Antimicrobial pharmacokinetics/pharmacodynamics US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Antimicrobial pharmacokinetics/pharmacodynamics. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Antimicrobial pharmacokinetics/pharmacodynamics US Medical PG Question 1: A 35-year-old woman is started on a new experimental intravenous drug X. In order to make sure that she is able to take this drug safely, the physician in charge of her care calculates the appropriate doses to give to this patient. Data on the properties of drug X from a subject with a similar body composition to the patient is provided below:
Weight: 100 kg
Dose provided: 1500 mg
Serum concentration 15 mg/dL
Bioavailability: 1
If the patient has a weight of 60 kg and the target serum concentration is 10 mg/dL, which of the following best represents the loading dose of drug X that should be given to this patient?
- A. 300 mg
- B. 450 mg
- C. 150 mg
- D. 1000 mg
- E. 600 mg (Correct Answer)
Antimicrobial pharmacokinetics/pharmacodynamics Explanation: ***600 mg***
- First, calculate the **volume of distribution (Vd)** using the provided data: **Vd = Total Dose / Serum Concentration**. Converting units: 15 mg/dL = 150 mg/L. Therefore, Vd = 1500 mg / 150 mg/L = **10 L** (for the 100 kg subject).
- Since the Vd value is for a 100 kg person, Vd per kg = 10 L / 100 kg = **0.1 L/kg**. For the 60 kg patient, the Vd = 0.1 L/kg × 60 kg = **6 L**.
- The **loading dose = Target Serum Concentration × Vd / Bioavailability**. Converting target concentration: 10 mg/dL = 100 mg/L. Therefore: (100 mg/L × 6 L) / 1 = **600 mg**.
*300 mg*
- This value is obtained if an incorrect **Vd** or target concentration was used, potentially through miscalculation or incorrect unit conversion.
- For instance, if the **Vd** was inaccurately calculated at 3 L (instead of 6 L), this could lead to the incorrect answer.
*450 mg*
- This result might occur if the **Vd calculation** was flawed or if the target concentration was incorrectly interpreted.
- A potential error could involve using a Vd of 4.5 L which would result in 450 mg, or if the drug amount was simply prorated by weight without properly considering the Vd per kg.
*150 mg*
- This value suggests a significant error in the calculation of the **volume of distribution** or the target concentration.
- It might be obtained if the **Vd** was mistakenly taken as 1.5 L or if the dose was divided by the original serum concentration without accounting for the new patient's weight and desired concentration.
*1000 mg*
- This value is significantly higher than the correct answer, indicating an overestimation of the **Vd** or target concentration.
- It could result from using the original dose (1500 mg) and attempting to scale it incorrectly by weight alone (1500 mg × 60/100 = 900 mg, close to 1000), or if unit conversions were mishandled during the Vd determination.
Antimicrobial pharmacokinetics/pharmacodynamics US Medical PG Question 2: Six days after undergoing an elective hip replacement surgery, a 79-year-old man develops dysuria, flank pain, and fever. His temperature is 38.5°C (101.3°F). Examination shows marked tenderness in the right costovertebral area. Treatment with an antibiotic is begun, but his symptoms do not improve. Further evaluation shows that the causal organism produces an enzyme that inactivates the antibiotic via phosphorylation. An agent from which of the following classes of antibiotics was most likely administered?
- A. Macrolides
- B. Tetracyclines
- C. Aminoglycosides (Correct Answer)
- D. Glycopeptides
- E. Fluoroquinolones
Antimicrobial pharmacokinetics/pharmacodynamics Explanation: ***Aminoglycosides***
- **Aminoglycosides** are commonly inactivated by bacterial enzymes through **phosphorylation**, acetylation, or adenylation, leading to resistance.
- The patient's lack of improvement despite antibiotic treatment and the mechanism of inactivation point towards this class of antibiotics.
*Macrolides*
- **Macrolide resistance** typically involves mechanisms such as modification of the ribosomal binding site (e.g., methylation), drug efflux pumps, or enzymatic inactivation by esterases, not phosphorylation.
- While macrolides can treat various infections, their inactivation mechanism is different from what is described.
*Tetracyclines*
- **Tetracycline resistance** is primarily mediated by bacterial efflux pumps that actively transport the antibiotic out of the cell, or by ribosomal protection proteins that interfere with drug binding.
