Oesophagus and its disorders Flashcards

1
Q

What does the oesophagus lie posterior to?

A

Lies posterior to the trachea

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2
Q

Where does the the esophagus begin and where does it join the stomach?

A

Begins at end of laryngopharynx and joins the stomach a few cm from
diaphragm (at the cardiac orifice of the stomach)

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3
Q

What muscles surround the upper third of the oesphagus?

A

Skeletal muscles surround the upper third of the oesophagus, below the
pharynx

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4
Q

What muscles surround the lower 2/3rds of the oesphagus?

A

Smooth muscles surround the lower two thirds

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5
Q

What muscle is the UOS made from?

A

Striated muscle

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6
Q

Why is the UOS constricted?

A

Constricted to avoid air entering the oesophagus

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7
Q

What muscle is the LOS made up of?

A

Smooth muscle

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8
Q

What is the intrinsic components of the LOS made up of and what is it under the influence of?

A

Intrinsic components of LOS: oesophageal muscles; under
neurohormonal influence

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9
Q

What is the extrinsic component of LOS made of?

A

Extrinsic components of LOS: diaphragm muscle

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10
Q

What muscle types is the intrinsic components of the LOS made up of?

A

Thick circular smooth muscle layers and longitudinal muscles

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11
Q

What are the muscle fibres like on the right side of the LOS? What activity keeps them running?

A

Clasp-like semi-circular smooth muscle fibres on the right side
– Myogenic activity (some resting tone initiated by the cells within), but
less ACh-responsive

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12
Q

What are the muscle fibres like on the left side of the LOS and how do they work and what do they prevent?

A

Sling-like oblique gastric (angle of His) muscle fibres on the left side
– Work in concert with the clasp like-semicircular smooth muscle fibres,
help to prevent regurgitation- responsive to cholinergic innervation

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13
Q

Why is reflux common in infants?

A

Angle of His is poorly developed in infants for it makes a vertical
junction with stomach, hence why reflux is common in infants

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14
Q

What part of the diaphragm encircles the LOS and what does this form?

A

Crural diaphragm encircles the LOS
-Forms channel through which oesophagus enters the abdomen

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15
Q

What type of action do the fibres of the crural portion of the diaphragm posses?

A

Fibres of the crural portion of the diaphragm possess a “pinchcock-like”
action (extrinsic sphincter; diaphragmatic sphincter)- myogenic tone

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16
Q

What is the upper part of the esophagus innervated by? What neurotransmitter is involved?

A

Striated muscle fibres in upper part:
-Nucleus ambiguus gives out somatic motor neurons from vagus nerve(splanchnic nerves)
-Ach

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17
Q

What is the lower part of the oesophagus innervated by? What neurotransmitter is involved?

A

Smooth muscles in lower part:
-Innervated by visceral motor neurons of the vagus nerve with interruptions
-synapse with postganglionic neurons; cell bodies in oesophagus and splanchnic plexus

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18
Q

What is the neural control of the oesophageal sphincters?

A

Oesophagus is encircled by nerves of the
oesophageal plexus

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19
Q

What neurotransmitters contract the intrinsic sphincters?

A

Acetylcholine & SP contract the intrinsic
sphincters

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20
Q

What neurotransmitters relax the intrinsic sphincters?

A

NO & VIP relax the intrinsic sphincters

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21
Q

What does gastrin do to intrinsic factors?

A

Gastrin contracts the intrinsic sphincters

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22
Q

What is the route of impulses during swallowing? BASIC

A

-Afferent impulses in the glossopharyngeal- vagal reflex
-Integration of impulses in the nucleus of tractus solitarius (NTS), nucleus
ambiguus (NA) and dorsal vagal nucleus
-Efferent impulses/motor pathways pass to the pharyngeal musculature, tongue, along the oesophagus; the LOS opens

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23
Q

Explain innervation of the oesophagus? DETAILED

A

-Afferent sensory pathways detect food in pharynx as well as oesophagus and crural part of diaphragm and transmit impulses which are integrated in the NTS
-This triggers phrenic nerve which has a motor innervation to the crural parts of diaphragm causing contraction
-Myenteric plexus is also innervated by vagus nerve which innervates the LOS

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24
Q

What is inhibited during swallowing?

A

Inhibition of respiration (breathing)- nasopharynx is closed off

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25
Q

What is closed during swallowing and what is this to prevent?

A

Closure of glottis (around the vocal cords) by epiglottis
– Prevents food from entering the trachea

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26
Q

What waves behind the food mass move the food towards the stomach and at what rate?

A

Ring of peristaltic waves (4cm/sec) behind the food mass moves it towards the stomach

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27
Q

What does the second wave of peristalsis do during swallowing?

A

A second wave of peristalsis moves any food remnants along the
oesophagus

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28
Q

What happens as soon as food passes the UOS and what does this cause?

