The Oesophagus Flashcards

(63 cards)

1
Q

What is GORD?

A

Reflux of the stomach contents into the oesophagus through the lower oesophageal sphincter

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2
Q

Epithelial lining of the oesophagus

A

Non keratinised stratified squamous epithelial

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3
Q

Causes/triggers of GORD

A
  • greasy + spicy foods
  • coffee + tea
  • alcohol
  • NSAIDs
  • stress
  • smoking
  • obesity
  • hiatus hernia
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4
Q

Presentation of GORD

A
  • dyspepsia
  • heartburn
  • acid regurgitation - acid taste in mouth
  • epigastric pain
  • bloating
  • nocturnal cough
  • hoarse voice
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5
Q

Investigations of GORD

A
  • 24 hour pH monitoring (gold standard)
  • endoscopy
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6
Q

Management of GORD

A
  • lifestyle changes - avoid triggers
  • medication review e.g. stop NSAIDS
  • antacids e.g. gaviscon, pepto-bismol - short term
  • PPIs e.g. omeprazole + Lansoprazole
  • H2 receptor antagonists e.g. famotidine, ranitidine
  • laparoscopic fundoplication
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7
Q

Mechanism of action of PPIs

A
  • Irreversibly inhibtis H+/K+ ATPase in gastric parietal cells > reducing gastric acid secretion
  • role of parietal cells is to secrete hydrochloric acid + intrinsic factor
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8
Q

Mechanism of action of H2 receptor antagonists

A

Inhibition of H2 receptors on gastric parietal cells
Local histamine release contributes to proton pump activation

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9
Q

What surgery is used in GORD?
Outline it

A

Laparoscopic fundoplication
Fundus is tied around the lower oesophageal sphincter to narrow it

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10
Q

Immediately after fundoplication, a patient reports difficulty belching, increased saliva + abdominal pain. What is the likely cause for symptoms?

A

fundus of stomach is too tightly wrapped around the gastro-oesophageal junction

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11
Q

What type of microorganism of H pylori?

A

Gram negative aerobic bacteria

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12
Q

What virulence factors does H pylori have?

A
  • Flagella - to propel itself
  • Lives in gastric mucosa - avoids acidic environment
  • produces ammonium hydroxide > neutralises acid around the bacteria
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13
Q

How does H pylori cause gastric damage?

A

produces ammonium hydroxide + toxins which damage the gastric mucosa

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14
Q

Investigations for H pylori

A
  • stool antigen test
  • urea breath test
  • H pylori antibody test - bood
  • rapid urease test during endoscopy
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15
Q

Preparation for H pylori test

A

2 weeks without using PPI before test

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16
Q

Outline rapid urease test

A
  • done during endoscopy
  • taking a small biopsy of the stomach mucosa
  • added to liquid containing urea
  • H pylori produces urease enzymes that convert urea > ammonia (alkaline)
  • pH indicator used
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17
Q

Treatment of H pylori

A

Triple therapy - PPI + 2 abx for 7 days
omoeprazole + amoxicillin + clarithromycin

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18
Q

What is Barrett’s oesophagus?

A

When the lower oesophageal lining changes from squamous to columnar epithelium via metaplasia due to chronic acid reflux

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19
Q

Stepwise progression of Barrett’s oesophagus

A
  • no dysplasia
  • low grade dysplasia
  • high grade dysplasia
  • adenocarcinoma
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20
Q

What type of cancer can Barrett’s oesophagus turn into?

A

Adenocarcinoma

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21
Q

Epithelium of Barrett’s oesophagus

A

Simple columnar epithelium

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22
Q

Investigations of Barrett’s oesophagus

A
  • biopsy
  • endoscopy - red + velvety appearance
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23
Q

Outline frequency of endoscopic monitoring of Barrett’s oesophagus based on the stage

A
  • no dysplasia: every 2-5 years
  • low grade dysplasia: every 6 months
  • high grade dysplasia: every 3 months
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24
Q

