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reflux Flashcards

1
Q

where does the oesophagus transport food from and to?

A

from pharynx to stomach

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2
Q

where does the oesophagus extend?

A

inferior border of cricoid cartilage to cardiac orifice of stomach (C6 to T11)

approx 25cm long

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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
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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

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5
Q

what is the second outermost layer of the oesophagus?

A

muscle layer

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6
Q

describe the structure of the muscle layer of the oesophagus.

A

external layer of longitudinal muscle

inner layer of circular muscle

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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
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8
Q

what is the third outermost layer of the oesophagus?

A

submucosa

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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)

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10
Q

how is food transported through the oesophagus?

A

peristalsis - rhythmic contractions of muscles propagating down oesophagus

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11
Q

what interferes with peristalsis and what can this lead to?

A

hardening of muscular layers

can cause difficulty swallowing (dysphagia)

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12
Q

what is the function of the upper oesophageal sphincter?

A

acts to prevent entry of air

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13
Q

what is the function of the lower oesophageal sphincter?

A

acts to prevent reflux of gastric contents

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14
Q

what kind of sphincter is the upper oesophageal sphincter?

A

anatomical

striated muscle sphincter produced by the cricopharyngeus muscle

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15
Q

where is the upper oesophageal sphincter located?

A

junction between pharynx and oesophagus

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16
Q

how does the upper oesophagul sphincter carry out its function?

A

constricted to prevent air entering oesophagus

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17
Q

where is the lower oesophageal sphincter located?

A

gastro-oesophageal junction (between stomach and oesophagus, to the left of T11 vertebra)

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18
Q

how is the gastro oesophageal junction marked?

A

by change from oesophageal to gastric mucosa

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19
Q

what kind of sphincter is the lower oesophageal sphincter?

A

physiological - no specific sphincteric muscle, formed from four phenomena

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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
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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

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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

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23
Q

what are the anterior relations of the cervical and thoracic oesophagus?

A
  • trachea
  • left recurrent laryngeal nerve
  • pericardium
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24
Q

what are the posterior relations of the cervical and thoracic oesophagus?

A
  • thoracic vertebral bodies
  • thoracic duct
  • azygous veins
  • descending aorta
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25
Q

what are the right relations of the cervical and thoracic oesophagus?

A
  • pleura

- terminal part of azygous vein

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26
Q

what are the left relations of the cervical and thoracic oesophagus?

A
  • subclavian artery
  • aortic arch
  • thoracic duct
  • pleura
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27
Q

what are the anterior relations of the abdominal oesophagus?

A
  • left vagus nerve

- posterior surface of heart

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28
Q

what are the posterior relations of the abdominal oesophagus?

A
  • right vagus nerve

- left crus of diaphragm

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29
Q

what is Barrett’s oeseophagus?

A

refers to metaplasia of lower oesophageal squamous epithelium to gastric columnar epithelium

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30
Q

how is Barrett’s oesophagus usually caused?

A

by chronic acid exposure resulting from malfunctioning lower oesophageal sphincter

acid irritates oesophageal epithelium, leading to metaplastic change

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31
Q

what is the most common symptom of Barrett’s oesophagus?

A

long term burning sensation of indigestion

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32
Q

how can Barrett’s oesophagus be detected?

A

endoscopy of oesophagus

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33
Q

what happens to any patients who are found to have Barrett’s oesophagus?

A

monitored for any cancerous changes

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34
Q

what are the 2 clinical features of an oesophageal carcinoma?

A

dysphagia (as tumour increases in size, passage of food is restricted further)

weight loss

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35
Q

what are the two major types of oesophageal carcinoma?

A

squamous cell carcinoma (most common)

adenocarcinoma

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36
Q

where does squamous cell carcinoma occur in the oesophagus?

A

any level

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37
Q

where does an adenocarcinoma occur in the oesophagus?

A

inferior third

associated with Barrett’s oesophagus - usually originates in the metaplastic epithelium

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38
Q

what are oesophageal varices?

A

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

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39
Q

when are oesophageal varices usually produced?

A

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)

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40
Q

what clinical feature do most patients with oesophageal varices present with and why?

A

haematemesis (vomiting blood)

varices predisposed to bleeding

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41
Q

what group of people are at high risk of developing oesophageal varices?