A

– UOS closes as soon as food passes
– Glottis opens
– Breathing resumes
– Coordinated peristalsis moves the food towards the LOS

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29
Q

What triggers secondary peristalsis?

A

Distension of the lumen of the oesophageal body by food remnants
stimulates the receptors → repeated waves of peristalsis (secondary
peristalsis)

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30
Q

What does secondary peristalsis ensure?

A

Secondary peristalsis ensures that all of the ingested food reaches the
stomach. Do not forget the role of vagal innervation - cholinergic (ACh, SP)
and non-cholinergic innervation (NO, VIP)
Introduction

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31
Q

What are the 3 mechanisms that prevent gastro-oesophageal reflux?

A
  1. LOS – closes after the food mass has passed
  2. “Pinchcock” effect of the diaphragmatic sphincter on the lower
    oesophagus (side-to-side compression between “2 pillars” of the crus)
  3. Plug-like action of the mucosal folds in the cardia– occludes the lumen
    of the gastro-oesophageal junction:
    – Intrabdominal pressure compresses the intra-abdominal parts of the
    oesophagus
    – Valve-like effect of oblique entry of oesophagus into stomach
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32
Q

What type of muscles are the sphincter muscles of the UOS and LOS and what do they act as?

A

Sphincter muscles of UOS and LOS = strong circular muscles
– Act as valves; and the law of the gut promotes and controls the movement
of the food mass aborally (movement towards the anus)

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33
Q

What is oropharyngeal dysphagia/aphagia? Why is it caused?

A

swallowing difficulty is caused by the
inability of the UOS to open or discoordination of the timing between the
opening of UOS and the pharyngeal push behind the ingested mass of food

34
Q

What is oesophageal spasm?

A

abnormal oesophageal contractions and food is not reaching the stomach effectively

35
Q

What is diffuse oesophageal spasm?

A

chest pain coming from oesophagus (angina-like pain)

36
Q

What is achalasia? And what needs to be assessed?

A

disorders of motility or peristalsis of oesophagus (assess the
motor function of the UOS, LOS and oesophageal body)

37
Q

What is regurgitation and what needs to be assessed?

A

reflux of stomach acids into oesophagus; weak LOS
(GORD); assess causes of regurgitation

38
Q

What may cause achalasia? And what does this result in?

A

Impaired LOS relaxation (spasms) -
* Can be accompanied by impaired
peristalsis (sphincter spasms);
* Food and liquids fail to reach the
stomach – delayed opening of LOS

39
Q

What is the aetiology of achalasia?

A
  1. Causes:
    -Viral triggers
    -Mutations and SNPs
    -HLA class II
  2. Results in:
    -Extracellular matrix turnover and wound repair
    -Inflammatory infiltrate
    -Humoral response(myenteric antibodies)
  3. Achalasia
    -Myenteric plexitis
    -Ganglion cell loss
    -Fibrosis
    -Impaired LOS
40
Q

What are the symptoms of achalasia?

A
  1. Dysphagia
  2. Vomiting/regurgitation
  3. Heartburn
    -Retrosternal burning sensation
    -Regurgitation
41
Q

How is achalasia diagnosed?

A
  1. Examine and take patients history
  2. Barium radiography
    -Dilation of oesphagus
    -Beak deformity at lower end
  3. Oesophageal manometry
    -Absent peristalsis
42
Q

Why is oesophageal manometry done?

A
  1. To determine cause of non-cardiac chest pain
  2. to determine cause of reflux
  3. To determine cause of swallowing difficulty
43
Q

Interpreting results of oesophageal manometry?

A

Pressure of LOS <26 mm Hg is normal; >100 mm Hg is considered achalasia; >
200 mm Hg is nut cracker achalasia

44
Q

What does a low LOS pressure in oesophageal manometry suggest?

A

Low LOS pressure suggests GORD

45
Q

What do normal results of oesophageal manometry show?

A
  • Normal LOS pressure and normal muscle contractions upon swallowing
  • The muscle contractions follow a normal pattern down the oesophageal body
  • Normal pressure of the LOS is about 15 mmHg
46
Q

What are abnormal results of oesophageal manometry characterised by?

A
  • Presence of muscle spasms in the oesophageal body
  • Presence of weak contractions along the length of the oesophagus
47
Q

What is achalasia characterised by and why?

A

Achalasia is characterised by high LOS pressure, the LOS fails to relax after
swallowing

48
Q

When does reflux in normal individuals occur?

A

Often occurs after meals in normal individuals (- due to transient
spontaneous LOS relaxation, tsr)

49
Q

What is an effective natural antacid in neutralise gastric acid?

A

Saliva is an effective natural antacid - dilutes and neutralises refluxed
gastric acid

50
Q

What can occur in normal individuals if there is a low rate of salivation or lack of ability to swallow own saliva during reflux?

