GIT Physiology

Dr Swapnil Pawar August 5, 2020 920

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GIT Physiology

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    GIT Physiology
    Dr Swapnil Pawar


Notes by Dr Madhuri Anupindi

Outline the physiology of swallowing:

There are three phases of swallowing; voluntary, pharyngeal, and oesophageal.

  • Voluntary
    • When food enters the mouth mastication begins via the chewing reflex and muscles innervated by the trigeminal nerve. The tongue and teeth make the food smaller and allow digestive enzymes within the mouth to begin the process of digestion
    • Food is rolled posteriorly into the pharynx by the tongue
  • Pharyngeal
    • Food enters the pharynx and stimulates the epithelial swallowing receptor areas. The soft palate elevates, closing the posterior nares and the palatopharyngeal folds are pulled medially forming a sagittal slit so that only small food boluses can enter.
    • The vocal cords are pulled together and the larynx moves upwards and anteriorly causing the epiglottis to swing over the laryngeal opening. The oesophageal opening is enlarged and the upper oesophageal sphincter relaxes. The wall of the pharynx contracts from superior to inferior causing a wave of peristalsis.
    • The most sensitive areas for initiating the pharyngeal phase of swallowing is around the pharyngeal opening and the tonsillar pillars. The stimuli is transmitted via the trigeminal and glossopharyngeal nerves to the medulla oblongata and into the swallowing centre which sends motor impulses via the 5th, 9th, 10th and 12th cranial nerves.
  • Oesophageal
    • This phase functions to transmit food rapidly from the pharynx to the stomach via peristalsis.
    • Two types of peristalsis
      • Primary peristalsis: continuation of the pharynx wave, lasts 8-10secs
      • Secondary peristalsis: activated if the primary peristaltic wave does not transmit all food into stomach activated by distension of oesophagus secondary to residual food initiated by myenteric plexus and also by reflexes from pharynx transmitted via vagal afferent fibres to medulla then back through CN 9 and 10.
    • Lower oesophageal sphincter and the stomach receptively relaxes when a peristaltic wave approaches

Describe the composition and regulation of gastric secretions

The stomach produces approximately 1.5 – 2.5L of gastric secretions a day. These secretions aid in digestion and help to protect the stomach. At rest, the lining of the stomach is coiled into folds called gastric rugae which contain microscopic invaginations known as gastric pits. Each gastric pit opens into several gastric glands which come in two varieties, oxyntic glands which make up 75% of the total number of glands, and pyloric glands which form the remainder. The entire surface of the stomach also contains surface mucus cells which secrete a large amount of alkali mucus that coats and lubricates the gastric surface. This helps to protect the gastric epithelium from hydrochloric acid, pepsin and other insults. Production is stimulated by contact with food or any chemical irritation.

Oxyntic glands are present in the fundus and proximal region of the stomach and contain:

  • Mucous neck cells: secrete mucus
  • Peptic or chief cells: secrete pepsinogen which has no digestive activity.
    • Pepsinogen is activated by hydrochloric acid to form pepsin and its function is optimized at acidic pHs of 1.8 – 3.5 and inactive at pH > 5.
    • Pepsin aids in the digestion of protein
    • Peptic cells are stimulated by acetylcholine from vagal nerves or from gastric enteric nervous plexus and from acid in the stomach.
    • Chief cells also secrete gastric lipase which aids in the digestion of lipids.
  • Parietal or oxyntic cells: secrete hydrochloric acid and intrinsic factor
    • Stimulated parietal cells produce hydrochloric acid from water and carbon dioxide under the influence of carbonic anhydrase. The carbonic acid that is formed dissociates into hydrogen and bicarbonate, the bicarbonate is exchanged with chloride from the blood which combines with hydrogen forming hydrochloric acid. The secretion of hydrogen is therefore accompanied by the release of the same number of bicarbonate ions into the bloodstream. This helps to neutralise the acid secreted into the blood later when the alkaline bicarbonate pancreatic secretions are produced.
    • Parietal cells secrete 1- 2L of 150-160mmol/L of hydrochloric acid a day. The HCL helps to denature ingested protein to make it more digestible and activates pepsinogen to pepsin. It also destroys some bacteria, stimulates the small intestinal mucosa to release secretin and cholecystokinin, and promotes the absorption of calcium and iron in the small intestine.
    • Hydrochloric acid secretion is stimulated by gastrin, histamine and acetylcholine and inhibited by low gastric pH and somatostatin. Histamine, gastrin and acetylcholine have synergistic effects on hydrochloric acid secretion.
    • Intrinsic factor is also secreted by parietal cells which is important for the absorption of vitamin B12
  • Enterochromaffin like cells: produce histamine
    • These cells lie in the deep recesses of oxyntic glands, in close contact with parietal cells, and release histamine
    • The rate of hydrochloric acid secretion is directly related to the amount of histamine released. Histamine secretion is stimulated mainly by gastrin, but also by acetylcholine from vagal nerves and hormones from the enteric nervous system. The most important inhibitor of the ECL cell is somatostatin

