Gastric Secretion, Mucosal Protection & Ulceration Flashcards
explain oxyntic glands
lines most of gastric body
contains surface mucous, mucous neck, parietal, chief, ECL, D and chief cells
explain pyloric glands
found in pylorus/antrum
contains surface mucous, mucous neck, enterochromaffin (ANP), D and G cells
what is the stimulus for acid secretion?
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
what is gastric acid secretion controlled by?
ACh (neuronal - parasympathetic)
histamine (ECL cell - paracrine)
gastrin (G cell - endocrine)
somatostatin (D cell - endocrine)
when are each gastric acid secretion regulator active?
Acetylcholine - cephalic phase
Histamine/Gastrin - in response to high pH (gastric phase)
somatostatin - in response to low pH (intestinal phase)
what are the components of gastric juice?
HCl
Pepsin
Mucin
Intrinsic Factor
what is the receptor of somatostatin?
CCK2
what is the receptor for ACh
M3
what epithelium is found in the stomach and lower oesophagus?
oesophagus - stratified squamous
stomach - simple columnar
what is the stomach’s defense against gastric acid
mucous
thick adherent layer, prostoglandin, rich in bicarbonate (neutralises)
what would a COX-1/COX-2 deficiency result in for gastric protection?
production of prostoglandins, reduction in mucosal protection
how does the oesophagus limit exposure to gastric acid as a defense?
gastro-oesophageal junction (LOS) sits at high tonic pressure reduces gastric content entering oesophagus
how does transient LOS relaxation prevent gastric acid damage in the oesophagus?
clears gastric acid with a non-swallowing wave of peristalisis when gas moves from stomach to oesophagus
what chemicals defend the oesophagus against acid damage?
saliva - alkaline/rich in bicarbonate, produce 1.5L daily, increased production during oesophageal acid exposure
what are the attacking causes of acid-peptic disease?
too much gastric acid production:
- zollinger ellison syndrome (rare benign gastrin producing tumour)
- helicobacter pylori antral gastritis
what are the weakened defense causes of acid peptic disease?
gastric/duodenal ulceration:
- NSAIDs
- stress ulceration
- H.Pylori corpus/pan gastritis
GORD:
- impaired physical anti-reflux barrier
what are the complications of peptic ulcer disease?
bleeding (erosion into blood vessel)
blood loss (fatigue etc.)
abdominal pain (perferation, erosion through serosa into peritoneum)
briedly describe H.Pylori
gram -ve bacillus, infects stomach in childhood
explain antero predominant gastritis
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
explain corpus predominant/pangastritis
parietal cells become atrophic and produce less acid, inflamed stomach lining, acid absense results in colonisation of bacteria, production of possible carcinogens (nitrosamines)
how does H.Pylori survive in low pH (stomach)?
urease - enzyme breaking down urea/water forming CO2/NH3
H.Pylori uses urease to surround itself in an alkaline environment buffering gastric acid
how can H.Pylori be detected?
blood test - serology for antibody
stool test for antigen in faeces
urease activity - urea breath test, rapid urease test from endoscopic biopsy
histological biopsy
what are the principles of the urea breath test?
patient ingests carbon isotope (urea) drink to enrich urea
urease breaks down urea into CO2/NH3 and enriched isotope CO2 is excreted in breath
describe a rapid urease test
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
