The Oesophagus and its Disorders Flashcards

1
Q

Describe the anatomy of the oesophagus.

A
  • it is a fibromuscular tube (25 cm) of striated squamous epithelium
  • it lies posterior (behind) to the trachea
  • it begins at the end of the laryngopharynx and joins the stomach a few centimetres from the diaphragm (at the cardiac orifice)
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2
Q

What promotes the transport of ingested food into the stomach?

A

The relaxation of the sphincters (UOS and LOS).
This is a highly coordinated muscular process; it involves contraction and relaxation of the oesophagus and transports the food through the GIT.

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3
Q

Describe the two sphincters of the oesophagus.

A

The oesophagus has two sphincters:
- UOS (upper oesophageal sphincter) = striated muscle
It has a musculo-cartilaginous structure, and it is constricted to avoid air entering the oesophagus.

  • LOS (lower oesophageal sphincter) = smooth muscle
    It is a high-pressure area. The LOS has extrinsic and intrinsic components to it. The intrinsic component is the oesophageal muscles, under neurohormonal influence(eg. NO, Ach controls the level of constriction). The extrinsic component is the diaphragm muscle.
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4
Q

Describe the components of the LOS.

A

INTRINSIC COMPONENTS:

  1. thick, circular smooth muscle layers.
  2. clasp-like, semicircular smooth muscle fibres (on the right-hand side)
    • it has myogenic activity (so some resting tone) but is less ACh-responsive
  3. Sling-like, oblique gastric (angle of His) muscle fibres on the left-hand side)
    • it is working in concert with the clasp-like smooth muscle fibres to help prevent regurgitation; it’s responsive to cholinergic innervation
    • the Angle of His is poorly developed in infants as it makes a vertical junction with the stomach, hence why reflux is common in infants

EXTRINSIC COMPONENTS:

  • The crural diaphragm encircles the LOS, and forms a channel through which the oesophagus enters the abdomen.
  • The fibres of the crural portion of the diaphragm posses a ‘pinchcock-like’ action to stop any reflux of acidic chyme into the oesophagus; if not treated, it leads to GORD, which can result in Barrett’s, then cancer.
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5
Q

Describe the neural innervation of the oesophageal sphincters.

A
  • acetylcholine, SP: contraction of intrinsic sphincters

- NO, VIP: relax the intrinsic sphincters

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6
Q

Describe the neural innervation of the oesophagus itself.

A

UPPER PART made up of STRIATED MUSCLE

  • supplied by somatic motor neurons of the vagus nerve without interruptions):
  • (so the vagus and splanchnic nerve)

LOWER PART made up of SMOOTH MUSCLE:

  • innervated by visceral motor neurons of the vagus nerve with interruptions
  • these synapse with postganglionic neurons; cell bodies in the oesophagus and splanchnic plexus
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7
Q

Describe oesophageal motor innervation.

A

The striated muscle of the upper oesophagus is innervated directly by the somatic efferent cholinergic fibres of the vagus nerve, originating from the nucleus ambiguus (releasing stimulatory ACh).

The smooth muscle of the of the distal oesophagus is innervated by the preganglionic vagus nerve fibres from the dorsal motor nucleus. ACh affects two types of post-ganglionic neurons in the myenteric plexus: excitatory cholinergic neurons and inhibitory nitrinergic neurons via NO and VIP.

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8
Q

List some functions of the oesophagus.

A
  • swallowing (deglutition)

- conveys food and fluids from the pharynx to the stomach

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9
Q

Describe the coordination of swallowing.

A

Swallowing is triggered by afferent impulses in the trigeminal, glossopharyngeal and vagus nerves.
The efferent impulses pass to the pharyngeal musculature and the tongue (the trigeminal, facial and vagus nerves supply the tongue muscles).

The integration of these impulses occurs in the nucleus tractus solitarius (NTS), the nucleus ambiguus (NA) and the dorsal vagal nucleus (DVN).

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10
Q

How is swallowing initiated?

A

1) VOLUNTARY actions, where we collect material on the tongue and push it backwards into the pharynx
2) waves of INVOLUNTARY contractions then push the material into the oesophagus

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11
Q

What ‘extracurricular’ events occur during swallowing?

A
  • inhibition of respiration, so the nasopharynx is closed off
  • closure of the glottis (around the vocal cords) by the epiglottis
  • a ring of peristaltic waves behind the material move it towards the stomach
  • a second wave of peristalsis moves any food remnants along
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12
Q

Why is secondary peristalsis necessary?

A

A large amount of food material does not reach the stomach after the first peristaltic wave.

Hence, there is stimulation of receptors upon distention of the lumen of the oesophagus by the food, which causes repeated waves of peristalsis, aka. secondary peristalsis.

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13
Q

What prevents the reflux of gastric contents?

A

1) LOS (closes after material passes)
2) the ‘pinchcock’ effect of the diaphragmatic sphincter on the lower oesophagus
3) the plug-like action of the mucosal folds in the cardia

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14
Q

Expand on the pathophysiology of achalasia.