A

alcoholics

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42
Q

what is reflux?

A

some of the acidic contents of the stomach come up the oesophagus towards the mouth

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43
Q

what are the symptoms of reflux?

A

heartburn - burning sensation behind breastbone because of the acid, may move up towards throat

unpleasant taste in mouth

dysphagia

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44
Q

what is the first treatment for reflux?

A

PPI (proton pump inhibitor) for 4-8 weeks depending on severity and response

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45
Q

what happens if the symptoms of reflux come back after taking a course of PPI?

A

PPI offered at lowest dose to control symptoms

taking it only when needed

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46
Q

what is used if PPI doesn’t work to treat reflux?

A

H₂ blocker

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47
Q

what is the first treatment for oesophagitis caused by reflux?

A

PPI (proton pump inhibitor) for 8 weeks

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48
Q

what happens if the symptoms of oesophagitis due to reflux come back after taking a course of PPI?

A

higher dose or treatment with different PPI

treatment taken for long time to control symptoms

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49
Q

what happens if PPI doesn’t work to treat oesophagitis cause by reflux?

A

reviw symptoms, lifestyle and treatments
(diferent PPI etc.)

may have specialist advice from gastroenterologist

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50
Q

when treating reflux, who is surgery appropriate for?

A

people who do not want to take medication long term

people with unpleasant side effects from medication

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51
Q

what is the most common type of surgery for reflux?

A

laparoscopic fundoplication

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52
Q

what takes place in laparoscopic fundoplication?

A

keyhole surgery

top of stomach stitched and folded just below where oesophagus meets it in order to create a smaller opening

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53
Q

what is the aim of laparoscopic fundoplication?

A

reduce amounts of stomach contents re-entering oesophagus

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54
Q

why should antacids not be taken long term for heartburn and reflux?

A

help symptoms short term but do not cure problem

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55
Q

mr mueller describes his symptoms as heartburn, how else could they be described?

A

reflux

indigestion

tummy ache

bloating

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56
Q

how would you describe the category of symptoms that mr mueller is describing?

A

dyspepsia

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57
Q

define dyspepsia.

A

recurrent epigastric pain, heartburn or symptoms of acid regurgitation

with or without bloating, nausea or vomiting

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58
Q

why is dyspepsia a better word to use than reflux, indigestion etc.?

A

there are no assumptions as to the cause

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59
Q

why may dyspepsia not be a better word to use than reflux, indigestion etc.?

A

lack of understanding from patient

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60
Q

what 5 possible diagnoses are possible for mr mueller’s dyspepsia?

A

GORD

gastritis

peptic ulcer disease

functional dyspepsia

stress

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61
Q

when the cause of dyspepsia is oesophageal reflux what other symptoms may be present?

A

belching

excess salivating in mouth (water brash)

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62
Q

when the cause of dyspepsia is gastroenteritis what other symptoms may be present?

A

vomiting

diarrhoea

fever

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63
Q

what is important about common differentials?

A

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

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64
Q

what is functional dyspepsia?

A

individual suffers from symptoms of dyspepsia but routine investigations do not reveal causative abnormalities

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65
Q

what is the relationship between gastritis and functional dyspepsia?

A

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

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66
Q

what does gastritis mean?

A

inflammation of gastric mucosa

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67
Q

what is the relationship between stress, gastritis/functional dyspepsia/peptic ulcers?

A

stress may contribute to development

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68
Q

what are the most common causes of dyspepsia?

A

oesophagitis (inflammation and irritation of oesophagus from acid)

peptic ulcer disease - gastric/duodenal

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69
Q

which of mr mueller’s symptoms are indicative of GORD?

A

getting worse after eating

especially when lying down, can feel like burning pain behind sternum

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70
Q

what is relevant about coeliac disease and inflammatory bowel disease?

A

alternative diagnoses; may be associated with systemic manifestations etc.

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71
Q

what is relevant about gall bladder/biliary disease?

A

linked with dypepsia

can be eliminated for now because pain is more colicky in nature

72
Q

what can cause colicky pain?

A

gallstones

renal stones

other intestinal obstructions

73
Q

what is colicky pain?

A

intermittent, spasmodic pain that occurs when it contracts usually in response to removing an obstruction

74
Q

what is relevant about pancreatitis?

