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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
Volume of distribution (Vd) plasma protein-bound can be alter by
liver and kidney disease --> low protein binding --> increased Vd
26
low Volume of distribution (Vd) - compartment and drug types
compartment: blood | Drug types: Large/charged molecules/plasma protein bound
27
Medium Volume of distribution (Vd) - compartment and drug types
compartment: ECF | Drug types: small hydrophilic molecules
28
High Volume of distribution (Vd) - compartment and drug types
compartment: all tissues including fat | Drug types: small lipohilic molecules, esp if bound to tissue protein
29
drug clearance (CL) - definition
the volume of PLASMA cleared of drug per unit
30
drug clearance (CL) - equation
CL = rate of elimination of drug / plasma drug concentration = Vd x Ke (elimination constant)
31
drug clearance (CL) may be impaired with
defects in cardiac, hepatic or renal function
32
drug - half-life (t1/2) - de
the time required to change the amount of drug in hte body by 1/2 during elimination
33
steady state of drug
amount of drug going in is the same as the amount of drug getting taken out
34
In first order kinetics - a drug infused at a constant rate takes .... to reach steady state
4-5 half-lives
35
In first order kinetics - a drug infused at a constant rate takes .... to reach 90% of the steady state
3.3 half lives
36
drug - half-life (t1/2) - equation in fist order elimination
t1/2 = (0.693xVd) / CL
37
1-4 half lives and % remaining of drugs
1 --> 50% 2 --> 25% 3 --> 12.5% 4 --> 6.25 %
38
Loading dose calculation
(Cp x Vd) / (F) | Cp = target plasma concentrations at steady state
39
Maintainne dose calculation
(Cp x CL x τ) / (F) Cp = target plasma concentrations at steady state τ = dosage interval (time between doses), if not administrated continuously
40
time to steady state depends primarily on .... and is independent of ...
depends: t 1/2 independent: dose and dosing frequency
41
renal or liver disease effects on loading and maintenance dose
loading dose --> unchanged | maintenance dose --> decreased
42
Types of drug interactions
1. additive 2. permissive 3. synergistic 4. Tachyphylactic
43
Types of drug interactions - definitions
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
Types of drug interactions - additive - definition and examples
effect of substance A and B together is equal to the sum of their individual effects --> aspirin and acetaminophen
45
Types of drug interactions - permissive - definition and examples
Presence of substance A is required for the full effects of substance B --> cortisol on catecholamine responsiveness
46
Types of drug interactions - synergistic - definition and examples
Effect on substance A and B together is greater than the sum of their individuals effects --> Clopidogrel and aspirin
47
Types of drug interactions - Tachyphylactic - definition and examples
acute decrease in response to a drug after initial / repeated administration --> MDMA and LSD
48
Elimination of drug - ways
1. Zero - order elimination | 2. First order elimination
49
Elimination of drug - zero order elimination?
