Fiser Chapter 30. STOMACH Flashcards
Stomach transit time
3-4 hours
Where in stomach does peristalsis occur?
Just antrum (distal stomach)
What sympathetic fibers does gastroduodenal pain get sensed?
T5-10
Blood supply of stomach
Celiac: left gastric, CHA, splenic (L gastroepiploic and short gastrics are branches of splenic)
Greater curvature: R and L gastroepiploics, short gastrics. (R gastroepiploic is a branch of GDA)
Lesser curvature: R and L gastrics, R is branch off CHA
Stomach mucosa hitso
Simple columnar epithelium
Cardia glands versus fundus and body glands
Cardia: mucus secreting
Fundus and body glands:
Chief cells pepsinogen
Parietal cells H+ and IF
Chief cells
Pepsinogen (1st enzyme in proteolysis)
Parietal cells
H+ and IF
What causes H+ release from parietal cells?
Ach (vagus)
Gastrin (G cells in antrum)
Histamine (from mast cells)
Phosphorylase kinase and protein kinase A
Achetylcholine and gastrin MoA to increase H+ release
Activates phospholipase (PIP) –> DAG + IP3 to increase calcium -> calcium-calmodulin activated phosphorylase kinase -> increased H+ relaease
Histamine MoA to increase H+ release
Histamine activates adenylate cyclase -> cAMP -> activates protein kinase A -> increased H+ release
Phosphorylase kinase and proteine kinase A MoA to increase H+ release
They phosphorylate H+/K+ ATPase to increase H+ secretion and K+ absorption
How does omeprazole work?
Blocks H+/K+ ATPase in parietal cell membrane (the final pathway for H+ release)
What are inhibitors of parietal cells (which release H+)?
Somatotatin
Prostaglandins (PGE1)
Secretin
CCK
What does intrinsic factor do?
Binds B12, and then the complex is reabsorbed in the TI
Fundus and body glands versus antrum and pylorus glands
Fundus and body: chief cells and parietal cells with pepsinogen and H+ and IF release
Antrum and pylorus: G cells (release gastrin in antrum) and mucus and HCO3- secreting glands; and D cells (secrete somatostatin)
Why is an antrectomy helpful for ulcer disease?
G cells release gastrin (taken out)
What inhibits and stimulates G cells
G cells release gastrin
Inhibited by H+ in duodenum
Stimulated by amino acids and acetylcholine
What do D cells do?
Secrete somatostatin, which inhibits gastrin and H+ release
What do Brunner’s glands do?
Secrete alkaline mucus
in duodenum
Antral and duodenal acidification causes what?
Somatostatin, CCK, and secretin release
MCC rapid and delayed gastric emptying
Rapid: previous surgery, ulcers
Delayed: DM, opiates, anticholinergics, hypothyroid
Trichobezoars and phytobezoars
Trychobezoars: Hair, hard to pull out, EGD generally inadequate and likely need gastrostomy and removal
Phytobezoars: Fiber, often in diabetics with poor gastric emptying, tx with enzymes, EGD and diet changes
Dieulafoy’s ulcer
vascular malformation that can bleed
Menetrier’s disease
Mucous cell hyperplasia, increased rugal folds
Nausea without vomiting, severe pains
Gastric volvulus, usually organoaxial
Associated with type 2 (paraesophageal) hernia
Tx: Reduction and Nissen
Hematemesis following severe retching
Mallory-Weiss tear
EGD with hemo-clips; Tear is usually on lesser curvature near GEJ
Bleeding often stops spontaneously, if continued bleeding may need gastrostomy and vessel oversewing
Truncal and proximal vagotomies
Both increase liquid emptying by removing vagally mediated receptive relaxation, causing increased gastric pressure that accelerates fluid emptying
Truncal (at level of esophagus): decreases solid emptying; add pyloroplasty to increase solid emptying
Proximal (high selective, divides individual fibers, preserves “crow’s foot”): Normal emptying of solids
Truncal vagotomy effects
decreased solid emptying (and increased liquid emptying like all vagotomies); decreases acid output by 90%, increases gastrin and gastrin cell hyperplasia; decreases exocrine pancreas function and postprandial bile flow; increases gallbladder volumes, and decreases release of vagally mediated hormons; diarrhea in 40% (most common problem after vagotomy) due to sustained MMCs forcing bile acids into colon
MCC problem after vagotomy
Diarrhea
Risk factors for UGIB
Prior UGIB, PUD, NSAIDs, smoking, liver dz, esophageal varices, splenic vein thrombosis, sepsis, burns, trauma, severe vomiting
Dx/Tx of UGIB
EGD, can potentially treat with hemo-clips, epi injection, cautery
Slow bleeding and having trouble localizing source?
Tagged RBCscan
Biggest risk factor for rebleeding at time of EGD
- Spurting blood vessel (60% chance)
- Visible vessel (40%)
- Diffuse oozing (30%)
HIghest risk factor for mortality with non-varicealm UGIB
Continued or rebleeding
Patient with liver failure MCC UGIB
Esophageal varices (NOT an ulcer)
Tx EGD with bands or sclerotherapy; TIPS if that fails
Duodenal ulcers cause
Increased acid production and less defese
Most common peptic ulcer
Duodenal
More common in men
Most common place for duodenal ulcer
Anterior, first part of duodenum
Anterior versus posterior duodenal ulcers
Anterior: Perforate
Posterior: Bleed from GDA
Epigastric pain radiating to the back, abates with eating but recurs 30 min after
Duodenal ulcer
Dx and Tx of duodenal ulcer
EGD; PPI, triple therapy for H pylori
Tripe therapy
Amoxicillin, Metronidazole/tetracyclene, PPI (PAM or PAT)
Surgery for ulcer?
Rarely indicated since PPIs
- Perforated
- Protracted bleeding despite EGD therapy
- Obstruction
- Intractability despite medical therapy
- Inability to rule out cancer (ulcer remains despite treatment) requires resection
- If a patient has been on a a PPI, an acid-reducing surgical procedure is required in addition to surgery for any complications
PUD mgt
Rule out gastrinoma in patients with complicated ulcer disease (ZES - gastric acid hypersecretion, peptic ulcers, and gastrinoma)
Surgical options for PUD (acid-reducing surgery)
Proximal vagotomy: lowest rate of complications, no need for antral or pylorus procedure; 10-15% ulcer recurrence and 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) and 2% mortality
Reconstruction after antrectomy: Roux-en-Y gastrojejunostomy is best: less dumping syndrome and reflux gastritis compared to Billroth I (gastroduodenal anastomosis) and Billroth II (gastrojejunal anastomosis)