A

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
Q

what is relevant about coronary heart disease?

A

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
Q

what is relevant about upper GI malignancy?

A

often presents with dyspepsia (may present with other symptoms)

77
Q

in which cases can gastritis be both symptomatic and problematic?

A

infection

medication

protecting mucus lining of stomach

alcohol excess

78
Q

how can you tell if a diagnosis will be very dangerous or not very dangerous?

A

look for signs of serious underlying pathology

79
Q

what term is used for associated symptoms that indicate serious underlying pathology?

A

red flag symptoms

80
Q

what are red flag symptoms?

A

signs found in patient history or clinical exams that could indicate a serious underlying conditions

81
Q

why are red flag symptoms important?

A

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
Q

which red flag symptoms may be important for back pain?

A

previous cancer

bowel issues

fever

very young or very old

leg weakness

83
Q

what are the high risk diagnoses for back pain?

A

spinal cord compression

malignancy

infection

84
Q

what are the high risk diagnoses for headaches?

A

meningitis

intra cerebral tumours

infection

acute bleed

85
Q

which red flag symptoms may be important for headaches if meningitis is suspected?

A

raised intra cranial pressure

meningism (signs of irritation in meninges)

particuarly severe and sudden headaches

86
Q

what is the high risk diagnosis for mr mueller’s dyspepsia?

A

upper GI cancer

87
Q

which red flag symptoms may be important for dyspepsia if checking for upper GI malignancies?

A

dysphagia

weight loss

anaemia

88
Q

why may vomiting or dyspepsia not be considered a red flag symptom for abdominal pain?

A

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
Q

when should a person with suspected upper GI malignancy be urgently referred (2 week wait) ?

A

if they have an upper abdominal mass consistent with stomach cancer

90
Q

to whom should an urgent endoscopy be suggested when upper GI cancer is suspected?

A

people with dysphagia

over 55 years with weight loss and upper abdominal pain/reflux/dyspepsia

91
Q

when should a non-urgent endoscopy be suggested if upper GI cancer is suspected?

A

presenting with haematemesis

over 55 years with any of:

  • low Hb level
  • raised platelet count
  • nausea and vomiting
92
Q

after having eliminated red flag symptoms for mr mueller, what tests should the GP do?

A

testing for H. pylori

FBC (full blood count)

LFTs (liver function test)

alcohol history

medication history

weight

ECG

93
Q

after having eliminated red flag symptoms for mr mueller, the GP would do 7 tests. which is prioritised first and why?

A

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
Q

after having eliminated red flag symptoms for mr mueller, the GP would do 7 tests. which is prioritised second and why?

A

weight

  • simple and free
  • monitoring; can compare with other results if needed
  • BMI; can discuss with patient
95
Q

after having eliminated red flag symptoms for mr mueller, the GP would do 7 tests. which is prioritised third and why?

A

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
Q

what is the recommended maximum alcohol intake per week?

A

14 units

97
Q

after having eliminated red flag symptoms for mr mueller, the GP would do 7 tests. which is prioritised fourth and why?

A

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
Q

after having eliminated red flag symptoms for mr mueller, the GP would do 7 tests. which is prioritised fifth and why?

A

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
Q

what is malt lymphoma?

A

lymphoma of mucosa associated lymphoid tissue

100
Q

after having eliminated red flag symptoms for mr mueller, the GP would do 7 tests. which is prioritised sixth and why?

A

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
Q

what causes elevated platelet count (thrombocytosis)?

A

release of cytokines that promote platelet production

102
Q

after having eliminated red flag symptoms for mr mueller, the GP would do 7 tests. which is prioritised seventh and why?

A

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
Q

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)?

A

if patient had

  • diarrhoea
  • fever
  • had travelled recently
  • a history in keeping with gastroenteritis
104
Q

when might an abdominal radiograph be done for another patients after red flag symptoms are eliminated/ why is this not suitable for mr mueller?

A
  • used only in more acute setting
  • used for suspected intestinal obstruction or perforation
  • more subtle findings not shown, e.g in soft tissues
105
Q

why would a CT scan not be suitable for mr mueller after red flag symptoms are eliminated?

A

radiation

expense

may not show any suspected diagnoses

106
Q

why would an echocardiogram not be suitable for mr mueller?

