Peptic ulcer disease

Question 1

Causes of peptic ulcers?

Answer 1

H. pylori
NSAIDs
Blood Group O have increased HCl production
Acid hypersecreters
Zollinger-Ellison syndrome –> gastrinoma

Question 2

Clinical features of duodenal peptic ulcer?

Answer 2

Epigastric pain relieved by eating, for ~2 hours
Nocturnal pain
Anorexia, vomiting, weight loss –> delayed gastric emptying

Question 3

Natural history of peptic ulcer disease?

Answer 3

Relapsing and remitting pattern

Question 4

Special investigations for peptic ulcer disease?

Answer 4

Endoscopy with biopsy x 4 quadrants
Breath urease for H. pylori (not necessarily needed)
Serum gastrin when suspecting Z-E syndrome (>500pg/ml is highly suspicious)
Barium meal - done uncommonly nowadays

Question 5

What is the empiric medical therapy of PUD?

Answer 5

PPI for 2 weeks
Abx for 1 week to eradicate H. pylori: amoxicillin 1g BD + metronidazole 400mg BD/clarithromycin 500mg BD
Stop NSAID use if using

Question 6

What are the complications of PUD?

Answer 6

SHOP:

• Stenosis [3]
• Haemorrhage (haematemesis, melaena, coffee grounds) [1]
• Obstruction [4]
• Perforation [2]

Question 7

What is the pathophysiology of duodenal stenosis following PUD?

Answer 7

• Large penetrating ulcers with associated inflammation and oedema
• Healed ulcer with fibrosis

Question 8

Clinical presentation of gastric ulcers?

Answer 8

Pain related to eating –> patient often afraid to eat
Vomiting –> dehydration
Epigastric pain radiating to the back

Question 9

What hormone do G cells produce?

Answer 9

Gastrin

Question 10

What hormone do D cells produce?

Answer 10

Somatostatin

Question 11

What do parietal cells produc?

Answer 11

HCl

Intrinsic factor

Question 12

What do Chief cells produce?

Answer 12

Pepsiongen

Question 13

What are protective factors against PUD?

Answer 13

Mucus layer
HCO3
Prostaglandin E2: augments mucus and HCO3, as well as increasing mucosal blood flow

Question 14

Mechanism of NSAIDs causing PUD?

Answer 14

Non-selective COX inhibitors:

• COX-2 inhibition reduces inflammation, pain in rest of body –> this is fine
• COX-1 inhibition inhibits PGE2 production –> this is a problem (see other card)

Question 15

Do posterior duodenal ulcers bleed or perforate more, and why?

Answer 15

They bleed, because the gastroduodenal artery runs posterior to D1

Question 16

Do anterior duodenal ulcers bleed or perforate more? What investigation shows this?

Answer 16

They perforate

Free air under the diaphragm

Question 17

What is the endoscopic/surgical management of a bleeding peptic ulcer?

Answer 17

• Gold probe coagulation + adrenalin/H20 tamponade + high dose PPI
• 2nd bleed: repeat scope
• 3rd bleed: surgery + H. pylori eradication therapy

Question 18

What is the surgical management of a perforated peptic ulcer?

Answer 18

Laparotomy + omental patch repair + PPI + Abx

Question 19

Clinical signs of gastric outlet obstruction?

Answer 19

Projectile vomiting
Succussion splash
Hypokalaemic hypochloraemic metabolic alkalosis

Question 20

What is the incisura angularis on the lesser curvature of the stomach?

Answer 20

The area of transition from parietal to G/D cells in the stomach

Question 21

Johnson classification of gastric ulcers: Class I

Answer 21

On the lesser curvature, within 2cm of incisura on pyloric side
Most common

Question 22

Johnson classification of gastric ulcers: Class II

Answer 22

Class I + a duodenal ulcer

Associated with high HCl output

Question 23

Johnson classification of gastric ulcers: Class III

Answer 23

Within 3cm of pyloris (pre-pyloric), anywhere

Associated with high HCl output

Question 24

Johnson classification of gastric ulcers: Class IV

Answer 24

High on the lesser curvature
(the higher the ulcer on the lesser curve, the more extensive the chronic gastritis)
Due to relative parietal cell loss, tend to have less HCl production

Question 25

Johnson classification of gastric ulcers: Class V

Answer 25

NSAID-associated: can be found anywhere