Pyloric glands are structurally similar to oxyntic glands but have few peptic cells and almost no parietal cells. They are located in the pylorus and the antrum. They contain

  • Mucous cells:
    • This is the main component of pyloric glands and secretes mucus and electrolytes
  • G cells: secrete gastrin
    • Gastrin is a peptide hormone which stimulates hydrochloric acid secretion by the parietal cells. It also stimulates pancreatic and biliary secretion and increases gastric and intestinal motility and gastric mucosal growth.
    • It is stimulated by vagal stimulation, proteins and amino acids in the stomach, gastric distension, and drugs such as alcohol.
    • It is inhibited by gastric acid, secretin, somatostatin and glucagon.
  • D cells: secrete somatostatin
    • Somatostatin decreases acid secretion by inhibiting parietal cells, decreasing histamine secretion from enterochromaffin-like cells and gastrin secretion from G cells.
    • Somatostatin release is stimulated by gastric acid secretion, the presence of gastrin and cholecystokinin.  It is inhibited by cholinergic stimulation

There are three phases of gastric secretion:

  • Cephalic
    • Sight, smell, taste and thought of food activate the cerebral cortex and appetite centres in the amygdala and hypothalamus which then activates the dorsal motor nuclei of the vagus nerve, and travels via the vagus to the stomach.
    • The greater the appetite, the greater the stimulus
    • Accounts for approximately 20% of gastric secretion
  • Gastric
    • Food enters the stomach and excites the long vasovagal reflexes from the stomach to the brain and back to the stomach, local enteric reflexes and gastrin release
    • Stretch receptors detect stomach distention, chemoreceptors detect increased pH and there is increased parasympathetic activity, all of which increase gastric secretions
    • This accounts for 70% of gastric acid secretion
  • Intestinal
    • Food in the upper intestine causes a small amount of gastric juice secretion and the release of secretin to stimulate the exocrine pancreas.
    • The duodenum initially enhances gastric secretion but later inhibits it as the acid and semi-digested fats trigger the enterogastric reflex. This reduces vagal stimulation of the stomach and sends inhibitory signals.

Describe the control of gastric emptying

Gastric emptying is a complex sequence of events that is controlled by myogenic, neural, hormonal and physicochemical mechanisms.

The stomach can be functionally divided into two regions:

  • The proximal stomach: cardia, fundus and body, which is characterized by a thin layer of muscle that produces relatively weak contractions. After food is ingested, the proximal stomach exhibits receptive relaxation via vagal input, and there is minimal increase in intragastric pressure. This part of the stomach can act as a food reservoir.
  • The distal stomach: consists of antrum and pylorus. This portion has a thick muscular wall and controls digestion in the stomach. The pattern of distal stomach contraction regulates the rate of emptying of food contents into the duodenum.

Myogenic mechanisms:

  • GI smooth muscle has its own intrinsic rhythmicity generated by action potentials which results in approximately 3 waves/minute. These contractions generate a basal pressure within the stomach and a pressure gradient from the stomach to the small intestine.
  • Peristaltic contractions are initiated near the border of the fundus and the body and progress towards the pylorus, thus propelling food towards the duodenum
  • These contractions are produced by slow waves which arise from pacemaker cells called the interstitial cells of Cajal. These waves propagate more slowly in the proximal stomach thus allowing for mixing and storage of ingested food. The waves are stronger and faster within the distal stomach. When food reaches the pylorus, there is a forceful contraction of the antrum causing retropulsion of food and is known as the pyloric pump. This allows food to be digested into smaller fragments and mix with gastric secretions.

