Surgical Anatomy of the Stomach

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    SURGICAL ANATOMY OF THE STOMACH

    Dr.M.Ardaale

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    ANATOMY:

    The stomach J-shaped. The stomach has

    two surfaces (the anterior & posterior),

    two curvatures (the greater & lesser), two

    orifices (the cardia & pylorus).

    It has fundus, body and pyloric antrum.

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    STOMACH

    The lesser curvature :forms the right border &extends from the cardiac orifice to thepylorus.It is suspended from the liver by the

    lesser omentum.The greater curvature :forms the left border,

    the greater omentum extends from the lowerpart to the transverse colon& the gastro-splenic omentum extend from the upperpart to the spleen .

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    CONT..

    The mucus membrane forms many folds called

    rugaethat are longitudinal in direction.

    It has 3 muscular layers: longitudinal ,

    circular & oblique.

    The stomach function is :storage of food ,mix

    the food with gastric secretions to form

    chyme, & the delivery of the chyme to the

    small intestine.

    Capacity: 1.5 L food; max capacity 4L (1

    gallon)

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    BLOOD SUPPLY:

    . The left gastric artery

    . Right gastric artery

    . Right gastro epiploic artery

    . Left gastro epiploic artery

    . Short gastric arteries

    The corresponding veins drain into portalsystem. The lymphatic drainage of thestomach corresponding its blood supply.

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    DUODENUM

    The 2ndpart: is 8 cm long runs vertically downward infront of the right kidney & on right side of L1,2vertebrae. Its medial border receives the bile duct &the main pancreatic ducts in major duodenal papilla &receive the accessory panc. Duct higher up in the

    minor duod. Papilla.The 3rdpart: is 8 cm long ,runs horizontally to the left, in

    front of the vertebral column& the lower margin of thehead of panc.

    The 4thpart: is 5 cm long, runs upward & to the left tothe duodeno-jejunal flexure.

    The mucus memb. Is formed in circular folds calledPlicae circularis

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    BLOOD SUPPLY OF DUODENUM

    Blood supply:

    superior

    mesentericartery;

    Veins drain intohepatic portal

    vein

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    HISTOLOGY OF STOMACH

    Parietal cells:

    These are in the body (acid-secreting portion) of

    the stomach and line the gastric crypts, more

    abundant distally. These are responsible for the production of

    hydrogen ions to form hydrochloric acid, which

    has a pH of around 1.

    The hydrogen ions are actively pumped by the

    proton pump, a hydrogenpotassium APTase

    (Sachs) which exchanges intraluminal potassium

    for hydrogen ions.

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    CONT..

    a key factor in gastric acid secretion.

    In addition, there are large numbers of

    somatostatin-producing D cells throughout

    the stomach, and

    somatostatinhas a negative regulatory role.

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    DUODENUM

    The duodenum is lined by a mucus-

    secreting columnar epithelium.

    In addition, Brunners glands lie beneath

    the mucosa and are similar to the

    pyloric glands in the pyloric part of the

    stomach.

    Endocrine cells in duodenum produce

    cholecystokinin and secretin

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    PHYSIOLOGY OF THE STOMACH AND

    DUODENUM

    The stomach mechanically breaks upingested food and, together with

    the actions of acid and pepsin, forms

    chymethat passes into the duodenum. In contrast to the acidic environment of the

    stomach, that of the duodenum is alkaline,as a result of the secretion of bicarbonate

    ionsfrom both the pancreasand theduodenum.

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    CONT..

    This neutralisesthe acid chyme and adjusts

    the osmolarityto approximately that of

    plasma.

    Endocrine cells in the duodenum produce

    cholecystokininthat stimulates

    the pancreas to produce trypsinand the gall

    bladder to contract.

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    CONT..

    Secretinis also produced by the endocrine

    cells of the duodenum.

    This hormone inhibits gastric acid

    secretion and promotes production of

    bicarbonate by the pancreas.

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    GASTRIC ACID SECRETION

    The secretion of gastric acid and pepsin

    tends to run in parallel,

    although the understanding of the

    mechanisms of gastric acid secretion is

    considerably greater than that of pepsin.

    Numerous factors are involved

    to some degree in the production of the

    gastric acid.

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    CONT..

    These include neurotransmitters,

    neuropeptidesand peptide hormones, and

    several other factors.

    As mentioned above, hydrogen ions are

    produced by the parietal cell by the

    proton pump.

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    GASTRIC MUCUS AND THE GASTRIC MUCOSAL

    BARRIER

    The gastric mucous layer is essential to theintegrity of the gastric mucosa.

    It is a viscid layer of mucopolysaccharides

    produced by the mucus-producing cells ofthe stomach and the pyloric glands.

    Gastric mucus is an importantphysiological barrier to protect the gastricmucosa from mechanical damage, andalso the effectsof acid and pepsin.

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    CONT..

    Its consider-able bufferingcapacity is

    enhanced by the presence of bicarbonate

    ions within the mucous.

    Many factors can lead to the break down ofthis gastric mucous barrier.

