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(gastro) upper gastrointestinal tract Flashcards

1
Q

what two sphincters are present in the oesophagus?

A

upper oesophageal sphincter (true sphincter)

lower oesophageal sphincter (physiological sphincter)

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2
Q

what are the three divisions of the oesophagus?

A

cervical oesophagus, (upper, middle and lower) thoracic oesophagus, abdominal oesophagus

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3
Q

what type of muscle is present in the cervical oesophagus?

A

skeletal

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4
Q

what type of muscle is present in the upper thoracic oesophagus?

A

skeletal and smooth

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5
Q

what type of muscle is present in the lower thoracic oesophagus?

A

smooth

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6
Q

at which spinal level does the oesophagus start and at which does it end?

A

approx C5 to T10

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7
Q

at which spinal level does the diaphragm start?

A

approx T10

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8
Q

what is the upper 1/3 of the oesophagus called?

A

proximal oesophagus

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9
Q

what is the lower 1/3 of the oesophagus called?

A

distal oesophagus

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10
Q

differentiate between the upper and the lower esophageal sphincter

A

while the upper oesophageal sphincter is a true, anatomical sphincter, the LOS is a physiological sphincter

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11
Q

why is it important that the anatomical contributions to the lower oesophageal sphincter are kept intact?

A

if they are affected, sphincter function can be compromised

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12
Q

what are the four main anatomical contributions to the lower oesophageal sphincter?

A

approx 3-4cm of distal oesophagus is within abdomen

the LOS is surrounded by the diaphragm via the left & right crura

an intact phrenoesophageal ligament

angle of His

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13
Q

how does the abdominal location of the distal oesophagus help with LOS function?

A

any increase in intrabdominal pressure will cause an increase in LOS pressure, contributing to function (i.e. keeping it closed when required)

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14
Q

how does the diaphragm help with LOS function?

A

diaphragm contracts against the sphincter using the left and right crura (i.e. scissor-like contraction)

= contributes to LOS effectiveness

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15
Q

how does the intact phrenoesophageal ligament help with LOS function?

A

the ligament anchors the distal oesophagus to the diaphragmatic barrier and prevents reflex + allows movement during respiration & digestion

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16
Q

what is the phrenooesophageal ligament?

A

ligament that allows attachment of the diaphragm to the oesophagus to allow independent movement during respiration and swallowing

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17
Q

describe the superior limb of the phrenoesophageal ligament

A

attaches the lower oesophagus to the superior surface of the diaphragm

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18
Q

describe the inferior limb of the phrenoesophageal ligament

A

attaches the cardia region of the stomach to the inferior surface of the diaphragm at the cardiac notch of stomach

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19
Q

what is the angle of His?

A

acute angle between the distal abdominal oesophagus and the cardia of the stomach at the gastroesophageal junction

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20
Q

how does the angle of His contribute to LOS function?

A

awkward angle prevents the reflux of stomach acid, bile and digestive enzymes into the oesophagus

= prevents oesophageal inflammation + reflux disease

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21
Q

how does the fundus respond after a large meal to prevent reflux?

A

fundus extends from left to right and compresses the distal oesophagus, making it narrower

= prevents reflux disease

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22
Q

what is a physiological sphincter?

A

wherein its resting arrangement cannot be distinguished from adjacent tissue = sphincter non-recognisable

don’t have localised muscle thickening (unlike anatomical sphincters)

sphincteric action is achieved through muscle contraction around them

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23
Q

what are the four stages of swallowing?

A

stage 0: oral phase
stage 1: pharyngeal phase
stage 2: upper oesophageal phase
stage 3: lower oesophageal phase

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24
Q

what happens in stage 0 of swallowing?

A

oral phase

  • chewing & saliva prepare bolus
  • both oesophageal sphincters constricted
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25
Q

what is the state of the sphincters during the oral phase (phase 0)?

A

both oesophageal sphincters constricted

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26
Q

what happens in stage 1 of swallowing?

A

pharyngeal phase

pharyngeal musculature guides food bolus towards oesophagus

upper oesophageal sphincter opens reflexly

the lower oesophageal sphincter opened by vasovagal reflex (receptive relaxation reflex)

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27
Q

what happens in stage 2 of swallowing?

A

upper sphincter closes

superior circular muscle rings contract & inferior rings dilate

sequential contractions of longitudinal muscle

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28
Q

what happens in stage 3 of swallowing?

A

lower sphincter closes as food passes through

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29
Q

in swallowing, what guides the food bolus to the oesophagus?

A

pharyngeal musclulature contraction

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30
Q

in swallowing, how and when does the lower oesophageal reflect open?

A

during the pharyngeal phase

via the vasovagal reflex (receptive relaxation reflex)

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31
Q

how is the bolus of food pushed down the oesophagus in the upper oesophageal phase?

A

superior circular muscle rings contract & inferior rings dilate

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32
Q

compare the time and length of opening for the upper and lower oesophageal sphincters

A

UOS = opens in the pharyngeal phase and closes in the upper oesophageal phase

LOS = opens in the pharyngeal phase and closes only in the lower oesophageal phase, after the food passes out of the oesophagus

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33
Q

what is manometry?

A

diagnostic test to measures the strength, pressure and muscle coordination of your oesophagus when you swallow

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34
Q

why is manometry important?

A

used to investigate and identify pathologies related to oesophageal motility

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35
Q

how is manometry carried out?

A

thin, pressure-sensitive tube is passed through the nose, along the back of the throat, down the esophagus, and into the stomach

= the strength and pressure of contractions is investigated

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36
Q

what is the pressure of normal peristaltic waves?

