ATI RN
Chapter 26 principles of pharmacology Questions
Question 1 of 5
Match the drug product below with the type of controlled-release dosage form that it represents
Correct Answer: A
Rationale: A matrix device (A) matches Biphenamine Capsules (1), where drug release occurs via diffusion through an inert matrix (e.g., wax). Ion-exchange (B) fits Thorazine Spansule (2), releasing via resin binding. Hydrocolloid (C) suits Valrelease (3), swelling to control release. Osmotic system (D) matches Slow-K (4), using osmotic pressure. Coated granules (original E) are distinct. Matrix systems provide sustained release, balancing simplicity and efficacy, widely used for chronic conditions, minimizing peak-trough fluctuations.
Question 2 of 5
All of the following statements about plasma protein binding of a drug are true except
Correct Answer: D
Rationale: Option D is false; drugs highly bound to plasma proteins (e.g., warfarin) have a smaller V_D, as they stay in plasma, unlike tissue-bound drugs (e.g., digoxin, large V_D). Displacement increases V_D transiently (A), boosts free drug for filtration (B), and risks toxicity in highly bound drugs (C), all true. Option E (original) is replaced. Protein binding restricts distribution, reducing V_D, a key pharmacokinetic factor affecting free drug levels and potential interactions, critical in polypharmacy.
Question 3 of 5
Monomer units of proteins are known as
Correct Answer: C
Rationale: Amino acids (C) are the monomer units of proteins, linked by peptide bonds (e.g., glycine in collagen), forming polypeptides via translation. Monosaccharides (A) build carbohydrates. Prosthetic groups (B) are non-protein enzyme parts. Purines (D) and nucleosides (original E) relate to nucleic acids. This biochemical foundation underpins protein drugs (e.g., insulin), where sequence dictates function, essential in pharmacology for therapeutic protein design and metabolism studies.
Question 4 of 5
N-oxidation will be involved with the metabolism of following drugs, except
Correct Answer: C
Rationale: Phenytoin (C) does not undergo N-oxidation; it's metabolized via CYP2C9 hydroxylation to HPPH, unlike dapsone (A), meperidine (B), and chlorpheniramine (D), which form N-oxides via flavin monooxygenases or CYP450. No original E. N-oxidation, a phase I reaction, adds oxygen to nitrogen, increasing polarity (e.g., meperidine to normeperidine), but phenytoin's aromatic ring hydroxylation differs, impacting its nonlinear kinetics and therapeutic monitoring, distinct in drug metabolism pathways.
Question 5 of 5
A patient receives long-term, high-dose therapy with a sulfonamide. After approximately 3 weeks of therapy, the patient has a low-grade fever, rash, and muscle and joint pain. Which type of hypersensitivity accounts for these symptoms?
Correct Answer: C
Rationale: Type III hypersensitivity (C) accounts for these symptoms after 3 weeks of sulfonamide therapy, a serum sickness-like reaction from immune complexes depositing in tissues, causing inflammation (fever, rash, arthralgia). Type I (A) is immediate (e.g., anaphylaxis). Type II (B) is cytotoxic. Type IV (D) is delayed, T-cell mediated. No original E. This delayed onset, common with prolonged drug exposure, requires discontinuation and sometimes steroids, highlighting immune complex pharmacology in adverse reactions.