8th February 2024

Gastrointestinal Physiology

GI tract structure

Structure

The GI tract can be divided into multiple different layers. From inner to outer layers, these are:

• Epithelial cells (specialised in the role of either secretion or absorption, depending on the site of the GI tract)
• Lamina propria
• Muscularis mucosa (changes the surface area of the GI tract)
• Circular muscle (increases or decreases circumference of GI tract)
• Longitudinal muscle (increases or decreases length of GI tract)
• Submucosal plexus and Myenteric plexus (make up the enteric nervous system of the GI tract). The enteric nervous system coordinates and disseminates information from the sympathetic and parasympathetic systems.
  • Submucosal plexus- controls secretion and blood flow (via sensory input from chemoreceptors and mechanoreceptors in the GI tract).
  • Myenteric plexus- controls motility.

Image Source: Wikimedia Commons (2020). Layers of the GI Tract English, Licensed under a creative commons licence. Available for free at: https://upload.wikimedia.org/wikipedia/commons/3/31/Layers_of_the_GI_Tract_english.svg (Accessed: 4 January 2024).

GI tract hormones

Hormones and associated disorders

There are a myriad of hormones that are secreted by the GI tract. Most act locally within the GI tract to regulate the digestion process. We summarise the action of these hormones in the table below. 

Table 4: Summary of hormones secreted by the GI tract. Own table. 

In most conditions, pathology develops in excess of these hormones rather than deficiencies. Increased gastrin levels can be found in gastrinomas, Zollinger-Ellison syndrome, achlorhydria, vagotomy, short bowel syndrome and iatrogenic ( PPI/H2 antagonist). Increased VIP can be seen in VIPoma. Increased PP can be seen in pancreatic malignancies. Decreased gastrin levels can be found in fasting patients and conditions stimulating hyperacidity.

References

Tortora, G. J., & Derrickson, B. (2017). Tortora’s principles of anatomy and physiology. John Wiley and Sons.

Kumar, P. and Clark, M., (2012). Kumar & Clark’s clinical medicine. 8th ed.

Fairweather, J., Findlay, M., & Isles, C. (2020). Clinical companion in nephrology. Springer International Publishing. 

Stomach

Overview

Gastric motility is controlled by smooth muscle cells and allows mixing of food. This is mediated by the smooth muscle cells, and the parasympathetic nervous system stimulates increased contractility, while reduced contractility is seen with increased sympathetic stimulation. 

The stomach also relaxes and distends to receive ingested food, and CCK stimulates this. Gastric emptying is stimulated by stomach distension and gastrin while it is reduced by fatty acids, secretin, CCK and acidic environments in the duodenum. 

The stomach also produces gastric acid, mediated by the parietal cells. Secretion is stimulated by vagal stimulation, gastrin, and histamine (H2 receptors are found on parietal cells). Secretion is inhibited by low pH (<3), small intestine peptide/hormone (e.g., secretin, CCK, GIP), anticholinergics (e.g., atropine), H2 receptors antagonist (e.g., Cimetidine), proton pump inhibitors(e.g., omeprazole). The parietal cells also produce an intrinsic factor that is vital in the absorption of vitamin B12. 

Other cells within the stomach include:

• Mucosal cells (located in stomach antrum): produce mucous and HCO3-
• Chief cells (located in the stomach body): produce pepsinogen
• G cells (located in the stomach antrum): produce gastrin
• Neuroendocrine cells: produce multiple secretory products, e.g., somatostatin

References

Tortora, G. J., &amp; Derrickson, B. (2017). Tortora’s principles of anatomy and physiology. John Wiley and Sons.

Kumar, P. and Clark, M., (2012). Kumar & Clark’s clinical medicine. 8th ed.

Fairweather, J., Findlay, M., &amp; Isles, C. (2020). Clinical companion in nephrology. Springer International Publishing. 

Pancreas (Exocrine)

Overview

The pancreas’ primary secretion consists of high volume, isotonic, alkalotic fluid due to high concentration of HCO3- to neutralise the acidic chyme from the stomach. This also contains digestive enzymes for protein, carbohydrate, and fat (protease, amylase, and lipase). 

The acinar and ductal cells of the pancreas perform the exocrine function of the pancreas. Acinar cells secrete fluids rich in enzymes and electrolytes. Ductal cells modify the fluids by producing water and electrolytes. The islet cells perform the endocrine function of the pancreas ( see Endocrinology section for more details). 

Both gastric and intestinal stimuli stimulate the secretion of the pancreatic juices. Gastrin from the stomach stimulates enzyme secretion from the acinar cells. Intestinal hormones are stimulated by peptides, amino acids, fatty acids and H+ within the duodenum, and the main hormones involved are secretin and CCK. Secretin will stimulate the secretion of bicarbonate, while CCK will stimulate the secretion of enzyme secretions. 

Image Source: Wikimedia Commons (2013). Exocrine and Endocrine Pancreas, Licensed under a creative commons licence. Available for free at: https://upload.wikimedia.org/wikipedia/commons/a/ac/2424_Exocrine_and_Endocrine_Pancreas.jpg  (Accessed: 4 January 2024).

