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NRS 270: Pharmacology > Module 3: Drug Interactions and Therapeutic Monitoring > Flashcards

Module 3: Drug Interactions and Therapeutic Monitoring Flashcards

1
Q

Mechanisms of Drug Interaction

Pharmacodynamiscs vs Pharmacokinetics

A
  • Pharmacodynamics:
    • drugs influence each other’s effects directly
      • competition at receptors
      • 2 drugs having similar actions through different cellular mechanisms
  • Pharmacokinetics
    • drugs affecting absorption, distribution, metabolism, and excretion
      • affecting the effective concentration at their sites of action
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2
Q

Mechanisms of DDI:

Protein Binding

A
  • highly-protein bound drugs –> enhanced toxicity if binding sites of plasma become saturated with another drug
  • ex. Warfarin effects are enhanced when it is displaced from plasma proteins by valproic acid
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3
Q

Mechanisms of DDI:

Receptor Binding

A
  • drugs competing at the receptor level
  • ex. Buprenorphine (partial agonist/antagonist) binds to opioid receptors which prevents euphoria from opioid drug abuse
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4
Q

Mechanisms of DDI:

Therapeutic Action

A
  • 2 drugs work toward the same therapeutic actions
  • ex: ASA (acetylsalicylic acid [aspirin]) + Heparin = increase risk of bleeding
    • sulfonylureas(increase insulin release from beta cells of pancreas) + metformin (blood sugar regulator) = increase risk of hypoglycemia
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5
Q

Classification of Chemical Interactions

A
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6
Q

Pharmacodynamic Interactions:

Additive Effects

A
  • combination of drug leads to added effects
  • ex: sedatives–potentiate each others sedation effects
    • alcohol–potentiates the sedative effects of many drugs
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7
Q

Pharmacodynamic Interactions:

Synergistic Effects

A
  • combination of drugs multiply their effects
    • Ex. Anti-infectives: vancomycin and aminoglycosides
      • ritonavir(HIV antiviral) and atazanavir (HIV antiviral)
    • ex. Pain therapy
      • amitriptyline (antidepressent and nerve pain medication) and morphine
      • gabapentin and morphine
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8
Q

Pharmacodynamic Interactions:

Potentiation

A
  • the effect of one drug is greatly increased by the intake of another drug without noticeable effect of the second drug
    • ex. amoxicillin + clavulanate potassium enhances the activities of amoxicillin against bacteria
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9
Q

Pharmacodynamic Interactions:

Antagonistic

A
  • one drug impedes the effects of another drug
    • ex. NSAIDs and ACE inhibitors
      • Propranolol and albuterol
      • NSAIDs and ASA
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10
Q

Spironolactone Eplerenone

A

Blocks Na+/K+ ATPases pump synthesis

  • blocks the action of aldosterone
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11
Q

ACE Inhibitors and Aldosterone antagonist

A
  • aldosterone antagonist = spironolactone eplerenone
    • blocks Na+/K+ ATPase pump synthesis
  • 2 agents working on the same pathway
    • more potassium retention can lead to serious hyperkalemia
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12
Q

Pharmacokinetic Interactions:

Absorption

A
  • drug binding:
    • ex. calcium reduces absorption of alendronate (osteoporosis tx)
    • Tetracyclin (TCN) and quinolones (antibiotics) are prone to chelate with multivalent cations which reduces absorption
  • GI motility
    • ex. Metoclopramide (antiemetic and gut motility stimulator) increases GI motility which will lower the level of digoxin (antiarrhythmic, BP stabilizer, cardiac glycoside)
  • GI pH
    • most drugs are weak acids or bases, and pH can affect their solubility
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13
Q

