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NME > Upper GI Tract Disorders > Flashcards

Upper GI Tract Disorders Flashcards

1
Q

Gastric acid is produced by parietal cells under:

A
  • autonomic and hormonal influences
  • direct and indirect
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2
Q

Effect of acid suppression medication (omneprazole):

(side effects too)

A
  • proton pump inhibitor
  • direct inhibition of the proton pump
  • reduction in acid secretion
  • side effects rare:
    - diarrhoea
    - increased risk of GI infection
  • H2 receptor antagonist: reduces histamine
    stimulation
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3
Q

Gastro-oesophageal reflux disease (GORD)

A
  • reflux of gastric contents into the oesophagus
  • very common
  • caused by:
    - failure of gatekeeper:
    - lower oesophageal sphincter not closing fully
    (or frequent non-physiological temporary
    relaxations)
    - diaphragmatic sphincter
  • increased intr-abdominal pressure
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4
Q

Risk factors for GORD

A
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5
Q

GORD symptoms:

A
  • many are asymptomatic
  • dyspepsia “acid reflux”“heartburn”
  • burning discomfort in chest/trhoat
  • reflux of acid into mouth
  • upper abdo/chest pain
  • globus sensation
  • respiratory symptoms
  • persistent nausea
  • poor dentition
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6
Q

Diagnosis of GORD:

A
  • mostly clinical
  • endoscopy
  • oesophageal manometry and pH studies
  • faeces or breath testing for H.pylori
  • Xray contrast swallow/meal
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7
Q

Management of GORD:

A
  • lifestyle advice
  • acid suppresion therapy:
    • mainly PPI
    • H2 receptor antagonist
    • reduces acid but do not reduce reflux
  • heliobacter pylori eradication if relevant
  • surgery reserved for medical failure or where long
    term medical treatment is undesirable
  • proof of reflux usually required pH studies
  • restore normal anatomy

Fundoplication = wrap fundus around oesophagus to
stop reflux

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8
Q

hernia

A

protrusion of all or a part of a viscus through its coverings and into an abnormal position

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9
Q

hiatus hernia

A

protrusion of the stomach through the diaphragm and into the chest

can be sliding or rolling

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10
Q

sliding hiatus hernia

A
  • 85-95%
  • Gastrooesophageal junction is mobile:
    - part or all of stomach enters the chest
    - loss of diaphragmatic sphincter effect
    - negative thoracic pressure pulls gastric contents
    into the oesophagus
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11
Q

presentation of a sliding hiatus hernia:

A
  • mostly symptomatic
  • GORD symptoms
  • dysphagia
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12
Q

what type of hernia is depicted below?

A

sliding hiatus hernia

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13
Q

Rolling Hiatal hernia (paraoesophageal)

A
  • 5-15%
  • gastrooesophageal junction fixed in normal position
    below diaphragm:
    - gastric fundus is lead part of hernia
    - diaphragmatic and lower oesophageal sphincter
    working
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14
Q

Presentation of rolling hiatal hernia (paraoesophageal):

A
  • often asymptomatic
  • chronic, non-specific, difficult to diagnose
  • abdo pain, early satiety, anaemia, dysphagia
  • strangulation (1% risk)
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15
Q

Management of hiatus hernia:

A
  • conservative
  • medical
  • surgical:
    • reduce the hernia
    • close the defect
    • often combined with fundoplication hence
      increases the bulk of gastrooesophageal junction
      so improves the reflux symptoms
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16
Q

Barrett’s oesophagus:

A
  • metaplastic replacement of normal oesophageal
    squamous epithelium with columnar epithelium
    (intestinal metaplasia)
  • 1-2%
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17
Q

Barrett’s oesophagus: causes:

A
  • chronic reflux
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18
Q

Barrett’s Oesophagus: Diagnosis:

A

columnar epithelium identified at lower oesophagus

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19
Q

Barrett’s oesophagus is a malignant condition.

True or False?

A

False
is a pre-malignant condition
metaplasia leads to dysplasia which is the adenocarcinoma sequence

20
Q

Risk Factors for Barrett’s Oesophagus:

A
  • male
  • age
  • history of reflux: but symptoms may improve as
    Barrett’s develops due to metaplastic columnar
    mucosa being more acid resistant
  • obesity
  • smoking
  • family history
21
Q

Natural History of Barrett’s:

A
  • metaplasia = replacement of one type of specialised
    cell with another
  • dysplasia = disordered cell development/precursor to
    cancer
  • Low grade dysplasia = some will progress to HGD and
    cancer, most will not progress
    or will revert to non-dysplastic
    mucosa
  • High grade dysplasia = upto half already have
    invasive cancer if HDG
    detected, risk of developing
    cancer
22
Q

Management of Barrett’s Oesophagus:

A
  • metaplasia without dysplasia is surveillance only
  • LGD is surveillance mostly
  • HGD:
    - complex MDT management
    - radiofrequency ablation
    - endoscopic removal +/- ablation
    - surgery
  • PPI therapy may reduce progression
23
Q

Gastritis is a ——- gastric mucosal injury

A

multifactorial

24
Q

Causes of Gastritis:

