Upper GI Flashcards

1
Q

What is GORD

A

Gastro-oesophageal reflux disease (GORD) is where acid from the stomach refluxes through the lower oesophageal sphincter and irritates the lining of the oesophagus

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2
Q

What type of lining does the oesophagus have

A

squamous epithelium

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3
Q

What type of lining does the stomach have

A

columnar epithelium

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4
Q

What is the presentation of dyspepsia

A
Heartburn
Acid regurgitation
Retrosternal or epigastric pain
Bloating
Nocturnal cough
Hoarse voice
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5
Q

What can endoscopy be used to assess?

A

peptic ulcers
oesophageal or gastric malignancy
evidence of GI bleed

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6
Q

What are the key red flags for dyspepsia

A
Dysphagia (difficulty swallowing) at any age gets a two week wait referral
Aged over 55 (this is generally the cut off for urgent versus routine referrals)
Weight loss
Upper abdominal pain / reflux
Treatment resistant dyspepsia
Nausea and vomiting
Low haemoglobin
Raised platelet count
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7
Q

What lifestyle advice is given to patients with dyspepsia

A
Reduce tea, coffee and alcohol
Weight loss
Avoid smoking
Smaller, lighter meals
Avoid heavy meals before bed time
Stay upright after meals rather than lying flat
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8
Q

What are examples of acid neutralising medicines

A

Gaviscon

Rennie

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9
Q

What is the management of GORD

A
  • Lifestyle advice
  • Acid neutralising medications
  • PPIs
  • Ranitidine
  • Surgery: laparoscopic fundoplication
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10
Q

What is ranitidine

A

This is an alternative to PPIs
H2 receptor antagonist (antihistamine)
Reduces stomach acid

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11
Q

What is laparoscopic fundoplication

A

tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.

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12
Q

What is helicobacter pylori?

A
  • gram negative aerobic bacteria
  • Buries into gastric mucosa to avoid the exposing the epithelial tissue to the acid
  • Produces ammonia
  • Causes gastric ulcers and increases risk of stomach cancer
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13
Q

What does producing ammonia in the stomach mean

A

neutralises the acid

directly damages the epithelial cells of the stomach

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14
Q

How do we investigate for helicobacter pylori

A

Urea breath test using radio-labelled carbon 13
Stool antigen test
Rapid urease test

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15
Q

What is a rapid urease test

CLO test (Campylobacter-like organism test)

A
  • Performed during endoscopy
  • Small biopsy of stomach mucosa
  • add urea to sample, if H pylori present, urease enzymes will convert urea to ammonia
  • Ammonia makes pH more alkali
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16
Q

How do we eradicate H. pylori

A

triple therapy:

  • proton pump inhibitor (e.g. omeprazole)
  • 2 antibiotics (e.g. amoxicillin and clarithromycin) for 7 days.
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17
Q

What is Barretts Oesophagus?

A
  • Constant reflex of acid causes metaplasia of the squamous epithelium in the oesophagus to columnar
  • Considered pre-malignant
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18
Q

Why is Barretts Oesophagus considered pre-malignant

A

3-5% lifetime risk of developing into adenocarcinoma
From columnar epithelium to high grade dysplasia
Monitored with endoscopy

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19
Q

What is the treatment of Barretts Oesophagus

A
  • PPI
  • regular aspirin can reduce rate of cancer - not in guidelines yet
  • Ablation treatment
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20
Q

What is ablation treatment

A
  • Photodynamic therapy, laser therapy or cryotherapy destroys the epithelium so that it is replaced with normal cells during endoscopy
  • Only recommended if an element of dysplasia is present
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21
Q

What is a peptic ulcer

A

ulceration of the mucosa of the stomach (gastric ulcer) or the duodenum (duodenal ulcer). Duodenal ulcers are more common.

