Chapter 6: Gastroduodenal Disease Four layers of Gastric wall:  Mucosa  Submucosa  Muscularis propria  Serosa.

Peptic ulcer: Benign, localized defect due to acid & pepsin attack.Extends through muscularis mucosa into the submucous or muscularis layer unlike erorion Erosion: superficial mucosal defect. Etiology:  Hyperacidity:Zollinger-Ellison  Drugs: (NSAIDs) & Corticostroids  smoking, Alcohol  Rapid gastric emptying ( duodenal ulcer)  Personality and stress  Helicobacter pylori infection Gastric Peptic Ulcer: Type of Gastric Ulcer:  Type 1: low- normal acid output. occur within 1.5 cm of the histologic transition zone between the fundic and antral mucosa  Type 2: located in the body of the stomach in combination with a duodenal ulcer, associated with excess acid secretion.  Type 3: prepyloric ulcers, behave like duodenal ulcers and are associated with hypersecretion of gastric acid.  Type 4: lesser curvature near the GE junction,not associated with excess acid secretion. Similarities Of Gastric & Duodenal Ulcer:  Acid is an important cofactor  Difficult to cure, likely recurrence  Complicate with bleeding, obstruction, Perforation  Partial gastrectomy is effective similar

feel pain about 1-2h after food  Tenderness in mid.or left.potential cancerigen Diagnosis:  H. pylori : Invasive tests (biopsy through endoscope)  Rapid Urease Test (RUT)  Culture  Histology  Polymerase Chain Reaction (PCR) Non-Invasive tests  Urea Breath Tests (UBT)  Serological tests  13C bicarbonate assay  Salivary assay  Urine  Stool antigen tests Management: . rigidity Gastric Ulcer:  Pain: may be relieved by food .pylori  Barium meal contrast x-ray  Endoscopy  Biospy: bacteria and malignancy How To Diagnose H.Difference of Duodenal & Gastric Ulcer:  Age: >35 vs >40  Location: Bulb vs wide  Etiology: Nerve factor vs chronic gastritis  BAO/MAO/PAO: High vs Low  Mechanism: Vagus Nerve vs lowered mucosal defenses  Malignancy: None vs possible  Antacid Therapy: Effective vs Indistinct Clinical Manifestations: Duodenal Ulcer:  M>F  Abdominal pain: mid-epigastric. or reboundness. nocturnal pain relieved by food  Tenderness.epigastric  Easy to relapse. bleeding and perforation. well localized.

H2R-Blockers Medical Management 2: H.Pylori 1 Week Tripple therapy  PPI + Metronidazole + Clarithromicin  PPI + Amoxycillin + Clarithromicin  PPI + Metronidazole (Tinidalole) + Amoxycillin Surgical Procedures: 4 Classsic indications for surgery:  Perforation  Hemorrhage  Intractability(Resistance to cure . Caffeine .Behavior Control: Diet .PPI.relief or control)  Obstruction 1 Goal of Ulcer Surgery is to prevent acid secretion Complications of Gastro-duodenal ulcer:  Perforation-Peritonitis-Emergency  Bleeding-Chronic IDA(iron deficiency anemia)acute .Massive  Fibrosis-Stricture obstruction-Pyloric Stenosis  Gastric carcinoma Perforation: Location: Frequently in the anterior wall of duodenal bulb or gastric lesser curvature Sudden pouring of acid into peritoneal cavity leads to:  severe abdominal pain  shock  vomiting  marked abdominal rigidity  absent bowel sound  air under the diaphragm shown by X-ray examination  Chemical peritonitis-Bacterial peritonitis-Toxic shock Differential Diagnosis: Acute Pancreatitis Acute Cholicystitis Acute Appendicitis Non-operative Therapy:  Young Patient . Alcohol Medical management 1: Antacids.Short Ulcer History .Smoking.

Dry mouth . and blood pressure. Reduced flow of urine  Haemoglobin level below 90 mg/L If there are above presentations Immediate blood transfusion is indicated to expand the circulating volume. Endoscopy : Provides an opportunity to render treatment to reduce the chances of rebleeding:  Injection of a dilute solution of adrenalin  Thermal coagulation .Fluid Rescucitation and Antibacterial Therapy Endoscopy Examination after Healing Operative Therapy: Simple Patching Suture-Cover with great omentum-Fix Omentum Hemorrhage: Hematemesis: more severe than melaena alone. Irregular breathing . restore cardiac output. Weak rapid pulse .     Sealed Duodenal Perforation Empty stomach-mild Symptoms and Signs Observer 6-8Hrs without deterioration Nasogastric Tube Decompression. Melaena: Destiguinsh black tarry stool from bright red rectal bleeding or colonic lesions Hemorrhage Management :  Assessment of Severity  Rescucitation  Diagnosis of Cause of Hemorrhage  Observation  Specific Treatment Assessment and Resuscitation  Marked tachycardia (pulse > 110)  Hypotension (blood pressure < 110 systolic)  Signs of hypovolaemic shock . Dilated pupils . Cold sweaty pallid skin .

