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CMOD > Sweatman Drug-Drug interactions > Flashcards

Sweatman Drug-Drug interactions Flashcards

1
Q

How the drug affects the body

A

pharmacodynamics

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2
Q

how the body acts on the drug

A

pharmacokinetics
(L-ADME)
*lending to means of D-D interactions

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3
Q

1+ 1= 2

A

additivity

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4
Q

1+1=3

A

synergism

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5
Q

change in serum blood level

A

pharmacokinetics

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6
Q

receptor/non-receptor interactions

A

pharmacodynamics

*lending to means of D-D interactions

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7
Q

many drug-drug interactions are susceptible to control by

A

dose adjustment

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8
Q

co-admin of cyclosporin with erythromycin has what effect

A

increases cyclosporin levels and decreases its cost

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9
Q

are all D-D interaction bad

A

no

some actually beneficial

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10
Q

why are elderly, women and very young at increased risk for ADR’s

A

decreased capacity to metabolize and excrete drug, normonal changes, immature metobolic mechs etc

*Pharmacokinetics are different than in adults/ men

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11
Q

relationship b/w polypharmacy and incidence

A

greater number of concurrent drugs being taken–> increases likelihood of ADR’s
*greater drug exposure=greater likelihood of drug-drug interactions

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12
Q

therapeutic window

A

MTC-MEC

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13
Q

lag period on a dose concentration-time curve indicated

A

rate of uptake/distribution following adminstration for orally administered drugs

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14
Q

lag time for IV

A

NONE

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15
Q

duratio of action

A

time for which the plasma concentration is above the MEC for maximal action upon the recptor

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16
Q

drugs with smaller therapeutic windows are more likely to

A

exhibit adverse effects

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17
Q

if the plasma concetration remains within the therapeutic window when interacting with a concurrent drug…will it be apparent

A

NO–> this is why most D-D interaction go unoticed

only when it goes above MTC (toxic) or below MEC (loss of clinical efficacy–>will drug-drug interactions become notiecd

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18
Q

High suspicion of drugs affecting which three categories should be monitored for D-D interactions

A
  1. anticoag (thrombosis or hemorrhage)
  2. Cardiovascular (arrhythmogenic events)
  3. CNS (ability to cross BBB can cause sedative or seizure activity)
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19
Q

Classifications of Chemical (D-D) interactions

A
  1. additive
  2. synergistic
  3. potentiation
  4. antagonism
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20
Q

outcome of physical changes that occur in all of the four chemical interactions

A

functional changes
chemical changes
dispositional changes
receptor changes

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21
Q

women need lower doses bc

A

they tend to not clear the drug as rapidly

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22
Q

most common CYP’s

A

3A4 and 2D6–> expression varies up to 40 fold for 3A4 and these two cyps have MANY different SNP’s

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23
Q

atorvastatin MOA regarding CYP

A

Enters cell–>binds to nuclear receptor (PXR) which dimerizes with RXR–> binds DNA00> recruits coactivator which binds to TBP at the TATA box–> activates RNA POl II–> upregulates CYP3A4 transcription–> metabolizes Atorvastatin

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24
Q

atorvastatin induces

A

its OWN metabolism

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25
Q

A concurrent drug can impact the metabolism of other agents via

A

semi-selective nuclear effects–> bc the enzyme produced via ligan-NR transcription upregulation can metabolism MANY DIFFERENT DRUGS NOT JUST THE ONE THAT CAUSES THE UPREGULATION
*EX–> ATORVASTATIN LEADS TO CYP3A4 UPREG–> WHICH WOULD DECREASE ALL OTHER DRUGS BEING TAKEN THAT ARE SUBSTRATES FOR CYP3A4

26
Q

Semiselective nuclear effects can affect which phases of metabolism

A

phase I -cyp mediated

AND PHASE II–> GLUCORONOSYLTRANSFERASES

27
Q

WARFARIN-RIFAMPIN INTERACTION

A

BOTH HANDLED BY CYP3A4:
taken together–> rifambin induces CYP and warfarin concentration declines–> PRO-THROMBOTIC STATE no longer sufficiently anticoagulated

28
Q

ORAL CONTRACEPTIVES AND RIFAMPIN

A

RIFAMPIN INCUCES CYP3A4 AND NOW CONTRACEPTIVE LEVELS ARE LOW–> RESULTING IN PARENTHOOD

29
Q

RIFAMPIN AND CYCLOSPORIN AND TAC

A

RIFAMPIN INDUCES CYP3A4–> cyclosporin and Tac are substrates–> lower plasma levels of tac and clycosporin via increased Cyp activity–> organ rejection