A
  • ingested irritants: NSAIDs, alcohol, caustics
  • Non heliobacter pylori infections eg EBV
  • inflammatory conditions can be multisystem eg
    Crohns
  • stress
  • smoking

main cause: heliobacter pylori infection

25
Q

Gastritis symptoms

A
  • gnawing or burning stomach pain
  • abdo bloating
  • loss of appetite
  • frequent belching
  • indigestion
  • vomiting
  • hiccups
  • nausea or recurrent upset stomach
26
Q

Chronic gastritis can lead to

A

ulceration or even cancer

27
Q

Management of Gastritis:

A
  • remove causal agent if possible
  • acid suppression therapy (PPI)
28
Q

NSAIDs

A
  • reversible inhibition of cyclo-oxygenase (COX)
    enzymes:
    - COX 1 produces GI tract protective prostaglandins
    - COX 2 produces prostaglandins which mediate
    pain and inflammation
  • Loss of protective prostaglandins:
    - reduced gastric mucous and bicarb production
    - reduced gastric mucosal blood flow: reduce
    protection of gastric mucosa and ability to repair
    after injury
  • always consider need for gastric protection (PPI) with long term NSAID use
29
Q

Peptic ulceration: causes:

A
  • H. pylori involvement is high
  • NSAIDs account for most other causes
  • decreasing incidence with advent of H2 receptor
    antagonists and PPIs
  • Rarer causes:
    • stress ulceration
    • malignancy
    • Zollinger-Ellison syndrom
    • medications
30
Q

Zollinger-Ellison Syndrome

A
  • rare neuroendocrine tumour of G cells
  • most often of the pancreas
  • 1:100,000 people
  • secretes uncontrolled and excessive gastrin
  • excessive activity of gastric parietal cells
  • multiple UGI ulcers
  • detected by imaging pancreas and measuring gastrin
    levels
31
Q

What is a peptic ulcer?

A

A perforation or hole in the lining of the small intestine, lower oesophagus or stomach.

32
Q

Types of peptic ulcers (2):

A
  • Gastric ulcers
  • duodenal ulcers
33
Q

Gastric Ulcers:

A
  • most commonly lesser curve of stomach
  • more likely to be associated with cancer
34
Q

Duodenal Ulcers:

A
  • usually 1st part (superior)
  • four times more common than gastric ulcers
35
Q

Chronic ulcer presentation:

A
  • upper abdo pain
  • gastric ulcer pain often increases 2-3 hours after a
    meal due to increased gastric acid
  • duodenal ulcer pain often reduces after eating
    (increased pancreatic juices results in increased bicarb
    in duodenum which neutralises acid)
  • iron deficiency anaemia
  • weight change due to association between pain and
    food
36
Q

Acute ulcer presentation:

A
  • acute UGI bleeding:
    • haematemesis “coffee-ground” (vomiting blood)
    • melaena: dark sticky faeces due to internal
      bleeding so contains partially digested blood
    • sometimes rectal bleeding
  • perforation of ulcer:
    • peritonitis
    • systemically unwell
37
Q

Diagnosis of ulcers:

A
  • history and examination
  • endoscopy
  • H.pylori testing: stool/rapid urease test with gastric
    biopsy CLO test
38
Q

Treatment of ulcers:

A
  • PPI +/- H.pylori eradication (antibiotics?)
  • remove causal agents if possible
39
Q

Acute UGI bleeding:

A
  • bleeding from oesophagus, stomach, duodenum
  • mortality 2-10%
  • Variceal bleeding (11%):
    - aim to stop bleeding and reduce portal pressure:
    - beta blockers, endoscopic intervention
  • Non-Variceal bleeding (89%):
    - aim to stop bleeding and treat cause:
    - medication (PPI)
    - radiological or endoscopic intervention
40
Q

Duodenal ulcer and UGI bleeding:

A
  • gastroduodenal artery passes behind the 1st part of
    the duodenum
  • posterior ulcer can erode into the gastro-duodenal
    artery causing bleeding
  • if seen endoscopically can be treated, else radiological
    embolisation or surgery
41
Q

Management of perforated peptic ulcers:

A
  • occasionally can be managed without surgery:
    - omentum spontaneously seals hole
    - posterior duodenal ulcer?
  • otherwise surgery needed:
    - closure of ulcer is possible
    - omental patch
    - high dose PPI
42
Q

Heliobacter Pylori

A
  • gram negative
  • most common in childhood
  • cannot live in acidic conditions:
    - express urease
    - converts urea to ammonia plus CO2
    - raises surrounding pH
  • most colonised humans show no symptoms >70%
43
Q

Pathogenicity of CagA

A
  • cytotoxin-associated gene A (CagA) produced by some
    strains are associated with inflammation, increased
    risk of ulcers and cancers
  • vacuolating toxin A (VacA) causes cell damage
  • multiple other factors causing:
    - gastritis
    - peptic ulceration:
    - 70-85% gastric ulcers
    - 90-95% duodenal ulcers
  • gastric cancer:
    - adenocarcinoma
    - mucosa-associated lymphoid tissue lymphoma
    92-98%
44
Q

Testing for H. pylori:

A
  • uncomplicated but unresponsive dyspepsia
  • prior to NSAID use if pervious ulcers
  • unexplained iron deficiency anaemia if malignancy
    excluded

do not routinely tested:
- predominantly GORD symptoms
- within two weeks of PPI treatment
- following treatment, bar certain contexts

45
Q

What type of hernia is depicted below?

A

Rolling hiatal hernia

NME (52 decks)

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