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PCEUT 510 > Exam Review--Things to Know! > Flashcards

Exam Review--Things to Know! Flashcards

This is still being worked on!!!

1
Q

Object/Victim

[definition]

A

The drug that is BEING AFFECTED by the interaction

usually the Substrate for an enzyme

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2
Q

Precipitant/Perpetrator

[definition]

A

The drug CAUSING the interaction

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3
Q

What are the 6 factors influencing interaction outcomes: Object Drug?

A
  1. Narrow therapeutic range
  2. Pre-interaction drug concentration
  3. High first-pass metabolism
  4. Genetics-Enzyme & Transporter
  5. Alternative elimination pathways
  6. Disease states
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4
Q

What are the 4 factors influencing outcomes: Precipitant drug?

A
  1. Dose or concentration
  2. Genetics- enzyme & transporter
  3. Route and time of administration
  4. Order of administration
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5
Q

What are the 6 PATIENT FACTORS that create HIGH VARIABILITY in drug interaction outcomes?

A
  1. Genetics
  2. Diseases
  3. Diet/Nutrition
  4. Environment
  5. Smoking
  6. Alcohol
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6
Q

What are the 6 DRUG FACTORS that create HIGH VARIABILITY in drug interaction outcomes?

A
  1. Dose
  2. Duration
  3. Dosing time
  4. Sequence
  5. Route
  6. Dosage Form
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7
Q

2D6 DDI
Diphenhydramine + Metoprolol
Who is the Perpetrator/Precipitant?

A

Diphenhydramine

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8
Q

2D6 DDI
Diphenhydramine + Metoprolol
Who is the Object/Victim?

A

Metoprolol

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9
Q

2D6 DDI
Quinidine + Codeine
Who is the Perpetrator/Precipitant?

A

Quinidine

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10
Q

2D6 DDI
Diphenhydramine + Codeine
Who is the Object/Victim?

A

Codeine

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11
Q

Metoprolol is a

[Substrate/Inhibitor] of 2D6

A

Substrate

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12
Q

Codeine is a

[Substrate/Inhibitor] of 2D6

A

Substrate

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13
Q

Diphenhydramine is a

[Substrate/Inhibitor] of 2D6

A

Inhibitor

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14
Q

Quinidine is a

[Substrate/Inhibitor] of 2D6

A

Inhibitor

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15
Q

2C19 DDI
Fluvoxamine + Omeprazole
Who is the Perpetrator/Precipitant?

A

Fluvoxamine

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16
Q

2C19 DDI
Fluvoxamine + Omeprazole
Who is the Object/Victim?

A

Omeprazole

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17
Q

Fluvoxamine is a

[Substrate/Inhibitor] of 2C19

A

Inhibitor

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18
Q

Omeprazole is a

[Substrate/Inhibitor] of 2C19

A

Substrate

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19
Q

1A2 DDI
Fluvoxamine + Theophylline
Who is the Perpetrator/Precipitant?

A

Fluvoxamine

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20
Q

1A2 DDI
Fluvoxamine + Theophylline
Who is the Object/Victim?

A

Theophylline

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21
Q

Fluvoxamine is a

[Substrate/Inhibitor] of 1A2

A

inhibitor

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22
Q

Theophylline is a

[Substrate/Inhibitor] of 1A2

A

Substrate

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23
Q

[PM/EM] for OBJECT drug will NOT be affected by precipitant drugs( inhibitors/inducers)

A

PM

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24
Q

[PM/EM] for PRECIPITANT drug may have HIGHER concentrations of precipitant drug and LARGER magnitude of change in OBJECT drug CLEARANCE

A

PM

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25
Q

[PM/EM] for OBJECT drug will LARGEST magnitude of INCREASE when co-administered with an INHIBITOR

A

EM

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26
Q

[PM/EM] for PRECIPITANT drug may have LOWER magnitude effect on OBEJCT drug CLEARANCE

A

EM

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27
Q

Grapefruit Juice is a

[Substrate/inhibitor] of 3A4

A

Inhibitor

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28
Q

Verapamil is a

[Substrate/inhibitor] of 3A4

A

Inhibitor

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29
Q

Itraconazole is a

[Substrate/inhibitor] of 3A4

A

Inhibitor

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30
Q

Ketoconazole is a

[Substrate/inhibitor] of 3A4

A

Inhibitor

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31
Q

Clarithromycin is a

[Substrate/inhibitor] of 3A4

A

Inhibitor

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32
Q

Rifampin is a

[Substrate/inducer] of 3A4

A

Inducer

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33
Q

If a drug is an inhibitor or inducer of 3A4 it is a

[perpetrator/victim]

A

PERPETRATOR!

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34
Q

in patients with Rheumatoid arthritis what is the inflammatory cytokine that is elevated and affects regulation of CYP3A4?

A

IL-6

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35
Q

The 2 DDI parameters that we are most concerned with are?

