General Surgery The Stomach Kingdom of Bahrain Arabian Gulf University College of Medicine and Medical Sciences General Surgery The Stomach Ali Jassim Alhashli

Anatomy, Histology & Physiology of Stomach Stomach is composed of 5 parts: Cardia. Fundus Body. Antrum. Pylorus. Blood supply of the stomach: Lesser curvature: Right gastric artery: from hepatic artery. Left gastric artery: from celiac trunk. Greater curvature: Right gastroepiploic artery: from gastroduodenal artery. Left gastroepiploic artery: from splenic artery. Pylorus: gastroduodenal artery. Fundus: short gastric arteries. Innervation of the stomach: Sympathetic: T5-T10. Parasympathetic: Anterior gastric wall: left vagus nerve (gives hepatic branch). Posterior gastric wall: right vagus nerve (gives celiac branch).

Anatomy, Histology & Physiology of Stomach

Anatomy, Histology & Physiology of Stomach

Anatomy, Histology & Physiology of Stomach Cardia: glands secreting mucous. Fundus: Parietal cells: secreting HCl and intrinsic factor (which combines with vitamin B12 and facilitates its absorption in terminal ileum). Acid secretion is regulated by: Gastrin. Histamine (via H2-receptors). Vagal stimulation (via M3-receptors). Chief cells: secreting pepsinogen which is converted to pepsin by the acidic environment and digests protein. Antrum: G-cells: secreting gastrin which functions in: Stimulation of gastric acid secretion. Growth of gastric mucosa. Stimulation of pepsinogen secretion. Gastrin secretion is stimulated by Gastrin-Releasing Peptide (GRP) + presence of amino acids in the stomach. It is inhibited by somatostatin.

Cholecystokinin (CCK) GI Hormones Hormone Site of release Action Stimulated by Inhibited by Gastrin G-cells in antrum of stomach Acid secretion and growth of gastric mucosa Gastric distention, presence of amino acids in stomach and vagal stimulation Acidity and somatostatin Cholecystokinin (CCK) Duodenum Contraction of the gallbladder, relaxation of sphincter of Oddi and inhibition of gastric emptying Presence of fat in the duodenum Chymotrypsin and trypsin Secretin Stimulates pancreatic secretion of HCO3 and inhibits gastric acid secretion High acidity in the duodenum High duodenal pH (alkaline environment) Somatostatin Pancreas General inhibitory function of GI tract Catecholamines Acetycholine release Immunological function of small bowel: Secretion of IgA. MALT (Mucosal Associated Lymphoid Tissue) is composed of: mucosal lymphocytes, lymphoid nodules, isolated lymphoid folicles in appendix and mesenteric lymph nodes.

Peptic Ulcer Disease (PUD) – Introduction Definition of PUD = duodenal ulcer + gastric ulcer. Risk factors for development of PUD: Helicobacter pylori infection. NSAIDs (due to inhibition of PG which acts as a protective barrier of gastric mucosa) and corticosteroids. Smoking. Burns (curling ulcer): due to due to sluggish blood flow to gastric mucosa. Head trauma (cushing ulcer): due to increased vagal stimulation which in turn increases gastric acid production. Family history of PUD. Zollinger-Ellison syndrome. Complications of PUD: Bleeding (20%): Occurs with posterior ulcers. Gastric ulcer: left gastric artery. Duodenal ulcer: gastroduodenal artery. Signs and symptoms: dizziness, syncope, hematemesis/melena. Perforation (7%): Occurs with anterior ulcers. Characterized by sudden, severe epigastric pain radiating to the right shoulder + air under diaphragm (with x-ray). Valentino’s sign: RLQ pain/peritonitis as a result of succus collecting from a perforated peptic ulcer. What is a Graham patch? Piece of omentum incorporated into the suture closure of perforation.

Peptic Ulcer Disease (PUD) – Introduction

Peptic Ulcer Disease (PUD) – Duodenal Ulcer It occurs mainly in males and discovered 2 decades earlier than gastric ulcer. In duodenal ulcer, there is increased acid production and the most common location is posterior wall in the first 2 cm of the duodenum. Causes: Almost always caused by H.pylori infection which is a urease-producing organism that damages gastric mucosa. It can also be caused by NSAIDs/steroids. Suspect that patient has Zollinger-Ellison syndrome when there are recurrent duodenal ulcers not responding to H.pylori treatment. Signs and symptoms: Burning epigastric pain which is relieved by food. Nausea and vomiting. Association with blood type (O). Diagnosis: Mainly a clinical diagnosis. Endoscopy is done when there are alarming symptoms: bleeding/anemia, weight loss, dysphagia and recurrent vomiting. Detection of H.pylori infection: can be done with serology (IgG) or urea-breath test (ingestion of C13/14 labeled urea). When treatment to eradicate H.pylori infection is given to the patient, follow-up is with detection of stool antigen. Treatment: Medical: Stop smoking, NSAIDs and steroids + lifestyle modifications. Proton-Pump Inhibitors (PPIs: omeprazole): 90% cure after 4 weeks. H2-blockers (ranitidine): 85% cure after 8 weeks. Antacids: symptomatic relief. Eradication of H.pylori infection: Triple therapy (for 2 weeks): amoxicillin, clarithromycin and PPI. Quadraple therapy (for 2 weeks): bismuth, tetracycline, metronidazole and PPI. Surgical: Indicated when there is: hemorrhage, perforation or obstruction. Procedure: highly selective vagotomy. Peptic Ulcer Disease (PUD) – Duodenal Ulcer