- **Enzymatic inactivation via phosphorylation** is not a characteristic resistance mechanism for tetracyclines.
*Glycopeptides*
- **Glycopeptide resistance**, particularly to vancomycin, is mainly associated with alterations in the cell wall precursor target (e.g., D-Ala-D-Lac modification), which prevents the antibiotic from binding.
- This mechanism is distinct from enzymatic phosphorylation of the antibiotic molecule itself.
*Fluoroquinolones*
- **Fluoroquinolone resistance** primarily arises from mutations in the genes encoding bacterial DNA gyrase and topoisomerase IV, or via efflux pumps.
- There is no significant mechanism of resistance involving direct enzymatic phosphorylation of fluoroquinolone drugs.
Antimicrobial pharmacokinetics/pharmacodynamics US Medical PG Question 3: An 18-year old college freshman presents to his university clinic because he has not been feeling well for the past two weeks. He has had a persistent headache, occasional cough, and chills without rigors. The patient’s vital signs are normal and physical exam is unremarkable. His radiograph shows patchy interstitial lung infiltrates and he is diagnosed with atypical pneumonia. The patient is prescribed azithromycin and takes his medication as instructed. Despite adherence to his drug regimen, he returns to the clinic one week later because his symptoms have not improved. The organism responsible for this infection is likely resistant to azithromycin through which mechanism?
- A. Mutation in topoisomerase II
- B. Methylation of ribosomal binding site
- C. Presence of a beta-lactamase
- D. Decreased binding to RNA polymerase
- E. Insertion of drug efflux pumps (Correct Answer)
Antimicrobial pharmacokinetics/pharmacodynamics Explanation: ***Insertion of drug efflux pumps***
- **Azithromycin** is a macrolide antibiotic that inhibits bacterial protein synthesis by binding to the **50S ribosomal subunit**.
- In **Mycoplasma pneumoniae** (the most common cause of atypical pneumonia in young adults), the **most common** mechanism of macrolide resistance is through **efflux pumps**, particularly the **mef genes**.
- These efflux pumps actively transport macrolides out of the bacterial cell, reducing intracellular drug concentration and conferring resistance.
- This mechanism is responsible for the majority of macrolide-resistant *M. pneumoniae* isolates worldwide.
*Methylation of ribosomal binding site*
- **Methylation** of the ribosomal binding site (specifically the **23S rRNA** via erm genes) does prevent azithromycin from binding effectively.
- While this is a valid macrolide resistance mechanism seen in organisms like *Streptococcus pneumoniae* and *Streptococcus pyogenes*, it is **less common** in *Mycoplasma pneumoniae*.
- Efflux pumps (mef) are the predominant mechanism in *M. pneumoniae* resistant strains.
*Mutation in topoisomerase II*
- **Topoisomerase II** (DNA gyrase) is the target of **fluoroquinolone antibiotics**, not macrolides.
- Mutations in this enzyme lead to resistance against fluoroquinolones, such as **ciprofloxacin**.
*Presence of a beta-lactamase*
- **Beta-lactamase enzymes** inactivate **beta-lactam antibiotics** (e.g., penicillin, cephalosporins) by hydrolyzing their beta-lactam ring.
- Additionally, *Mycoplasma pneumoniae* **lacks a cell wall**, making it inherently resistant to all beta-lactam antibiotics regardless of beta-lactamase production.
*Decreased binding to RNA polymerase*
- **RNA polymerase** is the target for antibiotics like **rifampin**, which inhibits bacterial transcription.
- Decreased binding to RNA polymerase would lead to rifampin resistance, not azithromycin resistance.
Antimicrobial pharmacokinetics/pharmacodynamics US Medical PG Question 4: A 26-year-old nurse presents 12 hours after she accidentally stuck herself with a blood-contaminated needle. She reported the accident appropriately and now seeks post-exposure prophylaxis. She does not have any complaints at the moment of presentation. Her vital signs include: blood pressure 125/80 mm Hg, heart rate 71/min, respiratory rate 15/min, and temperature 36.5℃ (97.7℉). Physical examination is unremarkable. The nurse has prescribed a post-exposure prophylaxis regimen which includes tenofovir, emtricitabine, and raltegravir. How will tenofovir change the maximum reaction rate (Vm) and Michaelis constant (Km) of the viral reverse transcriptase?
