Stomach PDF

STOMACH OBJECTIVES Correlate gastric anatomy, histology and physiology to the diagnosis and management of gastric diseases Understand the basic pathology and management of common surgical gastric diseases STOMACH  Remarkable organ with important digestive, nutritional and endocrine...

STOMACH OBJECTIVES Correlate gastric anatomy, histology and physiology to the diagnosis and management of gastric diseases Understand the basic pathology and management of common surgical gastric diseases STOMACH  Remarkable organ with important digestive, nutritional and endocrine functions  Stores and facilitates digestion and absorption  Helps regulate appetite STOMACH: ANATOMY Parts of the stomach Cardia Fundus Body Pylorus Angle of His Where the fundus meets the left side of the GE junction STOMACH: ANATOMY Angularis Incissura Marks the beginning of the pyloric antrum (25-30% of the stomach) Lesser curvature Greater Curvature RELATIONS OF THE STOMACH Liver Left kidney Spleen Pancreas Omental bursa Hepatogastric ligament (lesser omentum) Gastrocolic omentum ARTERIAL AND VENOUS SUPPLY Right and left gastric artery Right and left gastroepiploic artery Short gastric arteries ARTERIAL AND VENOUS SUPPLY Right and left gastric vein Drains to the portal vein Right gastroepiploic vein Drains to the SMV Left gastroepiploic vein Drains to the splenic vein ARTERIAL AND VENOUS SUPPLY CLINICAL IMPORTANCE OF RICH VASCULAR SUPPLY: At least two arteries may be ligated with impunity E.g. gastrectomy, stomach as replacement for esophagus ARTERIAL AND VENOUS SUPPLY CLINICAL IMPORTANCE OF RICH VASCULAR SUPPLY: Angiographic control of gastric bleeding requires embolization of more than one feeding artery Can be used as shunt (splenorenal shunt) to decompress pts with portal HPN LYMPHATIC SUPPLY Cardia and medial half of corpus Drain along the left gastric and celiac axis Lesser curvature (antrum side) Right gastric and pyloric nodes LYMPHATIC SUPPLY Greater curvature (distal) Right gastroepiploic chain Greater curvature (proximal) Left gastroepiploic chain or splenic hilum LYMPHATIC SUPPLY Greater and lesser curvature Drain to the celiac nodal basin INNERVATION VAGUS NERVE Parasympathetic innervation Left anterior Right Posterior (LARP) Nerves of Latarjet Crow’s foot at the angularis incisura INNERVATION VAGUS NERVE Posterior vagus Sends fibers to the posterior fundus and is called Criminal nerve of Grassi INNERVATION SYMPATHETIC NERVE SUPPLY T5-T10 spinal nerve fibers to the splanchnic nerve to celiac ganglion HISTOLOGY MUCOSA Inner layer, lined with columnar glandular cells Gastric glands Surface epithelium, lamina propia and muscularis mucosae (microscopic boundary for invasive gastric carcinoma) HISTOLOGY GASTRIC GLAND: Gastric pit secretes bicarbonate Protects the stomach Parietal and Chief cells Fundus and body Parietal cells Secrete acid, intrinsic factor and bicarbonate Midportion of the gastric glands HISTOLOGY GASTRIC GLAND: Chief Cells Zymogenic cells Secrete predominantly pepsinogen I and some pepsinogen II (proenzymes) Gastrin-secreting G cells and somatostatin-secreting D cells Present in the antrum of the stomach HISTOLOGY GASTRIC GLAND: In normal stomach 13% oxyntic (parietal) cells 44% chief (zymogenic) cells 40% mucous cells 3% endocrine cells HISTOLOGY HISTOLOGY HISTOLOGY HISTOLOGY SUBMUCOSA