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Botany > pharmacodynamics > Flashcards

pharmacodynamics Flashcards

1
Q

Actions/effects of the drug on the body
Determines the group in which the drug is
classified and plays a major role in deciding
whether a group is appropriate therapy for
particular symptom or disease

A

pharmacodynamics

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2
Q

Specific molecules in a biologic system with
which drugs interact to produce changes in
the function of the system

A

RECEPTORS

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3
Q

Determine the quantitative relations between
dose or concentration of drug and
pharmacologic effects

A

RECEPTORS

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4
Q

Selective in choosing a drug molecule to bind
to avoid constant activation by promiscuous
binding of many different molecules

A

RECEPTORS

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5
Q

Changes its function upon binding in such a
way that the function of the biologic system
is altered in order to have pharmacologic
effect

A

RECEPTORS

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6
Q

Selective in ligand-binding characteristics
(respond to proper chemical signals and
not to meaningless ones)
Mediate the actions of both pharmacologic
agonists and antagonists

A

RECEPTORS

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7
Q

Majority are proteins which provide the
necessary diversity and specificity of
shape and electrical charge

A

RECEPTORS

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8
Q

Specific binding region of the macromolecule

High and selective affinity to the drug molecule

A

RECEPTOR SITE/RECOGNITION SITE

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9
Q

is the fundamental event that initiates the action

of the drug

A

Interaction between the drug and the receptor

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10
Q

CLASSIFICATION OF RECEPTORS

Best characterized drug receptors
Mediates the action of endogenous chemical
signals like neurotransmitters, autacoids and
hormones
Mediates the effects of the most useful
therapeutic agents

A

REGULATORY PROTEIN

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11
Q

CLASSIFICATION OF RECEPTORS

Inhibited (or less commonly, activated) by
binding a drug
Eg, dihydrofolate reductase, the receptor for
methotrexate

A

ENZYMES

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12
Q

CLASSIFICATION OF RECEPTORS

Eg, Na+/K+ ATPase, the membrane receptor
for digitali

A

TRANSPORT PROTEINS

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13
Q

CLASSIFICATION OF RECEPTORS

Eg, tubulin, the receptor for colchicine,
an anti-inflammatory drug

A

STRUCTURAL PROTEINS

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14
Q

Molecules that translate the drug-receptor
interaction into a change in cellular activity
Eg, adenyl cyclase

A

EFFECTORS

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15
Q 
Response of a particular receptor-effector
system is measured against increasing
concentration of a drug
Graph of the response versus the drug
dose
A

GRADED DOSE-RESPONSE CURVE

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16
Q 
Sigmoid curve
Efficacy (Emax) and potency (EC50) are
derived from this curve
The smaller the EC
50, the greater the
potency of the drug
A

GRADED DOSE-RESPONSE CURVE

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17
Q

Maximal response that can be produced
by a drug
All receptors are occupied
No response even if the dose is increased

A

Emax

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18
Q

Concentration of drug that produces
50% of maximal effect
Smaller EC
50–more potent

A

EC50

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19
Q

Total number of receptor sites

All receptors have been occupied

A

Bmax

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20
Q

Equilibrium dissociation constant
Concentration of drug required to
bind 50% of the receptors

A

KD

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21
Q

Measure of the affinity of a drug

for its binding site on the receptor

A

KD

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22
Q

Smaller KD

A

–greater affinity of drug to receptor

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23
Q

Transduction process between the occupancy
of receptors and production of specific effect
Highly efficient coupling can be elicited by a
full agonist and spare receptors

A

COUPLING

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24
Q

Maximal drug response is obtained at less
than maximal occupation of the receptors
Not qualitatively different from nonspare
receptors, not hidden or unavailable

A

SPARE RECEPTORS

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25
Q

Temporal in character, when occupied, they
can be coupled to respond, there is still effect
Drugs with low binding affinity for receptors
will be able to produce full response even at
low concentration

A

SPARE RECEPTORS

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26
Q

Compare concentration for 50% of maximal
effect (EC50) with concentration for 50%
maximal binding (KD)
KD > EC50 with spare receptors

A

SPARE RECEPTORS

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27
Q

Effect of the drug-receptor interaction may
persist for a longer time than the interaction
itself
Actual number of receptors may exceed the
number of effectors available

A

SPARE RECEPTORS

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28
Q

Non-regulatory molecules of the body
Binding with these molecules will result
to no detectable change in the function
of the biologic system

A

INERT BINDING SITES

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29
Q 
Buffers the concentration of the drug
Bound drugs do not contribute directly
to the concentration gradient that drives
diffusion
Eg, albumin
A

INERT BINDING SITES

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30
Q

Binds to the receptor and directly or
indirectly bring about an effect
Full activation of the effector system

A

AGONIST

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31
Q

Produces less than the full effect, even
when it has saturated the receptors
Acts as an inhibitor in the presence of
a full agonist

