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Pharmacology > pharmacokinetics + pharmacodynamics > Flashcards

pharmacokinetics + pharmacodynamics Flashcards

1
Q

Km in enzyme kinetics is AKA

A

the Michaelis-Menten constant

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2
Q

Michaelis Menten kinetics: Km is? (definition)

A

the substrate concentration at which the reaction rate is half of Vmax

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3
Q

Michaelis Menten kinetics: Vmax is? (definition)

A

represents the maximum rate achieved by the system, at maximum saturation of the substrate concentration

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4
Q

Michaelis Menten kinetics: Km is …. related to the ….

A

inversely related to the affinity of the enzyme for its substrate

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5
Q

Enzyme kinetics - curves?

A
  • Most enzymes reactions follow a hyperbolic curve (eg. Michaelis Menten kinetics)
  • enzymatic reactions that exhibit a sigmoid curve usually indicate cooperative kinetics (eg. hemoglobin)
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6
Q

Michaelis Menten kinetics - effects of noncompetitive inhibitors on the curve

A
  • platue is lower
  • V max is lower / V1/2 lower
  • Km is the same
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7
Q

Michaelis Menten kinetics - effects of competitive (reversible) inhibitors on the curve

A
  • platue is the same
  • V max is the same / V1/2 same
  • Km is increased
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8
Q

Lineweaver–Burk plot - axons?

A

X axon –> 1/(S)

Υ axon –> 1/(V)

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9
Q

Lineweaver–Burk plot - interceptions on axons

A

interception on y –> 1/Vmax

interception on x –> -1/km

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10
Q

Lineweaver–Burk plot - description

A
  1. higher y-intercept –> lower V max
  2. the further to the right the x-intercept (closer to zero), the greater the Km and the lower affinity
  3. slope = Km/Vmax
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11
Q

Lineweaver–Burk plot - slope

A

Km/Vmax

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12
Q

Lineweaver–Burk plot - reversible competitive inhibitor

A

bigger Km (closer to 0), same Vmax (the same interception on y axon) –> cross each other competitively

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13
Q

Lineweaver–Burk plot - non competitive inhibitor

A

start from the same point at X axon (same K) but passes from higher point at Y axon (smaller V max)

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14
Q

reversible competitive inhibitor vs irreversible competitive inhibitor vs noncompetitive inhibitor according to resemble substrate

A

reversible competitive inhibitor –> Yes
irreversible competitive inhibitor –> Yes
noncompetitive inhibitor –> no

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15
Q

reversible competitive inhibitor vs irreversible competitive inhibitor vs noncompetitive inhibitor according to overcoming by increased (S)

A

reversible competitive inhibitor –> yes
irreversible competitive inhibitor –> no
noncompetitive inhibitor –> no

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16
Q

reversible competitive inhibitor vs irreversible competitive inhibitor vs noncompetitive inhibitor according to binding on active site

A

reversible competitive inhibitor –> yes
irreversible competitive inhibitor –> yes
noncompetitive inhibitor –> no

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17
Q

reversible competitive inhibitor vs irreversible competitive inhibitor vs noncompetitive inhibitor according to effects on V max

A

reversible competitive inhibitor –> unchanged (but reach it slower)
irreversible competitive inhibitor –> lower
noncompetitive inhibitor –> lower

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18
Q

reversible competitive inhibitor vs irreversible competitive inhibitor vs noncompetitive inhibitor according to effects on Km

A

reversible competitive inhibitor –> higher
irreversible competitive inhibitor –> unchanged
noncompetitive inhibitor –> unchanged

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19
Q

reversible competitive inhibitor vs irreversible competitive inhibitor vs noncompetitive inhibitor according to pharmacodynamics

A

reversible competitive inhibitor –> decreases potency
irreversible competitive inhibitor –> decreases efficacy
noncompetitive inhibitor –> decreases efficacy

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20
Q

Bioavailability (F) - definition and symbol

A

Fraction of administrated drug reaching systemic circulation unchanged. symbol: F

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21
Q

Bioavailability (F) for IV dose vs orally (explain)

A

IV –> F=100% (all in the blood)

Orally –> F typixally less than 100% due to incomplete absorption and first pass metabolism

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22
Q

Volume of distribution definition and symbol

A

Theoretical volume occupied by total amount of drug in the body to its plasma concentration (drug may distribute in more thatn 1 comartment)
symbol: Vd

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23
Q

Volume of distribution (Vd) - equation

A

Vd = (amount of drug in the body) / (plasma drug concentration)

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24
Q

Volume of distribution (Vd) may alter - example

A

Apparent Vd of plasma protein-bound drugs can be altered by liver and kidney disease (low protein binding –> increased Vd)

