Oesophageal/gastric pathology

Question 1

Name some causes for dysphagia

Answer 1

Intramural:
-Food bolus/bezour

Intramural
-Pharyngeal pouch
-Plummer vinson syndrome
-Achalasia
-Schatzki ring
-Tumour

Extramural:
-Neurological: stroke/guillain-barre

Question 2

How will different causes of dysphagia present?

Answer 2

Achalasia: chest pain, regurgitation, progressive dysphagia to solids and liquids

Pharyngeal pouch: halitosis, regurgitation, aspiration and chest infection

Barrett’s: GORD

Cancer: weight loss, cachexia

Question 3

What are main features of achalasia?

Answer 3

Loss of myenteric plexus (between longitudinal/circular muscles)

Lower oesophagus does not dilate

Question 4

How would you investigate achalasia?

Answer 4

-Barium swallow
-OGD
-Manometry

Question 5

How could you manage achalasia?

Answer 5

-Botox
-Heller’s cardiomyotomy (results in reflux)

Question 6

What are the main features of oesophageal web (plummer vinson syndrome)

Answer 6

Triad: oesophageal web, dysphagia, iron deficiency anaemia

Other features: beefy red tongue, koilonychia, splenomegaly

Question 7

What factors are responsible for maintaining integrity of lower oesophageal sphincter?

Answer 7

1) lower gastro-mucosal folds
2) angle of his
3) intra-abdominal portion oesophagus (increased pressure)
4) R crus diaphragm

Question 8

Describe the metaplastic process in Barrett’s transformation in the oesophagus

Answer 8

Protective mechanism: body adapted to change of cell type in response to acid in oesophagus

Question 9

Risk factors for barrett’s

Answer 9

Smoking
hiatus hernia
eating large meals late at night

Question 10

What is the clinical definition of barrett’s oesophagus?

Answer 10

Metaplastic change: columnar metoplasia lower 1/3rd
Oesophagus: up to 1cm acceptable. >1cm abnormal

Question 11

What are the main histological subtypes of gastric cancer and why are they important?

Answer 11

Gastric
Intestinal metaplasia–> goblet cells (worse prognosis)

Question 12

What are theInvestigation/ management options for barrett’s metaplasia?

Answer 12

Lifestyle, PPI
24 hr ph monitoring (gold standard for GORD)
Manometry
OGD + biopsy –> 4 biopsies every 2cm from go junction

Question 13

What surveillance is required for barrett’s

Answer 13

Metaplasia <3cm from GO junction: OGD every 3-5 yrs
Metaplasia >3cm more frequent OGD (every 2 years)

Question 14

What are the management options for low grade dysplasia?

Answer 14

6 month –> annual OGD until -ve

Question 15

What are the management options for high grade dysplasia?

Answer 15

Submucosal resection/ablation

Question 16

Name premalignant conditions of oesophagus

Answer 16

pharyngeal pouch
plummer visnon
achalasia
Scleroderma
Gord (barrett’s)

Question 17

Risk factors for oesophageal ca

Answer 17

Advancing age
HPV (squamous cell)
Thoracic radiation
GORD

Question 18

What are the type of oesohpageal carcinomas?

Answer 18

Squamous most common wordlwide –> upper 2/3rd oesohpagus

Adenocarcinoma most common uk –> lower 1/3rd oesophagus

Question 19

What are the management principles of treating patients with oesophageal carcinomas?

Answer 19

Optimise–> nutrition
Neoadjuvant radiotherapy (if squamous)

Surgery
-Lower 1/3rd: Ivor lewis (laparotomy, R side thoracotomy, resect lower part, anastamosis in mediastinum
-Middle 1/3rd: mckewan oesohpagectomy (laparotomy, right thoracotomy, anastamosis in the neck)
-Upper 1/3rd Radiotherapy

Question 20

What are the key complications following oesophageal surgery?

Answer 20

-Thoracic duct injury (lymph in drain)–> low fat diet
-Lungs: pneumonia, pneumothorax
-Mediastinitis
-Phrenic nerve injury
-Dietary deficiency (PEG, TPN)
-Subclavian injury, brachial plexus injury

Question 21

Which is the most common site for gastric cancers

Answer 21

Pylorus (50%)
Lesser curvature (25%)

Question 22

What are the risk factors of gastric cancer?

Answer 22

Genetic: FAP, HNPCC, Blood group A

Modifiable: Cigarette, alcohol, H pylori

Gastric conditions: Autoimmune gastritis, pernicious anaemia, peptic ulcer

Question 23

What are the main types of gastric cancers?

Answer 23

Adenocarcinoma
GIST
Lymphoma
Gastrinoma
Carcinoid
Linitis plastica

Question 24

What is triple thearpy for H pylori?

Answer 24

Clarithromicin, amox, PPI

Question 25

How are gastruc cancers managed?

Answer 25

-Neoadjuvant chemo -Gastrectomy: partial or total -Pylorus/antrum: partial In middle: total

Question 26

What are the main complications following gastric surgery for cancers?

Answer 26

Dumping syndrome B12 deficiency (parietal cells, intrinsic factor) Malabsorption

Question 27

What is H Pylori?

Answer 27

-Helicobactor pylori is a gram-negative, microaerophilic spiral bacterium -stomach

Question 28

How does h pylori become colonised in the stomach?