A

relevance; not many presenting symptoms

no history of cardiac issues

abnormal ECG

will not add anything to management of presenting complaint

107
Q

why would a digital rectal exam not be suitable for mr mueller?

A

used to look for upper gastrointestinal bleeding, where it can identify melaena

108
Q

what is melaena?

A

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
Q

why would an upper gastrointestinal endoscopy/oesophago gastro duodenoscopy (OGD) not be suitable for mr mueller?

A

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
Q

where is the site of H. pylori infection and why is this important?

A

stomach

contains hydrochloric acid which usually kills ingested pathogens

111
Q

how is corrosion of the epithelial stomach lining prevented?

A

foveolar cells produce a layer of alkaline mucus to protect it

112
Q

how does H. pylori enter the stomach?

A

most likely ingestion

113
Q

how does H. pylori survive in the stomach?

A

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
Q

why and how does H. pylori reach the stomach lining?

A

pH of mucous lining is much lower (neutral close to epithelial cells)

flagella for locomotion

chemotaxic gradient for orientation

115
Q

what molecule helps H. pylori adhere to stomach lining once it has reached there?

A

LPS (lipopolysaccharide)

BabA

116
Q

H. pylori isn’t generally harmful - which toxin fits between cells in stomach lining, causing inflammation (gastritis)?

A

cagA

H. pylori strands can either be cagA+ or cagA-; cagA+ is more closely associated with gastric conditions

117
Q

H. pylori isn’t generally harmful - which toxin causes cells in the stomach lining to apoptose?

A

vacA

118
Q

why is the action of cagA and vacA damaging?

A

disrupts continuity of stomach lining

lining now exposed to action of HCl

can lead to ulcers

119
Q

mr mueller’s H. pylori diagnosis came from a stool antigen test - what are its advantages?

A

non invasive, simple, safe

high sensitivity and specificity

can be used for diagnosis and theoretically as a test of cure

120
Q

mr mueller’s H. pylori diagnosis came from a stool antigen test - what are its disadvantages?

A

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
Q

H. pylori can be detected by a carbon-13 urea breath test - what are its advantages?

A

non invasive, simple, safe

high sensitivity and specificity

can be used for diagnosis and as a test of cure

122
Q

H. pylori can be detected by a carbon-13 urea breath test - what are its disadvantages?

A

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
Q

H. pylori can be detected by a serum serology test - what are its advantages?

A

cheap, widely available

may be useful for diagnosing newly infected patients

124
Q

H. pylori can be detected by a serum serology test - what are its disadvantages?

A

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
Q

H. pylori can be detected by a CLO test - what are its advantages?

A

high sensitivity and specificity

instantaneous result

126
Q

H. pylori can be detected by a CLO test - what are its disadvantages?

A

if patient is on antibiotics or PPIs the results might be falsely negative

invasive

127
Q

how does a carbon-13 urea breath test for H. pylori work?

A

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
Q

how does a stool antigen test for H. pylori work?

A

looks for antigens associated with H. pylori in stool

129
Q

how does a serum serology test for H. pylori work?

A

enzyme linked immunosorbent assay to detect serum H. pylori–specific IgG and IgA antibodies using either a monoclonal or polyclonal enzyme immunoassay

130
Q

how does a CLO test for H. pylori work?

A

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
Q

why may a stool antigen test have been the best one for mr mueller?

A

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
Q

how does the human body make HCl for use in the stomach?

A

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
Q

how is the amount of HCl in the stomach reduced if needed?

A

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
Q

why are PPIs used against H. pylori?

A

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
Q

how many receptors are blocked by the use of PPIs?

A

80% - sometimes H₂ antagonists are also needed

136
Q

what are some examples of PPIs?

A

omeprazole

lansoprazole

137
Q

what are some examples of H₂ antagonists?

A

ranitidine

cimetidine

138
Q

what are some examples of antacids?

A

magnesium carbonate

aluminium hydroxide

139
Q

what treatment was used for mr mueller?

A

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
Q

why was a carbon-13 urea breath test used after mr mueller’s treatment with omeprazole, amoxicillin and clarithromycin to judge its effectiveness?

A

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
Q

why might false negatives for H. pylori be produced by stool antigen, carbon-13 urea and CLO tests after a course of antibiotics?

