The Oesophagus and Its Disorders Flashcards

1
Q

The oesophagus has 2 sphincters. Describe these.

A

Oesophagus has an upper and lower oesophageal sphincter

(UOS): striated, musculo-cartilaginous structure. Constricted to stop air entering the oesophagus

(LOS): smooth muscle; acts as a flap valve. An area of high pressure, and has intrinsic and extrinsic components

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2
Q

Describe and explain the intrinsic components of the LOS

A

Intrinsic components of LOS:
Thick circular smooth muscle layers and longitudinal muscles

Clasp-like semi-circular smooth muscle fibres on the right side. These are myogenic but less ACh-responsive

Sling-like oblique gastric (angle of His) muscle fibres on the left side. These work w the clasp semicircular smooth muscle to prevent regurgitation. ACh responsive

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3
Q

Describe and explain the extrinsic components of the LOS

A

Extrinsic components of LOS:
The crural diaphragm functions as an adjunctive external sphincter which encircles the oesophagus. It raises the pa in the LOS related to the movements of respiration.
Fibres of the crural diaphragm have myogenic “pinchcock-like” action, pressing against the sides of the oesophagus

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4
Q

Summarise oesophageal motor innervation

A

The striated upper oesophagus is innervated by somatic efferent cholinergic fibres of the vagus nerve. This vagus nerve originates from the nucleus ambiguus.

Distal, smooth muscle oesophagus is innervated by preganglionic vagus nerve fibres from the dorsal motor nucleus.

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5
Q

Describe the involvment of neurotransmitter in oesophageal innervation

A

ACh affects 2 post-ganglionic neurons in the myenteric plexus: excitatory cholinergic neurons and inhibitory nitrinergic neurons via NO, VIP.

Ach, SP and Gastrin is involved in contraction, NO/VIP is involved in relaxation of the intrinsic sphincters. Coordinated contraction and relaxation using these= peristalsis

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6
Q

Describe swallowing of food and subsequent peristalsis

A

Skeletal muscle pushes bolus into pharynx. Food moves to oropharynx → laryngopharynx→oesophagus and stomach

Closure of glottis by epiglottis prevents food entering the trachea
The dorsal vagal nucleus and the nucleus ambiguus mediates peristalsis and sphincter relaxation.

Vagal efferent fibres communicate w myenteric neurons that relax the LOS. LOS closes after the food mass has passed

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7
Q

Why is secondary peristalsis important?

A

Large food material doesn’t reach the stomach after the 1st peristaltic wave

Distension of the lumen of the oesophagus by food stimulates receptors to repeat waves of secondary peristalsis

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8
Q

How does the LOS and the diaphragmatic sphincter prevent reflux?

A

LOS – closes after the food mass has passed
“Pinchcock” effect of the diaphragmatic sphincter on the lower oesophagus

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9
Q

How do mucosal folds in the cardia, and sphincter muscles of the UOS and LOS prevent reflux?

A

Mucosal folds in the cardia closes the lumen of the gastro-oesophageal junction:
Intrabdominal pa compresses intra-abdominal parts of the oesophagus. This creates a valve-like, oblique entry of oesophagus into stomach (adults only)

UOS and LOS = strong circular muscles which act as valves
Prevent reflux by forming an opening when relaxed and closing completely when contracted

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10
Q

Determine the main causes of swallowing difficulties

A

Oropharyngeal dysphagia- inability of the UOS to open or discoordination between the opening of UOS and the pharyngeal push behind ingested food

Oesophageal spasm- abnormal oesophageal contractions. Food isn’t reaching the stomach effectively

Diffuse oesophageal spasm- chest pain coming from oesophagus (angina-like)

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11
Q

What is the pathophysiology of achalasia?

A

Findings may vary:
Impaired LOS relaxation (spasms)
Impaired peristalsis (sphincter spasms)
Food and liquids fail to reach the stomach due to delayed opening of LOS
This causes bird’s beak appearance on an oesophagram
Initiating factor for this is thought to be autoimmune or infection

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12
Q

What are the symptoms of achalasia?

A

Dysphagia: difficult/painful swallowing

Vomiting/regurgitation

Heartburn due to:
oesophageal dysmotility
Retention of ingested (acidic) food
Lactic acid generation during decomposition of retained food;
Retention of gastric acid refluxed in the oesophagus due to poor emptying and incomplete LOS relaxation

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13
Q

What steps would you take to diagnose achalasia?

A

Take: patient history and evaluate any swallowing disorders
Some swallowing abnormalities may be frequent in elderly- eg swallowing slowly/coughing
Barium swallow shows oesophageal dilation w lower end beak deformity
Evaluate the entire swallowing channel (mouth, pharynx, and oesophagus)
Carry out oesophageal manometry: absent peristalsis in the body of the oesophagus.

