أسئلة السابعة فارما PPPM (قبل التعديل)

How is the total clearance of a drug from the body typically determined?

A drug is metabolized by the liver and excreted by the kidneys. If the hepatic clearance is 3 L/h and the renal clearance is 1 L/h, what is the total body clearance?

Which factor does not directly influence the clearance of a drug by an organ?

If a drug's clearance rate doubles while the volume of distribution remains constant, how will the elimination half-life change?

Which of the following best describes the process of drug excretion?

A drug's elimination half-life is affected by the rate of both metabolism and excretion. If a patient has impaired kidney function, what effect would this MOST likely have on a drug primarily cleared renally?

A new drug is being developed. In preclinical studies, the liver clearance is high, yet the drug has a long half-life in humans. What is a plausible explanation?

Which of the following factors would MOST significantly affect the glomerular filtration rate (GFR) and subsequent renal excretion of a drug?

Active tubular secretion in the kidney is a key elimination process for some drugs. If Drug A and Drug B compete for the same active transport system in the renal tubules, what is the MOST likely outcome if both are administered concurrently?

A patient with liver cirrhosis may have impaired drug metabolism. How would this MOST likely affect the oral bioavailability of a drug that undergoes significant first-pass metabolism?

A patient experiences a side effect from a drug. Their plasma concentration is significantly higher than the expected steady-state concentration (Cpss). What is the most likely cause of this side effect?

A patient on a maintenance dose of a drug develops a new side effect. Upon measuring plasma drug concentration, it is found to be approximately equal to the expected steady-state concentration (Cpss). What does this suggest about the cause of the side effect?

A patient presents with symptoms of drug toxicity. Their plasma concentration is measured and found to be substantially higher than the expected steady-state concentration (Cpss). Which of the following actions is most appropriate?

A patient on a stable drug regimen complains of a new side effect. Plasma drug concentration is within the expected therapeutic range, but the patient has also recently been diagnosed with a kidney disease. How might the kidney disease be contributing to the side effect?

A drug's steady-state concentration (Cpss) is achieved in a patient. However, they unexpectedly develop a severe adverse reaction. Assuming adherence and proper dosage, what is the MOST probable cause of this reaction?

To increase the steady-state plasma concentration (Cpss) of a drug from 75 mg/L to 150 mg/L, what initial dose should be administered, assuming a maintenance dose of 2/3 x target Cpss is used?

A drug is administered at a certain dose, resulting in a Cpss of 150 mg/L. If the decision is made to reduce the Cpss to 75 mg/L, what dosage regimen should be followed?

A medication requires a target Cpss of 'X' mg/L to be effective. To reach the target Cpss rapidly, specifically within one half-life, what is the appropriate loading dose to administer initially?

Why is it necessary to wait approximately five half-lives after adjusting a drug's dosage to achieve a new steady-state concentration (Cpss)?

A patient is receiving a drug with a maintenance dose of 80 mg every half-life, achieving a steady-state plasma concentration. If the decision is made to increase the Cpss by 50%, what should the new maintenance dose be?

A drug exhibits saturation kinetics. What happens to the rate of elimination as the plasma concentration of the drug increases significantly?

For a drug that follows first-order kinetics, how does the rate of elimination change with increasing plasma concentration?

A new drug is being tested. At low doses, it follows first-order kinetics, but at high doses, the elimination process shifts to zero-order kinetics. Which statement explains this change?

A drug is administered intravenously. Initially, its elimination follows first-order kinetics. After several hours, the elimination kinetics switch to zero-order. What is the most likely reason for this change?

For a drug that follows zero-order kinetics, if the plasma concentration is doubled, what happens to the amount of drug eliminated per unit of time?

How does the half-life ($t_{1/2}$) of a drug change as the dose increases to 150 mg, assuming non-linear pharmacokinetics?

A drug transitions from first-order to zero-order kinetics as its concentration increases. Which statement accurately describes this transition's effect on the elimination rate?

A patient takes a drug that exhibits first-order elimination at low doses but shifts to zero-order elimination at high doses. What is the most likely cause of this kinetic shift?

