Lecture 49: Gastric, Pancreatic, & Bile Secretions Flashcards
What are the two paths of vagal stimulation?
- Vagus nerve to acetylcholine to parietal cells to HCl
- Vagus nerve to GRP to G cells
What is the indirect path of vagal stimulation (rest G cell path)?
Gastrin from G cells to systemic circulation to HCl from parietal cells
Why does atropine not block HCl secretion completely?
Only affects one small path
(atropine binds to muscarinic receptors)
What are the three phases of HCl secretion? What percentages of total HCl are secreted in each phase?
Cephalic phase- 30%
Gastric phase- 60%
Intestinal phase- 10%
What are the stimuli of the cephalic phase of HCl secretion?
Smelling, tasting, chewing, swallowing, conditioned reflexes
What are the stimuli of the gastric phase of HCl secretion?
Distension of the stomach and presence of AA peptides
What are the four mechanisms to promote HCl secretion in the gastric phase?
Distension- vagal stimulation
Indirect via gastrin
Distension of antrom to local reflexes to gastrin
Amino aids and peptides to gastrin
What is the stimulus of the intestinal phase of HCl secretion?
Stimulated by products of protein digestion
When does HCl need to be inhibited?
Inhibited when it is no longer needed for conversion of pepsinogen to pepsin (you need a low pH for conversion)
What are the three triggers of HCl inhibition?
1) Decreased pH of gastric contents (pH drops low when food enters the stomach, but food acts as a buffer, when food leaves the stomach the pH will drop again and this is when HCl secretion starts to be inhibited)
2) Somatostatin
Directly- binds parietal cells and antagonizes histamine pathway by decreasing cAMP
Indirectly- Inhibits both histamine and gastrin release
3) Prostaglandins antagonize histamine by reducing cAMP
What are the two barriers to acid and pepsin damage to gastric mucosa? How do these two prevent damage?
1) Bicarbonate- gastric epithelial cells and mucus neck cells secrete bicarb, the bicarb gets trapped in the mucus, acid is neutralized and pepsin will be deactivated
2) Mucus- mucus forms a barrier between the cells and lumen contents
What is peptic ulcer disease? What causes it?
Ulcerative lesion of gastric or duodenal mucosa
Caused by loss of mucus, have excessive H+ and pepsin secretion, or a combination of both (H. Pylori overgrowth and stress are other damaging factors)
Why do gastric ulcers form?
form because the mucosal barrier is defective
How does H. Pylori cause gastric ulcers (what is the mechanism)?
H. Pylori colonizes gastric mucus and attaches to epithelial cells, releases cytotoxins that break down the mucus barrier and epithelial cells
It survives in the acidic environment because it has the urease enzyme (converts urea to ammonia, which increases the pH of the local environment, binds cells instead of being shed)
What causes duodenal ulcers and Zollinger-Ellison syndrome (Gastrinoma)?
- Duodenal ulcers: occur when H+ secretory rate is higher than normal
- Zollinger-Ellison Syndrome: high rates of H+ secretion due to high gastrin, delivery of high H+ to duodenum, causes steatorrhea (low pH in SI inactivates lipases, so no fat digestion= fat in poop)
What is the structure of the exocrine glands of the pancreas?
Acinus liked with acinar cells (secrete enzymes)
Ducts lined with ductal cells
Centroacinar cells
