2017B Question 10
Describe the physiological processes that influence the rate of gastric emptying.
Examiner Report
29.2% of candidates achieved a pass in this question The main points expected are best organised into local, neural and humoral control of gastric emptying of chyme into the duodenum.Candidates with a clear understanding of the reason for the coordinated emptying scored better in this question, which had asked for a description of physiological processes. However, a number of candidates were also awarded marks for pathophysiological and pharmacological factors; if there was prior demonstration of knowledge of normal physiology. Only a few candidates correctly pointed out that pregnancy does not delay gastric emptying; but the stress of labour does.
Common mistakes were
- Answering in tabular format, which listed factors that increase or decrease gastric emptying without further discussion.
- Answering in a clinical approach (patient, surgical and anaesthetic factors), which led to omission of essential physiological facts.
- Confusion about the hormones that are involved and their exact effects on gastric emptying.
- Regurgitation of fasting guidelines for patients without explaining the physiological basis for these guidelines.
- Detailed discussion of gastric acid production or function of the lower oesophageal sphincter, which is not within the scope of this question.
Model Answer
Structure:
- Introduction
- Physicochemical
- Neural: Extrinsic and intrinsic
- Hormonal factors
Introduction
| Factor | Details |
|---|---|
| Significance | - Gastric emptying rate (GER) varies to ensure chyme adequately digested - Full stomach → ↑↑ Risk of aspiration under GA - GER highly variable → Important to assess for pain, opioid use, sepsis |
| Normal physiology | - Antral waves, 3 per minute - GER ∝ antral contraction freq and strength (AC) / pyloric resistance (PR) |
Physicochemical
| Factor | Details |
|---|---|
| Substrate | - Starch meal: ~2-3 hours - Proteinaceous meal: ~3-4 hours - Fatty meal: 6 hours |
| Form | - Liquid faster than solid |
| Concentration | - ↑ Osmolality → ↓ GER |
Neural Factors
| Intrinsic Factor | Stimulus | Effect |
|---|---|---|
Meissner’s plexus (Submucosal) |
- ?Distension - ?CHO, protein, fat |
- Controls local absorption, secretion, contraction |
Auerbach’s plexus (Between longitudinal and circular muscle layers) |
- ?Distension |
- Controls local contraction |
| Myenteric reflex | - Distension |
- Peristalsis (↑ AC) |
| Enterogastric reflex | - Duodenal distension, irritation, acid, fat, protein, high osmo |
- ↓ AC |
| Extrinsic Factor | Stimulus | Effect |
|---|---|---|
| PSNS: CNX via coeliac and superior mesenteric plexuses | - ?Distension - ?CHO, protein, fat |
- ↑ Local ACh release - ↑ AC, ↓ PR |
| SNS: T5-L1 via same plexuses | - Exercise, pain, anxiety/stress, - Labour (not pregnancy) |
- ↓ Local ACh release - ↓ AC, ↑ PR |
| Vago-vagal excitatory reflex: CNX only | - Gastric distension |
- Receptive relaxation - ↑ AC |
Hormonal Factors
| Stimulate Antral Contraction | Source | Release stimulus |
|---|---|---|
| Gastrin | - Gastric G cells |
- Duodenal protein - Gastric distension |
| Motilin | - Duodenal M cells |
- Duodenal fat, acid |
| Insulin | - Islet β cells |
- Hyperglycaemia |
| Serotonin | - Duodenal wall? |
| Inhibit antral contraction | Source | Release stimulus |
|---|---|---|
| CCK | - Duodenal I cells |
- Duodenal fat, protein, acid |
| Secretin (conflict) | - Duodenal S cell |
- Duodenal fat, acid |
| GIP | - Duodenal K cells |
- Duodenal fat, protein, CHO |