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RW Gastroenterology > Oesphagus/Stomach/Duodenum > Flashcards

Oesphagus/Stomach/Duodenum Flashcards

1
Q

Which type of epithelium is the oesophagus?

A

Stratified squamous epithelium

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2
Q

What additional features are present in the oesophageal epithelium?

A
  • Have a stem cell layer which move slowly to the surface to replace a cells that are lost
  • Submucosal mucous glands lubricate passage into the stomach
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3
Q

What are the main causes of acute oesophagits?

A

Corrosive following chemical ingestion (e.g. when children drink things they shouldn’t such as bleach) or infection in immunocompromised patients e.g. candidiasis, HIV

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4
Q

What is reflux oesophagitis?

A

Inflammation of oesophagus due to refluxed low pH gastric content

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5
Q

What are some of the causes of reflux?

A
  • Defective sphincter mechanism/Hiatus hernia
  • Abnormal oesophageal motility
  • Physiological reflux with increased abdominal pressure e.g. pregnancy
  • Obesity (one of the most common)
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6
Q

What would you see microscopically with reflux oesophagitis?

A
  • Basal zone epithelial expansion (in attempt to regenerate surface cells being eroded)
  • Inflammatory cell infiltrates
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7
Q

What are some of the complications of reflux oesophagitis?

A
  • Ulceration (bleeding)
  • Stricture – fibroblasts respond to inflammation and lay down collagen causing a scar
  • Barrett’s Oesophagus
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8
Q

What is Barrett’s Oesophagus?

A

Replacement of stratified squamous epithelium of the oesophagus by columnar epithelium characteristic of the stomach

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9
Q

Why does Barrett’s Oesophagus occur?

A

Due to persistant reflux and changes as part of a protective mechanism as gastric epithelium is better equipped to deal with excessive acid than oesophageal epithelium

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10
Q

What would you consider in oesophagi’s patients who weren’t getting better with reflux medication?

A

Allergic (‘eosinophilic’) oesophagitis

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11
Q

What is the characteristic macroscopic appearance of allergic oesophagitis?

A

Corrugated (feline-like) or ‘spotty’ oesophagus

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12
Q

What is the treatment for allergic oesophagitis?

A

Steroids/chromoglycate/montelukast

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13
Q

What is the most common benign oesophageal tumour?

A

Squamous papilloma (often HPV related)

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14
Q

What is the most common malignant oesophageal tumour?

A

Adenocarcinoma (Squamous cell carcinoma is the other main one)

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15
Q

What are some of the main risk factors for oesophageal squamous cell carcinoma?

A
  • Vitamin A/Zinc deficiency
  • Tannic acid/ Strong tea
  • Smoking, Alcohol
  • HPV
  • Oesophagitis
  • Genetic
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16
Q

What is the pathogenesis pathway for oesophageal adenocarcinoma?

A

1) Genetic factors, reflux disease etc
2) Chronic reflux oesophagitis
3) Barrett’s oesophagus
4) Low grade dysplasia
5) High grade dysplasia
6) Adenocarcinoma

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17
Q

What is the main symptom of oesophageal carcinoma?

A

Dysphagia (additionally, odynophagia - pain on swallowing)

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18
Q

In which areas of the oesophagus is squamous cell cancer most common?

A

Upper 2/3rds

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19
Q

In which areas of the oesophagus is Barrett’s and adenocarcinoma most common?

A

Lower 1/3rd

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20
Q

What are GISTs?

A

Gastrointestinal Stromal Tumours - tumours of the muscle layer

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21
Q

What is the primary investigation for suspected oesophageal cancer?

A

Urgent Upper GI Endoscopy

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22
Q

What is an EUS?

A

Endoscopic Ultrasound Scan

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23
Q

What is the most common palliative treatment of oesophageal cancer?

A

Stenting (then radiotherapy)

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24
Q

True or False: Prognosis is good for oesophageal and gastric carcinoma

A

False, unfortunately it is dismal as few will survive more than year

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25
Q

What percentage of the population suffer from reflux monthly?

A

40%

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26
Q

How is oeosphagitis graded?

A
  • Grade 1 – tiny erosions less than 5mm
  • Grade 2 - >5mm
  • Grade 3 – less than 70% of the circumference involved
  • Grade 4 - >70% of the oesophagus is affected
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27
Q

What are some of the main symptoms of reflux?

A
  • Pain in the chest or throat
  • Acid regurgitation (into mouth etc)
  • Reflux bronchitis – when it comes up when they are lying down causing coughing and SOB
  • Oesophageal spams (may mimic cardiac symptoms)
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28
Q

What are the main treatments of reflux?

