Gastric Secretions Flashcards
What is the enzyme that H pylori bacteria secrete that allow them to survive in the acidic environment of the stomach? What is the toxin they secrete?
Urease
Cytoxin = VacA
What are the cell types in the gastric pits?
Parietal cell
Chief cells
What do chief cells produce?
Pepsinogen
What do parietal cells secrete? Function?
HCl
Protein digestion, sterilization, nutrient absorption
What cells secrete intrinsic factor? Function?
Parietal cells
Vit B12 absorption
What cells secrete pepsinogen? Function?
Chief cells
Protein digestion
What cells secrete mucus and bicarb in the stomach?
Superficial epithelial cells
What cells produce histamine in the stomach? Function?
ECL cells
Promotes HCl production
What cells produce gastrin? Function?
G cells
Promotes HCl secretion
What cells produce Ach in the stomach? Function?
Nerve cells
Promotes mucus, bicarb, and HCl secretion
What cells produce somatostatin in the stomach? Function?
D cell
Suppresses HCl secretion
Are there any parietal cells in the cardia portion of the stomach? What is the function of this?
No, protects esophagus
What are the four cell types in the body of the stomach?
- Parietal cells
- Chief cells
- Neck cells
- Enterochromaffin cells (ECL)
What are the three cell types in the antrum of the stomach?
- Chief cells
- G cells
- D cells
What are the two fundamental types of secretion in the stomach? What cells produce each? What happens with increased stimulation of the stomach to the activity of each?
Na rich secretion from non-parietal cells–these decrease with increased stimulation of the stomach
H rich from parietal cells–these increase with stimulation of the stomach
What is the pump and enzyme utilized to make HCl?
H-K ATPase (proton pump)
Carbonic anhydrase
How large is the vesicular supply of proton pumps (relatively)?
Super large
What are the three pathways that acid secretion is stimulated through? Transmitter for each?
Paracrine (histamine)
Endocrine (gastrin)
Neuronal (Ach)
What is the effect of the low pH on bile and pancreatic enzyme flow?
increases
What are the receptors on the parietal cells for that regulate acid secretion?
Muscarinic (Ach)
H2 receptor (G protein)
Gastrin receptor
What are the two indirect pathways that acid secretion is regulated through?
Endocrine (gastrin, somatostatin)
Neuronal (Ach)
What are the cells that sense amino acids in the stomach? What does this cell type secrete? What does this cause?
G cells
Gastrin
Increases HCl secretion
What are the cells that sense low pH in the stomach? What does this cell secrete?
D cell
Somatostatin to reduce acid secretion
What is the protein that binds B12 in the intestine?
Intrinsic factor
Damage to the parietal cells will cause what two things?
Lower Vit B12 absorption
Increased pH of the stomach
What are the primary cells that secrete pepsinogen? What is the key neurotransmitter that stimulates pepsinogen release?
Chief cells
Ach (but others as well)
What cleaves pepsinogen to pepsin? How does the activity of pepsinogen change in response to lower/higher pHs?
HCl
Lower pH generally better and v.v.
What is the function of pepsin?
Destroys proteins (protease)
What are the protective factors against HCl and pepsin? (2)
Mucus (Mucin, phospholipids, electrolytes, water)
Bicarb
What is the pH near the epithelial cell layer of the stomach? How?
High d/t bicarb and mucus secretions
What is the neurocrine regulator of protective factor secretion? Paracrine? What does each do?
Neurocrine = Ach (promotes mucus and bicarb secretion) Paracrine = prostaglandins (ditto above, and suppress acid secretion)
What are the roles of prostaglandins in the stomach?
- Mucus and bicarb secretion
- Suppression of HCl secretion
- Increased gastric flow
What is gastritis?
Inflammation of the gastric lining
What is the MOA of increased number of parietal cells causing acid-peptic disease?
Increase HCl secretion
What is the MOA of high serum gastrin levels causing acid-peptic disease?
Increases acid secretion
What is the MOA of a loss of acid-mediated negative feedback on gastrin secretion causing acid-peptic disease?
