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Pharmacology > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

1
Q

Pharmacodynamics

A

the study of the relationship of drug concentrations to drug effects
D+R=>DR
biological effect correlates to amount of DR

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2
Q

Receptor

A

Proteins on the surface or within cell that recognize and bind w/ specific molecules that act as chemical signals
-bind ligands

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3
Q

Ligands

A
  • drugs

- endogenous signalling molecules (ie hormones and neurotransmitters)

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4
Q

How do drugs elicit their effects-undesirable or desirable?

A

By mimicking or blocking the actions of hormones and neurotransmitters

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5
Q

Agonist

A

-drug binds to receptor and causes same effect as endogenous substance

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6
Q

Antagonist

A
  • drug binds to receptor but doesn’t produce a response

- inhibitory effect since it prevents endogenous binding

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7
Q

Kd

A
  • equilibrium dissociation constant
  • drug conc. at which 1/2 of Bmax is achieved
  • measure of the affinity of DR
  • constant-not altered by conc of drug or receptor number
  • smalle kd= higher affinity
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8
Q

Emax

A

-the max response achieved by the drug

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9
Q

ED50

A
  • the drug dose at which 50% of Emax is achieved

- POTENCY

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10
Q

Graded Dose Response Curve

A

-infinite number of intermediate states

eg vessel dilation, bp change, heart rate change

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11
Q

Quantal dose response curves

A
  • all or none

eg. death, pregnancy, cure, pain relief, effect of given magnitude

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12
Q

Under what circumstances are quantal dose response curves particularly useful?

A
  • to describe pop response to drugs

- based on plotting cumulative frequency distribution of responders against the log drug dose

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13
Q

Potency

A
  • ED50

- related to the amount of agonist needed to produce an effect of a given magnitude

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14
Q

Efficacy

A

Emax

-related to the max effect that can be achieved w/ a particular agonist

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15
Q

Full agonist

A
  • high potency, max efficacy

- reduced potency, max efficacy

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16
Q

Partial agonist

A
  • high potency, reduced efficacy
  • reduced potency, reduced efficacy
  • have a lower functional impact on the receptor
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17
Q

Max. efficacy is defined by the max. effect achieved with ?

A

the endogenous R agonist

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18
Q

Constitutive Receptor Activation

A
  • agonist binding induces conformational change in the receptor from inactive to active
  • agonists stabilize the active state
  • spont. dissociation of agonist returns receptor to inactive state
  • conformational change to active state can also occur spot in the absence of agonist
  • -> constitutive receptor activation
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19
Q

Inverse Agonist

A
  • stabilizes the inactive state
  • destabilizes the active state
  • constitutive receptor activation
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20
Q

Draw diagram demonstrating experimental apparatus to measure constitutive receptor activity

A

Pharmacodynamics

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21
Q

What is the effect of agonists on receptors with constitutive activity?

A

-has an independent impact upon receptor activity

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22
Q

What is the effect of antagonists on receptors with constitutive activity?

A

-impacts receptor activity only in the presence of agonist (lacks efficacy)

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23
Q

What is the effect of inverse agonists on receptors with constitutive activity?

A
  • has an independent impact upon receptor activity

- produces an effect opposite to agonist

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24
Q

Chemical Antagonism

A

Direct interaction of 2 substances in solution such that the effect of one or both is lost

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25
Q

Example of Chemical Antagonism

A
  • protamine (acidic anticoagulant) and heparin (basic anticoagulant)
  • loss of activity of both drugs
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26
Q

Physiological Antagonism

A

Indirect interaction of 2 substances with opposing physiological actions

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27
Q

Example of Physiological Antagonism

A
  • histamine, lowers bp through vasodilation (H1 R)

- epinephrine raises bp through vasoconstriction (alpha1 adrenergic R)

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28
Q

Pharmacological Antagonism

A
  • bind to receptors but do not activate signal transduction mechanisms
  • biological effects from blocking ability of agonist to bind/activate R
29
Q

Example of Pharmacological Antagonism

A

cimetidine blocks binding of histamine to H2 R resulting in lower gastric acid secretion

30
Q

Competitive Antagonists

A

-bind reversibly to the receptor
-inhibition can be overcome by increasing agonist conc
AFFECTS AGONIST POTENCY

31
Q

Non-competitive Antagonists

A
  • bind irreversibly (e.g. covalently) to the R or reversibly/irreversibly to a site on the receptor different from agonist (allosteric)
  • inhibition cannot be overcome by increasing agonist conc
  • AFFECTS AGONIST EFFICACY
32
Q

Draw the dose response curve for agonist in the presence of competitive antagonist

A

Pharmacodynamics

33
Q

Draw the dose response curve for agonist in the presence of non competitive antagonist

A

Pharmacodynamics

34
Q

ED50 of antagonists

A
  • the antagonist dose at which 50% of Emax is achieved

- aka potency, ID50, IC50

35
Q

Emax of antagonists

A
  • max biological effect achieved by the antagonist

- NOT a measure of efficacy

36
Q

T or F: majority of endogenous receptor ligands are full agonists

A

True

37
Q

T or F: endogenous inverse agonists are common

A

False-rare

38
Q

What is an example of an endogenous inverse agonist?