Neurogenic control:

  • Extrinsic nervous system
    • Parasympathetic pathways are conveyed to the myenteric plexus throughout the stomach and upper intestine via the vagus nerve. Parasympathetic stimulation results in receptive relaxation of the proximal stomach as food enter the oesophagus and proximal stomach. This mechanism helps to control the rate of gastric emptying. The parasympathetic nervous system stimulates the pyloric pump and gastric motility
    • Sympathetic pathways come from T5-T10 of the spinal cord via the coeliac ganglia and under resting conditions have little influence on motility.
  • Enteric nervous system
    • Consists mainly of the myenteric plexus which helps control motility and the submucous plexus which helps regulate gastrointestinal blood flow.
    • The enteric neurons secrete a host of neurotransmitters which help to co-ordinate digestion and gastric motility
    • GIT distension, chemical irritation and hormones can activate the enteric nervous system and cause gastric emptying. Stimulation of the myenteric plexus causes increased tonic contraction, increased contraction intensity and increased conduction velocity. It also secretes inhibitory peptide which inhibits the intestinal sphincter muscles, thus allowing for less impediment to food passage. The myenteric plexus also causes receptive relaxation a few cms downstream from the food bolus.

Hormonal control:

  • Hormones that cause increased gastric emptying include gastrin, motilin, acetylcholine
  • Hormones that cause decreased gastric emptying include cholecystokinin, noradrenaline, vasoactive intestinal peptide, gastric inhibitor peptide and secretin

Physicochemical factors:

  • Liquids empty faster than solids
  • Increased gastric distension results in vago-vagal reflexes which increase pyloric pump activity and gastric emptying. Duodenal distension decreases gastric emptying.
  • High protein food stimulates gastrin secretion which enhances gastric emptying. Fats stimulate cholecystokinin which inhibits emptying
  • Iso-osmolar substances cause increased gastric emptying whereas hyperosmolar substances slow gastric emptying
  • High acidity and the presence of fat and protein breakdown in chyme stimulates the enterogastric reflex which inhibits gastric emptying

List the physiological factors that prevent gastro-oesophageal reflex

  • Lower oesophageal sphincter
    • This is the smooth muscle around the lowest 2-4cm of the oesophagus. It is composed of circular muscle and gastric sling muscle and is tonically contracted 15 – 25mmHg above stomach pressure.
  • The angle of His: the acute angle between esophagus and fundus of the stomach. This acts as a barrier to reflux by creating a valve that acts as a functional sphincter.
  • Unidirectional peristalsis wave
  • Regular gastric emptying
  • Diaphragm: the crural fibres serve as an extrinsic sphincter for the oesophagus
  • Low intra-abdominal pressure
  • Saliva and acid neutralisation which help to clear remaining acid after food bolus is swallowed

Briefly outline the digestion and fate of dietary triglycerides.

Triglycerides consist of 3 fatty acids bound to glycerol. A small amount of digestion of triglyceride occurs in the stomach by gastric lipase but the majority occurs in the small intestine.

The first step of triglyceride digestion is emulsification by bile acids and lecithin. This breaks the fat into smaller pieces allowing for increased mixing with digestive enzymes. This begins to occur in the stomach via agitation and then continues in the duodenum through the action of bile which contains bile salts and lecithin. The next step is digestion via lipase produced by the pancreas which digests triglycerides into free fatty acids and 2-monoglyceride. The bile salts combine with monoglycerides and fatty acids to form micelles which transfer the fat to the intestinal epithelial cells where they enter the enterocytes.  Within the enterocytes, the fatty acids and monoglyceride are transported into the endoplasmic reticulum where they are packaged with cholesterol and lipoproteins to form chylomicrons. A small number of fatty acids are absorbed directly into the portal blood and bound to albumin. The chylomicrons are then transported in the lymphatics to the liver or to muscle and adipose tissue. These tissues contain lipoprotein lipase which hydrolyses the triglycerides in the chylomicron, thus releasing fatty acids and glycerol which can be used as energy – the glycerol can enter the glycolytic pathway to form glucose, and the fatty acids can undergo beta-oxidation to form acetyl CoA and then enter the citric acid cycle. If excess acetyl CoA is produced it can be used for fatty acid synthesis, cholesterol formation, protein acetylation or formation of ketone bodies.


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