Rich in blood vessels, lymphatics, collagen and Meissner’s autonomic submucosal plexus HISTOLOGY MUSCULARIS PROPRIA Muscularis externa Inner oblique layer, complete middle circular layer and complete outer longitudinal layer Rich network of autonomic ganglia; Auerbach’s plexus; Interstitial cells of Cajal (pacemaker) HISTOLOGY SEROSA Visceral peritoneum Provides tensile strength PHYSIOLOGY FUNCTIONS: Stores food (receptive relaxation and accommodation) and facilitates digestion (mixing and grinding, controlled emptying) Secretory functions (acid, pepsin, IF, mucus, hormones) PHYSIOLOGY ACID SECRETION HCL + pepsin =biochemical breakdown of food Facilitates proteolysis Inhibits proliferation of ingested pathogens PHYSIOLOGY PARIETAL CELL Oxyntic cells (~1 billion) Stimulated by gastrin, acetylcholine and histamine to secrete acid H+/K+ - ATPase is the proton pump (site of the PPIs) Packed with energy producing mitochondria PHYSIOLOGY PARIETAL CELL Gastrin binds to type B cholecystokinin receptor Acetylcholine binds to M3 muscarinic receptors Histamine binds to H2 receptors PHYSIOLOGY PHYSIOLOGIC ACID SECRETION Food ingestion is the physiologic stimulus for acid secretion Three phases: Cephalic (30%) Gastric (60%) Intestinal (10%)  PHYSIOLOGY PHYSIOLOGIC ACID SECRETION Cephalic (30%) Thought, smell and /or taste of food Gastric (60%) Amino acids stimulate gastrin Proximal gastric distention stimulates acid secretion via vagovagal reflex arc (abolished by truncal or HSV) Antral distention also stimulates gastrin  PHYSIOLOGY PHYSIOLOGIC ACID SECRETION Gastrin Major hormonal regulator of the gastric phase of acid secretion Stimulated by amino acids, inhibited by luminal acid Histamine Released by ECL Principle mediator of acid secretion  PHYSIOLOGY PHYSIOLOGIC ACID SECRETION Intestinal (10%) Poorly understood condition Thought to be mediated by a hormone released from the proximal small bowel in response to intraluminal chyme 10% of acid production H. pylori Inhibits the function of D cells (releases somatostatin) resulting to an exaggerated acid secretion PHYSIOLOGY PEPSINOGEN SECRETION Food ingestion stimulates chief cells Chief cells produces pepsinogen I → pepsin (at pH2.5) INTRINSIC FACTOR Secreted by parietal cells Binds to luminal Vit B12 PHYSIOLOGY GASTRIC MUCOSAL BARRIER Durability of the stomach to autodigestion Restitution Any sloughed or denuded SECs are repidly replaced by migration of adjacent cells PHYSIOLOGY GASTRIC MUCOSAL BARRIER Mucosal blood flow When “barrier-breakers” (aspirin or bile) lead to increased back diffusion of H ions from the lumen to the lamina propria and submucosa, there is a protective increase in the mucosal blood flow Mediators help maintain this protective response PHYSIOLOGY GASTRIC MUCOSAL BARRIER Sucralfate Acts locally to enhance mucosal defenses PHYSIOLOGY GASTRIC HORMONES Gastrin Antrum Leptin Major hormonal stimulant of acid Made by the chief cells secretion during gastric phase Decrease food intake Somatostatin Satiety signal hormone D cells Inhibits acid secretion from parietal Ghrelin cells and gastrin release from G Appetite stimulant cells PHYSIOLOGY INTRINSIC GASTRIC INNERVATION Enteric nervous system Excitatory Neurotransmitters Acetylcholine Tachykinins Substance P Neurokinin A Inhibitory Neurotransmitters Nitric oxide Vasoactive Intestinal