, H.
pylori can also colonize the rest of the stomach.
The inflammatory response caused by bacteria colonizing near the pyloric antrum
induces G cells in the antrum to secrete the hormone gastrin , which travels
through the bloodstream to parietal cells in the fundus.
Gastrin stimulates the parietal cells to secrete more acid into the stomach lumen,
and over time increases the number of parietal cells, as well.
The increased acid load damages the duodenum, which may eventually result in
ulcers forming in the duodenum.
When H. pylori colonizes other areas of the stomach, the inflammatory response
can result in atrophy of the stomach lining and eventually ulcers in the stomach.
This also may increase the risk of stomach cancer.

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3.4-Environmental Factors

The appearance of a multitude of factors contribute to the environment.
So smoking is considered a major risk factor for ulcerative disease, for healing, for
slowing the appearance of relapse and failure of ulcer. The mechanism of this action
include decreasing the production of prostaglandins, the appearance of low tide,
stimulating the production of bile acid and altered blood flow in the gastric mucosa.
Another factor for the emergence of significant exogenous ulcerous lesion
isconsumption of medicines non-steroidal anti -inflammatory DRUGS (NSAIDS).
Acute Ulcer produced by NSAIDS occurs more frequently in the stomach than
thethe duodenum, but complications caused by NSAIDS have equal frequency for
bothlocales. These substances acts through the inhibition of prostaglandin formation
about systemic and mucosal erosions are superficial, deep ulceration and bleeding.
Psychological Factor it is very important in the emergence of disease, being sure that
thestress significantly increases the secretion of hydrochloric acid and pepsin. Same
concept explains the pathogenesis of stress ulcer, experimentally proven fact yet now
two decades.
All exogenous fa ctors that have been incriminated in ulcerous disease
emergence inadequate nutrition, alcohol consumption, chronic infections, liver chronic
disease

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3.5-Genetic Factor
The presence of numerous cases of ulcerative disease in families raises the
question
genetic predisposition. Hereditary Membership in the pathogenesis of ulcer
patients can be
increased parietal cell mass and the fragility of the digestive mucosa —
factors
histologici genetically conditioned. However family aggregation of disease c an
be explained in part by the living arrangements and dietary habits and
poor behavior.
Another element that supports the role of the genetic factor in
ulcerogenesis isestablishment of the relationship between ulcerative
disease blood group 0 and (I), especially for
duodenal ulcer. It also reported increased frequency of presence
Antigen HLA -B5 histocompatibility in patients with duodenal ulcer.

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3.6-Path alogical Anatomy

 The characteristic histological finding of PUD is full ulceration of the gastric or
small intestinal mucosa to the level of the submucosa. Although the term
ulceration typically refers to any erosion of the surface epithelium, the term
"Peptic Ulcer" is reserved for deeper extents of erosion, into the submucosa. Such
a special meaning of "Ulcer" in the gastric and small intestinal context is used as
purely epithelial erosions are healed rapidly whereas deeper erosions into the
submucosa typically take weeks or months to heal. Classically, peptic ulcers
display a smooth base and perpendicular, punched out margins. They must be
distinguished from gastric carcinomas of 'excavated' morphology which display an
irregular base and heaped -up margins. Nearly all small intestinal ulcers occur in
the first part of the duodenum and are five times more common that gastric ulcers.

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CHAPTER IV
Diagnosis

-Clinical Diagnosis

Epigastric pain is the most common symptom of both gastric and duodenal ulcers.
It is characterized by a gnawing or burning sensation and occurs after meals —
classically, shortly after meals with gastric ulcer and 2 -3 hours afterward with
duodena l ulcer. Food or antacids relieve the pain of duodenal ulcers but provide
minimal relief of gastric ulcer pain.
Duodenal ulcer pain often awakens the patient at night. About 50 -80% of patients
with duodenal ulcers experience nightly pain, as opposed to onl y 30-40% of
patients with gastric ulcers and 20 -40% of patients with nonulcer dyspepsia
(NUD). Pain typically follows a daily pattern specific to the patient. Pain with
radiation to the back is suggestive of a posterior penetrating gastric ulcer
complicate d by pancreatitis.
Patients who develop gastric outlet obstruction as a result of a chronic, untreated
duodenal ulcer usually report a history of fullness and bloating associated with
nausea and emesis that occurs several hours after food intake. A common
misconception is that adults with gastric outlet obstruction present with nausea
and emesis immediately after a meal.
Other possible manifestations include the following:
 Dyspepsia, including belching, bloating, distention, and fatty food intolerance
 Heartburn
 Chest discomfort