A

approx 40 mmHg

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37
Q

why is there a migration of peristaltic waves during swallowing?

A

to propel and propagate the bolus of food down the oesophagus

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38
Q

what is the lower oesophageal sphincter resting pressure?

A

approx 20 mmHg

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39
Q

when does the LOS resting pressure change and how?

A

decreases by approx 5mmHg during receptive relaxation reflex in the pharyngeal phase of swallowing phase

= to allow the LOS to open

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40
Q

why does the LOS resting pressure decrease during receptive relaxation?

A

in order to allow the LOS to open and allow the bolus of food to enter the stomach

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41
Q

what stimulates the decrease in LOS resting pressure?

A

mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurones of the myentiric plexus

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42
Q

what are NCNA neurones?

A

noncholinergic nonadrenergic (NCNA) neurones

part of the myenteric plexus

responsible for stimulating a decrease in LOS resting pressure

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43
Q

what is the function of NCNA neurones in swallowing?

A

stimulate a decrease in LOS resting pressure to enable the LOS to open in the pharyngeal phase of swallowing

= allows food bolus to exit the oesophagus and enter the stomach

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44
Q

which neurones carry out the antagonistic action to NCNA neurones and how?

A

cholinergic fibres which, if excited, will cause muscle shortening, and prevent the relaxation of the LOS so the bolus of food cannot exit the oesophagus

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45
Q

how is oesophageal motility investigated?

A

using manometry

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46
Q

what form do functional disorders of the esophagus usually take?

A

strictures that can be either benign or malignant

(must be excluded first before diagnosing anything else)

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47
Q

besides strictures, what are the functional disorders of the oesophagus caused by?

A

1) abnormal oesophageal contraction: hypermotility, hypomotility, disordered contraction
(2) failure of protective mechanisms against reflux: GORD

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48
Q

what condition is most commonly caused by LOS dysfunction?

A

GORD

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49
Q

define dysphagia

A

fficulty in swallowing

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50
Q

define odynophagia

A

pain on swallowing

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51
Q

define regurgitation

A

return of oesophageal contents from above an obstruction

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52
Q

define reflux

A

passive return of gastroduodenal contents to the mouth

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53
Q

differentiate between reflux and vomiting

A

reflux is the passive return of gastroduodenal contest to the mouth whereas vomiting is the forceful throwing up of stomach contents

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54
Q

what must you clarify when taking a dysphagia history?

A

localisation (i.e. cricopharyngeal sphincter - UES - or more distal)

type (for soids/fluids, intermittent/progressive)

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55
Q

what are the two types of regurgitation?

A

function or mechanical regurgitation

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56
Q

differentiate between regurgitation and reflux

A

while regurgitation = return of oesophageal contents from above an obstruction (functional or mechanical), reflux = passive return of gastroduodenal contents to tehmouth

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57
Q

what is a stricture?

A

an abnormal narrowing of a bodily passage (as from inflammation, cancer, or the formation of scar tissue)

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58
Q

give an example of mechanical regurgitation

A

something being swallowed and getting stuck in the oesophagus, causing an obstruction

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59
Q

what is hypermotility?

A

abnormally increased or excessive activity or movement, particularly in the digestive tract

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60
Q

give an example of a oesophageal disease of hypermotility

A

achalasia

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61
Q

what causes achalasia?

A

due to the progressive degeneration & loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall

= decreased activity of inhibitory NCNA neurones.
= increase LOS pressure
= failure of LOS relaxation + impaired peristalsis in the distal oesophagus

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62
Q

what happens as a result of achalasia?

A

decreased activity of inhibitory NCNA neurones.

= increase LOS pressure
= failure of LOS relaxation + impaired peristalsis in the distal oesophagus

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63
Q

what is the proposed model of achalasia pathophysiology?

A

environemntal trigger + genetic predisposition

release of inflammatory infiltrates

extracellular turnover, wound repair and fibrosis

loss of immunological tolerance

apoptosis of neurones

absence of peristalsis + failure of LOS relaxation (+ humoral response of antimyenteric antibody production)

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64
Q

what are the two types of achalasia?

A

primary achalasia (aetiology unknown)

secondary achalasia

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65
Q

what are the causes of primary achalasia?

A

the aetiology of the condition is unknown

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66
Q

what are the causes of secondary achalasia?

A

diseases causing oesophageal motor abnormalities similiar to primary achalasia

e. g.
- Chagas’ disease
- protozoa infection
- amyloid/sarcoma/eosinophilic oesophagitis

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67
Q

in achalasia, which cells are affected and how?

A

ganglion cells of the Auerbach’s myenteric plexus in the LOS wall

= progressive degeneration OR loss of cells leads to reduced inhibitory NCNA neurone activity

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68
Q

how are NCNA neurones affected as a result of achalasia and what are the implications of this?

A

progressive loss and degeneration of the inhibitory NCNA neurones in Auerbach’s myenteric plexus

= so reduced inhibitory activity so increased pressure of the LOS

= reduced relaxation of the LOS

= impairs effective passage of food bolus from the oesophagus into the stomach

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69
Q

what are two possible causes of the hypermobility seen in achalasia?

A

either (1) diminished activity of the inhibitory NCNA neurones in the LOS wall OR (2) increased neuronal activity of the cholinergic neurones

= both acting to increase LOS pressure

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70
Q

what are two possible causes of the hypermotility seen in achalasia?