A

PARTIAL AGONIST

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32
Q

Binds but do not activate the receptors

Blocks or competes with agonist

A

ANTAGONIST

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33
Q

CLASSIFICATION

Competes with agonist receptor
Binds to the receptor reversibly without
activating the effector system

A

COMPETITIVE ANTAGONIST

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34
Q

CLASSIFICATION

Antagonist increases the agonist concentration
needed for a given degree of response
Concentration-effect curve is shifted to higher
doses (ie, horizontally to the right of the dose
axis)
Same maximal effect is reached

A

COMPETITIVE ANTAGONIST

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35
Q

CLASSIFICATION

Effects are overcomed by adding more agonist
Increases the median effective dose
ED50

A

COMPETITIVE ANTAGONIST

36
Q

2 THERAPEUTIC IMPLICATIONS

produced by the competitive antagonist depends on the

A

(1) Degree of inhibition

37
Q

2 THERAPEUTIC IMPLICATIONS
concentration of antagonist (eg, propranolol)
depends on the concentration of agonist that
is competing for binding to the receptor

A

(2) Clinical response to a competitive antagonist

38
Q

CLASSIFICATION

Binds with the receptor via covalent bonds
Antagonist’s affinity to the receptor maybe so high
Receptor is not available to bind the agonist

A

IRREVERSIBLE ANTAGONIST

39
Q

CLASSIFICATION

Concentration-effect curve moves downward
No shift of the curve in the dose axis
Emax is not reached
No increase in median effective dose (ED50)
unless there are spare receptors

A

IRREVERSIBLE ANTAGONIST

40
Q

CLASSIFICATION

Duration of action is relatively independent
of its own rate of elimination
More dependent on the rate of turnover of
receptors
Eg, phenoxybenzamine binding with alpha
receptors

A

IRREVERSIBLE ANTAGONIST

41
Q 
Does not depend on interaction with the
agonist’s receptor
Drug that interacts directly with the drug
being antagonized to remove it or to
prevent it from reaching its target
A

CHEMICAL ANTAGONISM

42
Q

Eg, protamine used to counteract the
effect of heparin making it unavailable
for interaction with proteins involved in
the formation of blood

A

CHEMICAL ANTAGONISM

43
Q 
Makes use of the regulatory pathway
Effects that are less specific and less
easy to control
Binds to a different receptor producing
an effect opposite to that produced by
the drug it is antagonizing
A

PHYSIOLOGIC ANTAGONISM

44
Q

5 BASIC TRANSMEMBRANE SIGNALING
MECHANISMS
crossing the plasma membrane and acts on intracellular
receptor (eg, steroids)

A

(1) Lipid soluble drug

45
Q

5 BASIC TRANSMEMBRANE SIGNALING
MECHANISMS

intracellular enzymatic activity is
regulated by a ligand that binds to
the protein’s extracellular domain

A

(2) Transmembrane receptor protein

46
Q

5 BASIC TRANSMEMBRANE SIGNALING
MECHANISMS
that binds and stimulates a protein tyrosine
kinase (eg, insulin)

A

(3) Transmembrane receptor

47
Q 
5 BASIC TRANSMEMBRANE SIGNALING
MECHANISMS
 which regulates the opening
of the ion channel (eg, GABA, excitatory
acetylcholine)
A

(4) Ligand-gated transmembrane ion

channel

48
Q

5 BASIC TRANSMEMBRANE SIGNALING
MECHANISMS
is coupled with an effector enzyme by G protein
which modulates production of an intracellular second messenger
[eg, cathecolamine (epinephrine)]

A

(5) Transmembrane receptor

49
Q

INTRACELLULAR 2ND MESSENGERS

Mediates hormonal responses
Mobilization of stored energy
(breakdown of carbohydrates in the liver stimulated by cathecolamines
Conservation of water by the kidneys
mediated by vasopressin
A

A. cAMP

50
Q

INTRACELLULAR 2ND MESSENGERS

Bind to receptors linked to G proteins while others bind to receptor tyrosine kinases

A

B. CALCIUM AND PHOSPHOINOSITIDES

51
Q

INTRACELLULAR 2ND MESSENGERS

Crucial step is the stimulation of membrane enzyme phospholipase C

A

B. CALCIUM AND PHOSPHOINOSITIDES

52
Q

INTRACELLULAR 2ND MESSENGERS

Few signaling roles in a few cell types like the intestinal mucosa and vascular smooth muscle cells

A

C. cGMP

53
Q

INTRACELLULAR 2ND MESSENGERS

Causes relaxation of vascular smooth
muscles by a kinase-mediated mechanism

A

C. cGMP

54
Q

Response gradually diminishes even if the
drug is still there (after reaching an initial
high level of response)
Reason is not known

A

RECEPTOR DESENSITIZATION

55
Q

STRUCTURE ACTIVITY RELATIONSHIP

A

Cells use more than one signaling mechanism

to respond to the drug

56
Q

Graph of the fraction of a population that
shows a specified response to increasing
doses of a drug

