Physiology
Gastrointestinal
Gastric secretion is:
Answer:
The cephalic phase is initiated by the sight, smell and taste of food. Acid secretion is upregulated by acetylcholine released from postganglionic parasympathetic fibres in the myenteric plexus which acts directly by stimulating parietal cells and indirectly by stimulating the release of gastrin (from antral G -cells) and histamine (from enterochromaffin-like cells) which themselves also upregulate acid secretion from parietal cells. A low pH in the stomach inhibits gastrin secretion, therefore when the stomach is empty or when acid has been secreted for some time after food has entered it, there is inhibition of acid secretion. Secretin is released in response to acid stimulation in the duodenum which reaches the stomach via the bloodstream and inhibits the release of gastrin and thus gastric acid.Phases of Gastric Secretion
Physiology / Gastrointestinal / Stomach
Last Updated: 26th July 2024
Stimulation of gastric secretion occurs in three phases.
Cephalic Phase
The cephalic phase is the shortest phase and is initiated by the sight, smell and taste of food, mediated by the activation of the vagus nerve and its action on the enteric plexus. It usually begins before the meal and lasts up to 30 minutes into the meal.
Acid secretion is upregulated by acetylcholine released from postganglionic parasympathetic fibres in the myenteric plexus which acts directly by stimulating parietal cells and indirectly by stimulating the release of gastrin (from antral G -cells) and histamine (from enterochromaffin-like cells) which themselves also upregulate acid secretion from parietal cells.
Gastric Phase
The gastric phase is the longest phase, lasting for up to 3 hours after the start of the meal. It is triggered by distension of the stomach and the chemical composition of the food. Most acid secretion takes place during this phase, and the food in the stomach is converted to chyme.
Mechanoreceptors in the stomach wall are stretched and set up local myenteric and central vagovagal cholinergic reflexes. Both cause the release of acetylcholine which stimulates the release of gastrin, histamine, and in turn, acid, pepsinogen and mucus. Stimulation of the vagus nerve also stimulates the release of gastrin-releasing peptide (GRP), which mainly acts directly on G-cells to release gastrin.
Whole proteins do not affect gastric secretions directly but the presence of their break-down products, amino acids and peptides, directly stimulates gastrin release from antral G-cells.
A low pH in the stomach inhibits gastrin secretion, therefore when the stomach is empty or when acid has been secreted for some time after food has entered it, there is inhibition of acid secretion. However, when food first enters the stomach, the pH rises, and this leads to release of the inhibition and causes a maximum secretion of gastrin. Thus gastric acid secretion is self-regulating.
Intestinal phase
The intestinal phase is brought about by chyme entering the duodenum through the pyloric sphincter. Initially, there is a continuation of gastric stimulation due to the activation of intestinal G cells by amino acids and peptides in chyme with subsequent gastrin release.
However, this is short lived as the duodenum becomes more distended with further gastric emptying and a series of reflexes (enterogastric reflex) is initiated which inhibits further release of gastric secretion. Secretin is released in response to acid stimulation which reaches the stomach via the bloodstream and inhibits the release of gastrin. The presence of fatty acids in the duodenum itself stimulates the release of gastric inhibitory peptide (GIP) and cholecystokinin (CCK), which inhibit the release of both gastrin and acid.
Together with mechanoreceptors in the duodenum via vagal and local reflex pathways, the release of secretin and cholecystokinin also plays a role in the regulation of gastric emptying.
Phases of Gastric Secretion. (Image by OpenStax College [CC BY 3.0 , via Wikimedia Commons)
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