A

either (1) diminished activity of the inhibitory NCNA neurones in the LOS wall OR (2) increased neuronal activity of the cholinergic neurones

= both acting to increase LOS pressure

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71
Q

how and why does the resting pressure of the LOS change in hypermotility?

A

increased resting pressure of the LOS in hypermobility

= the inhibitory action of the NCNA neurones is lost due to damage to the ganglion cells of Auerbach’s myenteric plexus

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72
Q

in achalasia, how does the pressure of the LOS compare to that of the stomach?

A

the pressure of the LOS is significantly higher than that of the stomach

(during the receptive relaxation reflex of the pharyngeal phase of swallowing normally but sets in later in achalasia)

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73
Q

what is the impact of the failed relaxation of the LOS on the oesophagus?

A

swallowed food collects in oesophagus causing increased pressure throughout with dilation of the oesophagus

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74
Q

what are the possible complications of achalasia?

A

oesophagitis and pneumonia

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75
Q

explain how achalasia can lead to oesophagitis and pneumonia

A

damage to ganglion cells of Auerbach’s myenteric plexus

reduced inhibition of the NCNA neurones

increased LOS resting pressure (too high)

= weight loss (as food cannot enter and be digested efficiently by the stomach), dysphagia, pain

= oesophagitis, pneumonia results

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76
Q

what are the implications of failed LOS opening in achalasia?

A

weight loss (as food cannot enter the stomach and remaining GI tract to be digested and absorbed)

dysphagia

pain

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77
Q

why and how is the propagation of peristaltic waves lost in achalasia?

A

increased resting pressure = i.e. up at 82 but should be 20 so food cannot properly enter the stomach

= build-up SO over time, lose propagation of swallowing waves

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78
Q

why is pneumonia a complication of achalasia?

A

patients can aspirate oesophageal contents that contain bacteria (as food bolus cannot move past contracted LOS)

= pneumonia

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79
Q

what is the onset of achalasia like?

A

insidious onset

i.e. symptoms for years prior to seeking help

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80
Q

how does achalasia progress without treatment?

A

progressive oesophageal dilation

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81
Q

how does achalasia affect oesophageal cancer risk?

A

oesophageal cancer risk increased x28 times

(but over incidence is low at 0.34%)

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82
Q

how does achalasia affect oesophageal cancer risk?

A

oesophageal cancer risk increased x28 times

(but overall incidence is low at 0.34%)

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83
Q

what is the main treatment for achalasia?

A

pneumatic dilatation (PD)

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84
Q

what is pneumatic dilatation?

A

endoscopic procedure wherein an balloon is used to inflate the LOS opening by circumferential stretching and muscle fibre tearing, forcing the LOS itself open, allowing food boluses to pass into the stomach

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85
Q

how is pneumatic dilation carried out?

A

endoscopist passes a catheter with a deflated balloon through the mouth and into the stomach

balloon is centered over the lower esophageal sphincter and inflated with air, expanding the LOS

restoration of the flow of food boluses into the stomach

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86
Q

why does pneumatic dilation work to treat achalasia?

A

as PD weakens the LOS that fails to open up by circumferential stretching and sometimes, by tearing of the muscle fibres too

= restores latency of LOS

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87
Q

what is the efficacy of PD?

A

approx 71 - 90% of patients respond initially but many patients subsequently relapse

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88
Q

how is achalasia treated surgically?

A

Heller’s myotomy - cutting the musculature of the oesophagus, leaving just the mucosa exposed for a continuous 6cm of the distal oesophagus and 3cm of the stomach

followed by a

dor fundoplication - wherein the anterior fundus is folded over the oesophagus and sutured to the right side of the myotomy, covering it

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89
Q

what is a Heller’s myotomy?

A

cutting the musculature of the oesophagus, leaving just the mucosa exposed for a continuous 6cm of the distal oesophagus and 3cm of the stomach

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90
Q

what is a dor fundoplication?

A

anterior fundus is folded over the oesophagus and sutured to the right side of the myotomy, covering it

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91
Q

what are the risks of surgically treating achalasia?

A

oesophageal & gastric perforation (10 – 16%)

division of vagus nerve – rare

splenic injury – 1 – 5%

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92
Q

what is hypomotility?

A

decreased contractile forces or slower transit in the gastrointestinal tract

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93
Q

give an example of a oesophageal disease of hypomotility

A

scleroderma

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94
Q

why is hypomotility caused?

A

neuronal defects cause atrophy of the smooth muscle of the oesophagus

= so peristalsis ceases completely in the distal oesophagus

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95
Q

what is scleroderma and why does it cause hypomotility?

A

autoimmune disease

= causes progressive atrophy and collagenous fibrous replacement of the muscularis (most commonly affects the distal oesophagus|)

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96
Q

what is the impact of hypomotility on the smooth muscle of the oesophagus?

A

hypomotility caused by atrophy of the smooth muscle in the oesophagus due to scleroderma causes

= complete inhibition of peristalsis
AND
= reduced resting pressure of the LOS (due to neuronal defects)

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97
Q

what is the impact of hypomotility on peristalsis?

A

causes complete inhibition of peristalsis

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98
Q

what is the impact of hypomotility on the resting pressure of the LOS?

A

reduces the resting pressure of the LOS

(increased relaxation of the LOS so increased risk of GORD)

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99
Q

what are the impacts of a reduced resting pressure of the LOS in scleroderma?