A
  1. Cmax

2. AUC

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36
Q

Toxicities are usually associated with [victim/perpetrator] drugs

A

Victim/object drugs

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37
Q

Do PPIs [increase/decrease] solubility?

A

Decrease

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38
Q

IL-6 is elevated in what disease state?

What role does the elevation of IL-6 play on CYP3A4 and Simvastatin AUC?

A

Rheumatoid arthritis
Suppresses CYP3A4,
Decreasing CL of Simvastatin Causing increased AUC

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39
Q

What effect does and IL-6 antagonist used for RA treatment have on Simvastatin?

A

IL-6 antagonism decrease IL-6 levels in the body

Decreasing CYP3A4 suppression = increased CL and Decreased AUC & Cmax for Simvastatin

40
Q

What 2 drugs produce STRONG anticholinergic side effects?

What is the side effect?

A
  1. Diphenhydramine (H1-antagonist)
  2. Amitriptyline( TCA)
    DECREASE GI motility
41
Q

How does SLOW GI motility affect bioavailability?

A

Slow motility = increased residence time = increase extent of absorption= INCREASED bioavailability

42
Q

Increased gastric pH leads to:
[increased/Decreased] ionization of BASIC drugs, which [slows/promotes] dissolution and [reduces/accelerates] BIOAVAILIBILITY?

A

DECREASED ionization
SLOWS dissolution
REDUCES bioavailability

ex:
Itraconazole-antacid

43
Q

Increased gastric pH leads to:
[increased/Decreased] ionization of ACIDIC drugs, which [slows/promotes] dissolution and [reduces/accelerates] ABSORPTION?

A

INCREASED ionization
PROMOTES dissolution
ACCELERATES absorption

ex: Sulfonylurea antidiabetic drugs

44
Q

What 3 POORLY SOLUBLE, BASIC drug classes are victims of PPI’s elevation of gastric pH?

A 
1. antifungals
[ketoconazole, itraconazole] 
2. tyrosine kinase inhibitors 
3. protease inhibitors
[indinavir, atazanavir]
45
Q

Itraconazole + Omeprazole DDI who is the [victim/object]?

How are they affected?

A

Itraconazole

Decreased AUC/bioavailability

46
Q

Itraconazole + Omeprazole DDI whos is the [perpetrator/precipitant]?

A

Omeprazole

47
Q

Why is FLUCONAZOLE NOT affected by increased gastric pH and not a concern when used with PPIs?

A

It is SOLUBLE and NOT very BASIC

48
Q

Tyrosine Kinase Inhibitors + PPIs DDI who is the [victim/object]?
How are they affected?

A

Tyrosine Kinase Inhibitors [all end in TINIB]

Decreased Cmax and AUC

49
Q

The reduction of Ketoconazole absorption by omeprazole can be reversed by what?

A
  1. Drinking with Coca-Cola!!

2. Changing to formulation to solution

50
Q

What role does Coca-Cola play in the DDI between azole antifungals and PPIs?

A

It reverses the effects of the PPI due to its acidity.

increasing the AUC of azole antifungals in the presence of PPIs.

51
Q

What affect does dietary fat have on fat-soluble drugs?

A

INCREASES solubility

52
Q

Orlistat prevents the break down of dietary fat because it is a ___________ inhibitor.

A

Pancreatic LIPASE inhibitor

53
Q

Orlistat [reduces/increases] absorption of Fat-soluble drugs?

A

REDUCES absorption

54
Q 
All of the following are Fat-soluble drugs EXCEPT? 
A. Cylosporine
B. Atenolol 
C. Amiodarone 
D. Levothyroxine
A

B is incorrect, atenolol is water-soluble

55
Q

Orlistat + Cyclosporine

who is the [victim/object]?

A

Cyclosporine

Fat-soluble

56
Q

Orlistat + amiodarone

who is the [victim/object]?

A

amiodarone

Fat-soluble

57
Q

Orlistat + levothyroxine

who is the [victim/object]?

A

levothyroxine

Fat-soluble

58
Q

What effect do antacids have on drug absorption?

A

SLOWS down rate of absorption of lumen

59
Q

Aluminum containing antacids + levothyroxine DDI who is the[victim/object]?
What effect does this have on bioavailability?

A

Levothyroxine

DECREASES bioavailability

60
Q

What is the concern with antacid metal ions and antibiotics?

A

antibiotics CHELATE to Al3+ and Mg2+ containing antacids & form NON-absorbable complexes = SEVERE bioavailability problems

61
Q

Aluminum containing antacids + ciprofloxacin DDI who is the[victim/object]?
What effect does this have on bioavailability?

A

Ciprofloxacin

DECREASES bioavailability

62
Q

How does Al3+ effect GI motility?

A

Slows motility

63
Q

How does Mg2+ effect GI motility?

A

Accelerates motility

64
Q

T/F
Sevelamer is a phosphate binder used to treat increased phosphate in ESRD. It can interfere with the oral absorption of Acidic drugs

A

True

Sevelamer is an ANION exchange resin
negatively charged drugs

65
Q

What 3 drugs will Sevelamer interfere with oral absorption?