    These include bile, nonsteroidal anti-

    inflammatory drugs (NSAIDs), alcohol,trauma and shock.

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    CONT..

    The stomach is the most sensitive to

    ischaemia following a hypovolaemic insult

    and also the slowest to recover.

    This may explain the high incidence of

    stress ulceration in the stomach.

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    PEPTIDES AND NEUROPEPTIDES IN THE

    STOMACH AND DUODENUM

    Many peptides recognized as hormones

    may also be produced by neurons, hence the

    term neuropeptides.

    The term messenger can be used to

    describe all such products.

    There are three conventional modes of

    action which overlap.

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    CONT..

    The autocrinemode of action should be

    mentioned for completeness.

    Here messengers are released from cell to

    act on receptors on the same cells surfacemembrane.

    Many growth factors such as epidermal

    growth factor and transforming growthfactors alpha and beta work in this way.

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    INVESTIGATION OF THE STOMACH AND

    DUODENUM

    Flexible endoscopy

    Amongst all of the methods used toinvestigate and image the stomach

    and duodenum, flexible endoscopy is nowthe gold standard.

    The original gastroscopes were fibre-optic

    (Hirschowitz), but now most use a solid-state camera mounted at the

    instruments tip.

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    ULTRASONOGRAPHY

    Standard ultrasound imaging can be used toinvestigate the stomach, particularly inpatients with neoplasia.

    Thickening of the gastric wall can be seen in malignancy, some assessment

    made of local invasion, and liver andperitoneal diseaseis often detected.

    However, used, conventionally, it is lesssensitive than other modalities.

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    CONT..

    By contrast, endoluminal ultrasound and

    laparoscopic ultrasound are probably the

    most sensitive techniques available in the

    preoperative staging of gastric

    cancer. In endoluminal ultrasound the

    transduceris usually attached to

    the distal tip of the instrument.

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    CONT..

    Five layers of the gastric wall may beidentified on endoluminal ultrasound andthe depth of invasion of a tumour can be

    assessed with exquisite accuracy (90 percent accuracy for the T

    component of the staging). Enlarged lymphnodes can also be identified

    and the techniques accuracy in thissituation is about 80 pet cent.

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    OTHER INVESTIGATIONS

    Laparoscopy: (gastric cancer, peritoneal

    Disease such as patients ascitesor bulkyintraperitoneal disease)

    Gastric emptying studies:(gastricdysmtility disorders, follow gastric surgery)

    Tests of gastric acid secretion and of pH

    monitoring(gastric acid secretion commonlyfound in patients with duodenal ulcerdisease)

    24-hour intragastric pH monitoring

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    MEASUREMENT OF PLASMA GASTRIN

    The measurement of plasma gastrin by

    radioimmunoassay is of use in the diagnosis

    of gastrinoma (ZollingerEllison syn-

    drome). In most assays the normal fasting gastrin

    level is about 50 ng/litre, but in gastrinomas

    very high levels, some-times manythousands of ng/litre, can be found.

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    CONT..

    the other common cause of

    hypergastrinaemia is hypochlorhydria

    associated with gastric atrophy and very

    high gastrin levels are found in perniciousanemia.

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    CONT..

    In some cases there seems to be a familial

    association.

    In such families the mother has suffered

    from the condition in 50 per cent of cases,

    and 10 per cent of male siblingsand 2 per

    cent of female siblings are affected.

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    PATHOLOGY

    The classical feature is that the musculature

    of the pylorusand adjacent antrum is

    grossly hypertrophied,

    the hypertrophy being maximum in the

    pylorus itself.

    The mucosa is compressed such that only

    a probe can be inserted.

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    CLINICAL FEATURES

    First-born male child that is most

    commonly affected.

    This condition is seen at 4 weeks after birth

    ranging from the third week to, on rare

    occasions, the seventh.

    A premature infant will also develop the

    condition at about 4 weeks after birth.

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    CLINICAL PRESENTATIONS

    Vomiting is the presenting symptom that

    after 23 days becomes forcible and

    projectile.

    The child vomits milk and no bile ispresent. Immediately after vomiting the baby

    is

    usually hungry.

    Weight loss is a striking feature and rapidly

    the infant becomes emaciated and de-

    hydrated.

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    DIAGNOSIS

    Feeding tube (NG tube)

    This may produce characteristic peristaltic

    wavesthat can be seen to pass across the

    upper abdomen.

    At the same time, using a warm hand, the

    abdomen is palpated to detect the lump

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    PYLORIC STENOSIS CONT.

    Signs:

    1.Vis ib le per istal t ic waves pass ing from lef t to

    right across the upper abdomen (golf ball

    waves).

    2.A palpable tumor in the

    epigastr ium or r ight

    hypochondr ium (most important).

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    IMAGING

    Ultrasonographyis the investigation ofchoice as it can, with-out difficulty, detect the

    classical features in the pyloric canal.

    Differential diagnosis:

    GERD

    UTI

    Intestinal obstruction

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    TREATMENT

    Correct dehydration level (with low sodium,chloride and potassium, and a metabolic

    alkalosis).

