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MedEd Lectures > Upper GI > Flashcards

Upper GI Flashcards

1
Q

What is dyspepsia

A

A combination of symptoms indicating an upper GI problem

Typically:

  1. epigastric pain
  2. early satiety and post-prandial fullness
  3. Belching
  4. bloating
  5. nausea
  6. discomfort in the lower abdomen
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2
Q

What is peptic ulcer disease

A

Break in the epithelial lining of the stomach or duodenum

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3
Q

What are the symptoms of peptic ulcer disease

A
  1. Recurrent epigastric pain related to eating (described as gnawing or burning)
  2. early satiety
  3. nausea and vomiting
  4. potential anorexia & weight loss
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4
Q

What are the signs for peptic ulcer disease

A
  1. epigastric tenderness

2. pointing sign (pts are able to point to where the pain is)

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5
Q

How is the pain of duodenal ulcers described

A

the abdominal pain may be severe and radiate through to the back as a result of penetration of the ulcer posteriorly into the pancreas

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6
Q

Difference between gastric and duodenal ulcers: Pain

A

Duodenal ulcers: 2-3 hours after eating

Gastric ulcers: immediately after eating

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7
Q

Difference between gastric and duodenal ulcers: Antacid relief

A

duodenal ulcers: yes

gastric ulcers: minimal

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8
Q

Difference between gastric and duodenal ulcers: eating

A

duodenal ulcers: overeating - weight gain

gastric ulcers: avoids eating - weight loss

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9
Q

A 45 year old woman presents with a 2 month history of upper abdominal pain, occurring 2 – 3 hours after meals. The GP orders some blood tests, with the relevant results shown below:

[reduced RBC, HCT, MCV]

Which of these is the most likely diagnosis?

GORD
Duodenal ulcer
Gastric ulcer
Biliary colic 
Cholecystitis
A

Duodenal ulcer

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10
Q

What are the 2 main risk factors in ulcer development

A
  1. NSAIDs

2. H. pylori

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11
Q

What are the risk factors for ulcer development

A
  1. NSAIDs
  2. H. pylori
  3. smoking
  4. Zollinger Ellison syndrome
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12
Q

Name 3 NSAIDs

A
  1. ibuprofen
  2. Naproxen
  3. Aspirin
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13
Q

What is the prevalence of Helicobacter Pylori

A

Prevalent in 50% of the population

10% of these may develop an ulcer

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14
Q

What are the investigations for H pylori

A
  1. Breath test

2. stool antigen test

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15
Q

What is the management for H Pylori

A

triple therapy:

  1. PPI
  2. Clarithromyocin
  3. amoxicillin or metronidazole
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16
Q

What is Zollinger-Ellison syndrome

A

Neuroendocrine tumour in pancreas
produces gastrin
which leads to increased gastric acid secretion
consequently 90% patients will develop gastric and duodenal ulcers

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17
Q

What is a gastrinoma

A

A neuroendocrine tumour in pancreas seen in Zollinger-Ellison Syndrome

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18
Q

What gene is a risk factor of a gastrinoma (seen in Zollinger Ellison syndrome)

A

MEN1

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19
Q

What are the investigations for Zollinger-Ellison syndrome

A
  1. Fasting serum gastrin
  2. serum calcium
  3. gastric acid secretory tests, stimulation tests, imaging
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20
Q

What is the treatment of Zollinger-Ellison Syndrome

A
  1. PPI

2. Surgical resection if needed

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21
Q

What are Cushing ulcers

A

Harvey Cushing (neurosurgeon) found patients suffering from head trauma developed peptic ulcers

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22
Q

How to Cushing ulcer’s come about

A

Raised ICP (due to brain trauma) stimulates the vagus nerve - leads to increased gastric secretion

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23
Q

What are curling ulcers

A

Ulcer following severe burns

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24
Q

How to Curling ulcers come about

A

These are ulcers following burns

The reduced plasma volume leads to ischaemia and necrosis of gastric mucosa

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25
Q

Peptic ulcer: if patient is under 55 with no red flag symptoms, what investigations are done