A

increased relaxation of the LOS so increased risk of GORD

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100
Q

explain how scleroderma can lead to GORD

A

autoimmune damage to the musculature of the oesophagus

neuronal defects

= atrophy of the smooth muscle of the oesophagus

= peristalsis inhibited in the distal oesophagus AND resting pressure of the LOS is significantly reduced

= overrelaxation of the LOS so increased risk of GORD

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101
Q

how does LOS resting pressure compare in both achalasia and scleroderma?

A

achalasia = hypermotility SO the LOS resting pressure is significantly increased = reduced relaxation of the LOS

scleroderma = hypomotility SO the LOS resting pressure is significantly reduced = increased relaxation of the LOS

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102
Q

what is GORD associated with?

A

the symptoms of CREST syndrome

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103
Q

what is CREST syndrome?

A

Calcinosis
Raynaud’s phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasia

= specific type of scleroderma that affects your digestive tract

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104
Q

what are the treatment options for scleroderma?

A

(1) exclude organic obstruction (i.e. ensure there is no malignancy)
(2) improve force of peristalsis by giving prokinetics (e.g. cisapride - but not very effective)

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105
Q

how can peristaltic failure be corrected?

A

once peristaltic failure occurs = usually irreversible

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106
Q

what is calcinosis?

A

deposition of calcium in the peripheral tissues (e.g. fingers)

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107
Q

what is Raynaud’s phenomenon?

A

constriction of peripheral blood vessels = white or cold skin on the hands and feet when you’re cold or stressed

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108
Q

what is oesophageal dysmotility?

A

problems swallowing and/or reflux

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109
Q

what is sclerodactyly?

A

tightness and thickening of finger or toe skin

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110
Q

what is telangiectasia?

A

dilation of the capillaries

= red spots on the hands, palms, forearms, face, and lips

111
Q

give an example of a oesophageal disease of disordered coordination

A

corkscrew oesophagus

112
Q

what is a corkscrew oesophagus?

A

oesophagus that looks like a corkscrew (curling)

= the result of diffuse oesophageal spasm reflecting uncoordinated oesophageal contractions

113
Q

how is a corkscrew oesophagus caused?

A

completely disordered coordination of oseophageal muscle contraction (i.e. diffuse oesophageal contraction)

= causes hypertrophy of the circular muscle resulting in a marked curled corkscrew shape

114
Q

what are the additional symptoms of a corkscrew oesophagus?

A

shape causes dysphagia and chest pain

115
Q

what pressures are common in a corkscrew oesophagus?

A

approx 400-500 mmHg

116
Q

what does a corkscrew oesophagus look like?

A
117
Q

how is a corkscrew oesophagus treated?

A

can try PD (peristaltic dilation) of the cardia - may respond if carried out in a forceful manner

(results not as predictable as achalasia)

118
Q

what is a diffuse oesophageal spasm

A

characterised by uncoordinated contractions of the esophagus

119
Q

what is an oesophageal perforation?

A

hole in the oesophagus

120
Q

what are the three areas of anatomical constriction in the oesophagus?

A

cricopharyngeal constriction

aortic & bronchial constriction

diaphragmatic (and ‘sphincter’) constricton

121
Q

what types of constriction can take place in the oesophagus?

A

anatomical (pre-existing)

pathological (cancer, foreign body etc)

122
Q

give examples of pathological constriction that can occur in the the oesophagus

A

cancer, foreign body, physiological dysfunction

123
Q

what are the possible causes of oesophageal perforations?

A

iatrogenic (OGD) = >50%

spontaneous (Boerhaave’s) = 15%

foreign body = 12%

trauma = 9%

intraoperative - 2%

malignant - 1%

124
Q

what is the most common cause of oesophageal perforation and what is the implication of this?

A

iatrogenic via OGD (endoscopic procedure)

= so only carry out endoscopic procedure if really required

125
Q

what is Boerhaave’s syndrome?

A

spontaneous perforation of the oesophagus

(that results from a sudden increase in intraesophageal pressure combined with negative intrathoracic pressure - vomiting, childbirth, defecation etc)

126
Q

explain how oesophageal perforations can be caused iatrogenically

A

usually at OGD + more common in the presence of diverticula (bulging pouches) or cancers

127
Q

which medical conditions increase the risk of oesophageal perforations during an OGD?

A

diverticula (bulging pouches that can form in the GI tract)

cancer (i.e. tumours)

128
Q

how can an oesophageal perforation be caused in an OGD?

A
129
Q

how does the risk of oesophageal perforation change with level of intervention in an OGD?

A

just OGD = 0.03%

OGD for stricture dilatation = 0.1-2%

OGD for sclerotherapy = 1-5%

OGD for achalasia dilatation = 2-6%

130
Q

explain why Boerhaave’s is caused

A

sudden increase in intra-oesophageal pressure with negative intrathoracic pressure - vomiting, retching, defecation, childbirth)

(e.g. vomiting against a closed glottis)

131
Q

how common is Boerhaave’s syndrome?

A

3.1 per 1,000,000

132
Q

what is the most common site of perforation in Boerhaave’s?

A

left posterolateral aspect of the distal oesophagus

133
Q

give examples of foreign bodies that can cause oesophageal perforations

A

disk batteries (can cause electrical burns if embedded in the mucosa)

magnets

sharp objects

dishwasher tablets

acid/alkali

134
Q

how can an oesophageal perforation be caused in trauma?

A 
neck = penetrating 
thorax = blunt force trauma
135
Q

what are the common symptoms of oesophageal perforation caused by trauma?

A

dysphagia

blood in saliva

haematemesis

surgical empysema

136
Q

define haematemesis

A

vomiting blood

137
Q

define surgical emphysema and describe how it is detected

A

presence of gas in the subcutaneous soft tissues

detection = swelling of affected area OR crepitus on palpation

138
Q

how do patients with oesophageal perforation commonly present?

