reflux Flashcards
1
Q
where does the oesophagus transport food from and to?
A
from pharynx to stomach
2
Q
where does the oesophagus extend?
A
inferior border of cricoid cartilage to cardiac orifice of stomach (C6 to T11)
approx 25cm long
3
Q
describe the anatomical course of the oesophagus.
A
- begins in neck (C6), continuous superiorly with laryngeal part of pharynx
- descends into superior mediastinum of thorax positioned between trachea and vertebral bodies of T1 to T4
- enters abdomen via oesophageal hiatus at T10 level (opening in diaphragm)
- abdominal portion of oesophagus approx 1.25cm, terminates by joining cardiac orifice of stomach at T11
4
Q
what is the outermost layer of the oesophagus?
A
adventitia - outer layer of connective tissue
very distal and intraperitoneal part of oesophagus have serosa instead of adventitia
5
Q
what is the second outermost layer of the oesophagus?
A
muscle layer
6
Q
describe the structure of the muscle layer of the oesophagus.
A
external layer of longitudinal muscle
inner layer of circular muscle
7
Q
describe the structure of the external layer of longitudinal muscle in the muscle layer of the oesophagus.
A
different muscle types in each third
- superior third - voluntary striated
- middle third - voluntary striated and smooth
- inferior third - smooth
8
Q
what is the third outermost layer of the oesophagus?
A
submucosa
9
Q
what is the fourth and innermost layer of the oesophagus?
A
mucosa - non keratinised stratified squamous epithelium (contiguous with columnar epithelium of stomach)
10
Q
how is food transported through the oesophagus?
A
peristalsis - rhythmic contractions of muscles propagating down oesophagus
11
Q
what interferes with peristalsis and what can this lead to?
A
hardening of muscular layers
can cause difficulty swallowing (dysphagia)
12
Q
what is the function of the upper oesophageal sphincter?
A
acts to prevent entry of air
13
Q
what is the function of the lower oesophageal sphincter?
A
acts to prevent reflux of gastric contents
14
Q
what kind of sphincter is the upper oesophageal sphincter?
A
anatomical
striated muscle sphincter produced by the cricopharyngeus muscle
15
Q
where is the upper oesophageal sphincter located?
A
junction between pharynx and oesophagus
16
Q
how does the upper oesophagul sphincter carry out its function?
A
constricted to prevent air entering oesophagus
17
Q
where is the lower oesophageal sphincter located?
A
gastro-oesophageal junction (between stomach and oesophagus, to the left of T11 vertebra)
18
Q
how is the gastro oesophageal junction marked?
A
by change from oesophageal to gastric mucosa
19
Q
what kind of sphincter is the lower oesophageal sphincter?
A
physiological - no specific sphincteric muscle, formed from four phenomena
20
Q
what are the four phenomena that form the lower oesophageal sphincter?
A
- oesophagus enters stomach at an acute angle
- walls of intra-abdominal section of the oesophagus are compressed when there is a positive intra-abdominal pressure
- folds of mucosa present aid in occluding the lumen at the gastro-oesophageal junction
- right crus of the diaphragm has a “pinch-cock” effect
21
Q
how does the lower oesophageal sphincter carry out its function?
A
during peristalsis the sphincter is relaxed to allow food to enter the stomach
at rest the sphincter prevents reflux of acidic gastric contents into the oesophagus
22
Q
where are the four physiological constrictions in the lumen of the oesophagus? (ABCD)
A
Arch of aorta
Bronchus (left main stem)
Cricoid cartilage
Diaphragmatic hiatus
23
Q
what are the anterior relations of the cervical and thoracic oesophagus?
A
- trachea
- left recurrent laryngeal nerve
- pericardium
24
Q
what are the posterior relations of the cervical and thoracic oesophagus?
A
- thoracic vertebral bodies
- thoracic duct
- azygous veins
- descending aorta
25
what are the right relations of the cervical and thoracic oesophagus?
- pleura
| - terminal part of azygous vein
26
what are the left relations of the cervical and thoracic oesophagus?
- subclavian artery
- aortic arch
- thoracic duct
- pleura
27
what are the anterior relations of the abdominal oesophagus?
- left vagus nerve
| - posterior surface of heart
28
what are the posterior relations of the abdominal oesophagus?
