(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)
2
Q
what are the three divisions of the oesophagus?
A
cervical oesophagus, (upper, middle and lower) thoracic oesophagus, abdominal oesophagus
3
Q
what type of muscle is present in the cervical oesophagus?
A
skeletal
4
Q
what type of muscle is present in the upper thoracic oesophagus?
A
skeletal and smooth
5
Q
what type of muscle is present in the lower thoracic oesophagus?
A
smooth
6
Q
at which spinal level does the oesophagus start and at which does it end?
A
approx C5 to T10
7
Q
at which spinal level does the diaphragm start?
A
approx T10
8
Q
what is the upper 1/3 of the oesophagus called?
A
proximal oesophagus
9
Q
what is the lower 1/3 of the oesophagus called?
A
distal oesophagus
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
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
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
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)
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
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
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
17
Q
describe the superior limb of the phrenoesophageal ligament
A
attaches the lower oesophagus to the superior surface of the diaphragm
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
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
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
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
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
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
24
Q
what happens in stage 0 of swallowing?
A
oral phase
- chewing & saliva prepare bolus
- both oesophageal sphincters constricted
25
what is the state of the sphincters during the oral phase (phase 0)?
both oesophageal sphincters constricted
26
what happens in stage 1 of swallowing?
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)
27
what happens in stage 2 of swallowing?
upper sphincter closes
superior circular muscle rings contract & inferior rings dilate
sequential contractions of longitudinal muscle
28
what happens in stage 3 of swallowing?
lower sphincter closes as food passes through
29
in swallowing, what guides the food bolus to the oesophagus?
pharyngeal musclulature contraction
30
in swallowing, how and when does the lower oesophageal reflect open?
during the pharyngeal phase
via the vasovagal reflex (receptive relaxation reflex)
31
how is the bolus of food pushed down the oesophagus in the upper oesophageal phase?
superior circular muscle rings contract & inferior rings dilate
32
compare the time and length of opening for the upper and lower oesophageal sphincters
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
33
what is manometry?
diagnostic test to measures the strength, pressure and muscle coordination of your oesophagus when you swallow
34
why is manometry important?
used to investigate and identify pathologies related to oesophageal motility
35
how is manometry carried out?
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
36
what is the pressure of normal peristaltic waves?
approx 40 mmHg
37
why is there a migration of peristaltic waves during swallowing?
to propel and propagate the bolus of food down the oesophagus
38
what is the lower oesophageal sphincter resting pressure?
approx 20 mmHg
39
when does the LOS resting pressure change and how?
decreases by approx 5mmHg during receptive relaxation reflex in the pharyngeal phase of swallowing phase
= to allow the LOS to open
40
why does the LOS resting pressure decrease during receptive relaxation?
in order to allow the LOS to open and allow the bolus of food to enter the stomach
41
what stimulates the decrease in LOS resting pressure?
mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurones of the myentiric plexus
42
what are NCNA neurones?
noncholinergic nonadrenergic (NCNA) neurones
part of the myenteric plexus
responsible for stimulating a decrease in LOS resting pressure
43
what is the function of NCNA neurones in swallowing?
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
44
which neurones carry out the antagonistic action to NCNA neurones and how?
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
45
how is oesophageal motility investigated?
using manometry
46
what form do functional disorders of the esophagus usually take?
strictures that can be either benign or malignant
(must be excluded first before diagnosing anything else)
47
besides strictures, what are the functional disorders of the oesophagus caused by?
1) abnormal oesophageal contraction: hypermotility, hypomotility, disordered contraction
(2) failure of protective mechanisms against reflux: GORD
48
what condition is most commonly caused by LOS dysfunction?