A 
pain = 95 % 
fever = 80 % 
dysphagia = 70 % 
emphysema = 35 %
139
Q

which investigation are carried out to assess an oesophageal perforation?

A

CXR

CT scan

swallow test using gastrograffin (contract medium)

OGD (endoscopic investigation only if essentially required)

140
Q

what does the following CXR show?

A

left pleural effusion with the oesophageal and gastic contents leaking out to the left

141
Q

what does the following CXR show?

A

mediastinal emphysema = air escaping from right side

142
Q

why is surgery important to treat an oesophageal perforation?

A

is a surgical emergency

(x2 mortality of 24h delay in diagnosis)

143
Q

what is the initial management of an oesophageal perforation?

A

NBM (nil-by-mouth)
IV fluids
broad-spectrum antibiotics & anti-fungals

ITU/HDU level care

bloods (including G&S)

referral to tertiary care centre

144
Q

when is conservative management of the oesophageal perforation recommended and how is it carried out?

A

with a covered oesophageal metal stent

= only recommended very rarely if the perforation is small and does not leak

145
Q

what is better than conservative management for an oesophageal perforation?

A

operative management

146
Q

what are the two forms of operative management for an oesophageal perforation?

A

primary repair = stitch the mucosa and musculature closed

oesophagectomy = remove entire oesophagus (definitive solution)

147
Q

in what state is the LOS usually found and why?

A

usually closed as barrier against reflux of harmful gastric juices, containing pepsin & HCl

148
Q

what does a closed LOS pretect against?

A

barrier against reflux of harmful gastric juices, containing pepsin & HCl

149
Q

when and why can LOS pressure increase?

A

(hypermotility, achalasaia) increased pressure in the oesophageal sphincter, possibly due to:

ACh, hormones, alpha-adrenergic agonists, protein-rich food, histamine, high intrabdominal pressure, PGF2a

150
Q

which substances can increase LOS pressure?

A

ACh, hormones, alpha-adrenergic agonists, protein-rich food, histamine, high intrabdominal pressure, PGF2a

151
Q

what is the implication of increased LOS pressure?

A

inhibits reflux and there is reduced relaxation of the LOS = reduced risk of GORD

(due to lack of inhibitory NCNA neuronal action)

152
Q

when and why can LOS pressure decrease?

A

(hypomotility, scleroderma) decreased lower oesophageal sphincter pressure possibly due to:

beta-adrenergic agonists, hormones, dopamine, NO, PGI2, PGE2, chocolate, acidic gastric juice, fat, smoking

153
Q

which substances can decrease LOS pressure?

A

beta-adrenergic agonists, hormones, dopamine, NO, PGI2, PGE2, chocolate, acidic gastric juice, fat, smoking

154
Q

what is the implication of decreased LOS pressure?

A

promotes reflux and there is increased/over-relaxation of the LOS = increased risk of GORD

(due to atrophy of smooth muscle AND neuronal defects leading to hypomotility)

155
Q

what is sporadic reflux?

A

bouts of acid reflux (occur randomly from time to time)

156
Q

what are the three causes of sporadic reflux?

A

unexpected pressure on a full stomach

swallowing

transient sphincter opening (sphincter relaxation induced without swallowing)

157
Q

what are the three mechanisms of protection following oesophageal reflux?

A

volume clearance (i.e. oesophageal peristalsis reflex to clear acidic oesophageal contents)

pH clearance w saliva

barrier properties of epithelium

158
Q

what is volume clearance?

A

uses swallowing and esophageal peristalsis (reflex) to empty the esophagus of reflux bolus and virtually all acid

159
Q

what is the oesophageal peristalsis reflex and why is it important in reflux?

A

reflex that causes oesophageal peristalsis to empty the oesophagus fully of the reflux bolus and all acidic content

160
Q

why is saliva an important protective mechanism against reflux?

A

saliva has a neutral pH that neutralises and prevets the decrease in oesophageal pH due to acidic reflux

161
Q

why is the epithelium an important protective mechanism against reflux?

A

the epithelium has barrier properties to protect against acidic reflux

162
Q

what is reflux oesophagitis?

A

reflux oesophagitis is an inflammation of the lining of the gullet caused by acidic reflux from the stomach

163
Q

what does reflux oesophagitis lead to?

A

epithelial metaplasia

which can develop into a carcinoma

164
Q

what are the causes of reflux oesophagitis?

A

reduced sphincter pressure

increased transient sphincter opening (air, CO2)

reduced volume clearance (abnormal peristalsis)

reduce pH clearance (reduced saliva production, reduced buffering capacity of saliva)

hiatus hernia

defective musosal protective mechanism (alcohol)

165
Q

what are the possible causes of reduced volume clearance?

A

abnormal peristalsis

166
Q

what are the possible causes of reduced pH clearance?

A

reduced saliva production (in sleep, xerostomia - dry mouth)

reduced buffering capacity of saliva (e.g. through smoking)

167
Q

summarises the possible causes of GORD

A
168
Q

what can cause reduced saliva production?

A

xerostomia (i.e. dry mouth)

in sleep

169
Q

what can cause reduced buffering capacity of saliva?

A

smoking

170
Q

what can cause defects in the muscosal protective mechanism?

A

alcohol

171
Q

what is a hiatus hernia?

A

upper part of your stomach bulges through the diaphragm into your chest due to weakened musclulature

172
Q

what are the two types of hiatus hernia?

