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PBL PY2 Fall > Dyslipidemia PK > Flashcards

Dyslipidemia PK Flashcards

1
Q

what factors make a patient more likely to experince the myopathy of statins?

A

old age, female, low BMI, chronic renal or liver disease, CYP3A4 inhibitors

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2
Q

what is Ka?

A

absorption rate constant = the fraction of drug absorbed into systemic circulation per unit time (NOT THE AMOUNT ABSORBED PER UNIT TIME)

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3
Q

rate of absorption is indicated by ___

A

Ka

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4
Q

if Ka increases, what happens to Tmax and Cmax?

A

Tmax decreases and C max increases

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5
Q

what is bioavailability?

A

the fraction of unchanged drug absorbed into the systemic circulation

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6
Q

F ranges from ___ to ___ and has no units

A

0-1

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7
Q

F is reflected by the ____ of the concentration vs time curve

A

area under the curve (AUC)

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8
Q

absolute F compares ____

A

AUC of a doasge form with the AUC of an IV reference standard for the same drug in the same person

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9
Q

relative F compares ___

A

to another non-IV dosage form (containing the same drug)

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10
Q

how to calculate absolute bioavailability

A

[AUC/Dose tablet A] divided by AUC/ IV ref standard

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11
Q

how to calculate relative bioavailability

A

(AUC/Dose tablet X) divided by (AUC/dose tablet A)

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12
Q

what is the first pass effect?

A

decrease in an orally administered drug at various sites (mainly small intestines and liver) before reaching the systemic circulation

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13
Q

reasons for decreased parent drug in the GI tract?

A

poor absorption, metabolism, and or efflux (reverse transport) at intestinal enterocytes

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14
Q

reasons for decrease in parent drug in the liver

A

drugs with high first pass metabolism, rapid and extensive loss (by metabolic elimination in the liver) of some drugs during their first pass through the liver (portal vein pre-systemic elimination) before reaching the systemic circulation

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15
Q

why do statins have lo oral F?

A

they are high first pass metabolism

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16
Q

for 2 products to be bioequivalent, the ratio for the ____ and ___ of test to reference need to be within 80-125%

A

AUC and Cmax

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17
Q

what uptake transpoters are statins substrates for?

A

OAT1B1 & OAT2B1

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18
Q

statins are substrates of whihc efflux trnasporters?

A

PGP and breast cancer resitance protein

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19
Q

fluvastatin, rosuvastatin, cerivastatin, and atorvastatin form metabolites in a ___ manner

A

parallel

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20
Q

lovastatin and simvastatin form metabolites in a ___ manner

A

parallel and consecutive

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21
Q

give 2 examples of phase 1 metabolic reactions

A

oxidation and hydrolysis

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22
Q

given some examples of phase 2 metabolic reactions?

A

conjugation with glucuronic acid, sulphate, acetyl coA, glutathione

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23
Q

where are CYP enzymes primarily found in the tissues?

A

mostly in the liver, also in the intestinal mucosa, kidney, lung, brain etc.

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24
Q

where are CYP enzymes primarily found in the subcellular level?

A

mainly in the smooth endoplasmic reticulum (microsomes)

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25
Q

what are UDP glucuronyltransferases (UGTs)?

A

superfamily of enzymes, major phase 2 enzymes that conjugate glucuronic acid to substrates

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26
Q

what are the families and subfamilies of UGTs?

A
  1. UGT1 A and B

2. UGT2 A and B

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27
Q

where in the tissues are UGT enzymes found?

A

liver, intestinal mucosa, kindney

28
Q

where in the subcellular are UGTenzymes found?

A

mainly in endoplasmic reticulum (microsomes)

29
Q

in most cases, the relationship between rate of drug metabolism and drug concentrations follows ____ kinetics

A

michaelis menton

30
Q

what is Km?

A

substrate (drug) concentration at which the rate of reaction is one-half of the maximal

31
Q

what does Km reflect?

A

the binding affinity for the enzyme

32
Q

what does a smaller Km mean?