A
  1. Breath test/stool antigen

2. FBC, stool occult, serum gastrin

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26
Q

Peptic ulcer: if patient is above 55, red flag symptoms are present or treatment has failed, what are the investigations

A
  1. OGD endoscopy
  2. Histology + biopsy urease testing
  3. repeat endoscopy after 6-8 weeks
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27
Q

What are red flag symptoms

A
  1. weight loss
  2. bleeding
  3. anemia
  4. vomiting
  5. early satiety
  6. dysphagia
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28
Q

What is the management for a peptic ulcer (where H pylori is not responsible)

A

PPI (omeprazole) or H2 antagonist (ranitidine)

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29
Q

Peptic ulcers: what are the complications

A
  1. bleeding

2. perforation

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30
Q

Peptic ulcer: management for bleeding

A
  1. endoscopy +/- therapy e.g. adrenaline
  2. IV PPI
  3. +/- blood transfusion
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31
Q

Peptic ulcer: management for perforation

A
  1. Nil by mouth
  2. IV antibiotics
  3. surgery
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32
Q

what is the most common type of gastric cancer

A

adenocarcinoma

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33
Q

What are symptoms of gastric cancer

A
  1. Epigastric pain
  2. Nausea, vomiting +/- blood
  3. Weight loss - anorexia
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34
Q

What are the risk factors for gastric cancer

A
  1. Smoking
  2. H Pylori
  3. Chronic gastritis - and therefore peptic ulcer disease
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35
Q

What are the clinical signs of gastric cancers

A
  1. palpable epigastric mass
  2. Virchow’s node/Troisier’s sign
  3. Sister Mary Joseph node - metastatic nodule on umbilicus
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36
Q

What are the investigations for gastric cancer

A
  1. endoscopy

2. biopsy + histology

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37
Q

A 61 year old man presents to his GP with a 3 month history of upper abdominal pain following meals. On questioning, he describes this pain as burning and is able to point to the pain on his abdomen. He reports having noticed his clothes have been looser recently, and has a long standing history of headaches. Which of these is the most important investigation to arrange?

H. Pylori breath test
Full Blood Count
OGD Endoscopy 
Trial of Proton pump inhibitor (PPI)
Abdominal X-ray
A

OGD Endoscopy

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38
Q

What is Gastro-oesophageal Reflux Disease (GORD)

A

Reflux of stomach contents into the oesophagus

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39
Q

What are the symptoms of GORD

A
  1. Heartburn
  2. Regurgitation
  3. Dysphagia
  4. Coughing and/or wheezing
  5. Hoarseness, sore throat
  6. Non-cardiac pain
  7. enamel erosion
  8. enamel erosion or other dental manifestations
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40
Q

What are the risk factors for GORD

A
  1. Increased intra-abdominal pressure:
    - obesity
    - pregnancy
  2. Lower oesophageal sphincter hypotension
    - Drugs: anti-muscarinics, CCB, nitrates, smoking
    - Treatment of achalasia (back up of food due to failure of the lower oesophageal sphincter to open)
    - hiatus hernia
  3. Gastric hyper-secretion
    - Diet
    - Smoking
    - Zollinger Ellison’s syndrome
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41
Q

What is a hiatus hernia

A

portion of the stomach prolapses through the diaphragmatic oesophageal hiatus

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42
Q

What are the complications of a hiatus hernia

A

predisposing patient to reflux or worsening existing reflux

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43
Q

What are the risk factors for a hiatus hernia

A
  1. raised intra-abdominal pressure

2. defect in the wall

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44
Q

What are the symptoms of a hiatus hernia

A

Most are asymptomatic and are discovered incidentally

otherwise patient is likely to present with symptoms of GORD

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45
Q

What are the investigations for a hiatus hernia

A
  1. Barium swallow
  2. Chest X ray
  3. Endoscopy
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46
Q