- right vagus nerve
| - left crus of diaphragm
29
what is Barrett's oeseophagus?
refers to metaplasia of lower oesophageal squamous epithelium to gastric columnar epithelium
30
how is Barrett's oesophagus usually caused?
by chronic acid exposure resulting from malfunctioning lower oesophageal sphincter
acid irritates oesophageal epithelium, leading to metaplastic change
31
what is the most common symptom of Barrett's oesophagus?
long term burning sensation of indigestion
32
how can Barrett's oesophagus be detected?
endoscopy of oesophagus
33
what happens to any patients who are found to have Barrett's oesophagus?
monitored for any cancerous changes
34
what are the 2 clinical features of an oesophageal carcinoma?
dysphagia (as tumour increases in size, passage of food is restricted further)
weight loss
35
what are the two major types of oesophageal carcinoma?
squamous cell carcinoma (most common)
adenocarcinoma
36
where does squamous cell carcinoma occur in the oesophagus?
any level
37
where does an adenocarcinoma occur in the oesophagus?
inferior third
associated with Barrett's oesophagus - usually originates in the metaplastic epithelium
38
what are oesophageal varices?
abnormally dilated sub mucosal veins in wall of oesophagus that lie in the anastomosis formed by the oesophagus draining into both the systemic and portal circulation
39
when are oesophageal varices usually produced?
when pressure in portal system increases beyond normal (portal hypertension - usually occurs secondary to chronic liver disease including cirrhosis or obstruction of the portal vein)
40
what clinical feature do most patients with oesophageal varices present with and why?
haematemesis (vomiting blood)
varices predisposed to bleeding
41
what group of people are at high risk of developing oesophageal varices?
alcoholics
42
what is reflux?
some of the acidic contents of the stomach come up the oesophagus towards the mouth
43
what are the symptoms of reflux?
heartburn - burning sensation behind breastbone because of the acid, may move up towards throat
unpleasant taste in mouth
dysphagia
44
what is the first treatment for reflux?
PPI (proton pump inhibitor) for 4-8 weeks depending on severity and response
45
what happens if the symptoms of reflux come back after taking a course of PPI?
PPI offered at lowest dose to control symptoms
taking it only when needed
46
what is used if PPI doesn't work to treat reflux?
H₂ blocker
47
what is the first treatment for oesophagitis caused by reflux?
PPI (proton pump inhibitor) for 8 weeks
48
what happens if the symptoms of oesophagitis due to reflux come back after taking a course of PPI?
higher dose or treatment with different PPI
treatment taken for long time to control symptoms
49
what happens if PPI doesn't work to treat oesophagitis cause by reflux?
reviw symptoms, lifestyle and treatments
(diferent PPI etc.)
may have specialist advice from gastroenterologist
50
when treating reflux, who is surgery appropriate for?
people who do not want to take medication long term
people with unpleasant side effects from medication
51
what is the most common type of surgery for reflux?
laparoscopic fundoplication
52
what takes place in laparoscopic fundoplication?
keyhole surgery
top of stomach stitched and folded just below where oesophagus meets it in order to create a smaller opening
53
what is the aim of laparoscopic fundoplication?
reduce amounts of stomach contents re-entering oesophagus
54
why should antacids not be taken long term for heartburn and reflux?
help symptoms short term but do not cure problem
55
mr mueller describes his symptoms as heartburn, how else could they be described?
reflux
indigestion
tummy ache
bloating
56
how would you describe the category of symptoms that mr mueller is describing?
dyspepsia
57
define dyspepsia.
recurrent epigastric pain, heartburn or symptoms of acid regurgitation
with or without bloating, nausea or vomiting
58
why is dyspepsia a better word to use than reflux, indigestion etc.?
there are no assumptions as to the cause
59
why may dyspepsia not be a better word to use than reflux, indigestion etc.?
lack of understanding from patient
60
what 5 possible diagnoses are possible for mr mueller's dyspepsia?
GORD
gastritis
peptic ulcer disease
functional dyspepsia
stress
61
when the cause of dyspepsia is oesophageal reflux what other symptoms may be present?
belching
excess salivating in mouth (water brash)
62
when the cause of dyspepsia is gastroenteritis what other symptoms may be present?
vomiting
diarrhoea
fever
63
what is important about common differentials?