Peptic Ulcer Disease (PUD) – Gastric Ulcer There is decreased acid production and damage to mucosal protective mechanisms (↓ mucous and bicarbonate production). Causes: H.pylori infection. NSAIDs/ steroids. Smoking. Signs and symptoms: Burning epigastric pain which is increased by food. Therefore, patient will avoid eating and this will result in weight loss. Nausea and vomiting. Association with blood type (A). Diagnosis: When clinically suspected, you have to do endoscopy and take a biopsy because here there is a risk of gastric adenocarcinoma and you want to rule it out. Treatment: depends on classification of gastric ulcers Peptic Ulcer Disease (PUD) – Gastric Ulcer Type Location Treatment I Most common; lesser curvature Distal gastrectomy with ulcer excision II Associated with DU Antrectomy + ulcer excision + truncal vagotomy III Prepyloric IV Near gastroesophageal junction Distal gastrectomy + ulcer excision + esophagogastrojejunostomy

Gastritis Definition: It is acute or chronic inflammation of gastric lining. Causes: “GNASHING” G: Gastric reflux. N: Nicotine. A: Alcohol. S: Stress. H: H.pylori. I: Ischemia. N: NSAID’s. G: Glucocorticoids. There are 2 types: Type-A (fundal): autoimmune destruction of parietal cells of the stomach resulting in pernicious anemia and achlorhydria. Type-B (antral): H.pylori infection. Diagnosis: endoscopy. Treatment: same as medical treatment for PUD. Complications: Gastric atrophy. Gastric metaplasia: with increased risk of MALT lymphoma and gastric adenocarcinoma.

Post-Gastrectomy Complications Dumping syndrome: It results from unregulated movement of gastric contents to small intestine. There are 2 types: Early dumping syndrome: 5-15 minutes post-prandially; due to high osmolar load reaching small intestine. Late dumping syndrome: 2-4 hours postprandially; due to hypoglycemia. Signs and symptoms: flushing, sweating, tachycardia/palpitations, nasuea/vomiting, diziness/syncope and diarrhea. Treatment: Small, frequent meals (low in carbohydrates and fat). Avoid excessive fluid intake. Alkaline reflux gastritis: Presents with: postpradial pain + bilious vomiting. Treatment: Roux-en-Y gastrojejunostomy. Nutritional deficiencies: vitamin B12 deficiency anemia and iron deficiency anemia. Afferent loop snydrome. Postvagotomy diarrhea.

Gastric Outlet Obstruction Causes: Tumors of the stomach or head of the pancreas. Ulcers (especially duodenal ulcers). Notice that chronic ulcers can result in scarring and edema which obstruct the lumen. Symptoms: Early: abdominal distention, gastric reflux and early satiety. Late: vomiting, dehydration, hypokalemic hypochloremic metabolic alkalosis with paradoxical aciduria, weight loss. Diagnosis: Barium meal. Endoscopy. Treatment: NG tube (for gastric decompression). After 7 days → truncal vagotomy and gastrojejunostomy.

Definition: bleeding which occurs proximal to ligament of Treitz. Differentials: Esophagus: Mallory-Weiss syndrome: post-emetic (mucosal tear) in gastroesophageal junction which resolves spontaneously. Boerhaave syndrome: post-emetic (rupture) in posterolateral aspect (left) of the esophagus near gastroesophageal junction. Esophagitis. Esophageal varices (in patient suffering from liver cirrhosis and portal hypertension). Esophageal cancer. Stomach and duodenum: PUD (gastric or duodenal ulcers). Gastritis. Gastric cancer. Signs and symptoms: Hematemesis (bright red blood or coffee ground). Melena (black, tarry stool occurs when bleeding is more than 60 cc). If there is profuse upper GI bleeding, patient can present with hematochezia (bright red blood per rectum). Signs of hypovolemic shock (hypotension and tachycardia). Diagnosis: CBC: check Hb and Hct; blood type and cross-match. Check for coagulation profile. NG tube aspirate. Endoscopy. Rate of bleeding ≥ 0.5 ml/minute: bleeding scan. Rate of bleeding ≥ 1 ml/minute: arteriography. Treatment: IV fluids + blood products then search for the cause. Upper GI Hemorrhage

Bariatric Surgery Definition: weight reduction surgery for morbidly obese patients. How to calculate BMI (Body Mass Index)? BMI = weight (kg) / height (m)2 What are the indications for bariatric surgery? BMI ≥ 35 with other diseases (such as diabetes or hypertension). BMI ≥ 40 with or without other diseases but there has to be a participation in a dietary program with no results. What are the medical conditions which are associated with morbid obesity: Diabetes mellitus. Hypertension. Coronary Artery Disease. Obstructive sleep apnea. Mention the types of bariatric surgery: Restrictive: reducing quantitiy of food which you can eat Gastric sleeve resection. Band placement. Malabsorptive: liming absorption by bypassing duodenum and small intestine: Gastrojejunostomy.

