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16 Sep 2014, 02:01
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Although the class of anti-inflammatory drugs known as COX-2 inhibitors has proven successful at reducing pain and swelling, a series of clinical trials has shown that these drugs come with potentially harmful side effects. Anti-inflammatory drugs act on prostaglandins, hormone-like substances with a general regulatory role in the body – controlling blood flow to the kidneys or prompting contraction of the uterus during childbirth, for example – in addition to bearing the primary responsibility for causing pain and inflammation. Prostaglandins are the result of a process by which a type of acid in the cell membrane is transformed by two enzymes both known as cyclooxygenase, or COX-1 and COX-2. Older anti-inflammatory medications such as aspirin and ibuprofen stop pain by blocking the action of both COX enzymes. Researchers have long been aware, however, that the simultaneous repression of both COX-1 and COX-2 halts production of all prostaglandins, including those not responsible for pain.
Researchers who developed COX-2 inhibitors hoped to avoid negative side effects by blocking only one of the two COX enzymes. After a series of trials, drugs such as Vioxx and Celebrex entered the market in the 1990s. This approach, unfortunately, soon presented its own drawbacks. Although COX-2 inhibitors do in fact prevent production of prostaglandin E2 (PGE2), which is responsible for causing pain and inflammation, they also inhibit production of various other substances in the body, including prostacyclin (PGI2), which dilates blood vessels and prevents clots. On the other hand, COX-2 inhibitors do not prevent the production of thromboxane, another prostaglandin that constricts vessels and helps blood platelets clump. There is widespread agreement that the next step for researchers is to develop anti-inflammatory drugs that target specific prostaglandins rather than the enzymes that produce them.
According to the passage, a problem with COX-2 inhibitors arises for which of the following reasons?
COX-2 inhibitors
A. often conflict with older types of anti-inflammatory medication.
B. cause the production of an excessive amount of prostaglandin E2.
C. do not suppress an excessive amount of thromboxane, which causes blood clots.
D. block both COX enzymes, stopping the production of all prostaglandins.
E. inhibit production of substances that help maintain normal bodily functions.
Researchers who developed COX-2 inhibitors hoped to avoid negative side effects by blocking only one of the two COX enzymes. After a series of trials, drugs such as Vioxx and Celebrex entered the market in the 1990s. This approach, unfortunately, soon presented its own drawbacks. Although COX-2 inhibitors do in fact prevent production of prostaglandin E2 (PGE2), which is responsible for causing pain and inflammation, they also inhibit production of various other substances in the body, including prostacyclin (PGI2), which dilates blood vessels and prevents clots. On the other hand, COX-2 inhibitors do not prevent the production of thromboxane, another prostaglandin that constricts vessels and helps blood platelets clump. There is widespread agreement that the next step for researchers is to develop anti-inflammatory drugs that target specific prostaglandins rather than the enzymes that produce them.
According to the passage, a problem with COX-2 inhibitors arises for which of the following reasons?
COX-2 inhibitors
A. often conflict with older types of anti-inflammatory medication.
B. cause the production of an excessive amount of prostaglandin E2.
C. do not suppress an excessive amount of thromboxane, which causes blood clots.
D. block both COX enzymes, stopping the production of all prostaglandins.
E. inhibit production of substances that help maintain normal bodily functions.
16 Sep 2014, 02:01
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Bookmarks
Official Solution:
Although the class of anti-inflammatory drugs known as COX-2 inhibitors has proven successful at reducing pain and swelling, a series of clinical trials has shown that these drugs come with potentially harmful side effects. Anti-inflammatory drugs act on prostaglandins, hormone-like substances with a general regulatory role in the body – controlling blood flow to the kidneys or prompting contraction of the uterus during childbirth, for example – in addition to bearing the primary responsibility for causing pain and inflammation. Prostaglandins are the result of a process by which a type of acid in the cell membrane is transformed by two enzymes both known as cyclooxygenase, or COX-1 and COX-2. Older anti-inflammatory medications such as aspirin and ibuprofen stop pain by blocking the action of both COX enzymes. Researchers have long been aware, however, that the simultaneous repression of both COX-1 and COX-2 halts production of all prostaglandins, including those not responsible for pain.