A
  1. digoxin
  2. warfarin
  3. ciprofloxacin
66
Q

Estrogen Containing OC + antibiotic DDI is due to what?

A

Bacteria responsible for OC metabolism&raquo_space; metabolites enter enterohepatic circulation

Antibiotics kill bacteria&raquo_space; NO enterohepatic circulation

67
Q

Sulfasalazine undergoes AZO-reduction by gut flora, ampicillin has what effect on the efficacy of this prodrug?

A

Ampicillin wipes out flora responsible for azo-reduction
DECREASING efficacy of Sulfasalazine in the treatment of IBS
(Prodrug activation is decreased)

68
Q

Primary active transporters

[definition]

A

Generate energy themselves (ATP hydrolysis)

69
Q

Pgp is what type of membrane transporter?

A

Primary active transporter

70
Q

Secondary active transporters

[definition]

A

Utilizes energy stored in voltage and ion gradients generated by a primary active transporter (Na+/K+ ATPase)

71
Q

T/F

Renal OAT is an example of a primary active transporter that relies on the maintenance of Na+ gradient by Na/K/ATPase

A

False

Primary does NOT use energy stored by a gradient!

72
Q

OATs are what kind of transporter?

A

Secondary active transporter driven by ion gradient

73
Q

What does Ki mean?

A

Binding affinity/potency of the inhibitor

Small Ki = strong binding affinity of inhibitor

74
Q

Pgp mediated transport in the intestine is on the [apical/basolateral] side

75
Q

Pgp mediated transport in the kidney is on the [apical/basolateral] side?

76
Q

Pgp mediated transport in the Liver is on the [Apical/basolateral] side?

77
Q

Pgp mediated transport in BBB is on the [apical/basolateral] side?

78
Q

Who is the object/victim drug in Pgp DDIs?

79
Q

Who is the precipitant/perpetrator drug in Pgp DDIs?

A

Any Pgp Inhibitor/inducer

80
Q

There are two drugs that have dual effects in Pgp DDIs depending on dosing regimen, what are they?

A
  1. rifampin

2. ritonavir

81
Q

Pgp DDI
Digoxin + clarithromycin
Who is the [precipitant/perpetrator]?
What is the effect?

A

Clarithromycin via
inhibition
INCREASED bioavailability of DIGOXIN

82
Q

Pgp DDI
Digoxin + itraconazole
Who is the [precipitant/perpetrator]?
What is the effect?

A

itraconazole via
inhibition
INCREASED bioavailability of DIGOXIN

83
Q

Pgp DDI
Digoxin + atorvastatin
Who is the [precipitant/perpetrator]?
What is the effect?

A

atorvastatin via
inhibition
INCREASED bioavailability of DIGOXIN

84
Q

Pgp DDI
Digoxin + rifampin
Who is the [precipitant/perpetrator]?
What is the effect?

A

Rifampin via
induction
DECREASED bioavailability of DIGOXIN

85
Q

Pgp DDI
Digoxin + quinidine
Who is the [precipitant/perpetrator]?

A

quinidine

inhibition

86
Q

Pgp DDI
Digoxin + verapamil
Who is the [precipitant/perpetrator]?

A

Verapamil

inhibition

87
Q

Pgp DDI
Digoxin + cyclosporine
Who is the [precipitant/perpetrator]?

A

Cyclosporine

inhibition

88
Q

Rifampin inhibits which OATP in the liver in the Biphasic DDI seen with REPAGLINIDE?

89
Q

What is a dosing strategy to overcome the biphasic DDI of Rifampin + Repaglinide?

A
  1. To minimize powerful inductive effect = give rifampin in the morning
  2. Give Repaglinide dosing before each meal through out the day while inhibition is present
  3. be aware of full emergency of inductive effect when rifampin is discontinued
  4. Close monitoring
90
Q

The OCT2 transporter is located on the [apical/basolateral] side of the renal tubule?

A

Basolateral

91
Q

The MATE2 transporter is located on the [apical/basolateral] side of the renal tubule?

92
Q

Cimetidine + Metformin DDI

Who is the [perpetrator/precipitant]?

A

Cimetidine

93
Q

Cimetidine + Metformin DDI who is the [object/victim]?

94
Q

Cimetidine + Metformin DDI what is it?

A

Cimetidine INHIBITS efflux of MATE at apical membrane of renal tubule inhibiting Cl of Metformin = INCREASED AUC

95
Q

Methotrexate + PPI DDI?

What is the interaction & effect?

A

PPI inhibits BCRP at apical membrane in KINDEYS = DECREASED elimination of METHOTREXATE = increased risk of toxicities

96
Q

[Li] is often elevated in Pts receiving concomitant thiazide because?

A

Increased renal reabsorption of LI results in the DECREASED CL of Li = precipitate retention of LI & Toxicities

97
Q

Li + thiazide DDI

Who is the [perpetrator/precipitant]

PCEUT 510 (12 decks)

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