GORD
gastritis
peptic ulcer disease
```
functional dyspepsia (most common)
all have same common differentials
```
but could also be signs of something serious but less common like upper GI malignancy
64
what is functional dyspepsia?
individual suffers from symptoms of dyspepsia but routine investigations do not reveal causative abnormalities
65
what is the relationship between gastritis and functional dyspepsia?
gastritis - common, usually resolves itself, doesn't always explain symptoms of dyspepsia
in an endoscopy for functional dyspepsia an element of gastritis may be revealed (~70% of those with functional dyspepsia)
even is gastritis is present it does not necessarily correlate with the degree of symptoms so functional dyspepsia is attributed as the cause
66
what does gastritis mean?
inflammation of gastric mucosa
67
what is the relationship between stress, gastritis/functional dyspepsia/peptic ulcers?
stress may contribute to development
68
what are the most common causes of dyspepsia?
oesophagitis (inflammation and irritation of oesophagus from acid)
peptic ulcer disease - gastric/duodenal
69
which of mr mueller's symptoms are indicative of GORD?
getting worse after eating
especially when lying down, can feel like burning pain behind sternum
70
what is relevant about coeliac disease and inflammatory bowel disease?
alternative diagnoses; may be associated with systemic manifestations etc.
71
what is relevant about gall bladder/biliary disease?
linked with dypepsia
can be eliminated for now because pain is more colicky in nature
72
what can cause colicky pain?
gallstones
renal stones
other intestinal obstructions
73
what is colicky pain?
intermittent, spasmodic pain that occurs when it contracts usually in response to removing an obstruction
74
what is relevant about pancreatitis?
signs of pancreatic insufficiency such as steatorrhea or diabetes?
linked with dypepsia
can be eliminated for now because steatorrhea and diabetes are common symptoms
75
what is relevant about coronary heart disease?
important to consider
he has risk factors; stressful job, smoking history
in some patients cardiac ischaemia can present as dyspepsia rather than angina-type pain; risk of misdiagnosis
76
what is relevant about upper GI malignancy?
often presents with dyspepsia (may present with other symptoms)
77
in which cases can gastritis be both symptomatic and problematic?
infection
medication
protecting mucus lining of stomach
alcohol excess
78
how can you tell if a diagnosis will be very dangerous or not very dangerous?
look for signs of serious underlying pathology
79
what term is used for associated symptoms that indicate serious underlying pathology?
red flag symptoms
80
what are red flag symptoms?
signs found in patient history or clinical exams that could indicate a serious underlying conditions
81
why are red flag symptoms important?
can assess risk level of patients relative to each other if needed especially if complaint is common
can get early investigation and management to those that need it
unnecessary time and money not taken
82
which red flag symptoms may be important for back pain?
previous cancer
bowel issues
fever
very young or very old
leg weakness
83
what are the high risk diagnoses for back pain?
spinal cord compression
malignancy
infection
84
what are the high risk diagnoses for headaches?
meningitis
intra cerebral tumours
infection
acute bleed
85
which red flag symptoms may be important for headaches if meningitis is suspected?
raised intra cranial pressure
meningism (signs of irritation in meninges)
particuarly severe and sudden headaches
86
what is the high risk diagnosis for mr mueller's dyspepsia?
upper GI cancer
87
which red flag symptoms may be important for dyspepsia if checking for upper GI malignancies?
dysphagia
weight loss
anaemia
88
why may vomiting or dyspepsia not be considered a red flag symptom for abdominal pain?
if it only lasts for a little while it may be due to something acute e.g acute gastroenteritis
if it continues for a while and does not respond to treatment it could become a red flag (especially if over 55 years for dyspepsia)
89
when should a person with suspected upper GI malignancy be urgently referred (2 week wait) ?
if they have an upper abdominal mass consistent with stomach cancer
90
to whom should an urgent endoscopy be suggested when upper GI cancer is suspected?
people with dysphagia
over 55 years with weight loss and upper abdominal pain/reflux/dyspepsia
91
when should a non-urgent endoscopy be suggested if upper GI cancer is suspected?
presenting with haematemesis
over 55 years with any of:
- low Hb level
- raised platelet count
- nausea and vomiting
92
after having eliminated red flag symptoms for mr mueller, what tests should the GP do?
testing for H. pylori
FBC (full blood count)
LFTs (liver function test)
alcohol history
medication history
weight
ECG
93
after having eliminated red flag symptoms for mr mueller, the GP would do 7 tests. which is prioritised first and why?
