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PK > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

How are NRTIs affected by CYP 450 enzymes?

A

They are not

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2
Q

Which NRTIs have pre-dominantly non-renal clearance?

A

ABC and ZDV

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3
Q

How are most NRTIs eliminated?

A

Renal

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4
Q

What is the half-life of the triphosphates?

A

Variable

3-40 hours

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5
Q

How are EFV/NVP/RVP affected by CYP 450 enzymes?

A

Substrates, inhibitors, and inducers of 3A4

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6
Q

What are ETV affected by CYP 450 enzymes?

A

Substrate for 3A4, 2C9, and 2C19
Inducer of 3A4
Inhibitor of 2C9 and 2C19

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7
Q

How are PIs affected by CY{ 450 enzymes?

A

Extensive metabolism - substrates, inhibitors and inducers

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8
Q

How are PIs affected by P-gp enzymes?

A

Substrates and inhibitors

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9
Q

How is ritonavir affected by P-gp enzymes?

A

Inhibitor

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10
Q

How is enfuviritide affected by enzymes?

A

Enfuviritide is a peptide and gets broken down enzymatically to aa’s that are then recycled into the body pool

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11
Q

How is Maravaroc affected by CYP 450 enzymes?

A

3A4 substrate

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12
Q

What enzymes affect INSTIs

A

RAL: glucuronidated by UGT 1A1
EVG: CYP 450 substrate
DTG: mainly glucuronidated, some 3A4

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13
Q

How are PK enhancers affected by enzymes?

A

Inhibitors of:
3A4 and 2A6
P-gp, BCRP, OATP1A1, OATP1B3

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14
Q

What is the PK result of EFV/NVP + rifampin and how do you change the dose?

A

Decreased [EFV/NVP]

Increase EFV

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15
Q

What is the PK result of EFV/NVP + statins and what do you do?

A

Decreased [statin]

Monitor cholesterol closely/more aggressive statin dose

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16
Q

What is the PK result of RPV + PPIs and what do you do?

A

Decreased RPV

Avoid PPIs w/RPV

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17
Q

What is the PK result of ETV + certain boosted PIs (ATV/r, FPV/r, TPV,r)

A

Decreased [PI]

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18
Q

What is the PK result of ETV + warfarin and what do you do?

A

Increased [warfarin]

Monitor INR

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19
Q

What is the PK result of PIs + rifampin?

A

Decreased [PI]

Increased [RIF]

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20
Q

What are the 6 contraindicated drugs with PIs?

A 
RIF
Midazolam/triazolam
Ergot derivatives
St. John's Wort
Lovastatin/simvastatin
Pimozide
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21
Q

What is the PK result of PIs + midazolam/triazolam?

A

Increased [midaz/triaz]

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22
Q

What are the PK results of PIs + ergot derivatives?

A

Increased [ergots]

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23
Q

What are the PK results of Pis + St. John’s Wort?

A

Decreased [PI]

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24
Q

What are the PK results of PIs + lovastatin/simvastatin?

A

Increased [Lovastatin/simvastatin]

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25
Q

What are the PK results of PIs + pimozide?

A

Increased [pimozide]

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26
Q

What are the PK results of ATV + PPIs and what do you do?

A

Decreased [ATV]
Max omeprazole 20mg/d equivalent
Aalways boost w/RTV
Avoid in experienced pts with resistance

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27
Q

What are the PK results of Pis + amiodarone, lidocaine, ruinide, bepridil and what do you do?

A

Increased [anti-arrhythmics]
Avoid if possible
TDM

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28
Q

What are the PK results of PIs + trazodone and what do you do?

A

Increased [trazodone]

Use lowest dose possible

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29
Q

What are the PK results of PIs + immunosuppressants and what do you do?

A

Increased [immuno.]

TDM

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30
Q

What are the PK results of PIs + statins and what do you do?

A

Increased [statins]

Prava/atorv preferred (+/- rosuv)

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31
Q

What are the PK results with fusion inhibitor interactions?

A

There are none

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32
Q

What are the PK results of MVC + inducers and what do you do?

A

Decreased [MVC]

Double MVC dose

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33
Q

What are the PK results of MVC + inhibitors and what do you do?

A

Increased [MVC]

1/2 MVC dose

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34
Q

What are the PK results of RAL + rifampin and what do we do?

A

Decreased [RAL]

Double RAL dose

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35
Q

What are the PK results of RAL + pheny/phenobarb and what do we do?

A

Potential decreased [RAL]

Use with caution

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36
Q

What are the PK results of elvitegravir with interacting drugs?