GORD
49
define dysphagia
fficulty in swallowing
50
define odynophagia
pain on swallowing
51
define regurgitation
return of oesophageal contents from above an obstruction
52
define reflux
passive return of gastroduodenal contents to the mouth
53
differentiate between reflux and vomiting
reflux is the passive return of gastroduodenal contest to the mouth whereas vomiting is the forceful throwing up of stomach contents
54
what must you clarify when taking a dysphagia history?
localisation (i.e. cricopharyngeal sphincter - UES - or more distal)
type (for soids/fluids, intermittent/progressive)
55
what are the two types of regurgitation?
function or mechanical regurgitation
56
differentiate between regurgitation and reflux
while regurgitation = return of oesophageal contents from above an obstruction (functional or mechanical), reflux = passive return of gastroduodenal contents to tehmouth
57
what is a stricture?
an abnormal narrowing of a bodily passage (as from inflammation, cancer, or the formation of scar tissue)
58
give an example of mechanical regurgitation
something being swallowed and getting stuck in the oesophagus, causing an obstruction
59
what is hypermotility?
abnormally increased or excessive activity or movement, particularly in the digestive tract
60
give an example of a oesophageal disease of hypermotility
achalasia
61
what causes achalasia?
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
62
what happens as a result of achalasia?
decreased activity of inhibitory NCNA neurones.
= increase LOS pressure
= failure of LOS relaxation + impaired peristalsis in the distal oesophagus
63
what is the proposed model of achalasia pathophysiology?
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)
64
what are the two types of achalasia?
primary achalasia (aetiology unknown)
secondary achalasia
65
what are the causes of primary achalasia?
the aetiology of the condition is unknown
66
what are the causes of secondary achalasia?
diseases causing oesophageal motor abnormalities similiar to primary achalasia
e. g.
- Chagas' disease
- protozoa infection
- amyloid/sarcoma/eosinophilic oesophagitis
67
in achalasia, which cells are affected and how?
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
68
how are NCNA neurones affected as a result of achalasia and what are the implications of this?
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
69
what are two possible causes of the hypermobility seen in achalasia?
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
70
what are two possible causes of the hypermotility seen in achalasia?
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
71
how and why does the resting pressure of the LOS change in hypermotility?
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
72
in achalasia, how does the pressure of the LOS compare to that of the stomach?
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)
73
what is the impact of the failed relaxation of the LOS on the oesophagus?
swallowed food collects in oesophagus causing increased pressure throughout with dilation of the oesophagus
74
what are the possible complications of achalasia?
oesophagitis and pneumonia
75
explain how achalasia can lead to oesophagitis and pneumonia
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
76
what are the implications of failed LOS opening in achalasia?
weight loss (as food cannot enter the stomach and remaining GI tract to be digested and absorbed)
dysphagia
pain
77
why and how is the propagation of peristaltic waves lost in achalasia?
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
78
why is pneumonia a complication of achalasia?
patients can aspirate oesophageal contents that contain bacteria (as food bolus cannot move past contracted LOS)
= pneumonia
79
what is the onset of achalasia like?
insidious onset
i.e. symptoms for years prior to seeking help
80
how does achalasia progress without treatment?
progressive oesophageal dilation
81
how does achalasia affect oesophageal cancer risk?
oesophageal cancer risk increased x28 times
(but over incidence is low at 0.34%)
82
how does achalasia affect oesophageal cancer risk?
oesophageal cancer risk increased x28 times
(but overall incidence is low at 0.34%)
83
what is the main treatment for achalasia?
pneumatic dilatation (PD)
84
what is pneumatic dilatation?
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
85
how is pneumatic dilation carried out?
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
86
why does pneumatic dilation work to treat achalasia?
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
87
what is the efficacy of PD?
approx 71 - 90% of patients respond initially but many patients subsequently relapse
88
how is achalasia treated surgically?
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
89
what is 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
90
what is a dor fundoplication?
anterior fundus is folded over the oesophagus and sutured to the right side of the myotomy, covering it
91
what are the risks of surgically treating achalasia?
oesophageal & gastric perforation (10 – 16%)
division of vagus nerve – rare
splenic injury – 1 – 5%
92
what is hypomotility?
decreased contractile forces or slower transit in the gastrointestinal tract
93
give an example of a oesophageal disease of hypomotility
scleroderma
94
why is hypomotility caused?
neuronal defects cause atrophy of the smooth muscle of the oesophagus
= so peristalsis ceases completely in the distal oesophagus
95
what is scleroderma and why does it cause hypomotility?
autoimmune disease
= causes progressive atrophy and collagenous fibrous replacement of the muscularis (most commonly affects the distal oesophagus|)
96
what is the impact of hypomotility on the smooth muscle of the oesophagus?