 severe bleeding and the signs of oligaemic shock regardless of their age. continued or recurrent bleeding. Definite Operations: Vagotomy: Truncal vagotomy: Both vagal trunks are divided at the esophageal hiatus.Surgery :  >60 years with chronic peptic ulcers. antrum. Subtotal gastrectomy: Rarely performed for peptic ulcer Indications:  Underlying malignancies. Highly selective vagotomy: Innervation of the antropyloric region and the hepatic and celiac branches is preserved. Recurrent Ulcerations  Following Truncal vagatomy and Antrectomy  Medical Therapy Unable to Heal  Zollinger-Ellison Syndrome . The vagal branches to the gastric cardia. fundus. the presence of recurrent or continued bleeding. and pylorus are divided.

vomiting. salted) Lack of refrigeration Poor drinking water (well water) Smoking Medical Prior gastric surgery H.diarrhea Postgastrectomy Syndromes :  Secondary to Gastric Resection Dumping syndrome Metabolic Disturbances  Related to Gastric Reconstruction Afferent Loop syndrome Efferent Loop Obstruction Alkaline Reflux Gastritis : (most common) Biliary Reflux ->Postprandial epigastric pain.Subtotal gastrectomy-Billroth II (Gastrojejunostomy w/closures of duodenal stumpincreased risk of blind loop syndrome) Anastomosis following antrectomy Blind Loop Syndrome-Bacterial overgrowth is closed loop. pylori infection Gastric atrophy and gastritis Adenomatous polyps Male gender Social Low social class .weight loss  Postvagotomy Syndromes Postvagotomy Diarrhea Postvagotomy Gastrictomy Gastric Malignant Tumors: Factors associated with increased risk of developing stomach cancer: Nutritional Low fat or protein consumption Salted meat or fish High nitrate consumption High complex-carbohydrate Environmental Poor food preparation (smoked. nausea .interferes wsith Folate and B12 absoprtion->+schilling.

Type A blood Location: Majority proximal stomach Pathologic classification (Bormann’s ) • Type I: polypoid or fungating lesions (Least common) • Type II : ulcerating lesions surrounded by elevated borders (most common) • Type III: ulcerating lesions with infiltration into the gastric wall (most common) • Type IV: diffusely infiltrating lesions (Linitis plastica) (worst Prognosis)  95% are caused by adenocarcinoma (Malignant) Spread of Gastric Cancer . pylori due to the result of free radicals  Hypochlorhydria: occurs in gastric atrophy and promotes bacterial growth in stomach  Epstein-Barr virus  Chronic atrophic gastritis  Having had a Billroth 2 procedure  Genetic factors include: First degree relatives . 60% gastric carcinomas result from H.

 Direct invasive  Lymph node metastasis  Vascular metastasis  Peritoneum planting Krukenberg tumor : Spread of Gastric cancer to Ovaries TNM staging: T stage : defined by depth of penetration into the gastric wall. .

 Stage III & IV cannot be cured. different strategies to treat the cancer. .N and M staging  At different staging.  Stage I & II can be cured. but we can make patients live better.

E  Enhanced CT  Chest X ray/ CT  EUS Nausea/vomiting Obstructive symptoms Iron deficiency/anemia Palpable epigastric mass Enlarged lymph nodes Weakness/fatigue Progressive weight loss Radiographic assessment: .B12 and iron absorption)  Stool positive for occult blood(+stool guaic) In Advanced stages:  Hypoalbuminemia  Bilirubin and alkaline phosphate will be abnormal  Increased level of carcinoembryonic antigen Diagnosis: Histology:  Upper GI Endoscopy(Ulcer and early stage of tumor at duodenum & stomach can be treated by endoscope) Stage  P.Clinical presentation: Early gastric cancer:  No specific symptoms in early stage Advanced stage: Little chance to cure at advanced stage        Labs:  Decreased hematocrit and hemoglobin  Macrocytic or microcytic anemia (decreased vit.

Systemic Therapy:  Postoperative chemoradiation to the treatment of patients with resectable gastric adenocarcinoma. and HER2-neu expression (for adenocarcinoma only) Best Supportive Care:  20% to 30% of gastric cancer patients present with stage IV disease . malignant ascites staging Double contrast upper GI radiology (90% diagnostic accuracy) Endoscopic ultrasound (EUS): the extent of gastric wall invasion. Laparoscopy: smaller macrometastases on the peritoneal surface or liver  Laparoscopic ultrasonography  Cytologic analysis of peritoneal fluid Surgical management: A :Subtotal gastrectomy with a Billroth II anastomosis. B:Total gastrectomy with a Roux-en-Y anastomosis. medical comorbidities. toxicity profile.    Upper GI Endoscopy: histologic diagnosis (98% diagnostic accuracy) C T : visceral metastatic.  Neoadjuvant chemotherapy is currently under investigation  Regimens should be chosen in the context of performance status. evaluate local nodal status.

 palliative treatment is for relief of symptoms n complications with minimal morbidity. endoscopic. or radiotherapeutic techniques.  Nonoperative therapies include laser recanalization and endoscopic dilation .  Method: resection or bypass alone or in conjunction with percutaneous.

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