A

Similar interactions with ritonavir

See PIs/cobi

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37
Q

What are the PK results of DTG + dofetilide and what do you do?

A

Increased [dofetilide]

CONTRAINDICATED

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38
Q

What are the PK results of DTG + rifampin and what do you do?

A

Decreased [DTG]

Increase DTG dose

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39
Q

What are the PK results of DTG + cations and what do you do?

A

Decreased [DTG]

Take DTG 2h before/6h after cations

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40
Q

Which drugs are contraindicated for use with PK enhancers?

A 
COBI + rifampin
COBI + ergot derivatives
COMI + St. John's Wort
COBI + lova/simva
COBI + sildenafil for PAH
COBI + PO triaz/midaz
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41
Q

What are the PK results of COBI + sildenafil for PAH?

A

Increased [sildenafil]

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42
Q

What is the most common type of PD?

A

CAPD: Continuous ambulatory peritoneal dialysis

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43
Q

What GFR rate do patients receiving peritoneal dialysis act like?

A

10-20 ml/min

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44
Q

How is PD added to a patient?

A

Invovles surgical insertion of a catheter in the lower abdomen in to the peritoneal cavity

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45
Q

Is HD or PD more efficient?

A

HD is more efficient

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46
Q

What is a common infxn in PD?

A

Peritonitis

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47
Q

What is the most common continuous renal replacement?

A

CVVH

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48
Q

Which dialysis is considered “low-flux”?

A

HD

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49
Q

Which dialysis removes larger molecules?

A

Continuous renal replacement

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50
Q

In continuous renal replacement, is the fraction of drug removed bound or unbound?

A

Unbound

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51
Q

How does the patient’s GFR behave in continuous renal replacement?

A

~30 ml/min

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52
Q

How does HD work?

A

Blood is pumped out of the patient, cleaned, then returned

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53
Q

How does MW affect dialysis?

A

“Low-flux” have relatively small p[ores.

Small drug molecules (< 500 daltons) tend to be eliminated by dialysis.

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54
Q

How does water/lipid solubility affect dialysis?

A

Drugs that have a high degree of water solubility tend to partition into water-based dialysis fluids, whereas lipid-soluble drugs tend to remain in the blood

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55
Q

How does plasma protein binding affect dialysis?

A

Only unbound drug molecules are able to pass through the pores.
Drugs that are not highly plasma protein-bound have high free fractions of drug in the blood and are prone to better dialysis clearance

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56
Q

How does Vd affect dialysis?

A

Medication with large Vd’s are principally located at tissue binding sites and not in the blood, where dialysis can remove the drug.
< 1 L/kg more likely to be removed (AGs, theophylline)

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57
Q

How does inherent clearance (route and rate) affect dialysis?

A

If kedney is the primary route of elimination - higher likelihood that drug will be removed by dialysis

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58
Q

What are the critically dosed agents?

A

CsA
TAC
SIR
Everolimus

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59
Q

What are the critically-dosed NTI ratios?

A

< 2 fold difference b/n LD50 and ED50
OR
< 2 fold difference in min. toxic conc. and min. effective conc.
AND
Safe and effective use requires careful titration and patient monitoring

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60
Q

What are the goals of critically-dosed agents?

A

Optimize drug therapy for individual patients
Minimize risk of allograft rejection
Minimize risk of dose-related adverse events
Optimize immunosuppressive therapy

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61
Q

What is the indication for critically dosed immunosuppressants?

A

Prevention of allograft rejection

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62
Q

What is the Tmax for CsA?

A

2-4 hours

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63
Q

What is F for CsA?

A

5-70%; average 30%

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64
Q

What is Vd for Csa?

A

3-7 L/kg

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65
Q

What percent of CsA is bound to erythrocytes in blood?

A

70%

Preferred sampling matrix

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66
Q

What is CsA bound to in plasma?

A

Associated with lipoproteins

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67
Q

What is the metabolism of CsA?

A

By hepatic and intestinal 3A4 and transport by P-gp

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68
Q

What are variables that modulate CsA oral bioavailability?

A

intestinal P-gp and 3A4 activity

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69
Q

Is CsA renally eliminated?

A

Minimally

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70
Q

What is the half-life of CsA?

A

12-16 hours

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71
Q

What is F for TAC IR?

A

5-67%, average 27%

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72
Q

What is Tmax for TAC IR?

A

2-4 hours

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73
Q

What is F for TAC XR?

A

~50% higher than with immediate formulation (healthy subjects)
F is better on an empty stomach and in the morning hours

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74
Q

What is F for TAC XL?