- A. Vm will decrease, Km will increase
- B. Vm and Km will both decrease
- C. Vm will stay the same, Km will increase
- D. Vm and Km will both increase
- E. Vm will decrease, Km will stay the same (Correct Answer)
Antimicrobial pharmacokinetics/pharmacodynamics Explanation: ***Vm will decrease, Km will stay the same***
- **Tenofovir** is a **nucleotide reverse transcriptase inhibitor (NtRTI)** that acts as a **competitive substrate analog**. Once phosphorylated to **tenofovir diphosphate**, it competes with natural deoxyadenosine triphosphate (dATP) for incorporation into the viral DNA chain.
- Upon incorporation, tenofovir acts as a **chain terminator** because it lacks a 3'-hydroxyl group necessary for further DNA elongation. This **irreversibly inactivates** the enzyme-DNA complex, effectively reducing the **maximum reaction rate (Vm)** by decreasing the amount of functional enzyme available.
- Since tenofovir competes with natural nucleotides but doesn't affect the enzyme's affinity for its natural substrates, the **Michaelis constant (Km) remains unchanged**. The inhibition pattern shows characteristics of competitive inhibition with irreversible chain termination.
*Vm will decrease, Km will increase*
- This pattern is characteristic of a **mixed inhibitor**, where the inhibitor can bind to both the free enzyme and the enzyme-substrate complex, reducing Vm while also decreasing substrate affinity (increasing Km).
- While tenofovir does reduce Vm through chain termination, it does not significantly alter the enzyme's affinity for natural nucleotide substrates. Tenofovir diphosphate **competes directly** with dATP rather than binding to an allosteric site, so Km remains unchanged rather than increasing.
*Vm and Km will both decrease*
- This effect is typical of an **uncompetitive inhibitor**, which binds only to the **enzyme-substrate complex**. Uncompetitive inhibitors decrease both Vm and Km, implying increased apparent substrate affinity.
- Tenofovir does not function as an uncompetitive inhibitor. As a **nucleotide analog**, it competes for the active site and gets incorporated into DNA, causing chain termination. This mechanism does not involve preferential binding to the enzyme-substrate complex that would decrease Km.
*Vm will stay the same, Km will increase*
- This describes **pure reversible competitive inhibition**, where the inhibitor competes with substrate for the active site but can be overcome by increasing substrate concentration, leaving Vm unchanged.
- While tenofovir diphosphate does **compete with natural nucleotides**, it acts as a **suicide substrate** that causes irreversible chain termination once incorporated. This **permanently inactivates** the enzyme-DNA complex, reducing the pool of functional enzyme and thus decreasing Vm, distinguishing it from simple reversible competitive inhibition.
*Vm and Km will both increase*
- An increase in both Vm and Km is not a standard pattern for enzyme inhibition and would suggest **reduced substrate affinity** with paradoxically increased catalytic capacity, which is inconsistent with any inhibitory mechanism.
- This scenario contradicts the **intended therapeutic effect** of tenofovir, which is to inhibit HIV reverse transcriptase activity and prevent viral replication, not to enhance enzyme function.
Antimicrobial pharmacokinetics/pharmacodynamics US Medical PG Question 5: An experimental drug, ES 62, is being studied. It prohibits the growth of vancomycin-resistant Staphylococcus aureus. It is highly lipid-soluble. The experimental design is dependent on a certain plasma concentration of the drug. The target plasma concentration is 100 mmol/dL. Which of the following factors is most important for calculating the appropriate loading dose?
- A. Volume of distribution (Correct Answer)
- B. Half-life of the drug
- C. Therapeutic index
- D. Clearance of the drug
- E. Rate of administration
Antimicrobial pharmacokinetics/pharmacodynamics Explanation: **Volume of distribution**
- The **loading dose** is primarily determined by the desired **plasma concentration** and the **volume of distribution (Vd)**, as it reflects how extensively a drug is distributed in the body.
- The formula for loading dose is: Loading Dose = (Target Plasma Concentration × Vd).
*Half-life of the drug*
- The **half-life** is crucial for determining the **dosing interval** and the time it takes to reach **steady-state concentrations**, not the initial loading dose.
- It reflects the rate at which the drug is eliminated from the body.
*Therapeutic index*
- The **therapeutic index** is a measure of a drug's relative safety, indicating the ratio between the **toxic dose** and the **effective dose**.