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)
97
what is the impact of hypomotility on peristalsis?
causes complete inhibition of peristalsis
98
what is the impact of hypomotility on the resting pressure of the LOS?
reduces the resting pressure of the LOS
(increased relaxation of the LOS so increased risk of GORD)
99
what are the impacts of a reduced resting pressure of the LOS in scleroderma?
increased relaxation of the LOS so increased risk of GORD
100
explain how scleroderma can lead to GORD
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
101
how does LOS resting pressure compare in both achalasia and scleroderma?
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
102
what is GORD associated with?
the symptoms of CREST syndrome
103
what is CREST syndrome?
Calcinosis
Raynaud's phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasia
= specific type of scleroderma that affects your digestive tract
104
what are the treatment options for scleroderma?
(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)
105
how can peristaltic failure be corrected?
once peristaltic failure occurs = usually irreversible
106
what is calcinosis?
deposition of calcium in the peripheral tissues (e.g. fingers)
107
what is Raynaud's phenomenon?
constriction of peripheral blood vessels = white or cold skin on the hands and feet when you're cold or stressed
108
what is oesophageal dysmotility?
problems swallowing and/or reflux
109
what is sclerodactyly?
tightness and thickening of finger or toe skin
110
what is telangiectasia?
dilation of the capillaries
= red spots on the hands, palms, forearms, face, and lips
111
give an example of a oesophageal disease of disordered coordination
corkscrew oesophagus
112
what is a corkscrew oesophagus?
oesophagus that looks like a corkscrew (curling)
= the result of diffuse oesophageal spasm reflecting uncoordinated oesophageal contractions
113
how is a corkscrew oesophagus caused?
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
what are the additional symptoms of a corkscrew oesophagus?
shape causes dysphagia and chest pain
115
what pressures are common in a corkscrew oesophagus?
approx 400-500 mmHg
116
what does a corkscrew oesophagus look like?
117
how is a corkscrew oesophagus treated?
can try PD (peristaltic dilation) of the cardia - may respond if carried out in a forceful manner
(results not as predictable as achalasia)
118
what is a diffuse oesophageal spasm
characterised by uncoordinated contractions of the esophagus
119
what is an oesophageal perforation?
hole in the oesophagus
120
what are the three areas of anatomical constriction in the oesophagus?
cricopharyngeal constriction
aortic & bronchial constriction
diaphragmatic (and 'sphincter') constricton
121
what types of constriction can take place in the oesophagus?
anatomical (pre-existing)
pathological (cancer, foreign body etc)
122
give examples of pathological constriction that can occur in the the oesophagus
cancer, foreign body, physiological dysfunction
123
what are the possible causes of oesophageal perforations?
iatrogenic (OGD) = \>50%
spontaneous (Boerhaave’s) = 15%
foreign body = 12%
trauma = 9%
intraoperative - 2%
malignant - 1%
124
what is the most common cause of oesophageal perforation and what is the implication of this?
iatrogenic via OGD (endoscopic procedure)
= so only carry out endoscopic procedure if really required
125
what is Boerhaave's syndrome?
spontaneous perforation of the oesophagus
(that results from a sudden increase in intraesophageal pressure combined with negative intrathoracic pressure - vomiting, childbirth, defecation etc)
126
explain how oesophageal perforations can be caused iatrogenically
usually at OGD + more common in the presence of diverticula (bulging pouches) or cancers
127
which medical conditions increase the risk of oesophageal perforations during an OGD?
diverticula (bulging pouches that can form in the GI tract)
cancer (i.e. tumours)
128
how can an oesophageal perforation be caused in an OGD?
129
how does the risk of oesophageal perforation change with level of intervention in an OGD?
just OGD = 0.03%
OGD for stricture dilatation = 0.1-2%
OGD for sclerotherapy = 1-5%
OGD for achalasia dilatation = 2-6%
130
explain why Boerhaave's is caused
sudden increase in intra-oesophageal pressure with negative intrathoracic pressure - vomiting, retching, defecation, childbirth)
(e.g. vomiting against a closed glottis)
131
how common is Boerhaave's syndrome?