A

sliding hiatus hernia

rolling/paraoesophageal hiatus hernia

173
Q

what is a sliding hiatus hernia?

A

most common type of hiatus hernia associated with symptoms of GORD

174
Q

what causes a sliding hiatus hernia?

A

ligament holding the distal oesphagus gives way and the whole stomach slides up pushing the distal oesophagus upwards

175
Q

what is a rolling hiatus hernia?

A

less common type of hiatus hernia that is much riskier

176
Q

what causes a rolling hiatus hernia?

A

distal oesophagus held in place by ligament but portion of stomach slips up the side through defect in the diaphragm (hole in diaphragm)

177
Q

what do the following abdominal CTs show?

A

sliding hiatus hernia

(stomach positioned much higher than it should be)

178
Q

what does the following barium scan show?

A

rolling/paraoesophageal hiatus hernia

179
Q

what does a sliding hiatus hernia contribute to?

A

contributes significantly to GORD

180
Q

what are the implications of a rolling/paraoesophageal hernia?

A

portions of the bowel or the viscus can herniate through and can

1) cause a blockage or obstruction
2) can become strangulated (i.e. blood supply compromised SO tissue becomes ischaemic and dies)

181
Q

which type of hiatus hernia is more common?

A

sliding hiatus hernia much more common than rollling/paraoesophageal

182
Q

which type of hiatus hernia is more risky?

A

rolling hiatus hernia as

1) other organs can protrude and herniated through the hole e.g. pancreas, liver, small intestine
2) protruding organs can cause an obstruction/blockage

183
Q

how is a hiatus hernia investigated?

A

OGD

oesophageal manometry

24-hr oesophageal pH recording

184
Q

why is an OGD done to investigate a hiatus hernia?

A

to exclude cancer

to investigate and either exclude/confirm the presence of oesophagitis, peptic stricture and Barrett’s oesophagus

185
Q

how is a hiatus hernia treated?

A

medically
- lifestyle changes (weight loss, smoking, alcohol reduction)

surgically

  • peptic stricture dilation
  • laparascopic Nissen’s fundoplication
186
Q

how is a hiatus hernia treated?

A

medically

  • lifestyle changes (weight loss, smoking, alcohol reduction, remove aggravating factors)
  • PPIs

surgically

  • peptic stricture dilation
  • laparascopic Nissen’s fundoplication
187
Q

how is a hiatus hernia treated medically?

A
  • lifestyle changes (weight loss, smoking, alcohol reduction, remove aggravating factors)
  • PPIs
188
Q

how is a hiatus hernia treated surgically?

A
  • peptic stricture dilation
  • laparascopic Nissen’s fundoplication
189
Q

describe how Nissen’s fundoplication is carried out

A

defect is where the diaphragm loops around the oesophagus

fix defect

reinforce fixed defect by wrapping the fundus of the stomach around the oesophagus

190
Q

why is a fundoplication important when treating a hiatus hernia?

A

prevents acidic reflux

191
Q

when carrying out Nissen’s fundoplication, what must you be careful not to do?

(common complication?)

A

cannot suture the reinforcement of the stomach fundus too tightly as this can significantly impair swallowing

192
Q

describe the structure of the stomach

A
193
Q

what are the functions of the stomach?

A

breaks food into smaller particles (acid & pepsin)

holds food, releasing it in controlled steady rate into duodenum

kills parasites & certain bacteria

194
Q

what is produced in the cardia and pyloric regions?

A

mucus only

195
Q

what is produced in the body and fundus of the stomach?

A

mucus, HCl, pepsinogen

196
Q

what is produced in the antrum?

A

gastrin

197
Q

what is gastritis?

A

inflammation of the lining of the stomach

198
Q

what are the four types of gastritis?

A

erosive & haemorrhagic gastritis

non-erosive, chronic active gastritis

atophic (fundal gland) gastritis

reactive gastriris

199
Q

what are the causes of erosive & haemorrhagic gastritis?

A

NSAIDs, alcohol, multi-organ failure, burns, trauma, ischaemia

200
Q

what happens as a result of erosive & haemorrhagic gastritis?

A

acute ulcer formation which can lead to perforation and massive bleeding

201
Q

what happens as a result of erosive & haemorrhagic gastritis?

A

acute ulcer formation which can lead to perforation and massive bleeding

(can also lead to reactive gastritis = carcinoma)

202
Q

which part of the stomach are most affect by acute ulcers?

A

can occur anywhere in the stomach

203
Q

what is the most common cause of acute ulcers?

A

increased intake of NSAIDs

204
Q

what are the causes of chronic active non-erosive (antral) gastritis?

A

helicobacter pylori infection

205
Q

what is the causes of chronic active non-erosive (antral) gastritis?

A

helicobacter pylori infection

206
Q

what can non-erosive chronic active gastritis lead to and why?

A

gastric and duodenal ulcers due to increased gastrin and therefore increased acid secretion

(and reactive gastritis = carcinoma)

207
Q

differentiate between acute ulcers and gastric/duodenal ulcers

A

acute ulcer = result of erosive & haemorrhagic gastritis

gastric & duodenal ulcer = result of non-erosive antral chronic gastritis

208
Q

what is common between gastric/duodenal ulcers and acute ulcers?

A

both cause reactive gastritic

= causes epithelial metaplasia
= carcinoma

209
Q

why do gastric and duodenal ulcers form in non-erosive antral chronic gastritis?