- While important for drug safety, it does not directly determine the magnitude of the loading dose itself.
*Clearance of the drug*
- **Clearance** is the rate at which the drug is removed from the body and is a primary determinant of the **maintenance dose** required to sustain a desired plasma concentration.
- It does not directly calculate the initial loading dose needed to achieve an immediate target concentration.
*Rate of administration*
- The **rate of administration** (e.g., infusion rate) primarily influences how quickly the drug reaches its target concentration, but not the total quantity of drug needed for the initial loading dose.
- It affects the kinetics of how the loading dose achieves the target concentration, rather than defining the dose amount.
Antimicrobial pharmacokinetics/pharmacodynamics US Medical PG Question 6: A scientist is studying the mechanisms by which bacteria become resistant to antibiotics. She begins by obtaining a culture of vancomycin-resistant Enterococcus faecalis and conducts replicate plating experiments. In these experiments, colonies are inoculated onto a membrane and smeared on 2 separate plates, 1 containing vancomycin and the other with no antibiotics. She finds that all of the bacterial colonies are vancomycin resistant because they grow on both plates. She then maintains the bacteria in liquid culture without vancomycin while she performs her other studies. Fifteen generations of bacteria later, she conducts replicate plating experiments again and finds that 20% of the colonies are now sensitive to vancomycin. Which of the following mechanisms is the most likely explanation for why these colonies have become vancomycin sensitive?
- A. Point mutation
- B. Gain of function mutation
- C. Viral infection
- D. Plasmid loss (Correct Answer)
- E. Loss of function mutation
Antimicrobial pharmacokinetics/pharmacodynamics Explanation: ***Plasmid loss***
- The initial **vancomycin resistance** in *Enterococcus faecalis* is often mediated by genes located on **plasmids**, which are extrachromosomal DNA.
- In the absence of selective pressure (vancomycin), bacteria that lose the plasmid (and thus the resistance genes) have a **growth advantage** over those that retain the energetically costly plasmid, leading to an increase in sensitive colonies over generations.
*Point mutation*
- A **point mutation** typically involves a change in a single nucleotide and could lead to loss of resistance if it occurred in a gene conferring resistance.
- However, since there was no selective pressure for loss of resistance, it is less likely that 20% of the population would acquire such a specific point mutation to revert resistance.
*Gain of function mutation*
- A **gain of function mutation** would imply that the bacteria acquired a *new* advantageous trait, not the *loss* of resistance.
- This type of mutation would not explain why some colonies became sensitive to vancomycin after the drug was removed.
*Viral infection*
- **Viral infection** (bacteriophages) can transfer genes through transduction or cause bacterial lysis, but it's not the primary mechanism for a widespread reversion of resistance in the absence of antibiotic pressure.
- It would not explain the observed increase in vancomycin-sensitive colonies due to evolutionary pressure.
*Loss of function mutation*
- While a **loss of function mutation** in a gene conferring resistance could lead to sensitivity, it's generally less likely to explain a 20% shift without selective pressure than **plasmid loss**.
- Plasmids are often unstable and are easily lost in the absence of selection, whereas a specific gene mutation causing loss of function would need to arise and become prevalent in the population.
Antimicrobial pharmacokinetics/pharmacodynamics US Medical PG Question 7: A 67-year-old male with a past medical history of diabetes type II, obesity, and hyperlipidemia presents to the general medical clinic with bilateral hearing loss. He also reports new onset vertigo and ataxia. The symptoms started a day after undergoing an uncomplicated cholecystectomy. If a drug given prophylactically just prior to surgery has caused this patient’s symptoms, what is the mechanism of action of the drug?
- A. Formation of free radical toxic metabolites that damage DNA
- B. Inhibition of the formation of the translation initiation complex (Correct Answer)
- C. Inhibition of DNA gyrase
- D. Inhibition of cell wall synthesis
- E. Inhibition of DNA-dependent RNA polymerase
Antimicrobial pharmacokinetics/pharmacodynamics Explanation: **Correct: Inhibition of the formation of the translation initiation complex**
- The symptoms of **bilateral hearing loss**, **vertigo**, and **ataxia** point to **ototoxicity** and **vestibulotoxicity**, which are classic side effects of **aminoglycoside antibiotics**.