3.1 per 1,000,000
132
what is the most common site of perforation in Boerhaave's?
left posterolateral aspect of the distal oesophagus
133
give examples of foreign bodies that can cause oesophageal perforations
disk batteries (can cause electrical burns if embedded in the mucosa)
magnets
sharp objects
dishwasher tablets
acid/alkali
134
how can an oesophageal perforation be caused in trauma?
```
neck = penetrating
thorax = blunt force trauma
```
135
what are the common symptoms of oesophageal perforation caused by trauma?
dysphagia
blood in saliva
haematemesis
surgical empysema
136
define haematemesis
vomiting blood
137
define surgical emphysema and describe how it is detected
presence of gas in the subcutaneous soft tissues
detection = swelling of affected area OR crepitus on palpation
138
how do patients with oesophageal perforation commonly present?
```
pain = 95 %
fever = 80 %
dysphagia = 70 %
emphysema = 35 %
```
139
which investigation are carried out to assess an oesophageal perforation?
CXR
CT scan
swallow test using gastrograffin (contract medium)
OGD (endoscopic investigation only if essentially required)
140
what does the following CXR show?
left pleural effusion with the oesophageal and gastic contents leaking out to the left
141
what does the following CXR show?
mediastinal emphysema = air escaping from right side
142
why is surgery important to treat an oesophageal perforation?
is a surgical emergency
(x2 mortality of 24h delay in diagnosis)
143
what is the initial management of an oesophageal perforation?
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
when is conservative management of the oesophageal perforation recommended and how is it carried out?
with a covered oesophageal metal stent
= only recommended very rarely if the perforation is small and does not leak
145
what is better than conservative management for an oesophageal perforation?
operative management
146
what are the two forms of operative management for an oesophageal perforation?
primary repair = stitch the mucosa and musculature closed
oesophagectomy = remove entire oesophagus (definitive solution)
147
in what state is the LOS usually found and why?
usually closed as barrier against reflux of harmful gastric juices, containing pepsin & HCl
148
what does a closed LOS pretect against?
barrier against reflux of harmful gastric juices, containing pepsin & HCl
149
when and why can LOS pressure increase?
(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
which substances can increase LOS pressure?
ACh, hormones, alpha-adrenergic agonists, protein-rich food, histamine, high intrabdominal pressure, PGF2a
151
what is the implication of increased LOS pressure?
inhibits reflux and there is reduced relaxation of the LOS = reduced risk of GORD
(due to lack of inhibitory NCNA neuronal action)
152
when and why can LOS pressure decrease?
(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
which substances can decrease LOS pressure?
beta-adrenergic agonists, hormones, dopamine, NO, PGI2, PGE2, chocolate, acidic gastric juice, fat, smoking
154
what is the implication of decreased LOS pressure?
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
what is sporadic reflux?
bouts of acid reflux (occur randomly from time to time)
156
what are the three causes of sporadic reflux?
unexpected pressure on a full stomach
swallowing
transient sphincter opening (sphincter relaxation induced without swallowing)
157
what are the three mechanisms of protection following oesophageal reflux?
volume clearance (i.e. oesophageal peristalsis reflex to clear acidic oesophageal contents)
pH clearance w saliva
barrier properties of epithelium
158
what is volume clearance?
uses swallowing and esophageal peristalsis (reflex) to empty the esophagus of reflux bolus and virtually all acid
159
what is the oesophageal peristalsis reflex and why is it important in reflux?
reflex that causes oesophageal peristalsis to empty the oesophagus fully of the reflux bolus and all acidic content
160
why is saliva an important protective mechanism against reflux?
saliva has a neutral pH that neutralises and prevets the decrease in oesophageal pH due to acidic reflux
161
why is the epithelium an important protective mechanism against reflux?
the epithelium has barrier properties to protect against acidic reflux
162
what is reflux oesophagitis?
reflux oesophagitis is an inflammation of the lining of the gullet caused by acidic reflux from the stomach
163
what does reflux oesophagitis lead to?
epithelial metaplasia
which can develop into a carcinoma
164
what are the causes of reflux oesophagitis?
