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621 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What happens to the PK parameters with the administration of a competitive inhibitor of renal secretion?

A

-clearence decrease
-V=no change
-increase half life
-decrease Fe
-no change in oral bioavailibility`

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2
Q

What problem do antacids propose?

A

-increase gastric pH
-decrease bioavailibility(rate and extent of absorption)

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3
Q

How to fix antacid problem?

A

-seperate medication and antacid by at lease 2 hours

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4
Q

medications that interact with antacids

A

-atenolol
-ciprofloxacin
-enoxacin
-isoniazid
-ketoconazole
-norflloxacin
-ofloxacin
-tetracycline

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5
Q

Which enzyme are in higher concentration in upper GI?

A

-CYP3A4
-do most of drug metabolism

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6
Q

Transporters in DDI

A

-control the concentration of drugs accross membrances
-drugs can induce or inhibit them

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7
Q

OATP

A

-polymorphs in this transportes
-variability in the HMG-CoA reductase inhibitors(AKA statins)

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8
Q

OAT transporters

A

-anion transporter in the kidneys
-remove foreign chemicals from the body

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9
Q

OCT transporters

A

-organic cation transporters
-passivly remove chemicals from the body

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10
Q

ABCB Family

A

-AKA multidrug resistance/transporters associated with atigen processing(MDR/TAP)
-P-gp(MDR1/ACBC)

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11
Q

P-gp(MDR1/ACBC)

A

-efflux transporter expressed in most cancer cells
-limits drugs that cross the BBB

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12
Q

what does it mean to be multidrug resistant?

A

they are cancer cells that pump medications out of affected cells

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13
Q

P-gp inducers

A

-decrease drug concentration
-Carbamzepine
-Phenytoin
-Rifampin
-St Johns Wort
-Ritonavir
-Tipanavir
-Avasimbe

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14
Q

P-gp inhibitors

A

-increase drug concentration
-Cyclosporin
-Quinidine
-Verapamil
-Amiodarone
-Erthromycin
-Claritromycin
-Azithromycin

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15
Q

Factors that affect drug distribution

A

-protein binding
-transporters

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16
Q

Factors that affect metabolism

A

-enzyme induction depends on activation of transcription factors
-PXR
-CAR
-AhR
-Estrogen
-Glucocorticoid

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17
Q

Broad spectrum enzyme inducers

A

-carbamzepine
-phenytoin
-phenobarbital
-rifampin

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18
Q

Selective 3A4 inducers

A

-Felbamate
-topiramate
-oxcarbazepine
-Griseofulvin
-Nevirapine
-St Johns wort

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19
Q

Selective 1A2 inducers

A

smoking

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20
Q

Selective 2E1 inducers

A

alcohol

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21
Q

Selective UGT inducers

A

-lamotrigine
-oxcarbazepine
-oral contraceptives

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22
Q

Strong enzyme inducers

A

> 80% decrease in AUC

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23
Q

moderate inducers

A

50-80% decrease in AUC

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24
Q

weak inducers

A

<50% decrease in AUC

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25
Q

UGT1

A

conjugate variety of drugs

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26
Q

UGT2

A

glucornidation of steriods and bile acids as well as some other drugs

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27
Q

substrates of UGT2

A

morphine, valproate, zidovudine, lorazepam, oxazepam, lamotrigrine

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28
Q

Oxidation

A

-NADPH dependent
-CYP450 reductase: seven enzymes responsible for most metabolism

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29
Q

Name the 7 enzymes responsible for most drug metabolism via oxidation

A

-1A2
-2C8
-2C9: has polymorphisms
-2D6: has polymorphisms
-2E1: has polymorphisms
-3A4

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30
Q

polymorphisms

A

genetic variability

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31
Q

Inhibitors of 3A4

A

-ketokonazole
-erthromycin
-verapamil
-grapefruit juice

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32
Q

Inducers of 3A4

A

-phenytoin
-carbanazepine
-rifampin
-St Johns wort

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33
Q

3 types of inhibition

A

-competitive at hepatic enzyme sites
-non-competitive
-mechanism based inhibition

