B5-032 Gastric Ulcer Flashcards
main hormone produced by antral cells to stimulate parietal cells to produce acid
gastrin
main inhibitor of gastric acid secretion
somatostatin
main neurotransmitter secreted by vagus nerve to regulate acid secretion
ACh
promotes mucus secretion
prostaglandin
main risk factors for ulcers
2
H. pylori
NSAIDs
how does H. pylori cause ulcers in a majority of cases?
pangastritis of antral and fundic mucosa, causing reduced mucous production
how does H. pylori cause duodenal ulcers in a minority of patients?
causes antrum predominant gastritis which results in high gastric acid secretion
describe the characteristics of H. pylori bacterium
gram stain, shape, etc.
gram negative
helical rod shape
flagellae
major characteristics of peptic ulcer disease
periodic epigastric pain
(may be relieved with food or antacids)
pain occuring every 6-12 weeks, if on NSAIDs may have no pain
imaging modality of choice to diagnose peptic ulcer disease
EGD
CT if perforated
risk factors for peptic ulcer disease
4
- Type A personality
- steroids
- NSAIDs
- Zollinger Ellison
mucosal protective agents
3
- sucralfate
- pepto-bismol
- misprostrol
identify the image
gastric ulcer
how might an ulcer present in an older person?
bleeding/perforation symptoms without preceding pain
what is the diagnostic modality of choice when perforated ulcer is suspected?
CT scan
what symptoms may lead you to suspect perforation?
severe abdominal pain
abdominal wall rigidity
what country has a highest incidence of H. pylori?
China
Hong Kong specifically, may be relevant to patient’s hx
how does H. pylori cause ulcers?
- causes inflammation
- activates T cells
- chronic cellular damage
- worsened by acid
- H. pylori proteins channel into gastric epithelial cells
how do NSAIDs cause ulcers?
- block COX-1 from synthesizing prostaglandings
- decrease mucous barrier
- worsened by acid
which form of gastritis is more likely to cause an ulcer in the stomach and not the duodenum?
pangastritis
what kinds of cells are in the gastric antrum?
4
- G cells
- D cells
- mucous neck cells
- surface mucous cells
why does antral gastritis cause duodenal ulcers?
decreased somatostatin causes increased gastric acid –> duodenal ulcer
H. pylori attaches to receptors called […] in the gastric mucosa
Lewis antigens
does H pylori invade gastric cells?
no
attaches to lewis antigen receptors
genes within this island form a special apparatus to transport bacterial product inside the host cell
cag pathogenicity island
treatment of H. pylori peptic ulcer disease
3 things
- remove offending agent
- acid suppression
- mucosal protective agent
why is ischemia of the stomach rarely seen?
heavily vascularized
descibe the neural pathway of acid secretion
ACh from gastric enteric neurons -> M3 receptors -> intracellular Ca+ -> H+
descibe the hormonal pathway of acid secretion
Gastrin from antral G cells -> CCK2 receptors -> intracellular Ca+ -> H+
describe the paracrine pathway of acid secretion
histamine released from oxyntic ECL cells -> H2 receptors -> cAMP pathway
inhibited by somatostatin
inhibits the paracrine pathway of gastric acid secretion
somatostatin
how do PPIs block the proton pump?
sulfenamide binds to cysteine in HKATPase
what is the duration of treatment for ulcers?
12 or more weeks
how do you establish a refractory ulcer?
- ensure patient has stopped NSAIDs
- ensure H. pylori is cleared
- ensure patient has been compliant with treatment
- counsel about smoking
how do gastrinomas cause ulcers?
increased gastrin -> increased gastric acid
how does systemic mastocytosis cause ulcers?
excessive histamine –> increased gastric acid production
oncologic gastric ulcers
3
- MALT lymphoma
- gastric adenocarcinoma
- metastatic disease (breast cancer)
symptoms of systemic mastocytosis
associated with gastric ulcers
pruritis, flushing, syncope, nausea, vomiting, diarrhea, fibromyalgia
symptoms of Churg-Strauss
associated with gastric ulcers
eosinophilia, asthma, peripheral neuropathy, palpable purpura
options of surgical treatment of gastric ulcers
rare but happens, 3
- vagotomy
- antrectomy
- subtotal gastrectomy (both body and antrum)
or combination of above
what is the main inhibitory method against acid secretion?
somatostatin
H. pylori can lead to gastric ulcer in some, but duodenal ulcer in others. Why?
depends on if H. pylori infects the entire stomach or just the antrum
how do NSAIDs cause gastric ulcers?
decreased mucous production by inhibiting COX-1 with reduced prostaglandin secretion
what will happen when a tumor starts producing excess gastrin?
- the basal and maximal acid output is increased because parietal cells secrete more acid
- ulcers will develop in unusual locations
primary gastric cells that secrete acid
parietal cells
neurogenic control of acid secretion
vagus via ACh
primary gastric cells that secrete gastrin
G cell in antrum
primary cells that secrete somatostatin
D cells
primary gastric cells that secrete pepsin
chief cells
primary gastric cells to secrete histamine
ECLs
final common pathway to secrete acid
H+K+ATPase
indomethacin is an NSAID, which blocks
COX-1
COX-1 inhibitors cause
decreased production of prostaglandins
multiple, recurrent ulcers in unsual locations
gastrinoma
a serum gastrin level can help rule in/out
2
gastrinoma
Zollinger Eillison
what can be measure to determine if a patient is unknowingly taking NSAIDs?
serum salicylate
older people who take NSAIDs can develop complications of ulcer disease without
prior symptoms
side effect of Pepto Bismol
black stools
enzymes responsible for production of prostaglandins in the stomach
COX 1 & 2
constitutively expressed in the stomach and helps in the production of mucus and maintaining the integrity of the gastric mucosa
COX-1
surgery that will remove gastrin producing antral G cells
distal gastrectomy
surgery to decrease the parietal cell mass but with leaves the antrum intact
proximal gastrectomy
acid secretion will continue
what two surgical options significantly decrease acid production?
- vagotomy
- distal gastrectomy