Rate of elimination is constant regardless to Cp (target plasma concentrationsat steady state) --> constant AMOUNT of drug eliminated per unit
50
Zero order elimination - effects on Cp (target plasma concentrationsat steady state)
decreases linearly with time
51
Zero order elimination - examples of drugs
1. Phenyntoin (at high or toxic high concentrations) 2. Ethanol (at all clinically important concentrations) 3. Aspirin (at high or toxic high concentrations)
52
Elimination of drug - First order elimination
rate of elimination is directly proportional to drug concentration --> constant FRACTION of drug eliminated per unit time
53
First order elimination - effects on Cp (target plasma concentrationsat steady state)
decreases exponentially per time
54
First order elimination - examples of drugs
applies to more drugs
55
First vs Zero order elimination according to t1/2
zero: time of t1/2 decreases as concentration decreases first: time of t1/2 is constant as concentration decreases
56
Urine pH and drug elimination - explain
- ionized species are trapped in urine and cleared quickly | - Neutral forms can be reabsorbed
57
Urine pH and drug elimination - weak acids - explain
ROOCH RCOO- + H+ (lipid soluble) (trapped) Trapped in basic environment
58
Urine pH and drug elimination - weak bases - explain
RNH3+ RNH2 + H+ | Trapped in acidic environment
59
Urine pH and drug elimination - weak bases vs acids according to trapping environment
acid --> Trapped in basic environment | bases --> Trapped in acidic environment
60
weak acids - examples of drugs and treatment of overdose
1. phenobarbital 2. methotrexate 3. aspirin treat overdose with biocarbonate (alkalization)
61
weak basis - examples of drugs and treatment of overdose
1. amphetamines 2. TCAs treat with ammonium chloride (acidification)
62
drug metabolism involves 2 major chemical pathways
phase I | phase I
63
drug metabolism - phase I
Reduction, oxidation, hydrolysis with cytochromic P-450 usually yield slightly polar, water-soluble metabolites (often still alive)
64
drug metabolism - phase II
Conjugation (methylation, Glucuronidation, Acetylation, Sulfation) usually yields vere polar inactive metabolies (renally excreted)
65
drug metabolism - phase I vs II according to geriatric patients
geriatric patietns lose phase I first
66
slow acetylators - drug elimination
Patients who are slow acetylators have increased side effects from certain drugs because of lower rate of metabolism
67
efficacy vs potency according to definition
efficacy --> maximal effect a drug can produce | potency --> amount of drug needed for a given effect
68
graphic - maximal effect (%) on y, Log (drug dose) on x - efficacy vs potency
efficacy --> y value (V max) --> increase y = increased efficacy potency --> x value (EC50) --> left shifting = lower EC50 and higher potency (lower drug needed)
69
drug - EC50 - definition, relationhip with potency
- Effective concentration - drug dose for 50% of maximal effect - low EC50 --> high potency --> little drug need
70
Partial vs full agonists according to efficacy
partial agonists has less efficacy than full agonist
71
efficacy and potency - relationship
unrelated: - efficacious drug can have high or low potency - potent drug can have high or low efficacy
72
high potency vs drug needed
high potency --> little drug need
73
agonists with competitive antagonist - effect
lower potency, no change in efficacy (shift curve right)
74
agonists with competitive antagonist - overcome
can be overcome by increasing the concentration of agonist substrate
75
agonists with competitive antagonist - example
diazepam (agonist) + flumazenil (competitive antagonist) on GABA receptor
76
agonist with noncompetitive antagonist - effect
lower efficacy, no change on potency (shift curve down)
77
agonist with noncompetitive antagonist - example
Norepinephrine (agonist) + phenoxybenzamine (noncompetitive antagonist)
78
Partial agonist (alone) - compare to full agonist
lower maximal effect (lower efficacy) | potency is an independent variable
79
agonist vs partial agonist - example
morphine (full agonist) vs buprenorphine (partil agonist) at opioid μ-receptors
80
Therapeutic index is a measurement of
drug safety
81
Therapeutic index calculation
TD50 / ED 50 = median toxic dose / median effecive dose
82
Therapeutic window?
dosage range that can safely and effectively treat disease
83
therapeutic index in safety drugs
higher
84
Drugs with lower therapeutic index --> (and example of drugs)
require monitoring | eg. digoxin, lithium, theophiline, warfarin
85
example of drugs with low therapeutic index
1. digoxin 2. lithium 3. theophiline 4 warfarin
86
therapeutic index in animals
TD50 is replaced by lethal median dose (LD50)
87
Pharmacokinetics vs pharmacodynamics according to definition
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
Drug absorption - first-pass effect
elimination that occurs when a drug is first absorbed from the intestine and passes through liver --> decrease availability
89
Distribution of a drug depends on
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
Receptors types
1. steroid 2. ion channel 3. transmembrane tyrosine kinase 4. JAK-STAT 5. G protein-coupled
91
pharmacology - physiologic antagonism
binding of an agonist drug to a receptor that produces effects opposite to the effect of another agonist acting at a 2nd receptor
92
stage of drug development before clinical trials
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
Human trials requiring approval of an
investigational new drug exemption application (IND)
94
marketing for human use (phase 4) requires approval of an
New drug application (NDA)

Pharmacology (9 decks)

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