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DT4- Exam 3 > Valentovic- Drug Interactions - Leah :) > Flashcards

Valentovic- Drug Interactions - Leah :) Flashcards

1
Q

What patients are predisposed to DD interactions? (5)

A
  • multiple meds
  • female (OCPs + CYP inducer–> ineffective)
  • age extremes
  • major organ/metabolic/ endocrine dysfxn
  • genetic polymorphisms
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2
Q

3 examples of drugs that effect OCP efficacy?

A
  • Rifampin, St. Johns Wart (CYP inducers–> less effective)

- Abx (alters gut flora)

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3
Q

Define pharmacokinetics + dynamics:

A

-pharmacokinetics= what body does to drug
-pharmacodynamics= what drug does to body
(Dynamic= D= “D”rug action on body)

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4
Q

Describe the difference between precipitant and object drugs:

A
  • precipitant: effects body
    (i. e. alcohol = more NAPQI production)
  • object drug: drug effected by initial modification
    (i. e. acetaminophen)
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5
Q

What are three types of pharmacodynamic interactions?

A
  • additive (alcohol + BDZ = ^^ resp depression)
  • antagonistic (BDZ + flumazenil)
  • synergistic (aminoglycoside + succinylcholine = ^^ resp depression during surgery)
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6
Q

How do aminoglycosides interact with succinylcholine in surgery?
How do you reverse these effects?
What kind of interaction is this?

A

This is an example of synergistic pharmacodynamic interaction:

-further increase respiratory depression
(presynaptic acetylcholine synthesis decreased by AGs)
-neostigmine can reverse these effects
-pharmacodynamic interaction
(precipitant = AG; object drug= succinylcholine)

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7
Q

What two types of interactions effect the absorption of a drug? How do we work around this?

A

-drug-drug
-drug-food
(altered pH, chelation, transport, metabolism)
-should stagger drugs or drugs/ meals

Ex: cholestyramine should be staggered with food

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8
Q

Antacids:
What can they contain?
What drug can they prevent from being absorbed?

A
  • Ca, Mg, Al

- Complex with TCN –> tetracycline excreted in feces

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9
Q

Cholestyramine effects the absorption of what two drugs? Via what mechanism?

A

-digoxin
-warfarin
(forms complex)

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10
Q

Mycophenolate mofteil:

  • MOA
  • COMPLEXES with what drugs? (2)
A

-Immunosuppressant: Inosine monophosphate dehydrogenase (IMPDH) inhibitor

  • ferrous sulfate/ iron 2+ containing vitamins and Ca, Mg, Al (antacids)
  • NOT influenced by pH; don’t interact w/ bicarb*
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11
Q

How do drugs that decrease GI motility affect absorption? What drugs slow motility? (2)

A
  • slow peak time, but not extent of absorption (bioavailability)
  • morphine/ amitryptilline + other tricyclics
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12
Q

How do drugs that increase GI motility affect absorption?

What drug increases GI motility?***

A
  • shorter peak time, but no change in extent of absorption

- metaclopromide

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13
Q

How do H2 antagonists (–idines) and PPis (–prazole) effect ketaconazole/ itraconazole absorption?

A
  • INCREASE stomach pH –> decreased absorption and levels of ketaconazle/ itraconazole
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14
Q

In addition to azoles, what drug also has decreased bioavailability when taken with PPis?

A

-atazanavir (HIV protease inhibitor)

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15
Q
  • ATP dependent transporters known as the “gatekeepers of metabolism” are called___?
  • What specifically is their function?
  • Where in the intestine are p glycoproteins found?
A
  • P glycoproteins
  • transport lipophilic substances out of the brain, liver, etc –> to bile, gut lumen, urine (excrete lipophilic substances)
  • Enterocytes of small intestine
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16
Q

What 4 substances are known to inhibit P glycoproteins?

What drugs will be “object” drugs when taking a P glycoprotein inhibitor? What will be the effect?

A
  • ketaconazole
  • Erythro, clarithromycin
  • Grapefruit juice
    (Many CYP3A4 also = P glycoprotein inhibitors; may balance effects…)

-Drugs that are P glycoprotein substrates will be “object” drugs (i.e. cyclosporin) and have ^^^^ absorption

17
Q

How is the efficacy of:
-OCPs
-digoxin
Changed when taking abx?

A
  • OCP efficacy decreased

- Digoxin efficacy ^^ (^^^ blood levels due to ^^^ enterohepatic circulation when gut bacteria are killed)

18
Q

Which drugs have drug-drug binding displacement interactions?
What happens to the “object” drug?

