Stomach transit time 3–4 hours
Peristalsis – occurs only in distal stomach (antrum)
Gastroduodenal pain sensed through afferent sympathetic fibers T5–10
Blood supply
• Celiac trunk – left gastric, common hepatic artery, splenic artery
• Left gastroepiploic and short gastric are branches of splenic artery
• Greater curvature – right and left gastroepiploics, short gastrics
• Right gastroepiploic is a branch of gastroduodenal artery
• Lesser curvature – right and left gastrics
• Right gastric is a branch off the common hepatic artery
• Pylorus – gastroduodenal artery
Mucosa – lined with simple columnar epithelium
![](https://i0.wp.com/basicmedicalkey.com/wp-content/uploads/2017/06/image00586.gif?w=960)
Cardia glands – mucus secreting
Fundus and body glands
• Chief cells – pepsinogen (1st enzyme in proteolysis)
• Parietal cells – release H+ and intrinsic factor
• Acetylcholine (vagus nerve), gastrin (from G cells in antrum), and histamine (from mast cells) cause H+ release
• Acetylcholine and gastrin activate phospholipase (PIP → DAG + IP3 to ↑ Ca); Ca-calmodulin activates phosphorylase kinase →↑ H+ release
• Histamine activates adenylate cyclase → cAMP → activates protein kinase A →↑ H+ release
• Phosphorylase kinase and protein kinase A phosphorylate H+/ K+ ATPase to ↑ H+ secretion and K+ absorption
• Omeprazole blocks H+/K+ ATPase in parietal cell membrane (final pathway for H+ release)
• Inhibitors of parietal cells – somatostatin, prostaglandins (PGE1), secretin, CCK
• Intrinsic factor – binds B12 and the complex is reabsorbed in the terminal ileum
Antrum and pylorus glands
• Mucus and HCO3– secreting glands – protect stomach
• G cells release gastrin – reason why antrectomy is helpful for ulcer disease
• Inhibited by H+ in duodenum
• Stimulated by amino acids, acetylcholine
• D cells – secrete somatostatin; inhibit gastrin and acid release
Brunner’s glands – in duodenum; secrete alkaline mucus
Somatostatin, CCK, and secretin – released with antral and duodenal acidification
Rapid gastric emptying – previous surgery (#1), ulcers
Delayed gastric emptying – diabetes, opiates, anticholinergics, hypothyroidism
Trichobezoars (hair) – hard to pull out
• Tx: EGD generally inadequate; likely need gastrostomy and removal
Phytobezoars (fiber) – often in diabetics with poor gastric emptying
• Tx: enzymes, EGD, diet changes
Dieulafoy’s ulcer – vascular malformation; can bleed
Ménétrièr’s disease – mucous cell hyperplasia, ↑ rugal folds
GASTRIC VOLVULUS
Associated with type II (paraesophageal) hernia
Nausea without vomiting; severe pain; usually organoaxial volvulus
Tx: reduction and Nissen
MALLORY–WEISS TEAR
Secondary to forceful vomiting
Presents as hematemesis following severe retching
Bleeding often stops spontaneously
Dx/Tx: EGD with hemo-clips; tear is usually on lesser curvature (near GE junction)
If continued bleeding, may need gastrostomy and oversewing of the vessel
VAGOTOMIES
Vagotomy – both truncal and proximal forms ↑ liquid emptying → vagally mediated receptive relaxation is removed (results in ↑ gastric pressure that accelerates liquid emptying)
Truncal vagotomy – divides vagal trunks at level of esophagus; ↓ emptying of solids
Proximal vagotomy (highly selective) – divides individual fibers, preserves “crow’s foot”; normal emptying of solids
Addition of pyloroplasty to truncal vagotomy results in ↑ solid emptying
Other alterations caused by truncal vagotomy:
• Gastric effects – ↓ acid output by 90%, ↑ gastrin, gastrin cell hyperplasia