A

Low rate of salivation or the lack of ability to swallow own saliva may
cause the prolongation of contact of refluxed gastric juice with
oesophagus → GORD

51
Q

What is GORD?

A

GORD is the retrograde movement of gastric content into oesophagus, due
to prolonged relaxation of the LOS

52
Q

What are factors that contribute to the severity of GORD?

A
  1. Weak or uncoordinated oesophageal contractions/ poor oesophageal motor activity
  2. Length of time the oesophagus is exposed to gastric acid
  3. Amount of pressure placed on the anti-reflux barrier
53
Q

What are factors associated with GORD?

A
  1. Pregnancy or obesity
  2. Less functional LOS
  3. Food
    -Large meals, fat, chocolate, coffee
  4. Drugs
    -Alcohol
    -Cigarette
54
Q

What is the pathophysiology of GORD?

A
  • 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
55
Q

What are the symptoms of GORD?

A
  • Heartburn and acid regurgitation
  • Wake up at night – reflux irritates the larynx
  • Belching
  • Dysphagia
56
Q

How would we investigate GORD?

A
  • Low dose proton pump inhibitor (PPI) challenge is 1st line
  • Upper GI endoscopy
  • Manometry
  • 24-hr ambulatory pH monitoring
57
Q

How do the findings from continuous pH monitoring work?

A
  • 24 hr hour pH monitoring shows that most normal individuals (non-refluxers) reflux on a daily basis
  • But, GORD implies not just the presence of
    reflux, but reflux in excess of that experienced by non-refluxers
58
Q

Why is there an increased chance of GORD in last trimester of pregnancy?

A

Last trimester of pregnancy is associated with increased abdominal
pressure which forces gastric contents into oesophagus

59
Q

What does a foetus do to the abdominal contents?

A

Foetus increases pressure on abdominal contents
– Pushes terminal segments of oesophagus into thoracic cavity

60
Q

Why does heartburn subside in last months of pregnancy?

A

Heartburn subsides in the last months of pregnancy as uterus descends
into pelvis

61
Q

What is the general mechanism of antacids?

A

-Neutralise gastric acid
-Increase pH of gastric acid

62
Q

What can prolonged dosing of antacids lead to?

A

-Can lead to healing of duodenal ulcers
-Less effective for gastric ulcers

63
Q

What does bismuth chelate protect?

A

Protects gastric mucosa

64
Q

How does bismuth chelate work?

A

– Forms a base over crater of the ulcer
– Adsorbs pepsin
– ↑ HCO3- and PG secretion

65
Q

What is bismuth chelate and therefore what can it be used for?

A

Toxic against H. pylori – used as part of triple therapy to eradicate it

66
Q

What does bismuth chelate blacken?

A

Blackens stool and tongue

67
Q

What children can bismuth chelate not be used it and why so?

A

NOT use in children with chicken pox or
flu-like symptoms as can cause Reye’s
syndrome.

68
Q

What is cimetidine?

A

H2 receptor antagonist

69
Q

What is omeprazole?

A

Proton pump inhibitor

70
Q

What do H2 receptor antagonists and proton pump do?

A

↓ acid secretion and help heal the ulce

71
Q

The removal of what is essential to prevent ulcers returning when using H2 receptor antagonists and proton pump inhibitors and how is this done?

A

removal
of H. pylori (bacteria) is essential to stop the ulcer returning; for that,
combination therapy including antibiotics have to be used

72
Q

What is the mechanism of action for H2 receptor antagonists?

A
  • Inhibit histamine-, ACh- and gastrin-stimulated acid secretion
  • Reduce gastric acid secretion and as a consequence reduce pepsin
    secretion
73
Q

What do H2 receptor antagonists promote healing of?

A

Promote the healing of duodenal ulcers

74
Q

What can H2 receptor antagonists be used for?

A
  • Peptic ulcer
  • Reflex oesophagitis
75
Q

What are examples of non-pharmacological treatment of GORD?

A
  1. Lifestyle changes
  2. Avoid large meals
  3. Avoid lying down after meals
  4. Avoid smoking and drugs
76
Q

What is a possible surgical treatment of GORD?

A

Anti-reflux surgery (fundoplication – wrap fundus around LOS)

77
Q

What can fundoplication cause?

A

Fundoplication can cause dysphagia as it can reduce the
distensibility of LOS

78
Q

What does acid reflux do to squamous mucosa?

A

Acid reflux → desquamation of oesophageal cells (injury of squamous
mucosa

79
Q

What does increased cell loss in oesophagus cause?

A

↑ cell loss → basal cell hyperplasia

80
Q

What can excessive desquamation result in?

A

Excessive desquamation → ulceration

81
Q

What may happen to ulcers if they worsen and what can this lead to?

A

Ulcers may haemorrhage, perforate or heal by fibrosis with strictures
- Leads to barrett’s oesophagus and oesophageal cancer