Physiology and Biochemistry of upper GI tract
Stimulation of saliva formation:
Saliva is formed first and then it’s modified, the modification depends on the rate of flow/rate of
saliva production. Saliva production is mainly stimulated by the parasympathetic nervous system,
but it needs a small amount of sympathetic to stimulate the production of saliva. So cholinergic and
muscarinic receptors are activated which increase ion flow into the acinus. Also, when producing
saliva, we need to increase blood flow so parasympathetic peptides (VIP and Bradykinin) are
released from nerves which cause vasodilation. As a you get a movement of ions, especially Cl- into
the acinar cells via channels associated with cystic fibrosis (CFTR – NKCC1). So, this results in the
acinus becoming negative which causes Na+, HCO3- and water to move in to maintain isotonicity as
the concentration of primary secretion resemble that of plasma. Then, salivary secretion is modified
as it travels through the duct. So as the saliva travels down the duct (impermeable to water) – the
Na+ and chloride are removed from channels where HCO3- comes in for Cl- and K+ for Na+. The
amount of removal of this depends on the rate of flow. So, when the flow rate is slowed down as
salivary glands less stimulated – the Na+ and Cl- concentration in saliva falls as slow travel allows
greater time for exchange, making saliva hypoosmotic. The constituents of saliva i.e. Na+ and Cl- also
respond to aldosterone (Crohn’s and Addison’s disease).
Swallowing Reflex: once mastication is complete the bolus has been formed, it is swallowed. Food
passes posteriorly into the oropharynx and then into the laryngopharynx.
The first (oral) phase of swallowing is voluntary but the subsequent pharyngeal and oesophageal
phase are under involuntary (autonomic) control. Neurons in the medulla and lower pons mediate
the involuntary phase of swallowing. During the first (oral) phase the tip of the tongue is placed
against the hard palate and the tongue contracts to force the food bolus into the oropharynx. The
pharynx is richly dense with mechanoreceptors and, when food stimulates these receptors – it
initiates a sequence of events which complete the swallowing process.
Information form the mechanoreceptors passes via afferents in cranial nerve IX to sensory nuclei in
the brain stem + also spreads via interneurons to motor nucleus ambiguus in the medulla. Motor
impulses travel from here to the muscles of the pharynx, palate and upper oesophagus via CN IX and
X. Lesions of the control centres involved in swallowing e.g. CN IX and X leads to dysphagia.
The efferent response begins with contractions of the superior constrictor muscle, which raises the
soft palate towards the posterior pharyngeal wall to prevent food entering the nasopharynx. It also
initiates a wave of peristaltic contraction that propels the bolus through the relaxed upper
oesophageal sphincter into the oesophagus. The larynx is raised to allow the epiglottis to close of
the opening to the trachea. At the same time as this is happening, respiration is inhibited
(deglutition apnoea).
In the final phase of swallowing, oesophageal phase the wave of peristaltic contractions that was
initiated in the pharynx continues along the oesophagus. If this wave to propel bolus into the
stomach, distention of the oesophagus initiates a vaso-vagal reflex which triggers a secondary
peristaltic wave.
The oesophageal submucosa contains glands that secrete mucous in response to pressure from the
bolus. This mucous helps to lubricate the oesophagus and helps transport of food. Movement down
oesophagus is also aided by gravity. At the junction of oesophagus and stomach there is the lower
oesophageal sphincter which acts as a valve and remains closed when food is being swallowed thus
, preventing reflux back into the oesophagus. Just before the peristaltic wave/bolus reaches the end
of the oesophagus, the sphincter opens to allow food to enter the stomach. This is the same case
with the upper sphincter which opens before the bolus reaches it.
Oesophageal phase begins with relaxation of upper sphincter but normally, both sphincters
are closed – prevent reflux.
Upper third of oesophagus is striated muscle and lower two thirds is smooth muscle. We
don’t have control over any of these muscles. The striated muscle is peristalsis organised by
brainstem and smooth muscle is peristalsis organised via ENS. So, both are autonomic.
Lower oesophageal sphincter displays receptive relaxation which involves inhibitory
interneurons. The sphincters have the most stable muscle tone compared to that of at rest
and the lower sphincter helps to maintain resting tone.
Within the gastric glands found in the deep mucosa there are cells which produce certain chemicals:
G cells release the hormone gastrin (located at pyloric antrum of stomach)
D cells release somatostatin
H-cells (ECL) release histamine (binds to h2 receptors to potentiate effect of gastrin)
Chief cells produce pepsinogen
Parietal cells produce HCl
ACH, histamine and gastrin stimulate parietal cells lots of HCl made
As parietal cells secrete HCl, they have tubulovesicles when at rest which has the H+/K+ ATP-ase on
membrane and when the cells are activated e.g. by gastrin, these tubulovesicles fuse to form
canaliculus which have a greater surface area and display more proton pumps on surface ready for
gastric secretion.