Treatment of Barrett’s oesophagus

A
  • endoscopic monitoring for progression
  • PPIs
  • endoscopic ablation
  • endoscopic mucosal resection
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25
Use of ablation in Barrett’s oesophagus
Destroys abnormal columnar epithelial cells > replaced by normal squamous epithelial cells
26
What is Zollinger-Ellison syndrome?
Rare condition where duodenal or pancreatic tumour secretes excessive gastrin > increases stomach acid > dyspepsia, diarrhoea + peptic ulcers
27
What red flag symptoms require further investigation for suspected upper GI malignancy
- dysphagia - >55 with weight loss + upper abdominal pain, dyspepsia or reflux - persistent symptoms despite conservative management - new anaemia
28
Parts of the oesophagus
cervical thoracic abdominal
29
Where are the physiological constrictions of the oesophagus?
ABCD - **A**rch of aorta - **B**ronchus (left) - **C**ricoid cartilage - **D**iaphragmatic hiatus
30
arterial blood supply to the oesophagus
- **thoracic**: branches of thoracic aorta + inferior thyroid artery - **abdominal**: left gastric artery + left inferior phrenic artery
31
Venous drainage of the oesophagus
- **thoracic**: azygous vein + inferior thyroid vein - **abdominal**: mixed venous drainage: left gastric vein to portal circulation or azygous vein to systemic circulation > form a porto-systemic anastamosis
32
Types of oesophageal cancer
squamous cell carinoma adenocarinoma
33
outline squamous cell carcinoma of the oesophagus incl risk factors
- affects upper 2/3rds - risk factors: smoking, alcohol use, hot beverages
34
outline adenocarcinoma of oesophageal cancers incl risk factors
- affects lower 1/3rd due to dysplasia from Barrett's oesophagus - risk factors: obesity, GORD
35
Clinical presentation of oesophageal cancer
- progressive dysphagia (initally solids difficult > progresses to liquids too) - odynophagia - unexplained weight loss
36
Red flags of oesophageal cancer
- progressive dysphagia ALARM - **A**naemia - **L**oss of weight - **A**norexia - **R**ecent onset of progressive symptoms - **M**alaena
37
Investigations for oesophageal cancer
- upper GI endoscopy 2WW + biopsy - endoscopic USS - bloods - CT chest-abdo-pelvis + PET scan
38
Management of oesophageal cancers
- most present with advanced disease > palliative care > *oesophageal stents, radio/chemotherapy, nutritional support - thickened fluids + supplements* - SS: chemo-radiotherapy - adenocarcinoma: neoadjuvant chemo(radio)therapy followed by oesophageal resection - oesophagectomy
39
outline an oesophagectomy
removal of tumour, top of stomach + surrounding lymph nodes
40
types of oesophageal tears
**Mallory Weiss tears** - superficial mucosa **Boerhaave syndrome** - full thickness rupture
41
what is a mallory weiss tear
tear in the superficial oesophageal mucosa occurs after heavy vomiting
42
What is Boerhaave syndrome?
spontaneous full thickness rupture of oesophagus secondary to severe vomiting episodes
43
Causes of oesophageal tears
- iatrogenic *e.g. endoscopy* - after severe forceful vomiting
44
Most common location for oesophageal tear
left postero-lateral position just above diaphragm
45
Presentation of oesophageal tears
- retrosternal chest pain - respirotary distress - haematemesis - SC emphysema
46
invesitgations of oesophageal tears
- routine bloods incl G&S - CXR - **CT chest abdo pelvis with IV + oral contrast** (gold standard) - urgent endoscopy in theatre
47
Management of oesophageal tears
- fluid resuscitation - **thoracotomy** to control leak + eradication of mediastinal + pleural contamination - wash out - decompress oesophagus via trans-gastric drain or endoscopically placed NG tube - nutritional support TPN - nil by mouth for 1-2 weeks
48
What are oesophageal motility disorders?
group of conditions characterised by abnormailites in oesophageal peristalsis
49
Causes of oesophageal dysmotility
achalasaia diffuse oesophageal spasm
50
muscular composition of the oesophagus
- upper third - skeletal muscle - middle third - transition zone of both skeletal + smooth muscle - lower third - smooth muscle
51
Muscular composition of oesophageal sphincters
- upper oesophageal sphincter - skeletal muscle - lower oesophageal sphincter - smooth muscle
52
Outline the peristalic waves of the oesphagus
- controlled by oesophageal myenteric neurones - primary wave - controlled by swallowing - secondary wave - activated in response to distention
53
What is achalasia
- primary motility disorder of the oesophagus - characterised by failure of relaxation of lower oesophageal sphincter + absence of peristalsis along the oesophageal body
54
Histological feature of achalasia
progressive destruction of ganglion cells in myenteric plexus
55
clinical features of achalasia
- progressive dysphagia - regurgitation of food - noctural cough - aspiration - chest pain - dyspepsia - weight loss
56
Investigations of achalasia
- upper GI endoscopy OGD - **oesophageal manometry** (gold standard) - barium swallow
57
Features of achalasia in barium swallow
bird's beak appearance due to failure of relaxation lower oesophageal sphincter
58
Key features of oesophageal manometry of achalasia
- absence of oesophageal peristalsis - failure of relaxation of lower oesophageal sphincter - high resting lower oesophageal sphincter tone
59
Management of Achalasia
- sleeping with multiple pillows - eating slowly + chew food thoroughly - plenty of fluids with meals - CCBs to inhibit LOS contraction - botox injection into LOS via endoscopy - laparoscopic heller myotomy - per oral endoscopic myotomy - endoscopic balloon dilatation - oesophagectomy - end stage
60
what is diffuse oesophageal spasm
- disease characterised by multifocal high amplitude contractions of oesophagus - due to dysfunction of oesophageal inhibitory nerves
61
Clinical features of diffuse oesophageal spams
- severe dysphagia to both solids + liquids - central chest pain exacerbated by food
62
Investigations + findings of diffuse oesophageal spasm
**Manometry**: - repetitive, simultaneous + ineffective contractions of oesophagus
63
management of diffuse oesophageal spasm
- CCBs first line - pneumatic dilatation - Heller myotomy