A circumscribed ulceration of the gastrointestinal mucosa occurring in areas exposed to acid and pepsin and most often caused

by Helicobacter pylori infection.

stomach is readily recognizable as the asymmetrical, pearshaped, most proximal abdominal organ of the digestive tract stomach attached to the esophagus is called the cardia. distal end, the pyloric sphincter connects the stomach to the proximal duodenum

bounded superiorly by the diaphragm and laterally by the spleen body of the stomach contains most of the parietal (oxyntic) cells

stomach is the most richly vascularized portion of the alimentary tube large majority of the gastric blood supply is from the celiac axis .

Both the extrinsic and intrinsic innervation of the stomach play an important role in gastric secretory and motor function. The vagus nerves provide the extrinsic parasympathetic innervation to the stomach, and acetylcholine is the most important neurotransmitter. extrinsic sympathetic nerve supply to the stomach originates at spinal levels T5 through T10

The stomach stores food and facilitates digestion through a variety of secretory and motor functions. Important secretory functions include the production of acid, pepsin, intrinsic factor, mucus, and a variety of GI hormones. Important motor functions include food storage (receptive relaxation and accommodation), grinding and mixing, controlled emptying of ingested food, and periodic interprandial "housekeeping."

Hydrochloric acid in the stomach hastens both the physical and (with pepsin) the biochemical breakdown of ingested food. In an acidic environment, pepsinand acid facilitate proteolysis. Gastric acid also inhibits the proliferation of ingested pathogens, which protects against both infectious gastroenteritides and intestinal bacterial overgrowth.

The parietal cell is stimulated to secrete acid when one or more of three membrane receptor types is stimulated by acetylcholine (from vagal nerve fibers), gastrin (from D cells), or histamine (from ECL cells).

Gastrin is produced by antral G cells and is the major

hormonal stimulant of acid secretion during the gastric phase. Luminal peptides and amino acids are the most potent stimulants of gastrin release, and luminal acid is the most potent inhibitor of gastrin secretion. Gastrin-stimulated acid secretion is significantly blocked by H2 antagonists, suggesting that the principal mediator of gastrin-stimulated acid production is histamine from mucosal ECL cells

SOMATOSTATIN Somatostatin is produced by D cells located throughout the gastric mucosa. The predominant form in humans is somatostatin 14, though somatostatin 28 is present as well. The major stimulus for somatostatin release is antral acidification; acetylcholine from vagal nerve fibers inhibits its release. Somatostatin inhibits acid secretion from parietal cells and gastrin release from G cells. It also decreases histamine release from ECL cells. The proximity of the D cells to

PHYSIOLOGIC ACID SECRETION

Food ingestion is the physiologic stimulus for acid secretion described in three phases: cephalic, gastric, and intestinal

large majority of duodenal and gastric ulcers are caused by H. pylori infection and/or NSAID, the final common pathway to ulcer formation is acid-peptic injury of the gastroduodenal mucosal barrier. Thus, the adage "no acid, no ulcer" .

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 100,000

cases. Mortality rate has decreased dramatically in the past 20 years

approximately 1 death per 100,000 cases

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.

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

Epigastric tenderness Guaic-positive stool resulting from occult blood loss Succussion splash resulting from scaring or edema due to partial or complete gastric outlet obstruction
A succussion splash describes the sound obtained by

shaking an individual who has free fluid and air or gas in a hollow 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 splashing noise is heard, either with or without a stethoscope. It is not valid if the pt has eaten or drunk fluid within the last three hours.

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 urease test on a biopsy sample. Upper GI Endoscopy: Any pt >50 yo with new onset of symptoms or those with alarm markings including 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 and rapid urease tests for testing for H. Pylori.

Medications: Triple therapy for 14 days is considered the treatment 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 or Rabeprazole (Aciphex): 20 mg PO bid for 14 d or Esomeprazole (Nexium): 40 mg PO qd for 14 d plus Clarithromycin (Biaxin): 500 mg PO bid for 14 and Amoxicillin (Amoxil): 1 g PO bid for 14 d Can substitute Flagyl 500 mg PO bid for 14 d if allergic to PCN

inhibitor therapy for additional 2 weeks. Goal: complete elimination of H. Pylori. Once achieved reinfection rates are low. Compliance!

