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A circumscribed ulcerationof the gastrointestinal

mucosa occurring in areasexposed to acid and pepsinand most often caused byHelicobacter pyloriinfection.

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stomach is readily recognizable

as the asymmetrical, pear-shaped, most proximalabdominal organ of the digestivetract

stomach attached to theesophagus is called the cardia.

distal end, the pyloric sphincterconnects the stomach to theproximal duodenum

bounded superiorly by thediaphragm and laterally by thespleen

body of the stomach containsmost of the parietal (oxyntic) cells

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stomach is the most

richly vascularizedportion of thealimentary tube

large majority of thegastric blood supplyis from the celiac axis.

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Both the extrinsic and intrinsicinnervation of the stomach play

an important role in gastricsecretory and motor function.

The vagus nerves provide the

extrinsic parasympatheticinnervation to the stomach, andacetylcholine is the mostimportant neurotransmitter.

extrinsic sympathetic nervesupply to the stomach originatesat spinal levels T5 through T10

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The stomach stores food and facilitates digestion through avariety of secretory and motor functions. Important secretoryfunctions include the production

of acid, pepsin, intrinsic factor, mucus, and a variety of GIhormones. Important motor functions include food storage(receptive relaxation and

accommodation), grinding and mixing, controlled emptyingof ingested food, and periodic interprandial "housekeeping."

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Hydrochloric acid in the stomachhastens both the physical and (withpepsin) the biochemical breakdown ofingested food. In an acidic environment,pepsinand acid facilitate proteolysis.Gastric acid also inhibits the proliferationof ingested pathogens, which protectsagainst both infectious gastroenteritidesand

intestinal bacterial overgrowth.

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The parietal cell is stimulated to secrete acid whenone or more of three membrane receptor types isstimulated by acetylcholine (from vagal

nerve fibers), gastrin (from D cells), or histamine(from ECL cells).

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Gastrin is produced by antral G cells and is the majorhormonal stimulant of acid secretion during the gastricphase.

Luminal peptides and amino acids are the most potentstimulants of gastrin release, and luminal acid is the mostpotent inhibitor of gastrin secretion.

Gastrin-stimulated acid secretion is significantly blocked byH2 antagonists, suggesting that the principal mediator of

gastrin-stimulated acid production is histamine from mucosalECL cells

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SOMATOSTATIN

Somatostatin is produced by D cells locatedthroughout the gastric mucosa. The

predominant form in humans is somatostatin14, though somatostatin 28

is present as well. The major stimulus forsomatostatin release is antral acidification;

acetylcholine from vagal nerve fibers inhibits itsrelease. Somatostatin inhibits acid secretionfrom parietal cells and gastrin release from Gcells. It also decreases histamine release fromECL cells. The proximity of the D cells to

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PHYSIOLOGIC ACID SECRETION

Food ingestion is the physiologic stimulus for acid secretion

described in three phases:

cephalic, gastric, and intestinal

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large majority of duodenal and gastriculcers are

caused by H. pylori infection and/orNSAID, the final common pathway toulcer formation is acid-peptic injury ofthe gastroduodenal mucosal barrier.Thus, the adage "no acid, no ulcer" .

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Higher prevalence in developing countries H. Pylori is sometimes associated with

socioeconomic status and poor hygiene

In the US: Lifetime prevalence is ~10%.

PUD affects ~4.5 million annually.

Hospitalization rate is ~30 pts per 100,000cases.

Mortality rate has decreased dramaticallyin the past 20 years

approximately 1 death per 100,000 cases

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A peptic ulcer is a mucosal break, 3 mm or greater,that can involve the stomach or duodenum.

The most important contributing factors are H

pylori, NSAIDs, acid, and pepsin. Additional aggressive factors include smoking,

ethanol, bile acids, aspirin, steroids, and stress.

Important protective factors are mucus,bicarbonate, mucosal blood flow, prostaglandins,

hydrophobic layer, and epithelial renewal. Increased risk when older than 50 d/t decrease protection

When an imbalance occurs, PUD might develop.

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Paingnawing, aching, or burning

Duodenal ulcers: occurs 1-3 hours after a meal and

may awaken patient from sleep. Pain is relieved by

food, antacids, or vomiting. Gastric ulcers: food may exacerbate the pain while

vomiting relieves it.

Nausea, vomiting, belching, dyspepsia,

bloating, chest discomfort, anorexia,hematemesis, &/or melena may also occur.

nausea, vomiting, & weight loss more common with

Gastric ulcers

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Epigastric tenderness

Guaic-positive stool resulting from occult blood loss

Succussion splash resulting from scaring or edema

due to partial or complete gastric outletobstruction A succussion splash describes the sound obtained by

shaking an individual who has free fluid and air or gas in ahollow organ or body cavity.