- Aminoglycosides, such as gentamicin, are known to **inhibit bacterial protein synthesis** by binding to the **30S ribosomal subunit**, thereby **inhibiting the formation of the translation initiation complex**. They are sometimes used prophylactically, though less commonly for cholecystectomy.
*Incorrect: Formation of free radical toxic metabolites that damage DNA*
- This mechanism is characteristic of **nitrofurans** (e.g., nitrofurantoin) and some **antimalarials**, which are not typically used for surgical prophylaxis.
- While these drugs can cause various adverse effects, this specific mechanism does not lead to the described triad of ototoxicity and vestibulotoxicity.
*Incorrect: Inhibition of DNA gyrase*
- This is the mechanism of action for **fluoroquinolone antibiotics** (e.g., ciprofloxacin, levofloxacin).
- While fluoroquinolones can cause adverse effects like tendinopathy and CNS disturbances, they are not typically associated with the pronounced ototoxicity and vestibulotoxicity seen in this patient.
*Incorrect: Inhibition of cell wall synthesis*
- This is the mechanism of action for **beta-lactam antibiotics** (e.g., penicillin, cephalosporins) and **vancomycin**, which are common choices for surgical prophylaxis.
- Though some of these drugs can have side effects (e.g., vancomycin's "red man syndrome" or ototoxicity in specific cases), the combination of bilateral hearing loss, vertigo, and ataxia is not their characteristic adverse effect profile.
*Incorrect: Inhibition of DNA-dependent RNA polymerase*
- This is the mechanism of action for **rifamycins** (e.g., rifampin).
- Rifampin is primarily used for tuberculosis and some other serious infections, not typically for routine surgical prophylaxis, and its side effect profile does not include this specific constellation of ototoxicity and vestibulotoxicity.
Antimicrobial pharmacokinetics/pharmacodynamics US Medical PG Question 8: A 51-year-old man is admitted to the hospital because of a 2-day history of fever, nausea, and abdominal pain. His temperature is 39.4°C (102.9°F) and pulse is 106/min. Physical examination shows tenderness in the right upper quadrant. Blood cultures grow nonhemolytic, gram-positive cocci that grow in hypertonic saline. Antibiotic sensitivity testing of the isolated organism shows that gentamicin has a minimum inhibitory concentration (MIC) of 16 μg/mL. The addition of ampicillin, which has an MIC of 2 μg/mL alone, decreases the MIC of gentamicin to 0.85 μg/mL. The decrease in the MIC of gentamicin with the addition of ampicillin is most likely due to which of the following mechanisms?
- A. Increase in the intracellular uptake of gentamicin (Correct Answer)
- B. Sequential block of essential micronutrient synthesis
- C. Inhibition of the acetylation of gentamicin
- D. Additive bacteriostatic effect of ampicillin
- E. Stabilization of gentamicin binding at the target site
Antimicrobial pharmacokinetics/pharmacodynamics Explanation: ***Increase in the intracellular uptake of gentamicin***
- This scenario describes **synergism**, where ampicillin (a cell wall synthesis inhibitor) damages the bacterial cell wall, allowing better penetration of gentamicin (an aminoglycoside) into the cell. Aminoglycosides require **active transport** across the bacterial cell membrane, which is enhanced by cell wall disruption.
- The significant reduction in gentamicin's MIC when combined with ampicillin demonstrates that ampicillin facilitates gentamicin's access to its **ribosomal target**, leading to a more potent bactericidal effect.
*Sequential block of essential micronutrient synthesis*
- **Sequential block** typically refers to the synergistic action of drugs like trimethoprim and sulfamethoxazole, which inhibit different steps in the **folic acid synthesis pathway**.
- This mechanism is not directly applicable to the combination of a cell wall inhibitor and an aminoglycoside, which target different cellular processes.
*Inhibition of the acetylation of gentamicin*
- **Acetylation** is a common mechanism of aminoglycoside inactivation by bacterial enzymes (aminoglycoside-modifying enzymes).
- Ampicillin does not primarily work by inhibiting these enzymes; its main action is on **peptidoglycan synthesis** in the bacterial cell wall.
*Additive bacteriostatic effect of ampicillin*
- Ampicillin is a **bactericidal antibiotic** that works by inhibiting cell wall synthesis, not typically bacteriostatic in its primary action, especially against susceptible organisms.