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 Hematemesis or melena resulting from gastrointestinal bleeding. Melena may be
intermittent over several days or multiple episodes in a single day.
 Rarely, a briskly bleeding ulcer can present as hematochezia.
 Symptoms consistent with anemia (eg, fatigue, dyspnea) may be present
 Sudden onset of symptoms may indicate perforation.
 NSAID -induced gastritis or ulcers may be silent, especially in elderly patients.
 Only 20 -25% of patients with symptoms suggestive of peptic ulceration are found
on investigation to have a peptic ulcer.
Alarm features that warrant prompt gastroenterology referral[1] include the
following:
 Bleeding or anemia
 Early satiety
 Unexplained weight loss
 Progressive dysphagia or odynophagia
 Recurrent vomiting
 Family history of GI cancer

4.1 -Laboratory diagnosis

Testing for H pylori infection is essential in all patients with peptic ulcers. In most
patients with uncomplicated peptic ulcer disease (PUD), routine laboratory tests
usually are not helpful. Documentation of PUD depends on radiographic and
endoscopic confirmation.

29
If the diagnosis of PUD is suspected, obtaining CBC count, liver function tests
(LFTs), amylase, and lipase may be useful. CB C count and iron studies can help
detect anemia, which is an alarm signal that mandates early endoscopy to rule out
other sources of chronic GI blood loss.
Upper GI endoscopy is the preferred diagnostic test in the evaluation of patients
with suspected PUD . It is highly sensitive for the diagnosis of gastric and
duodenal ulcers, allows for biopsies and cytologic brushings in the setting of a
gastric ulcer to differentiate a benign ulcer from a malignant lesion, and allows for
the detection of H pylori infect ion with antral biopsies for a rapid urease test and/or
histopathology in patients with PUD
In patients presenting acutely, a chest radiograph may be useful to detect free
abdominal air when perforation is suspected. On upper GI contrast study with
water -soluble contrast, the extravasation of contrast indicates gastric perforation.
Double -contrast radiography performed by an experienced radiologist may
approach the diagnostic accuracy of upper GI endoscopy. However, it has been
replaced largely by diagnosti c endoscopy, when available. An upper GI series is
not as sensitive as endoscopy for establishing a diagnosis of small ulcers (< 0.5
cm). It also does not allow for obtaining a biopsy to rule out malignancy in the
setting of a gastric ulcer or to assess fo r H pylori infection in the setting of a
gastroduodenal ulcer.
Angiography may be necessary in patients with a massive GI bleed in whom
endoscopy cannot be performed. An ongoing bleeding rate of 0.5 mL/min or more
is needed for the angiography to be able to accurately identify the bleeding source.
Angiography can depi ct the source of the bleeding and can help provide needed
therapy in the form of a direct injection of vasoconstrictive agents.

30
A fasting serum gastrin level should be obtained in certain cases to screen for
Zollinger -Ellison syndrome. Such cases include the following:
 Patients with multiple ulcers
 Ulcers occurring distal to the duodenal bulb
 Strong family history of PUD
 Peptic ulcer associated with diarrhea, steatorrhea, or weight loss
 Peptic ulcer not associated with H pylori infection or NSAID use
 Peptic ulcer associated with hypercalcemia or renal stones
 Ulcer refractory to medical therapy
 Ulcer recurring after surgery

A secretin stimulation test may be required if the diagnosis of Zollinger -Ellison
syndrome cannot be made on the basis of the seru m gastrin level alone. This test
can distinguish Zollinger -Ellison syndrome from other conditions with a high
serum gastrin level, such as use of antisecretory therapy with a proton pump
inhibitor, renal failure, or gastric outlet obstruction.

A single bi opsy offers 70% accuracy in diagnosing gastric cancer, but 7 biopsy
samples obtained from the base and ulcer margins increase the sensitivity to 99%.
Brush cytology has been shown to increase the biopsy yield, and this method may
be useful particularly whe n bleeding is a concern in a patient with coagulopathy.

