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

  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

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

•  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

Stay updated, free articles. Join our Telegram channel

Join