A

Better on an empty stomach and in the morning hours

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75
Q

What is Tmax for TAC XR?

A

6-8 hours

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76
Q

What is Tmax for TAC XL?

A

2-4 hours

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77
Q

What is Vd for TAC?

A

5-6 L/kg

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78
Q

How is TAC bound in the blood?

A

70-80% erythrocytes

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79
Q

How is TAC bound in plasma?

A

88% albumin and alpha-1 acid glycoprotein

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80
Q

How is TAC metabolized?

A

Hepatic and intestinal 3A4 and transported by P-gp

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81
Q

How is TAC eliminated?

A

Minimal renal elimination (< 5%)

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82
Q

What is the half-life of TAC IR?

A

3.5-40.5 hours, average 12 hours

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83
Q

What is the half-life of TAC XR?

A

31 +/- 8 hours

84
Q

What is the half-life of TAC XL?

A

38 +/- 3 hours

85
Q

What is F for SIR?

A

15%

Poorly absorbed

86
Q

What is Tmax for SIR?

A

1.42 +/- 1.2 hours

87
Q

What is Vd for SIR?

A

14 L/kg (range 4-20)

88
Q

How is SIR bound in blood?

A

95% RBCs

89
Q

How is SIR bound in plasma?

A

40% lipoproteins

90
Q

How is SIR metabolized?

A

3A4 and transported by P-gp

91
Q

How is SIR eliminated?

A

< 2.2% renally

92
Q

What is the half-life of SIR?

A

57-63 hours (need LD and MD)

93
Q

What is F for Everolimus?

A

30% (reduced with meals)

94
Q

What is Tmax for Everolimus?

A

1-2 hours

95
Q

What is the Vd for Everlimus?

A

2-5 L/kg

96
Q

How is Everolimus bound in the body?

A

~70% plasma protein

97
Q

How is Everolimus metabolized?

A

Substrate for 3A4 and P-gp

98
Q

How is Everolimus eliminated?

A

Feces (80%)

Minimal renal elimination (5%)

99
Q

What is the half-life for Everolimus?

A

30 hours

100
Q

What is the standard of care at most hospital for CsA?

A

Pre-dose trough whole blood concentrations

101
Q

What is the new option for CsA administration?

A

Single point sampling 2 hours after drug administration

102
Q

Which weight do we use for CsA?

A

ABW

103
Q

What is the dosing for CsA?

A

Initial 2.5 mg/kg PO q12h, then titrated based on SS trough blood levels

104
Q

How often do we monitor CsA levels?

A

3x/wk for 1st month, then 2x/wk for the next 2 months, then weekly for 3 months, then monthly thereafter or after any dose change

105
Q

How do we adjust CsA doses?

A

25-50mg PO q12 to achieve therapeutic levels

106
Q

What is the PO:IV conversion of TAC?

A

3:1 PO:IV

107
Q

What is monitored for TAC dosing?

A

High correlation between trough, Cmax, and AUC0-4.

Pre-dose trough whole blood concentration is the standard of care.

108
Q

What is TAC IR dosing?

A

0.075 mg/kg PO q12 then titrated based on SS trough blood levels

109
Q

What is TAC XR dosing

A

Conversion from IR to XR: 80% of the daily dose

110
Q

What is TAC XL dosing?

A

Conversion from IR to XL: 1:1

111
Q

When do we monitor SS levels?

A

2-3x/wk for the 1st month, then 2x/wk for the next 2 months, then weekly for 3 months, then monthly thereafter or after any dose change

112
Q

How are TAC doses adjusted?

A

IR: Adjust doses by 1-2mg PO q12 to achieve therapeutic levels
XR/XL: no clear guidance; take into account that it takes 7 days to acheive SS

113
Q

How is SRL monitored?

A

High correlation between SS and AUC

Whole blood trough monitoring is standard of care

114
Q

How do we calculate LD for SRL?

A

LD should be 3x MD

115
Q

What is SRL dosing for low-moderate immunologic risk?

A

6mg LD, followed by 2mg daily

116
Q

What is SRL dosing for high-immunologic risk?

A

15mg LD, followed by 5mg daily

117
Q

How do we monitor SRL?

A

Very long half-life
Adjusting doses before SS is reached can lead to over- or under-dosing
Weekly for the 1st month post-transplant then monthly/every 3 months thereafter or after any dosing change

118
Q

How do we adjust SRL dosing?

A

By 1-2 mg/d

119
Q

What are the strategies for Everolimus monitoring?