The histology of gastric ulcer depends on its chronicity. The surface is covered
with slough and inflammatory debris. Beneath this neutrophilic infiltration, active
granulation with mononuclear leuko cytic infiltration and fibrinoid necrosis may be
seen. In chronic superficial gastritis, lymphocytes, monocytes, and plasma cells
often infiltrate the mucosa and submucosa .

31

4.2-Differential Diagnosis

 Acute Coronary Syndrome
 Aneurysm, Abdominal
 Cholangitis
 Cholecystitis
 Cholecystitis and Biliary Colic in Emergency Medicine
 Cholelithiasis
 Diverticular Disease
 Esophageal Perforation, Rupture and Tears
 Esophagitis

32
 Gastritis, Acute
 Gastritis, Chronic
 Gastroenteritis
 Gastroesophageal Reflux Disease
 Inflammatory Bowel Disease
 Viral Hepatitis

4.3-Locating recess

After locating recess Requires special mentionduodenal ulcerpostbulbar.It is
Located distal to the bulb on the fixed portion of segment D1 (from right front of
gastroduodenal artery), on the Upper Reaches of the duodenum or
kneesupra vateriana segment in D2. Exceptionally it can locate and subvaterian.
This type of ulcer has a long evolution, with variable times symptomatic,
Sometimes for many years.
Periulcer inflammatory reaction causes damage retractile, with penetration in the
pancreas and ampulla Vater Involvement and even hepatic p edicle. Therefore
symptoms may include vomiting, jaundice and angiocholitis. The same anatomical
feature – location near the duodenal papilla niche – can cause biliary -digestive
fistulas installation of choices duodenal (duodeno -common bile duct or
duodeno ¬veziculrazation ). Postbulbar ulcer frequently causes complications such
as bleeding and stenosis, and usually penetrates the pancreas. Ulcer duodenal
papilla located distal stenosis can cause subvateriana .

33
Diagnosis is made by radiological examination – image typical "wire brushes" –
and endoscopic, although not rare that lesion location specified by intraoperative
exploration.
Another special form of a duo denal ulcers are multiple. Thus
Double duodenal ulcers can coexist with locating recess on the front and
posterior bulb, described as "kissing ulcer". Their evolution can be severe, marked
both perforation (previous injury) as well as hemorrhage (lesionrear).
The association with gastric ulcer, duodenal ulcer is
frequency, as a consequence of gastric lesions gastric emptying disorders
due to duodenal location. A special case of multiple ulcers is found in
Zollinger -Ellison syndrome, to be presented later.
All a particular form of giant duodenal ulcer is.
The lesion is located on the rear wall of the bu lb or postbulbar and can reach
in its evolution sizes 3 to 6 cm. Giant ulcer penetrates deep into
pancreas, producing a marked inflammatory reaction. From the clinical point of
view,
These morphological characters continue generating intense pain with radi ation
back, with vomiting and weight loss. Endoscopic appearance is
giant crater, while giant niche radiological barium examination may be
confused with duodenal bulb image

34
4.4-Age of the patient

Particular forms of ulcer can be described according to patient age. Thus pediatric
disease is common and may be atypical manifestations with predominant vomiting,
diffuse abdominal pain and refusing food.
The elderly, ulcer occurs mainly due to decrease both gastric and duodenal mucosal
resistance due to at herosclerotic lesions of vessels that supply the mucosa as well as
digestive wall structures due to involution. Pathology of chronic degenerative
rheumatism frequently encountered in these patients involves frequent administration
of NSAIDs and other chron ic diseases – hypertension, ischemic heart disease, liver
cirrhosis, BPOS – causes metabolic changes that affect the digestive mucosa.

35

CHAPTER V
Treatment
5.1 Treatment igienodietetic

1 Avoid smoking, alcohol, irritating food (spices, too cold, too hot).
2 repair teeth, chewing properly, drink water before and during meals.
3 Giving as much as possible to ulcerogenic drugs (aspirin, indomethacin,
corticosteroids).
4 Hygiene Plan – the regular hours, 4 -6 times daily with food that reduce effort
and neutralizes acid secretion: milk, butter, cream or soft raw egg, cheese, rice,
pasta.