What is management of a hiatus hernia

A
  1. conservative - risk factors modification
  2. pharmacological (PPI)
  3. Surgery - Nissen fundoplication
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47
Q

What are the investigations for GORD

A
  1. Clinical diagnosis
  2. trial of PPI
  3. OGD endoscopy
  4. biopsy (if endoscopy shows presence of oesophagitis or Barrett’s)
  5. consider other tests
48
Q

In GORD, what investigations do you do if endoscopy is unrevealing

A
  1. ambulatory pH monitoring
  2. oesophageal manometry
  3. Barium swallow
  4. oesophageal capsule endoscopy
49
Q

A 40 year old lady presents to her GP with heartburn and problems swallowing. She reports that the heartburn worsens at night, and is often accompanied by a ‘funny taste’ in her mouth and cough. She reports no change in weight or systemic symptoms. Which of these should be the next step?

UGI endoscopy
Barium Swallow
Manometry 
Serum gastrin levels
Trial of Proton pump inhibitor (PPI)
A

Trial of Proton pump inhibitor (PPI)

50
Q

What is the conservative management for GORD

A
  1. Diet: avoid precipitants and loose weight
  2. Sleep: head of bed elevation
  3. Stop smoking
51
Q

What is the pharmacological management for GORD

A
  1. PPI (omeprazole 20mg daily)

2. H2 antagonist (ranitidine )

52
Q

What is the surgical management for GORD

A
  1. Nissen fundoplication
53
Q

What is the complications of GORD

A

GORD leads to Barrett’s which leads to adenocarcinoma

54
Q

What is Barrett’s oesophagus

A

Metaplasia of the oesophagus due to chronic oesophagitis

55
Q

What are the histological changes in Barrett’s oesophagus

A

Metaplasia

Squamous epithelium changes to columnar epithelium

56
Q

What are the complications of Barrett’s oesophagus

A

11 x increased risk of oesophageal cancer

57
Q

What is the initial management for Barrett’s oesophagus

A

Regular surveillance: endoscopy and biopsy

58
Q

Barrett’s oesophagus: management for high grade dysplasia

A
  1. Radio-frequency ablation

2. PPI

59
Q

Barrett’s oesophagus: management for a nodule

A
  1. endoscopic mucosal resection

2. PPI

60
Q

What are the 2 types of oesophageal cancer

A
  1. Adenocarcinoma

2. Squamous cell

61
Q

What are the symptoms of oesophageal cancer

A
  1. Progressive dysphagia from solids to liquids
  2. Burning chest pain
  3. Red flag symptoms - particularly weight loss, anaemia
62
Q

oesophageal cancer: what is the location and risk factor for adenocarcinoma

A
  1. Lower third

2. Barrett’s

63
Q

oesophageal cancer: what is the location and risk factor squamous cell carcinoma

A
  1. middle third

2. smoking + alcohol

64
Q

What are the investigation s for oesophageal cancer

A
  1. OGD endoscopy and biopsy to diagnose/grade

2. CT to stage cancer

65
Q

A 59 year old man presents with severe retrosternal burning pain. Upper GI endoscopy shows ‘metaplastic changes within the epithelium’. Which of these is the most likely diagnosis?

Gastric ulcer 
Gastric carcinoma 
Oesophageal carcinoma
GORD
Barrett’s oesophagus
A

Barrett’s oesophagus

66
Q

What us dyspepsia

A

indigestion

67
Q

What are the differential diagnosis of dyspepsia

A
  1. PUD
  2. Gastric cancer
  3. GORD
  4. Oesophageal cancer
  5. biliary pancreatic pathology
68
Q

A patient comes in to the clinical with dyspepsia, what treatment algorithm do you use

A

<55 y/o, no red flag symptoms:

  1. Life style changes and drug review
  2. Trial of PPI/triple therapy

> 55 y/o and/or red flags

  1. UGI endoscopy
  2. Biopsy and histology
69
Q

What is dysphagia

A

difficulty swallowing

70
Q

What is high dysphagia

A

Associated with neuromuscular disase

[Think higher functions]