Researchers who developed COX-2 inhibitors hoped to avoid negative side effects by blocking only one of the two COX enzymes. After a series of trials, drugs such as Vioxx and Celebrex entered the market in the 1990s. This approach, unfortunately, soon presented its own drawbacks. Although COX-2 inhibitors do in fact prevent production of prostaglandin E2 (PGE2), which is responsible for causing pain and inflammation, they also inhibit production of various other substances in the body, including prostacyclin (PGI2), which dilates blood vessels and prevents clots. On the other hand, COX-2 inhibitors do not prevent the production of thromboxane, another prostaglandin that constricts vessels and helps blood platelets clump. There is widespread agreement that the next step for researchers is to develop anti-inflammatory drugs that target specific prostaglandins rather than the enzymes that produce them.
According to the passage, a problem with COX-2 inhibitors arises for which of the following reasons?
COX-2 inhibitors
A. often conflict with older types of anti-inflammatory medication.
B. cause the production of an excessive amount of prostaglandin E2.
C. do not suppress an excessive amount of thromboxane, which causes blood clots.
D. block both COX enzymes, stopping the production of all prostaglandins.
E. inhibit production of substances that help maintain normal bodily functions.
Answer: E. The question asks for a problem identified in the passage. COX-2 inhibitors reduce pain and inflammation, but their effects are not limited to those intended benefits: they also interfere with substances that perform useful regulatory functions.
A. Incorrect. The passage compares older anti-inflammatory medications with COX-2 inhibitors, but it does not discuss what happens when the two types are used together. There is no support for the claim that they conflict with each other.
B. Incorrect. The passage states that COX-2 inhibitors prevent the production of prostaglandin E2, which is responsible for pain and inflammation. This choice reverses that relationship by claiming that the drugs cause excessive production of the substance.
C. Incorrect. The unsupported detail is an excessive amount of thromboxane. The passage says that COX-2 inhibitors do not prevent thromboxane production; it does not say that the amount produced is excessive. Blocking prostacyclin, which prevents clots, could leave thromboxane’s clot-promoting effects less opposed. However, that is different from establishing that too much thromboxane is produced. The explanation for rejecting C is therefore not that E describes a larger problem, but that C adds a claim the passage does not support.
D. Incorrect. Blocking both COX enzymes and stopping the production of all prostaglandins describes the older medications, such as aspirin and ibuprofen. The passage explicitly states that COX-2 inhibitors were developed to block only one of the two enzymes.
E. Correct. The passage identifies prostacyclin, or PGI2, as a substance that dilates blood vessels and prevents clots. COX-2 inhibitors inhibit its production along with that of substances responsible for pain and inflammation. Thus, the drugs can interfere with normal bodily regulation, which is the problem described by this choice.
Answer: E
Although the class of anti-inflammatory drugs known as COX-2 inhibitors has proven successful at reducing pain and swelling, a series of clinical trials has shown that these drugs come with potentially harmful side effects. Anti-inflammatory drugs act on prostaglandins, hormone-like substances with a general regulatory role in the body – controlling blood flow to the kidneys or prompting contraction of the uterus during childbirth, for example – in addition to bearing the primary responsibility for causing pain and inflammation. Prostaglandins are the result of a process by which a type of acid in the cell membrane is transformed by two enzymes both known as cyclooxygenase, or COX-1 and COX-2. Older anti-inflammatory medications such as aspirin and ibuprofen stop pain by blocking the action of both COX enzymes. Researchers have long been aware, however, that the simultaneous repression of both COX-1 and COX-2 halts production of all prostaglandins, including those not responsible for pain.
Researchers who developed COX-2 inhibitors hoped to avoid negative side effects by blocking only one of the two COX enzymes. After a series of trials, drugs such as Vioxx and Celebrex entered the market in the 1990s. This approach, unfortunately, soon presented its own drawbacks. Although COX-2 inhibitors do in fact prevent production of prostaglandin E2 (PGE2), which is responsible for causing pain and inflammation, they also inhibit production of various other substances in the body, including prostacyclin (PGI2), which dilates blood vessels and prevents clots. On the other hand, COX-2 inhibitors do not prevent the production of thromboxane, another prostaglandin that constricts vessels and helps blood platelets clump. There is widespread agreement that the next step for researchers is to develop anti-inflammatory drugs that target specific prostaglandins rather than the enzymes that produce them.
According to the passage, a problem with COX-2 inhibitors arises for which of the following reasons?