A

stronger the binding affinity

33
Q

in 1st order kinetics, the rate of metabolism roughly approximates ___

A

drug concentration

34
Q

apsrin, theophylline and phenytoin follow what type of metabolism kinetics?

A

capacity limited (saturable) kinetics

35
Q

in saturable kinetics, what changes after saturation?

A

T 1/2

36
Q

give an example of active parent drug being turned into aninactive metabolite

A

lactonization of atorvastatin to atorvastatin lactone

37
Q

give an example of inactive parent drug (prodrug) being turned into an active metabolite

A

lovastatin lactone beinf turned into lovastatin

38
Q

give an example of active parent drug beinf turned into active metabolite

A

hydroxylation of atoravastatin to make ortho and para atoravstatin

39
Q

give an example of active parent drug being metabolized into a reactive metabolite (may cause toxicity)

A

oxidation of acetaminophen to reactive metabolite that leads to hepatic necrosis

40
Q

lovastatin and simvastatin are prodrugs that are converted to their active acid forms by what process?

A

ester hydrolysis

41
Q

esterases belong to hat family?

A

carboxyesterase families

42
Q

give 2 examples of esterases and where they are located

A

CES1 mainly in the liver; CES2 mainly in the intestines and colon

43
Q

what enzymes metabolize gemfibrozil?

A

UDP UGTs (UGT1A1 and UGT1A3)

44
Q

gemfibrozil inhibits what enzymes?

A

CYP2C9 and CYP2C8

45
Q

fenofibrate is a prodrug that is metabolized int the active form ___, which can then be further metabolized to the inactive metabolite ___

A

fenobric acid; fenobric acid glucuronide

46
Q

fenofibrate is metabolized by what enzymes?

A

UGT2B7 and UGT1A9

47
Q

what is the half life of fenobric acid>

A

20hrs

48
Q

formulation of lipidil micro

A

micronized

49
Q

formulation of lipidil supra

A

microcaoted micronized form (particles coated with micronized fenofibrate)

50
Q

formulation of lipidil EZ

A

film coated tablet of nano crystals

51
Q

describe pk drug interaction

A

drug A affects the plasma levels of drug B (affectes ADME,)

52
Q

describe PD drug interaction

A

drug A affects the pharmalogical response of drug B

53
Q

strong CYP3A4 inhibitors can cause how large of an increase in AUC?

A

5-fold or greater

54
Q

moderate CYP3A4 inhibitors can cause how large of an increase in AUC?

A

between 2-5 fold increase

55
Q

weak CYP3A4 inhibitors can cause how large of an increase in AUC?

A

1.25-2.5 fold increase

56
Q

competitive inhibition

A

reversible; a drug binds to an enzyme and prevents another drug’s access to the binding substrate

57
Q

non-competitive inhibition

A

reversible; a drug binds to a site other than the binding site

58
Q

irreversible inhibition or inactivation

A

can be time dependent of mechanism based inactivation. Enzyme metabolizes drug to form a reactive metabolite which binds irreversibly to the enzyme

59
Q

competitive inhibitors have the same ___ and different ___

A

Vmax; Km

60
Q

noncompetitive inhibitors have the same ___ and different ___

A

Km; Vmax

61
Q

in irrversible mechanism based inactivation reversed once the drug has been completely eliminated?

A

no; need new enzymes to be made (depends on turnover or recovery half-life of the enzyme)

62
Q

what is the name of the phyochemical in GFJ that causes the interactions?

A

furanocoumarins

63
Q

GFJ affects ___, but not ____

A

F; systemic metabolism/clearance

64
Q

GFJ is a potent CYP3A4 ____ (inhibitor/inducer)

A

inhibitor

65
Q

aside from CYP3A4, what else does GFJ inhibit?

A

PGP

66
Q

describe the interaction between gemfribrozil and statins

A

statins metabolized by CYP3A4 & CYP2C8; gemfibrozil inhibits CYP2C8, so statin can build up and cause myopathy

67
Q

are there interactions between fenofibrate and rosuvastatin

A

no

PBL PY2 Fall (21 decks)

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