- The dramatic drop in gentamicin's MIC suggests more than just an additive bacteriostatic effect; it indicates a **synergistic interaction** leading to enhanced bactericidal activity.
*Stabilization of gentamicin binding at the target site*
- Gentamicin binds to the bacterial **30S ribosomal subunit**, inhibiting protein synthesis.
- Ampicillin's mechanism of action is on the **bacterial cell wall**, and it does not directly stabilize the binding of gentamicin to the ribosome. Its role is to facilitate gentamicin's entry into the cell.
Antimicrobial pharmacokinetics/pharmacodynamics US Medical PG Question 9: An investigator is studying a strain of bacteria that retains a blue color after crystal violet dye and acetone are applied. The bacteria are inoculated in a petri dish containing hypotonic saline. After the addition of an antibiotic, the bacteria swell and rupture. This antibiotic most likely belongs to which of the following classes?
- A. Macrolide
- B. Cephalosporin (Correct Answer)
- C. Sulfonamide
- D. Fluoroquinolone
- E. Tetracycline
Antimicrobial pharmacokinetics/pharmacodynamics Explanation: ***Cephalosporin***
- This scenario describes a **Gram-positive bacterium** (retains blue color) which, after antibiotic treatment, swells and lyses in a hypotonic solution. This indicates a defect in the **peptidoglycan cell wall**.
- **Cephalosporins** are **β-lactam antibiotics** that inhibit bacterial cell wall synthesis by interfering with **peptidoglycan cross-linking**, leading to osmotic lysis in hypotonic environments.
*Macrolide*
- Macrolides like **azithromycin** and **erythromycin** inhibit bacterial **protein synthesis** by binding to the 50S ribosomal subunit.
- They do not directly target the cell wall, so they would not cause immediate osmotic lysis in this manner.
*Sulfonamide*
- Sulfonamides inhibit bacterial **folic acid synthesis** by acting as a competitive inhibitor of dihydropteroate synthase, disrupting DNA and RNA production.
- Their mechanism of action does not involve direct cell wall disruption or osmotic lysis.
*Fluoroquinolone*
- Fluoroquinolones interfere with bacterial **DNA replication and transcription** by inhibiting **DNA gyrase** and **topoisomerase IV**.
- This class of antibiotics does not primarily target the cell wall, and therefore would not lead to prompt osmotic swelling and rupture.
*Tetracycline*
- Tetracyclines inhibit bacterial **protein synthesis** by binding to the 30S ribosomal subunit, preventing the attachment of aminoacyl-tRNA.
- They do not affect the cell wall, so they would not cause the observed osmotic lysis.
Antimicrobial pharmacokinetics/pharmacodynamics US Medical PG Question 10: An experimental infusable drug, X729, is currently being studied to determine its pharmacokinetics. The drug was found to have a half life of 1.5 hours and is eliminated by first order kinetics. What is the minimum number of hours required to reach a steady state concentration of >90%?
- A. 6 (Correct Answer)
- B. 3
- C. 7.5
- D. 1.5
- E. 4.5
Antimicrobial pharmacokinetics/pharmacodynamics Explanation: ***6***
- For a drug eliminated by **first-order kinetics**, approximately **4 to 5 half-lives** are required to reach **steady-state concentration**.
- To reach >90% of steady-state, at least **4 half-lives** are needed, where **93.75%** of the steady state is achieved.
- The time taken would be **4 half-lives × 1.5 hours/half-life = 6 hours**, making this the **minimum time** to exceed 90%.
*3*
- This represents only **2 half-lives** (2 × 1.5 hours = 3 hours), which would achieve roughly **75%** of the steady-state concentration.
- This is insufficient to reach >90% of the steady-state concentration.
*7.5*
- This time point represents **5 half-lives** (5 × 1.5 hours = 7.5 hours), which would achieve approximately **97%** of the steady-state concentration.
- While this does exceed 90%, the question asks for the **minimum** number of hours required, and 90% is already exceeded at 6 hours (4 half-lives).
*1.5*
- This is only **1 half-life**, which would achieve approximately **50%** of the steady-state concentration.
- This is far too early to reach a >90% steady-state concentration.
*4.5*
- This represents **3 half-lives** (3 × 1.5 hours = 4.5 hours), achieving approximately **87.5%** of the steady-state concentration.
- While close to 90%, it does not quite reach "greater than 90%".
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