36
5.2-Complex treatment issues

As developed scientific data regarding the etiopathogenesis of ulcers was
identified new substances which can be used in anti -ulcer therapy to achieve two
main objectives: relieve pain and promote healing of the lesion. Various drug
classes acting either at the receptor, antagonize the action of histamine, gastrin and
acetylcholine or inhibits the parietal cell proton pump or by adding or improving
gastric mucosal defense means. The disease is chronic and progressive treatment
addresses acute flares improve

5.3-Antagonisti receptor H2

Histamine causes the production of acid in the gastric parietal cells occupying a
membrane receptor and stimulate adenylate cyclase. Blocking histamine H2
receptors inhibits cups so as basal gastric secretion and stimulated. In this group
are summarized fannacologit Cimetidine , Ranitidine, Famotidine, and nizatidine.
Cimetidine has been the first product from the group of H2 -receptor antagonists
used in the treatment of duodenal ulcers. Administered at a dose of 400 mg every
12 hours or 800 mg single dose at bedtime for 4 to 8 weeks, this substance
significantly reduces basal acid secretion and stimulated secretion and causes
scarring of ulcerous lesion. The further treatment with 400 mg at bedtime for
several months significantly decreased the incidence of relapses.
Ranitidine is 6-8 times more intense action than cimetidine, resulting in a dose
corresponding in practice to obtain an equivalent effect. The dose of ranitidine is
150 mg twice daily or 300 mg once in the evening and the night 1ntreținere is
150 mg.

37
Famotidine is 8 -10 times more active in inhibiting acid secretion than ranitidine.
It is administered as a single dose 40 mg in the evening and the maintenance
dose is 20 mg.
Nizatidine is also very active, with biochemical structure similar to that of
famotidine, the ini tial dose is 300 mg at bedtime, single dose, continue taking
150mg.
Efficiency ulcer therapy with H2 receptor antagonists is uncertain, demonstrating
that the endoscopic ulcer disappears after 8 weeks of treatment in 85 -90% of
patients. This medication doe s not influence the "voice ulceroas'ă" recurrence,
less than half of the patients in the year following discontinuation .

5.4-anticholinergic

These substances inhibit gastric acid secretion blocking muscarinic acetylcholine
receptors situated in the parietal cells. Atropine action is not as strong as that of
H2 receptor antagonists, and side effects are unpleasant (visual disturbances,
urinary r etention). Anticholinergic substances have been identified as pirenzepine,
to muscarinic M1 receptor selectivity for the postganglionic nerve fibers which
innervate the stomach and inhibiting the action of the vagal stimulation of acid
secretion, and at th e same time having minimal effects

38

5.5-Proton Pump Inhibitor

Gastric acid secretion by parietal cells via an active transport of hydrogen ions
from the cytoplasm into the secretory canaliculi of potassium ions instead. Ion
exchange is mediated by an enzyme – ATPase – acting as a "proton pump".
Substance has been identified which inhibit the ATPase specific lowered
intensively acid production, called omeprazole. Anti acids omeprazole produced is
substantially complete, therefore this product should not be long -term. therapeutic
dose is 20 -30 mg / day, Zollinger -Ellison syndrome requiring only one dose of 60
mg up to 100 mg / day and more.
From the group of drugs that reduce gastric secretion by inhibiting the proton
pump part substance called Pantoprazo le (Controloc). Administer 40mg once daily
(1 tb.) Before or during breakfast, and in patients with severe hepatic impairment
rate of administration is two days. The duration of treatment is 2 to 4 weeks.

5.6-Anti Acids
The use of these substances in the therapy of ulcer was decreased in recent years
due to the identification of drug groups described before. Aluminum hydroxide
mixtures or preparations containing magnesium (hydroxide or thiosulphate),
calcium sodium carbon ate or bicarbonate may contribute to ulcer healing, but
especially the suppression of pain. These substances are not recommended as a
sole treatment or inilial, but can complete the effect, the antisecretoarelor ulcer.

