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Questions and Answers
What primarily determines the rate of gastric emptying?
Which factor is NOT associated with gastric emptying?
Which substance is particularly potent in delaying gastric emptying?
What is the role of enterogastrones released from the duodenum?
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What occurs when the duodenum is not ready to receive chyme?
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What is the role of H+/K+ ATPase in parietal cells?
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Which neurotransmitter is released by parasympathetic cholinergic neurons to stimulate parietal cells?
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How does gastrin affect parietal cells?
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What is the source of histamine in the gastric glands?
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Which cellular process occurs when parietal cells are stimulated?
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Which factor does NOT stimulate histamine secretion?
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What mechanism initiates the transport of H+ into the gastric lumen by parietal cells?
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What effect does the activation of PLC have on parietal cells?
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What area of the stomach is primarily responsible for producing hydrochloric acid?
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What is the role of pepsinogen in the stomach?
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Which cell type in the gastric glands is primarily responsible for producing gastrin?
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What function does hydrochloric acid (HCl) serve in the gastric secretions?
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Identifying the components of gastric mucosa, which area includes the chief cells?
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The pyloric gland area is specifically located in which part of the stomach?
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What does somatostatin do in the context of gastric secretions?
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Which of the following is NOT a component of the gastric mucosa?
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What is the role of the vagus nerve in gastric function?
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How does gastrin affect parietal cells?
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Which of the following mechanisms does NOT contribute to the stimulation of parietal cells?
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What triggers the activation of enteric neurones through mechanoceptors?
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Which neurotransmitter is directly released by enteric neurones to stimulate parietal cells?
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What is the function of somatostatin in this context?
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How does the presence of food affect gastric phase activity?
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Which cell is primarily responsible for the release of histamine in the stomach?
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Which aspect is NOT directly related to the gastric phase of digestion?
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What is the role of GRP in gastric function?
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What is the primary function of HCO3- in the duodenum?
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Which transporter is responsible for HCO3- secretion at the basolateral membrane of pancreatic duct cells?
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What is a possible consequence of cystic fibrosis concerning pancreatic duct cells?
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What role does Cl- play in HCO3- secretion at the apical membrane?
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What is the effect of HCO3- on pancreatic enzyme function?
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At what secretion rates is the HCO3- content highest?
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Which mechanism describes the entry of Na+ into pancreatic duct cells?
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What happens to H2CO3 in the pancreatic duct cells?
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Study Notes
Parietal Cell Stimulation and HCl Secretion
- The parietal cell is stimulated by three main mechanisms:
- Acetylcholine (ACh) released from parasympathetic cholinergic neurons binds to muscarinic (M3) receptors on parietal cells, leading to the activation of phospholipase C (PLC).
- Gastrin released from G cells binds to CCK2 receptors on parietal cells, also activating PLC.
- Histamine secreted by enterochromaffin-like (ECL) cells in the gastric glands is stimulated by acetylcholine and locally activates parietal cells.
- When stimulated, the parietal cell transports H+ into the gastric lumen using the H+/K+ ATPase on the apical membrane.
Control of Stomach Emptying
- Gastric emptying is controlled by the strength of the antral wave and the opening of the pyloric sphincter.
- The rate of gastric emptying depends on the volume of chyme in the stomach.
- Distension of the stomach increases motility, due to:
- Stretch of smooth muscle
- Stimulation of intrinsic nerve plexuses
- Increased vagus nerve activity and gastrin release.
- Distension of the stomach increases motility, due to:
- The consistency of chyme influences emptying, with thin liquid chyme being emptied faster.
### Duodenal Factors Affecting Emptying
- The duodenum regulates the rate of emptying by delaying it when not ready to receive chyme.
- This delay is mediated by:
- Enterogastric reflex: Neuronal signals from intrinsic nerve plexuses and the autonomic nervous system (ANS) decrease antral activity.
- Hormonal response: Enterogastrones like cholecystokinin (CCK) released from the duodenum inhibit stomach contraction.
- Stimuli in the duodenum that trigger these responses include:
- Fat: Fat delays gastric emptying to allow time for digestion and absorption in the small intestine.
- Acid: Time is needed for neutralization of gastric acid by pancreatic bicarbonate, crucial for proper function of pancreatic enzymes.
- Hypertonicity: Digestion products of carbohydrates and proteins are osmotically active, drawing water into the small intestine. This can lead to reduced plasma volume and dangerous circulatory disturbances, like 'dumping syndrome'.
- Distension: Duodenal distension also contributes to the control of gastric emptying.
Gastric Mucosa
- The gastric mucosa is divided into two regions:
- Oxyntic gland area (OM): Proximal stomach, including the fundus and body.
- Pyloric gland area (PGA): Distal stomach, also known as the antrum.
- The gastric mucosa is composed of three layers:
- Surface lining: Lines the stomach.
- Pits: Invaginations of the surface lining.
- Glands: At the base of the pits, responsible for secretion.
Gastric Secretions
- Different cell types within the gastric glands produce various secretions:
-
Oxyntic mucosa:
- Parietal cells: Produce HCl, intrinsic factor, and gastroferrin.
- Chief cells: Produce pepsinogen.
-
Pyloric gland area:
- G cells: Produce gastrin.
- D cells: Produce somatostatin.
- Enterochromaffin-like (ECL) cells: Produce histamine.
-
Oxyntic mucosa:
Functions of Gastric Secretions
-
HCl:
- Activates pepsinogen to pepsin.
- Denatures proteins.
- Kills most microorganisms ingested with food.
- Pepsinogen: Inactive precursor of the peptidase, pepsin.
Regulation of Gastric Secretion
- The vagus nerve stimulates enteric neurons, which in turn:
- Release acetylcholine (ACh) directly activating parietal cells (neurotransmitter action).
- Release gastrin-releasing peptide (GRP), leading to the release of gastrin from G cells into the systemic circulation, activating parietal cells (endocrine action).
- Release histamine from ECL cells, locally activating parietal cells (paracrine action).
- Inhibit D cells, reducing the inhibitory effect of somatostatin (SS) on G cells.
Gastric Phase of Digestion
- The gastric phase is triggered by:
- Distension of the stomach.
- Protein digestion products.
- Smell and taste of food.
- This phase leads to the release of ACh, gastrin, and histamine, stimulating the secretion of HCl and pepsinogen.
Pancreatic Duct Cell Secretion
- Pancreatic duct cells are responsible for secreting bicarbonate (HCO3-), which is essential for neutralizing acidic chyme entering the duodenum.
- This neutralization:
- Provides the optimal pH for pancreatic enzyme function.
- Protects the mucosa from erosion by acid.
- HCO3- secretion occurs via a Cl-/HCO3- exchanger at the apical membrane facing the lumen of the pancreatic duct.
- Na+/K+ ATPase at the basolateral membrane facing the interstitium contributes to the supply of HCO3-.
- Some HCO3- secretion might also occur via the cystic fibrosis transmembrane conductance regulator (CFTR), although not depicted in the figure provided.
- Patients with cystic fibrosis, lacking functional CFTR, have reduced fluid secretion.
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Description
Test your understanding of parietal cell stimulation and HCl secretion, as well as the control of stomach emptying. This quiz covers key mechanisms and physiological processes involved in digestion. Prepare to explore important concepts related to gastric functions and the factors affecting them.