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25
Q

Volume of distribution (Vd) plasma protein-bound can be alter by

A

liver and kidney disease –> low protein binding –> increased Vd

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26
Q

low Volume of distribution (Vd) - compartment and drug types

A

compartment: blood

Drug types: Large/charged molecules/plasma protein bound

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27
Q

Medium Volume of distribution (Vd) - compartment and drug types

A

compartment: ECF

Drug types: small hydrophilic molecules

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28
Q

High Volume of distribution (Vd) - compartment and drug types

A

compartment: all tissues including fat

Drug types: small lipohilic molecules, esp if bound to tissue protein

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29
Q

drug clearance (CL) - definition

A

the volume of PLASMA cleared of drug per unit

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30
Q

drug clearance (CL) - equation

A

CL = rate of elimination of drug / plasma drug concentration = Vd x Ke (elimination constant)

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31
Q

drug clearance (CL) may be impaired with

A

defects in cardiac, hepatic or renal function

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32
Q

drug - half-life (t1/2) - de

A

the time required to change the amount of drug in hte body by 1/2 during elimination

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33
Q

steady state of drug

A

amount of drug going in is the same as the amount of drug getting taken out

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34
Q

In first order kinetics - a drug infused at a constant rate takes …. to reach steady state

A

4-5 half-lives

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35
Q

In first order kinetics - a drug infused at a constant rate takes …. to reach 90% of the steady state

A

3.3 half lives

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36
Q

drug - half-life (t1/2) - equation in fist order elimination

A

t1/2 = (0.693xVd) / CL

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37
Q

1-4 half lives and % remaining of drugs

A

1 –> 50%
2 –> 25%
3 –> 12.5%
4 –> 6.25 %

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38
Q

Loading dose calculation

A

(Cp x Vd) / (F)

Cp = target plasma concentrations at steady state

39
Q

Maintainne dose calculation

A

(Cp x CL x τ) / (F)
Cp = target plasma concentrations at steady state
τ = dosage interval (time between doses), if not administrated continuously

40
Q

time to steady state depends primarily on …. and is independent of …

A

depends: t 1/2
independent: dose and dosing frequency

41
Q

renal or liver disease effects on loading and maintenance dose

A

loading dose –> unchanged

maintenance dose –> decreased

42
Q

Types of drug interactions

A
  1. additive
  2. permissive
  3. synergistic
  4. Tachyphylactic
43
Q

Types of drug interactions - definitions

A
  1. additive –> effect of substance A and B together is equal to the sum of their individual effects
  2. permissive –> Presence of substance A is required for the full effects of substance B
  3. synergistic –> Effect on substance A and B together is greater than the sum of their individuals effects
  4. Tachyphylactic –> acute decrease in response to a drug after initial / repeated administration
44
Q

Types of drug interactions - additive - definition and examples

A

effect of substance A and B together is equal to the sum of their individual effects –> aspirin and acetaminophen

45
Q

Types of drug interactions - permissive - definition and examples

A

Presence of substance A is required for the full effects of substance B –> cortisol on catecholamine responsiveness

46
Q

Types of drug interactions - synergistic - definition and examples

A

Effect on substance A and B together is greater than the sum of their individuals effects –> Clopidogrel and aspirin

47
Q

Types of drug interactions - Tachyphylactic - definition and examples

A

acute decrease in response to a drug after initial / repeated administration –> MDMA and LSD

48
Q

Elimination of drug - ways

A
  1. Zero - order elimination

2. First order elimination

49
Q

Elimination of drug - zero order elimination?

A

Rate of elimination is constant regardless to Cp (target plasma concentrationsat steady state) –> constant AMOUNT of drug eliminated per unit

50
Q

Zero order elimination - effects on Cp (target plasma concentrationsat steady state)

A

decreases linearly with time

51
Q

Zero order elimination - examples of drugs

A
  1. Phenyntoin (at high or toxic high concentrations)
  2. Ethanol (at all clinically important concentrations)
  3. Aspirin (at high or toxic high concentrations)
52
Q

Elimination of drug - First order elimination

A

rate of elimination is directly proportional to drug concentration –> constant FRACTION of drug eliminated per unit time

53
Q

First order elimination - effects on Cp (target plasma concentrationsat steady state)

A

decreases exponentially per time

54
Q

First order elimination - examples of drugs

A

applies to more drugs

55
Q

First vs Zero order elimination according to t1/2

A

zero: time of t1/2 decreases as concentration decreases
first: time of t1/2 is constant as concentration decreases

56
Q

Urine pH and drug elimination - explain

A
  • ionized species are trapped in urine and cleared quickly

- Neutral forms can be reabsorbed

57
Q

Urine pH and drug elimination - weak acids - explain

A

ROOCH RCOO- + H+
(lipid soluble) (trapped)
Trapped in basic environment

58
Q

Urine pH and drug elimination - weak bases - explain

A

RNH3+ RNH2 + H+

Trapped in acidic environment

59
Q

Urine pH and drug elimination - weak bases vs acids according to trapping environment