A

QUANTAL DOSE-RESPONSE CURVE

57
Q

Minimum dose required to produce a specific
response is determined in each member of
the population
Sigmoid curve

A

QUANTAL DOSE-RESPONSE CURVE

58
Q

Median effective dose
50% of the individuals manifested
the desired therapeutic effect

A

ED50

59
Q

Median toxic dose

50% of the individuals manifested the toxic effects

A

TD50

60
Q

Median lethal dose

A

LD50

61
Q

Ratio of the TD
50 (or LD50 ) to the ED50 determined from the quantal dose-response curves
Increased therapeutic index-wide margin of
safety

A

THERAPEUTIC INDEX

62
Q

Represents an estimate of the safety of the
drug
A very safe drug might be expected to have
a very large toxic dose and a much smaller
effective dose
Eg, ED50 of 3mg and the LD50 is 150 mg
Therapeutic index is 50 (150/3)

A

THERAPEUTIC INDEX

63
Q 
Dosage range between the minimum
effective therapeutic concentration or
dose (MEC) and the minimum toxic
concentration or dose (MTC)
More clinically relevant index of safety
A

THERAPEUTIC WINDOW

64
Q

normal value MEC

A

7-10 mg/L (average of 8 mg/L)

65
Q

normal value Therapeutic window

A

8-18 mg/L

66
Q

normal value MTC

A

15-20 mg/L (average of 18 mg/L)

67
Q

ex of therapeutic window

A

theophylline

68
Q 
Maximal effect (Emax) an agonist can
produce if the dose is taken to very high
levels
Determined mainly by the nature of
receptors and its associated effectors
A

MAXIMAL EFFICACY

69
Q

Measured with a graded dose-response
curve but not with quantal dose-response
curve

A

MAXIMAL EFFICACY

70
Q

Amount of drug needed to produce a given
effect
In the graded dose-response curve, the effect
chosen is the 50% of the maximal effect and
the dose is (EC50)

A

POTENCY

71
Q

In the quantal dose-response curve, ED50,
TD50, and LD50 are variables in 50% of the
population

A

POTENCY

72
Q

VARIATION OF RESPONSES IN INDIVIDUALS

Caused by differences in metabolism (genetic)
or immunologic mechanisms
Response to the drug is unknown or unusual

A

IDIOSYNCRATIC RESPONSE

73
Q

VARIATION OF RESPONSES IN INDIVIDUALS

Intensity of the drug is decreased
Large dose of the drug is needed to have
an effect

A

HYPOREACTIVE RESPONSE

74
Q

VARIATION OF RESPONSES IN INDIVIDUALS

Intensity of the drug is increased or exaggerated

A

HYPEREACTIVE RESPONSE

75
Q

VARIATION OF RESPONSES IN INDIVIDUALS

Decreased sensitivity acquired as a result of
exposure to the drug

A

TOLERANCE

76
Q

VARIATION OF RESPONSES IN INDIVIDUALS

Tolerance develops after a few doses

A

TACHYPHYLAXIS

77
Q

VARIATIONS IN DRUG RESPONSIVENESS

that reaches the receptor due to absorption,
distribution and elimination differences

A
  1. Alteration on the concentration of the drugq
  2. Variation in the concentration of the endogenous
  3. Alterations in number/function of receptors
  4. Changes in 2nd messengers
  5. Clinical selectivity
78
Q

VARIATIONS IN DRUG RESPONSIVENESS

Drug has been taken for a long time, then
abruptly discontinued
Eg, propranolol (beta-blocker)
Gradual decrease of taking the drug by
decreasing/tapering the dose
A

OVERSHOOT PHENOMENON/

REBOUND HYPERTENSION

79
Q

VARIATIONS IN DRUG RESPONSIVENESS
3. Alterations in number/function of receptors

Decrease in # of receptors

A

DOWN REGULATION

80
Q

VARIATIONS IN DRUG RESPONSIVENESS
3. Alterations in number/function of receptors

Increase in the # of receptors

A

UP REGULATION

81
Q

WHAT TO DO TO AVOID/CIRCUMVENT

TOXIC EFFECTS

A

Give low doses
Carefully monitor the patient
Employ ancillary procedures

82
Q

VARIATIONS IN DRUG RESPONSIVENESS
Beneficial and toxic effects may be mediated
by the same receptor-effector mechanism
D + R DR X (beneficial/toxic)

A
  1. Clinical selectivity
83
Q

WHAT TO DO TO AVOID/CIRCUMVENT

TOXIC EFFECTS

A

Use a safer drug if possible
Beneficial and toxic effects are mediated
by identical receptors but in different ways

84
Q

Low doses for prevention of blood clots
Very high doses causes internal bleeding
Monitor PT, PTT and bleeding parameters

A

HEPARIN

85
Q 
Give lowest dose possible
Give adjunctive drugs
Anatomic selectivity (lungs-by inhalation)
A

STEROIDS

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