Increases acid secretion
What is the MOA of Rapid gastric empyting causing acid-peptic disease?
Too fast = not enough time to buffer
What is the MOA of H.Pylori infx causing acid-peptic disease?
Releases toxin and immune response
What is the MOA of NSAID use causing acid-peptic disease?
Inhibits PGE2, causing H2 receptor to be uninhibited
What are the degradation products of urea?
Bicarb
Ammonium ion
What causes the damage seen in H.pylori infx?
Inflammatory response to the H.Pylori colonization
What is the enzyme that NSAIDs inhibit that reduce prostaglandin synthesis?
COX1/2
What is the MOA of H2 inhibitors?
Blocks histamine, thereby decreasing HCl secretion
What is the MOA of pepto bismol (bismuth salts)?
Substitute for the mucus
Where do the Histamine and PGE2 receptors on the parietal cell converge? What is the consequence of this?
On the G protein receptors
Have opposite effects (PGE2 inhibits)
What are the histamine producing cells of the stomach? What neurotransmitters do these respond to?
ECL cells
Respond to ACh, and gastrin
Gastrin and ACh have both indirect and direct effects on HCl release. How?
Direct = receptors on parietal cells
Indirect = receptors on ECL cells that produce histamine (which also increases HCl production)
How do the gastric pits secrete acid to ensure that not all of the H+ ions secreted are buffered by the mucus/bicarb layer?
Contractile squirting into the lumen of the stomach
What are the three key roles of PGE2 production?
- Mucus and bicarb secretion
- Suppression of HCl
- Increased gastric blood flow
Why are PPIs chosen over H2 receptor antagonists?
Because PPIs regulate at the common pathway for all three ACh, H2, and Gastrin, thus hit three acid secreting receptors instead of just one
What is the secretion that non-parietal cells secrete at a basal level? What happens to this as the secretory rate of the stomach increases?
Na-rich secretion, which decreases with increased stimulation of the stomach
What are the four phases of acid secretions?
- Interdigestive phase
- Cephalic phase
- Gastric phase
- Intestinal phase
What is the interdigestive phase of gastric acid secretion?
Between digesting times, low acid secretion
What is the cephalic phase of gastric acid secretion?
This phase is activated by stimuli such as the sight or smell of food, which increases gastric acid secretion
What is the gastric phase of acid secretion?
Vagal stimulation to increase acid in response to distension/protein products of the stomach
What are the cells in the stomach that ensure that pH does not get too low? What chemical do they produce, and what is its effect?
D cells, which will secrete somatostatin to reduce gastric secretion
What is the intestinal phase of acid secretion?
Presence of peptides in the duodenum increases acid secretion via the release of gastrin from G cells
What cells in the duodenum sense the presence of protein? What do they secrete?
G cells– gastrin to increase the rate of acid secretion.
What cells produce IF?
Parietal cells
What cells produce the mucus lining of the stomach? Where in the stomach are these found?
Epithelial cells–everywhere
What are the two key neurotransmitters that stimulate epithelial and neck cells to produce mucus and HCO3 in the stomach?
ACh and Prostaglandins
A break in the protective mucosal lining of the lower esophagus, stomach, or duodenum = ?
Peptic ulcer
What ulcer occurs with the greatest frequency?
Duodenal ulcers
Peptic ulcer caused by illness, systemic trauma, neuronal injury, emotions = ?
Stress ulcer
What is a stress ulcer associated with head trauma or brain surgery?
Cushing ulcer
What are ulcers caused by hemorrhage, multi-system trauma, severe burns, heart failure, or sepsis?
Ischemic ulcers
What is Zollinger-Ellison syndrome?
gastrin-secreting tumor of the pancreas that stimulates the acid-secreting cells of the stomach (parietal cells) to maximal activity, with consequent gastrointestinal mucosal ulceration. ZES may occur sporadically or as part of an autosomal dominant familial syndrome called multiple endocrine neoplasia type 1 (MEN 1)