ECG
- quick and non invasive
- ideally during pain to see if there is any indication of cardiac ischaemia
- might highlight abnormalities - old myocardial infarcts,
94
after having eliminated red flag symptoms for mr mueller, the GP would do 7 tests. which is prioritised second and why?
weight
- simple and free
- monitoring; can compare with other results if needed
- BMI; can discuss with patient
95
after having eliminated red flag symptoms for mr mueller, the GP would do 7 tests. which is prioritised third and why?
alcohol history
- mr mueller has hinted that his alcohol intake may be over the limit
- risk factor for many clinical consequences; including dyspepsia, and in excess may cause problems such as alcoholic gastritis or liver damage etc.
- offer support even if not necessarily related to abdominal issue
96
what is the recommended maximum alcohol intake per week?
14 units
97
after having eliminated red flag symptoms for mr mueller, the GP would do 7 tests. which is prioritised fourth and why?
medication history
- including over the counter; may highlight meds that contribute to dyspepsia
e. g those that relax lower oesophageal sphincter, facilitating reflux - includes beta blockers, calcium channel blockers and nitrates
e.g those that affect gastric mucosa (protective mucous layer) - includes non steroidal anti inflammatory drugs, aspirin
98
after having eliminated red flag symptoms for mr mueller, the GP would do 7 tests. which is prioritised fifth and why?
testing for Helicobacter pylori
- common in dyspepsia - can cause many of the differentials for gastritis, peptic ulcer disease, gastric malignancies (including adenocarcinoma and malt lymphoma)
- infection of Helicobacter highly prevalent (~50% of worlds population have it living in stomach although it doesn't always cause symptoms)
99
what is malt lymphoma?
lymphoma of mucosa associated lymphoid tissue
100
after having eliminated red flag symptoms for mr mueller, the GP would do 7 tests. which is prioritised sixth and why?
FBC (full blood count)
- anaemia and high platelets (thrombocytosis); feature in referral guide for upper GI malignancies
- anaemia might be caused upper GI malignancies since GI cancers promote bleeding and cancer cells can impact RBC production due to interference with erythopoeitin action
101
what causes elevated platelet count (thrombocytosis)?
release of cytokines that promote platelet production
102
after having eliminated red flag symptoms for mr mueller, the GP would do 7 tests. which is prioritised seventh and why?
LFTs (liver function tests)
- biliary disease (unlikely from history, but not impossible)
- alcohol induced liver changes; opportunistic test
- no inconvenience as bloods are being done anyway
103
for another patient, what symptoms might be presenting for stool tests to be done after red flag symptoms are eliminated (MC+S and parasites, cysts and ova)?
if patient had
- diarrhoea
- fever
- had travelled recently
- a history in keeping with gastroenteritis
104
when might an abdominal radiograph be done for another patients after red flag symptoms are eliminated/ why is this not suitable for mr mueller?
- used only in more acute setting
- used for suspected intestinal obstruction or perforation
- more subtle findings not shown, e.g in soft tissues
105
why would a CT scan not be suitable for mr mueller after red flag symptoms are eliminated?
radiation
expense
may not show any suspected diagnoses
106
why would an echocardiogram not be suitable for mr mueller?
relevance; not many presenting symptoms
no history of cardiac issues
abnormal ECG
will not add anything to management of presenting complaint
107
why would a digital rectal exam not be suitable for mr mueller?
used to look for upper gastrointestinal bleeding, where it can identify melaena
108
what is melaena?
dark and offensive smelling faeces containing digestive blood from GI tract
mr mueller has no stool changes or haematemesis (only use if these are present or in an acute situation)
109
why would an upper gastrointestinal endoscopy/oesophago gastro duodenoscopy (OGD) not be suitable for mr mueller?
needed for certain causes of dyspepsia
requires referral to secondary care
invasive and requires sedation
not always necessary; in this case no symptoms concerning enough for OGD
110
where is the site of H. pylori infection and why is this important?
stomach
contains hydrochloric acid which usually kills ingested pathogens
111
how is corrosion of the epithelial stomach lining prevented?
foveolar cells produce a layer of alkaline mucus to protect it
112
how does H. pylori enter the stomach?
most likely ingestion
113
how does H. pylori survive in the stomach?
urease - enzyme that catalyses reaction to neutralise gastric acid surrounding it (urea + water---> carbon dioxide + ammonia)
ammonia is basic, therefore neutralises HCl, creating thin buffering layer around H. pylori
114
why and how does H. pylori reach the stomach lining?
pH of mucous lining is much lower (neutral close to epithelial cells)
flagella for locomotion
chemotaxic gradient for orientation
115
what molecule helps H. pylori adhere to stomach lining once it has reached there?