39

5.7-Sucralfatul

This substance is a basic aluminu m salt of sucrose octasulfat polymerized in the
gastric acid becomes viscous and adheres to the gastric mucosa in general and, in
particular ulcer base. This creates a protective blanket lining the lesion, resulting
in a barrier to acid and pepsin aggression and inactivation of bile acids. Sucralfate
also stimulates the production of prostaglandin E2 tissue, thus increasing the
capacity of defense of the gastric mucosa and increases the secretion of
bicarbonate. The recommended dose of 1 g four times daily one hour before
meals. The s ubstance has minimal absorption and thus systemic effects are
nonexistent.Bismuth compounds have similar action sucralfate. These substances
formed in the acid coagulation of proteins, a protective film against
clorhidropeptice action. Also these drugs d e ffect of H. pylori eradication, healing
determining

gastritis and ulcers associated with this germ.
Analogues of prostaglandin
Cytoprotective effect is known and the antisecretory of
prostaglandins. Were produced synthetically related substances
prostagl andin E 1 and E2. Of these the most used is Misoprostol in
200 g dose 4 times a day. Effectiveness in wound healing ulcer is
comparable to that of H2 receptor antagonists

40
5.8-Antimicrobian Treatment
For eradication of Helicobacter pylori have been proposed many
regimens cons isting in mono, bio or trittherapy .
The effective bismuth compounds include combinations – salicylates and
colloidal bismuth citrate In association with metronidazole, amoxicillin with or
without the addition of, or Tetracyclin e. We exemplify such an association noted
bismuth subcitrate administration (Denol) 2 tb. 2 times a day before meals for 6
weeks + metronidazole 250 mg three times a day for 2 weeks + Amoxicillin 500
mg three times a day, or tetracycline 500 mg 3 times a d ay for 2 weeks. This
triple therapy fails to cure Helicobacter pylori infection in 90% of cases, and the
association and H2 receptor antagonists or omeprazole increase the effectiveness
of antimicrobial therapy.
At the end of the presentation of these grou ps of antiulcer drugs must emphasize
that all are effective in healing duodenal ulcer and no evidence for superiority of
one to the other. Also not shown the need to involve them. Under their action
ulcers usually heal in 4 -6 weeks, in some cases requiring therapy longer than 8 –
nini. maintenance in cases extends to at least one year.
5.9-Surgical Treatment

Preoperative preparation:
 Rest digestive and gastric lavage
 infusion to fluid resuscitation hemodynamics and protein
 Analgesics
 correction of anemia

41

surgical Procedures
Increasingly in recent years has become a duodenal ulcer disease are cured by
medical treatment, surgery is reserved for complications (bleeding, stenosis,
perforation and lack of response to medical treatment). Surgical treat ment goals
are the achievement of a hypo gastric clearance, when possible, ulcerative lesion
and gastric drainage provision as close to normal physiology.
Reduce stomach acid secretion can be done by tapping in the brain (the various
types of vagotomy) or by combining the effects vagotomiei reducing acidity by
limited resection (bulbantrectomie). Reduce acidity exclusively
gastrinosecretante region wide resection (gastric antrum) and a portion of the
body containing the stomach secreting parietal cells, so -called gastric resections
3.2, provides a disfigurement that makes them no longer accepted by most
surgeons. They appear to have an indication for the treatment of duodenal ulcer,
only for those cases where the ulcer can not be resected (resection of exclu sion)
and while usually associated with truncal vagotomy.
Today increasingly more surgeons prefer intercepting nerve secretion by various
types of vagotomy or both secretory mechanisms by assigning a limited
resections (bulbantl'ectomie) with truncal vagot omy.

42
5.9.1-Troncular Vagatomy

Truncal vagotomy is performed by secțittnea subdiaphragmatic vagal trunks
both. Effect vagotomiei harsh stomach is hyperacidity , and motor denervation
which brings disorder exhaust vagal denervation of the biliary tract, pancreas,
and intestine.
For this reason it is necessary to associate vagotomiei truncal surgery to suppress
the pyloric sphincter function and called pyloroplasty. Among the many types of
pyloroplasty were described the Heineke -Mikulicz pyloroplast y is used. It
consists of a longitudinal section of the anterior wall of the antrum and
duodenum one (per cm 2 each of the pylorus), followed by suturing cross –
making to increase considerably the lumen of the pyloric canal. Are used in
practice and describ ed by Judd and Finney pyloroplasty.
All the operations of "drainage" of the stomach associated vagotomiei were
described gastroduodenostomiile performing a latero -lateral anastomosis
antroduodenală and performing drainage gastrojejunostomia stomach by
anastomosis antro jejunal that bypasses pylorus. Moreover, Professor Burlui
described previous pilorectomia antroduodenostomie latero -lateral lift has the
advantage of ulcers.
outside vagotomiei truncal been described and so -called selective vagotomy,
which cu t off all the branches that go to the stomach vagal preserve those that go
to the liver and celiac ganglia. And this type of surgery has many followers.
Lately it was done laparoscopic posterior truncal vagotomy combined with the
earlier sero myotomy for n ervous secreting regions of the stomach through an
incision sero muscular along the lesser curvature up to about 6 cm from the
pylorus. thereby kept innervation pylorus.