References

Tortora, G. J., &amp; Derrickson, B. (2017). Tortora’s principles of anatomy and physiology. John Wiley and Sons.

Kumar, P. and Clark, M., (2012). Kumar & Clark’s clinical medicine. 8th ed.

Fairweather, J., Findlay, M., &amp; Isles, C. (2020). Clinical companion in nephrology. Springer International Publishing. 

Biliary system

The liver produces bile, which is typically stored in the gallbladder. It comprises bile salts, bile pigments (bilirubin and biliverdin), phospholipids, cholesterol and protein. We will look at the metabolism of both bilirubin and bile salts. 

Bilirubin metabolism

Bilirubin is produced from the degradation of haemoglobin by the reticuloendothelial system. Red blood cells are broken down within the spleen, and haemoglobin is broken down into haem and globin. Haem is catabolised into bilirubin, while the globin is broken down into amino acids and recycled. Iron released from haem is also recycled. 

Bilirubin is bound to albumin and is transported to the liver. The liver conjugates bilirubin with glucuronic acid, forming conjugated bilirubin. This is done by glucuronyl transferase. The urine will directly excrete a portion of this, while some will enter the intestinal system via bile and will be deconjugated by the intestinal bacteria to form urobilinogen. 

At the terminal ileum, the enterohepatic circulation reabsorbs a portion of urobilinogen and will return to the liver. Some reabsorbed urobilinogen will re-enter bile while the kidneys will excrete the remainder.

Intestinal bacteria will break down the remainder of the urobilinogen within the large intestine into urobilin and stercobilin before being excreted by faeces.

Image Source: Degruyter (2021). almed-2021-0047, Licensed under a creative commons licence. Available for free at: https://www.degruyter.com/document/doi/10.1515/almed-2021-0047/html#APA   (Accessed: 9 January 2024).

Bile salts

Bile salts are constantly produced by the liver and are excreted by the large intestine. This consists of primary and secondary bile salts. Primary bile salts consist of cholic acid and chenodeoxycholic acid. They are synthesised from cholesterol by hepatocytes. Intestinal bacterial enzymes convert secondary bile salts from primary bile salts, consisting of deoxycholic acid and lithocholic acids.

Bile salts aim to solubilise dietary lipids by emulsifying fats into phospholipids and fatty acids. It also forms micelles to help solubilise cholesterol and fatty acids. This helps with the absorption of fatty acids, cholesterol and fat-soluble vitamins. 

CCK, gastrin and secretin stimulate the secretion of bile. CCK stimulates the contraction of the sphincter of Oddi, while gastrin and secretin stimulate the production of bile and HCO3-. Increased parasympathetic stimulation also increases the secretion of bile. 

References

Tortora, G. J., &amp; Derrickson, B. (2017). Tortora’s principles of anatomy and physiology. John Wiley and Sons.

Kumar, P. and Clark, M., (2012). Kumar & Clark’s clinical medicine. 8th ed.

Fairweather, J., Findlay, M., &amp; Isles, C. (2020). Clinical companion in nephrology. Springer International Publishing.

Small and large intestines

Small intestine

The small intestine has a wide range of functions from the duodenum, jejunum and ileum. The duodenum secretes various hormones, as highlighted in the sections above. It also continues the digestion processes from the stomach as it receives pancreatic and bile secretions. Paneth cells secrete watery secretions, while Brunner’s glands secrete an alkaline mucous. The enterocytes produce digestive enzymes. CCK, secretin and parasympathetic stimulation stimulate these, while they are inhibited by sympathetic stimulation. 

The majority of nutrient absorption occurs within the duodenum and upper jejunum. Specialised epithelium with brush borders is found in this area to help with absorption. The duodenum and upper jejunum absorb iron and calcium. Fatty acids, cholesterol and fat-soluble vitamins are passively absorbed, while carbohydrates (monosaccharides), proteins (amino acids), folic acid and water-soluble vitamins are absorbed through carrier proteins. 

As highlighted in previous sections, the terminal ileum also performs essential functions in absorbing vitamin B12 and bile salt reabsorption. 

Large intestine

The large intestine is the site of water reabsorption, digestion of chyme by bacterial intestines and formation and storage of faeces. It also acts as the site of vitamin K absorption, as the enteric bacteria produce this. 

Its motility is stimulated by parasympathetic stimulation, CCK, drugs (cholinergic, laxatives) and the gastrocolic reflex (food in the stomach increases motility and mass movement in the colon). Anticholinergics and sympathetic stimulation inhibit it. 

References

Tortora, G. J., &amp; Derrickson, B. (2017). Tortora’s principles of anatomy and physiology. John Wiley and Sons.

Kumar, P. and Clark, M., (2012). Kumar & Clark’s clinical medicine. 8th ed.

Fairweather, J., Findlay, M., &amp; Isles, C. (2020). Clinical companion in nephrology. Springer International Publishing.