Answer 28

-Is able to detect ph -Uses flagella to swim away from acidic luminal contents -Adheres to more neutral epithelial lining To avoid being carried away in the lumen, H pylori is able to detect pH and uses its flagella to swim away from the acidic contents of the lumen and adheres to the more neutral epithelial lining of the stomach.

Question 29

How does H Pylori survive the acidic conditions in the stomach?

Answer 29

-Produces urease -Urea --> CO2 + ammonia -Ammonia + H + --> ammonium, neutralises gastric acid H. pylori produces the enzyme urease. This converts urea to carbon dioxide and ammonia. The ammonia then binds with H+ to form ammonium which neutralizes gastric acid.

Question 30

How does H Pylori cause gastritis and ulcers?

Answer 30

-Proteases and phospholipases -ammonia from breakdown of urea -Damage to gastric mucosa -Leads to further damage due to loss of protective mechanisms from gastric acid H. Pylori produces certain proteases and phospholipases and these, together with the toxic ammonia produced from the breakdown of urea, damage the gastric mucosa leading to inflammation. Ulcers result when the protective mucosal layer is so damaged by inflammation that it is unable to combat the acid production in the stomach, leading to further tissue destruction and ulceration

Question 31

What is the lifetime risk of developing peptic ulcer disease with h pylori?

Answer 31

10 - 20%

Question 32

How can patients with H. Pylori present?

Answer 32

-Epigastric pain -nausea -dyspepsia -bloating -haematemesis and melaena

Question 33

Is everyone infected by the bacterium symptomatic?

Answer 33

No, 80% of individuals are asymptomatic

Question 34

Are there any other complications associated with H Pylori infection?

Answer 34

Gastric neoplasias -gastric adenocarcinomas -gastric mucosa-associated lymphoid tissue lymphomas

Question 35

What is the lifetime risk of H. Pylori associated gastric neoplasia?

Answer 35

1-2%

Question 36

How is H pylori diagnosed?

Answer 36

Via the CLO campylobacter-like organism) test which is dependent on urease production by H Pylori . A gastric mucosal biopsy is taken during gastroscopy and is placed into a medium consisting of urea and an indicator such as phenol red. Urease produced by H Pylori converts urea to ammonia which increases the pH changing the colour from yellow to red, hence a positive test.

Question 37

What is the eradication therapy?

Answer 37

7-day twice-daily course of treatment consisting of a: Full-dose PPI + metronidazole 400 mg and clarithromycin 250 mg OR amoxicillin 1 g and clarithromycin 500 mg

Question 38

A patient presents with dyspepsia to their general practice. Under what circumstances would you refer for an endoscopy?

Answer 38

ALARM Symptoms Anaemia Loss of weight Anorexia Recent onset of progressive sympsoms Malaena or haematemesis Swallowing difficulty Urgent specialist referral for endoscopic investigation is indicated for patients of any age with dyspepsia when presenting with any of the following: -chronic gastrointestinal bleeding -progressive unintentional weight loss -progressive difficulty swallowing -persistent vomiting -iron deficiency anaemia -epigastric mass Routine endoscopic investigation of patients of any age, presenting with dyspepsia and without alarm signs, is not necessary. However, in patients aged 55 years and older with unexplained and persistent recent-onset dyspepsia alone, an urgent referral for endoscopy should be made.

Question 39

Name some important aetiological factors in peptic ulcer disease

Answer 39

Infection with Heliobacter pylori NSAIDs Steroids Stress Smoking and alcohol

Question 40

Is H. Pylori more strongly associated with gastric or duodenal ulcers?

Answer 40

More commonly duodenal ulcers (95%) compared with gastric ulcers (80%)

Question 41

Describe how food consumption relates to pain for gastric ulcers versus duodenal ulcers

Answer 41

Duodenal ulcers: pain typical before meals and relieved by eating Gastric ulcers: pain often related to meals

Question 42

What are the main complications of peptic ulcer disease?

Answer 42

Bleeding Perforation Gastric outflow obstruction secondary to scarring/inflammation Small risk of malignant transformation (but common risk factors for both mailganacy and PUD e.g. H. Pylori, smoking, alcohol etc.)

Question 43

Which vessel is most commonly implicated in a bleed from a duodenal ulcer?

Answer 43

The gastroduodenal artery as it runs posteriorly to the duodenum

Question 44

From where does the gastroduodenal artery arise and what are its main terminal branches?

Answer 44

The gastroduodenal artery arises from the common hepatic branch of the celiac trunk Its two main terminal branches are the right gastroepiploic artery and the superior pancreatoduodenal artery

Question 45

What non surgical treatments are available for peptic ulcer disease?

Answer 45

Modification of behaviour e.g. NSAID use, smoking & alcohol H. Pylori eradication therapy Proton pump inhibitors and H2 receptor antagonists Antacids and alginates

Question 46

What are Billroth I and Billroth II operations?

Answer 46

Billroth I: partial gastrectomy with simple re-anastomosis Billroth II: partial gastrectomy with the duodenal stump oversewn (leaving a blind loop) and anastomosis is to the proximal jejunum

Question 47

Vagotomies can also be used for peptic ulcer disease. What is the action of the vagus nerve on the stomach?

Answer 47

The vagus nerve releases acetylcholine which increases the release of acid, gastrin and histamine and decreases somatostatin release. It also increases gastric emptying.