71
Q

What is low dysphagia

A

Dysphagia due to obstruction or achalasia

72
Q

Dysphagia: what is a functional abnormality

A

the muscles or the nerves supplying them are not functioning properly

73
Q

Dysphagia: what is a structural abnormality

A

something in the way

74
Q

What does intermittent dysphagia suggest

A

motility issue/neurological

75
Q

What does progressive dysphagia suggests:

A

structural blockage

76
Q

What does dysphagia with both solids and liquid suggest

A

functional abnormality (high dysphagia: Stroke, Parkinson’s; low dysphagia: achalasia)

77
Q

What does dysphagia which progresses to from solid to liquid suggest

A

structural abnormality (cancer)

78
Q

What are the symptoms of achalasia

A
  1. Dysphagia (solids and liquids)
  2. Regurgitation
  3. Dyspepsia
  4. weight loss
79
Q

What is the aetiology of achalasia

A
  1. absence of oesophageal peristalsis

2. failure of lower oesophageal sphincter (LOS) to relax

80
Q

Lower oesophageal sphincter is hypertensive in 50% of patients, what does this mean

A

Smooth muscle contracted too much

leading to failure of lower oesophageal sphincter to open and absence of oesophageal peristalsis

81
Q

New-onset dysphagia in patients over 55 is what until proven otherwise

A

oesophageal cancer

82
Q

How is dysphagia investigated

A
  1. barium swallow
  2. endoscopy
  3. Videofluroscopy
  4. Manometry
83
Q

Dysphagia: why is a barium swallow conducted

A

For:
high dysphagia: avoid perforation on endoscopy
Low dysphagia: suspect achalasia

84
Q

What is the first line investigation for low dysphagia (obstruction - cancer )

A

Endoscopy

85
Q

In achalasia, what is the sign on a barium swallow

A

Bird’s beak

86
Q

What is the pathophysiology of achalasia

A

Absence of ganglion cells in myenteric plexus
A-peristalsis
failure of LOS to relax

87
Q

What are the investigations for achalasia

A

Barium swallow + manometry

88
Q

A 28 year old lady presents with a 2-year history of mild dysphagia to both solids and liquids. She has no weight loss, but symptoms of heartburn and nocturnal cough. PPIs and bronchodilators haven’t helped. She is systemically well, and her examination is unremarkable. A “bird’s beak” appearance is noted on barium swallow. What is the most likely diagnosis?

Achalasia
Benign stricture
Plummer-Vinson syndrome
Oesophageal spasm
Stroke
A

Achalasia

89
Q

A 76-year old retiree visits her GP with difficulty swallowing solids. She says this has been getting progressively worse over 1 month. There is no coughing, choking or heartburn. She reports food getting “stuck” 2-3 seconds after swallowing. She attributes her weight loss to not eating properly, and also thinks this has caused loose, brown-black stools. She feels tired. Bloods show a microcytic anaemia. Select the likely diagnosis:

Stroke
Oesophageal cancer
Pharyngeal pouch
Plummer-Vinson syndrome
Benign stricture
A

Oesophageal cancer

Although appropriate age for a stroke, the dysphagia is to solids and progressive, suggesting a obstructive course, not functional one. This is supported by absence of cough or choking. Pharyngeal pouch or benign stricture would not be accompanied by weight loss, tiredness and IDA.
Although Plummer Vinson may explain IDA, it wont account for melaena, it also would not typically be getting progressively worse.
Given systemic symptoms and age, plus other red flag symptoms proceed on suspicion of oesophageal cancer.

