Upper GI Tract Flashcards
Function of mouth
receive food by ingestion, break it into small particles by mastication, and mix it with saliva produced by the salivary glands that open into the oral cavity. During swallowing, the soft palate and uvula move upward to direct food away from the nasal cavity and into the oropharynx.
Function of pharynx
Food is forced into the pharynx by the tongue. When food reaches the opening, sensory receptors around the fauces respond and initiate an involuntary swallowing reflex. The uvula is elevated to prevent food from entering the nasopharynx. The epiglottis drops downward to prevent food from entering the larynx and trachea in order to direct the food into the esophagus. Peristaltic movements propel the food from the pharynx into the oesophagus
Function of oesophagus
collapsible muscular tube that serves as a passageway between the pharynx and stomach. It passes through an opening in the diaphragm, called the oesophageal hiatus, and then empties into the stomach. The mucosa has glands that secrete mucus to keep the lining moist and well lubricated to ease the passage of food. Upper and lower oesophageal sphincters control the movement of food into and out of the oesophagus
Function of stomach
food enters the stomach, which is the primary site of digestion. It is also involved in storage of food. The secretions of the exocrine gastric glands - composed of the mucous, parietal, and chief cells - make up the gastric juice. Mucus neck cells secrete a lubricatory, acid-resistant mucus; parietal cells produce HCl and chief cells produce pepsinogen and lipase. Relaxation of the pyloric sphincter allows chyme to pass from the stomach into the small intestine
Function of duodenum
After foods mix with stomach acid, they move into the duodenum, where they mix with bile from the gallbladder and digestive juices from the pancreas. The absorption of vitamins, minerals, and other nutrients begins in the duodenum. Specific functions of the duodenum include:
-Receiving the mixed, churned small pieces of food from the stomach
-Neutralising the acidity (pH level) in chyme
-Advancing the digestive process with bile from the liver, digestive enzymes from the pancreas, and intestinal juices secreted by the duodenum walls and other digestive organs
-Preparing the chyme for further digestion by mixing in bile to help break down fats
-Absorbing certain nutrients, such as folate, iron, and vitamin D
anatomy of the upper GI tract (pharynx, oesophagus, stomach and duodenum) including the course through the thoracic cavity
The upper GI tract begins with the oral cavity, which contains the tongue, teeth, gums and ducts of salivary glands. When food is swallowed, the soft palate contracts to close off the nasopharynx from the oropharynx and the epiglottis covers the trachea to prevent aspiration of food or liquid. Food then enters the oropharynx to the laryngopharynx before entering the oesophagus. The oesophagus is a muscular tube which rhythmically contracts (peristalsis) to move food down into the stomach. It then moves through the cardiac sphincter into the cardia region of the stomach. The stomach is divided into 4 cavities: cardia, fundus, body, pylorus. It then leaves the pylorus via the pylorus sphincter into the duodenum
Slow waves
generated and propagated by interstitial cells of Cajal, which initiate motility, NOT smooth muscle
Spikes
true action potentials occurring automatically when GI smooth muscle becomes move positive than -40mV
GI syncytium
Smooth muscle of the GI tract acts as a syncytium: muscle fibres connected by gap junctions allow electrical signals to initiate muscle contraction from one muscle fibre to the next rapidly along the length of the bundle.
2 types of waves contributing to membrane potential in gastro-oesophageal motility
Slow waves
Spikes
Oesophageal motility
propels food bolus from the pharynx to the stomach: the food bolus is formed in the oral cavity and when the upper oesophageal sphincter opens, it passes from the pharynx into the upper oesophagus. The upper oesophageal sphincter closes and then primary peristaltic contraction begins. A series of coordinated sequential contractions cause each segment of the oesophagus to contract which creates an area of high pressure behind the bolus, pushing it down the oesophagus. If not all food is pushed down, there is distension of the oesophageal wall and activation of mechanoreceptors in the mucosal layer. This relays afferent sensory information to the enteric nervous system and myenteric plexus, which coordinates muscle contractions above the site of distension and relaxation below it- the secondary peristaltic wave.
• the primary peristaltic wave travels approximately 3cm/sec and so solid food takes around 10s to travel from the cervical region to the stomach, and liquid takes around 1-2s.