A
  • drugs that are more than 90% protein bound can have drug-drug binding displacement interactions
  • one of the two drugs will have a higher free fraction that normal (important when drug normally has a very SMALL free fraction)
19
Q

***Example of a drug-drug binding displacement interaction

A
  • Warfarin = 99% protein bound

- TMP-SMX displaces warfarin and can ^^ INR to 6 (normal is below 3)

20
Q

Five drugs known to DECREASE/ INHIBIT
cyp450 activity?

KNOW THESE FOREVER

A
  • ketaconazole (3A4)
  • erythromycin (3A4)
  • clarithromycin
  • grape fruit juice
  • cimetidine (ALL CYPs)

(INCREASE availability of drugs that are cyp 450 metabolites, i.e. warfarin)

21
Q

Four drugs known to INCREASE CYP 450 acitvity?
Which cyps for each drug?

KNOW THESE FOREVER

A
  • St Johns Wart
  • Rifampin (3A4, 2C9, 2C19)
  • Phenytoin (3A4)
  • Carbamazepine (3A4)

(DECREASE availability of drugs that are cyp450 metabolites, i.e. warfarin)

22
Q

CYP 1A2 is induced by ____/_____ and its substrate is____.

A
  • cigarette smoke, phenobarbital
  • theophylline

***You had phenytoin, and that might have been right but I am going off of the chart on slide 19; I might be misreading it or I might have missed this elsewhere in the notes.

23
Q

How are opioids effected when combined with abs?

Which two antibiotics in particular will affect their metabolism?

A

Decreased clearance with erythromycin and clarithromycin = ^^ risk of oxycodone OD due to P450 inhibition

24
Q

Which CYP metabolizes warfarin?

A

CYP3A4

25
Q

There are no known inducers/ few inhibitors of CYP2D6, so why is it important?

A
  • 33% drugs metabolized by this cyp

- Many POLYMORPHISMS: AA > whites > asians

26
Q

How is CYP2D6 implicated in therapy with tamoxifen?

A
  • Slow CYP2D6 metabolizers get less active metabolite formation = drug is not effective
  • siX= tamoXifen
27
Q

Clopidigrel metabolism is dependent on which CYP?

Population this should be considered in?

A
  • 2C19; 2”C”19= “C”lopidigrel
  • Less effective in slow metabolizers because drug requires formation of active metabolite
  • 20% Asians are SLOW CYP2C19 metabolizers
28
Q

Two ways renal elimination may be involved with DD interactions:

A
  • altered tubular secretion

- altered tubular reabsorbtion

29
Q

Give two examples of DD interactions in which the “object drug” has inadequate “renal secretion”.

A
  • increase penicillin t1/2 by giving probenecid (probenecid more tightly binds secretion transporters= penicillin cant be secreted)
  • Giving bactrim will ^^ methotrexate by the same mechanism
30
Q

How does bactrim effect renal reabsorption of electrolytes?

A

-High dose bactrim (HIV) inhibits Na ATPase and sodium reabsorption at distal tubule–> HYPERkalemia

(Do not mistake for renal failure)

31
Q

How can NSAIDs/ diuretics effect renal reabsorption of electrolytes and lithium?

Which diuretics are especially implicated?

A

-NSAIDs and diuretics (esp THIAZIDES) increase Na/Water reabsorption as well as LITHIUM reabsorption

NOTE: Uworld question- Thiazide + Lithium can = acute lithium toxicity (see tremor, ataxia —> coma)

32
Q

What drug interaction occurs by inhibiting p-glycoprotein at the kidney?

A

-Quinidine blocks renal p glycoprotein —> ^^^ levels of digoxin

33
Q

How does urine pH effect renal excretion of drugs?

A
  • nonionized drugs all reabsorbed
  • low pH = basic drugs ionized and excreted
  • high pH= acidic drugs ionized and excreted
34
Q

How does acetazolamine effect blood/urine pH and how do these changed effect excretion of quinidine/amphetamines?

A
  • Acidifies blood (^^^ HCO3- excretion in PT)

- Alkalinize urine –> unionized quinidine + amphetamine–> ^^ reabsorption

35
Q

How does acetazolamide effect levels of aspirin in the blood?

A

^^ HCO3 excretion–> ACIDIFICATION of blood–> ^^ aspirin toxicity–> ^^ unionized ASA freely crosses BBB

36
Q

Which macrolides have a greater potential to interact with other drugs and why?

A

-erythromycin and clarithromycin are more likely than azithromycin to cause DDis because they are CYP inhib’s

37
Q

Which H2 inhibitor is most likely to cause DDis? Least?

A
  • cimetidine most (inhibits all CYPs)

- ranitidine least

38
Q

Which statins are most likely to cause DDIs? Least?

A
  • lovastatin and atorvastatin most likely (prodrugs)

- fluva, prava, rosuva least likely (not pro-drugs)

DT4- Exam 3 (14 decks)

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