Usually elicited to confirm intestinal or pyloric obstruction. Done by gently shaking the abdomen by holding either

side of the pelvis. A positive test occurs when a splashingnoise is heard, either with or without a stethoscope. It is notvalid if the pt has eaten or drunk fluid within the last threehours.

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Stool for fecal occult blood

Labs: CBC (R/O bleeding), liver function test,amylase, and lipase.

H. Pylori can be diagnosed by urea breath test,blood test, stool antigen assays, & rapid ureasetest on a biopsy sample.

Upper GI Endoscopy: Any pt >50 yo with new

onset of symptoms or those with alarm markingsincluding anemia, weight loss, or GI bleeding. Preferred diagnostic test b/c its highly sensitive for dx of

ulcers and allows for biopsy to rule out malignancy andrapid urease tests for testing for H. Pylori.

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Medications:Triple therapy for 14 days is considered thetreatment of choice.

Proton Pump Inhibitor + clarithromycin and amoxicillin

Omeprazole (Prilosec): 20 mg PO bid for 14 d or

Lansoprazole (Prevacid): 30 mg PO bid for 14 d orRabeprazole (Aciphex): 20 mg PO bid for 14 d orEsomeprazole (Nexium): 40 mg PO qd for 14 d plusClarithromycin (Biaxin): 500 mg PO bid for 14 andAmoxicillin (Amoxil): 1 g PO bid for 14 d

Can substitute Flagyl 500 mg PO bid for 14 d if allergic to PCN

In the setting of an active ulcer, continue qd proton pumpinhibitor therapy for additional 2 weeks.

Goal: complete elimination of H. Pylori. Once achievedreinfection rates are low. Compliance!

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Medicationstreat with Proton PumpInhibitors or H2 receptor antagonists to

assist ulcer healing H2: Tagament, Pepcid, Axid, or Zantac for up

to 8 weeks

PPI: Prilosec, Prevacid, Nexium, Protonix, or

Aciphex for 4-8 weeks.

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Discontinue NSAIDs and use Acetaminophenfor pain control if possible.

Acid suppression--Antacids

Smoking cessation No dietary restrictions unless certain foods are

associated with problems.

Alcohol in moderation Men under 65: 2 drinks/day

Men over 65 and all women: 1 drink/day

Stress reduction

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Consider prophylactic therapy for the following patients: Pts with NSAID-induced ulcers who require daily NSAID

therapy Pts older than 60 years

Pts with a history of PUD or a complication such as GIbleeding Pts taking steroids or anticoagulants or patients with

significant comorbid medical illnesses

Prophylactic regimens that have been shown todramatically reduce the risk of NSAID-induced gastric and

duodenal ulcers include the use of a prostaglandinanalogue or a proton pump inhibitor. Misoprostol (Cytotec) 100-200 mcg PO 4 times per day Omeprazole (Prilosec) 20-40 mg PO every day Lansoprazole (Prevacid) 15-30 mg PO every day

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Perforation & Penetrationintopancreas, liver and retroperitoneal

space Peritonitis

Bowel obstruction, Gastric outflowobstruction, & Pyloric stenosis

Bleeding--occurs in 25% to 33% of casesand accounts for 25% of ulcer deaths.

Gastric CA

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INDICATIONS

1. INTRACTABLE PAIN INSPITE OF MEDICAL

TREATMENT2. FREQUENT RELAPSES

3. COMPLICATIONS

GASTRIC OUTLET OBSTRUCTION HAEMORRHAGE

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Sub-total gastrictomy:BILLROTH 1Stomach to duodenum (Gastroduodenostomy

)

BIILROTH 2Stomach to jejunum ( Gastrojejunostomy )

Total gastrictomy:ANTRECTOMY - Removal of lower portion of the stomach.

PYLOPLASTY - Incision is made into the pylorus to enlarge

ten outlet& relax the muscle to enhance emptying

VAGOTOMYInterruption of vagus nerve to decreasegastric

secretion.

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AIM; EXCLUDING THE DAMAGING EFFECTSOF ACIDS FROM THE DUODENUM

1. BILLROTH 2 GASTRECTOMY2. GASTROJEJUNESTOMY

3. TRUNCAL VAGOTOMY AND DRAINAGE

4. HIGHLY SELECTIVE VAGOTOMY5. TRUNCAL VAGOTOMY AND

ANTRECTOMY

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AIM ; EXCLUDE THE DAMAGING EFFECTS OFACID AS WELL AS REMOVAL OF

DECEASED TISSUE BILLROTH 1 GASTRECTOMY

BILLROTH 2 GASTRECTOMY

VAGOTOMY, PYLOROPLASTY AND ULCEREXCISION

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1. Failure of the stomach or stomach remnant to emptyoccurs after any procedure. It was formerly commonafter vagotomy and drainage. Causes are:

A. Prolonged paralysis of stomach (doubtful)

B. Edema at a stoma

C. Fluid and electrolyte disorder, especially

hypokalaemia.

