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CSI > CSI 8 Acid Reflux > Flashcards

CSI 8 Acid Reflux Flashcards

1
Q

Oesophagus begins at?

A

inferior border of cricoid cartilage (C6)

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2
Q

Oesophagus ends at?

A

cardiac orifice of the stomach (T11)

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3
Q

How does oesophagus enter the abdomen?

A

-through oesophageal hiatus in diaphragm (T10)

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4
Q

Structure of oesophagus?

A

Adventitia → muscle layer → submucosa → mucosa

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5
Q

Structure and function of upper oesophageal sphincter?

A

anatomical, striated, between pharynx and oesophagus, constricted to stop air getting in

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6
Q

Structure and function of lower oesophageal sphincter?

A

physiological/functional, in GOJ, at rest prevents reflux

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7
Q

4 phenomena forming lower oesophageal sphincter?

A
  1. oesophagus enters stomach at acute angle
  2. +ve intra-abdominal pressure so oesophageal wall compressed
  3. mucosal folds occlude lumen
  4. pinch cock effect of right crus of diaphragm
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8
Q

4 areas where there are constrictions in oesophageal lumen?

A

Arch of aorta, Bronchus, Cricoid cartilage, Diaphragmatic hiatus

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9
Q

What is dyspepsia?

A

recurrent epigastric pain, heartburn or symptoms of acid regurgitation, with or without bloating, nausea or vomiting

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10
Q

How may patients describe dyspepsia?

A

heartburn, indigestion, chest pain, reflux, tummy ache, bloating

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11
Q

What is reflux?

A

acidic stomach contents come back up oesophagus towards mouth - can cause feeling of heartburn

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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

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13
Q

Other symptoms of heartburn and reflux?

A

unpleasant taste in mouth, swallowing problems

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14
Q

Most common causes of dyspepsia?

A

functional dyspepsia, gastritis, GORD, peptic ulcer disease

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15
Q

What is functional dyspepsia?

A

individual symptoms of dyspepsia but no causative abnormalities in investigations

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16
Q

What is gastritis?

A

inflammation of gastric mucosa

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17
Q

Potential causes of gastritis?

A

infection, medications like NSAIDs (affecting integrity of stomach’s mucous lining) or alcohol excess

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18
Q

What can severe cases of gastritis lead to?

A

ulceration

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19
Q

What is GORD?

A

gastro-oesophageal reflux disease → reflux of gastric contents

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20
Q

GORD can cause?

A

oesophagitis (due to irritation)

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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

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22
Q

What does peptic ulcer disease refer to?

A

gastric ulceration or duodenal ulceration

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23
Q

What is an ulcer?

A

sore on lining of stomach or duodenum

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24
Q

What are some less likely causes of dyspepsia?

A
  • coeliac disease
  • inflammatory bowel disease
  • pancreatitis
  • medication side effects
  • gallbladder disease
  • gastroenteritis
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25
Q

What can coeliac disease and IBD be associated with?

A

systemic symptoms

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26
Q

What signs and symptoms of pancreatic insufficiency would you see in pancreatitis?

A

steatorrhoea or diabetes

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27
Q

What type of pain is associated with gallbladder disease?

A

colicky pain

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28
Q

What is colicky pain?

A

intermittent spasmodic pain when hollow tube contracts to try and relieve an obstruction

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29
Q

What additional symptoms alongside dyspepsia would you see in gastroeneteritis?

A

fever, vomiting, diarrhoea

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30
Q

What are some potential dangerous causes of dyspepsia?

A

upper GI malignancy, coronary heart disease (atypical pain often misdiagnosed)

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31
Q

What are red flags?

A

used for associated symptoms that indicate a more serious underlying pathology

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32
Q

What are some red flags for upper GI cancers?

A

dysphagia, weight loss, haematemesis

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33
Q

What are some other potential red flags for upper GI cancer?

A

treatment-resistant dyspepsia, low Hb levels or raised platelet count, nausea and vomiting (normally w/other symptoms)

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34
Q

Important investigations for dyspepsia?

A

Testing for H. Pylori, FBC, LFTs, alcohol history, medication history, weight, ECG

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35
Q

What does H. Pylori use to neutralise stomach acid?

A

urease

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36
Q

What does H. Pylori use for locomotion?

A

flagella

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37
Q

What does urease do?

A

converts urea + water into ammonia and CO2

38
Q

How does H. Pylori adhere host cells?

A

LPS/BabA

39
Q

What H. Pylori toxin disrupts tight junctions between cells in stomach lining, leading to gastritis?

A

cagA (can be +ve or -ve)

40
Q

What H. Pylori toxin causes cells of stomach lining to undergo apoptosis and die?

A

vacA

41
Q

What strain of H. Pylori is more often associated with gastric diseases?

A

CagA +ve

42
Q

What 4 tests can be used to detect H. Pylori?

A

C-13 urea breath test, stool antigen test, serum serology test, CLO test

43
Q

What test does NICE recommend to detect H. Pylori?

A

C-13 urea breath test

44
Q

What does the C-13 urea breath test and CLO test look for?

A

urease protein

45
Q

What does the stool antigen test detect?

A

antigens produced by H. Pylori e.g. catalase

46
Q

What does the serum serology test detect for?

A

antibodies made as result of H. Pylori exposure

47
Q

What cell secretes acid in the stomach?

A

parietal cell

48
Q

How do parietal cells secrete HCl?

A

(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
Q

3 types of receptors on parietal cell?

A

H2 receptor
ACh receptor
Gastrin receptor

50
Q

3 types of drugs that decrease acid secretion?

