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Pharmacology > Pharmacokinetics > Flashcards

Pharmacokinetics Flashcards

1
Q

Pharmacokinetics

A

Study of how body impacts drugs

  1. Absorbed
  2. Distributed
  3. Eliminated
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2
Q

Standard drug dose

A

Based on trials in healthy ind. w/ average physiology

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3
Q

Therapeutic window

A

Increased effectiveness

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4
Q

Adverse response

A

Toxicity

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5
Q

Pharmacokinetics affected by

A
  1. Age
  2. Liver and renal function
  3. Fat/lean tissue
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6
Q

Physiological barriers to drugs

A
  1. Cell membrane
  2. Large, polar molecules
    A. Protein pores/channels
    B. Facilitated (SLC transporters) or active carriers (ABC)
    **many drugs work on membrane receptors outside cell
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7
Q

Drug diffusion

A
  1. Effects of charge
    A. Most drugs charged (acids/bases)
    B. PH/ion trapping: pKa < pH = charged; pKa > pH = uncharged
    C. Clinical application: inc. drug clearance
    1. Alkaline urine -> excrete weak acids (pKa= pH + log [HA/A-])
    2. Acidic urine -> excrete weak bases (pKa= pH + log [BH+/B])
  2. Blood brain barrier
    A. Tight junctions prevent passive diffusion
    B. CNS drugs hydrophobic
    C. Intrathecal administration
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8
Q

Absorption

A
  1. Enteral
  2. Paraenteral
  3. Mucous membrane
  4. Transdermal
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9
Q

Enteral absorption

A 
Pros:
 1. Easy
 2. Inexpensive
 3. No injection
Cons:
 1. Harsh GI tract
 2. 1st pass metabolism
 3. Slow distribution
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10
Q

Paraenteral absorption

A 
Pros:
 1. Rapid delivery
 2. High bioavailability
 3. No 1st pass metabolism
Cons:
 1. Irreversible => dose important
 2. Infection
 3. Pain/fear
 4. Skilled personnel required
Routes:
 1. Subcutaneous
 2. Intramuscular
 3. Intrathecal
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11
Q

Mucous membrane absorption

A 
*example: nitroglycerin
Pros: 
 1. Rapid delivery
 2. No 1st pass metabolism
 3. Simple/convenient
Cons:
 1. Few drugs
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12
Q

Transdermal absorption

A 
Pros:
 1. Simple/convenient
 2. Painless
 3. Continuous/prolonged administration
 4. No 1st pass metabolism
Cons:
 1. Requires highly lipophilic
 2. Slow delivery
 3. Possibly irritating
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13
Q

First pass metabolism

A
  • liver
    1. Oral drugs only
    2. Dec. amt reaching tissue by inactivating drug
    3. Pro-drugs: activated by 1st pass metabolism
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14
Q

Bioavailability (F)

A
  1. Fraction of unchanged drug reaching circulation
  2. 0 < F < 100
  3. Factors:
    A. Absorption
    B. 1st pass metabolism
  4. Routes:
    A. IV = 100%
    B. IM = 75-100%
    C. SubQ = 75-100%
    D. Oral = 5-100%
    E. Rectal = 30-100%
    F. Inhalation = 5-100%
    G. Transdermal = 80-100%
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15
Q

Bioequivalence

A

Drugs with same system bioavailability and predictable drug response

  1. Generic and brand name
  2. Same amt. active ingredient
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16
Q

Loading dose

A

Initial dose administered to compensate for distribution

  1. Dependent on Vd
  2. Gets into therapeutic range faster
    * *w/o loading dose takes 3-5 half-lives to get to steady state
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17
Q

Steady state

A

Therapeutic dosing maintained between peak and through

1. Takes 3-5 half-lives to achieve

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18
Q

Maintenance dose

A

Maintains steady state concentrations

  1. Subsequent doses replace drug metabolized or excreted
  2. Dosing schedule
  3. Dependent on clearance
    * clearance= (metabolism + excretion)/([drug]plasma)
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19
Q

Distribution

A

Drug must reach target organs at therapeutic dose
1. Sanctuary compartments: tight junctions don’t allow drug in/out
A. BBB and testes (BTB)
2. [Drug]plasma correlates w/ [Drug]tissue
3. Tissues vary
A. H2O soluble: blood
B. Fat soluble: cell membrane, adipose, fat-rich areas
*marijuana

20
Q

Volume of distribution (Vd)

A

Fluid volume required to contain total amt. absorbed drug at uniform concentration
1. Vd = (amt. drug in body (mg))/([Drug]plasma (mg/L))
2. Extrapolated, not physical volume => can exceed body volume
3. Can’t be lower than plasma volume (4L)
4. Predicts whether drug will reside in blood or tissue
A. Small Vd -> blood
B. Large Vd -> tissues
5. Total body H2O and Vd
A. Vd=4 (low) - blood (heparin)
B. Vd=10 (medium) - ECF (mannitol)
C. Vd=42 (med-high) - total body H2O (alcohol)
D. Vd >42 (high) - in specific cells/tissues (chloroquine, azithromycin, digoxin)
6. Tissue distribution and Vd
A. Rate of accumulation depends
1. Blood flow to organ
2. Chem of drug
3. Plasma
B. Adipose can act as reservoir
C. Vd takes distribution to different tissues into account