A drug's plasma concentration declines non-linearly with increasing doses. How does this affect the predictability of drug accumulation with repeated dosing?

Aspirin exhibits first-order elimination at low doses and zero-order elimination at high doses. Which of the following best describes how to adjust the dosing regimen to maintain therapeutic drug levels and avoid toxicity?

A drug is administered via constant intravenous infusion. After approximately how many half-lives will the plasma concentration (Cp) approach steady-state?

A drug with a half-life of 6 hours is administered as a continuous infusion. Approximately how long will it take for the drug to reach 75-80% of its steady-state plasma concentration?

A drug is administered via continuous intravenous infusion, and after 24 hours, the plasma concentration is measured to be 60% of the expected steady-state concentration. What is the approximate half-life of this drug?

A constant infusion of a drug is started. After achieving steady-state plasma concentrations, the infusion rate is doubled. How will the time required to reach the new steady-state compare to the time it took to reach the initial steady-state?

A drug is administered via continuous infusion to a patient with impaired renal function, resulting in a prolonged half-life. How would this altered half-life affect the time required to reach steady-state plasma concentrations, compared to a patient with normal renal function?

In a patient with compromised liver function, which route of drug elimination would be least affected?

A drug is primarily eliminated through saliva and sweat. What implications does this have for drug dosing in patients with impaired renal function?

A drug is known to be significantly excreted in breast milk. Which of the following factors would MOST increase the infant's exposure to the drug?

Why is it clinically important to understand the primary route of elimination for a drug when prescribing to a patient with organ dysfunction?

A drug undergoes significant first-pass metabolism in the liver and is also excreted in bile. In a patient with both hepatic impairment and cholestasis (reduced bile flow), what is the MOST likely outcome?

Why does drug accumulation frequently occur when drug concentrations increase?

What is the primary implication of non-linear pharmacokinetics regarding drug dosing?

A drug exhibits saturation kinetics. How will the area under the plasma concentration-time curve (AUC) change as the dose is increased?

A drug that follows Michaelis-Menten kinetics is administered. Which of the following changes would MOST likely cause a transition from first-order to zero-order kinetics?

Under what specific condition is a drug considered to have reached a steady-state level in plasma?

What is the clinical significance of achieving a steady-state concentration of a drug in a patient's plasma?

How does the predictability of achieving and maintaining therapeutic drug concentrations change when a drug exhibits non-linear pharmacokinetics?

A patient has been receiving a drug at a constant dose for a period slightly shorter than five half-lives. Which of the following statements accurately describes the drug concentration in the plasma?

A physician notices that a patient's symptoms fluctuate significantly, despite consistent drug dosing. Assuming adherence, what aspect of pharmacokinetics should the physician investigate first to explain the variability?

In what scenario would achieving steady-state be MOST critical for therapeutic efficacy?

A drug transitions from first-order to zero-order kinetics as its concentration increases. How does this affect the predictability of drug accumulation with repeated dosing?

To rapidly achieve a target steady-state plasma concentration (Cpss) of 75 mg/L for a drug, what initial dosing strategy should be employed, assuming a maintenance dose of 50 mg is used after one half-life?

A drug requires a Cpss of 75 mg/L. If the maintenance dose needed to sustain this Cpss is approximately 50 mg, and a loading dose of 100mg is administered, how long will it take to reach the Cpss if the drug follows first-order kinetics?

A medication requires a target Cpss of 75 mg/L to be effective. If the decision is made to administer a loading dose of 100mg, followed by a maintenance dose of 50 mg after one half-life, how does this strategy primarily affect the time to reach the target Cpss?

A drug is administered with a loading dose to achieve a Cpss of 75 mg/L, followed by a maintenance dose of 50 mg. Assuming the half-life of the drug is 4 hours, how long after the loading dose should the first maintenance dose be administered to maintain the target Cpss?

A patient needs to achieve a Cpss of 75 mg/L rapidly. A loading dose of 100 mg is given, followed by a maintenance dose of 50 mg after one half-life. What is the MOST critical assumption about the drug's pharmacokinetics that justifies this approach?