When pH is high, how will it affect the number of ionic species of a weak acid

A
  • when pH is high, more ionic species are present
    • Ex. Methotrexate (MTX– cancer therapy) + coca cola can reduce urine pH (less ionic species) which leads to reduced elimination and increases the MTX level which can lead to toxicity
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14
Q

urinary pH and elimination in the presence of a weak acid

A
  • higher urinary pH = more elimination in the urine (i.e. lower plasma concentration)
  • lower urinary pH = less elimination in the urine (i.e. higher plasma concentraion
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15
Q

weak bases, pH, and number of ionic species

A
  • when pH is low, more ionic species are present for a weak base
  • ex. levothryoxine (pKa = 10)– TSH increases after proton pumo inhibitor was introduced for 2-6 months leads to increased gastric pH and the average dose of levothryoxine had to be increased 35%
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16
Q

Pharmacokinetic Interactions:

Inhibition interactions

A
  • certain drugs will inhibit CYP450 which can lead to serious DDI
  • ex. Floconazole (antifungal) inhibits CYP2C9 which increases warfarin bioavailability
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17
Q

Pharmacokinetic Interactions:

Induction Interactions

A
  • influenced by biotransformation of a drug
    • inducing CYP450 will reduce the effect of the drug that is metabilized by that liver enzyme
    • ex. carbamazepine + warfarin will lead to reduced INR
18
Q

Pharmacokinetic Interactions:

DDI affecting elimination

A
  • ex. Vitamin C reduces urine pH
    • this will reduce excretion of acidic drugs (i.e. ASA)
    • this will also increase excretion of basic drugs (i.e. pseudoephedrine)
19
Q

P-glycoproteins

A
  • when induced, they accelerate efflux transporters
    • leads to sub-therapeutic concentration
  • when inhibited, they deccelerate efflux transporters
    • leads to toxicity
  • aka p-gp
20
Q

ABCC2

A
  • ATP-binding cassette = ABC transporter
  • type of efflux drug transporter

these use energy to pump drugs out of the cell before the drugs can elicit their effects

21
Q

ABCG2

A
  • BCRP = breast cancer resistance protein
  • type of efflux drug transporter

these use energy to pump drugs out of the cell before the drugs can elicit their effects

22
Q

MRP2

A
  • multi-drug resistance protein
  • type of efflux drug transporter

these use energy to pump drugs out of the cell before the drugs can elicit their effects

23
Q

Pharmacokinetic Interactions:

Induction of p-gp

A
  • induction of p-glycoprotein accelerates the efflux transport of the drug and leads to sub-therapeutic concentrations (decrease bioavailability)
24
Q

Pharmacokinetic Interactions:

inhibition of efflux transporters

A
  • when efflux transporters are inhibited, they cannot pump out the drug, thereby increasing the bioavailability and potentially leading to toxicity
25
Q

Lab Tests and Therapeutic Monitoring:

Carbamazepine

A
  • anticonvulsant
  • therapeutic range: 4-12 mmcg/mL
  • comments:
    • toxic level: >12mcg/mL
    • half-life: 10-26 hours in adults (repeated dosing)
    • half-life: 25-65 hours (initial doses)
  • Time to steady state: >4 weeks due to autoinduction
  • Monitoring: draw trough immediately prior to next dose
  • CAN AUTO-INDUCE!
26
Q

Lab Tests and Therapeutic Monitoring:

Digoxin

A
  • anti-arrhythmic and blood pressure support, cardiac glyoside
  • therapeutic range: 0.8 to 2.0 ng/mL
  • comments:
    • toxic level >2.4ng/ml
    • half life: 33-51 hours
    • steady state: 7-10 days (possibly longer)
  • Monitoring: draw serum digoxin levels:
    • at least 4 hours after an IV dose OR
    • 6 hours after an oral dose to allow sufficient time for drug distribution
27
Q

Lab Tests and Therapeutic Monitoring:

Lithium

A
  • antimanic, regulates glutamate
  • therapeutic range: 0.5-1.2mEq/L
  • comments:
    • potentially toxic level: > 1.5mEq/L
    • half life: 17-36 hours
  • Monitoring- draw levels:
    • just prior to the next dose OR
      • at least 6-12 hours after the last dose
28
Q

Lab Tests and Therapeutic Monitoring:

Phenobarbital

A
  • anticonvulsant, barbiturates
  • therapeutic range: 15 - 40 mcg/mL
  • comments:
    • steady state: 15-25 days
    • toxic level >40mcg/mL
      • half life: 1.5-3 days
  • Monitoring: draw levels:
    • during peak: 4-12 hours after dose
    • trough: immediately prior to next dose
29
Q

