Chapter 30 - Stomach Flashcards
What is the transit time of the stomach?
3-4h
What level of afferent sympathetic fibers sense gastroduodenal pain?
T5-10
What type of mucosa does the stomach have?
Simple columnar epithelium
What do the cardia glands secrete?
Mucus
What do Chief cells secrete? Location?
Pepsinogen; fundus and body
What do Parietal cells secrete? Location?
H+ and intrisic factor; fundus and body
What stimulates HCl release?
Gastrin, ACh, histamine
What mediator does ACh and gastrin work on to inc. HCl?
Phospholipase –> PIP –> DAG + IP3 –> inc. Ca, activates phosphorylase kinase
Histamine acts on what mediator to inc. HCl?
Adenylate cyclase –> cAMP –> protein kinase A
What are inhibitors of parietal cells?
Somatostatin, PGE1, secretin, CCK
What is the response to intrinsic factor?
Binds B12 and the complex is reabsorbed in the terminal ileum
G cells release what? Location?
Gastrin; Antrum and pylorus
G cells inhibited by? Stimulated by?
Inhibited by H+ in duodenum; stimulated by amino acids, ACh
D cell secrete what? Location?
Somatostatin; antrum and pylorus
Response to somatostatin in the stomach?
Inhibit gastrin and acid release
Brunner’s glands secrete what? Location?
Pepsinogen and alkaline mucus; duodenum
DDx for elevated acid and gastrin?
ZES, antral cell hyperplasia, retained antrum, renal failure, gastric outlet obstruction, short bowel syndrome
DDx for elevated gastrin and normal/decreased acid?
Pernicious anemia, chronic gastritis, gastric ca, postvagotomy, medical acid suppression
DDx for rapid gastric emptying?
1 previous surgery, ZES, ulcers
DDx for delayed gastric emptying?
Opiates, anticholinergics, myxedema, hyperglycemia, diabetes
Components of Billroth I?
Antrectomy with gastroduodenal anastamosis
Components of Billroth II?
Antrectomy with gastrojejunal anastamosis
What is a trichobezoar? Treatment?
Hair, hard to pull out; EGD inadequate, likely need gastrostomy and removal
What is a phytobezoar? Treatment?
Fiber, often in diabetics with poor gastric emptying; enzymes, EGD, diet changes
What is Dieulafoy’s ulcer?
Vascular malformation
What is Menetrier’s disease?
Mucous cell hyperplasia, increased rugal folds
Gastric volvulus is associated with what condition?
Type II hernia
Symptoms of gastric volvulus? Treatment?
Nausea without vomiting, severe pain; usually organoaxial volvulus; reduction and Nissen
What is a Mallory-Weiss tear? Presentation?
Secondary to forceful vomiting; hematemesis following severe retching
Diagnosis of Mallory-Weiss? Treatment?
EGD; tear usually near lesser curve of stomach, PPE, transfusion; if continued bleeding, may need gastrostomy and oversewing of the vessel
Effects of all forms of vagal denervation?
Increased liquid emptying; vagally mediated receptive relaxation is removed; results in increased gastric pressure that accelerates liquid emptying
Where is the denervation in truncal vagotomy? Effect on solid emptying?
Divides vagal trunks at level of esophagus; decreased emptying of solids
Where is the level of denervation in selective vagotomy? Effect on solid emptying?
Divides nerves of Latarjet; decreased emptying of solids
Where is the level of denervation in highly-selective vagotomy? Effect on solid emptying?
Divides individual fibers, preserves “crow’s foot”; normal emptying of solids
What are the gastric effects of truncal vagotomy?
Dec. acid output by 90%, increased gastrin, gastrin cell hyperplasia
What are the nongastric effects of truncal vagotomy?
Decreased exocrine pancreas function, decreased postprandial bile flow, increased gallbladder volumes, decreased release of vagally mediated hormones
What is the most common problem following vagotomy?
Diarrhea (30-50%), caused by sustained MMCs forcing bile acids into colon
Risk factors for upper GI bleed?
Previous UGI bleed, PUD, NSAIDs, smoking, liver disease, esophageal varices, splenic v thrombosis, sepsis, burn injuries, trauma, severe vomiting
Treatment for UGI bleed?
1st EGD; can potentially treat if due to bleeding ulcer; if pt hypotensive despite resuscitation, go to OR
Risk factors for rebleeding at time of EGD?
1 spurting blood vessel (60%), #2 visible blood vessel (40%), #3 diffuse oozing (30%)
Likely source of UGI bleed in liver failure patient? Treatment?
Bleeding from esophageal varices; EGD with sclerotherapy, TIPS, not OR
What is the cause of duodenal ulcers?
Increased acid production, decreased host defense
Most common location of duodenal ulcers?
1st part of duodenum, usually anterior
Most common presentation of anterior duodenal ulcers? Posterior?
Anterior: perforation, posterior: bleed
Treatment of duodenal ulcers?
H2 blockers, PPI, triple therapy for pts with H. pylori
Surgical indications for duodenal ulcer?
Perforation, protracted bleeding despite EGD therapy, obstruction, intractability despite medical therapy, inability to r/o cancer
Surgical options for duodenal ulcers?
Truncal vagotomy and pyloroplasty, truncal vagotomy and antrectomy with BI or BII
Ulcer surgery with lowest rate of recurrence?
Truncal vagotomy and antrectomy with BI/BII
Ulcer surgery with lowest rate of complications?
Proximal or highly selective vagotomy
What is the most frequent complication of duodenal ulcers?
Bleeding
Surgical options for bleeding duodenal ulcer?
Duodenostomy and GDA ligation (careful to avoid CBD), if pt was on PPI, needs surgical ulcer procedure
What is the initial treatment of choice for obstruction secondary to duodenal ulcers?
Serial dilation