In the setting of an active ulcer, continue qd proton pump

Medicationstreat with Proton Pump Inhibitors 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.

Discontinue NSAIDs and use Acetaminophen for 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

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 GI bleeding Pts taking steroids or anticoagulants or patients with significant comorbid medical illnesses Prophylactic regimens that have been shown to dramatically reduce the risk of NSAID-induced gastric and duodenal ulcers include the use of a prostaglandin analogue 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

Perforation & Penetrationinto pancreas, liver and retroperitoneal space Peritonitis Bowel obstruction, Gastric outflow obstruction, & Pyloric stenosis Bleeding--occurs in 25% to 33% of cases and accounts for 25% of ulcer deaths. Gastric CA

INDICATIONS 1. INTRACTABLE PAIN INSPITE OF MEDICAL TREATMENT 2. FREQUENT RELAPSES 3. COMPLICATIONS GASTRIC OUTLET OBSTRUCTION HAEMORRHAGE

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Sub-total gastrictomy:

BILLROTH 1Stomach to duodenum (Gastroduodenostomy ) BIILROTH 2 Stomach 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 VAGOTOMY Interruption of vagus nerve to decrease gastric secretion.

AIM; EXCLUDING THE DAMAGING EFFECTS OF ACIDS FROM THE DUODENUM 1. BILLROTH 2 GASTRECTOMY 2. GASTROJEJUNESTOMY 3. TRUNCAL VAGOTOMY AND DRAINAGE 4. HIGHLY SELECTIVE VAGOTOMY 5. TRUNCAL VAGOTOMY AND ANTRECTOMY

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AIM ; EXCLUDE THE DAMAGING EFFECTS OF ACID AS WELL AS REMOVAL OF DECEASED TISSUE BILLROTH 1 GASTRECTOMY BILLROTH 2 GASTRECTOMY VAGOTOMY, PYLOROPLASTY AND ULCER EXCISION

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1. Failure of the stomach or stomach remnant to empty occurs after any procedure. It was formerly common after 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.

2. Intestinal obstruction. Causes are: A. Adhesive. B. As a consequences: (a) Twisting of the loop of a gastrojejunostomy after polya gastrectomy. (b) Herniation of loops through a mesenteric defect. (c) Retrograde intussusception of the efferent loop of a gastrojejunostomy (rare). Treatment: operative

3.

Fistulae. Can occur after any operation, which involves a suture line. Most usual sites are: 1. After polya gastrectomy i. Duodenal stump ii. Pancreases from trying to dissect out a difficult ulcer 2. Occasionally at a Pyloroplasty

4. Acute pancreatitis. May follow any procedure. Its etiology is unknown, but some cases are traumatic

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 a suture exposed as a consequence of ulceration from another cause. Prophylaxis: adequate primary treatment. Management is related to cause and requires investigation to ascertain the level of acid secretion or the completeness of vagotomy. Recurrence after vagotomy is best managed by polya gastrectomy.

2. Gastrojejunocolic fistulae. Occurs when a recurrent ulcer after gastrojejual anastomosis penetrates into the colon. It should arouse the suspicion of Zollinger-Ellison syndrome. Clinical features: Severe diarrhea occurs due to enteritis caused by cronic contents passing 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 and the construction of a higher gastrectomy. 2. Poor risk patient. A staged procedure: (a) Stage 1: Proximal colostomy which, diverts the faecal stream from the fistula and thus stops the enteritis. (b) Stage 2: Excision of fistula and its visceral components and the construction of a higher gastrectomy and colonic anastomosis. (c) Stage 3: Closure of colostomy.

The stomach is a reservoir and the pylorus meters food rendered iso-osmotic with plasma into the small bowel for further digestion and absorption. Consequently, ablation of gastric areas plus, as is always the case, loss or bypass of the pylorus allows the entry of hyperosmolal, 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 which aggravates the bulk problem and may also reduce blood volume so creating vasomotor instability-the patient feels faint and tremulous after a meal. These features constitute the dumping syndrome which is aptlynamed because it does result from dumping a large volume of hypertonic liquid into the jejunum.

