Gastrointestinal physiology acid production Flashcards
(20 cards)
What is the main function of parietal cells in the stomach, and how do they accomplish it?
Parietal cells are specialized epithelial cells in the stomach that secrete hydrochloric acid (HCl). They accomplish this using the proton pump (H⁺/K⁺ ATPase) located on their apical membrane. This pump uses ATP to actively transport hydrogen ions into the stomach lumen in exchange for potassium ions, contributing to the highly acidic gastric environment.
Which three stimulatory pathways increase gastric acid secretion, and what receptors are involved?
The three main stimulatory pathways are:
Acetylcholine from the enteric and parasympathetic nervous systems, acting on M3 muscarinic receptors (Gq-coupled).
Histamine from ECL cells, acting on H2 receptors (Gs-coupled).
Gastrin from G cells, acting on CCKB receptors (Gq-coupled).
All these pathways enhance proton pump activity through increased intracellular calcium or cyclic AMP.
How do somatostatin and prostaglandins inhibit gastric acid secretion?
Both somatostatin (from D cells) and prostaglandins inhibit gastric acid secretion by binding to Gi-coupled receptors on parietal cells. This inhibits adenylate cyclase activity, leading to reduced cyclic AMP levels and decreased proton pump activity, thus lowering acid secretion.
Why can chronic NSAID use lead to stomach ulcers?
Chronic NSAID use inhibits cyclooxygenase (COX) enzymes, which are needed to produce prostaglandins. Since prostaglandins normally inhibit gastric acid secretion and help maintain the protective mucosal layer, their reduction can lead to excessive acid production and mucosal damage, increasing the risk of stomach ulcers.
What are the pharmacological strategies used to reduce gastric acid secretion, and how do they work?
Pharmacological strategies include:
Proton Pump Inhibitors (e.g., omeprazole): Directly inhibit the H⁺/K⁺ ATPase pump.
H2 Receptor Antagonists (e.g., cimetidine): Block histamine from binding to H2 receptors.
Anticholinergics (e.g., atropine): Block acetylcholine at M3 receptors.
Each of these drugs reduces stimulation of the proton pump, lowering acid secretion.
What protects the gastric mucosa from the acidic environment of the stomach?
A mucosal surface layer with a near-neutral pH (~7) protects the underlying gastric mucosa from the highly acidic gastric contents (pH ~1.2).
What is the role of the proton pump in parietal cells?
The proton pump (H⁺/K⁺ ATPase) moves hydrogen ions into the stomach lumen in exchange for potassium ions, a key step in producing hydrochloric acid.
Which ions are secreted by parietal cells to form hydrochloric acid?
Hydrogen (H⁺) and chloride (Cl⁻) ions are secreted separately and combine in the stomach lumen to form hydrochloric acid (HCl).
How does acetylcholine stimulate parietal cells?
Acetylcholine binds to M3 muscarinic receptors on parietal cells, which are Gq-coupled, leading to increased intracellular calcium and enhanced proton pump activity.
What is the function of enterochromaffin-like (ECL) cells?
ECL cells secrete histamine, which binds to H2 receptors on parietal cells to stimulate acid secretion.
What type of receptor does histamine bind to in parietal cells, and what is its effect?
Histamine binds to H2 receptors (Gs-coupled) on parietal cells, increasing cyclic AMP and stimulating the proton pump.
What stimulates the release of gastrin, and what cells release it?
G cells release gastrin in response to the presence of food in the stomach.
What receptor does gastrin bind to on parietal cells?
Gastrin binds to the CCKB receptor, which is Gq-coupled, leading to increased calcium and proton pump activity.
How does somatostatin inhibit acid secretion?
Somatostatin binds to Gi-coupled receptors on parietal cells, inhibiting adenylate cyclase, decreasing cyclic AMP, and reducing proton pump activity.
What enzyme do NSAIDs inhibit, and what is the consequence in the stomach?
NSAIDs inhibit cyclooxygenase (COX) enzymes, reducing prostaglandin production, which normally inhibits acid secretion—leading to increased acid and risk of ulcers.
Why don’t common antihistamines like loratadine affect stomach acid secretion?
Because they block H1 receptors (involved in allergic responses), not H2 receptors, which mediate acid secretion in the stomach.
How do prostaglandins suppress acid secretion in the stomach?
They bind to Gi-coupled receptors on parietal cells, reducing cyclic AMP and decreasing proton pump activity.
What are the two sources of acetylcholine that stimulate parietal cells?
Acetylcholine is released by the enteric nervous system (submucosal plexus) and the parasympathetic nervous system.
How does the submucosal plexus contribute to acid secretion during the gastric phase?
It detects stretch and pH changes, signaling via acetylcholine to stimulate parietal cells and ECL cells.
Name three drug classes that inhibit gastric acid secretion and their mechanisms.
Proton Pump Inhibitors – directly block H⁺/K⁺ ATPase.
H2 Receptor Antagonists – block histamine’s effect on H2 receptors.
Anticholinergics – block acetylcholine from binding to M3 receptors.
