Lec 3 Flashcards
During what stages of digestion is acid secreted?
cephalic, gastric, and intestinal phases
Where are chief and parietal cells located in gastric fundic gland?
- chief cells near base
- parietal cells in middle below mucous neck cells
What substances are secreted by gastric fundic gland mucosa?
HCl
Pepsinogen
Intrinsic Factor
What is the function of the stomach?
- mechanical churning
- initiate protein/fat digestion
- produce intrinsic factor for vit B12 absorption
What does “the stomach as two organs” mean?
1st organ = secretes stuff = fundus and body + cardia
2nd organ = antrum = mixes and grinds
What is motilin?
hormone made in duodenum
binds receptors on smooth muscle throughout gut and pro-motility
–> increases phase III contractions of migrating motor complex [MMC]
What is effect of erythromycin on GI?
motilin agonist –> increase contraction of bowel
What do stretch receptors on stomach act on?
- increase secretion of gastrin by G cells
- increase secretion of acid/pepsin
- activate vagus
Where is histamine released from?
ECL cells in gastric fundus
What is action of histamine in GI?
- binds H2 receptors on parietal cells
- stimulates parietal to secrete HCl
What causes histamine to be released by ECL cells?
- ACh and gastrin
What is gastrin?
a hormone released by G cells in the antrum –> goes through bloodstream to reach parietal cells in stomach fundus
What is action of gastrin?
binds gastrin receptors [CCK-b} on parietal cells
stimulates parietal to secrete HCl
Where is gastrin released from?
G cells in gastric antrum
What is action of ACh in stomach?
released by vagus nerve and binds muscarinic M3 receptors on parietal cell
stimulates parietal cell to secrete acid
also stimulates ECL cell to release histamine
What causes parietal cell to release HCl?
- ACh from vagus
- gastrin from G cells
- histamine from ECL cells
- stretch
What are 2 effects of ACh on stomach?
- stimulates parietal cells to release acid
- stimulates ECL to release histamine
What cells release somatostatin?
D cells in the antrum
When is somatostatin released?
D cells sense low pH –> causes them to release somatostatin
What is action of somatostatin?
- acts on G cells to inhibit gastrin release
- inhibits ECL cells and parietal cells directy
Where is pepsinogen released from?
chief cells in the fundus
gets converted to pepsin in the acidic stomach
How does acid get into the lumen of stomach?
in exchange for K through the H-K ATPase pump
What makes up the mucus-bicarbonate barrier of stomach? What induces their secretion?
- mucus secreted by surface epithelium
- bicarbonate is within the mucus
their secretion is stimulated by prostaglandins
What causes duodenal ulcers?
hypersecretion of acid
What causes gastric ulcers?
disurption of mucus barriers [by NSAIDS, aspirin, etc]
What are some things that cause peptic ulcer disease?
- H pylori
- NSAIDS, aspirin
- stress [due to ischemia]
- gastrinoma
cigarettes and alcohol may aggravate but are not independent risk factors
Where does h pylori infect?
only colonizes gastric-type epithelium [not intestinal or squamous]
WHat is use of h pylori urease?
protects the h pylori from the acid in gastric lumen
What is the H pylori toxin that causes peptic ulcers?
CagA
How are some common complications of h pylori?
- gastritis
- peptic ulcer
- associated w/ gastric adenocarcinoma and lymphoma
What are x mech of action by which H pylori injures the mucosa?
- directly releases cytokines on epithelial cells
- disrupts mucous layer by production of proteases
- stimulates host pro-inflammatory cytokines
- inhibits somatostatin by antral D cells –> thus more gastrin –> acid hypersecretion
What is presentation of peptic ulcer disease?
- pain [may be relieve by food, may bore into back]
- bleeding [melena, hematemesis]
- gastric outlet obstruction
- perforation
- penetration
What is most common cause of acute infectious gastritis?
h pylori
What causes non-infectious acute gastritis?
aspirin, NSAIDS
severe physical stress, radiation
How do NSAIDS cause gastritis?
inhibit mucosal prostaglandin synthesis
How does esophagus protect itself from acid?
LES excludes acid/pepsin from refluxing; esophageal motility keeps contents moving distally
How does duodenum protect itself from acid?
neutralizes acid/pepsin with duodenal/pancreatic/biliary bicarbonate
What are 3 basic types of treatment for peptic ulcer disease?
- remove inciting agent
- medication
- surgery
What medications are used for peptic ulcer disease?
- antacids to neutralize acid
- PPIs and H2 blcoekrs to block acid production
- enhance prostaglandin production [sucralfate]
How does a highly selective vagotomy work?
- eliminate cholinergic stimulus to parietal cells
How does an antrectomy work?
remove gastrin-producing area and the are most susceptible to ulcer
anatomosis either by Billroth I or Billroth II
How does a subtotal gastrectomy work?
remove antrum and most of the body to the stomach; eliminates gastrin secretion and most of the parietal cells
What is difference Billroth I and Billroth II?
Billroth I = hook up the duodenum to the fundus of the stomach; only works if top of duodenum is in good shape
Billroth II = hook up the middle of the duodenum to the fundus of the stomach; leaves the top of the duodenum but its kind of off to the side
What happens if you leave some of the antrum during billroth surgery?
you will have G cells there making gastrin but they are no longer in contact with the lumen so don’t get turned off by low acid
its like having a gastrinoma –> get hypersecretion of acid.
What are major causes of hypergastrinemia?
- insufficient amount of luminal acid [due to destruction of parietal cells in pernicious anemia OR use of PPIs/H2 blockers]
- overproduction of gastrin [antral G hyperplasia, retained antrum]
- ectopic production of gastrin [gastrinoma]
What is pernicious anemia?
autoimmune destruction of parietal cells leads to loss of acid secretion
anti parietal cell and anti IF antibodies
What is zollinger-ellison?
gastrin producing neuroendocrinetumor n pancrea or duodenal wall
autonomously produces gastrin –> acid hypersecretion by parietal cells
