CSI 8 Acid Reflux Flashcards
1
Q
Oesophagus begins at?
A
inferior border of cricoid cartilage (C6)
2
Q
Oesophagus ends at?
A
cardiac orifice of the stomach (T11)
3
Q
How does oesophagus enter the abdomen?
A
-through oesophageal hiatus in diaphragm (T10)
4
Q
Structure of oesophagus?
A
Adventitia → muscle layer → submucosa → mucosa
5
Q
Structure and function of upper oesophageal sphincter?
A
anatomical, striated, between pharynx and oesophagus, constricted to stop air getting in
6
Q
Structure and function of lower oesophageal sphincter?
A
physiological/functional, in GOJ, at rest prevents reflux
7
Q
4 phenomena forming lower oesophageal sphincter?
A
- oesophagus enters stomach at acute angle
- +ve intra-abdominal pressure so oesophageal wall compressed
- mucosal folds occlude lumen
- pinch cock effect of right crus of diaphragm
8
Q
4 areas where there are constrictions in oesophageal lumen?
A
Arch of aorta, Bronchus, Cricoid cartilage, Diaphragmatic hiatus
9
Q
What is dyspepsia?
A
recurrent epigastric pain, heartburn or symptoms of acid regurgitation, with or without bloating, nausea or vomiting
10
Q
How may patients describe dyspepsia?
A
heartburn, indigestion, chest pain, reflux, tummy ache, bloating
11
Q
What is reflux?
A
acidic stomach contents come back up oesophagus towards mouth - can cause feeling of heartburn
12
Q
What is heartburn?
A
burning sensation in chest due to acid in stomach - pain felt in chest behind breastbone, may move towards throat
13
Q
Other symptoms of heartburn and reflux?
A
unpleasant taste in mouth, swallowing problems
14
Q
Most common causes of dyspepsia?
A
functional dyspepsia, gastritis, GORD, peptic ulcer disease
15
Q
What is functional dyspepsia?
A
individual symptoms of dyspepsia but no causative abnormalities in investigations
16
Q
What is gastritis?
A
inflammation of gastric mucosa
17
Q
Potential causes of gastritis?
A
infection, medications like NSAIDs (affecting integrity of stomach’s mucous lining) or alcohol excess
18
Q
What can severe cases of gastritis lead to?
A
ulceration
19
Q
What is GORD?
A
gastro-oesophageal reflux disease → reflux of gastric contents
20
Q
GORD can cause?
A
oesophagitis (due to irritation)
21
Q
What are some additional symptoms of GORD alongside dyspepsia?
A
belching, water brush (excessive salivation in mouth), discomfort worse after eating and on lying down, burning pain behind sternum
22
Q
What does peptic ulcer disease refer to?
A
gastric ulceration or duodenal ulceration
23
Q
What is an ulcer?
A
sore on lining of stomach or duodenum
24
Q
What are some less likely causes of dyspepsia?
A
- coeliac disease
- inflammatory bowel disease
- pancreatitis
- medication side effects
- gallbladder disease
- gastroenteritis
25
What can coeliac disease and IBD be associated with?
systemic symptoms
26
What signs and symptoms of pancreatic insufficiency would you see in pancreatitis?
steatorrhoea or diabetes
27
What type of pain is associated with gallbladder disease?
colicky pain
28
What is colicky pain?
intermittent spasmodic pain when hollow tube contracts to try and relieve an obstruction
29
What additional symptoms alongside dyspepsia would you see in gastroeneteritis?
fever, vomiting, diarrhoea
30
What are some potential dangerous causes of dyspepsia?
upper GI malignancy, coronary heart disease (atypical pain often misdiagnosed)
31
What are red flags?
used for associated symptoms that indicate a more serious underlying pathology
32
What are some red flags for upper GI cancers?
dysphagia, weight loss, haematemesis
33
What are some other potential red flags for upper GI cancer?
treatment-resistant dyspepsia, low Hb levels or raised platelet count, nausea and vomiting (normally w/other symptoms)
34
Important investigations for dyspepsia?
Testing for H. Pylori, FBC, LFTs, alcohol history, medication history, weight, ECG
35
What does H. Pylori use to neutralise stomach acid?
urease
36
What does H. Pylori use for locomotion?
flagella
37
What does urease do?
converts urea + water into ammonia and CO2
38
How does H. Pylori adhere host cells?
LPS/BabA
39
What H. Pylori toxin disrupts tight junctions between cells in stomach lining, leading to gastritis?
cagA (can be +ve or -ve)
40
What H. Pylori toxin causes cells of stomach lining to undergo apoptosis and die?
vacA
41
What strain of H. Pylori is more often associated with gastric diseases?
CagA +ve
42
What 4 tests can be used to detect H. Pylori?
C-13 urea breath test, stool antigen test, serum serology test, CLO test
43
What test does NICE recommend to detect H. Pylori?
C-13 urea breath test
44
What does the C-13 urea breath test and CLO test look for?
urease protein
45
What does the stool antigen test detect?
antigens produced by H. Pylori e.g. catalase
46
What does the serum serology test detect for?
antibodies made as result of H. Pylori exposure
47
What cell secretes acid in the stomach?
parietal cell
48
How do parietal cells secrete HCl?
(1) CO2 diffuses in, combines w/H2O using carbonic anhydrase to form carbonic acid
(2) carbonic acid dissociates into bicarbonate and H+
(3) H+ goes through proton pump to apical side
(4) bicarbonate chloride antiporter - Cl- into cell
(5) Cl- through Cl- channel --> to apical side
(6) H+ + Cl- --> HCl
49
3 types of receptors on parietal cell?