Management is conservative with NG suction, fluid,electrolyte and nutritional replacement.

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2. Intestinal obstruction.Causes are:

A. Adhesive.

B. As a consequences:

(a) Twisting of the loop of a gastrojejunostomyafter polya gastrectomy.

(b) Herniation of loops through a mesentericdefect.

(c) Retrograde intussusception of the efferentloop of a gastrojejunostomy (rare).

Treatment: operative

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3. Fistulae. Can occur after anyoperation, which involves a suture line.Most usual sites are:

1. After polya gastrectomy

i. Duodenal stump

ii. Pancreases from trying todissect out a

difficult ulcer2. Occasionally at a Pyloroplasty

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4. Acute pancreatitis. May follow any

procedure. Its etiology is unknown, but

some cases are traumatic

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1. Anastomotic and recurrent ulceration

Causes:

a. Inadequate resection of parietal cell mass.

b. Isolated antrum left after polya gastrectomy.

c. Incomplete vagotmy.

d. Persistent suture in the anastomosis. More usually this is merely asuture exposed as a consequence of ulceration from anothercause.

Prophylaxis: adequate primary treatment.

Management is related to cause and requires investigation toascertain the level of acid secretion or the completeness ofvagotomy. Recurrence after vagotomy is best managed bypolya gastrectomy.

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2. Gastrojejunocolic fistulae.

Occurs when a recurrent ulcer after gastrojejual anastomosis penetrates into thecolon. It should arouse the suspicion of Zollinger-Ellison syndrome.

Clinical features: Severe diarrhea occurs due to enteritis caused by cronic contentspassing directly into the small bowel and acidosis, dehydration, potassium loss,anaemia and cachexia will result in death if the fastula is not interrupted

surgically.

Treatment:

1. Good risk patient. Excision of the gastric, jejunal and colonic components andthe construction of a higher gastrectomy.

2. Poor risk patient. A staged procedure:

(a) Stage 1: Proximal colostomy which, diverts the faecal stream from the fistulaand thus stops the enteritis.

(b) Stage 2: Excision of fistula and its visceral components and the construction ofa higher gastrectomy and colonic anastomosis.

(c) Stage 3: Closure of colostomy.

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The stomach is a reservoir and the pylorus meters food

rendered iso-osmotic with plasma into the small bowel forfurther digestion and absorption.

Consequently, ablation of gastric areas plus, as is always thecase, loss or bypass of the pylorus allows the entry ofhyperosmolal, large volume loads into the jejunum. Two things

follow: The bulk stimulates peristalsis and results in pain, rapid transit

and thus occasionally diarrhea.

The hyperosmolity draws fluid into the gut lumen whichaggravates the bulk problem and may also reduce blood

volume so creating vasomotor instability-the patient feels faintand tremulous after a meal.

These features constitute the dumping syndrome which isaptlynamed because it does result from dumping a largevolume of hypertonic liquid into the jejunum.

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Partial gastrectomy and polya

reconstruction interferes with duodenalabsorption of iron and a macrocyticanemia may result

More rarely, sufficient stomach has beenremoved to cause failure of release ofintrinsic factor and thus a macrocyticanemia

Malnutrition may contribute to both.

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Particulary after partial gastrectomywhen patients are unwilling to eatsufficiently, weight loss is common

Severe malnutrition is rare, but there isan increased risk of nutrition-associated diseases such as

tuberculosis.

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Any operation which, destroys or

bypasses the pylorus allows bile to reachthe stomach. Not only does this produce atrophic

gastritis but also it may be associated with

bilious vomiting. This is more likely after a polya

gastrectomy where characteristically apatient eats a meal and some to 10 to 20

minutes later vomits bile only. In severe cases, either normal anatomy

should be restored or the bile divertedmore distally into the intestine.

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Apart from the dumping syndrome, allvagotomies except highly selectiveones seem to cause diarrhea

Matters are made worse ifcholecystectomy has been done or issubsequently done

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H. Pylori Positive: retesting for tx efficacy Urea breath testno sooner than 4 weeks

after therapy to avoid false negative results

Stool antigen testan 8 week interval must beallowed after therapy.

H. Pylori Negative: evaluate symptomsafter one month. Patients who are

controlled should cont. 2-4 more weeks. If symptoms persist then refer to specialist

for additional diagnostic testing.