22
Q

What are the causes of a stomach ulcers

A

Breakdown of the protective layer of the stomach and duodenum
Increase in stomach acid
Medications (e.g. steroids or NSAIDs)
Helicobacter pylori

23
Q

What can increase acid production

A
Stress
Alcohol
Caffeine
Smoking
Spicy foods
24
Q

What is the presentation of peptic ulcers

A

Epigastric discomfort or pain
Nausea and vomiting
Dyspepsia
Bleeding causing haematemesis, “coffee ground” vomiting and melaena
Iron deficiency anaemia (due to constant bleeding)

25
Q

What type of ulcer causes more pain on eating

A

gastric ulcers

26
Q

What type of ulcer improves pain on eating

A

duodenal

27
Q

What investigations should be carried out for ? peptic ulcers

A
  • Endoscopy
  • rapid urease test (CLO test)
  • Biopsy to rule out malignancy
28
Q

What is the management of peptic ulcer disease

A
  • High dose PPIs
29
Q

What are the complications of peptic ulcers

A
  • Bleeding
  • Perforation
  • Scarring and stricture: can lead to pyloric stenosis
30
Q

What are the symptoms of pyloric stenosis

A
  • upper abdominal pain
  • distention
  • nausea and vomiting, particularly after eating.
31
Q

What is an upper GI bleed

A

Bleeding from the oesophagus, stomach or duodenum

32
Q

What are the key causes of Upper GI bleed

A

Oesophageal varices
Mallory-Weiss tear, which is a tear of the oesophageal mucous membrane
Ulcers of the stomach or duodenum
Cancers of the stomach or duodenum

33
Q

What is the presentation of an Upper GI bleed

A
  • Haematemesis (vomiting blood)
  • Malaena
  • Haemodynamic instability
  • Epigastric pain and dyspepsia in peptic ulcers
  • Jaundice for ascites in liver disease with oesophageal varices
34
Q

What is haematemesis

A

“Coffee ground” vomit. This is caused by vomiting digested blood that looks like coffee grounds.

35
Q

What is malaena

A

tar like, black, greasy and offensive stools caused by digested blood

36
Q

What is the Glasgow Blatchard Score?

A
  • scoring system in suspected upper GI bleed on their initial presentation
  • Establishes risk of Upper GI bleed
37
Q

Why does urea rise in upper GI bleed

A

blood in the GI tract gets broken down by the acid and digestive enzymes. One of the breakdown products is urea and this urea is then absorbed in the intestines.

38
Q

What is the management of an Upper GI bleed?

A

A - ABCDE
B – Bloods
A – Access (ideally 2 large bore cannula)
T – Transfuse
E – Endoscopy (arrange urgent endoscopy within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)
NB. it is NOT recommended to give PPI prior to endoscopy

39
Q

What is the Rockalls Score?

A

Used in patients that have had an endoscopy to calculate their risk of rebleeding and overall mortality

40
Q

What bloods must you send off in an acute Upper GI bleed

A
Haemoglobin (FBC)
Urea (U&Es)
Coagulation (INR, FBC for platelets)
Liver disease (LFTs)
Crossmatch 2 units of blood
41
Q

What is the difference between group and save and a cross-match?

A

“Group and save” is where the lab simply checks the patients blood group and keeps a sample of their blood saved incase they need to match blood to it. “Crossmatch” is where the lab actually finds blood, tests that it is compatible and keeps it ready in the fridge to be used if necessary.

42
Q

In a massive heamorrhage, what should be transfused

A

blood, platelets and clotting factors (fresh frozen plasma)

43
Q

When should platelets be given in an Upper GI bleed

A

Active bleeding and thrombocytopenia (platelets < 50)

44
Q

If a patient is on warfarin and is actively bleeding what should be given

A

Prothrombin complex concentrate

45
Q

What additional steps should be taken if oesophageal varices are suspected

A
  • Terlipressin
  • Prophylactic broad spectrum antibiotics
  • oesophagogastroduodenoscopy (OGD) to provide interventions that stop the bleeding
46
Q

Features of achlasia

A
  • Difficulty swallowing solids and fluids
  • retrosternal chest pain
  • regurgitation (usually bland)
  • gradual weight loss
47
Q

what do you see in barium swallowin achlasia

A

birds peak

48
Q

what is the management of a barium swallow

A
  • intra-sphincteric injection of botulinum toxin
  • Heller cardiomyotomy
  • pneumatic (balloon) dilation
  • Nifidipine bridges until definitive surgery/not fit for surgery
49
Q

Investigations for achlasia

A
  • manometry: excessive LOS tone which doesn’t relax on swallowing
  • barium swallow shows grossly expanded oesophagus, fluid level, ‘bird’s beak’ appearance
  • CXR: wide mediastinum, fluid level
50
Q

Which ulcer is relieved on eating

A

duodenal ulcer

51
Q

What is Zollinger-Ellison syndrome

A

rare cause of ulcers characterised by excessive levels of gastrin, usually from a gastrin secreting tumour