H. pylori infection and stomach cancer
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H. pylori infection and stomach cancer
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[post_date] => 2024-12-23 18:27:15
[post_date_gmt] => 2024-12-23 23:27:15
[post_content] => Practice Passage (Question 1-6)
*This passage is the property of Khan Academy and has been reformatted into an AAMC-style interface in their entirety by MedLife Mastery. MedLife Mastery does not endorse and is not an affiliate of Khan Academy.
Helicobacter pylori (H. pylori) is a Gram-negative, microaerophilic bacterium characterized by its ability to survive in highly acidic conditions. Infection with H. pylori can lead to peptic ulcer disease (PUD); in fact, the bacterium is responsible for the development of 70% of gastric ulcers and an estimated 80-95% of duodenal ulcers, which may in turn lead to the development of certain cancers.
Once H. pylori bacteria reach the stomach, they burrow through the protective mucosal layer and adhere to the gastric epithelium, causing local cell destruction and inflammation. H. pylori most commonly colonizes the antrum of the stomach—the distal end of the stomach which connects to the opening to the small intestine, the pyloric sphincter.
Microscopic analysis of stomach mucosa in patients afflicted by PUD reveals a marked destruction in somatostatin-producing D cells (also known as delta cells). The decreased presence of D cells relative to other cell types within the stomach is accompanied by measurable increases in gastric acid production, and a decrease in luminal pH. H. pylori is capable of surviving in these harsh conditions by two mechanisms. First, the mucous layer through which it burrows to reach the epithelial surface is characterized by a more neutral pH than the gastric lumen. Second, the organism is capable of producing the enzyme urease, the effect of which is to produce a more neutral environment in the area immediately surrounding the bacterium.
A strong association between chronic H. pylori infection and the development of gastric cancer has been demonstrated, though few studies have been able to accurately assess whether this risk is more strongly associated with specific subtypes of cancer or their anatomical distribution. A 2001 review of twelve prospective studies attempted to illustrate the association between gastric cancer risk and anatomical distribution (cardia vs. non-cardia) in patients with a known H. pylori infection. The results of this study are shown in Figure 2, which maps the odds ratios (a measure of association wherein a ratio not equal to 1 denotes an association) and 95% confidence intervals for the relationship between cancer development and H. pylori for cardia vs. non-cardia anatomical areas.
Figure 1 Matched odds ratios (ORs) and 95 percent confidence intervals for associations between H. pylori infection and non-cardia cancer (Panel A) and cardia cancer (Panel B). The area of the black squares is proportional to the study size. The white diamond shows the OR value for all studies combined, with the 95% confidence interval represented by horizontal spread.
Data adapted from: Webb, P. M., Law, M., Varhese, C., & Forman, D. Gastric cancer and Helicobacter pylori : a combined analysis of 12 case control studies nested within prospective cohorts. Gut, 49, 347-353.
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[question] => Under normal conditions, what stimulates the release of somatostatin from Antral D-cells?
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[answer] => 3
[description] => Reason for Correct Answer:
Somatostatin is an inhibitory hormone produced by delta-cells or D cells in the antrum of the stomach. The passage states that “The decreased presence of D cells relative to other cell types within the stomach is accompanied by measurable increases in gastric acid production, and a decrease in luminal pH.”
If you are unsure of somastatin’s function in the stomach, this passage info should give you a hint that D cells and somatostatin usually function to decrease stomach acid production.
In fact, in the stomach, somatostatin acts directly on the acid-producing parietal cells via a G-protein coupled receptor to reduce acid secretion. Somatostatin can also indirectly decrease stomach acid production by preventing the release of other hormones (including gastrin, secretin, and histamine), which effectively slows down the digestive process.
Since somatostatin acts to decrease stomach acid production, it makes sense that its release from D cells is triggered by high stomach acid, or low gastric pH.
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[answers] => Array
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[0] => Array
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[each_answer] => A. Low fat content in gastric chyme
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[1] => Array
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[each_answer] => B. Distention of the stomach
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[each_answer] => C. Low gastric pH
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[3] => Array
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[each_answer] => D. Acetylcholine
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[1] => Array
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[quiz_unique_key] => 1403770772
[question] => What is the most likely sequence in generating the decreased luminal pH following the destruction of antral D cells in H. pylori infection?
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[answer] => 2
[description] => Reason for Correct Answer:
Somatostatin does not have any autocrine activity, i.e. it does not exert feedback inhibition on itself. However, somatostatin inhibits other cells. With less somatostatin, essentially all other gastric cells are free to operate with relatively greater freedom.
Chief cells are responsible for producing pepsinogen and gastric lipase.
G cells produce gastrin.
Gastrin promotes release of HCl from parietal cells in addition to stimulating parietal cell maturation and growth.
Therefore, it makes most sense that somatostatin would normally decrease stomach acid by inhibiting gastrin production by G cells, leading to a decrease in HCl production by parietal cells.
Conversely, with less somatostatin, there is less G cell inhibition, more gastrin release, and more maturation and HCl production by parietal cells.