LPS (lipopolysaccharide)
BabA
116
H. pylori isn't generally harmful - which toxin fits between cells in stomach lining, causing inflammation (gastritis)?
cagA
H. pylori strands can either be cagA+ or cagA-; cagA+ is more closely associated with gastric conditions
117
H. pylori isn't generally harmful - which toxin causes cells in the stomach lining to apoptose?
vacA
118
why is the action of cagA and vacA damaging?
disrupts continuity of stomach lining
lining now exposed to action of HCl
can lead to ulcers
119
mr mueller's H. pylori diagnosis came from a stool antigen test - what are its advantages?
non invasive, simple, safe
high sensitivity and specificity
can be used for diagnosis and theoretically as a test of cure
120
mr mueller's H. pylori diagnosis came from a stool antigen test - what are its disadvantages?
patients might prefer other tests
samples need refrigeration
if patient is on antibiotics or PPIs the results might be falsely negative
lacking sufficient evidence to use as a test of cure
121
H. pylori can be detected by a carbon-13 urea breath test - what are its advantages?
non invasive, simple, safe
high sensitivity and specificity
can be used for diagnosis and as a test of cure
122
H. pylori can be detected by a carbon-13 urea breath test - what are its disadvantages?
specialist analysis equipment needed, samples may need to be sent away
if patient is on antibiotics or PPIs the results might be falsely negative
requires fasting conditions
123
H. pylori can be detected by a serum serology test - what are its advantages?
cheap, widely available
may be useful for diagnosing newly infected patients
124
H. pylori can be detected by a serum serology test - what are its disadvantages?
IgM poorly sensitive for new infection
IgG does not tell you if infection is current (remains positive after infection is cleared)
cannot test for cure
125
H. pylori can be detected by a CLO test - what are its advantages?
high sensitivity and specificity
instantaneous result
126
H. pylori can be detected by a CLO test - what are its disadvantages?
if patient is on antibiotics or PPIs the results might be falsely negative
invasive
127
how does a carbon-13 urea breath test for H. pylori work?
provide 2 breath samples by blowing into an
empty test tube through a straw
drink a solution containing 13 Carbon Urea and wait for 30 mins
asked to blow into another 2 test tubes and you will then be allowed to go home
carbon dioxide produced by the action of urease on ammonia will have different isotopes of carbon; mass spectrometry is used to detect this
128
how does a stool antigen test for H. pylori work?
looks for antigens associated with H. pylori in stool
129
how does a serum serology test for H. pylori work?
enzyme linked immunosorbent assay to detect serum H. pylori–specific IgG and IgA antibodies using either a monoclonal or polyclonal enzyme immunoassay
130
how does a CLO test for H. pylori work?
biopsy of mucosa taken from stomach, and is placed into a medium containing urea and an indicator such as phenol red
urease produced by H. pylori hydrolyzes urea to ammonia, which raises the pH of the medium, and changes the colour of the specimen from yellow (NEGATIVE) to red (POSITIVE)
131
why may a stool antigen test have been the best one for mr mueller?
serum serology tests for specific human proteins in serum - serum antibody level rises in response to H. pylori antigens, but infection may have been in the past and not necessarily be current
carbon-13 urea breath test, stool antigen test and CLO test all probe for H. pylori proteins
BUT carbon-13 breath test and CLO test test for molecules that result from the presence of H. pylori
stool antigen test tests directly for H. pylori antigens
NICE recommends stool antigen test or carbon-13 urea breath test as first option but carbon-13 breath test requires specialist equipment
132
how does the human body make HCl for use in the stomach?