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14
Q

Why should oesophageal manometry be carried out?

A

To determine the cause of non-cardiac chest pain
To evaluate the cause of reflux (GORD? Or achalasia?)
To determine the cause of swallowing difficulty (does UOS/LOS contract and relax in a coordinated fashion?)

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15
Q

How would you interpret the results of oesophageal manometry?

A

Normal LOS pa=15 mmHg, but when the LOS relaxes to let food into the stomach, pa is <10 mmHg

If LOS pa is < 10mmHg in the absence of food into the stomach, GORD can be suspected. Other manometric findings:
LOS fails to relax upon wet swallow (<75% relaxation)
LOS pa>100 is achalasia because the LOS fails to relax after swallowing. > 200 is nut cracker achalasia
Aperistalsis in oesophageal body
Relative increase in intra-oesophageal pa compared w intra-gastric pa

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16
Q

Describe the oesophageal manometry procedure

A

Local anaesthetic
Lubricated catheter is inserted into the nostril→ throat → oesophagus → stomach
Patient takes a deep breath and swallows water.
The catheter measures strength and coordination of muscle contractions as well as strength and relaxation function of the LOS
Catheter is slowly removed at the end

17
Q

What is GORD

A

Gastro oesophageal reflux disease/GORD: movement of gastric content into oesophagus due to prolonged LOS relaxation

Reflux is more frequent, causing oesophageal irritation and damage

18
Q

What are the causes of gastro oesophageal reflux disease (GORD)

A

Transient spontaneous LOS relaxation (tsr)
Resting LOS pa is too weak to resist the pressure within the stomach
Sudden, sustained relaxation of the LOS that is not induced by swallowing
Malfunction of extrinsic and intrinsic components of LOS

Factors associated inc pregnancy/obesity which increases abdominal pa, large meals, tomatoes, orange juice, cigs and alcohol, anticholinergic drugs

19
Q

Give the pathophysiology of GORD

A

Resting LOS tone= low/absent
LOS tone fails to increase when lying flat or during pregnancy
Poor oesophageal peristalsis →↓ clearance of gastric acid
A hiatus hernia (impairs the functioning of LOS and diaphragm closing mechanisms)
Delayed gastric emptying

20
Q

Give the symptoms of GORD

A

Heartburn and acid regurgitation
Wake up at night – reflux irritates the larynx
Belching
Dysphagia

21
Q

How would you investigate GORD?

A

Low dose proton pump inhibitor (PPI) to see if the body responds
Upper GI endoscopy
Manometry
24-hr ambulatory pH monitoring would show excess reflux

22
Q

How can general antacids be used to treat GORD?

A

Antacids contain Sodium alginate, Sodium bicarbonate,
Calcium carbonate to neutralise gastric acid (peptic activity stops at pH 5)
Alginic acid + saliva float on gastric lumen content and protects the oesophageal mucosa from reflux
Prolonged dosing can heal duodenal ulcers, but less effective for gastric ulcers

Magnesium salts→ diarrhoea
Aluminium salts→ constipation
Use a mixture of 2 to ensure bowel function

23
Q

Give an example of an antacid with cytoprotective effects

A

Bismuth chelate:
Protects gastric mucosa
Forms a base over crater of the ulcer
Adsorbs pepsin
↑ HCO3- and PG secretion
Toxic against H. pylori – used as part of triple therapy to eradicate it

But blackens stool and tongue, do not use in children w chicken pox or flu-like symptoms as can cause Reye’s syndrome.

24
Q

What are H2 receptor antagonists and how can they be used to treat GORD?

A

H2 receptor antagonists: ranitidine, cimetidine, famotidine, nizatidine

Inhibit histamine, ACh and gastrin stimulated acid secretion
Reduce gastric acid secretion and therefore reduces pepsin secretion
Promote the healing of duodenal ulcers

25
Q

Give non pharmacological treatments for GORD

A

Life-style changes: raise head of bed at night, weight loss, modify food
Lose weight if overweight
Avoid foods that increase gastric acidity or that slow gastric emptying e.g fatty foods
Avoid some drugs/smoking
Anti-reflux surgery (fundoplication – wrap fundus around LOS)
Caution: Fundoplication can cause dysphagia as it can reduce LOS distensibility

26
Q

What are the complications and long term effects of GORD?

A

Oesophagus has squamous mucosa
Acid reflux → desquamation of oesophageal cells (injury of squamous mucosa)
↑ cell loss, causing basal cell hyperplasia
Excessive desquamation → ulceration
Ulcers may haemorrhage, perforate or heal by fibrosis with strictures
This leads to Barrett’s oesophagus and oesophageal cancer