• The movement is accelerated by gravity eg faster if sitting or standing compared to lying supine
As the food bolus approaches the lower oesophageal sphincter, it opens by peptidergic fibres of the vagus nerve and the release of vasoactive intestinal peptide (VIP), causing the smooth muscle to relax. At the same time, the cardia region of the stomach relaxes, causing the pressure to decreases and so the food bolus is propelled into the stomach. The lower oesophageal sphincter closes immediately and returns to high pressure resting tone- this prevents reflux.
Speed of primary peristaltic wave
3 cm/s
Time for solid food to travel from cervical region to stomach
10s
Time for liquid to travel from cervical region to stomach
1-2s
What increases the speed of movement of food down oesophagus
Gravity
eg faster if sitting or standing compared to lying supine
Primary peristaltic wave
Oesophageal motility propels food bolus from the pharynx to the stomach: the food bolus is formed in the oral cavity and when the upper oesophageal sphincter opens, it passes from the pharynx into the upper oesophagus. The upper oesophageal sphincter closes and then primary peristaltic contraction begins. A series of coordinated sequential contractions cause each segment of the oesophagus to contract which creates an area of high pressure behind the bolus, pushing it down the oesophagus.
Secondary peristaltic wave
If not all food is pushed down, there is distension of the oesophageal wall and activation of mechanoreceptors in the mucosal layer. This relays afferent sensory information to the enteric nervous system and myenteric plexus, which coordinates muscle contractions above the site of distension and relaxation below it- the secondary peristaltic wave.
What prevents reflux
The lower oesophageal sphincter closes immediately and returns to high pressure resting tone
What cause the smooth muscle of the lower oesophageal sphincter to relax
peptidergic fibres of the vagus nerve and the release of vasoactive intestinal peptide (VIP)
3 components of gastric motility
Receptive relaxation
Gastric contractions
Gastric emptying
Receptive relaxation
• relaxation of the lower oesophageal sphincter and cardia region of stomach to receive food bolus from oesophagus
• Stomach can accommodate up to 1.5L of food
How many L of food can the stomach accommodate
1.5 L
Gastric contractions
break up the bolus and mix it with gastric secretions to initiate digestion
• Contraction begins in middle stomach body- progressively increases strength as food approaches pylorus
• Most gastric contents undergo retropulsion (propelled back into stomach for further mixing)
Retropulsion
propelled back into stomach for further mixing
Frequency and force of contraction increased by:
parasympathetic stimulation, gastrin, motilin
Frequency and force of contraction decreased by:
sympathetic stimulation, secretin, gastric inhibitory peptide (GIP)
Gastric emptying
• propelling chyme into the small intestine
• Rate hormonally determined to allow adequate time for small intestine neutralisation of stomach acid, digestion and absorption
• Emptying stomach of 1.5L can take approximately 3 hours
How long can emptying 1.5L from the stomach take
3 hours
Physiology of acid production
Parietal cells in the body and fundus of the stomach secrete HCl which forms a gastric content pH of 1-2 in order to convert inactive pepsinogen into active pepsin for protein digestion, inactivate amylase, denature proteins, as well as kill ingested bacteria. The apical membrane if the gastric gland has 2 transporters:
1. H+-K+ ATPase: H+ is secreted into the stomach lumen against its electrochemical gradient- it is a primary active process
2. Cl- channel: Cl- follows H+ into lumen- passive process
The basolateral membrane cells contain carbonic anhydrase, so H+ is then secreted with Cl- into the lumen of the stomach and HCO3 - is absorbed into the blood (alkaline tide). As a result, there is an overall NET HCl secretion and NET HCO3 - absorption
HCl secretion is increased by gastrin, which is secreted into systemic circulation by gastric antral G cells, histamine and ACh. It is decreased by production of somatostatin from D cells to inhibit gastrin secretion, cholecystokinin, secretin and GIP.