43

5.9:2 -Supraselective Vagatomy

Intersects only fibers innervating the stomach secretoarea region. Are
preserved both celiac and hepatic vaga l branches and those that go to antro –
pyloric region. For this reason, it is not necessary to asso ciate
vagotomiei supraselective drainage surgery. By this technique are cut
branches gastri c vagal about 5 cm proximal to the pylo rus, along the lesser
curvature of stomach.
-Advantage – suppresses secretion clorhidropeptică preserving antrum
motility and pylorus function.

44
-Disadvantages – technically more difficult and there is always the safety of
extirpation all interested vagal branc hes clorhidropeptică secretion.

5.9:3 -Troncular Vagatomy Asociation wit h Bulbanterctomy

It is considered as the most effe ctive surgical treatment option of ulcer as it
adds to the effect of denervation on the extirpation of the gastric antrum and
duodenal bulb with the source of gastrin. In general, caution, surgeons
performed a gastrectomy wider than a antrectomie that hemigastrectomie
call. This intervention appears to have the most followe rs, being burdened by
the small number of recurrences.
Restoration of digestive continuity is achieved by local technical conditions
by gastroduodenal anastomosis end -to-end (Nan – Bilroth I), preferably
through functional advantages of keeping the duodenu m in transit. It can be
done and anastomosis gastrojejunală terminolaterală (Bilroth II) with several
variants, depending on the transition transmezocolic or precolic anastomotic
loop mode after performing anastomosis with jejunum using whole tranche
gastr ic (Reichel – Polya) or only a portion of them (Hoffmeister – Finsterer).

45
Duodenal ulcer surgery performed gastric physiology changes with
beneficial clinical effects, but also undesirable. The vagotomy reduces
cholinergic stimulation of gastric parietal c ells and their sensitivity to the
action of gastrin and histamine. There are no significant differences between
the results vagotomiei supraselective to truncal vagotomy in the remaining
acid. Antrectomiei association with truncal vagotomy causes a greater
decrease

acid secretion in gastrin -stimulated acid yielding maximum flow decreased
by 85% compared to preoperatively.
Due vagotomiei install and impaired gastric emptying, supraselectivă
vagotomy inhibits vagal mediated muscle relaxation. Thus the pa ssage of
food, especially liquids, into the duod enum is accelerated, the damage region
proximal stomach motility. Gastric emptying is faster if vagotomiei
associated practice and pyloroplasty.

46
Other effects of the vagotomy extragastric truncal refers to th e function of
pancreatic exocrine secretion is reduced postprandial. It also decreases the
secretion of bicarbonate, enzymes, bile and gall bladder relaxes.

5.9:4 -Gastric Resection

Resection gastric ulcer disease is to create a anacid stomach or the removal of distal
hypo 02.03 (classic resection) or 3/4 of the stomach Along initial portion of the
duodenum, made so removing gastrino¬formatoare area, as well as the a large part of
the acid -secretotrie. Food transit recovery is made after two basic methods: gastro –
duodenal anastomosis (type Pean -Bilroth I) that keep transit blo ck-duodeno –
pancreatic biliary and gastro -jejunal (Bilroth type II) using whole tranche gastric
(Reichel – Polya process ) or only the lower tranche (Hoffmeister -Finsterer method).
Jejunal gastrointestinal anastomosis can be transmezocolic the transverse mes o or
precolic • When operating the corresponding loop requires a long anastomosis with
the efferent to avoid stasis related 1n (BrauntBalfoux).
Limited resection (antrectomia) is 1n removal of antral portion (gastrin mechanism)
and duodenal bulb (bulboantr ectomia) due to secretion
at the level of the duodenal gastrin. Antrectomia associated vagotomiilor is pathogenic
operation of choice in the treatment of duodenal ulcer as the main component
suppresses the excitosecreție (vagueness and antrum) resection is limited (too much
unaltered reservoir capacity of the stomach) and duodenal Gastrointestinal
anastomosis allowed that restores digestive transit normal; such function is taken from
the pylorus abolished cudurile duodenal with its anatomy and its physiolog ical
sphincters