A

Agouti Related peptide (AGRP)

  • reduces constitutive R activity of melanocortin R
  • increases food intake and reduces energy expenditure
39
Q

T or F: Endogenous pure antagonists are rare

A

True

40
Q

What is an example of an endogenous pure antagonist?

A

Kynurenic acid

  • NMDA receptor antagonist
  • physiological role unclear but may play a role in neurotransmission and neuropathologies
41
Q

? is a full agonist that mimics epinephrine at cardiac Beta1R

A

Isoproterenol

42
Q

? is a partial agonist that mimics endogenous endorphins at u opiod R

A

-buprenorphine

43
Q

Why is buprenorphine safer than morphine

A

-reduced risk with of respiratory depression with overdose

44
Q

Superagonists

A

> 100% Emax

-uncommon in clinical practice

45
Q

Drug Desensitization

A

-effect of a drug often diminishes when given continuously or repeatedly

46
Q

Receptor Mediated Desensitization (2)

A
  • loss of receptor fxn

- reduction of receptor number

47
Q

How does loss of receptor function cause desensitization?

A
  • rapid desensitization due to change in receptor conformation
  • usually due to feedback of cellular effects of agonist
48
Q

How does reduction of receptor number cause desensitization?

A
  • slower, long term desensitization due to change in receptor number
  • usually due to feedback of cellular effects of agonist
49
Q

What is an example of desensitization caused by loss of receptor function?

A

Phosphorylation of specific amino acids in GPCRs blocks coupling to G proteins

50
Q

What is an example of desensitization caused by reduction of receptor number?

A

-Phosphorylation of specific aa’s in GPCRs causes removal from cell surface

51
Q

What are the 3 types of non receptor mediated desensitization?

A
  1. reduction of receptor coupled signalling components
  2. increased metabolic degradation
  3. biological adaptation
52
Q

How does reduction of receptor coupled signalling cause desensitization?

A

-depletion of signaling molecules required for biological response

53
Q

What is an example of reduction of receptor coupled signalling desensitization?

A

-prolonged stimulation of G-protein coupled receptors can lead to depletion of intracellular secondary messengers
ie cellular stores of ATP depleted by prolonged cAMP production

54
Q

How does increased metabolic degradation cause desensitization?

A
  • increase in the rate of metabolism and/or elimination of drug
  • lowers plasma drug concentrations
55
Q

What is an example of desensitization caused by increased metabolic degradation?

A

-barbiturates induce the expression of metabolic enzymes that degrade these drugs

56
Q

How does increased physiological adaptation cause desensitization?

A
  • reduction or amelioration of drug effects due to opposing homeostatic response
  • very few well characterized mechanisms
57
Q

What are the 3 adverse drug effects?

A
  1. side effects
  2. toxic reaction
  3. allergic reaction
58
Q

Side Effect

A
  • dose dependent
  • not directly related to desired effect of drug
  • action of drug at other sites to produce undesirable effects
59
Q

Toxic Reaction

A
  • dose dependent
  • directly related to desired effect of drug
  • excessive action of drug at intended target site
60
Q

Allergic Reaction

A
  • not dose dependent
  • not related to desired effect of drug
  • immunologic response to drug (largely unpredictable)
61
Q

What is the desirable therapeutic effect of cyclosporine?

A
  • promotes survival of transplanted organs

- magnitude of effect is dose dependent

62
Q

What are the toxic effects of cyclosporine?

A
  • increased susceptibility to infection
  • consequence of intended pharmacological action (immunosuppression)
  • dose dependent
63
Q

What are the side effects of cyclosporine?

A
  • kidney damage
  • not related to intended pharmacological activity
  • dose dependent
64
Q

What are the allergic effects of cyclosporine?

A
  • rash, hives, itching, breathing difficulties
  • not related to intended pharmacological activity
  • not dose dependent
65
Q

T or F: the nature of the drug determines toxicity

A

False-the amount determines toxicity

66
Q

Therapeutic Index

A

-a measure of drug safety
-dose required for a toxic/ adverse drug effect vs that required for beneficial effect
TI=Toxic ED50/Beneficial ED50
-larger TI indicates a clinically safer drug

67
Q

Therapeutic Window-Relationship to blood levels

A

-considers a range of blood concentrations assoc. with toxic effects, therapeutic benefit or lack of effect within a pop.

68
Q

Therapeutic Window-Relationship to dose

A

-considers the range of dosages assoc. with toxic effects, therapeutic benefit or lack of effect within a pop.

Pharmacology (9 decks)

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