Gastric, Pancreatic, & Bile Secretions Flashcards
Trace the direct path of vagal stimulation for HCl secretion. (2 pathways)
vagus nerve —> Ach —> parietal cells —> HCl
vagus nerve —> GRP —> G cells (first part)
Trace the indirect path of vagal stimulation for HCl secretion.
gastrin from G cells —> systemic circulation —> HCl from parietal cells (rest of pathway)
Why won’t atropine block HCl secretion completely?
you have GRP in the G cell path
T/F: The cephalic phase is the primary phase of HCl secretion at 60%
FALSE - only 30%
What are the stimuli for the cephalic phase in HCl secretion?
smelling, tasting, chewing, swallowing, conditioned reflexes
What are 2 mechanisms in the cephalic phase that promote HCl secretion?
- direct stimulation by vagus n - Ach
- indirect via gastrin
What are the stimuli for the gastric phase in HCl secretion?
distention of stomach and presence of aa and peptides (PROTEIN)
What are the 4 mechanisms in the gastric phase that promote HCl secretion?
- distention - vagal stimulation
- indirect via gastrin
- distention of antrum - local reflexes of gastrin
- amino acids and peptides - gastrin
What are the phases in HCl secretion?
cephalic
gastric
intestinal
What is the stimuli for the intestinal phase?
products of protein digestion
What inhibits HCl secretion?
decreased pH of gastric contents
somatostatin - directly and indirectly
prostaglandins
How does somatostatin DIRECTLY inhibit HCl secretion?
binds parietal cells
antagonizes histamine pathway by decreasing cAMP
How does somatostatin INDIRECTLY inhibit HCl secretion?
inhibits both histamine and gastrin release
What helps prohibit acid and pepsin damage to gastric mucosa?
bicarbonate
mucus
How does HCO3 help inhibit gastric mucosa damage?
gastric epithelial cells and neck cells that secrete HCO3- get trapped in mucus
acid is then neutralized
pepsin deactivated
What is peptic ulcer disease caused by?
loss of mucus
excessive H+ and pepsin secretion
combination of both factors
Peptic ulcer disease is classified as either
gastric or duodenal ulcers
Why do gastric ulcers occur?
mucosal barrier is defective - H+ ions and pepsin digest mucosa
What is one cause of gastric ulcers? (Hint: colonizes)
H. pylori colonizes gastric mucus and attaches to epithelial cells
releases cytotoxins
Why does H. pylori survive in acidic environments?
converts urea to ammonia which increases pH of local environment
binds cells inside of being shed
Why do duodenal ulcers occur?
when H+ secretory rate is higher than normal
overwhelming buffering capacity
What is Zollinger-Ellison syndrome?
high rates of H+ secretion due to high gastrin
delivery of H+ to duodenum
causes steatorrhea
Why does steatorrhea occur in Zollinger-Ellison syndrome?
low pH in the small intestine inactivates lipases, so there is no fat digestion
T/F: The exocrine pancreas comprises 90% of the pancreas
TRUE
The exocrine pancreas has ______ and _______ components
aqueous
enzymatic
There is a high amount of _____ to neutralize acid in the pancreas
HCO3-
The enzymatic components of the exocrine pancreas digest what
digest carbohydrates, proteins, and fat