What increases HCl secretion
gastrin, which is secreted into systemic circulation by gastric antral G cells, histamine and ACh
What decreases HCl secretion
production of somatostatin from D cells to inhibit gastrin secretion, cholecystokinin, secretin and GIP.
pH of gastric contents
1-2
Function of low pH in gastric contents
convert inactive pepsinogen into active pepsin for protein digestion
inactivate amylase
denature proteins
kill ingested bacteria
defences of the gastric and duodenal mucosa against acid damage
Gastric mucus is a gel-mucous barrier secreted by epithelial cells and glandular cells in the stomach wall which acts as part of a barrier that protects the stomach wall from the acid and digestive enzymes. It is also made up of a bicarbonate secretion and the tightly joined epithelial cells. Mucus is secreted by mucus neck cells in all regions of the stomach. The mucus is around 95% water and 5% polymers which give it a more gel-like viscosity (the viscosity is dynamic and can be altered by the rate of secretion from glandular cells or the rate of breakdown by proteolytic enzymes within the stomach lumen). The bicarbonate element of the mucus allows an increased pH local to the epithelial cells, protecting them from the highly acidic stomach environment. This also blocks gastric enzymes that have their optima in the acid range of pH. The secretion of bicarbonate from the pancreas is stimulated by secretin. An increase in mucus production is signalled by stimulation of the vagus nerve and is mediated by prostaglandins in response to external factors such as mechanical stress and elements of cephalon and gastric digestion phases.
What increase mucus secretion
signalled by stimulation of the vagus nerve and is mediated by prostaglandins in response to external factors such as mechanical stress and elements of cephalic and gastric digestion phases.
Dyspepsia
broad term often used to describe functional gastrointestinal disorders of the stomach and oesophagus. These fall into three main categories: gastroesophageal reflux disease (GORD), peptic ulcer disease and functional dyspepsia. The term “dyspepsia” refers to a group of symptoms, for example upper belly pain, belching, bloating and feeling full- it is also known as indigestion.
GORD
failure of the lower oesophageal sphincter: either poor closure or inappropriate relaxation (poor tone) which causes the stomach contents to re-enter the oesophagus. It is typically associated with oesophageal motility, gastric outlet obstruction and hiatal hernia. This results in inflammation to the oesophageal mucosa.
The main signs and symptoms are: acid taste in mouth, heartburn, retrosternal chest pain, early satiety, regurgitation, odynophagia (pain when swallowing), increased salivation, postprandial nausea and vomiting, sore throat, sensation of lump in throat, tooth decay, coughing and wheezing. The majority of these symptoms are often felt shortly after eating meals and are worse after large meals or when lying down.
Risk factors for reflux
• overweight
• Smoking
• heavy alcohol consumption
• Male gender
• Eating large, high fat meals
• Family history
• anti-inflammatory drugs - inhibit mucus secretion
• Pregnancy
Hiatus hernia- part of stomach above diaphragm
Physiological basis for symptoms of GORD
When acid reflux occurs, food or fluid can be tasted in the back of the mouth. When refluxed stomach acid touches the lining of the oesophagus it may cause a burning sensation in the chest or throat called heartburn or acid indigestion. Inflammation of the oesophagus from refluxed stomach acid can damage the lining and cause bleeding or ulcers, also called oesophagitis. Scars from tissue damage can lead to strictures, narrowing the oesophagus that makes swallowing difficult. Some people develop Barrett’s oesophagus, in which cells in the oesophageal lining take on an abnormal shape and colour. Over time, the cells can lead to oesophageal cancer, which is often fatal
Bicarbonate element of mucus
allows an increased pH local to the epithelial cells, protecting them from the highly acidic stomach environment. This also blocks gastric enzymes that have their optima in the acid range of pH.
What stimulates section of bicarbonate from the pancreas
Secretin
Main signs and symptoms of GORD
acid taste in mouth, heartburn, retrosternal chest pain, early satiety, regurgitation, odynophagia (pain when swallowing), increased salivation, postprandial nausea and vomiting, sore throat, sensation of lump in throat, tooth decay, coughing and wheezing.
The majority of these symptoms are often felt shortly after eating meals and are worse after large meals or when lying down.
Why is smoking a risk factor for GORD
Weakens oesophageal sphincter
Why is alcohol a risk factor for GORD
Damages oesophageal and gastric mucosa
How long must symptoms of GORD be present before being worrying
> 4 weeks
What is the outermost tissue layer of the gastrointestinal tract
Serosa
What is the outermost tissue layer of the gastrointestinal tract
Serosa