• Nongastric effects – ↓ exocrine pancreas function, ↓ postprandial bile flow, ↑ gallbladder volumes, ↓ release of vagally mediated hormones
• Diarrhea (40%) – most common problem following vagotomy
• Caused by sustained MMCs (migrating motor complex) forcing bile acids into the colon
![](https://i0.wp.com/basicmedicalkey.com/wp-content/uploads/2017/06/image00587.gif?w=960)
![](https://i0.wp.com/basicmedicalkey.com/wp-content/uploads/2017/06/image00588.gif?w=960)
UPPER GASTROINTESTINAL BLEEDING (UGI BLEEDING)
Risk factors: previous UGI bleed, peptic ulcer disease, NSAID use, smoking, liver disease, esophageal varices, splenic vein thrombosis, sepsis, burn injuries, trauma, severe vomiting
Dx/Tx: EGD (confirm bleeding is from ulcer); can potentially treat with hemo-clips, Epi injection, cautery
![](https://i0.wp.com/basicmedicalkey.com/wp-content/uploads/2017/06/image00589.gif?w=960)
• Slow bleeding and having trouble localizing source → tagged RBC scan
• Biggest risk factor for rebleeding at the time of EGD – #1 spurting blood vessel (60% chance of rebleed), #2 visible blood vessel (40% chance of rebleed), #3 diffuse oozing (30% chance of rebleed)
• Highest risk factor for mortality with non-variceal UGI bleed – continued or re-bleeding
• Patient with liver failure is likely bleeding from esophageal varices, not an ulcer → Tx: EGD with variceal bands or sclerotherapy; TIPS if that fails
DUODENAL ULCERS
From ↑ acid production and ↓ defense
Most common peptic ulcer; more common in men
Usually in 1st part of the duodenum; usually anterior
• Anterior ulcers perforate
• Posterior ulcers bleed from gastroduodenal artery
Symptoms: epigastric pain radiating to the back; abates with eating but recurs 30 minutes after
Dx: endoscopy
Tx: proton pump inhibitor (PPI; omeprazole), triple therapy for Helicobacter pylori → bismuth salts, amoxicillin, and metronidazole/tetracycline (BAM or BAT)
Surgery for ulcer rarely indicated since PPIs
Need to rule out gastrinoma in patients with complicated ulcer disease (Zollinger-Ellison syndrome – gastric acid hypersecretion, peptic ulcers, and gastrinoma)
Surgical indications:
• Perforation
• Protracted bleeding despite EGD therapy
• Obstruction
• Intractability despite medical therapy
• Inability to rule out cancer (ulcer remains despite treatment) → requires resection of ulcer
• If patient has been on a PPI, an acid-reducing surgical procedure is required in addition to surgery for any complications
Surgical options (acid-reducing surgery)
• Proximal vagotomy – lowest rate of complications, no need for antral or pylorus procedure; 10%–15% ulcer recurrence; 0.1% mortality
• Truncal vagotomy and pyloroplasty – 5%–10% ulcer recurrence, 1% mortality
• Truncal vagotomy and antrectomy – 1%–2% ulcer recurrence (lowest rate of recurrence), 2% mortality
• Reconstruction after antrectomy – Roux-en-Y gastro-jejunostomy (best)
• Less dumping syndrome and reflux gastritis compared to Billroth I (gastro-duodenal anastomosis) and Billroth II (gastro-jejunal anastomosis)
Bleeding
• Most frequent complication of duodenal ulcers
• Usually minor but can be life threatening
• Major bleeding – > 6 units of blood in 24 hours or patient remains hypotensive despite transfusion
• Tx: EGD 1st – hemoclips, cauterize, Epi injection
• Surgery – duodenotomy and gastroduodenal artery (GDA) ligation
• Avoid hitting common bile duct (posterior) with GDA ligation
• If patient has been on a PPI, need acid-reducing surgery as well
![](https://i0.wp.com/basicmedicalkey.com/wp-content/uploads/2017/06/image00590.gif?w=960)
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