A

increased gastrin production SO increased acid secretion + H.pylori infection

= gastric & duodenal ulcers

210
Q

whre does non-erosive, antral chronic gastritis occur?

A

antrum

211
Q

where does non-erosive, antral chronic gastritis occur?

A

antrum

212
Q

how is a H.pylori infection treated?

A

treatment w triple antibiotics

(amoxicillin, clarithromycin, pantoprazole)

213
Q

where does atrophic gastritis occur?

A

fundus

214
Q

what is the causes of atrophic gastritis?

A

autoantibodies produced against parts of a parietal cell (H+K+ ATPase, gastrin receptor) OR products of parietal cell function (IF)

215
Q

in atropic gastritis, autoantibodes against what are produced?

A

against parts of a parietal cell = H+K+ ATPase, gastrin receptor

products of parietal cell function = intrinsic factore

216
Q

what can atrophic gastritis lead to and why?

A

pernicious anaemia = reduced IF secreteion and so reduced cobalamin absorption (i.e. cobalamin deficiency)

carcinoid + carcinoma (from epithelial metaplasia) = reduced acid secretion so increased gastrin

217
Q

how is pernicious anaemia caused in atrophic gastritis?

A

reduced IF secreteion and so reduced cobalamin absorption = cobalamin deficiency

218
Q

how are carcinomas (and carcinoid) caused in atrophic gastritis?

A

reduced acid secretion so increased gastrin = increase G cell hyperplasia = epithelial metaplasia = carcinoma

if increased ECL hyperplasia = carcinoid

219
Q

what happens to parietal cells in atrophic gastritis>?

A

parietal cell atrophy

220
Q

what happens to acid and IF secretion in atrophic gastritis?

A

reduced IF and acid secretion

221
Q

why is the function of parietal cells essential?

A

release pepsin and acid (H+)

= essential for protein digestion in the stomach

222
Q

what stimulates parietal cells to release pepsin and HCl?

A

neural
- ACh (postganglionic transmitter of vagal parasympathetic fibres)

endocrine
- gastrin (G cells of antrum)

paracrine
- histamine (ECL cells & mast cells of gastric wall)

223
Q

what inhibits parietal cells to release pepsin and HCl?

A

endocrine
- secretin (small intestine)

paracrine
- somatostatin (SIH)

paracrine & autocrine
- PGs (E2 & I2), TGF-α & adenosine

224
Q

what stimulates parietal cells to release pepsin and HCl?

A

neural
- ACh (postganglionic transmitter of vagal parasympathetic fibres)

endocrine
- gastrin (G cells of antrum)

paracrine
- histamine (ECL cells & mast cells of gastric wall)

225
Q

what inhibits parietal cells to release pepsin and HCl?

A

endocrine
- secretin (small intestine)

paracrine
- somatostatin (SIH)

paracrine & autocrine
- PGs (E2 & I2), TGF-α & adenosine

226
Q

explain how parietal cells are stimulated neurally

A

ACh (postganglionic transmitter of vagal parasympathetic fibres)

227
Q

explain how parietal cells are stimulated via endocrine pathways

A

gastrin (G cells of antrum)

228
Q

explain how parietal cells are stimulated via paracrine pathways

A

histamine (ECL cells & mast cells of gastric wall)

229
Q

explain how parietal cells are stimulated via endocrine pathways

A

secretin (small intestine)

230
Q

explain how parietal cells are stimulated via paracrine pathways

A

somatostatin (SIH)

231
Q

explain how parietal cells are stimulated via paracrine & autocrine pathways

A

PGs (E2 & I2), TGF-α & adenosine

232
Q

summarise how parietal cells are stimulated and inhibited

A
233
Q

what effect does increased acid have on gastrin production?

A

gastrin stimulates acid secretion which in turn shuts off gastrin secretion

(via somatostatin)

234
Q

what are the four ways in which the mucosa is already protected?

A

1) overlying protective mucus film
2) HCO3- secretion
3) epithelial barrier
4) mucosal blood perfusion

235
Q

explain how the mucosa is protected by a mucus film

A

the overlying mucus film is approximately 1-1.5cm thick, protecting the mucosa from damage due to hydrogen to pepsinogen

236
Q

explain how the mucosa is protected by HCO3- secretion

A

epithelial cells produce bicarbonate (HCO3- ions) that buffer the acidic H+ ions (producing water)

= production propagated by prostaglandins

237
Q

explain how the mucosa is protected by an epithelial barrier

A

the physical barrier of the epithelial cell membrane prevents entry of H+ ions and any damage caused by them

238
Q

explain how the mucosa is protected by mucosal blood perfusion

A

any H+ ions that enter the epithelial cells are rapidly taken away via the basolateral sodium-hydrogen exchange

= so they do not remain within the epithelial cells long enough to cause damage

239
Q

what does the mucus film specifically protect against?

A

hydrogen ions an dpepsinogen

240
Q

why are bicarbonate ions produced by the epithelial cells?

A

to buffer the H+ ions (producing water)

241
Q

what is required for the production of bicarbonate ions?

A

prostaglandins

242
Q

how can NSAIDs impair mucosal protection in the upper GI tract?

A

NSAIDs will impair prostaglandin production by inhibiting the normal functioning of the COX enzyme

so reduced prostaglandin results in less propagation of bicarbonate ion production

so reduced bicarbonate ion concentration so less buffering of H+ ions

243
Q

which transporter is responsible for removing H+ ions from the epithelial cells?

A

sodium-hydrogen co-transporter/

244
Q

how will ischaemia affect mucosal protection in the upper GI tract?