A

antacids, proton pumps inhibitors, H2 antagonists

51
Q

Examples of antacids?

A

aluminium hydroxide

magnesium carbonate

52
Q

Examples of proton pump inhibitors?

A

omeprazole

lansoprazole

53
Q

Examples of H2 antagonists?

A

ranitidine

cimetidine

54
Q

Non drugs treatment of dyspepsia?

A

lifestyle measures, assess for stress, anxiety, depression, endoscopic investigation if meeting urgent criteria

55
Q

What criteria is there for urgent endoscopic investigation with dyspepsia?

A
  • patients w/dysphagia
  • sig. acute GI bleeding
  • age >55 w/unexplained weight loss, symptoms of upper abdominal pain, reflux or dyspepsia
56
Q

Lifestyle changes to ease heartburn and acid reflux?

A
  • 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
Q

How can stress influence composition of GI bacteria?

A

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
Q

What can long term use of PPIs cause?

A

hypergastrinaemia, pneumonia, c difficile, hypomagnesmia, vit B12 deficiency, acute interstitial nephritis, dementia, subacute cutaneous lupus erythrematous, drug interactions

59
Q

What is the initial management of uninvestigated dyspepsia?

A

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
Q

What is the initial management of functional dyspepsia?

A

test for H. Pylori and treat if positive. In patients -ve for H. Pylori use PPI or H2 receptor antagonist for 4 weeks

61
Q

What can antacids relieve symptoms in?

A

ulcer dyspepsia and non-erosive gastro-oesophageal reflux

62
Q

Which antacids can promote ulcer healing?

A

liquid Mg-Al

63
Q

What is the function of simeticone in antacids?

A

added to antacid as anti-foaming agent to relieve flatulence

64
Q

What is the function of alginates taken with an antacid?

A

increase viscosity of stomach contents and protect oesophageal mucosa from acid reflux, some form a gel that floats on stomach contents

65
Q

What might cause persistent dyspepsia symptoms despite treatment?

A

large hiatus hernia, insufficient acid suppression by current medication, functional dyspepsia diagnosis, uncommon scenario of non-acid reflux

66
Q

What would management be in non-acid reflux?

A

identification of diagnosis with special test e.g. gastro-oesophageal pH monitoring, treatment w/alginates better

67
Q

What is a hiatus hernia?

A

occur when part of abdominal viscera herniate through oesophageal opening in diaphragm

68
Q

What are some risk factors for developing a hiatus hernia?

A

male gender, obesity, age, pregnancy, genetic predisposition

69
Q

Why can a hiatus hernia occur?

A

widening of diaphragmatic hiatus
pulling up of stomach (e.g. oesophageal shortening)
pushing up of stomach (e.g. increased intra-abdominal pressure)

70
Q

What are hiatus hernias a common cause of and why?

A

Common cause of GORD due to loss of function of lower oesophageal sphincter

71
Q

What are the 2 types of hiatus hernia?

A

sliding and rolling

72
Q

What is the most common type of hiatus hernia?

A

sliding (85 - 95% of cases)

rolling (5 - 15% of cases)

73
Q

What is a sliding hiatus hernia?

A

gastro-oesophageal junction moves upwards, predominantly causes symptoms of GORD

74
Q

What is a rolling hiatus hernia?

A

GOJ stays in place, portion of stomach, bowel, pancreas or spleen herniated into chest next to GOJ

75
Q

What is Barrett’s oesophagus?

A

repeated exposure of stomach content causes change in cell type in oesophagus

76
Q

Causes of Barrett’s oesophagus?

A

main cause is GORD w/risk factors for reflux being:

  • overweight
  • smoking
  • drinking excess alcohol
  • eating spicy, acidic, fatty foods
  • hiatus hernia
77
Q

For people with reflux, who is more likely to develop Barrett’s oesophagus?

A

people who smoke, men and people >50

78
Q

How is Barrett’s oesophagus diagnosed?

A

usually during endoscopy as Barrett’s has no symptoms but GORD symptoms may be present

79
Q

What would be seen on a biopsy of Barrett’s oesophagus?

A

intestinal metaplasia and/or cardiac metaplasia

80
Q

What change in cell type occurs in Barrett’s oesophagus?

A

stratified squamous epithelium turns into columnar epithelium

81
Q

What is intestinal metaplasia?

A

characterized by columnar epithelium and distinctive intestinal goblet cells

82
Q

What is cardiac metaplasia?

A

sometimes considered precursor to intestinal metaplasia

83
Q

What does Barrett’s oesophagus look like macroscopically?

A

more red and velvety

84
Q

Why can the cellular changes in Barrett’s oesophagus become dangerous?

A

due to excessive growth factors etc. metaplastic ells are vulnerable to abnormalities

85
Q

What can Barrett’s oesophagus progress into?

A

high grade dysplasia

86
Q

What can high grade dysplasia confined to cells above BM can be called?

A

stage 0 cancer, intraepithelial tumour, carcinoma in situ

87
Q

What is carcinoma in situ?

A

abnormal cells staying where they first formed, may spread and become cancer

88
Q

What can high grade dysplasia progress into?

A

invasive adenocarcinoma (cancer of glandular cells invading BM)

89
Q

What is cancer?

A

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
Q

What is the management/treatment of Barrett’s oesophagus?

A
  • surveillance
  • lifestyle changes
  • medicines
  • fundoplication
  • removing the affected area
91
Q

How can the affected area of Barrett’s oesophagus be removed?

A
  • endoscopic mucosal resection
  • radiofrequency ablation
  • oesophagectomy

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