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[answers] => Array
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[0] => Array
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[each_answer] => A. Decreased production of somatostatin→ decreased inhibition of chief cells→ increased gastric acid production by chief cells
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[each_answer] => B. Decreased production of somatostatin→ decreased inhibition of G cells→ increased gastrin production→ increased numbers of mature parietal cells
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[2] => Array
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[each_answer] => C. Decreased production of somatostatin→ decreased inhibition of parietal cells→ increased gastrin production by parietal cells
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[each_answer] => D. Decreased production of somatostatin→ decreased inhibition of D cells→ increased gastric acid production by D cells
)
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[2] => Array
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[quiz_unique_key] => 1403770772
[question] => Which of the following characteristics does H. pylori likely demonstrate?
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[answer] => 2
[description] => Reason for Correct Answer:
The passage states that “Helicobacter pylori (H. pylori) is a Gram-negative, microaerophilic bacterium.”
The Gram stain is positive (dark colored) only if a large amount of peptidoglycan is available to bind. Therefore, Gram-positive bacteria have thick peptidoglycan layers. In Gram-negative bacteria, there is a thinner layer sandwiched between two lipid bilayers.
https://commons.wikimedia.org/wiki/File:Bacterial_cell_walls.jpg
Teichoic acids are an important part of a Gram-positive organism’s cell wall and serve an integral function in the organism’s adherence and penetrative properties. They are not present on Gram-negative bacteria.
Aerophilic organisms, such as H. pylori, are capable of utilizing oxygen for their survival (in contrast to anaerobic bacteria).
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[answers] => Array
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[0] => Array
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[each_answer] => A. Thick peptidoglycan layer
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[each_answer] => B. Oxygen utilization
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[each_answer] => C. Teichoic acids
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[each_answer] => D. Single lipid bilayer
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[quiz_unique_key] => 1403770772
[question] => What is the best conclusion to draw from the data shown in Figure 2?
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[answer] => 4
[description] => Reason for Correct Answer:
The squares and diamonds on Figure 1 show estimated odds ratios (ORs) for the correlation of gastric cancers and H. pylori infection. An OR greater than 1 implies a positive correlation between an exposure and a disease.
The lines on Figure 1 show the 95% confidence interval. In other words, they show data ranges in which they are 95% confident that the true odds ratio lies. An OR is generally considered significant only if its 95% confidence interval does not include 1, reflecting a level of certainty similar to the commonly used p-value threshold of 0.05.
Panel A shows that, for non-cardia cancer patients, the estimated ORs and 95% confidence intervals are mostly greater than 1. Panel B shows that, for cardia cancer patients, most of the 95% confidence intervals include positive and negative values, with only two being positive or negative.
This suggests that H. pylori is positively correlated with the formation of non-cardia gastric cancers and is not correlated with the formation of cardia gastric cancers.
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[answers] => Array
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[0] => Array
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[each_answer] => A. H. pylori is positively associated with the formation of cardia gastric cancers and negatively associated with the formation of non-cardia gastric cancers
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[1] => Array
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[each_answer] => B. H. pylori is positively associated with the formation of non-cardia gastric cancers and negatively associated with the formation of cardia gastric cancers
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[2] => Array
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[each_answer] => C. H. pylori is positively correlated with the formation of cardia gastric cancers and is not correlated with the formation of non-cardia gastric cancers
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[each_answer] => D. H. pylori is positively correlated with the formation of non-cardia gastric cancers and is not correlated with the formation of cardia gastric cancers
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[4] => Array
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[quiz_unique_key] => 1403770772
[question] => What is the function of urease?
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[answer] => 3
[description] => Reason for Correct Answer:
The passage describes an overall decrease in somatostatin due to the destruction of D cells; this does not involve the urease that the bacteria produces.
Recall that the function of an enzyme is often denoted by its name. The root of an enzyme, followed by the suffix “-ase,” often describes the substance that an enzyme degrades, so, in this instance, ‘urease’ must be an enzyme which catalyzes the degradation of urea.
The passage describes urease as a protective mechanism which neutralizes the acidic environment. Intuitively, its product should have a net basic effect. CO2 is slightly acidic, but ammonia is more strongly basic than CO2 is acidic, so the breakdown of urea to ammonia and CO2 makes the most sense.
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[answers] => Array
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[0] => Array
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[each_answer] => A. Catalyzes the formation of urea from ammonia and CO₂
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[1] => Array
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[each_answer] => B. Catalyzes the formation of somatostatin from urea and CO₂
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[2] => Array
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[each_answer] => C. Catalyzes the degradation of urea to ammonia and CO₂
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[3] => Array
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[each_answer] => D. Catalyzes the degradation of somatostatin to urea and CO₂
)
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[5] => Array
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[quiz_unique_key] => 1997864699
[question] => Decreased secretions from which cell type would leave the stomach lining more susceptible to decreases in pH that accompany PUD?
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[answer] => 1
[description] => Reason for Correct Answer:
For this question, you’re looking for a cell type that secretes something that would normally protect the stomach lining.
Here is a list of these cell types and their secretions.
Of the answer choices, only secretions from goblet cells, which secrete mucus, would directly protect against the drop in pH seen in PUD. Notice that both parietal cells and G cells secrete more acid, which would worsen things, and chief cells secrete a protease precursor, pepsinogen, which would not help.
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[0] => Array
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[each_answer] => A. Goblet cells
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[each_answer] => B. Parietal cells
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[each_answer] => C. Chief cells
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[each_answer] => D. G cells
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Figure 1