30
Q

Herbal remedies can cause what problems

A
  1. can affect CYP activity–> indirect drug interactions
  2. some are anticoagulant which can have an ADDITIVE EFFECT
  3. Some possess CNS activity–> additive or antagonistic effects on CNS
31
Q

three forms of CYP inhibition

A

reversible (most common)-
quasi irreversible
irreversible

32
Q

most cyp inhibition is

A

competitive and reversible

33
Q

most cyp inhibitors contain

A

Nitrogen–>simultaneously binds prosthetic heme iron and lipophillic region of protein
*inhibitor potency determined by lipophillicity and strength of bonds

34
Q

Both reversible and quasi-irreversible inhibition is caused by

A

formation of reactive metabolites that covalently bind to the active site for ever (irreversible) or apprently/effectively forever (quasi)

*require at least 1 cycle of CYP catalytic processes

35
Q

STATINS in too high concentrations can cause

A

Rhabdomyolysis–> breakdown of muscle tissue
muscle pain and acute renal failure

*monitor via CPK and aldolase

36
Q

so Erythromycin and Statin doctor should–>

A

Erythromycin–> CYP3A4 inhibitor–> rhabdomyolysis

  • ->consider another macrolide such as azithromycin which is not a CYP3A4 inhibitor
  • ->reduce dose of either
  • ->monitor for muscle enzymes
  • ->change statin
37
Q

only statins which are substrates CYP3A4

A

simvastatin
lovastatin
atorvastatin

38
Q

ranitidine interaction MOA

A

affects absorption of other drugs

–> raises stomach pH which would caused increased absoprtion of basic drugs

39
Q

ranitidine increases uptake of…

A

triazolam–> benzo sedative agent

*increases bioavailabiltiy

40
Q

bile sequesterant agents will bind up and decrease absorption of

A

propanolol–> a beta blocker

*decreases bioavailability

41
Q

heavily protein bound drugs should not be given with…

A

other protein bound drugs

*warfarin and valproic acid

42
Q

Conditions leading to toxicity/overdose of heavily protien bound drugs

A
  • -> when protein sites become saturated
  • ->physiologic/pathologic states causing hypo-albuminemia
  • -> when protein bound fraction is altered and more free drug enters the plasma
43
Q

agents that bind up a toxin and promote safe renal elimination

A

chelating agens

–> for toxic agents such as iron, mercury etc

44
Q

what is important about wafarin and chronic NSAID use

A

DUPLICATION OF OVERALL EFFECT

both produce anti-coag state–> but through different effects–> increased bleeding risk

45
Q

MEASURABLE CHARACTERISTIC OF WARFARIN PLUS NSAIDS

A

INCREASD INR

46
Q

SSRI’S SHOULD NOT BE GIVEN WITH

A

other drugs or herbal remedies that increase serotinin levels

  • -> drugs than inhibit CYP metabolism
  • ->TRYPTANS–RECEPTOR ANTAGONISTS WHICH MAKE SEROTONINE MORE POTENT
  • CAN LEAD TO SEROTONIN SYNDROME AND HTN CRISIS WITH NON-SELECTIVE MAOI’S
47
Q

DIFFERENT TARGETS, UNRELATED PATHWAYS

*beneficial

A

AMOXICILLIN + CLAVULANATE

48
Q

DIFFERENT TARGETS, RELATED PATHWAYS
*beneficial

synergistic

A

salmeterol + fluticasone

salmeterol–> agonist on beta 2 receptors
fluticasone upregulates beta 2 receptors
*synergistic T-cell activation and apoptosis induction

49
Q

Upstream-Downstream targets
*beneficial
synergistic

A

sulfamethexazole + trimethoprim

50
Q

facilitated action

A

erythromycin + penicillin

*penicillin weakens cell wall (increases effectiveness of erythromycin) and erythromycin is able to penetrate better

51
Q

indirect ineraction with caffeine

A

xanax and echinacea

52
Q

indirect effect of signalling cytokine

A

lisinopril and aspirin–> removed PG’s

–>coupling effect is removed and Lisinopril effect not as large

53
Q

penicillin ad plavix both have affects on

A

platelets

54
Q

Enhanced distribution/localization

*potentiation effect

A

ergotamine and caffeine

caffiene increases water solubility of ergoteramine thus increasing its absorption

55
Q

additive equivalent action

A

niacin (b3) + simvastatin

–> both drugs either decrease secretion or decrease synthesis–> lowering LDL

56
Q

captopril leads to what

A

retension of potassium–> pro-arrhythmogenic

ACE inhbitor

57
Q

Same target different binding site

A

cisplatin + cyclophosphamide

–> compliment each others actions

58
Q

Same target: increases capalities

A

methotrexate + flourouracil

M binds to F when bound to thymydylate synthase–> increase activity

59
Q

Same target: Pharmacologic antagonism

A

propanolol + salmterol

–> taking propanolon cannot respond to salmeterol bc the B2 adrenergic receptor is blocked by propanolon (non-specific beta blocker)

60
Q

when a previously stable pt. starts a new drug and new symptoms start what is assumed to be responsible

A

the new drug!

CMOD (19 decks)

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