Stomach Flashcards
what are the 4 areas of the stomach
fundus
body
antrum
pylorus
where does the oesophagus meet the stomach
cardia
what is the main function of the stomach
mixing of gastric secretions into chyme
what happens in the orad region of the stomach
no slow wave activity
weak tonic contractions move gastric contents into the caudad region
what happens in the caudad region of the stomach
slow wave activity occurs
peristalsis pushes chyme along pylorus then retropulsion occurs
what is retropulsion
rebound of chyme against distal antrum into the body to allow further mixing of chyme into small particles
where in the stomach does most of the mixing of chyme take place
antrum
what factors promote the emptying of the stomach (gastric factors)
large volume of chyme
thin consistency of chyme
what factors delay the release of chyme (duodenal factors)
enterogastric reflexes
hormonal response - CCK and secretin
what is the enterogastric reflex
duodenum signals to the stomach that it has enough chyme causing peristalsis to slow down
where are the pyloric gland and oxyntic glands located
pyloric - antrum
oxyntic - fundus and body
what cells are within pyloric gland and what do they secrete
D cells - somatostatin
G cells - gastrin
what cells are within oxyntic gland and what do they secrete
parietal cells - HCl and intrinsic factor
enterochromaffin like cells - histamine
chief cells - pepsinogen
what does intrinsic factor do
binds to vitamin B12 to help with digestion
what do gastrin and histamine do
stimulate secretion of HCl
what does somatostatin do
inhibit secretion of HCl
how is HCl secreted from gastrin and histamine
CO2 and H2O form carbonic anhydrase - dissociates into H+ and HCO3
HCO3 is pumped out via antiporter exchanged for Cl-
Cl- is pumped out via CFTR channel
H+ leaves via proton pump and H+ and Cl- bind
what are secretagogues and give examples
substances that stimulate production of HCl
eg histamine, gastrin and ACh
what are the 3 phases of gastric secretions
cephalic phase
gastric phase
intestinal phase
describe the cephalic phase
stomach prepared for good. conditioned by chewing/swallowing, causes increased gastric secretions from secretagogues
describe the gastric phase
when food is in the stomach
distension of stomach causes mechanoceptors to increase secretions
describe the intestinal phase
once the food has left the stomach
gastric secretions stopped through the release of CCK and somatostatin
name groups of drugs that influence gastric acid secretion
PPIs
H2 receptor antagonists
Muscarinic receptor antagonists
NSAIDs
what is contained within normal gastric mucosa to prevent irritation
contains mucus as physical barrier
contains HCO3 to buffer the mucosa
what effect does prostaglandin have on mucosa
increases mucus and HCO3 production and increases blood flow therefore preventing gastric irritation
what effect do NSAIDs have on gastric mucosa
inhibit prostaglandin production though COX1 causing less mucus and decreased blood flow - increases change of developing peptic ulcer and bleeding
give an example of a PPI and when/route of administration
omeprazole
orally before breakfast
how to PPIs work
inhibit the proton pump preventing secretion of acid
only active at low pH
give an example of a H2 receptor antagonist and when to administer
ranitidine or cimetidine
take orally once/twice daily
how do H2 receptor antagonists work
competitive antagonist of H2 receptor which reduces acid secretion from ACh
what are the causes of acute gastritis
irritants/chemicals
trauma
severe burns
what are the symptoms of acute gastritis
sudden onset of epigastric pain
vomiting (possibly with blood)
what are the causes of chronic gastritis
autoimmune
bacterial - H. Pylori
chemical - NSAIDs alcohol
what autoimmune conditions are associated with chronic gastritis
anti-parietal and anti-intrinsic factor antibodies - increased risk of malignancy with these conditions
what are the symptoms of chronic gastritis
epigastric pain
reflux
vomiting
feeling full after eating
what are 4 complications of chronic gastritis
ulceration
perforation
bleeding
stenosis
what investigations are recommended for chronic gastritis
endoscopy
test for H. pylori
what is the treatment for chronic gastritis
antacids, PPIs
antibiotics if H. Pylori
eat smaller more frequent meals
what are benign gastric tumours known as
polyps - most common is adenoma
what are the symptoms of polyps
usually asymptomatic but if perforate may cause bleeding
what causes gastric polyps
chronic gastritis
familial adenomatous polyposis (FAP genetic condition)
drugs triggers typically PPIs
do polyps need removed and why
yes - metastatic tissue that does have malignant potenial
removed at endoscopy on biopsy
what types of malignant gastric cancers can arise
adenocarcinoma
lymphomas from MALT - mucosal associated gut lymphoid tissue
what are the main symptoms of gastric cancer
weight loss
anaemia
haematemesis
palpable mass
how does H. pylori increase risk of developing cancer
H pylori - chronic gastritis - metaplasia - dysplasia - adenocarcinoma
how and where is gastric adenocarcinoma likely to spread to
lymph nodes
haematogenous - liver metastases
direct invasion - ovaries and peritoneal cavity
what is the treatment for gastric cancer
no mets - curative surgery
mets - palliation as chemo has little success
what is gastroparesis
delayed gastric emptying
what causes gastroparesis
idiopathic diabetes cannabis drugs eg opiates systemic disease (sclerosis)
what are the classical symptoms of gastroparesis
feeling full easily
nausea/vomiting
upper abdominal pain
weight loss
what is the main treatment for gastroparesis
remove precipitating factor
liquid diet/small portion
pro-motility drug
define peptic ulcer disease
breach in gastric mucosa by acid/pepsin due to imbalance of gastro-protective factors and mucosal injurious substances
what are the main causes of peptic ulcer disease
H. Pylori infection
NSAIDs
idiopathic associated with IBS
what are the symptoms of peptic ulcer disease
epigastric pain (radiates to back)
relapsing/remitting symptoms
pain relieved by eating - gastric ulcer
pain on eating - duodenal ulcer
what sort of bacterium is H. Pylori and how does it cause peptic ulcer disease
grame -ve flagellated bacillus
increases acid secretion causing erosion of the stomach
how is H. Pylori spread
faecal-oral or oral-oral
acquired in infancy but doesnt cause disease until later life
what investigations are required for diagnosing H. Pylori
urease breath test
serology for IgA
stool sample for FAT (faecal antigen test)
possible endoscopy and biopsy
if someone has H. pylori -ve peptic ulcer disease what is the treatment
anti-secretory therapy eg PPI and antacid
remove NSAIDs
if someone has H. pylori +ve peptic ulcer disease what is the treatment
triple therapy
PPI + amoxicillin + clarythromycin for 1 week
what are the main complications of peptic ulcer disease
bleeding
perforation
anaemia
where in the GI tract is a peptic ulcer more likely to arise
duodenum followed by stomach
functional dyspepsia is more common than organic dyspepsia true/false
true
which individuals are at risk of developing GI infections
malnutrition deficiencies immunocompromised individuals closed communities eg ward extremes of age gastric acid secretion suppression
what is dysentry
inflammation of the intestine esp colon
causes bloody diarrhoea with mucus and associated with gastroenteritis
name some organisms causing gastroenteritis that have short incubation times (1-6 hours)
staph aureus
bacillus cereus
name some organisms causing gastroenteritis that have medium incubation times (12-48 hours)
salmonella
C. perfringes
name some organisms causing gastroenteritis that have long incubation times
campylobacter
E. Coli 0157