A
  • Proton Pump Inhibitors e.g. Omeprazole are best
  • H2 receptor antagonists e.g. cimetidine or ranitidine (But histamine isn’t the only thing stimulating gastric acid, so eventually the body adapts and simply promotes it through gastrin and ACh etc)
  • Anti-acids e.g. aluminium/magenesium hydroxide
  • Surgically tightening the LOS laprascopically
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29
Q

What occurs in achalasia?

A

Sphincter has increased tone and spasming so the food cant get into the stomach and oesophagus has poor or no motility (no peristalsis)

30
Q

What is the definitive test for achalasia?

A

Oesophageal manometry (Tube is passed through nose into oesopagus to measure pressures on swallowing)

31
Q

What are the surgical treatments for achalasia?

A
  • Pneumatic dilation (mechanical dilatation of the lower oesophageal sphincter using a balloon)
  • Laprascopic Cardiomyotomy (surgery to cut the LOS)
  • Botox injections to paralyse the LOS muscles by blocking nerves
32
Q

What are 3 main types of chronic gastritis?

A

1) Autoimmune (rarest)
2) Bacterial (H. pylori) - most common
3) Chemical (NSAIDs, alcohol, reflux etc)

33
Q

Which antibodies are involved in autoimmune gastritis?

A

Anti-parietal and anti-intrinsic factor antibodies

34
Q

What is meant by peptic ulceration?

A

A breach in the gastrointestinal mucosa as a result of acid and pepsin attack

35
Q

At which site of the stomach do gastric ulcers most often occur?

A

Junction between antrum and body and gastro-oesophageal junction

36
Q

What is the morphology of peptic ulcers?

A
  • 2-10 cm across
  • Edges are clear cut, punched out
  • Layered Appearance:
    • Floor of necrotic fibrinopurulent debris
    • Base of inflamed Granulation tissue
    • Deepest layer is fibrotic scar tissue
37
Q

What are the 3 main types of gastric tumours?

A

1) Adenocarcinomas (95%)
2) Lymphomas
3) GISTs

38
Q

What is the major risk factor for gastric cancers?

A

H. pylori infection (Pts with anti-H. pylori antibodies carry a greater risk)

39
Q

What is the pathogenesis pathway for gastric adenocarcinoma?

A

1) H. pylori infection
2) Chronic gastritis
3) Intestinal metaplasia/atrophy
4) Dysplasia
5) Adenocarcinoma

40
Q

What are the subtypes of gastric carcinoma?

A

1) Intestinal type (the end-result of an inflammatory process that progresses from chronic gastritis to atrophic gastritis and finally to intestinal metaplasia and dysplasia)
2) Diffuse type (characterized by the development of linitis plastica, is associated with an unfavourable prognosis)

41
Q

What are gastric lymphomas derived from?

A

Mucosa associated lymphoid tissue (hence also known as Maltomas)

42
Q

What causes a gastric lymphomas?

A

H. pylori infection can cause continuous inflammation which induces an evolution into a clonal B-cell proliferation (low grade lymphoma). If unchecked evolves into a high grade B-cell lymphoma.

43
Q

What is dyspepsia?

A

Dyspepsia is defined as having epigastric pain or discomfort, which can involve postprandial fullness and early satiety (aka indigestion)

44
Q

What does heartburn generally refer to?

A

GORD

45
Q

What is the difference between dyspepsia and GORD?

A

Dyspepsia is a symptom whereas GORD represents a collection of diseases caused by gastro-oesophageal reflux.

46
Q

Which criteria is used to define dyspepsia?

A

Rome III criteria (2006):

1) Epigastric pain or discomfort
2) Postprandial fullness ( Can eat all their meal but then don’t feel great)
3) Early satiety (Can’t eat whole meal)

47
Q

What are the 2 main types of causes for dyspepsia, and give examples of each

A
  • 1) Organic causes (25%)
    • Peptic ulcer disease
    • Drugs (NSAIDs, COX2 inhibitors etc)
    • Gastric cancer
  • 2) Functional casuses (75%)
48
Q

What are the overall 5 main causes of dyspepsia?

A

1) Functional dyspepsia
2) Medication - induced
3) GORD
4) Peptic ulcer disease
5) Malignancy

49
Q

What is functional dyspepsia?

A

Defined as dyspepsia symptoms of greater than 3 months duration, with onset at least 6 months prior to diagnosis and without any anatomical, systemic and metabolic abnormality.

There is a large overlap with irritable bowel syndrome (IBS).

50
Q

What is the difference between dyspepsia (indigestion) and heartburn (reflux)?

A

Heartburn/reflux is a retrosternal burning sensation, while dyspepsia/indigestion is an epigastric pain or burning

51
Q

What would be found on examination of uncomplicated dyspepsia?

A

Epigastric tenderness

52
Q

What may be found on examination of complicated dyspepsia?