47

5.9:5 -Exclusive resection

Exclusive resection is necessary intervention with leaving ulcers on the spot;
Gastric ulcers can be practiced juxta cardial (Madlener technique) or duod enal
ulcers and hard postbulbar removed. The operation consists of partial gastric
resection and suturing antrum preserving Mucus and gastro¬jejunostomy +
bilateral truncalvagotomy (technical Finster, Willmans, PLENK).
Surgical treatment of duodenal ulcer particular forms In the final c hapter surgical
treatment we humans refer to some particular therapeutic issues that address
specific forms of ulcer.

48

5.9:6 -Doudenal ulcer postbulbar treatment

The main feature of these ulcers is a tendency to break 1n neighboring organs and
anatomical structures (pancreas, liver pedicle, liver). Relations with the bile duct,
pancreas and liver pedicle do that most times their surgical excision fle not possible.
in these cases, most authors opt for maximum interception of both secretory
mechanisms, involving resection gastric 3.2 of 'exclusion' of the ulcers with truncal
vagotomy and obviously to restore transit through end -to-side gastrojejunostomy –
anastomosis .. special mention worth ulcers postbulbare below Vater ampulla which
tend to duodenal lumen stenosis. their treatment will always be a 2/3 gastrectomy
exclusion ulcer with truncal vagotomy. Restoration transit will b e achieved using a
jejunal anastomosed e nd-to-side to the gastric stump.

5.9:7 -Giant Duodenal ulcer
Usually these ulcers are located in the duodenal bulb, rear wall, penetrating in
pancreas, which performs a real crater bounded by an intense local inflammatory

49
reaction. This type of ulcer treatment creates technical difficulties, most surgeons
prefer to join a hemigastrectomie with truncal vagotomy and duoden um preserving 1n
transit suture being made in the posterior d uodenal wall in the lower right ulcer crater.

5.9:8 -Multiple endocrine ulcers

If the location of gastrinoma was possible preoperatively
The treatment consists of the removal of the tumor without having to
gastrectomy (35 -40%
of cases). If the tumor is malignant, and hepatic metastases, as far as
which is technically possible, it is recommended their resection.
Where gastrinoma location could not be determined preoperatively
or intraoperative exploration is recommended total gastrectomy
followed by a
esojejunostomy a jejunal loop "Y", 50 -60 cm long, in order to
prevent
bile reflux into the esophagus. Lately total gastrectomy was replaced
by
perform a subdiaphragmatic truncal vagotomii associated with
pyloroplasty,
which significantly reduces the necessary amount of antisecretory
drugs control the symptoms

50

5.9:9 -Possible postoperative complications

I. Complications and consequences of trauma postanestezice operator: – shock; pulmonary
atelectasis; pneumonia:
II. Early postoperative complications:
bleeding into the abdominal cavity;
bleeding into the lumen of the digestive tract;
duodenal stump dehiscence;
anastomosis dehiscence:
a) gastroduodenoanastomosis (GDA);
b) gastroenteroanastomo sis (GEA);
c) eso -gastroanastomosis (EGA)
d) eso -jejunoanastomosis (EJA)
gastric stump necrosis (NBG);
iatrogenic biliary tract;
disorders of gastric discharge stump;
postvagotomice early complications; Postoperative acute pancreatitis; peritonitis;

51
postoperative intestinal obstruction;
III. Late postoperative:
– BSO;
intestinal obstruction adherents; – Late abdominal abscesses; – Eventrations postoperative
abdominal wall;

