D
Man, you have to choose INCORRECT answer
drdg wrote: My answer goes to A "Detection of H. pylori antibody in the serum is sufficient for a diagnosis of peptic ulcer disease. " is not correct. Since many people have H.Pylori infections but no peptic ulcer disease.
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| darkhorse
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The answer is D.
Helicobacter pylori is a spiral-shaped, microaerophilic gram-negative rod that is found in 95%
of duodenal ulcers and 75 to 85% of gastric ulcers. However, only 15% of infected individuals
with documented H. pylori infections develop peptic ulcer disease over the course of their
lifetimes. H. pylori colonization of the gastric mucosa is promoted by the organism's production
of urease, which hydrolyzes urea to ammonium ion and carbon dioxide. This increases the
gastric pH and helps the organism avoid the harmful effects of gastric acid. H. pylori further
promotes inflammation in the gastric mucosa by means of the generation of inflammatory
cytokines and increased generation of hydrogen ions created by the breakdown of ammonium
ion. Furthermore, the organism produces proteases and phospholipases that cause degradation
of the mucus gel layer that protects the gastric mucosa from the stomach acid. The reason for
H. pylori–mediated duodenal ulcer is unclear. One possibility is that H. pylori infection causes
gastric metaplasia in the duodenum and thus creates an environment for infection. Another
possibility is that H. pylori infection in the stomach increases acid secretion and decreases
duodenal pH, causing duodenal ulceration. Detection of H. pylori antibody in the serum of
someone suspected of having a duodenal or gastric ulcer is insufficient for the diagnosis as this
only signifies prior infection. Demonstration of organisms on biopsy, detection by the urease
breath test, or detection of H. pylori in the stool is needed for the diagnosis. Treatment of H.
pylori requires triple-drug therapy, with a variety of regimens available. All include some form
of acid suppression in the form of bismuth sulfate or proton pump inhibitors. The 1-year
relapse rate of duodenal ulcers after eradication of H. pylori is less than 15%
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