A

High correlation between trough, Cmax and AUC 0-4

Pre-dose trough whole blood concentration is the standard of care

120
Q

How do we dose Everolimus in liver transportation, rejection prophylaxis?

A

1mg BID, then titrate as needed at a 4-5 day interval

121
Q

How do we dose Everolimus in kidney transplantation, rejection prophylaxis?

A

0.75mg BID, then titrate as needed at a 4-5 day interval

122
Q

What is the therapeutic range for Everolimus?

A

3-5 ng/ml, when given in conjunction with a calcineurin inhibitor

123
Q

How do we monitor SS levels?

A

1-2x/wk for the 1st month, then as clinically indicated

124
Q

How do we adjust Everolimus doses?

A

0.25-0.5mg PO q12 to achieve therapeutic levels

125
Q

What are some 3A4/P-gp inhibitors?

A

Macrolides (except zithro)
Non-dihydropyridine CCBs
Azole antifungals
PIs, cobi

126
Q

What are some 3A4/P-gp inducers?

A

Phenytoin
Phenobarbital
Rifampin, Rifabutin
Carbamazepine

127
Q

How do statins interact with immunosuppressants?

A

3A4 substrate
CsA is a substrate and inhibitor of 3A4
TAC/SRL substrates and weak inhibitors of 3A4
Potential to increase statin concentrations with concomitant use

128
Q

How does grapefruit juice affect immunosuppressants?

A 
Inhibit P-gp and 3A4 in the gut
Increased Cmax and AUC
No change in CL or half-life
Increased C0 concentrations by 77%
Increased CSA/TAC/SRL/EVR drug concentrations
129
Q

How does St. John’s Wort affect immunosuppressants?

A

Induce intestinal/hepatic 3A4
Induce P-gp in gut (decreased drug absorption = decreased bioavailability)
Decreased CSA/TAC/SRL/EVR drug concentrations

130
Q

Which drugs increase the risk of nephrotoxicities when taken with immunosuppressants?

A

AG
Ampho. B
Vanc
NSAIDs

131
Q

How often do we monitor CSA/TAC trough levels?

A

2-3 days after drug initiation and adjust dose appropriately

132
Q

How do we monitor ARL trough levels?

A

1 week after drug initiation and adjust dose accordingly

133
Q

How do we monitor EVR trough levels?

A

4-5 days after drug initiation and adjust dose

134
Q

What is Harvoni’s Tmax?

A

4 hours

135
Q

Which drugs are in Harvoni?

A

SOF and LDV

136
Q

What is SOF?

A

NS5B nucleotide polymerase inhibitor

137
Q

What is LDV?

A

NS5A inhibitor

138
Q

How is SOF distributed?

A

65% bound to human plasma protein

139
Q

How is LDV distributed?

A

> 99% bound to plasma proteins

140
Q

How is SOF metabolized?

A

Hydrolysis and phosphorylation to an active metabolite

141
Q

How is LDV metabolized?

A

Via oxidative metabolism

142
Q

How is SOF cleared?

A

Renally (80%)

143
Q

What is the half-life of SOF?

A

25 hours

144
Q

How is LDV eliminated?

A

Biliary/feces

145
Q

What is the half-life of LDV?

A

47 hours

146
Q

What drugs are in epclusa?

A

SOF and VEL

147
Q

What is VEL?

A

NS5A inhibitor

148
Q

What is Tmax of Epclusa?

A

3 hours

149
Q

How is VEL distributed?

A

> 99% bound to plasma proteins

150
Q

How is VEL metabolized?

A

2B6, 2C8, 3A4

151
Q

How is VEL eliminated?

A

Biliary/feces

152
Q

What is the half-life of VEL?

A

15

153
Q

What drugs are in Viekira XR?

A

Omb, Pari, Ritonavir, Das

154
Q

What is Omb?

A

NS5A inhibitor

155
Q

What is pari?

A

NS3/4A protease inhibitor

156
Q

What is ritonavir?

A

PK enhancer

157
Q

What is Das?

A

NS5B

158
Q

What is the Tmax of Viekira XR?

A

4-8 hours

Should be taken with food

159
Q

How is Viekira XR distributed?

A

Highly bound to human plasma proteins

160
Q

What is Vd of Viekira XR?

A

High apparent Vd (V/F) for all 4 components

161
Q

How is Omb metabolized?

A

Amide hydrolysis, followed by oxidative metabolism

162
Q

How is Pari metabolized?

A

3A4 (major)

163
Q

How is ritonavir metabolized?