90
Q

What is the best way to diagnose a pharyngeal punch

A

barium swallow

91
Q

What is plummer vinson syndrome

A

combination of oesophageal wells (resulting in dysphagia) and iron deficiency anaemia

92
Q

What are signs or severe iron deficiency anaemia

A
  1. Cheilosis (painful inflammation and cracking of the corners of the mouth)
  2. atrophic glossitis (soreness and redness of the tongue)
  3. Koilonychia (spoon-like nails)
93
Q

What are 2 obscure causes of dysphagia

A
  1. limited cutaneous scleroderma

2. oesophageal spasm

94
Q

What is a Mallory Weiss Tear

A

a tear in mucosal layer if the oesophagus

95
Q

What can cause a Mallory Weiss Tear

A

Can occur after any event raising intragastric pressure, particularly vomiting

Following episode of severe vomiting due to alcohol, bulimia

96
Q

How does a Mallory Weiss tear present

A

Blood streaked in vomit

remember: vomiting precedes bleeding

97
Q

How is a Mallory-Weiss Tear diagnosed

A

endoscopy

98
Q

What is the treatment for a Mallory-Weiss Tear

A

Resolves itself within 24-48 hrs

May need to be admitted if actively bleeding

99
Q

What is Boerhaave syndrome

A

Full tear in the oesophageal wall

100
Q

How do you diagnose Boerhaave syndrome

A

CXR/CT

will show pneumomediastinum

101
Q

What is management for Boerhaave syndrome

A

Surgical management

102
Q

What are the complications of Boerhaave syndrome

A

35% mortality

103
Q

What is the clinical sign of pneumomediastinum on ascultation

A

Hamman’s sign: crunching sound on auscultation

104
Q

What are oesophageal varices

A

extremely dilated sub-mucosal veins in lower third of oesophagus

105
Q

What causes oesophageal varices

A

consequence of portal hypertension due to cirrhosis

106
Q

What are the complications of oesophageal varices

A

Strong tendency to bleed - occurs in 10% of cirrhosis patients each year

107
Q

What are the symptoms of oesophageal varices

A
  1. extreme haematemesis
  2. maybe unconscious or in shock (dropped bp)
  3. malaena
108
Q

What are the investigations for oesophageal varices

A
  1. FBC (macrocytic anaemia, reduced platelets)
  2. LFTs (increased GGT and bilirubin and reduced albumin)
  3. U&Es (increased urea)
109
Q

What is the management for an oesophageal varices

A
  1. ABCDE approach
  2. Fluids, regular monitoring
  3. Reduce portal HTN: Terlipressin
  4. Endoscopy: Band ligation is first line
110
Q

What is the first line management of oesophageal varices

A

Endoscopy: band ligation

111
Q

What drug is given to reduce portal HTN (in oesophageal varices)

A

Terlipressin

112
Q

How does a ruptured peptic ulcer present

A

Coffee ground emesis

Malaena

113
Q

What are the risk factors for a ruptured peptic ulcer

A

Background of PUD

  • long term NSAID use
  • H pylori infection
114
Q

What are the investigations for a ruptured peptic ulcer

A

Observations: reduced blood pressure

FBC + LFTs are normal

115
Q

What is the management of a ruptured peptic ulcer

A
  1. endoscopy: IM adrenaline at site of ulcer
  2. PPI e.g. Omprazole
  3. Triple therapy (if H pylori)
116
Q

A 53-year old man staggers into A&E having vomited 6 times in 2 hours. He is intoxicated and jaundiced. His friend said his vomit was initially “normal”, but after the first couple of episodes had fresh blood in it. His blood pressure is 120/90 and HR 70 bpm. What is the most likely diagnosis?

Ruptured oesophageal varices
Mallory-Weiss tear
Ruptured peptic ulcer
Boerhaave syndrome
Oesophagitis
A

Mallory-Weiss tear

117
Q

A 47 year old man is brought into A&E having vomited blood. His wife reports he developed food poisoning 2 days ago. Suddenly this morning he experienced extreme chest pain and began to vomit blood. His HR is 110 and BP 85/60. On auscultation of his chest you hear a crackling sound and his CXR shows pneumomediastinum. What is the most likely diagnosis?

Ruptured oesophageal varices
Mallory-Weiss tear
Ruptured peptic ulcer
Boerhaave syndrome
Myocardial Infarction
A

Boerhaave syndrome

MedEd Lectures (15 decks)

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