Esophageal Motility Flashcards
First 2 steps in processing of food
Chewing and swallowing
Chewing functions
Chewing:
- reduces the size of the food particles,
- increases surface area,
- mixes them with saliva to start the process of carbohydrate digestion (salivary amylase),
- and lubricates them to facilitate swallowing.
Swallowing phases
- Oral Phase (or voluntary phase) – the tip of the tongue
separates a bolus of food and forces it back toward the
pharynx. This stimulates the somatosensory receptors
initiating an involuntary swallowing reflex. - Pharyngeal phase – the food is propelled from the mouth
through the pharynx to the esophagus by several events
(all of which occur in less than 2 seconds). During this
phase respiration is reflexly inhibited.
These first two phases of swallowing are coordinated by the
swallowing center (located in the medulla) via a number of
cranial nerves.
- Esophageal Phase – the food is propelled through the esophagus to the stomach (controlled primarily by the swallowing center).
Upper esophageal sphincter fx.
prevents the entry of air at the top of the esophagus
lower esophageal sphincter (LES) fx.
prevents reflux of the gastric contents back into the
esophagus.
Outer muscle layer of esophagus distribution
- The pharynx, UES and the upper one third of the esophagus are composed of skeletal muscle.
- The middle one third is a transitional area and has both skeletal and smooth muscle.
- The lower one third of the esophagus and the LES are smooth muscle.
Primary vs. Secondary peristaltic waves
The swallowing center
then initiates a primary peristaltic wave that
sweeps the length of the esophagus.
Propulsion of food by this peristaltic
movement is active and is not influenced by
gravity (although liquids will travel faster due
to the additional effects of gravity).
If a bolus fails to travel the length of the
esophagus under these circumstances,
mechanosensory afferents are stimulated and
these initiate a secondary peristaltic wave to
finish the process. Secondary peristaltic waves do not involve the swallowing center and a person is
generally unaware that they are occurring. Peristalsis in the esophagus is largely a circular muscle
phenomenon. Although the longitudinal muscle is involved in peristalsis the driving force for moving
a bolus towards the stomach comes from circular muscle contraction.
Skeletal muscle vs. smooth muscle peristalsis
regions containing skeletal muscle the
control of motor activity that drives the peristaltic
wave is the result of coordinated firing of
extrinsic excitatory nerves via the nucleus
ambiguus (thus CNS is required).
In the smooth muscle portion of the esophagus the myenteric plexus controls coordination of peristalsis (thus CNS is not required).
Smooth muscle layers and their types of contractions
- Longitudinal muscle contracts in response to electrical stimulation of its intrinsic nerves and remains contracted until the stimulus is terminated (i.e. a duration response). This is a cholinergic phenomenon.
- Circular muscle exhibits a small contraction at the onset of stimulation of its intrinsic nerves (on response). At the end of stimulus there is a larger contraction (off response). The time between the end of the stimulus and the off response (latency) increases going from the proximal to the distal smooth muscle esophagus. This relates to the amount of nitric oxide (NO) being released from the myenteric plexus. Peristaltic waves are propagated in the smooth muscle portion of the esophagus because of this latency gradient.
- The LES is a tonically contracted region of increased pressure at the distal end of the esophagus. In response to electrical stimulation of its intrinsic nerves it relaxes. The LES therefore relaxes with swallowing. This precedes the peristaltic wave and the relaxation is maintained until the wave has passed.
Inhibition of LES tone (tonicity)
The tone of the LES is due to intrinsic muscle activity and is not blocked by neural inhibitors (e.g. TTX) or vagotomy but is decreased by calcium channel blockers (e.g. verapamil) and metabolic poisons such as cyanide (CN-).
Mechanism of LES relaxation
The mechanism of LES relaxation is unclear but is certainly neural in origin because it is blocked by TTX. As relaxation of the LES is not affected by cholinergic or adrenergic antagonists it is known as an NANC (Non-Adrenergic, Non-Cholinergic) response.
LES relaxation is mediated via nitric oxide (NO).
Agents that increase LES pressure
- Neurotransmitters - alpha-adrenergic agonists (norepinephrine), cholinergic agents and anticholinesterases.
- Hormones - gastrin, motilin, substance P and bombesin
- Other agents – protein, antacids, prostaglandin F2
Agents that decrease LES pressure:
• Neurotransmitters - beta-adrenergic agonists (isoproterenol), alpha-adrenergic antagonists
(phentolamine), anticholinergics (atropine) and dopamine.
- Hormones – progesterone, estrogen, secretin, CCK, glucagon, VIP, CGRP, somatostatin
- Other agents – fat, chocolate, ethanol, peppermint, smoking, nitrites, theophylline, calcium channel blockers, prostaglandin E2
DIFFUSE ESOPHAGEAL SPASM
an abnormal response to esophageal distension resulting in
uncoordinated, powerful and sustained contractions
of the muscles of the esophagus. This produces
severe chest pain (which may be confused with
cardiac arrest or angina pectoris).
NUTCRACKER ESOPHAGUS
(hypertensive peristalsis) is caused by abnormal, high
amplitude peristaltic waves in the distal esophagus. This condition is also painful.
ACHALASIA
results in a failure of the lower esophageal sphincter to open during swallowing. This results in severe esophageal distension (as much as 1 liter of decomposing food may accumulate) and an increased risk of aspiration pneumonia.
Achalasia may be caused by the lack of a functional myenteric plexus in the region of the lower esophageal sphincter (and loss of NO and VIP). Although achalasia may be painful, the pain involved is secondary to other symptoms and would ordinarily not be misdiagnosed as being related to the heart.
Esophageal ulceration, rupture, and death can occur.
GASTROESOPHAGEAL REFLUX
resulting from contents of the stomach refluxing into the
esophagus. Due to the intrathoracic location of the esophagus the pressure in the thoracic esophagus is close to intrathoracic pressure which is less than abdominal pressure.
Normally the UES will prevent air from entering the upper esophagus, and the LES will prevent the acidic contents of the stomach from entering the lower esophagus.
Gastroesophageal reflux disease (GERD)
is a chronic problem that should not be confused with
the intermittent episodes of “heartburn” that everyone experiences from time to time. The pathophysiological basis of GERD appears to be an incompetent lower esophageal sphincter. That
is to say, there is an absence of a fully functional gastroesophageal barrier.
However, it is now believed that the symptoms actually occur when the balance between “aggressive forces” (reflux and the potency of the refluxate) and “defensive forces” (esophageal acid clearance and mucosal integrity) moves in favor of the aggressive forces.
The symptoms of GERD include regurgitation, non-cardiac chest
pain, cough and bronchospasm. Unlike heartburn, chronic esophageal reflux ultimately causes damage of the esophageal epithelium by acid and pepsin in the refluxate. This can lead to epithelial destruction associated with neutrophil and eosinophil infiltration of the mucosa. Glandular, columnar epithelium (Barrett’s epithelium) occurs and this is now recognized as being a major risk factor for Barrett’s esophagus and adenocarcinoma.
COMMON DIAGNOSTIC TESTS
Endoscopy - visual examination (inflammation, tumors etc)
Barium studies - radiography, swallowing, clearance studies
Manometry - esophageal pressures
pH monitoring - acid monitoring