    The child should be rehydrated withdextrosesaline and potassium (2.5 per

    cent dextrose plus 0.45 per cent sodium

    chloride plus 1 g of potassium chloride per500 ml of

    fluid).

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    DEFINITIVE MANAGEMENT(SURGERY)

    Ramstedtsoperation:

    it is important that the stomach is emptied

    and washed out with saline, and that

    hypothermia is avoided.

    Procedure:transverse incision placed

    in the upper abdomen over the right rectus

    sheath, which is opened in the same line.

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    Treatment :

    Treatment is theoperation of

    pyloromyotom

    (Ramstedts

    operation).

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    CONT..

    The rectus muscle is then split along theline of its fibresand the posterior rectus

    sheath opened in the line of the skin incision.

    The hypertrophied pylorus is delivered androtated so that its superior surface comes

    into view .

    Thus, the least vascular portion can beselected for incision.(Pyloratomy).

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    DUODENAL ATRESIA

    This occurs at the point of fusion betweenthe foregut and midgut, and therefore lies in

    the neighborhood of the ampulla of Vater.

    There is a diaphragm, which is usuallycomplete, across the duodenum at this point

    and the condition is frequently accompanied

    by other defects.

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    CONT..

    The diagnosis is now made antenatally inmost cases through the use of

    ultrasound.

    This shows the characteristic appearanceof a

    dilated stomach and first part of the

    duodenum (double bubble). The child vomits from birth and the vomitus

    is bile stained.

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    DIFFERENTIAL DIAGNOSIS

    High intestinal obstruction

    Pyloric stenosis

    Treatment:(surgery)

    operation of the

    duodenoduodenostomyin which the

    dilated proximal duodenum isanastomosedto the atrophic distal

    duodenum.

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    GASTRITIS

    Type A gastritis:

    This is an autoimmune condition in which

    there are circulating antibodies to the parietal

    cell.

    This results in the atrophy of the parietal

    cell mass, hence hypochlorhydria and

    ultimately achlorhydria.

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    CONT..

    As intrinsic factor is also produced by theparietal cell there is malabsorption of vitaminB12,

    which, if untreated, may result in perniciousanaemia.

    In type A gastritis the antrum is not affectedand the hypochlorhydria leads to the

    production of high levels of gastrin from theantral G cells.

    This results in chronic hypergastrinaemia.

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    TYPE B GASTRITIS

    Most commonly type B gastritis affects

    the antrum, and it is these patients who are

    prone to peptic ulcer disease.

    Helicobacter-associated pangastritisis also

    a very common manifestation of infection,

    but gastritis affecting the corpus alone

    does

    not seem to be associated.

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    CONT..

    Patients with pangastritis seem to be mostprone to the development of gastric cancer.

    Intestinal metaplasia is associated with

    chronic pangastritis with atrophy.Although intestinal metaplasiaper se is

    common, intestinal metaplasia associatedwith dysplasia has significant malignantpotential,

    and if this condition is identified the patientshould be regularly screened

    endoscopically.

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    EROSIVE GASTRITIS

    This is caused by agents which disturb thegastric mucosal barrier; NSAIDs andalcohol are common causes.

    The nonsteroidal-induced gastric lesion isassociated with inhibition of the cyclo-oxygenase type 1

    (Cox 1) receptor enzyme, hence reducing theproduction of cytoprotectiveprostaglandins in the stomach.

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    STRESS GASTRITIS

    This is a common sequel of serious illnessor injury and is characterized by a reduction

    in the blood supply to superficial mucosa

    of the stomach.

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    MNTRIERS DISE SE

    This is an unusual condition characterized bygross hyper-trophy of the gastric mucosal

    folds, mucus production and

    hypochlorhydria. The condition is premalignant and may

    present with hypoproteinaemia and

    anaemia. There is no treatment other than a

    gastrectomy.

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    CONT..

    The disease seems to be caused by over_expressionof transforming growth factor

    alpha (TGF-alpha).

    Like epidermal growth factor (EGF), this

    peptide also binds to the EGF receptor.

    The histological features of Mntriers

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    LYMPHOCYTIC GASTRITIS

    This type of gastritis is seen rarely.

    It is characterizedby the infiltration of

    the gastric mucosa by T cells and is

    probably associated with H. pylori infection.

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    OTHER FORMS OF GASTRITIS

    Eosinophilic gastritis appears to have an allergicbasis, and is treated with steroids andchromoglycate. Granulomatous gastritis isseen rarely in Crohnsdisease and also may be

    associated with tuberculosis.Acquired immunodeficiency syndrome (AIDS)

    gastritis is secondary to infection withcryptospirodiosis.

    Phlegmonous gastritis is a rare bacterialinfectionof the stomach found in patients withsevere intercurrent illness.It is usually anagonal event.

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    ASSIGNMENTS

    Duodenal ulceration

    Gastric ulcers

    Malignancy in gastric ulcers

    Operations for duodenal/Gastric

    ulceration

    Small stomach syndrome

    Haematemesis and melaena