A

acid –> Trapped in basic environment

bases –> Trapped in acidic environment

60
Q

weak acids - examples of drugs and treatment of overdose

A
  1. phenobarbital
  2. methotrexate
  3. aspirin
    treat overdose with biocarbonate (alkalization)
61
Q

weak basis - examples of drugs and treatment of overdose

A
  1. amphetamines
  2. TCAs
    treat with ammonium chloride (acidification)
62
Q

drug metabolism involves 2 major chemical pathways

A

phase I

phase I

63
Q

drug metabolism - phase I

A

Reduction, oxidation, hydrolysis with cytochromic P-450 usually yield slightly polar, water-soluble metabolites (often still alive)

64
Q

drug metabolism - phase II

A

Conjugation (methylation, Glucuronidation, Acetylation, Sulfation) usually yields vere polar inactive metabolies (renally excreted)

65
Q

drug metabolism - phase I vs II according to geriatric patients

A

geriatric patietns lose phase I first

66
Q

slow acetylators - drug elimination

A

Patients who are slow acetylators have increased side effects from certain drugs because of lower rate of metabolism

67
Q

efficacy vs potency according to definition

A

efficacy –> maximal effect a drug can produce

potency –> amount of drug needed for a given effect

68
Q

graphic - maximal effect (%) on y, Log (drug dose) on x - efficacy vs potency

A

efficacy –> y value (V max) –> increase y = increased efficacy
potency –> x value (EC50) –> left shifting = lower EC50 and higher potency (lower drug needed)

69
Q

drug - EC50 - definition, relationhip with potency

A
  • Effective concentration
  • drug dose for 50% of maximal effect
  • low EC50 –> high potency –> little drug need
70
Q

Partial vs full agonists according to efficacy

A

partial agonists has less efficacy than full agonist

71
Q

efficacy and potency - relationship

A

unrelated:
- efficacious drug can have high or low potency
- potent drug can have high or low efficacy

72
Q

high potency vs drug needed

A

high potency –> little drug need

73
Q

agonists with competitive antagonist - effect

A

lower potency, no change in efficacy (shift curve right)

74
Q

agonists with competitive antagonist - overcome

A

can be overcome by increasing the concentration of agonist substrate

75
Q

agonists with competitive antagonist - example

A

diazepam (agonist) + flumazenil (competitive antagonist) on GABA receptor

76
Q

agonist with noncompetitive antagonist - effect

A

lower efficacy, no change on potency (shift curve down)

77
Q

agonist with noncompetitive antagonist - example

A

Norepinephrine (agonist) + phenoxybenzamine (noncompetitive antagonist)

78
Q

Partial agonist (alone) - compare to full agonist

A

lower maximal effect (lower efficacy)

potency is an independent variable

79
Q

agonist vs partial agonist - example

A

morphine (full agonist) vs buprenorphine (partil agonist) at opioid μ-receptors

80
Q

Therapeutic index is a measurement of

A

drug safety

81
Q

Therapeutic index calculation

A

TD50 / ED 50 = median toxic dose / median effecive dose

82
Q

Therapeutic window?

A

dosage range that can safely and effectively treat disease

83
Q

therapeutic index in safety drugs

A

higher

84
Q

Drugs with lower therapeutic index –> (and example of drugs)

A

require monitoring

eg. digoxin, lithium, theophiline, warfarin

85
Q

example of drugs with low therapeutic index

A
  1. digoxin
  2. lithium
  3. theophiline
    4 warfarin
86
Q

therapeutic index in animals

A

TD50 is replaced by lethal median dose (LD50)

87
Q

Pharmacokinetics vs pharmacodynamics according to definition

A

Pharmacokinetics –> describes the action of biological systems on drugs icluding ADME (absorption, distribution, elimination, metabolism)
Pharmacodynamics –> describes the detailed actions of drugs on living system

88
Q

Drug absorption - first-pass effect

A

elimination that occurs when a drug is first absorbed from the intestine and passes through liver –> decrease availability

89
Q

Distribution of a drug depends on

A
  1. Blood flow to the tissue
  2. Size of the organ
  3. Solubility of the drug
  4. Binding (on macromolecules)
    5 .Volume of distribution
90
Q

Receptors types

A
  1. steroid
  2. ion channel
  3. transmembrane tyrosine kinase
  4. JAK-STAT
  5. G protein-coupled
91
Q

pharmacology - physiologic antagonism

A

binding of an agonist drug to a receptor that produces effects opposite to the effect of another agonist acting at a 2nd receptor

92
Q

stage of drug development before clinical trials

A

all in animals

  1. pharmacologic profile –> determine all useul or toxic actions and the mechanism
  2. Reproductive toxicity –> fertility, teratogenic, mutagenic etc
  3. Chronic toxicity –> long term testing for toxic effects
93
Q

Human trials requiring approval of an

A

investigational new drug exemption application (IND)

94
Q

marketing for human use (phase 4) requires approval of an

A

New drug application (NDA)

Pharmacology (9 decks)

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