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H. Pylori Positive: retesting for tx efficacy Urea breath testno sooner than 4 weeks

after therapy to avoid false negative results

Stool antigen testan 8 week interval must beallowed after therapy.

H. Pylori Negative: evaluate symptomsafter one month. Patients who are

controlled should cont. 2-4 more weeks. If symptoms persist then refer to specialist

for additional diagnostic testing.

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End

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PRINCIPLE ; SECTION OF VAGUS NERVE ,WHICH ARE CRITICALLY INVOLVED TO THESECRETION OF GASTRIC ACID , REDUCESTHE MAXIMAL ACID OUTPUT BYAPPROXIMATELY 50 %.

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PARIETAL CELL VAGOTOMY

PROXIMAL GASTRIC VAGOTOMY

ONLY THE PARIETAL CELL MASS OF THE

STOMACH ARE DENERVATED.

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ADDITION TO TRUNCAL VAGOTOMY , THEANTRUM OF THE STOMACH IS REMOVED ,THUS REMOVING THE SOURCE OFGASTRIN.

- LEAST RECURRENCE RATE

- 3-4 % MORTALITY RATE

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PARTIAL GASTRECTOMY IS DONEINCLUDING REMOVAL OF ULCERFOLLOWED BY GASTRODUODENALANASTOMOSIS.

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People who do not respond to medication, orwho develop complications: Vagotomy - cutting the vagus nerve to interrupt

messages sent from the brain to the stomach toreducing acid secretion.

Antrectomy - remove the lower part of the stomach(antrum), which produces a hormone that stimulatesthe stomach to secrete digestive juices. A vagotomyis usually done in conjunction with an antrectomy.

Pyloroplasty - the opening into the duodenum andsmall intestine (pylorus) are enlarged, enablingcontents to pass more freely from the stomach. Maybe performed along with a vagotomy.

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The stomach is a reservoir and the pylorus meters food

rendered iso-osmotic with plasma into the small bowel forfurther digestion and absorption.

Consequently, ablation of gastric areas plus, as is always thecase, loss or bypass of the pylorus allows the entry ofhyperosmolal, large volume loads into the jejunum. Two things

follow: The bulk stimulates peristalsis and results in pain, rapid transit

and thus occasionally diarrhea.

The hyperosmolity draws fluid into the gut lumen whichaggravates the bulk problem and may also reduce blood

volume so creating vasomotor instability-the patient feels faintand tremulous after a meal.

These features constitute the dumping syndrome which isaptlynamed because it does result from dumping a largevolume of hypertonic liquid into the jejunum.

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Partial gastrectomy and polya

reconstruction interferes with duodenalabsorption of iron and a macrocyticanemia may result

More rarely, sufficient stomach has beenremoved to cause failure of release ofintrinsic factor and thus a macrocyticanemia

Malnutrition may contribute to both.

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Particulary after partial gastrectomywhen patients are unwilling to eatsufficiently, weight loss is common

Severe malnutrition is rare, but there isan increased risk of nutrition-associated diseases such as

tuberculosis.

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Any operation which, destroys or

bypasses the pylorus allows bile to reachthe stomach. Not only does this produce atrophic

gastritis but also it may be associated with

bilious vomiting. This is more likely after a polya

gastrectomy where characteristically apatient eats a meal and some to 10 to 20minutes later vomits bile only.

In severe cases, either normal anatomyshould be restored or the bile divertedmore distally into the intestine.

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Apart from the dumping syndrome, allvagotomies except highly selectiveones seem to cause diarrhea

Matters are made worse ifcholecystectomy has been done or issubsequently done

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H. Pylori Positive: retesting for tx efficacy Urea breath testno sooner than 4 weeks

after therapy to avoid false negative results

Stool antigen testan 8 week interval must beallowed after therapy.

H. Pylori Negative: evaluate symptomsafter one month. Patients who are

controlled should cont. 2-4 more weeks. If symptoms persist then refer to specialist

for additional diagnostic testing.

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Sub-total gastrictomy:BILLROTH 1Stomach to duodenum (Gastroduodenostomy )

BIILROTH 2Stomach to jejunum ( Gastrojejunostomy )

Total gastrictomy:ANTRECTOMY - Removal of lower portion of the stomach.

PYLOPLASTY - Incision is made into the pylorus to enlarge ten

outlet& relax the muscle to enhance emptying

VAGOTOMYInterruption of vagus nerve to decrease gastric

secretion.

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Neoplasm of the stomach

Pancreatitis

Pancreatic cancer

Diverticulitis Nonulcer dyspepsia (also called functional

dyspepsia)

Cholecystitis

Gastritis

GERD

MInot to be missed if having chest pain