Bariatric Surgery

Malignant Tumors Adenocarcinoma (95%): Incidence increases with advanced age (< 60 years). It is more common among males and blacks. In addition, it is considered to be the leading cause of cancer-related deaths in Japan. Risk factors: Familial adenomatous polyposis. Chronic atrophic gastritis. H. pylori infection. Smoked food. Smoking. Pathological types: Polypoid (25-50%). Ulcerative (25-50%): with sharp margins. Superficial spreading (3-10%): involves mucosa and submucosa only; has the best prognosis. Linitis plastica (7-10%): involves all the layers; extremely poor prognosis. Histologic types: Intestinal: well-differentiated, distal, progressing to cancer slowly, secondary to environmental factors, usually 1 mass identified. Diffuse: poorly-differential, proximal, aggressive, congenital, characterized by generalized gastric hypertrophy. Signs and symptoms: Constant epigastric pain which increases with food. Hematemesis. Melena. Weight loss and anorexia. Blumer’s shelf: metastasis to pelvic cul-de-sac; felt by digital rectal examination. Krukenberg’s tumor: metastasis to ovaries. Virchow’s node: metastasis to left supraclavicular lymph node. Sister Mary Joseph’s nodule: periumbilical metastatic nodule. Irish’s node: left axillary adenopathy from gastric cancer. Malignant Tumors

Malignant Tumors

Malignant Tumors

Malignant Tumors Adenocarcinoma (continued): Diagnosis: Best: upper GI endoscopy with biopsy. Endoscopic ultrasound. Abdomino-pelvic CT-scan: for staging. Staging (TNM): Tumor: Tx: tumor cannot be assessed. T0: no evidence of tumor. Tis: carcinoma in situ. T1: involving submucosa. T2: reaching muscularis propria. T3: subserosal, not reaching adjacent structures. T4: involving adjacent structures. Nodes: Nx: lymph nodes cannot be assessed. N0: no evidence of lymph node involvement. N1: 1-2 regional lymph nodes. N2: 3-6 regional lymph nodes. N3: ≥ 7 regional lymph nodes. Metastasis: Mo: no distant metastasis. M1: distant metastasis. Treatment (gastrectomy with lymph node disection + chemotherapy/radiation): Proximal and midbody tumors: total gastrectomy. Antrum tumor: distal subtotal gastrectomy. Prognosis: tumor markers (not specific) → CEA and CA 19-9 Malignant Tumors

Malignant Tumors Gastric lymphoma (4%): Most are non-Hodgkin B-cell type. Risk is increased with H.pylori infection. Signs and symptoms (non-specific): abdominal pain, bleeding/anemia, nausea/vomiting and weight loss/anorexia. Diagnosis: Upper endoscopy with biopsy. Bone marrow aspiration and gallium bone scan (for metastasis). Treatment: Low-grade MALT: treat H.pylori infection. High-grade MALT or non-MALT: radiation/chemotherapy ± surgical resection (which is preserved for those with perforation or hemorrhage). GIST (1%) Gasto-Intestinal Stromal Tumor: Arising from cells of Cajal, submucosal, slow growing. Stomach is the most common site. Expression of c-kit (CD 117) which has tyrosine kinase activity. Treatment: surgical removal + imatinib (inhibits tyrosine kinase receptor). Malignant Tumors

Benign Lesions Menetier’s disease: Definition: it is hypertrophic gastropathy in which glandular cells will replace parietal and chief cells resulting in protein deficiency. Signs and symptoms: Middle-aged male who presents with epigastric pain, anorexia/weight loss, diarrhea and hypoproteinemia. Diagnosis: Endoscopy with biopsy. Barium swallow: shows thickened rugae. Treatment: Anticholinergics and H2-blockers to reduce protein loss. High-protein diet. Dieulafoy’s lesion: Definition: mucosal end artery which causes pressure necrosis, erodes into the stomach and ruptures. Signs and symptoms: recurrent, massive, painless hematemesis. Diagnosis: upper GI endoscopy. Treatment: endoscopic sclerosing therapy or electrocoagulation. Gastric volvulus: Definition: twisting of the stomach around its long axis. This is associated with paraesophageal hernia. It is characterized by Brochardt’s triad: Inability to vomit. Difficulty in passing NG tube. Intermittent, severe epigastric pain and distention. Diagnosis: upper GI contrast study. Surgical repair of associated paraesophageal hernia. Gastropexy: fixation of stomach to anterior abdominal wall. Benign Lesions