H2 receptor
ACh receptor
Gastrin receptor
50
3 types of drugs that decrease acid secretion?
antacids, proton pumps inhibitors, H2 antagonists
51
Examples of antacids?
aluminium hydroxide
| magnesium carbonate
52
Examples of proton pump inhibitors?
omeprazole
| lansoprazole
53
Examples of H2 antagonists?
ranitidine
| cimetidine
54
Non drugs treatment of dyspepsia?
lifestyle measures, assess for stress, anxiety, depression, endoscopic investigation if meeting urgent criteria
55
What criteria is there for urgent endoscopic investigation with dyspepsia?
- patients w/dysphagia
- sig. acute GI bleeding
- age >55 w/unexplained weight loss, symptoms of upper abdominal pain, reflux or dyspepsia
56
Lifestyle changes to ease heartburn and acid reflux?
- eat smaller more frequent meals
- raise 1 end of bed
- try to lose weight if overweight
- try to find ways to relax
- don't eat/drink trigger foods
- don't eat 3-4 hrs before bed
- don't wear clothes tight around waist
- don't smoke
- don't drink too much alcohol
57
How can stress influence composition of GI bacteria?
altered levels of glucocorticoids (e.g. cortisol) leads to modulated immune response --> higher levels of pro-inflammatory cytokines alter gut microbiota --> changes in levels of neuroactive molecules released by gut bacteria --> directly or indirectly (via altered immune response) influence brain function + interaction with gut
58
What can long term use of PPIs cause?
hypergastrinaemia, pneumonia, c difficile, hypomagnesmia, vit B12 deficiency, acute interstitial nephritis, dementia, subacute cutaneous lupus erythrematous, drug interactions
59
What is the initial management of uninvestigated dyspepsia?
PPI for 4 weeks, test for H. Pylori and treatment if positive, patients @ high risk of H. pylori tested first or in parallel w/PPI course
60
What is the initial management of functional dyspepsia?
test for H. Pylori and treat if positive. In patients -ve for H. Pylori use PPI or H2 receptor antagonist for 4 weeks
61
What can antacids relieve symptoms in?
ulcer dyspepsia and non-erosive gastro-oesophageal reflux
62
Which antacids can promote ulcer healing?
liquid Mg-Al
63
What is the function of simeticone in antacids?
added to antacid as anti-foaming agent to relieve flatulence
64
What is the function of alginates taken with an antacid?
increase viscosity of stomach contents and protect oesophageal mucosa from acid reflux, some form a gel that floats on stomach contents
65
What might cause persistent dyspepsia symptoms despite treatment?
large hiatus hernia, insufficient acid suppression by current medication, functional dyspepsia diagnosis, uncommon scenario of non-acid reflux
66
What would management be in non-acid reflux?
identification of diagnosis with special test e.g. gastro-oesophageal pH monitoring, treatment w/alginates better
67
What is a hiatus hernia?
occur when part of abdominal viscera herniate through oesophageal opening in diaphragm
68
What are some risk factors for developing a hiatus hernia?
male gender, obesity, age, pregnancy, genetic predisposition
69
Why can a hiatus hernia occur?
widening of diaphragmatic hiatus
pulling up of stomach (e.g. oesophageal shortening)
pushing up of stomach (e.g. increased intra-abdominal pressure)
70
What are hiatus hernias a common cause of and why?
Common cause of GORD due to loss of function of lower oesophageal sphincter
71
What are the 2 types of hiatus hernia?
sliding and rolling
72
What is the most common type of hiatus hernia?
sliding (85 - 95% of cases)
| rolling (5 - 15% of cases)
73
What is a sliding hiatus hernia?
gastro-oesophageal junction moves upwards, predominantly causes symptoms of GORD
74
What is a rolling hiatus hernia?
GOJ stays in place, portion of stomach, bowel, pancreas or spleen herniated into chest next to GOJ
75
What is Barrett's oesophagus?
repeated exposure of stomach content causes change in cell type in oesophagus
76
Causes of Barrett's oesophagus?
main cause is GORD w/risk factors for reflux being:
- overweight
- smoking
- drinking excess alcohol
- eating spicy, acidic, fatty foods
- hiatus hernia
77
For people with reflux, who is more likely to develop Barrett's oesophagus?
people who smoke, men and people >50
78
How is Barrett's oesophagus diagnosed?
usually during endoscopy as Barrett's has no symptoms but GORD symptoms may be present
79
What would be seen on a biopsy of Barrett's oesophagus?
intestinal metaplasia and/or cardiac metaplasia
80
What change in cell type occurs in Barrett's oesophagus?
stratified squamous epithelium turns into columnar epithelium
81
What is intestinal metaplasia?
characterized by columnar epithelium and distinctive intestinal goblet cells
82
What is cardiac metaplasia?
sometimes considered precursor to intestinal metaplasia
83
What does Barrett's oesophagus look like macroscopically?
more red and velvety
84
Why can the cellular changes in Barrett's oesophagus become dangerous?
due to excessive growth factors etc. metaplastic ells are vulnerable to abnormalities
85
What can Barrett's oesophagus progress into?
high grade dysplasia
86
What can high grade dysplasia confined to cells above BM can be called?
stage 0 cancer, intraepithelial tumour, carcinoma in situ
87
What is carcinoma in situ?
abnormal cells staying where they first formed, may spread and become cancer
88
What can high grade dysplasia progress into?
invasive adenocarcinoma (cancer of glandular cells invading BM)
89
What is cancer?
term for diseases in which abnormal cells divide w/o control and can invade near tissues, can also spread to other parts of the body via blood or lymph (metastasis)
90
What is the management/treatment of Barrett's oesophagus?
- surveillance
- lifestyle changes
- medicines
- fundoplication
- removing the affected area
91
How can the affected area of Barrett's oesophagus be removed?
- endoscopic mucosal resection
- radiofrequency ablation
- oesophagectomy