COX-2 inhibitors
A. often conflict with older types of anti-inflammatory medication.
B. cause the production of an excessive amount of prostaglandin E2.
C. do not suppress an excessive amount of thromboxane, which causes blood clots.
D. block both COX enzymes, stopping the production of all prostaglandins.
E. inhibit production of substances that help maintain normal bodily functions.
Answer: E. The question asks for a problem identified in the passage. COX-2 inhibitors reduce pain and inflammation, but their effects are not limited to those intended benefits: they also interfere with substances that perform useful regulatory functions.
A. Incorrect. The passage compares older anti-inflammatory medications with COX-2 inhibitors, but it does not discuss what happens when the two types are used together. There is no support for the claim that they conflict with each other.
B. Incorrect. The passage states that COX-2 inhibitors prevent the production of prostaglandin E2, which is responsible for pain and inflammation. This choice reverses that relationship by claiming that the drugs cause excessive production of the substance.
C. Incorrect. The unsupported detail is an excessive amount of thromboxane. The passage says that COX-2 inhibitors do not prevent thromboxane production; it does not say that the amount produced is excessive. Blocking prostacyclin, which prevents clots, could leave thromboxane’s clot-promoting effects less opposed. However, that is different from establishing that too much thromboxane is produced. The explanation for rejecting C is therefore not that E describes a larger problem, but that C adds a claim the passage does not support.
D. Incorrect. Blocking both COX enzymes and stopping the production of all prostaglandins describes the older medications, such as aspirin and ibuprofen. The passage explicitly states that COX-2 inhibitors were developed to block only one of the two enzymes.
E. Correct. The passage identifies prostacyclin, or PGI2, as a substance that dilates blood vessels and prevents clots. COX-2 inhibitors inhibit its production along with that of substances responsible for pain and inflammation. Thus, the drugs can interfere with normal bodily regulation, which is the problem described by this choice.
Answer: E
16 Feb 2015, 21:52
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I got tricked (and I partly do not agree with some of the responses/explanations)
- by the V04-11 question because:
For answer E, the correct one, the text states "also drastically reduce the amount of various other substances in the body, including prostacyclin (PGI2)," - So drastically reduce BUT NOT BLOCK - Should we actually infer that drastically reduce = block? (I have not seen this before)
While C is supported by the text: "do not prevent the production of thromboxane, another prostaglandin that constricts vessels and helps blood platelets clump." it is considered by the response key as "less larger problem" - How do we account for that?
- by question V04-12 because:
I did not manage to infer that the effects of the 2 substances balance. While I can agree that "It can be concluded, then, that their functions balance each other.", but is it safe to infer that their effects balance as well? (Since we don't know the quantities, how can we infer that the effects balance? In the V04-11 we considered that one is less important than other, then can we safely say that they balance?)
- and by question V04-13 because:
I think we can equally infer that COX-2 can accidentally disrupt constriction of blood vessels for the reason: "COX-2 inhibitors do not prevent the production of thromboxane, another prostaglandin that constricts vessels and helps blood platelets clump". Since the inhibitors do not prevent the production of thromoxane, then the inhibitors permit the the constriction of blood vessels, right?
Thanks for clarifying!
- by the V04-11 question because:
For answer E, the correct one, the text states "also drastically reduce the amount of various other substances in the body, including prostacyclin (PGI2)," - So drastically reduce BUT NOT BLOCK - Should we actually infer that drastically reduce = block? (I have not seen this before)
While C is supported by the text: "do not prevent the production of thromboxane, another prostaglandin that constricts vessels and helps blood platelets clump." it is considered by the response key as "less larger problem" - How do we account for that?
- by question V04-12 because:
I did not manage to infer that the effects of the 2 substances balance. While I can agree that "It can be concluded, then, that their functions balance each other.", but is it safe to infer that their effects balance as well? (Since we don't know the quantities, how can we infer that the effects balance? In the V04-11 we considered that one is less important than other, then can we safely say that they balance?)
- and by question V04-13 because:
I think we can equally infer that COX-2 can accidentally disrupt constriction of blood vessels for the reason: "COX-2 inhibitors do not prevent the production of thromboxane, another prostaglandin that constricts vessels and helps blood platelets clump". Since the inhibitors do not prevent the production of thromoxane, then the inhibitors permit the the constriction of blood vessels, right?
Thanks for clarifying!