Peptide (VIP) PHYSIOLOGY INTRINSIC GASTRIC INNERVATION INTERSTITIAL CELLS OF CAJAL Amplify both cholinergic (excitatory) and nitrergic (inhibitory) input to stomach Cells of origin of GIST PHYSIOLOGY GASTRIC EMPTYING PYLORUS is the effective regulator of gastric emptying Also an effective barrier in duodenogastric reflux PHYSIOLOGY GASTRIC EMPTYING Liquid emptying Half time emptying is 12 minutes Varies depending on caloric density, osmolarity, nutrient composition of liquids Solid emptying Half time is 2 hours Function of meal particle size, caloric content and composition BENIGN DISEASES OF THE STOMACH  PEPTIC ULCER DISEASE (PUD) One of the most common GI disorders 2% prevalence in the US, 10% lifetime cummulative prevalence Peak age: 70 years old Decline in incidence in the advent of the H2 blockers and PPIs PEPTIC ULCER DISEASE (PUD) Focal defects in the gastric or duodenal mucosa that extend into the submucosa or deeper “NO acid, no ulcer” Caused by imbalance between mucosal defenses and Acid/peptic injury ETIOLOGY NSAIDS Compromise of mucosal barriers H. pylori infection (90%) Predisposes to ulceration by acid hypersecretion and compromise of mucosal defense mechanisms Others: Zollinger-Ellison syndrome, drugs, trauma, burns, stress, cigarette smoking ETIOLOGY H. pylori infection Occurs in 90% of patients with duodenal ulcers, 70-90% of patients with gastric ulcers With specialized flagella and rich supply of urease Urease → converts urea to ammonia and bicarbonate that buffers the acid of the stomach Ammonia→ damages the surface epithelial cells Flagella → helps the bacteria to navigate and attach to the mucus layer ETIOLOGY H. pylori infection Mechanism: disturbance in gastric acid secretion via inhibitory effect of H. pylori to the somatostatin secreting antral D cells (due to alkalinization of the antrum) Results to hypergastrinemia and acid hypersecrection Inflammation→ metaplasia → dysplasia → neoplasia ETIOLOGY ETIOLOGY ETIOLOGY H. pylori infection Strong evidence exists on the development and recurrence of PUD 75% recurrence rate if treated only with PPIs 45 y.o. with epigastric pain, alarm symptoms DIAGNOSIS ENDOSCOPY (ESOPHAGOGASTRODUODENOS COPY) All gastric ulcer should be biopsied Presence of H. pylori Can control bleeding of ulcers if present Complications: perforation (rare) DIAGNOSIS Plain abdominal films/ chest xray upright Detect pneunoperitoneum in perforated peptic ulcer (PPU) MEDICAL MANAGEMENT SURGICAL MANAGEMENT INDICATIONS: Perforation Bleeding Obstruction Intractability or nonhealing SURGICAL MANAGEMENT BLEEDING Endoscopic control: clipping, electrocauterization, epinephrine Surgery: oversewing of bleeders Early operation for >60 y.o. Shock >4 units of blood in 48 hrs Rebleeding Ulcer >2cm SURGICAL MANAGEMENT SURGICAL MANAGEMENT PERFORATION Second most common complication Omental patching Biopsy of the ulcer SURGICAL MANAGEMENT OBSTRUCTION Endoscopic dilatation Surgery 5% of patients with PUD Inflammation and ulcer cicatrixation Nonbilious vomiting Hypokalemic, hypochloremic MA Antrectomy + vagotomy SURGICAL MANAGEMENT SURGICAL MANAGEMENT INTRACTABILITY/ NONHEALING Noncompliant Missed cancer SURGICAL MANAGEMENT TRUNCAL VAGOTOMY HIGHLY SELECTIVE VAGOTOMY SURGICAL MANAGEMENT PYLOROMYOTOMY SURGICAL MANAGEMENT SURGICAL MANAGEMENT RECONSTRUCTION: ROUX-EN-Y GASTROJEJUNOSTOMY