Parietal cell
Secrete HCl stored in vesicles
Respond to gastrin, Ach from enteric neurons, and histamine
Gastrin
Released by G cells
Stimulates parietal acid release
Stimulates ECL (enterochromaffin like) cells to release histamine to H2 receptors
D cells
Release inhibitory somatostatin
Greatest effect is on inhibition of histamine, not gastrin
Decrease in response to Ach, increase in response to VIP
Stomach distention
Low grade = somatostatin release, inhibition of acid secretion
High grade = increased gastrin, less somatostatin
Prostaglandins
Inhibit acid secretion
Inhibit histamine stimulated parietal function
Inhibit gastrin stimulated histamine release
In particular, all of these pharmacologic causes are made worse in conjunction with the use of NSAIDs
This equates to a population burden of ~115 million people!
However, the prevalence of actual PUD in these carriers is usually quite low, around 1-2%; thus, no need for mass screening program of asymptomatic carriers of H pylori
Classic dyspepsia pain pattern
Gastric ulcers: more closely timed to meals
Duodenal ulcers: typically 2-5 hours after a meal, as well as at night when circadian stimulation of acid secretion is at its max
Alarm symptoms such as these typically need workup with endoscopy on a more urgent basis to identify underlying etiology
Other things to look out for in history
Smoking
Comorbid diseases
H pylori that has escaped detection, make sure off PPI/ABX/Bismuth
Biopsy ulcers
Crack cocaine/amphetamines that can cause vascular compromise
H pylori testing
Urea breath test more accurate in hospitalized patients with acute bleeding
Stool studies not as accurate if acute bleeding, blood can cause cross reactivity
If initial testing negative, f/u in 4 weeks
Also need eradication testing 4+ weeks after completion of therapy
If patient had a CT performed for their dyspepsia, and it showed benign appearing duodenal ulcer with no alarm features, no need to EGD for diagnosis
However, EGD necessary for all gastric ulceration
All ulcers with malignant features should be biopsied for further evaluation
Both PPI and H2 antagonists may be effective, but healing rates with PPI after 8 weeks of treatment were significantly higher
Frequently recurrent = >2 documented cases per year
This is called the clarithromycin based concomitant therapy, usually used after failure of bismuth quadruple therapy
Treatment timing: some studies say 10-14 days, but in practice most patients are placed on therapy for 14 days
Levofloxacin triple therapy: levo, amox/flagyl, PPI
High dose dual therapy: amoxicillin, PPI
Rifabutin therapy: Rifabutin, amoxicillin, PPI
Clarithromycin concomitant therapy: clarithro, amox, flagyl, PPI
Bleeding: often managed with fluids, transfusion, PPI, endoscopy; surgery may be necessary if refractory
Perforation: Generally in the context of sudden onset severe, diffuse, abdominal pain
GOO: for those with refractory disease not amenable to medical treatment, most associated with duodenal or pyloric channel ulcers
