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Pharm > 1: Pharmacodynamics 1 > Flashcards

1: Pharmacodynamics 1 Flashcards

1
Q

pharmacodynamics vs. pharmacokinetics

A

dynamics: drug effects on the body - dose-response relationships and drug-receptor interactions
kinetics: the body’s effects on the drug - ADME (absorption, distribution, metabolism, elimination) - [plasma] over time

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2
Q

what is biopharmaceutics?

A

science of how you package a drug to get it where it needs to go (we won’t talk about this much)

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3
Q

what is the cornerstone of pharmacology?

A

the receptor = drug target

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4
Q

definition of drug side effect

A

an unwanted or bothersome effect of a drug usually related to the main effect

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5
Q

definition of drug toxic effect

A

a harmful or adverse effect of a drug

  • generally not related to the main effect
  • often related to excessively high drug concentration
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6
Q

factors that affect the magnitude of response to drug therapy

A
  • dose administered
  • concentration at site of action
  • duration in which the drug remains at the site of action
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7
Q

time-action curve: two important questions for every drug

A
  1. How quickly will the drug act?
  2. How long will the drug effect last?
    • time to onset of therapeutic effect
    • minimum effective concentration
    • peak concentration
    • duration of action
    • residual effect
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8
Q

what type of function do drugs modify?

A

cellular function only

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9
Q

3 potential types of sites of drug action

A
  1. extracellular
  2. intracellular
  3. on the cell surface
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10
Q

examples of extracellular sites

A
  • neutralization of excessive gastric acid by antacids

- heparin in preventing blood coagulation

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11
Q

examples of intracellular sites

A
  • drugs used to treat infections
  • drugs used for cancer chemotherapy
  • hormones such as estrogen
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12
Q

examples of cell surface sites

A

many drugs act by combining with receptors on the cell surface

  • ACh and muscarinic receptors
  • catecholamines and alpha- and beta-receptors
  • histamine and H2 receptors
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13
Q

what determines the quantitative relationship b/w dose/concentration of drug and pharmacologic effects?

A

receptors

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14
Q

what determines the selectivity of drug action?

A

receptors - size, shape, and electrical charge of a drug molecule + changes in the chemical structure of a drug

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15
Q

definition of agonists

A

drugs that bind to a receptor and stimulate a biological response

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16
Q

definition of antagonists

A

drugs that bind to a receptor without altering receptor function, but prevent other drugs/substances from binding (such as agonists)

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17
Q

definition of inverse agonists

A
  • look like antagonist, but changes receptor to inhibit basal activity of that receptor
  • not many drugs use this action
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18
Q

macromolecular nature of most drug receptors

A

proteins

  • regulatory proteins (GPCRs, ion channels, transporters)
  • enzymes
  • transport proteins
  • structural proteins
19
Q

concentration-effect curves of agonists

A
  • responses to [low] increase proportionally (graded response - but there are some exceptions (bimodals))
  • as doses increase, the incremental response decreases
  • may become saturated = hallmark of a receptor-mediated response
20
Q

definition of effective concentration

A

EC50

-concentration at which you get 50% of the maximal response

21
Q

law of mass action for drugs

A

[D] + [R] [DR] –> effect
k1 = association rate constant
k-1 = dissociation rate constant

the effect of a drug is directly proportional to the amount of drug-receptor complex formed

22
Q

rate of association? rate of dissociation?

A

association: k1 [D][R]
dissociation: k-1 [DR]

23
Q

definition of dissociation constant

A

KD
-measure of how tightly the drug binds to the receptor
= [D][R]/[DR] = k-1/k1 (in moles)
-at KD, half the receptors are bound by drug
-allows you to compare affinities of different drugs

24
Q

the lower the KD, the ______ the affinity

A

higher

25
Q

relationship between occupied receptor B and drug concentration C

A

occupied receptor B = (C x Bmax)/(C + KD)

26
Q

law of mass action: assumptions (3)

A
  • the binding is totally reversible
  • D and R only exist as free and bound
  • all receptor sites are considered to have equivalent affinity for D and to be independent
27
Q

definition of potency

A
  • the dose of a drug required to produce a particular effect of given intensity
  • comparison based on doses that produce the SAME effect (usually ED50)
28
Q

definition of affinity

A
  • the ability of the drug to interact with the receptor
  • measured by KD
  • one of the determinants of potency
29
Q

definition of efficacy

A
  • the biological response resulting from the drug-receptor interaction/ magnitude of response from drug-receptor interaction
  • maximal efficacy is often limited by toxicity
  • includes how well the enzyme can convert the DR combo into the final product
30
Q

which is more important as a drug property: potency or efficacy?