A

H. pylori are still present but their activity is lessened

142
Q

what does NICE recommend to prevent false negatives in carbon-13 urea tests after a course of antibiotics?

A

no PPIs for 2 weeks before test

no antibiotics for 4 weeks before test

143
Q

why is mr mueller’s dyspepsia classed as treatment resistant?

A

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
Q

what is the next step for treatment after mr mueller’s dyspepsia has been classed as treatment resistant?

A

in case of over 55 years and treatment resistant dyspepsia NICE recommends referral for non-urgent upper GI endoscopy

145
Q

what does mr mueller’s OGD report say after his upper GI endoscopy?

A

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
Q

what is a sliding hiatus hernias?

A

when part of the abdominal viscera herniate through an opening in the diaphragm

147
Q

what are the risk factors for a sliding hiatus hernia?

A

male

obesity

pregnancy

genetic predisposition

148
Q

why do sliding hiatus hernias occur?

A

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
Q

what is the effect of a sliding hiatus hernia?

A

function of lower oesophageal sphincter is lost - stomach contents allowed to reflux back into oesophagus

therefore a common cause of GORD

150
Q

what are the two types of hiatus hernia?

A

sliding and rolling

151
Q

what is the most common type of sliding hiatus hernia?

A

sliding (85-95%)

152
Q

what happens to the GOJ in a sliding hiatus hernia?

A

moves upwards

153
Q

how common is a rolling hiatus hernia?

A

5-15%

154
Q

what happens to the GOJ in a rolling hiatus hernia?

A

remains in place

155
Q

what does a sliding hiatus hernia predominantly cause symptoms of?

A

GORD

156
Q

what happens in a rolling hiatus hernia?

A

portion of stomach, bowel, pancreas or spleen herniates into chest next to GOJ

157
Q

what are the constituents of refluxed material?

A

stomach acid

at times, ingested food

rarely, if bile has entered from duodenum it might also be refluxed

158
Q

what is the pH of refluxed material?

A

ingested food may buffer the acid to make it less acidic and lower the pH

159
Q

what are some reasons for continuation of symptoms despite use of a PPI?

A

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
Q

how would non acid reflux be treated?

A

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
Q

GORD may lead to oesophagitis, which has a 10% chance of developing into Barrett’s oesophagus - why might this be dangerous?

A

risk of developing oesophageal cancer

1-5% of those with Barrett’s oesophagus develop it

162
Q

how does the tissue in the oesophagus change in Barrett’s oesophagus?

A

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
Q

how can an area of high grade dysplasia in the oesophagus also be descibed?

A

carcinoma in situ

intra epithelial neoplasia

stage 0 cancer

164
Q

how is carcinoma in situ defined?

A

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
Q

where can carcinoma in situ occur?

A

breast ducts

oesophagus

bladder

cervix

skin

166
Q

what are the treatment options for Barrett’s oesophagus?

A

endoscopic ablation

oesophagectomy

167
Q

when is it likely that someone with GORD will develop Barrett’s oesophagus?

A

family history of GORD, Barrett’s or oesophageal cancer

medical history of gastroenteric issues

168
Q

what lifestyle changes should mr mueller make to ease his symptoms and to reduce further risk later?

A

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

169
Q

why is losing weight an important lifestyle change to make when treating GORD?

A

more weight on abdomen means more intra abdominal pressure, increasing risk of reflux (use BMI)

170
Q

why is managing stress an important lifestyle change to make when treating GORD?

A

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)
171
Q

why is not smoking an important lifestyle change to make when treating GORD?

A

nicotine may relax lower oesophageal sphincter

172
Q

why is reducing alcohol intake an important lifestyle change to make when treating GORD?

A

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
173
Q

why is eating smaller, less frequent meals an important lifestyle change to make when treating GORD?

A

less acid production

less increase in intra abdominal pressure

174
Q

what foods are likely to trigger GORD symptoms?

A

spicy food

coffee

acidic fruits (e.g citrus)

175
Q

why may not eating 3-4 hours before bed be an important lifestyle change to make when treating GORD?

A

gives stomach time to digest and empty before lying down

176
Q

why are lifestyle changes important in treating GORD?

A

helps symptoms

reduces risk of further complications with oesophagus through exposure to refluxed contents

CSI (9 decks)

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