Partial gastrectomy and polya reconstruction interferes with duodenal absorption of iron and a macrocytic anemia may result More rarely, sufficient stomach has been removed to cause failure of release of intrinsic factor and thus a macrocytic anemia Malnutrition may contribute to both.

Particulary after partial gastrectomy when patients are unwilling to eat sufficiently, weight loss is common

Severe malnutrition is rare, but there is an increased risk of nutritionassociated diseases such as tuberculosis.

Any operation which, destroys or bypasses the pylorus allows bile to reach the 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 a patient 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 diverted more distally into the intestine.

Apart from the dumping syndrome, all vagotomies except highly selective ones seem to cause diarrhea

Matters are made worse if cholecystectomy has been done or is subsequently done

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 be allowed after therapy.

H. Pylori Negative: evaluate symptoms after one month. Patients who are controlled should cont. 2-4 more weeks. If symptoms persist then refer to specialist for additional diagnostic testing.

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 be allowed after therapy.

H. Pylori Negative: evaluate symptoms after one month. Patients who are controlled should cont. 2-4 more weeks. If symptoms persist then refer to specialist for additional diagnostic testing.

End

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PRINCIPLE ; SECTION OF VAGUS NERVE , WHICH ARE CRITICALLY INVOLVED TO THE SECRETION OF GASTRIC ACID , REDUCES THE MAXIMAL ACID OUTPUT BY APPROXIMATELY 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 , THE ANTRUM OF THE STOMACH IS REMOVED , THUS REMOVING THE SOURCE OF GASTRIN. LEAST RECURRENCE RATE 3-4 % MORTALITY RATE

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PARTIAL GASTRECTOMY IS DONE INCLUDING REMOVAL OF ULCER FOLLOWED BY GASTRODUODENAL ANASTOMOSIS.

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People who do not respond to medication, or who develop complications:

Vagotomy - cutting the vagus nerve to interrupt

messages sent from the brain to the stomach to reducing acid secretion. Antrectomy - remove the lower part of the stomach (antrum), which produces a hormone that stimulates the stomach to secrete digestive juices. A vagotomy is usually done in conjunction with an antrectomy. Pyloroplasty - the opening into the duodenum and small intestine (pylorus) are enlarged, enabling contents to pass more freely from the stomach. May be performed along with a vagotomy.

The stomach is a reservoir and the pylorus meters food rendered iso-osmotic with plasma into the small bowel for further digestion and absorption. Consequently, ablation of gastric areas plus, as is always the case, loss or bypass of the pylorus allows the entry of hyperosmolal, 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 which aggravates the bulk problem and may also reduce blood volume so creating vasomotor instability-the patient feels faint and tremulous after a meal. These features constitute the dumping syndrome which is aptlynamed because it does result from dumping a large volume of hypertonic liquid into the jejunum.

Partial gastrectomy and polya reconstruction interferes with duodenal absorption of iron and a macrocytic anemia may result More rarely, sufficient stomach has been removed to cause failure of release of intrinsic factor and thus a macrocytic anemia Malnutrition may contribute to both.

Particulary after partial gastrectomy when patients are unwilling to eat sufficiently, weight loss is common

Severe malnutrition is rare, but there is an increased risk of nutritionassociated diseases such as tuberculosis.

Any operation which, destroys or bypasses the pylorus allows bile to reach the 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 a patient 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 diverted more distally into the intestine.

Apart from the dumping syndrome, all vagotomies except highly selective ones seem to cause diarrhea

Matters are made worse if cholecystectomy has been done or is subsequently done

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 be allowed after therapy.

H. Pylori Negative: evaluate symptoms after one month. Patients who are controlled should cont. 2-4 more weeks. If symptoms persist then refer to specialist for additional diagnostic testing.

Sub-total gastrictomy:
BILLROTH 1Stomach to duodenum (Gastroduodenostomy ) BIILROTH 2 Stomach 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 VAGOTOMY Interruption of vagus nerve to decrease gastric secretion.

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