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Foundations > Exam 1: Pharm > Flashcards

Exam 1: Pharm Flashcards

1
Q

Effect of inducers on pharmacokinetic/dynamic parameters

A

REDUCED t1/2
INCREASED Ke
INCREASED Cl

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2
Q

Effect of inhibitors on pharmacokinetic/dynamic parameters

A

INCREASED t1/2
REDUCED Ke
REDUCED Cl

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3
Q

Relative duration and onset of inducers?

A

Slow onset, long duration. Liver must synthesize new hepatic enzymes (relatively slow process), but they persist relatively long time.

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4
Q

Relative duration and onset of inhibitors?

A

Fast onset, short duration. No synthesis required: inhibitors competitively/noncompetitively inhibit a specific hepatic enzyme’s function. Once these are knocked off or degraded, though, function returns to baseline quickly.

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5
Q

Formula for half-life given Ke

A

T1/2 = (0.693/Ke)

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6
Q

Formula for half-life given Vd or Cl

A

T1/2 = (0.693)(Vd/Cl)

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7
Q

Relationship between T1/2 and Cl?

A

Inverse: as Cl increases, half-life decreases. As Cl decreases, half-life increases.

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8
Q

Relationship between T1/2 and Vd?

A

Direct: as Vd increases, half-life increases. As Vd decreases, half-life decreases.

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9
Q

What is the function of an inducer?

A

Stimulates the liver to create more hepatic enzyme, resulting in faster biotransformation of the associated substrate. (5 cups of coffee will feel like 1 in presence of inducer)

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10
Q

What is the function of an inhibitor?

A

Competitively and noncompetitively inhibits function of an hepatic enzyme, resulting in slower biotransformation. (1 cup of coffee will feel like 5 in presence of inhibitor)

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11
Q

What is the result of biotransformation?

A

Drug becomes more water soluble and more suitable for elimination, sometimes via Phase I and/or Phase II biotransformation

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12
Q

Phase I Biotransformation is…:

A

“Non-synthetic” or “preparatory”: bonds are changed, functional groups are eliminated, etc. Nothing is added. Prepares molecule for elimination or for Phase II biotransformation. Might result in an active metabolite.

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13
Q

Phase II Biotransformation is…:

A

“Synthetic”: something is added to molecule, resulting in it being more water soluble.

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14
Q

Relationship between loading dose and Cl?

A

Nothing! Trick question. Loading dose doesn’t care about clearance.

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15
Q

% of drug eliminated after 1, 2, 3, 4, and 5 half-lives

A

50%; 75%; 87.5%; 93.75%; 97% elimination (consider drug eliminated after 5th half-life)

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16
Q

Multiple to find original administered dose after 1, 2, 3, 4, or 5 half-lives:

A

Current amount in body x (2; 4; 8; 16; or 32) = original administered dose

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17
Q

In 70 kg man, what are some representative VD of different compartments?

A

42 L total body water: 28 L intracellular volume + 14 L extracellular volume.
Of extracellular: 10 L interstitial volume + 4 L plasma volume.

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18
Q

If Vd exceeds total body volume, what can be inferred?

A

If VD exceeds 42 L (total body volume) or the volume of any single compartment, we can assume the drug distributes widely into tissue. Especially true of lipid-soluble drugs, which can distribute into fat.

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19
Q

If the peak concentration of a drug after one half-life is measured at 2mg/L and it is administered at a frequency equal to its half-life, what will its concentration be when it reaches steady state concentration? How long will that take?

A

Css will be reached in 5 half-lives and will peak at 4 mg/L.

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20
Q

If the trough concentration of a drug after one half-life is measured at 0.5mg/L and it is administered at a frequency greater than its half-life, what will its concentration be when it reaches steady state concentration? How long will that take?

A

Steady state will be reached in 5 half-lives and will trough at a level greater than 1mg/L.

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21
Q

What are the determining factors of drug accumulation?

