Chapter 30: Stomach Flashcards
Stomach transit time
3-4 hours
Where does stomach peristalsis occur?
Distal stomach (antrum)
How is gastroduodenal pain sensed
Through afferent sympathetic fibers T5-T10
Components of the celiac trunk
Left gastric
Common hepatic artery
Splenic artery
Branches of the splenic artery that supply the stomach
Left gastroepiploic and short gastric
Blood supply to the greater curvature
Right and left gastroepiploics, short gastrics
What is the right gastroepiploic a branch of?
Gastroduodenal artery
Blood supply of lesser curvature
Right and left gastrics
What is the right gastric a branch off?
The common hepatic artery
Blood supply of the pylorus
Gastroduodenal artery
Mucosa lining the stomach
Simple columnar epithelium
What do cardia glands secrete?
Mucus
Fundus and body glands
Chief cells
Parietal cells
Produces pepsinogen (1st enzyme in proteolysis)
Chief cells
Release hydrogen and intrinsic factor
Parietal cells
What stimulates parietal cells?
Acetylcholine (vagus nerve), gastrin (from G cells in antrum), and histamine (from mast cells) cause H+ release
What is the pathway of acetylcholine (vagus nerve) and gastrin?
Activates phospholipase (PIP -> DAG + IP3 + Increase Ca); Ca-calmodulin activates phosphorylase kinase -> H+ release
What is the pathway of histamine?
Activates adenylate cyclase -> cAMP -> activates protein kinase A -> increased H+ release
How do phosphorylase and protein kinase A work?
Phosphorylate H+/K+ ATPase to increase H+ secretion and K+ absorption
Blocks H+/K+ ATPase in parietal cell membrane (final pathway for H+ release)
Omeprazole
Inhibitors of parietal cells
Somatostatin, prostaglandins (PGE1), secretin, CCK
Binds B12 and the complex is reabsorbed in the terminal ileum
Intrinsic factor
Antrum and pylorus glands
Mucus and HCO3- secreting glands. G cells (gastrin). D cells (somatostatin)
Secreting glands - protect stomach
Mucus and HCO3- (Antrum and pylorus glands)
Release gastrin - reason why antrectomy is helpful for ulcer disease
G cells
What inhibits G cells?
H+ in duodenum
What stimulates G cells?
Amino acids, acetylcholine
Secrete somatostatin, inhibit gastrin and acid release
D cells
In duodenum; secrete alkaline mucus
Brunner’s glands
Released with antral and duodenal acidification
Somatostain, CCK, and secretin
What are the causes of rapid gastric emptying?
Previous surgery (#1), ulcers
What are the causes of delayed gastric emptying?
Diabetes, opiates, anticholingerics, hypothyroidism
(Hair) - hard to pull out
Tx?
Trichobezoars
- Tx: EGD generally inadequate; likely need gastrostomy and removal
(fiber) - often in diabetics with poor gastric emptying
Tx?
Phytobezoars (fiber)
Tx: enzymes, EGD, diet changes
Vascular malformation; can bleed
Dieulafoy’s ulcer
Mucous cell hyperplasia, increased rugal folds
Menetrier’s disease
- Associated with type II (paraesophageal) hernia
- Nausea without vomiting; severe pain; usually organoaxial volvulus
Treatment?
Gastric volvulus
Tx: reduction and Nissen
- Secondary to forceful vomiting
- Presents as hematemesis following severe retching
- Bleeding often stops spontaneously
Mallory-Weiss tear
What type of volvulus is a gastric volvulus?
Organoaxial volvulus
Dx/Tx: Mallory Weiss Tear
EGD with hemo-clips; tear is usually on the lesser curvature (near GE junction)
Where is the Mallory Weiss Tear located?
Usually on the lesser curvature (near GE junction)
What if you have continued bleeding after EGD with hemo-clips for Mallory Weiss tear?
If continued bleeding, may need gastrostomy and oversewing of the vessel.
What is the physiologic effect of vagotomy?