A

Mostly 3A4

To a lesser extent 2D6

164
Q

How is Das metabolized?

A

Mostly 2C8

To a lesser extent 3A4

165
Q

How is Viekira XR eliminated?

A

Predominantly feces

Minimal renal elimination

166
Q

What is the half-life of Omb?

A

21-25 hours

167
Q

What is the half-life of Pari?

A

5.5 hours

168
Q

What is the half-life of ritonavir?

A

4 hours

169
Q

What is the half-life of Das?

A

5.5-6 hours

170
Q

What drugs are in Zepatier?

A

Elb and Graz

171
Q

What is Elb?

A

NS5A inhibitor

172
Q

What is Graz?

A

NS3/4A protease inhibitor

173
Q

What is the Tmax of Elb?

A

3-6 hours

174
Q

What is the Tmax of Graz?

A

0.5-3 hours

175
Q

How is Zepatier distributed?

A

> 97% bound to plasma proteins

High Vd

176
Q

How is Zepatier metabolized?

A

Primarily 3A4

177
Q

What is the only DAA that is approved for patients with all CrCl?

A

Zepatier

178
Q

How is Zepatier eliminated?

A

Predominantly via feces

Minimal renal elimination

179
Q

What is the half-life of Elb?

A

24 hours

180
Q

What is the half-life of Graz?

A

31 hours

181
Q

What drugs are not recommended to be taken with Harvoni or Epclusa?

A

Amiodarone
P-gp inducers: rifampin, St. John’s Wort
Anticonvulsants

182
Q

What drugs are contraindicated with Viekira XR?

A

Anticonvulsants: carbamazepine, phenytoin, phenobarbital

183
Q

How does ritonavir affect 3A4

A

Inhibitor of 3A4

184
Q

What drugs are contraindicated with Zepatier?

A

Anticonvulsants: Phenytoin, carbamazepine
Antimycobacterial: rifampin
Herbal: St. John’s Wort
HIV meds: CsA

185
Q

What drugs are not recommended with Zepatier?

A

3A4 inducers: nafcillin

3A4 inhibitors: ketoconazole, cobi

186
Q

What is a post-antibiotic effect?

A

Continued suppression of bacterial growth after a short exposure to antimicrobial agents

187
Q

What is a time-dependent ABX?

A

Amount of microbial killing depends on the time the drugs stays above the MIC
T > MIC

188
Q

What is a concentration-dependent ABX?

A

Amount of microbial killing depends on the max concentration of drug above the MIC

189
Q

What is the goal of therapy for time-dependent an minimal PAE abx when T > MIC?

A

Maximize duration of exposure

190
Q

What is the goal of therapy for time dependent and minimal PAE of abx when 24h-AUC/MIC

A

Maximize amount of drug

191
Q

What is an example of ABX for time-dependent and minimal PAE with T > MIC?

A

PCN

192
Q

What is an example of ABX for time-dependent and minimal PAE with 24h-AUC/MIC?

A

Vancomycin

193
Q

What is an example of ABX for time-dependent and moderate to prolonged PAE?

A

Azithromycin

194
Q

What is the goal of therapy for time dependent and moderate to prolonged PAE?

A

Maximize amount of drug

195
Q

What is an example of concentration-dependeMICnt and prolonged PAE?

A

FQs

196
Q

What is the goal of therapy for concentration-dependent and prolonged PAE?

A

Maximize concentrtaion

197
Q

What is fT > MIC?

A

Amount of time the free or non-protein bound drug concentrations exceeds the

198
Q

What are the advantages for using extended infusions of ABX?

A

Superior PD profile (more fT > MIC)
Allows for time between doses for administrations of drugs through the same IV line
Cost saving

199
Q

What is the rationale for using ABX drug combinations?

A 
Broad-spectrum empiric  therapy
Polymicrobial infections
Decrease resistance
Decrease dose-related toxicity
Increase inhibition or killing
200
Q

What are some examples of antagonism?

A

Vanc + linezolid

Two beta-lactams

201
Q

What mechanism does Bactrim work?

A

Blockade of sequential steps in a metabolic sequence

202
Q

What mechanism do beta-lactam/B-lactamse combos work?

A

Inhibition of enzymatic inactivation

203
Q

What mechanism do PCN G and gent work by?

A

Enhancement of abx uptake

204
Q

By what mechanism does vanc + linezolid inhibit each other?

A

Inhibition of cidal activity by static agents

205
Q

By what mechanism does two beta-lactams inhibit each other?

A

Induction of enzymatic inactivation

PK (6 decks)

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