Kingdom of Bahrain Arabian Gulf University College of Medicine and Medical Sciences

1. Kingdom of BahrainArabian Gulf UniversityCollege of Medicine and Medical Sciences GI System – Review Problem (4) – Stomach Ali Jassim Alhashli, BSc www.alhashli.com

2. 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).

3. Anatomy, Histology & Physiology of Stomach

4. Anatomy, Histology & Physiology of Stomach

5. Anatomy, Histology & Physiology of Stomach • Histology: • 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.

6. Anatomy of Duodenum • Anatomy: • General: • Length of small bowel: 5-10 m • Consists of: duodenum, jejunum and ileum. • Duodenum is a retroperitoneal structure (except for the first 2 cm), while jejunum and ileum are intraperitoneal structures. • Duodenum: • Composed of 4 parts: • First part: 5 cm, common site for ulcers. • Second part: 10 cm, curves around head of pancreas. • Third part: 10 cm, anterior to aorta and IVC, posterior to superior mesenteric vessels. • Fourth part: 5 cm, forming duodenojejunal junction which is suspended by ligament of Treitz. • Blood supply: • Arterial: • Proximal (up to ampulla of Vater): gastroduodenal artery through anterior and posterior superior pancreaticoduodenal arteries. • Distal (below ampulla of Vater) superior mesenteric artery through anterior and posterior inferior pancreaticoduodenal arteries. • Venous drainage: through superior mesenteric vein which joins splenic vein behind the neck of the pancreas forming the portal vein.

7. Anatomy of Duodenum

8. Anatomy and Embryology

9. GI Hormones • 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.

10. Gastroschisis and Omphalocele • Gastroschisis: • Congenital, full-thickness defect of the abdominal wall which is found right to the umbilicus and resulting in exposed bowel (with no covering). • Diagnosis: • Often detected by pre-natal ultrasound. • Associated with ↑ alpha-fetoprotein (AFP). • Not associated with other anomalies. • Treatment: • Temperature regulation. • Sterile covering with a plastic wrap. • NG decompression with Total Parenteral Nutrition (TPN). • Broad-spectrum antibiotics. • Surgical correction and closure of the abdomen. • Prognosis: 20% of cases are complicated with necrotizing enterocolitis. • Omphalocele: • Herniation of abdominal contents into the base of umbilical cord (with a covering made of peritoneum and amnion). • Associated anomalies: • Beckwith-Wiedmann syndrome (gigantism, macroglossia, hypoglycemia, umbilical defect and organomegaly). • Trisomy 13 and 18. • Extrophy of urinary bladder. • There are two types: • Small: containing only intestine. • Large: liver, spleen and GI tract. • Treatment: • Intact sac: not urgent. • Ruptured sac: similar to gastroschisis. Emergency surgical repair is required.

11. Pyloric Stenosis • Pyloric stenosis: • Definition: it is the narrowing of pyloric canal due to hypertrophy of smooth muscle. This is more common among males, those with family history and firstborn males. • Signs and symptoms: • They will appears between 2 weeks – 2 months of age. • Olive-like mass in the midepigastric area. • Projectile, non-bilious vomiting obstruction is proximal to ampulla of vater). • Visible peristalsis. • Hypokalemic, hypochloremic metabolic alkalosis with paradoxical aciduria. • Diagnosis: ultrasound which will show: • Elongation of pyloric canal (< 14 mm). • Thickened pyloric wall (< 4 mm). If ultrasound is not diagnostic, barium swallow shows string sign. • Treatment: • Fluid replacement, correction of electrolytes and acid-base disturbance. • Surgery: Ramstedtpyloromyotomy. Remember that vein of Mayo crosses the pylorus.

12. 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.

13. 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. • Smoking. • 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.

14. Peptic Ulcer Disease (PUD) – Introduction

15. 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 ureas-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.

16. 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

17. Gastric Adenocarcinoma • 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 adenomatouspolyposis. • 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. • Linitisplastica (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 axillaryadenopathy from gastric cancer.

18. Gastric Adenocarcinoma

19. Gastric Adenocarcinoma

20. 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 muscularispropria. • 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 Gastric Adenocarcinoma