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34
Q

strong inhibitor

A

> 5 fold increase in AUC

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35
Q

moderate inducer

A

2-<5 fold increase in AUC

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36
Q

weak inhibitor

A

1.25-<2 increase in AUC

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37
Q

UGT Inhibitors

A

-VPA
-Lamotrigrine
-Lorazepam

38
Q

OAT inhibitors

A

-Probenecid
-NSAIDs
-indomethacin
-didanosine
-salicylate

39
Q

OCT inhibitors

A

-cimetidine
-cisplatin
-famotidine
-ranitidine
-certirizine

40
Q

Dihydropyridine(calcium channel blockers) DDI

A

-interact with CYP3A4 sybstrates
-deceased drug level

41
Q

warfarin DDI

A

-antizeziure medications that affect 3A4 and 2C9 alter warfain levels

42
Q

Characteristics of non-linear PK

A

1)one or more ADME process are saturable
2) dose and concentration are not proportional
3) PK parameters change with dose

43
Q

How do you accomadate saturable kinetics?

A

-divide daily dose
-slow release formulations: crystal size, osmotic pump, staggered-dissolution granules

44
Q

Protien binding

A

-doesn’t typically affect unbound Css
-highly bound drugs with low V(<0.2 L/Kg) DO AFFECt Css

45
Q

What is the effect of a larger dose in saturable kinetics?

A

-increase time to steady state
-increase Css disproportionally

46
Q

What factors alter absorption in Peds?

A

-gastric pH: increase ionization at higher pH for weak acids
-gastric emptying
-intestinal transit
-larger small intestine area
-reduced bile production

47
Q

How is percutaneous absorption different in kids?

A

-Higher BSA
-thinner stratum corneum
-greater skin perfusion and hydration

48
Q

Why is percutaneus absorption in kids important to know?

A

higher systemic exposure to topical medications
-Can be DANGEROUS

49
Q

IM ingections in kids considerations

A

-reduced muscle mass
-feeble muscle contractions
-prefer thigh inj. because of increased movement
-volume limit
(0.5 mL for neonates, 1 mL for infants)

50
Q

Drug distribution in peds

A

-water bags
-distribution of hydrophillic and lipophillic drugs is affected

51
Q

Gentamycin dosing in peds

A

-hydrophillic
-need a higher dose(4-5 mg/kg) in neonates than in adults
-need a longer dosing interval because of reduced renal function

52
Q

Albumin in peds

A

-reduced amount in neonates and infants
-bilirubin elevated in neon.
-compete for drug binding: increase unbound drug concentrations

53
Q

What drugs pose a risk of causing kinicterus in peds?

A

-ceftriaxone: < 6 weeks
-Bactrim: <2 months
-because they displace bilirubin into the bloodstream: can cause jaundice and kinicterus

54
Q

Which phase I enzymes are high at birth, then rapidly decline?

A

-CYP3A7
4A1

55
Q

Which phase I enzymes are expressed in early neonates?

A

2D6
2E1

56
Q

Which phase I enzymes are expressed in late neonates?

A

3A4
2C family
1A2

57
Q

Caffiene metabolism in children

A

-neonates/infants: 2E1, 3A, renal excretion
->4 months: CYP1A2\
-increased half life in neonates so you need a loading dose to reach therapeutic concentration quickly

58
Q

Phenobarbital metabolism in peds

A

-CYP2C9
-half life is decrease in kids 1-12 so a higher dose is needed

59
Q

UDT glucornidation/Phase II metabolism in kids

A

-limited at birth
-adult level 2-6 months

60
Q

Chloramphenicol in peds

A

-metabolized in liver by UGT: slower in peds
0can accumulate to toxic levels and penetrate BBB
-Gray baby syndrome
-do NOT use in preterm and neonates