BILLROTH I AND II BENIGN DISEASES OF THE STOMACH Gastritis Lipoma Lyieyomyoma Zollinger-Ellison Syndrome/gastrinoma Bezoars Gastric Varices Deilafoy’sLesion Hypertropic Gastropathy MALIGNANT NEOPLASMS OF THE STOMACH GASTRIC NEOPLASMS 3 most common primary malignant neoplasm: Adenocarcinoma (95%) Lymphoma (4%) Malignant GIST (1%) GASTRIC CANCER 4th most common type of cancer 2nd leading cause of cancer death Disease of the elderly In young patients: usually of the diffuse type (linitis plastica) ETIOLOGY Higher incidence in patients with pernicious anemia, blood group A, family history of gastric cancer ETIOLOGY Environmental factors Diet Smoking H. pylori infection EBV (10%) ETIOLOGY GENETIC FACTORS Most common genetic abnormalitites: p53 COX-2 genes CDH1 ETIOLOGY Premalignant conditions Hyperplastic polyp Gastric adenomas (FAP) PATHOLOGY DYSPLASIA Universal precursor to gastric adenocarcinoma EARLY GASTRIC CANCER Limited to the mucosa and submucosa HISTOLOGY PROGNOSTIC INDICATORS: Lymph node involvement Depth of tumor invasion Tumor grade (well diff, mod diff, poorly diff) PATHOLOGIC STAGING CLINICAL MANIFESTATION Usually asymptomatic until late in the disease (stage III) Common symptoms: Weight loss Anorexia Early satiety Abdominal pain (often ignored) Nausea, vomiting, bloatedness UGIB (melena, hematemesis-5%) CLINICAL MANIFESTATION PHYSICAL EXAMINATION Typically normal Incurable disease may show: Virchow’s node (supraclavicular nodes), cervical, axillary nodes Sister Mary Joseph’s nodule (umbilical nodule) Abdominal mass Krukenberg tumor (ovarian tumor) Ascites Rectal exam: drop metastasis in the pouch of Douglas (nodularity), dark stools (positive for occult blood) DIAGNOSTIC EVALUATION EGD/ENDOSCOPY Dyspepsia symptoms Differentiate between PUD and carcinoma Alarm symptoms for age 45 and above Family history of gastric cancer “Gold standard”: Direct visualization and histopathological evidence (biopsy) DIAGNOSTIC EVALUATION PRE-OPERATIVE STAGING Abdominal CT scan with contrast MRI Endoscopic Ultrasound (EUS) Depth of the tumor (80%) PET SCAN Distant metastasis and locoregional staging May be combined with CT scan (PET-CT) Staging Laparoscopy and cytology TREATMENT Surgical resection is the ONLY curative treatment for gastric cancer GOAL OF SURGERY: CURATIVE resection Resection of all tumor plus margins (5 cm) Adequate lymphadectomy (15 lymph nodes) TREATMENT RADICAL SUBTOTAL GASTRECTOMY Involves ligation of right and left gastric and gastroepiploic arteries at the origin Enbloc removal of the distal 75% of the stomach including pylorus and 2 cm of the duodenum, greater and lesser omentum and all associated lymphatic tissue TREATMENT RADICAL SUBTOTAL GASTRECTOMY Reconstruction with Roux-en-Y gastrojejunostomy or Billroth II gastrojejunostomy TREATMENT TOTAL GASTRECTOMY For proximal tumors Roux-en-Y reconstruction TREATMENT EXTENT OF LYMPHADENECTOMY D1 Stations 1, 3, 4sb, 4d, 5,6,7 D2 Stations additional station 8a, 9, 10, 11 p and 12a TREATMENT CHEMOTHERAPY AND RADIATION Added survival benefit Radiation usually for palliation of bleeding 5-FU, cisplatin, doxorubicin, taxanes, methotrexate, camptothecin Targeted molecular agents Her2 testing Use of trastuzumab TREATMENT ENDOSCOPIC MUCOSAL RESECTION (EMR) For early gastric cancer Minimally invasive procedure Curative intent for tumors