A

Dosing interval and half-life. Half-life is in turn dependent on clearance and volume of distribution.

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22
Q

What are the units of clearance?

A

L/hr

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23
Q

What are the units of concentration?

A

mg/L

24
Q

What are the units of maintenance dose rates?

A

mg/hr

25
Q

How does clearance affect maintenance dose frequency and accumulation?

A

Accumulation is dependent on half-life and half-life is dependent on clearance. A drug’s half-life will shorten as the rate of clearance increases, which means that dosing frequency will increase.

26
Q

Relate Cl to AUC:

A

Cl = Dose/AUC

27
Q

Calculate maintenance dose

A

MD = (Css)(Cl) / F

28
Q

A patient who has kidney disease MUST be administered a drug that is cleared 30% by the liver. What impact can be expected?

A

This drug will clear ~70% through the kidneys, which are in a diseased state. This will reduce rate of elimination, and therefore Cl. This in turn will increase the half-life of the drug. Since Cl is reduced, we should expect that a lower maintenance dose will be needed at longer intervals to maintain Css.

29
Q

A patient consumes a large, fatty meal before taking a drug. How will this impact drug absorption?

A

A large meal will cause an initial increase in rate of gastric emptying, and then a period of decreased emptying. The high fat content will result in a decreased emptying rate. This (net) decrease in gastric emptying will slow drug absorption, as drugs are absorbed primarily in the small intestine.

30
Q

How does viscosity impact gastric emptying?

A

Increased viscosity slows emptying.

31
Q

Do liquids or solids empty more quickly from the stomach to the small intestine?

A

Liquids.

32
Q

How does osmotic pressure impact gastric emptying?

A

Slows it.

33
Q

Name 5 drugs that slow gastric emptying, and two that speed it.

A

Opioids, anticholinergics, ethanol, bile salts, and acidification slow gastric emptying.
Bicarbonate and metoclopramide speed gastric emptying.

34
Q

8 factors that impact drug absorption:

A

Molecular weight: less permeable at >350 g/mole
Blood flow: faster in sm intestine vs stomach
Solubility: Aq > oil solutions > suspensions > solids
Concentration
Disintegration and dissolution
Partition Coefficient (how a substance distributes itself between two immiscible solvents – water and octanol) ie: lipid solubility (greater lipid solubility = extensive distribution)
Transporters involved
pH partition theory: uncharged are able to move compartments

35
Q

Your patient has a mental illness and has been noncompliant with their medication, claiming that taking it twice per day is too much to remember so they take a double dose in the morning (when they remember). The drug has been ineffective for them since. What kind of formulation might work better for this patient?

A

A modified release preparation with a slower absorption could help maximize compliance because it could reduce the dosing frequency needed to reach steady state concentration.

36
Q

What is bioavailability determined by?

A

Extent of absorption (AUC) and rate of absorption (tmax and Cp max).

37
Q

When are two formulations bioequivalents?

A

When there is no significant difference in their respective bioavailabilities.

38
Q

Compare absolute bioavailability to relative bioavailability.

A

Absolute bioavailability (“F”) is the fraction of drug administered which becomes systemically available. AUC(PO)/AUC(IV). Always 1 for an IV-administered drug.

Relative bioavailability compares two formulations or two conditions under which a drug is administered. For example, a generic to a name brand, both administered PO, would be assessed AUC(test)/AUC (std).

39
Q

Between the following tissues, which perfuse the fastest? The slowest?
Muscle; Liver; Fat

A

Liver > Muscle > Fat

40
Q

A PA wants to prescribe a drug that is a weak base to a breast-feeding woman. Knowing that breast milk is slightly acidic, could this pose a problem?

A

Yes, if the drug passes into the milk. A weakly basic drug is more likely to concentrate in the milk due to ion trapping. Once in the milk, the drug will become charged (due to the acidic pH) and less able to pass into another compartment.

