Case 11- Physiology and SPA Flashcards
Layers of the Oesophagus
- Mucosa-stratified squamous epithelium
- Submucosa-mucous glands
- Muscular layer-containing inner circular and outer longitudinal muscle fibres
- Serosal layer
- Submucosal plexus (Meissner’s)- within the submucosa it controls secretion, absorption and local muscle movement
- Myenteric plexus (Auerbach’s)- between the circular and longitudinal muscle layers, controls the tone of the gut.
How food moves down the Oesophagus
Once we have chewed our food it moves into the pharynx, causing distention of the pharynx. The epiglottis and glottis close so food doesn’t enter the respiratory tract. The nasopharynx is closed to stop reflux. When we swallow a signal is generated in the brainstem via Vagal nerves. This causes the upper oesophageal sphincter to open so food can move into the oesophagus. There is a wave of relaxation followed by contraction of circular muscles behind the food to squeeze the bolus along, this is peristalsis.
Oesophagus- Peristalsis is triggered by
- Primary peristalsis- swallowing reflex
* Secondary peristalsis- distension of the oesophagus due to the food bolus
Neuronal control in the upper third of the Oesophagus
Contains striated muscle.
Primary Peristalsis- Sequential firing from the Nucleus ambigus (NA) within the Medulla activates the lower motor fibres of the Vagus nerve. This generates timed contraction of the striated muscle allowing peristalsis to occur.
Secondary peristalsis- distension of the oesophagus is detected by the CNS via the afferent vagus nerves. This generates sequential firing to cause muscle contraction.
Neuronal control in the lower third of the oesophagus
Contains smooth muscle. Control of smooth muscle contraction is via the dorsal motor nucleus (DMN) in the medulla. Primary peristalsis is controlled by vagal nerves via the enteric nervous system. Secondary peristalsis is locally controlled
Neuronal control in the lower third of the oesophagus- Excitatory pathway
Primary peristalsis- preganglionic motor nerves originate from the rostral part of the DMN synapse in the myenteric plexus. The activation of the postganglionic fibres cause a release of acetylcholine and substance P. This causes contraction of the smooth muscle behind the bolus.
Neuronal control in the lower third of the oesophagus- Inhibitory pathway
Primary peristalsis- preganglionic motor nerves originate from the caudal part of the DMN synapse in the myenteric plexus. The activation of the postganglionic fibres cause a release of nitric oxide, vasoactive intestinal peptide and ATP. This causes a relaxation of the smooth muscle in front of the bolus.
The lower third of the Oesophagus- Secondary Peristalsis
The submucosal plexus between the mucosa and the inner circular muscle layer senses the distension of the oesophagus. It then forms a connection with the myenteric plexus motor fibres to generate smooth muscle contraction. The lining of the oesophagus at the bottom contains mechanoreceptors which sense stretch. This then signals to the enteric nervous system which triggers an enteric nervous system response.
Why is muscle contraction controlled in the Oesophagus
Behind the trigger there will be contraction due to excitatory response. In front of the trigger there will be relaxation due to an inhibitory response.
The fundus and proximal bodies of the stomach
They act as reservoirs. Two major types of motility occur here: receptive relaxation and gastric accommodation.
Fundus and proximal bodies of the stomach- Receptive relaxation
Receptive relaxation in anticipation of food- controlled by the Vago-vagal reflex. The lower oesophageal sphincter and proximal stomach relax in anticipation of contents.
Fundus and proximal bodies of the stomach- Gastric accomodation
Gastric accommodation- mechanoreceptors sense the stretch in the wall of the stomach when food enters. This causes relaxation of the stomach. It is controlled by the ENS with vagal involvement. If there was no relaxation there would be an increase in intra-gastric pressure putting a greater strain on the sphincters, potentially resulting in reflux. So gastric accommodation causes no change in intra-gastric pressure.
Roles of the distal body and antrum
Has roles in mixing and emptying
Mechanism of action of the distal body and antrum
- Propulsion- peristaltic contractions which move food towards the pyloric sphincter and antrum. There will be occlusion of the pylorus.
- Grinding- the antrum is thick and muscular and crushes and grinds the food. Only particles below 2mm in diameter pass through the pylorus.