Stimulation of saliva formation:
Saliva is formed first and then it’s modified, the modification depends on the rate of flow/rate of
saliva production. Saliva production is mainly stimulated by the parasympathetic nervous system,
but it needs a small amount of sympathetic to stimulate the production of saliva. So cholinergic and
muscarinic receptors are activated which increase ion flow into the acinus. Also, when producing
saliva, we need to increase blood flow so parasympathetic peptides (VIP and Bradykinin) are
released from nerves which cause vasodilation. As a you get a movement of ions, especially Cl- into
the acinar cells via channels associated with cystic fibrosis (CFTR – NKCC1). So, this results in the
acinus becoming negative which causes Na+, HCO3- and water to move in to maintain isotonicity as
the concentration of primary secretion resemble that of plasma. Then, salivary secretion is modified
as it travels through the duct. So as the saliva travels down the duct (impermeable to water) – the
Na+ and chloride are removed from channels where HCO3- comes in for Cl- and K+ for Na+. The
amount of removal of this depends on the rate of flow. So, when the flow rate is slowed down as
salivary glands less stimulated – the Na+ and Cl- concentration in saliva falls as slow travel allows
greater time for exchange, making saliva hypoosmotic. The constituents of saliva i.e. Na+ and Cl- also
respond to aldosterone (Crohn’s and Addison’s disease).
Swallowing Reflex: once mastication is complete the bolus has been formed, it is swallowed. Food
passes posteriorly into the oropharynx and then into the laryngopharynx.
The first (oral) phase of swallowing is voluntary but the subsequent pharyngeal and oesophageal
phase are under involuntary (autonomic) control. Neurons in the medulla and lower pons mediate
the involuntary phase of swallowing. During the first (oral) phase the tip of the tongue is placed
against the hard palate and the tongue contracts to force the food bolus into the oropharynx. The
pharynx is richly dense with mechanoreceptors and, when food stimulates these receptors – it
initiates a sequence of events which complete the swallowing process.
Information form the mechanoreceptors passes via afferents in cranial nerve IX to sensory nuclei in
the brain stem + also spreads via interneurons to motor nucleus ambiguus in the medulla. Motor
impulses travel from here to the muscles of the pharynx, palate and upper oesophagus via CN IX and
X. Lesions of the control centres involved in swallowing e.g. CN IX and X leads to dysphagia.
The efferent response begins with contractions of the superior constrictor muscle, which raises the
soft palate towards the posterior pharyngeal wall to prevent food entering the nasopharynx. It also
initiates a wave of peristaltic contraction that propels the bolus through the relaxed upper
oesophageal sphincter into the oesophagus. The larynx is raised to allow the epiglottis to close of
the opening to the trachea. At the same time as this is happening, respiration is inhibited
(deglutition apnoea).
In the final phase of swallowing, oesophageal phase the wave of peristaltic contractions that was
initiated in the pharynx continues along the oesophagus. If this wave to propel bolus into the
stomach, distention of the oesophagus initiates a vaso-vagal reflex which triggers a secondary
peristaltic wave.
The oesophageal submucosa contains glands that secrete mucous in response to pressure from the
bolus. This mucous helps to lubricate the oesophagus and helps transport of food. Movement down
oesophagus is also aided by gravity. At the junction of oesophagus and stomach there is the lower
oesophageal sphincter which acts as a valve and remains closed when food is being swallowed thus
, preventing reflux back into the oesophagus. Just before the peristaltic wave/bolus reaches the end
of the oesophagus, the sphincter opens to allow food to enter the stomach. This is the same case
with the upper sphincter which opens before the bolus reaches it.
Oesophageal phase begins with relaxation of upper sphincter but normally, both sphincters
are closed – prevent reflux.
Upper third of oesophagus is striated muscle and lower two thirds is smooth muscle. We
don’t have control over any of these muscles. The striated muscle is peristalsis organised by
brainstem and smooth muscle is peristalsis organised via ENS. So, both are autonomic.
Lower oesophageal sphincter displays receptive relaxation which involves inhibitory
interneurons. The sphincters have the most stable muscle tone compared to that of at rest
and the lower sphincter helps to maintain resting tone.
Within the gastric glands found in the deep mucosa there are cells which produce certain chemicals:
G cells release the hormone gastrin (located at pyloric antrum of stomach)
D cells release somatostatin
H-cells (ECL) release histamine (binds to h2 receptors to potentiate effect of gastrin)
Chief cells produce pepsinogen
Parietal cells produce HCl
ACH, histamine and gastrin stimulate parietal cells lots of HCl made
As parietal cells secrete HCl, they have tubulovesicles when at rest which has the H+/K+ ATP-ase on
membrane and when the cells are activated e.g. by gastrin, these tubulovesicles fuse to form
canaliculus which have a greater surface area and display more proton pumps on surface ready for
gastric secretion.
