The correct answer is D. Gastric acid is produced by parietal cells located in the gastric fundus. Acid production is regulated neurally (vagus nerve) and chemically via hormones and paracrines.
- Gastrin, acetylcholine (ACh), and histamine all increase secretion rates.
- Prostaglandin E2, somatostatin, secretin, and glucose-dependent insulinotropic polypeptide (GIP, also known as gastric inhibitory peptide) all decrease secretion rates.
The factors that decrease parietal cell activity are all products of the duodenum, and their release normally provides a negative feedback pathway that protects the duodenal mucosa and digestive enzyme function from being overwhelmed by gastric acid entering via the pyloric sphincter. Thus, duodenal resection and loss of these feedback pathways will increase gastric acid production.
Pancreatic lipases and bile salts are required for digestion and absorption of lipids. Since cholecystokinin (CCK) stimulates the release of both enzymes and bile, lipid absorption rates will be decreased, not increased, following surgery (choice A).
CCK is a product of I cells located in the duodenum and jejunum and is released in response to the presence of fatty acids and amino acids in the small intestine. CCK secretion will thus be decreased, not increased (choice B), following duodenal resection.
CCK has three principal functions. It stimulates digestive enzyme release by the pancreas, it facilitates bile release by stimulating gallbladder contraction and by promoting sphincter of Oddi relaxation, and it delays gastric emptying to allow time for digestive enzymes to degrade nutrients arriving via the pyloric sphincter. Duodenal resection will, therefore, decrease rather than increase the stimulus for gallbladder contraction (choice C).
Secretin is produced by S cells that localize to the small intestine, so duodenal resection will decrease, not increase net secretin secretion (choice E). Secretin normally stimulates bicarbonate release from the pancreas when duodenal pH is lowered, or when fatty acids are present. Secretin also decreases acid production by parietal cells through suppression of gastrin release and stimulation of somatostatin release from D cells in the duodenum and stomach.
This is a multi-step question.
What is the question asking?
This question is asking us to identify a physiologic effect of duodenal resection.
What is the first step?
The first step is to recognize the role of the duodenum. The duodenum is responsible for the breakdown of many macromolecules and coordinating the release of appropriate enzymes for digestion. It does this through the secretion of hormones such as cholecystokinin, secretin, somatostatin, prostaglandin E2, and glucose-dependent insulinotropic polypeptide (GIP, also known as gastric inhibitory peptide).
What is the next step?
The next step is identifying which of the answer choices will be increased by the loss of the hormones produced by the duodenum. Many duodenal hormones (secretin, somatostatin, prostaglandin E2, and GIP) participate in the duodenal negative feedback on stomach acid by decreasing acid secretion from parietal cells. Duodenal resection will decrease levels of these hormones, which will increase gastric acid secretion (choice D).
Can other answers be eliminated?
The other answer choices would be decreased (not increased) in a patient who has undergone duodenal resection:
- Cholecystokinin (CCK) is released by I cells in the duodenum and jejunum. Its functions include bile salt by causing contraction of the gallbladder and the release of pancreatic lipases. Both of these aid lipid digestion and absorption. Thus, duodenal resection will decrease CCK secretion (choice B) and gallbladder contraction (choice C) which decreases absorption of lipids (choice A).
- Secretin is produced by S cells in the duodenum, therefore duodenal resection will decrease secretin secretion (choice E).
What is the single best answer and why?
The single best answer is gastric acid secretion (choice D) because the duodenum normally provides negative feedback to gastric acid secretion. The loss of this feedback will increase gastric acid production.
MedEssentials (4th Ed.): pp. 346
First Aid (2019): pp. 365.1
First Aid (2018): pp. 365.1
First Aid (2017): pp. 356.1