A
  • Cachexia (weight loss)
  • Mass
  • Evidence gastric outflow obstruction (e.g. abdominal distension)
  • Peritonism
53
Q

What are the alarm symptoms of dyspepsia, that would trigger a referral for endoscopy?

A
  • Dysphagia
  • GI Blood loss
  • Vomiting
  • Weight loss
  • Upper abdominal mass
54
Q

What are the steps for management of dyspepsia?

A

(If no alarm symptoms)

  • 1) Lifestyle changes, stop causative medications and start anti-acids/H2 receptor agonists
  • 2) If not, ‘test & treat approach’: check h. pylori status and eradicate if positive
  • 3) If negative:
    • If <55 manage as function dyspepsia with PPIs and other meds
    • If >55 refer to specialist for endoscopy
55
Q

With functional dyspepsia there are no structural causes, so what are some of the suggested causes?

A
  • Visceral hypersensitivity ( people have different pain tolerance in gut)
  • Psychosocial factors – when people are in a bad place then any pain/symptoms are worse
  • Genetic factors
  • Altered brain-gut interactions
  • Disrupted gut-immune interactions
56
Q

Which factors in a history would indicate peptic ulcer disease as the cause of dyspepsia?

A
  • Pain predominant dyspepsia (radiating to back)
  • Often also nocturnal – keeping them up at night
  • Aggravated or relieved by eating
  • Relapsing & remitting chronic illness
  • Lower socio-economic groups
  • Family history common
57
Q

True or False: Gastric ulcers are relieved on eating

A

True, with gastric ulcers when you are fasting then the acid is non-diluted and will cause more pain

58
Q

True or False: Duodenal ulcers are relieved on eating

A

False, with duodenal ulcers then there is no acid or stimulation of the area until you start eating

59
Q

What are the 2 main causes of peptic ulcer disease?

A

1) H. pylori (95% of duodenal ulcers, 75% of gastric ulcers)
2) NSAIDs

60
Q

What kind of bacteria is H. Pylori?

A

Gram -ve microaerophilic flagellated bacillus

61
Q

What is the mode of transmission of H. pylori?

A

Oral-oral / faecal oral spread (most people get it in infancy)

62
Q

How can H. pylori cause ulcers?

A
  • It is within the mucous gel layer where it is protected, and secretes inflammatory agents, weakening the mucosal barrier - leaving the submucosa exposed to HCl and pepsin.
  • It also produces ammonia and proteases which breakdown the epithelium and cause ulcers.
  • It also decreases somatostatin realises, increasing acid secretion
63
Q

How is acid secretion normally controlled?

A

1) - Normally, G cells produce gastrin in response to a higher pH
2) Gastrin then stimulates parietal cells to produce acid
3) Presence of acid then inhibits G cells as a negative feedback

64
Q

How would you test for H. pylori infection?

A
  • 1) FAT (faecal antigen test)
  • 2) Carbon 13 (C-13) urea breath test (CUBT) (H. pylori causes the reaction urea > ammonia bicarbonate + CO2 using urease - breath test detects CO2)
  • 3) Serology (IgA antibodies)
  • Gastric biopsy
    • Urease test/CLO test - tests the pH produced by the urease released by H.Pylori - shows as raised pH
    • Histology – often need to actually stain for H. pylori
    • Culture/sensitivity
65
Q

What is the treatment of peptic ulcer disease?

A
  • ALL antisecretory therapy (PPI/H2 antagonists)
  • ALL tested for presence of H pylori
    • H pylori +ve - eradicate and confirm
    • H pylori -ve - antisecretory therapy
  • Withdraw NSAIDs
  • Lifestyle (difficult)
  • Surgery - infrequent
66
Q

What does H. Pylori eradication therapy entail?

A

Generally triple therapy for 1 week:

  • PPI + amoxycillin 1g bd + clarithromycin 500mg bd
  • PPI + metronidazole 400mg bd + clarithromycin 250mg bd
67
Q

What are the main complications of peptic ulcer disease?

A
  • Anaemia
  • Bleeding
  • Perforation
  • Gastric outlet/duodenal obstruction - fibrotic scar
68
Q

Achlorhydria or hypochlorhydria =

A

States where the production of hydrochloric acid in gastric secretions of the stomach and other digestive organs is absent or low, respectively

69
Q

True or False: Achlorhydria (reduced HCl in gastric secretions) increases risk of gastric cancer

A

True

70
Q

How can H. Pylori cause achlorhydria (decreased gastric acid secretion)?

A

H. Pylori infection stimulated IL-1 beta production which is powerful inhibitor of acid secretion

71
Q

Which host gene is associated with the achlorhydria/hypochlorhydric response to H. Pylori?

A

IL- 1B gene

RW Gastroenterology (13 decks)

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