61
Q

GFR in peds

A

-renal system beveloped by 36 weeks gestation
-blood frow improve after birst
-GFR: rises rapidly first 2 weeks, adult level 8-12 months

62
Q

Inplications of reduced renal function in peds

A

-may need longer dosing intervals because of reduced CL

63
Q

Simple Dirrect Effect(rapid)

A

plasma drug concentrations are in rapid equillibrium with the effect site

64
Q

Hysteresis

A

-response and concentration do not match with time
-detect time delay or other mechanism

65
Q

Counter clockwise hysteris

A

-time delay: active metabolite, biophase distribution, turnover process
-Dose-response curve shifts left: lower concentrations needed to achieve the same effect after a time delay

66
Q

Clockwise hystersis

A

-tolerance effect: curve shifts right
-need higher concentrations to reach same effect

67
Q

Direct delayed model

A

-biological effect lag behind plasma concentration: bc of delayed distribution
-effect corrlates with the concentration in the biophase rather than plasma concentration

68
Q

Indirect, reversible basic turnover model

A

-Kin: drug input, zero order
-Kout: first order elimination, proportional to drug conc., exponential decay

69
Q

Warfarin inhibition

A

-inhibits VKORC1
-reduces vitamin K dependent proteins
delayed response of drug effect

70
Q

Omeprazole inhibition

A

-irreversible inactivation of proton pump receptor
-slow restoration of gastric acd secretion(3 days)
-slow synthesis of new receptor

71
Q

How does CL relate to organ blood flow?

A

CLb approached organ blood flow as E approaches 1

72
Q

components of the nephron

A

-GLOMERULUS
-tubule
-bowman’s space/capsule

73
Q

glomerular filtration barrier

A

-driving force for filtration is the large hydrostatic pressure created by kidney blood flow

74
Q

renal flow and filtration

A

-firtration increases moderatly with increased plasma flow
-filtration decreases GREATLY with decreaing plasma flow

75
Q

What passes through the filtration barrier?

A

-MW<5.5 kDA
-NOT albumin
-macromolecules: positive charge>neutral>negative, flexible molecules, small molecules

76
Q

Active tubular

A

-secretion requires energy
-need transport systems to work againist concentration gradient

77
Q

Reabsorption in the kidneys

A

-passive process
-prefers lipophillic, low MW, unionized drugs

78
Q

Why is inulin a good glomerular marker?

A

-Only filtered, not secreted or reabsorbed
-it is not synthesized or metabolized by the kidney

79
Q

PAH

A

-filtered and secreted

80
Q

drug used to increase pH

A

sodium bicarbonate

81
Q

drug used to decreae pH

A

Ammonium chloride

82
Q

Very polar: reabsorption

A

-minimal reabsorption
-urine pH dependent

83
Q

Nonpolar weak base(pKa less than 7): reabsorption

A

-extensive reabsorption

84
Q

Non polar strong base: reabsorption

A

minimal reabsorption

85
Q

Non-polar weak base(pka 7-12)

A

-reabsorption ranges from extensive to minimal
-pH sensitive

86
Q

Diuresis

A

increased urine flow
-increase fluid intake or diuretic

87
Q

When is forced diuresis useful?

A

-increase urine flow
-dilute urine
-decrease drug concentration in the tubule
-DECREASE REABSORPTION

88
Q

What drugs can be cleared with forced diuresis?

A

-Drugs primarily eliminated by renal excretion AND
-drugs where reabsorption is extensive

89
Q

Crockroft-Gault

A

-not used for CKD
-estimates CrCL

90
Q

CKD-EPI

A

-calculate eGFR using normalized body surface area
-preferred in >18yrs old, diabetes, organ transplant, alcoholics

91
Q

MDRD

A

-valid in patients 18-70 with lowere GFR, non-diabetic, without kidney transplant
-ONLY use if eEFR< 60mL/min/1.73m2

92
Q

24 hour urine collection

A

-measure in lab
-useful when Scr change is due to change in muscle mass

621 (1 decks)

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