Both truncal and proximal forms increase liquid emptying -> vaguely mediated receptive relaxation if removed (results in increased gastric pressure that accelerates liquid emptying)
Vagotomy:
Divides vagal trunks at the level of the esophagus; decreases emptying of solids
Truncal vagotomy
Vagotomy:
- highly selective
- divides individual fibers, preserves “crow’s foot”, normal emptying of solids
Proximal vagotomy
Emptying of solids: truncal vs proximal vagotomy
Truncal: decreased emptying of solids
Proximal: normal emptying of solids
How can you increase solid emptying with truncal vagotomy?
Addition of pyloroplasty to truncal vagotomy results in increased solid emptying.
Physiologic effects of truncal vagotomy
- Gastric effects
- Nongastric effects
- Diarrhea
- Gastric: decreased acid output by 90%, increased gastrin cell hyperplasia
- Nongastric: decreased exocrine pancreas function, decreased postprandial bile flow, increased gallbladder volumes, decreased release of vaguely mediated hormones
- Diarrhea: MC problem following vagotomy
MC common problem following vagotomy
Diarrhea (40%)
What causes diarrhea following vagotomy?
Caused by sustained MMCs (migrating motor complex) forcing bile acids into the colon
Name that vagotomy: both nerve trunks are divided at the level of the diaphragmatic hiatus
Truncal vagotomy
Name that vagotomy: division of the vagal fibers that supply the gastric funds. Branches to the antropyloric region of the stomach are not transected, and the hepatic and celiac divisions of the vagus nerves remain intact.
Proximal gastric vagotomy
Risk factors: upper gastroinestinal bleeding
Previous UGIB, PUD, NSAIDs, smoking, liver disease, esophageal varices, splenic vein thrombosis, sepsis, burn injuries, trauma, severe vomiting.
Dx/Tx: UGIB
EGD (confirm bleeding is from ulcer); can potentially treat with hemo-clips, Epi injection, cautery
Mgmt: UGIB with slow bleeding and having trouble localizing source
Tagged RBC scan
UGIB: 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 UGIB
Continued or re-bleeding
Treatment: patient with liver failure is likely bleeding from esophageal varices, not an ulcer
EGD with variceal bands or sclerotherapy; TIPS if that fails
- From increased acid production and decreased defense
- Most common peptic ulcer; more common in men
Duodenal ulcers
Location of duodenal ulcers
Usually in 1st part of the duodenum; usually anterior.
Complications of duodenal ulcers:
- Anterior
- Posterior
- 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/Tx?
Duodenal ulcer
- Dx: endoscopy
- Tx: PPI, triple therapy for H. pylori -> bismuth salts, amoxicillin, and metronidazole/tetracycline (BAM or BAT)
What has decreased incidence of surgery for ulcer?
Surgery for ulcer rarely indicated since PPIs
What do you need to rule out in patients with complicated ulcer disease?
Need to rule out gastrinoma
Gastric acid hyper secretion.
Peptic ulcers.
Gastrinoma.
Zollinger-Ellison Syndrome
Surgical indications for duodenal ulcer
Perforation. Protracted bleeding despite EGD therapy. Obstruction. Intractability despite medical therapy. Inability to rule out cancer. PPI with duodenal ulcer complication.
Duodenal ulcer: if patient has been on a PPI and has complications
If a 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) for duodenal ulcers
- Proximal vagotomy
- Truncal vagotomy and pyloroplasty
- Truncal vagotomy and antrectomy
- Reconstruction after antrectomy - Roux-en-Y gastro-jejunostomy (best)
Surgery duodenal ulcer: lowest rate of complications, no need for astral or pylorus procedure; 10-15% ulcer recurrence, 0.1% mortality
Proximal vagotomy
Ulcer recurrence / mortality after proximal vagotomy
- 10-15% ulcer recurrence
- 0.1% mortality
Ulcer recurrence / mortality after truncal vagotomy and pyloroplasty
- 5-10% ulcer recurrence
- 1% mortality