21
Q

Drug-protein binding

A
  1. Usually reversible in plasma
  2. Binding proteins
    A. Albumin: most abundant, acid drug binding
    B. Alpha-1 acid glycoprotein: basic drug binding
    C. Lipoproteins: lipophilic drug binding
  3. Bound = inactive
  4. Importance
    A. Disease can dec. binding -> inc. free drug -> toxicity
    1. Hypoalbuminemia
    2. Ceftrioxone in neonates can make it worse
      B. Difficult to demonstrate clinical significance
    3. Monitor low clearance drugs:
      A. Warfarin: Vd=8L and PPB= 99%
      B. Phenytoin (anti-epileptic): PPB = 96%
      C. Tolbutamide (anti-diabetic): PPB= 96%
22
Q

Distribution w/ pediatric consideration

A

Neonates and infants

  1. Dosing (mg/kg)
  2. Inc total body H2O and ECF -> inc. Vd for hydrophilic drugs
  3. Dec. plasma protein -> inc. free drug %
  4. Dec. body fat -> dec. Vd lipid-soluble drugs
23
Q

Distribution w/ elderly consideration

A
  1. Dec. total body H2O -> dec. Vd hydrophilic
  2. Inc. fat -> inc. Vd lipid soluble and prolonged half-life
  3. Protein binding fairly constant
    A. Acute illness
    1. Dec. albumin -> inc. % free drug (acidic)
    2. Inc. alpha-1-acid glycoprotein -> inc. % free drug (basic)
24
Q

Cytochrome P450 enzyme system

A
  1. Superfamily of heme-protein monooxygenases
  2. SER of hepatocytes
  3. Mostly metabolize hydrophobic drugs (75% of drugs on market)
  4. 18 families, 6 important for metabolism
    A. CYP3A4 - inducer = St. John’s Wart, inhibitor = grapefruit
    B. CYP2D6
    C. CYP2C19
    D. CYP2C9
    E. CYP2E1 - inducer =ETOH
    F. CYP1A2 - inducer = tobacco smoke
  5. Genetic variation
    A. Polymorphism/mutations alter drug metabolism
    B. Pharmacogenomics
25
Q

Outcomes of drug metabolism

A
  1. Active drug -> inactive metabolite
  2. Unexcretable lipophilic drug -> excretable metabolite
  3. Active drug -> active metabolite (inc. effect)
  4. Inactive prodrug -> active drug
  5. Active drug -> toxic metabolite
26
Q

Drug metabolism Phase I reactions

A
  1. Redox reactions
  2. Purpose: uncover hydrophilic moeity-> inc. hydrophilicity for renal elimination
  3. Mediated by CYP450 in liver
  4. Enzymes dec. w/ age
27
Q

Drug metabolism Phase II reactions

A
  1. Conjugation/hydrolysis reaction
  2. Purpose: inc. polarity by adding hydrophilic moeity -> inactive metabolite
  3. Inc. urine and bile excretion
  4. Reactions:
    A. Glucuronidation
    B. Acetylation
    C. Sulfation
  5. Important in neonates
    A. Dec. UDP-glucuronyl transferase (UDPGT) -> inc. risk jaundice
28
Q

Renal excretion

A
  1. Major route
  2. Kidneys receive 25% systemic blood flow
  3. Rate elimination depends on:
    A. Drug filtered
    B. Reabsorbed
    C. Secreted
29
Q

Elimination kinetics

A
  1. Half-life: used to estimate dosing to maintain therapeutic levels
    A. First-order (95% drugs)
    **t1/2= (0.693 x Vd)/clearance
30
Q

Pharmacokinetics

A
  1. Biochem and physiological mechanism of drug actions
    A. Relate to molecular interactions between body constituents and drugs
  2. Determine efficacy, potency, and toxicity
  3. Dose-response relationships
31
Q

Dose-response relationships

A
  1. Emax = largest effect drug can produce
  2. ED50 = dose that produce therapeutic effect in 50% pop
  3. LD50 = dose lethal to 50% animals (adverse effect in humans)
  4. Therapeutic index (TI) = LD50/ED50
32
Q

Efficacy

A

Drug effectiveness

33
Q

Potency

A

Amt drug needed to produce same effect

34
Q

Ligand

A

Agonist or antagonist chemical that binds receptor

35
Q

Receptor

A

Target/site of drug action

36
Q

Affinity

A

Attraction of drug to receptor

37
Q

Selectively

A

Specific affinity for certain receptors

38
Q

Pharmacological agonists

A
  1. Mimic endogenous neurotransmitters

2. Inc. affinity and specificity

39
Q

Pharmacological antagonists

A

Block neurotransmitters

  1. Competitive: dec potency of agonist, Emax same
  2. Noncompetitive: potency same, dec. Emax
  3. Partial agonist: act as full agonist but dec. Emax
  4. Inverse agonist: causes opposite action
40
Q

Physiological antagonists

A
  1. Activate physiological responses that oppose agonist-mediated response
    * example: sympathetic NS vs. parasympathetic NS
41
Q

Receptor types

A
  1. Enzyme: linked to kinase -> phosphorylation reactions
  2. Ligand-gated ion channel: allows ion to pass through (nicotinic acetylcholine receptors)
  3. G-protein-coupled receptors: linked to G-proteins -> secondary messenger systems
  4. Transcription factors: intracellular, affects gene transcription => takes longer
  5. Characteristics:
    A. Specificity
    B. Sensitivity (up-regulation): antagonist -> inc receptors -> inc response after antagonist removed
    C. Tolerance (down-regulation): long-term agonist exposure -> dec receptors-> dec physiological response
42
Q

Additive interactions

A

Sum of effects

43
Q

Synergistic

A

Effect > sum

44
Q

Tachyphylaxis

A

Dec drug response

45
Q

Factors influencing drug response

A
  1. Prescribed dose
  2. Administered dose
  3. [Drug] at action site
  4. Drug effects

Pharmacology (4 decks)

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