gastric pits in lumen of stomach lead to gastric glands which are lined by several different types of cell including parietal cells that secrete HCl
apical side of parietal cell - lumen, gastric glands
basolateral side of parietal cell - interstitial fluid with direct access to blood capillaries
HCl travels to apical side
chloride ions come from blood (basolateral side)
hydrogen ions produced by:
carbon dioxide diffuse from interstitial fluid into parietal cell via cell membrane
carbonic anhydrase in parietal cells catalyses reaction of carbon dioxide + water to form carbonic acid
carbonic acid dissociates to form hydrogen ions and bicarbonate ions
chloride-bicarbonate exchanger in basolateral membrane of parietal cells uses ATP to exchange chloride and bicarbonate ions so that chloride ions move into the cell and bicarbonate ions move out
proton pump uses ATP in apical membrane exchanges potassium ions for hydrogen ions so they travel through to lumen and gastric glands on apical side
chloride channels in apical membrane of parietal cells allow chloride ions through apical membrane into the lumen and gastric glands
receptors that stimulate process:
- ACh receptors
- H₂ receptors (histamine receptors) - stimulate signalling cascade that move proton pumps to apical cell membrane
- gastrin receptors
133
how is the amount of HCl in the stomach reduced if needed?
drugs can only affect certain parts of the process producing HCl in a safe manner
PPIs inhibit proton pumps in apical membrane of parietal cells
H₂ antagonists inhibit H₂ receptors in basolateral membrane of parietal cells
antacids to neutralise HCl
134
why are PPIs used against H. pylori?
reduce level of HCl by inhibiting proton pumps in apical membrane of parietal cells
mild antibacterial effect against H. pylori
anti urease and anti ATPase activity
usually used in combination with antibiotics - antibacterial effect caused of antibiotics to be concentrated and thereby enhance their effectiveness
135
how many receptors are blocked by the use of PPIs?
80% - sometimes H₂ antagonists are also needed
136
what are some examples of PPIs?
omeprazole
lansoprazole
137
what are some examples of H₂ antagonists?
ranitidine
cimetidine
138
what are some examples of antacids?
magnesium carbonate
aluminium hydroxide
139
what treatment was used for mr mueller?
omeprazole (PPI)
amoxicillin
clarithromycin
carbon-13 urea breath test after treatment cam out negative (only method validated by NICE that gives test of cure)
140
why was a carbon-13 urea breath test used after mr mueller's treatment with omeprazole, amoxicillin and clarithromycin to judge its effectiveness?
carbon-13 urea breath test only method validated by NICE that gives test of cure
antibiotics used may have given false negatives for stool antigen, CLO and carbon-13
141
why might false negatives for H. pylori be produced by stool antigen, carbon-13 urea and CLO tests after a course of antibiotics?
H. pylori are still present but their activity is lessened
142
what does NICE recommend to prevent false negatives in carbon-13 urea tests after a course of antibiotics?
no PPIs for 2 weeks before test
no antibiotics for 4 weeks before test
143
why is mr mueller's dyspepsia classed as treatment resistant?
even though carbon-13 urea breath test showed that H. pylori was gone, dyspepsia still persisted
3 week course of omeprazole also did not have results
followed by a course of ranitidine which also did not have results
144
what is the next step for treatment after mr mueller's dyspepsia has been classed as treatment resistant?
in case of over 55 years and treatment resistant dyspepsia NICE recommends referral for non-urgent upper GI endoscopy
145
what does mr mueller's OGD report say after his upper GI endoscopy?
sliding hiatus hernia present with evidence of moderate oesophagitis
gastric mucosa macroscopically normal
duodenum normal
CLO test negative
recommend high dose omeprazole and repeat OGD after 3 months
146
what is a sliding hiatus hernias?
when part of the abdominal viscera herniate through an opening in the diaphragm
147
what are the risk factors for a sliding hiatus hernia?
male
obesity
pregnancy
genetic predisposition
148
why do sliding hiatus hernias occur?
widening of diaphragmatic hiatus
pulling up of the stomach (due to oesophageal shortening)
pushing up the stomach (e.g due to increased intra abdominal pressure)
149
what is the effect of a sliding hiatus hernia?
function of lower oesophageal sphincter is lost - stomach contents allowed to reflux back into oesophagus
therefore a common cause of GORD
150
what are the two types of hiatus hernia?
sliding and rolling
151
what is the most common type of sliding hiatus hernia?
sliding (85-95%)
152
what happens to the GOJ in a sliding hiatus hernia?
moves upwards
153
how common is a rolling hiatus hernia?
5-15%
154
what happens to the GOJ in a rolling hiatus hernia?
remains in place
155
what does a sliding hiatus hernia predominantly cause symptoms of?