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
what are the possible causes of reduced volume clearance?
abnormal peristalsis
166
what are the possible causes of reduced pH clearance?
reduced saliva production (in sleep, xerostomia - dry mouth)
reduced buffering capacity of saliva (e.g. through smoking)
167
summarises the possible causes of GORD
168
what can cause reduced saliva production?
xerostomia (i.e. dry mouth)
in sleep
169
what can cause reduced buffering capacity of saliva?
smoking
170
what can cause defects in the muscosal protective mechanism?
alcohol
171
what is a hiatus hernia?
upper part of your stomach bulges through the diaphragm into your chest due to weakened musclulature
172
what are the two types of hiatus hernia?
sliding hiatus hernia
rolling/paraoesophageal hiatus hernia
173
what is a sliding hiatus hernia?
most common type of hiatus hernia associated with symptoms of GORD
174
what causes a sliding hiatus hernia?
ligament holding the distal oesphagus gives way and the whole stomach slides up pushing the distal oesophagus upwards
175
what is a rolling hiatus hernia?
less common type of hiatus hernia that is much riskier
176
what causes a rolling hiatus hernia?
distal oesophagus held in place by ligament but portion of stomach slips up the side through defect in the diaphragm (hole in diaphragm)
177
what do the following abdominal CTs show?
sliding hiatus hernia
(stomach positioned much higher than it should be)
178
what does the following barium scan show?
rolling/paraoesophageal hiatus hernia
179
what does a sliding hiatus hernia contribute to?
contributes significantly to GORD
180
what are the implications of a rolling/paraoesophageal hernia?
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
which type of hiatus hernia is more common?
sliding hiatus hernia much more common than rollling/paraoesophageal
182
which type of hiatus hernia is more risky?
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
how is a hiatus hernia investigated?
OGD
oesophageal manometry
24-hr oesophageal pH recording
184
why is an OGD done to investigate a hiatus hernia?
to exclude cancer
to investigate and either exclude/confirm the presence of oesophagitis, peptic stricture and Barrett's oesophagus
185
how is a hiatus hernia treated?
medically
- lifestyle changes (weight loss, smoking, alcohol reduction)
surgically
- peptic stricture dilation
- laparascopic Nissen's fundoplication
186
how is a hiatus hernia treated?
medically
- lifestyle changes (weight loss, smoking, alcohol reduction, remove aggravating factors)
- PPIs
surgically
- peptic stricture dilation
- laparascopic Nissen's fundoplication
187
how is a hiatus hernia treated medically?
- lifestyle changes (weight loss, smoking, alcohol reduction, remove aggravating factors)
- PPIs
188
how is a hiatus hernia treated surgically?
- peptic stricture dilation
- laparascopic Nissen's fundoplication
189
describe how Nissen's fundoplication is carried out
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
why is a fundoplication important when treating a hiatus hernia?
prevents acidic reflux
191
when carrying out Nissen's fundoplication, what must you be careful not to do?
(common complication?)
cannot suture the reinforcement of the stomach fundus too tightly as this can significantly impair swallowing
192
describe the structure of the stomach
193
what are the functions of the stomach?
breaks food into smaller particles (acid & pepsin)
holds food, releasing it in controlled steady rate into duodenum
kills parasites & certain bacteria
194
what is produced in the cardia and pyloric regions?
mucus only
195
what is produced in the body and fundus of the stomach?
mucus, HCl, pepsinogen
196
what is produced in the antrum?
gastrin
197
what is gastritis?
inflammation of the lining of the stomach
198
what are the four types of gastritis?
erosive & haemorrhagic gastritis
non-erosive, chronic active gastritis
atophic (fundal gland) gastritis
reactive gastriris
199
what are the causes of erosive & haemorrhagic gastritis?
