Gastric Secretion, Mucosal Protection & Ulceration

Question 1

explain oxyntic glands

Answer 1

lines most of gastric body
contains surface mucous, mucous neck, parietal, chief, ECL, D and chief cells

Question 2

explain pyloric glands

Answer 2

found in pylorus/antrum
contains surface mucous, mucous neck, enterochromaffin (ANP), D and G cells

Question 3

what is the stimulus for acid secretion?

Answer 3

gastric pH rises due to buffering of acid by ingested food (protein)
acid secretion highest after eating
as meal clears stomach, buffering weakens and acid secretion reduces due to lower intragastric pH

Question 4

what is gastric acid secretion controlled by?

Answer 4

ACh (neuronal - parasympathetic)
histamine (ECL cell - paracrine)
gastrin (G cell - endocrine)
somatostatin (D cell - endocrine)

Question 5

when are each gastric acid secretion regulator active?

Answer 5

Acetylcholine - cephalic phase
Histamine/Gastrin - in response to high pH (gastric phase)
somatostatin - in response to low pH (intestinal phase)

Question 6

what are the components of gastric juice?

Answer 6

HCl
Pepsin
Mucin
Intrinsic Factor

Question 7

what is the receptor of somatostatin?

Answer 7

CCK2

Question 8

what is the receptor for ACh

Answer 8

M3

Question 9

what epithelium is found in the stomach and lower oesophagus?

Answer 9

oesophagus - stratified squamous
stomach - simple columnar

Question 10

what is the stomach’s defense against gastric acid

Answer 10

mucous
thick adherent layer, prostoglandin, rich in bicarbonate (neutralises)

Question 11

what would a COX-1/COX-2 deficiency result in for gastric protection?

Answer 11

production of prostoglandins, reduction in mucosal protection

Question 12

how does the oesophagus limit exposure to gastric acid as a defense?

Answer 12

gastro-oesophageal junction (LOS) sits at high tonic pressure reduces gastric content entering oesophagus

Question 13

how does transient LOS relaxation prevent gastric acid damage in the oesophagus?

Answer 13

clears gastric acid with a non-swallowing wave of peristalisis when gas moves from stomach to oesophagus

Question 14

what chemicals defend the oesophagus against acid damage?

Answer 14

saliva - alkaline/rich in bicarbonate, produce 1.5L daily, increased production during oesophageal acid exposure

Question 15

what are the attacking causes of acid-peptic disease?

Answer 15

too much gastric acid production:

• zollinger ellison syndrome (rare benign gastrin producing tumour)
• helicobacter pylori antral gastritis

Question 16

what are the weakened defense causes of acid peptic disease?

Answer 16

gastric/duodenal ulceration:
- NSAIDs
- stress ulceration
- H.Pylori corpus/pan gastritis

GORD:
- impaired physical anti-reflux barrier

Question 17

what are the complications of peptic ulcer disease?

Answer 17

bleeding (erosion into blood vessel)
blood loss (fatigue etc.)
abdominal pain (perferation, erosion through serosa into peritoneum)

Question 18

briedly describe H.Pylori

Answer 18

gram -ve bacillus, infects stomach in childhood

Question 19

explain antero predominant gastritis

Answer 19

inflammed antrum, reduces somatostatin, increases gastrin and gastric acid production causing ulceration (pylorus, antrum, duodenum)
normal/increased acid production, no increased risk of gastric cancer

Question 20

explain corpus predominant/pangastritis

Answer 20

parietal cells become atrophic and produce less acid, inflamed stomach lining, acid absense results in colonisation of bacteria, production of possible carcinogens (nitrosamines)

Question 21

how does H.Pylori survive in low pH (stomach)?

Answer 21

urease - enzyme breaking down urea/water forming CO2/NH3
H.Pylori uses urease to surround itself in an alkaline environment buffering gastric acid

Question 22

how can H.Pylori be detected?

Answer 22

blood test - serology for antibody
stool test for antigen in faeces
urease activity - urea breath test, rapid urease test from endoscopic biopsy
histological biopsy

Question 23

what are the principles of the urea breath test?

Answer 23

patient ingests carbon isotope (urea) drink to enrich urea
urease breaks down urea into CO2/NH3 and enriched isotope CO2 is excreted in breath

Question 24

describe a rapid urease test

Answer 24

biopsy placed in urea gel with coloured pH indicator
presence of H.Pylori will produce urease breaking down urea into NH3 causing a pH/colour change

Question 25

what are the symptoms and complications of GORD?

Answer 25

symptoms - heartburn, food/fluid regurgitation
complications - benign stricture formation (dysphagia), ulceration (bleeding/anaemia), columnar metaplasia (adenocarcinoma)

Question 26

what drugs act locally to treat symptoms of acid peptic disorders?

Answer 26

antacids (weak alkalis neutralising acids)
alginates/sucralfate (promotes mucosal resistance)

Question 27

describe the action of sucralfate

Answer 27

complex of aluminium hydroxide and sulphated sucrose
forms a viscous suspension in presence of acid
high affinity for damaged mucosa/ulcers (provides physical barrier)

Question 28

explain the mechanism of action of proton pump inhibitors

Answer 28

oral ingestion
absorbed via small intestine
only taken into parietal cell when proton pump is activated
short plasma half life (30-60 mins)

Question 29

what does surgical manages of reflux disease involve?

Answer 29

laparoscopic fundoplication - repair of anti-reflux barrier by wrapping fundus around gastro-oesophageal junction

SE - bloating, unable to belch, swallowing difficulties

Question 30

what are some of the possible side effects of PPIs?

Answer 30

diarrhoea
weaker nutrient/micronutrient absorption
weaker antimicrobial function