A

efficacy

however, you also hope for good efficacy b/c less chance for adverse effects

[D] + [R] [DR] —————> effect
(potency) (efficacy)

31
Q

definition of a partial agonist

A
  • elicits a biological response, but it is not a full response, even at full receptor occupancy
  • cannot produce same maximal effect as a full agonist, regardless of concentration used
  • may competitively inhibit the response of a full agonist
  • mechanisms complex, but probably related to drug binding in inactive form of receptor
32
Q

definition of receptor antagonism and three types

A

a drug-receptor interaction that interferes with or prevents the development of a drug response by an agonist

  • competitive
  • mixed
  • irreversible
33
Q

definition of competitive antagonism

A
  • antagonist combines with the same site on the receptor as the agonist
  • antagonism can be reversed by increasing dose of the agonist (outcompetes the antagonist)
  • has affinity but lacks significant intrinsic activity (efficacy)
34
Q

how does a competitive antagonist shift the dose-response curve?

A

shifts the curve to the right in a parallel fashion (shape does not change) - indicates a reduction in the effective potency of the agonist

magnitude of shift to the right is proportional to the [antagonist]

35
Q

concept of spare receptors

A
  • when the maximal response can be elicited by an agonist at a concentration that does not result in 100% occupancy of available receptors
  • important in the action of irreversible antagonists
36
Q

how does an irreversible antagonist shift the dose-response curve in the presence of spare receptors?

A
  • at lower [antagonist], you get a parallel, right shift and still get maximal response b/c there are more receptors present than are needed for full response
  • but reach a critical level of receptors required for maximal response: then as [antagonist] increases, the slope of the line decreases and you get a down shift (in a sense) of the line - with lessened maximal effect
37
Q

definition of noncompetitive antagonists

A
  • antagonist produces its effect at a site of the receptor other than the site used by the agonist
  • agonist and noncompetitive antagonist do NOT compete with one another for a single binding site
  • antagonism cannot be completely reversed by increasing the [agonist]
  • increasing [antagonist] increases KD and decreases Emax of the agonist
  • reduces both the efficacy and the affinity (increased KD) - right shift of the EC50
38
Q

describe the log dose-response curve in the presence of a noncompetitive antagonist

A
  • shifted to the right
  • as the dose of noncompetitive antagonist increases, the slope of the agonist curve and maximal response obtained are progressively decreased
  • at very high [antagonist], no amount of agonist can produce a response
39
Q

comparison of reversible vs. irreversible antagonists

A
  • an irreversible antagonist will usually bind to the same site as the agonist, but will not be readily displaced
  • irreversible inhibition is generally caused by covalent reaction b/w antagonist and receptor
  • inhibition persists even after an irreversible antagonist is removed
40
Q

definition of positive allosteric activators

A

=positive allosteric modulator (PAM)

  • can increase potency and/or efficacy
  • synergistic with agonists
41
Q

definition of negative allosteric activators

A

= negative allosteric activator/modulator

  • can decrease potency and/or efficacy
  • ex: noncompetitive antagonists
42
Q

definition of functional/physiological antagonism + example

A
  • two drugs influence a physiological system but in opposite directions
  • each drug is unhindered in the ability to elicit its own characteristic response

ex: ACh on BP (lowers it) vs. epinephrine on BP (raises it)

43
Q

definition of chemical antagonism

A
  • a chemical reaction occurs b/w an agonist and an antagonist to form an inactive product
  • agonist is inactivated in direct proportion to the extent of the chemical reaction with the antagonist

ex: Ca-antacids chelate tetracycline antibiotics; sodium nitrite inactivates cyanide

Pharm (19 decks)

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