A

ischaemia can impair blood flow to the epithelial cells so the H+ ions that enter the cells cannot effectively be removed into the bloodstream

(due to impaired blood supply)

245
Q

what mechanisms exist to repair epithelial defects?

A

migration

gap closed by cell growth

acute wound healing

246
Q

explain how migration repairs epithelial defects

A

adjacent epithelial cells flatten to close gap via sideward migration along the basement membrane

247
Q

explain how cell growth repairs epithelial defects

A

covering defect through cell division

wherein cell growth is stimulated by EGF, TGFa, IGF-1, GRP, and gastrin

248
Q

explain how wound healing repairs epithelial defects

A

if basement membrane destroyed

= attraction of leukocytes & macrophages + phagocytosis of necrotic cells + angiogenesis + regeneration of ECM after repair of BM

= epithelial closure by restitution & cell division

249
Q

what are possible causes for ulcer formation?

A

H. pylori infection

increased secretion of gastric juices

decreased HCO3- secretion

decreased cell formation

decreased blood perfusion

250
Q

explain how H. pylori can lead to ulcer formation

A

infection w H. pylori (can lead to gastritis and) disrupts barrier function

= epithelial damage

251
Q

what are NSAIDs?

name some common examples

A

non-steroidal anti-inflammatory medicines
= used to relieve pain, reduce inflammation, and bring down a high temperature

e.g. diclofenac, ibuprofen, acetylsalicylic acid (ASA = aspirin), indomethacin

252
Q

explain how NSAIDs can lead to ulcer formation

A

NSAIDs inhibit the COX enzyme, impairing prostaglandin synthesis

less prostaglandin is therefore available to propagate HCO3- secretion in epithelial cells

less buffering of the acidic H+ contents occurs due to the reduced HCO3- concentration

= increased H+ concentration increases risk of ulcer formation

253
Q

explain how stress can lead to ulcer formation

A

stress from major surgery/trauma/lifestyle

= reduced blood perfusion and sometimes increased H+ and pepsinogen secretion

= increased chemical aggression

= epithelial damage are exposed to more H+ ions, increasing risk of ulcer formation

254
Q

explain how smoking or gastrinomas can lead to ulcer formation

A

smoking and gastrinomas can lead to increased H+ and pepsinogen secretion

= increased chemical aggression

= epithelial damage are exposed to more H+ ions, increasing risk of ulcer formation

255
Q

what are gastrinomas?

A

rare tumours that start in the neuroendocrine cells that make large amounts of the hormone gastrin

256
Q

in which age group are gastrinomas the most likely cause of ulcer formation and why?

A

commonly diagnosed between the ages of 20 and 50

(mainly young people)

257
Q

what are the two ways in which the epithelium can be damaged?

A

barrier function disturbed

epithelial damage

258
Q

what are the possible clinical outcomes of H. pylori infection?

A

>80% = asymptomatic or chronic gastritis

15-20% = chronic atrophic gastritis, intestinal metaplasia OR (less commonly) gastric or duodenal ulcer

<1% = gastric cancer or MALT lymphoma

259
Q

what proportion of H. pylori patients are asymptomatic?

A

approx 80%

260
Q

what proportion of H. pylori patients get chronic atrophic gastritis, intestinal metaplasia OR gastric or duodenal ulcers?

A

approx 15-20%

261
Q

what proportion of H. pylori patients get gastric cancer/MALT lymphoma?

A

approx <1%

262
Q

what is the treatment for ulcers?

A

primarily medical = PPI/H2 blocker + triple Abx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days

most ulcers heal within 12 weeks but if they don’t = change medication + observe another 12 weeks

263
Q

is surgery common for ulcers?

A

rare as most uncomplicated ulcers will heal within 12 weeks

if they don’t = change medication and observe for another 12 weeks

264
Q

how long do ulcers take to heal?

A

uncomplicated ulcers = approx 12 weeks

265
Q

what must you do if ulcers do not heal within the first 12 weeks?

A

change medication and observe for another 12 weeks

check serum gastrin

OGD

266
Q

why must you check serum gastrin levels in patients that have ulcers that are not healing well?

A

they may have antral G-cell hyperplasia

OR

may be due to a gastrinoma (Zollinger-Ellison syndrome)

267
Q

why must you do an OGD in patients that have ulcers that are not healing well?

A

must biopsy all four quadrant of the ulcer to rule out malignancy

268
Q

what are some reasons for abnormally high serum gastrin levels?

A

antral G-cell hyperplasia

gastrinoma i.e. Zollinger-Ellison syndrome (ZES)

269
Q

what does an OGD rule out?

A

malignant ulcers

270
Q

what are the possible indications for surgery of an ulcer?

A

1) intractability (i.e. difficult or impossible to control despite therapy)
2) if they cannot be conservatively managed = e.g. require continuous NSAIDs/steroid therapy for another medical condition
3) complications = haemorrhage, obstruction, perforation

271
Q

what are the possible complications of ulcers?

A

haemorrhage, obstruction, perforation

272
Q

what is Zollinger-Ellison syndrome?

A

characterised by the development of a tumour (gastrinoma) or tumours that secrete excessive levels of gastrin, a hormone that stimulates the production of acid by the stomach

excess gastric acid leads to the formation of peptic ulcers

273
Q

what are peptic ulcers?

A

sores or raw areas within the digestive tract where the lining has been eroded by stomach acid and digestive juices

274
Q

what does the following scan show?

A

barium swallow to show oesophageal dilation as a result of achalasia (hypermotility)

brs (phase 1b) (71 decks)

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