gastric and duodenal ulcers

Question 1

effect of H. pylori (70-80% cause of peptic ulcers) on GI environment

Answer 1

increases gastric acid formation, causes gastric metaplasia, decreases defence factors

Question 2

what activates the proton pump which causes H+ secretion

Answer 2

increased Ca2+ and cAMP

Question 3

effect of histamine released from enterochromaffin-like cells

Answer 3

bind to H3 receptors and increase cAMP

Question 4

presentation of peptic ulcer

Answer 4

simple is most common: epigastic pain, burning sensation occuring after meals

Question 5

2 investigations needed to make H. pylori positive peptic ulcer diagnosis

Answer 5

carbon-urea breath test (detects H. pylori), stool antigen test (confirms H. pylori)

Question 6

structure of gastric antrum stomach

Answer 6

epithelial cells produce mucus layer to protect against acid

Question 7

effect of H. pylori on mucosal layer to cause peptic ulcer

Answer 7

dissolves in pockets, so epithelial cells more likely to get damaged and die following acid exposure, causing peptic ulcer formation

Question 8

besides epigastric pain, what is an emergency symptom due to severe peptic ulceration

Answer 8

severe blood loss

Question 9

treatment for underlying cause of H. pylori peptic ulcer

Answer 9

2 antibiotics (amoxicillin and clarithromycin/metronidazole)

Question 10

3rd treatment for H. pylori peptic ulcer

Answer 10

proton pump inhibitor to reduce acid production

Question 11

features of H. pylori and significance

Answer 11

generally commensal gram -ve (treatment) and motile (causes multiple peptic ulcers)

Question 12

how does H. pylori dissolve mucosal layer

Answer 12

increases gastric acid formation by increasing production of gastrin or preventing production of somatostatin

Question 13

what else does H. pylori do

Answer 13

causes gastric metaplasia (excessive acid exposure) and downregulates defence factors (epidermal growth factor, bicarbonate production)

Question 14

virulence of H. pylori

Answer 14

produces urease which catalyses urea into ammonium chloride and monocloramine, which damages epithelial cells

Question 15

feature of urease

Answer 15

antigenic so evokes immune response (can be detected in stool)

Question 16

what do other virulent strains of H. pylori produce

Answer 16

CagA (antigenic) or VacA (cytotoxic), causing more intesne tissue inflammation

Question 17

presentation and investigations of chronic peptic ulcer

Answer 17

same as acute (acute treatment has failed)

Question 18

how does H. pylori cause epithelial cell death besides dissolving mucosa to expose epithelia to acid

Answer 18

exotoxins and inflammation

Question 19

antibiotic treatment for chronic peptic ulcer

Answer 19

switch one of the 2 antibiotics, and consider using quinolone or tetracycline, with the addition of chelating agents such as bismuth and sucralfate (lower acidity to prevent bacterial access to mucosa and reducing inflammation around epithelium)

Question 20

other treatment for peptic ulcer

Answer 20

proton pump inhibitor e.g. omeprazole

Question 21

how do proton pumps expressed on secretory vesicles within parietal cells work

Answer 21

H+-K+-ATPase pump H+ out and K+ in

Question 22

mechanism by which proton pumps secrete H+

Answer 22

stimuli -> increase [Ca2+]i -> increase cAMP (linked to Gs protein) -> translocation of secretory vesicles to parietal cell apical surface -> H+ secretion (for K+ influx)

Question 23

proton pump activity in ulcer formation

Answer 23

increase, increasing H+ secretion and reducing gastric pH

Question 24

investigation and diagnosis for negative carbon-urea breath test and negative stool antigen test (not H. pylori)

Answer 24

determine whether NSAID use, which is positive

Question 25

how to NSAIDs cause peptic ulcers

Answer 25

directly cytotoxic (irreversible inhibition of COX enzymes which produce protective effect by reducing proton pump expression), reduce mucus production, increase likelihood of bleeding, increase acidity

Question 26

treatment for NSAID-causing peptic ulcer

Answer 26

remove NSAID (not always possible), use proton pump inhibitor or histamine H2 antagonist e.g. ranitidine

Question 27

effect of H2 receptor, and antagonist

Answer 27

increase acid secretion, so antagonist reduces acid secretion

Question 28

what causes increased expression of proton pumps: ACh

Answer 28

ACh released from neurones (vagus/enteric) on M3 muscarinic receptors, increases [Ca2+]

Question 29

what causes decreased expression of proton pumps: prostaglandins

Answer 29

prostaglandins released from local cells act on EP3 receptors, decreasing cAMP

Question 30

what causes increased expression of proton pumps: histamine

Answer 30

histamine released from enterochromaffin-like cells act on H2 receptors, increasing cAMP

Question 31

what causes increased expression of proton pumps: gastrin

Answer 31

gastrin released from G-cells and acts on cholecystokinin B receptors, increase [Ca2+]

Question 32

effect of increases in [Ca2+] and cAMP on gastric acid secretion

Answer 32

translocation of secretory vesicles containing proton pumps to parietal cell apical surface, increasing H+ secretion

Question 33

effect of somatostain on gastric acid secretion

Answer 33

peptide that inhibits G-cells, enterochromaffin-like cells and parietal cells, reducing acid secretion