Ex. 2 Practice Questions Flashcards
L1: T/F: Higher dose is expected to show greater drug accumulation (i.e. higher accumulation index)
False - greater not dose dependent
L1: When you switch dosage regimen from 10mg q12h to 10mg 24h, what happens to: Fluctuation?
Goes up
L1: When you switch dosage regimen from 10mg q12h to 10mg 24h, what happens to:
Average CSS?
Lower
Because CSSave is (dose/T)/CL
L1: When you switch dosage regimen from 10mg q12h to 10mg 24h, what happens to:
TSS
Same
L1: When you switch dosage regimen from 10mg q12h to 10mg 24h, what happens to: Accumulation index?
Lower
L3: “A” (close to top) is called the distribution phase
True
L3: “B” (mid-line) is called the elimination phase
True
L3: The data show a drug following a one-compartment model (slight curve at beginning, then linear throughout)
False - two compartment
L3: This happens (bi-phasic) because drug distribution to/from tissue is slow
True
L4: After IV admin, Drug A and Drug B show MRT values of 1 and 5 hr respectively. Which drug is eliminated faster?
- A
- B
- Not enough info given
Drug A
MRT is mean residence time; lower time = faster elimination
L4: After 1 gram of drug C is admin intravenously, the following concentration time profile is obtained:
(Straight line, no curve)
T/F
1: AUC can be estimated
2. AUMC can be estimated
3. MRT can be estimated
4. CL can be estimated
5. Vdss can be estimated
- True
- True
- True
- True
- True
L4: After 1 gram of drug C is admin intravenously, the following concentration time profile is obtained:
(Curvy line)
T/F
1: AUC can be estimated
2. AUMC can be estimated
3. MRT can be estimated
4. CL can be estimated
5. Vdss can be estimated
- True
- True
- True
- True
- True
L5: What is rate-limiting step that determines metabolite amount in the body?
Kf = 0.0.5
K(m) = 1.2
Kf = 0.05 formation of metabolite (slower step)
L5: What is the apparent t/12 of parent drug from the body?
Kf = 0.05
k(m) = 1.2
T1/2 = 0.693/k
0.693/0.05 = 14 hr
parent drug = Kf
L5: What is the apparent t1/2 of metabolite from the body after administration of the parent drug?
Kf = 0.05
k(m) = 1.2
0.693/k
0.693/0.05hr
L5: What would be the true t1/2 of metabolite from the body (i.e., t1/2 obtained by administering the metabolite)
Kf = 0.05
K(m) = 1.2
0.693/k= 0.693/1.2 = 0.6 hr
L5: What is the rate-limiting step that determines metabolite amount in the body?
Kf = 1.2
K(m) = 0.05
Elimination of metabolites (0.05)
L5: What is the apparent t1/2 of parent drug from the body?
t1/2 = 0.693/k
Kf = 1.2
K(m) = 0.05
t1/2 = 0.693/k
0.693/1.2 = 0.6 hr
L5: What is the apparent t1/2 of metabolite from the body after administration of parent drug?:
Kf = 1.2
K(m) = 0.05
t1/2= 0.693/k
0.693/0.05 = 14 hr
L5: What would be the true t1/2 of metabolite from the body (i.e., t1/2 obtained by administering the metabolite)
Kf = 1.2
K(m) = 0.05
t1/2 = 0.693/k
0.693/0.05 = 14 hr
L5: Q1 Tolbutamide is a low EH drug, and its fe = 0. What would happen to the half-life of tolbutamide when it is combined with rifampin, an inducer of CYP2C9 expression?
Rifampin will increase CYP2C9 level, increase the rate of formation, increase clearance, increase K, =
t1/2 will decrease
L5: What would happen to half-life of hydroxytolbutamide when tolbutamide is combined with rifampin, an inducer of CYP2C9 expression?
Decreased t1/2
Governed by formation
L5: Shown is a graph of formation rate limited
T/F:
1.This is likely represents a kinetic profile of pro-drugs
- It demonstrates “metabolite formation rate-limited” kinetics
- The “true” t1/2 of metabolite (i.e. the t1/2 obtained after administration of metabolite, assuming its commercial availability) would be much shorter than t1/2 estimated from this graph
- This occurs when elimination rate of metabolite is faster than its formation rate
- False
- True
- True
- True
L5: Shown is a graph that is elimination rate limited
T/F:
- This likely represents a kinetic profile of pro-drugs
- It demonstrates “metabolite formation rate-limited kinetics”
3.The “true” t/2 of metabolite (i.e. the t1/2 obtained after admin of metabolite, assuming its commercial availability) would be much shorter than the t1/2 estimated from this graph
- This occurs when elimination rate of metabolite is faster than its formation rate
T/F: Drugs of High EH are associated with low F. A prodrug that has a high EH would exhibit minimal/no pharmacological activity after oral dosing
- True
- False
- False
- True
- False
L6: T/F: Inhibition of P-gp in cancer cell is expected to improve anticancer drug efficacy by increasing intracellular drug concentrations
True
L6: T/F inhibition of Pgp in brain is expected to increase the penetration of Pgp substrates into brain
True
L6: T/F: HIV-associated Neurocognitive Disorders occur when HIV enters the nervous system and impacts the health of nerve cell. Combining HIV Protease inhibitors (p-gp susbtrates) with P-gp inhibitors will likely increase brain distribution of anti-HIV drugs
True
L6: T/F: Combining paclitaxel with a P-gp inhibitor will likely decrease biliary excretion of paclitaxel
True
Biliary excretion major form of elimination - inhibit pgp
L6: T/F: Biliary excretion of paclitaxel is its major elimination route. Combining paclitaxel with a P-gp inhibitor will likely decrease paclitaxel elimination from the body and increase systemic drug concentration
True
L6: T/F: P-gp inhibitors will likely increase the passage of P-gp substrates across placenta, leading to increased fetal drug levels
True
L6: T/F: OATP1B1 inhibition will likely decrease the intrahepatic concentration OATP1B1 substrates
True
L6: Which of the following is NOT the expected biological consequence of a P-gp substrate drug when it is co-administered with a pgp inhibitor?
A. Increased brain distribution
B. Increased biliary excretion
C. Increased intestinal absorption
D. Increased drug transfer to fetus
B - increased biliary excretion
L6: which one of the following transporters is responsible for increased absorption of valacyclovir as compared to acyclovir?
A. Pgp
B. OATP1B1
C. PEPT1
D. OCT1
C - PEPTI
L6: Which one of the following transporters is responsible for hepatic uptake of statins?
A. Pgp
B. OATP1B1
C. PEPT1
D. OCT1
B. OATP1B1
L6: Genetic polymorphisms of OATP1B1 that are associated with nonfunctional transporter activity would lead to:
A. Increased hepatoxicity of statins
B. Decreased efficacy of statins
C. Decreased myopathy of statins
E. None of the above
B - decreased efficacy of statins