GORD
156
what happens in a rolling hiatus hernia?
portion of stomach, bowel, pancreas or spleen herniates into chest next to GOJ
157
what are the constituents of refluxed material?
stomach acid
at times, ingested food
rarely, if bile has entered from duodenum it might also be refluxed
158
what is the pH of refluxed material?
ingested food may buffer the acid to make it less acidic and lower the pH
159
what are some reasons for continuation of symptoms despite use of a PPI?
mr mueller - hernia caused symptoms and dose was not high enough to combat this
functional dyspepsia
non acid reflux - PPI will have no effect, better option is something like Gaviscon (an alginate - precipitates into a gel that forms a layer on top of stomach contents acting as a physical barrier against reflux despite it being acidic/non acidic)
specialist tests (e.g gastro oesophageal pH monitoring) by gastroenterologist team needed for treatment
160
how would non acid reflux be treated?
PPI will have no effect
better option is something like Gaviscon (an alginate - precipitates into a gel that forms a layer on top of stomach contents acting as a physical barrier against reflux despite it being acidic/non acidic)
161
GORD may lead to oesophagitis, which has a 10% chance of developing into Barrett's oesophagus - why might this be dangerous?
risk of developing oesophageal cancer
1-5% of those with Barrett's oesophagus develop it
162
how does the tissue in the oesophagus change in Barrett's oesophagus?
changes from stratified squamous epithelium, becomes columnar with goblet cells (metaplasia)
repeated exposure to stomach contents causes it to change
- biopsy would show intestinal metaplasia (goblet cells present) but it may not be distributed evenly in the same way as the columnar-lined eosophagus
- cardiac metaplasia (part of the stomach near the heart, not heart tissue) sometimes considered a precursor to intestinal metaplasia
but both are accepted as a diagnostic measure for Barrett's oesophagus
163
how can an area of high grade dysplasia in the oesophagus also be descibed?
carcinoma in situ
intra epithelial neoplasia
stage 0 cancer
164
how is carcinoma in situ defined?
a group of abnormal cells that remain in the place where they are first formed - they have not spread
these abnormal cells may become cancerous and spread into nearby normal tissue
165
where can carcinoma in situ occur?
breast ducts
oesophagus
bladder
cervix
skin
166
what are the treatment options for Barrett's oesophagus?
endoscopic ablation
oesophagectomy
167
when is it likely that someone with GORD will develop Barrett's oesophagus?
family history of GORD, Barrett's or oesophageal cancer
medical history of gastroenteric issues
168
what lifestyle changes should mr mueller make to ease his symptoms and to reduce further risk later?
raise one end of your bed 10-20 cm so that chest and head are above level of waist (stomach acid does not travel up towards chest) - especially since he has trouble sleeping because of symptoms
don't eat within 3-4 hours before bed
try to lose weight
try to find ways to relax
don't smoke
don't drink excessively
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why is losing weight an important lifestyle change to make when treating GORD?
more weight on abdomen means more intra abdominal pressure, increasing risk of reflux (use BMI)
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why is managing stress an important lifestyle change to make when treating GORD?
gut is connected to CNS - brain gut axis; exposure to stress alters this axis
clinical consequences that increase GORD effects-
- may relax lower oesophageal sphincter
- slow gastric emptying
- increasing susceptibility of oesophagus to damage and inflammatory pathways
- increasing oesophageal sensitivity to refluxed material (lowered threshold for symptoms)
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why is not smoking an important lifestyle change to make when treating GORD?
nicotine may relax lower oesophageal sphincter
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why is reducing alcohol intake an important lifestyle change to make when treating GORD?
chronic excess alcohol intake is associated with GORD
mechanisms include
- damage to gastric mucosa which triggers increased acid production
- inhibition of gastric emptying
- effect on functioning of oesophagus (especially lower oesophageal sphincter)
- may directly cause oesphageal mucosal damage
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why is eating smaller, less frequent meals an important lifestyle change to make when treating GORD?
less acid production
less increase in intra abdominal pressure
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what foods are likely to trigger GORD symptoms?
spicy food
coffee
acidic fruits (e.g citrus)
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why may not eating 3-4 hours before bed be an important lifestyle change to make when treating GORD?
gives stomach time to digest and empty before lying down
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why are lifestyle changes important in treating GORD?
helps symptoms
reduces risk of further complications with oesophagus through exposure to refluxed contents
