H. pylori and ulcers

Question 1

Percentage of world population with h.pylori infection

Answer 1

approx 50%
90% develop chronic inflam with persistent infection (gastritis)
15% will develop ulcers
Related to stomach carcinomas

Question 2

H. pylori

Answer 2

Gram negative bacteria
Spiral shape and flagella make it motile
Live in low pH of stomach
Transmission is fecal-oral and oral-oral

Question 3

How does it metabolise urea

Answer 3

Has urease enzyme which breaks down urea in stomach.
forms a buuble of ammonia, which is alkali, allowing it to live in acidic conditions.
likes the ANTRUM as lower pH

Question 4

Mechanism for h.pylroi infection

Answer 4

Can burrow thorugh mucosal layer in antrum, causing inflammation
Inhibits somatostatin release by damaging endocrine cells D cells
(somatostatin inhibits acid secretion by acting on G cells, ECL, parietal)
Therefore ACID SECRETION INCREASE

Question 5

Molecules on h.pylori

Answer 5

Has sugar bining adhesion molecules Saba and Baba genes (Leb and sialyl-lex, which these bind to, are present in mucus and epithelial cs)
Also has cagA and vacA genes

Question 6

cagA gene

Answer 6

Type IV secretion system
Disables epithelial tight junctions
Nod1 receptor recognises components of cell wall broken down and stimulates proinflam cytokine, causing gastric inflammation

Question 7

vacA gene

Answer 7

A cytotoxin

forms large vacuoles

Question 8

MUC5AC defence against H.pylori

Answer 8

Has glycoproteins Leb and sialyl-lex which h.pylori has sugar adhesins for. So h.pylori binds and gets stuck in this outer layer

Question 9

MUC6 defence against h.pylori

Answer 9

If it gets through, MUC6 has different set of sugars, a 1-4 GlcNAc) which interferes with cell wall synthesis of h.pylori

Question 10

MUC1 defence against h.pylori

Answer 10

If it gets past MUC6, then h.pylori will bind to the Leb and sialy-lex on MUC1
MUC1 will then be shed from the cell surface

Question 11

Diagnosis for H.pylori

non invasive tests

Answer 11

Noninvasive

• Serological tests for IgG antibodies
• 13C- urea breathing test
• stool antigen test

Question 12

Diagnosis for H.pylori

invasive

Answer 12

Require upper GI endoscopy and analysis of gastric biopsy

• biopsy urea test
• culture and histology

Question 13

Treating h.pylori infection

Answer 13

2 antibiotics (amoxicillin and clarithromycin)
1 acid secretion decreasor (HPPI or H2 antagonist)

IF the triple cocktail doesnt work (sucessful in 90%) then can give bismuth chelate which lines the stomach

Question 14

Causes of peptic ulcer disease

Answer 14

hyperacidity
h.pyloi infection
reflux of duodenal contents
NSAIDs
smoking (impairs mucus healing)
Genetics (blood O and 1degree relatives)
Males are 3 times more likely

Question 15

Types of PUD

Answer 15

Duodenal

Gastric (especially at junction of antrum and body)

Question 16

Duodenal ulcers

Answer 16

2-3 more common than gastric
15% of the population
90% of DU associated w h.pylori
Epigastric pain is relieved by food, exacerbated by hunger
Pain wakes them up at night
Vomiting infrequent but can relieve pain
Symptoms relapse and remit spontaneously

Question 17

Gastric ulcers

Answer 17

70% associated w h.pylori, the rest with NSAID use
Linked to Zollinger-Ellison syndrome
Epigastric pain associated with food intake

Question 18

Zollinger-Ellison syndrome

Answer 18

gastrin secreting pancreatic tumours that cause excess acid production, leading to acute ulcers

Question 19

Treatment of PUD

Answer 19

PPI for at least 2 months

Treatment for h.pylori if necessary

Question 20

Complications of PUD

Answer 20

• bleeding (most common)
• perforation, leading to peitonitis
• penetration into underlying tissue
• stricture, causig pyloric stenosis
• malignant change

Question 21

Perforation of ulcer

Answer 21

Contents of stomach enter peitoneal cavity

most common in DU

Question 22

Clinical signs of perforation

Answer 22

• Initial sudden, severe pain in upper abdomen that spreads (as gastric contents spead)
• shoulder tip pain due to diaphragm irritation
• shallow resp
• abdomen immobile (boardlike rigidity)
• bowel sounds absent
• after some hours sympotms may improve, but abdo rigidity remains.
• Later again deteriorates as peritonitis develops

Question 23

Treatment for perforation

Answer 23

Surgery to oversew

Question 24

What is dyspepsia

Answer 24

‘Indigestion’

upper abso symptoms like heartburn, acidity, pain, wind, fullness

Question 25

What are ‘alarm’ features

Answer 25

suggestive of cancer

• dysphagia
• weight loss
• protracted vomiting
• anorexia
• haematemesis/malaena

Question 26

Age differences for PUD treatment

Answer 26

If age under 55 with typical symps of PUD who are h.pylori positive can start eradication therapy immediately
If elderly then need confirmation of diagnosis and exclusion of cancer
If have ‘alarm’ signs then endoscopy

Question 27

Gastric Outlet Obstruction

Answer 27

Least common ulcer related problem
Pain worse with meals
Nausea
Vomiting of undigested food

Question 28

What is an ulcer

Answer 28

Eroded area of the mucosa

Caused by gastric juices and acid actions

Question 29

Gastric acid reflux

Answer 29

Causes dyspepsia (pain, inflammation and damage)
Backflow of stomach acid into the oesophagus

Question 30

Gastric oesophageal reflux disease (GORD)

Answer 30

Extreme cause of gasrtic acid reflux.
Can be associated with certain foods, medications and conditions
20% have heartburn

Question 31

Pathophys of GORD

Answer 31

• disturbances of normal anti reflux barrier

- weakness of LOS