Clinical case

A 53 -year-old man with a history of chronic myeloid leukemia in clinical
remission for three years, on maintenance therapy (100mg/day) with imatinib, was
admitted to our hospital to investigate a persistent fever. He reported the sudden
onset of an acute c hest pain with epigastric radiation 15 days before his hospital
admission. At that time, the referring physician excluded a pain of cardiac origin
based on normal electrocardiogram (ECG) findings and cardiac enzyme levels.
Three days later, our patient was febrile (38.5°C) and dyspnoic. Laboratory tests
revealed an elevated white blood cell count (13×103 cells/mL), and a chest X -ray
(not shown) was performed revealing an ill -defined hypolucency in the right lower
lobe. On the basis of these clinical and rad iological findings, a presumed diagnosis
of acute bronchopneumonia was made and our patient was given medical therapy
with antibiotics, non -steroidal anti -inflammatory and proton -inhibitor drugs.

52
At admission, our patient was febrile (38.5°C) with abdominal tenderness and
hypoactive bowel sounds. A plain abdominal X -ray film was then performed
. On the upright film a huge air -fluid level was clearly depicted in the right
subphrenic space. In the s upine position the extraluminal air appear to extend from
the right subphrenic to the subhepatic space and the hepatoduodenal fossa
(Figure 1B). Based on the X -ray findings, a con trast-enhanced multi -detector row
CT study was performed with a detector configuration of 1×32mm, a table feed of
36mm/s and a gantry rotation time of 0.75 (pitch factor=0.844), 120kVp and
automatic dose modulation. A monophasic acquisition was performed 8 0s after
intravenous bolus injection of 150cm3 of non -ionic iodinated contrast media
at a rate of 2cm3/s.

On contrast -enhanced MDCT, a right subphreni c abscess was clearly depicted The
huge air -fluid collection extended from the subphrenic
to the perihepatic space and extraluminal air bubbles could also be detected in the
fissure of Teres’ ligament
. On the coronal reformatted image extraluminal air could also be detected in the
hepatoduodenal ligament where extraluminal leakage of the water -solub le
iodinated contrast media could be seen after oral administration of 500cm3of 3
percent diluted diatrizoatemeglumine.

53
patient underwent surgery. During laparotomy, a huge abscess was found in both
the right subphrenic and the subhepatic spaces. After drainage, several attempts to
identify the site of leakage were made but were unsuccessful because of an
inflammatory block involving the lesser omentum, the duodenal bulb, the hepatic
flexure and the inferior margin of the left hepatic lobe . After extensive
adhesiolysis, the duodenal bulb was finally exposed and the site of the ulcer
identified by methylene blue administration through a nasogastric tube. The ulcer
was sutured.
Our patient had a largely uneventful recovery, with the only inci dents being a right
pleural fluid collection (600cm3) requiring thoracocentesis and small (<200cm3)
residual perihepatic fluid collections, which were monitored and managed
conservatively. He was discharged 12 days later.

Conclusion
case of a perforated duodenal ulcer complicated by a right subphrenic abscess,
first revealed on abdominal X -ray film and then confirmed by contrast -enhanced
MDCT. While subphrenic abscesses are well known complications of perforated
gastric or duodenal ul cers, they have nowadays become rare thanks to advances in
both diagnostic and therapeutic strategies for peptic ulcer disease. However, when
peptic ulcer disease is not clinically suspected, the contribution of imaging may be
substantial.

54

SUMMARY

This review includes findings which provide insight with regard to the triaging of
dyspeptic subjects, information on new PPI drugs and H pylori eradication 'rescue
regimens'. The COX -2 debacle is discussed and new data relating to the efficacy
of co -thera py strategies for the prevention of NSAID gastropathy are presented,
while the use of antiplatelet agents as 'safe' substitutes for aspirin
cardioprophylaxis is questioned. The important issue of PPI safety and NSAID
enteropathy are addressed.

 A Duode nal ulcer is a break in superficial epithelial cells penetrating down to
muscularis mucosa
 Duodenal > gastric ulcers
 Can be asymptomatic
 H pylori is a predominant risk factor
 H pylori diagnosed by c urea breath test, stool antigen or if validated
serology,
 Complications of PUD can lead to acute emergency of upper GI bleed And
Surgical Interventions
 Post Operative Complications and post OperativeTreamtent And Life Care
should be followed

55

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