- Retropulsion- any larger particles are moved into the body to break them down.
Stomach- intrinsic pacemaker
The interstitial cells of Cajal have an intrinsic pacemaker function generating a membrane potential. This is a sub threshold so requires a further stimuli to generate muscle contractions. This can be Ach and gastrin (excitatory). Or it can be inhibited by NO, VIP and ATP. It is the origin of phasic contractions in the greater curvature of the corpus.
Stomach= gastro-gastro reflexes
Via the enteric nervous system. Distension of the reservoir stimulates antral contractions in anticipation of churning up the food. When the antrum is distended relaxation of the reservoir is required to accommodate the food that will be pushed back in the area to be broken down further. Distension of the antrum leads to prolonged relaxation of the reservoir.
Controls of gastric emptying- Intestinal break
By delaying gastric emptying you give the intestine time to deal with the food that is already there
Control of gastric emptying- stomach contents
Emptying is inhibited by stomach contents (i.e. HCl, amino acids and long chain fatty acids) entering the small intestine. Endocrine cells sense the contents of the gut and release hormones to control their emptying. The hormones are Cholecystokinin (CCK), glucagon-like peptide (GLP-1) and peptide YY.
Control of gastric emptying= Entero-gastric neural reflexes
Receptors in the wall of the duodenum detect the contents of the duodenum, this is sent though afferent fibres to the enteric NS. Vagus nerves then control gastric emptying.
Gastric emptying- Secretin
Low pH causes S cells to release secretin causing bicarbonate secretion. This reduces acid production in the stomach and decreases gastric emptying. The duodenal chemoreceptors also cause more secretin to be released which decrease gastric emptying. The acid in the lumen also reduces gastrin production, inhibiting gastric motility.
Gastric emptying- CCK
I cells produce CCK in response to fat, this decreases gastric emptying. The I cells are a type of duodenal chemoreceptor.
Gastric emptying- Enteric NS
The enteric NS acts to reduce gastric emptying, it does this through contraction of sphincters.
Gastric emptying- Hypertonicity
Hypertonicity is detected by the duodenal chemoreceptors an unidentified hormone is then released to decrease gastric emptying. The Hypotonicity signal is also sent via chemoreceptor afferents to the intramural intrinsic which directly decreases gastric emptying and through the CNS. The CNS increases sympathetic activity and decreases parasympathetic activity in order to decrease gastric emptying.
Vomiting (emesis)
The forceful expulsion of gastrointestinal contents through the mouth. There is contraction of the intercostal muscles generating an increased intrathoracic pressure which squeezes on the stomach. There is no contraction of the stomach muscle itself.
Retching (dry heave)
Chyme moves into the oesophagus due to relaxation of the distal oesophagus but this is followed by immediate backflow. Contraction of the proximal oesophagus stops expulsion. The backflow is due to secondary peristalsis.
What part of the brain causes vomiting
The Medulla Oblongata in an area called the vomiting centre. Sends signals to the respiratory, abdominal and oesophageal muscles and the oesophageal sphincter generating emesis
The receptors which stimulate vomiting
- Higher brain centres respond to stress, severe pain or if you see/smell a certain trigger.
- The Chemical trigger zone is outside the blood brain barrier and is able to detect toxins in the blood and induce vomiting to clear them i.e. morphine.
- Labyrinthine receptors in the ear- the body interprets vertigo as being due to toxin intoxication. This is why people experience motion sickness.
- Touch receptors in the throat- gag reflex.
- Mechanoreceptors and chemoreceptors in the stomach respond to stretch and cytotoxic substances
Mechanism of vomiting
1) Retrograde contraction in the jejunum
2) Chyme moves from the proximal small intestine to the relaxed stomach through the open pylorus, causes nausea and increases saliva
3) Rhythmic respiratory movements against the closed glottis produce negative oscillations in the intrathoracic pressure.
4) This produces retching and the epiglottis and soft palate close.
5) The abdominal muscles and diaphragm contract to increase the intra-abdominal pressure. Squeezing the stomach and forcing its contents out of the mouth, there is opening of the oesophageal sphincters and pyloric contraction.
The micro skills involved in giving a good explanation
1) Giving the right types of information
2) Giving the right amount of information
3) Achieve accurate recall and understanding