41
Q

Equation for loading dose:

A

LD = (change in C x Vd)/F

42
Q

Equation for finding peak concentration (not from the triangle)

A

Cp = (F x Dose)/Vd

43
Q

An 80 kg patient receives a 12 mg/kg IV loading dose of a drug. When it is administered, the concentration = 240 mg/L. What is the drug’s Vd and to what compartment has it likely distributed?

A

Use equation Vd = Dose/Cp.

Dose is 80 kg x 12mg/kg = 960 mg.
Cp is 240 mg/L.

Vd = 4L. This is likely distributed to the plasma.

44
Q

What is the equation for Vd, given dose?

A

Vd = Dose/Cp

45
Q

Drug X is know to be 89% protein-binding. What percent of this drug is responsible for the drug’s action? What effect does protein binding have on the drug? Is this drug considered highly bound?

A

11% of the drug is responsible for its action. Protein binding makes the drug incapable of crossing membranes or binding to receptors. Drugs that are >90% bound are considered “highly bound”, so it is not considered highly bound.

46
Q

How do you differentiate between a drug that is a weak acid or a weak base by its name alone? Which part of the drug is active?

A

A weak acid forms a salt with NaOH, KOH, or Ca(OH)2 - for example, NaPenicillin. The active part is the anion.

A weak base forms a salt with HCl, H2SO4, HNO3. For example, diphenhydramine HCl. The active part is the cation.

47
Q

Order these compartments from most acidic to least acidic and give approximate values for each: Blood; Stomach; Bile; Urine.

A 
Most acidic:
Stomach (~ 1.5)
Urine (~5.7)
Bile (~6.9)
Blood (~7.4)
48
Q

What do drugs target to elicit cellular response?

A

Receptors, ion channels, enzymes, or transporters.

49
Q

If you’d like to study the maximal efficacy, potency, and selectivity of a drug, what would you study?

A

The graded dose response curve.

50
Q

If you’d like to examine how a proportion of individuals respond to a drug, what would you examine?

A

Quantal response curve.

51
Q

Therapeutic index vs. therapeutic window

A

Therapeutic index is a ratio at which 50% of subjects experience toxic effects and 50% experience therapeutic effects.

Therapeutic window deals only within a range of desired effects.

52
Q

Describe the difference between potency and efficacy, including how to determine their values on a plot.

A

Potency is RELATIVE and has to do with how much drug is needed to elicit the same effect. If two graphs are compared, the ED50 of the more potent drug would lay further to the left.

Efficacy is an intrinsic ability - the maximum effect a drug can have. This can be visualized as the y-axis peak.

53
Q

Describe full agonists, partial agonists, and inverse agonists. What is an example of a partial agonist?

A

Full agonist: binds a receptor and generates cellular response.

Partial agonist: binds a receptor but cannot achieve maximal efficacy even at highest drug concentration. Can be displaced. Chantix (varenicline) is an example.

Inverse agonist: Preferentially bind receptors in the resting state (antagonists bind equally); this reduces the availability of the receptor to full agonists.

54
Q

What is the difference between tachyphlaxis and tolerance?

A

Tachyphlaxis is a form of tolerance in which number of receptors rapidly synthesize on introduction of a substance, and then rapidly degrade upon withdrawal.

Tolerance is hypoactivity as a result of chronic drug exposure.

55
Q

What is the difference between a competitive and non-competitive antagonist?

A

A competitive antagonist binds at the same site that the agonist would (the active site). These can be overcome with sufficient [S] (reversible) or can be irreversible (as is the case with disulfide/covalent bonding).

A noncompetitive antagonist binds at a site removed from the active site. They cause a conformational change that prevents the agonist from eliciting the typical response.

56
Q

What happens to the log dose response curve if a reversible competitive antagonist is administered?

A

The curve has the same shape, but ED50 is shifted right. Emax remains the same.

57
Q

What happens to the log dose response curve if an irreversible competitive antagonist is administered?

A

Emax will be reduced.

Foundations (8 decks)

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