Lecture 5: Gastric, Pancreatic, Bile Secretions Flashcards
What are the direct paths of vagal stimulation?
Vagus nerve -> Parietal cells -> ACh -> HCl
Vagus nerve -> GRP -> G Cells
What are the indirect paths of vagal stimulation
Rest of G cell path
Gastrin from G cells -> Systemic circulation -> HCl from parietal cells
Which pathway will atropine block?
Vagus nerve -> Parietal cells -> ACh -> HCl
Why will atrophne not block HCl secretion completely?
Only affecting 1 of 3 pathways
Name the phases of gastric HCl secretion
Cephalic, gastric, intestinal
Which phase accounts for 30% of total HCl?
Cephalic
Which phase accounts for 60% of total HCl?
Gastric
Which phase accounts for 10% of total HCl?
Intestinal
What are stimuli for the cephalic phase?
Smelling, tasting, chewing, swallowing, conditioned reflexes
What are the mechanisms to promote HCl secretion in the cephalic phase?
Direct stimulation of parietal cells by vagus nerve
Indirect stimulation via gastrin
What are the stimuli for the gastric phase?
Distention of stomach and presence of AA and peptides
What are the mechanisms to promote HCl secretion in gastric phase?
- Distention -> Vagal nerve stimulation -> Parietal cells
- Indirect via gastrin
- Distention of antrum -> Local reflexes -> Gastrin release
- AA + Peptides -> G cells -> Gastrin
What is the intestinal phase stimulated by?
Products of protein digestion
What is the intestinal phase stimulated by?
Products of protein digestion
When is HCl secretion inhibited (why is it no longer needed)
No longer needed for conversion of pepsinogen to pepsin
Decreased what of gastric contents inhibits HCl secretion?
pH
How does somatostatin directly inhibit HCl secretion?
Binds parietal cells and antagonizes histamine pathway by decreasing cAMP
How does somatostatin indirectly inhibit HCl secretion?
Inhibits both histamine and gastrin release
How do prostaglandins antagonize histamine in the inhibition of HCl secretion?
Reducing cAMP
What are the barriers to acid and pepsin damage to gastric mucosa?
Bicarbonate and mucus
What is peptic ulcer disease?
Ulcerative lesion of gastric or duodenal mucosa
Name the causes of peptic ulcer disease
Could be 1 or both:
Loss of mucus
Excessive H+ and pepsin secretion
Why do gastric ulcers form?
Because mucosal barrier is defective, so H+ and pepsin digest mucosa
Why do duodenal ulcers form?
Occur when H+ secretory rate higher than normal, overwhelm buffering capacity of pancreas
What is the SNS innervation of the exocrine pancreas?
Celiac and superior mesenteric plexuses
What is the PNS innervation of the exocrine pancreas?
Vagal nerve
What effect does PSNS stimulation have on exocrine pancreas?
Stimulates secretion
What effect does SNS stimulation have on exocrine pancreas?
Inhibits secretions
Name the two components of pancreatic secretions
Enzymatic component
Aqueous component
What is the enzymatic component of pancreatic secretions responsible for digesting?
Carbs, proteins, lipids
Where are the enzymes of pancreatic secretion synthesized?
Rough ER of acinar cells
Where are the enzymes of pancreatic secretion stored?
On zymogens
What form are amylase and lipases secreted by pancreas?
Active
What form are proteases secreted by pancreas?
Inactive (known as zymogens)