3 ways poisoning occurs:

A
  1. Therapeutic drugs
  2. non-therapeutic drugs
  3. chemical exposures
  • 2 million estimated hospitalized pts / year due to serious adverse drug reactions
    • 100,000 of these cases are fatal
30
Q

Passive Poisoning Prevention Strategies

A
  1. Reduce manufacture/sale of poisons
  2. Decrease amount of posion in a consumer product
    1. limiting # of pills in a single bottle of baby aspirin
  3. Prevent access to poison
    1. the use of child-resistant packing
  4. Change product formulation
    1. Removing ethanol from mouthwash
31
Q

9-rights of Drug Administrion

A
  1. right drug
  2. right patient
  3. right dose
  4. right route
  5. right time
  6. right reasons
  7. right responses
  8. right documentation
  9. right of pt to refuse
32
Q

Acute Poisoning Treatment Goals

A
  • maintain vital physiological functions
  • keep concentration of poison in itssues as low as possible
    • preventing absorption
    • enhancing elimination
  • combat the toxicological effects of the posion at the effector site
33
Q

Decontamination Mechanisms

A

Dependent on route of exposure

  1. wash eyes and skin copiously, if needed
  2. GI decontamination
    1. gastric emptying
      1. induce vomiting
      2. gastric lavage
      3. whole bowel irrigation
    2. Catharsis - stimulate bowel evacuation
  3. Enhancing Elimination
    1. manipulating urinary pH
    2. multiple dose of activated charcoal
    3. hemodialysis
  4. Administering an antidote
34
Q

Lab Tests and Therapeutic Monitoring:

Phenytoin

A
  • anticonvulsant
  • Therapeutic Range:
    • total: 10-20mcg/mL
    • Free: 1-2mcg/ mL
    • ***NEED TO CORRECT FOR ALBUMIN**
35
Q

NAPQI

A
  • toxic intermediate in the metabolism of acetaminophen
  • occurs when acetaminophen is metabolized by CYP2E1
    • ethanol/alcohol induces this enzyme
      • increases levels of NAPQI to toxic levels that the body cannot clear
36
Q

Sedative/Hypnotic, Opioid, Cholinergic, and Ca2+ Channel Blockers will generally do what:

A

Induce suppressive responses

37
Q

Sympathomimetic, Anticholinergic, and Salicylate will generally do what

A

Induce high BP, high HR, increased temp, enlarged pupils

38
Q

NSAIDs and Diuretics

A
  • NSAIDs will reduce the effect of any diuretics
    • with ACE inhibitors, they both lower the GFR too much may induce kidney failure and stop the diuretic effects of the ACE inhibitor
  • NSAID = constricts the afferent arteriole of glomerulus = decreased GFR
  • ACE inhibitors = dilate the efferent arteriole of the glomerulus = also decreased GFR
39
Q

Functions COX-1

A
  • “Constitutive”
    • produced in a constant amount
  • enzyme
  • protects the GI mucosa
  • platelete formation and hemostasis
  • blocked by ASA and non-specific NSAIDs
40
Q

Functions COX-2

A
  • enzyme
  • inducible
  • mediate pain, inflammation, and fever
  • blocked by non-specific NSAIDs and COX-2 NSAIDs
41
Q

NSAIDs, ASA, and COX-1/2

A
  • Ibuprofen (non-specific NSAID) will outcompete ASA at the inhibition of COX-1
    • ibuprofen does not inhibit it as significantly as ASA
      • ASA is an irrereverisble antagonist and will totally “kill” the receptor.
      • decreased antiplatelete effects
        • decreased protection from CAD (coronary artery disease)
42
Q

SSRIs, platelet activation, and NSAIDs

A
  • platelets need to be activated by seratonin
  • non-specific NSAIDs inhibit COX-1
  • taking both an SSRI and non-specific NSAID can increase risk of GI bleeds

NRS 270: Pharmacology (14 decks)

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