NSAIDs, alcohol, multi-organ failure, burns, trauma, ischaemia
200
what happens as a result of erosive & haemorrhagic gastritis?
acute ulcer formation which can lead to perforation and massive bleeding
201
what happens as a result of erosive & haemorrhagic gastritis?
acute ulcer formation which can lead to perforation and massive bleeding
(can also lead to reactive gastritis = carcinoma)
202
which part of the stomach are most affect by acute ulcers?
can occur anywhere in the stomach
203
what is the most common cause of acute ulcers?
increased intake of NSAIDs
204
what are the causes of chronic active non-erosive (antral) gastritis?
helicobacter pylori infection
205
what is the causes of chronic active non-erosive (antral) gastritis?
helicobacter pylori infection
206
what can non-erosive chronic active gastritis lead to and why?
gastric and duodenal ulcers due to increased gastrin and therefore increased acid secretion
(and reactive gastritis = carcinoma)
207
differentiate between acute ulcers and gastric/duodenal ulcers
acute ulcer = result of erosive & haemorrhagic gastritis
gastric & duodenal ulcer = result of non-erosive antral chronic gastritis
208
what is common between gastric/duodenal ulcers and acute ulcers?
both cause reactive gastritic
= causes epithelial metaplasia
= carcinoma
209
why do gastric and duodenal ulcers form in non-erosive antral chronic gastritis?
increased gastrin production SO increased acid secretion + H.pylori infection
= gastric & duodenal ulcers
210
whre does non-erosive, antral chronic gastritis occur?
antrum
211
where does non-erosive, antral chronic gastritis occur?
antrum
212
how is a H.pylori infection treated?
treatment w triple antibiotics
| (amoxicillin, clarithromycin, pantoprazole)
213
where does atrophic gastritis occur?
fundus
214
what is the causes of atrophic gastritis?
autoantibodies produced against parts of a parietal cell (H+K+ ATPase, gastrin receptor) OR products of parietal cell function (IF)
215
in atropic gastritis, autoantibodes against what are produced?
against parts of a parietal cell = H+K+ ATPase, gastrin receptor
products of parietal cell function = intrinsic factore
216
what can atrophic gastritis lead to and why?
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
how is pernicious anaemia caused in atrophic gastritis?
reduced IF secreteion and so reduced cobalamin absorption = cobalamin deficiency
218
how are carcinomas (and carcinoid) caused in atrophic gastritis?
reduced acid secretion so increased gastrin = increase G cell hyperplasia = epithelial metaplasia = carcinoma
if increased ECL hyperplasia = carcinoid
219
what happens to parietal cells in atrophic gastritis\>?
parietal cell atrophy
220
what happens to acid and IF secretion in atrophic gastritis?
reduced IF and acid secretion
221
why is the function of parietal cells essential?
release pepsin and acid (H+)
= essential for protein digestion in the stomach
222
what stimulates parietal cells to release pepsin and HCl?
neural
- ACh (postganglionic transmitter of vagal parasympathetic fibres)
endocrine
- gastrin (G cells of antrum)
paracrine
- histamine (ECL cells & mast cells of gastric wall)
223
what inhibits parietal cells to release pepsin and HCl?
endocrine
- secretin (small intestine)
paracrine
- somatostatin (SIH)
paracrine & autocrine
- PGs (E2 & I2), TGF-α & adenosine
224
what stimulates parietal cells to release pepsin and HCl?
neural
- ACh (postganglionic transmitter of vagal parasympathetic fibres)
endocrine
- gastrin (G cells of antrum)
paracrine
- histamine (ECL cells & mast cells of gastric wall)
225
what inhibits parietal cells to release pepsin and HCl?
endocrine
- secretin (small intestine)
paracrine
- somatostatin (SIH)
paracrine & autocrine
- PGs (E2 & I2), TGF-α & adenosine
226
explain how parietal cells are stimulated neurally
ACh (postganglionic transmitter of vagal parasympathetic fibres)
227
explain how parietal cells are stimulated via endocrine pathways
gastrin (G cells of antrum)
228
explain how parietal cells are stimulated via paracrine pathways
histamine (ECL cells & mast cells of gastric wall)
229
explain how parietal cells are stimulated via endocrine pathways
secretin (small intestine)
230
explain how parietal cells are stimulated via paracrine pathways
somatostatin (SIH)
231
explain how parietal cells are stimulated via paracrine & autocrine pathways
PGs (E2 & I2), TGF-α & adenosine
232
summarise how parietal cells are stimulated and inhibited
233
what effect does increased acid have on gastrin production?
gastrin stimulates acid secretion which in turn shuts off gastrin secretion
(via somatostatin)
234
what are the four ways in which the mucosa is already protected?