A
  • impaired LOS relaxation
  • can be accompanied by impaired peristalsis (sphincter spasms)
  • foods and liquids fail to reach the stomach (delayed emptying of LOS)
  • results in dilatation of the oesophageal body with distal narrowing
  • long periods of sporadic dysphagia (difficulty swallowing)
  • regurgitation of food
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15
Q

List some causes of achalasia.

A
  • disorders of motility or peristalsis of the oesophagus
  • damage to the innervation of the oesophagus
  • degenerative lesions of the vagus nerve, and loss of the myenteric plexus ganglionic cells in the oesophagus
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16
Q

List some symptoms of achalasia.

A
  • dysphagia
  • vomiting
  • heartburn
17
Q

What are two tests used in the diagnosis of achalasia?

A

1) BARIUM RADIOGRAPHY: allows for the evaluation of the entire swallowing channel (mouth, pharynx and oesophagus)
2) OESOPHAGEAL MANOMETRY: checks to see if the oesophagus is contracting relaxing properly

18
Q

What different diseases do different LOS pressures indicate?

A

.Low LOS pressure suggests GORD (although GORD can occur in individuals with normal LOS pressure).

High LOS pressure suggests achalasia.

<26 mmHg = normal
>100 mmHg = achalasia
>200 mmHg = nut-cracker achalasia

19
Q

What do the results of oesophageal manometry suggest in each case?

A

Normal results of an oesophageal manometry would show:

  • the pressure of the muscle contractions that move food down the oesophagus is normal
  • the muscle contractions follow a normal pattern down the oesophagus

Abnormal results show/are characterised by:

  • the presence of muscle spasms in the oesophageal body
  • the presence of weak contractions along the length of the oesophagus
20
Q

Describe reflux in normal individuals.

A

The reflux is often brief, and relatively infrequent.

It often occurs after meals in normal individuals (due to transient spontaneous LOS relaxation, aka TSR).

The reflux usually stimulates salivation. Saliva is an effective natural antacid - it dilutes and neutralises the refluxed gastric contents.

21
Q

What is GORD?

A

GORD stands for Gastro-Oesophageal Reflux Disease. It is when reflux is more frequent and troublesome.

Also, there is sometimes a low rate of salivation. This leads to a lack of ability to swallow own saliva, which leads to the prolongation of contact of the refluxed material with the oesophagus. This results in oesophageal irritation and oesophageal damage.

22
Q

List some causes of reflux in those with GORD.

A

1) transient spontaneous LOS relaxation (TSR)
2) resting LOS pressure is too weak to resist the pressure within the stomach
3) sudden relaxation of the LOS that isn’t induced by swallowing

23
Q

What are some factors that could contribute to the severity of GORD?

A
  • weak or uncoordinated oesophageal contractions
  • length of time the oesophagus is exposed to gastric acid
  • amount of pressure placed on the anti-reflux barrier
24
Q

What are some factors associated with GORD?

A
  • pregnancy/obesity
  • fat, chocolate, coffee or alcohol ingestion
  • large meals, tomatoes, orange juice, onions, etc.
  • cigarettes
  • drugs (eg. anticholinergic agents, calcium channel clockers and nitrate drugs)
25
Q

What are some symptoms of GORD?

A
  • heartburn and acid regurgitation
  • waking up at night (the reflux irritates the larynx)
  • dysphagia (difficulty swallowing)
26
Q

How would you investigate GORD?

A
- low dose proton pump inhibitor (PPI) challenge is the first line
then:
- upper GI endoscopy
- manometry
- 24-hour ambulatory pH monitoring
27
Q

How does pregnancy affect GORD?

A

The foetus increases the pressure on the abdominal contents. It pushes the terminal segments of the oesophagus into the thoracic cavity.
The last trimester of pregnancy is associated with increased abdominal pressure, and this forces gastric contents into the oesophagus. The heartburn subsides in the last months of pregnancy as the uterus descends into the pelvis.

28
Q

What are some potential long-term effects of GORD?

A
  • oesophagitis (inflammation)
  • squamous cell carcinoma
  • Barrett’s Syndrome - this may predispose someone to oesophageal adenocarcinoma
  • oesophageal ulcer
29
Q

Describe the management and drug treatment of GORD.

A

There are some lifestyle changes that can help alleviate the symptoms of GORD. Examples include:
losing weight, avoiding food that increases gastric acidity, that slow gastric emptying, avoiding drugs and smoking, etc.

There is also the option of anti-reflux surgery (a fundoplication, where you wrap the fundus around the LOS).
Taking antacids is another option, H2-receptor antagonists and proton pump inhibitors.

30
Q

Describe a possible problem with the use of antacids in the treatment of GORD.

A

They neutralise gastric acid, increasing the pH of the gastric lumen. They inhibit peptic activity and stop acid secretion.

However, magnesium salts cause diarrhoea while aluminium salts cause constipation. We use a mixture of the two to ensure bowel function.

31
Q

Why do we study oesophageal disorders?

A

There are many complications of GORD.
(the oesophagus has squamous mucosa)

The acid reflux could lead to the desquamation of oesophageal cells. The increased cell loss causes basal cell hyperplasia.
The excessive desquamation causes ulceration. The ulcers may haemorrhage, perforate or heal by fibrosis with strictures.

This leads to Barrett’s oesophagus and oesophageal cancer.