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)
Which enzyme allows H. Pylori to survive the acidic environment of the stomach?
A) Protease
B) Urease
C) Lactase
D) Amylase
Urease
The exocrine pancreas comprises ___% of the pancreas.
90%
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
What is the innervation of the exocrine pancreas?
SNS: celiac and superior mesenteric plexuses
PNS: vagus nerve
The enzymes secreted by the pancreas are synthesized where?
On the rough ER of acinar cells- after synthesis they transfer to the golgi, proteases store as zymogens
The aqueous component of pancreatic secretions is produced where?
Centroacinar cells and ductal cells make the initial secretion, then modified by transport processes in ductal cells
What are the cephalic and gastric phases of pancreatic secretion initiated by?
Cephalic- initiated by smell, taste, conditioning (Vagus nerve)
Gastric- initiated by distention of stomach (vagus nerve)
Why is bile needed in the GIT?
needed for digestion and absorption of lipids
Lipids are insoluble in water
Why are bile salts an important component of bile?
Bile salts are emulsify lipids for digestion, solubilize products into micelles for absorption
CCK stimulates the contraction of what organ?
The gallbladder
Which ion varies with the flow rate of pancreatic juice?
A) Na+
B) Cl-
C) K+
D) H+
Cl-
Bile salts are amphipathic- what does this mean?
They have hydrophobic and hydrophilic ends, binds with lipids then they can dissolve in water
Bilirubin is the product of what?
Product of hemoglobin degradation