1) overlying protective mucus film
2) HCO3- secretion
3) epithelial barrier
4) mucosal blood perfusion
235
explain how the mucosa is protected by a mucus film
the overlying mucus film is approximately 1-1.5cm thick, protecting the mucosa from damage due to hydrogen to pepsinogen
236
explain how the mucosa is protected by HCO3- secretion
epithelial cells produce bicarbonate (HCO3- ions) that buffer the acidic H+ ions (producing water)
= production propagated by prostaglandins
237
explain how the mucosa is protected by an epithelial barrier
the physical barrier of the epithelial cell membrane prevents entry of H+ ions and any damage caused by them
238
explain how the mucosa is protected by mucosal blood perfusion
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
what does the mucus film specifically protect against?
hydrogen ions an dpepsinogen
240
why are bicarbonate ions produced by the epithelial cells?
to buffer the H+ ions (producing water)
241
what is required for the production of bicarbonate ions?
prostaglandins
242
how can NSAIDs impair mucosal protection in the upper GI tract?
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
which transporter is responsible for removing H+ ions from the epithelial cells?
sodium-hydrogen co-transporter/
244
how will ischaemia affect mucosal protection in the upper GI tract?
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
what mechanisms exist to repair epithelial defects?
migration
gap closed by cell growth
acute wound healing
246
explain how migration repairs epithelial defects
adjacent epithelial cells flatten to close gap via sideward migration along the basement membrane
247
explain how cell growth repairs epithelial defects
covering defect through cell division
wherein cell growth is stimulated by EGF, TGFa, IGF-1, GRP, and gastrin
248
explain how wound healing repairs epithelial defects
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
what are possible causes for ulcer formation?
H. pylori infection
increased secretion of gastric juices
decreased HCO3- secretion
decreased cell formation
decreased blood perfusion
250
explain how H. pylori can lead to ulcer formation
infection w H. pylori (can lead to gastritis and) disrupts barrier function
= epithelial damage
251
what are NSAIDs?
name some common examples
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
explain how NSAIDs can lead to ulcer formation
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
explain how stress can lead to ulcer formation
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
explain how smoking or gastrinomas can lead to ulcer formation
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
what are gastrinomas?
rare tumours that start in the neuroendocrine cells that make large amounts of the hormone gastrin
256
in which age group are gastrinomas the most likely cause of ulcer formation and why?
commonly diagnosed between the ages of 20 and 50
(mainly young people)
257
what are the two ways in which the epithelium can be damaged?
barrier function disturbed
epithelial damage
258
what are the possible clinical outcomes of H. pylori infection?
\>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
what proportion of H. pylori patients are asymptomatic?
approx 80%
260
what proportion of H. pylori patients get chronic atrophic gastritis, intestinal metaplasia OR gastric or duodenal ulcers?
approx 15-20%
261
what proportion of H. pylori patients get gastric cancer/MALT lymphoma?
approx \<1%
262
what is the treatment for ulcers?
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
is surgery common for ulcers?
rare as most uncomplicated ulcers will heal within 12 weeks
if they don't = change medication and observe for another 12 weeks
264
how long do ulcers take to heal?
uncomplicated ulcers = approx 12 weeks
265
what must you do if ulcers do not heal within the first 12 weeks?
change medication and observe for another 12 weeks
check serum gastrin
OGD
266
why must you check serum gastrin levels in patients that have ulcers that are not healing well?
they may have antral G-cell hyperplasia
OR
may be due to a gastrinoma (Zollinger-Ellison syndrome)
267
why must you do an OGD in patients that have ulcers that are not healing well?
must biopsy all four quadrant of the ulcer to rule out malignancy
268
what are some reasons for abnormally high serum gastrin levels?
antral G-cell hyperplasia
gastrinoma i.e. Zollinger-Ellison syndrome (ZES)
269
what does an OGD rule out?
malignant ulcers
270
what are the possible indications for surgery of an ulcer?
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
what are the possible complications of ulcers?
haemorrhage, obstruction, perforation
272
what is Zollinger-Ellison syndrome?
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
what are peptic ulcers?
sores or raw areas within the digestive tract where the lining has been eroded by stomach acid and digestive juices
274
what does the following scan show?
barium swallow to show oesophageal dilation as a result of achalasia (hypermotility)
