A 4-month-old infant has a viral illness with high fever and cough. The infant's parent asks the NP about what to give the infant to help with symptoms. The NP should prescribe which of the following?
- A. Aspirin to treat the fever
- B. Acetaminophen as needed
- C. Dextromethorphan for coughing
- D. An antibiotic to prevent increased infection
Correct Answer: B
Rationale: The correct answer is B because acetaminophen is safe for infants to reduce fever. Choice A is incorrect (aspirin risks Reye’s syndrome). Choice C is wrong (dextromethorphan risks respiratory depression). Choice D is inaccurate (antibiotics don’t treat viral illness).
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Which of the following statements about the major distribution barriers (blood-brain or fetal-placental) is true?
- A. Water soluble and ionized drugs cross these barriers rapidly.
- B. The blood-brain barrier slows the entry of many drugs into and from brain cells.
- C. The fetal-placental barrier protects the fetus from drugs taken by the mother.
- D. Lipid-soluble drugs do not pass these barriers and are safe for pregnant women.
Correct Answer: B
Rationale: Choice B is correct because the blood-brain barrier, with its tight junctions, slows entry of many drugs, especially water-soluble ones, protecting the brain. Choice A is incorrect as water-soluble, ionized drugs cross poorly due to barrier selectivity. Choice C is wrong because the fetal-placental barrier doesn't fully block drugs—many cross and affect the fetus. Choice D is incorrect since lipid-soluble drugs readily pass these barriers, posing risks in pregnancy.
An agonist activates a receptor and stimulates a response. When given frequently over time, the body may:
- A. Upregulate the total number of receptors
- B. Block the receptor with a partial agonist
- C. Alter the drug's metabolism
- D. Downregulate the numbers of that specific receptor
Correct Answer: D
Rationale: Choice D is correct because frequent agonist use can cause the body to downregulate receptors, reducing sensitivity to overstimulation as a compensatory mechanism. Choice A is incorrect as upregulation occurs with antagonists, not agonists. Choice B is wrong because partial agonists compete, not result from frequent use. Choice C is incorrect since metabolism changes aren't the primary receptor response.
Herbal products that may increase INR include:
- A. Ginkgo biloba
- B. St John's wort
- C. Valerian root
- D. All of the above
Correct Answer: A
Rationale: Choice A is correct because ginkgo biloba can increase INR by enhancing warfarin's effect through antiplatelet activity, risking bleeding. Choice B is incorrect as St John's wort induces CYP2C9, decreasing INR and warfarin efficacy. Choice C is wrong because valerian root doesn't significantly alter INR. Choice D is incorrect since only ginkgo biloba increases INR.
The U.S. Drug Enforcement Administration:
- A. Registers manufacturers and prescribers of controlled substances
- B. Regulates NP prescribing at the state level
- C. Sanctions providers who prescribe drugs off-label
- D. Provides prescribers with a number they can use for insurance billing
Correct Answer: A
Rationale: Choice A is correct because the DEA registers those handling controlled substances, issuing numbers for tracking and prescribing, its primary role. Choice B is incorrect as state boards, not the DEA, regulate NP prescribing. Choice C is wrong because off-label prescribing isn't DEA-regulated. Choice D is incorrect since the DEA number is for controlled substances, not insurance billing.
Drugs that are affected by genetic polymorphisms of UGT1A1 include:
- A. Warfarin
- B. Irinotecan
- C. Acetaminophen
- D. All of the above
Correct Answer: B
Rationale: Choice B is correct because irinotecan's active metabolite is glucuronidated by UGT1A1; poor function increases toxicity, requiring genetic consideration. Choice A is incorrect as warfarin's metabolism is via CYP2C9, not UGT1A1. Choice C is wrong because acetaminophen uses other UGT enzymes, not specifically UGT1A1 critically. Choice D is incorrect since only irinotecan is notably affected by UGT1A1 polymorphisms.
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