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Pharmacology > Pharmacodynamics II > Flashcards

Pharmacodynamics II Flashcards

1
Q

Spare receptors exist when

A

It is possible to elicit a maximum

biological response without occupying all of the available receptors.

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2
Q

When spare receptors exist, what happens to the concentration-response curve (EC50)?

A

EC50 is shifted to smaller concentrations (left)

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3
Q

When spare receptors exists, how is Kd effected?

A

Kd remains the same

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4
Q

If EC50 is lower than Kd then there are

A

Spare receptors

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5
Q

In the case of spare receptors, is the maximal response still produced?

A

Yes, the maximal response is still produced due to amplification of the cell signaling mechanism

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6
Q

What is the clinical implication of spare receptors?

A

Use a lower dose

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7
Q

How do competitive antagonists effect ED50 and Emax?

A

ED50 of agonist increases Emax does not change

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8
Q

How do non-competitive antagonists effect ED50 and Emax?

A

ED50 may/maynot change

Emax decreases

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9
Q

Do competitive antagonists bind to the same or different receptor site as agonist?

A

Bind to same receptor site as agonist

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10
Q

How do competitive antagonist effect affinity of an agonist for its receptor?

A

Decrease affinity (increase Kd) of an agonist for its receptor

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11
Q

What is the relationship between competitive antagonist and potency of agonist?

A

As antagonist concentration increases, potency of agonist decreases (increase EC50)

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12
Q

With the addition of a competitive antagonists would the curve for agonist shift to the left or right?

A

Right

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13
Q

Do competitive antagonists have an effect on maximal response?

A

No

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14
Q

Can the effects of a competitive antagonist be overcome?

A

Yes, effects can be overcome by increasing dose of agonist

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15
Q

What are the two mechanisms for non-competitive antagonists

A
  1. Inhibit agonist binding at active site by binding to a secondary site on the receptor (allosteric)
  2. Irreversibly (covalent) bind to the same site as an agonist
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16
Q

How do non-competitive antagonist effect affinity and potency of an agonist for its receptor?

A

Affinity (Kd) and potency (EC50) may or may not change

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17
Q

How do non-competitive antagonist effect Emax and Bmax?

A

Decreases Emax and Bmax

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18
Q

Can the effects of a non-competitive antagonist be overcome?

A

No

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19
Q

Explain physiologcial/functional antagonism and give an example

A

Two drugs that act on different receptors or by different mechanisms, to counteract effects of agonist

Ex: Reversing a fall in blood pressure produced by histamine with epinephrine

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20
Q

Explain chemical antagonism

A

Directly interacts with agonist and inactivates it

21
Q

Partial agonists have higher/lower efficacy than full agonist?

A

Lower efficacy (α); cannot produce the same maximal response as full agonists

22
Q

The dose response curve for a partial agonist will have higher/lower Emax and Bmax?

A

Lower Emax and Bmax

23
Q

What are the effects of a single concentration of full agonist and increasing concentrations of partial agonist?

A

Response caused by full agonist decreases
Response caused by partial agonist
increases
Total response gradually decreases

24
Q

Partial agonists can act as competitive antagonists in the presence of ____?

A

Full agonist

The particular agonist binds to the receptor, displacing the agonist, and the overall effect is lower.

25
Q

What is an example of molecule that binds to intracellular receptors and how do they work?

A

Lipid soluble ligands (hormones, steroids)

Modify gene transcription

26
Q

Are the effects of intracellular receptors

a) immediate or slow
b) short-term or long-lasting

A

a) Effects are not immediate

b) Effects are long lasting

27
Q

What is a common transmembrane receptor?

A

Tyrosine kinase receptors

28
Q

How do transmembrane receptors work?

A

Self phosphorylation

29
Q

Tyrosine kinase receptors activate what pathway?

What are examples?

A

Activate the Ras/Raf signaling pathway

  1. Insulin
  2. Epidermal and nerve growth factor
  3. Platelet-derived growth factor
30
Q

Cytokine receptors activate what pathway?

What are examples?

A

Activate JAK/STAT

  1. Growth hormone
  2. Erythropoietin
  3. Interferons and interleukins
31
Q

What are 2 examples of ligand ion channels?

A

Acetylcholine binding to nicotinic receptors

GABA (benzodiazepines, barbiturates, ethanol)

32
Q

Do ion channels have a slow or rapid response?

A

Very rapid response

33
Q

How do G-protein coupled receptors work?

A 
Signal amplification
Gs (stimulatory) increases cAMP
Gi (inhibitory) decreases cAMP
Gq activates PLC
       Ca2+ release
       DAG activates PKC
34
Q

Are βeta receptors activated by Gs, Gi, or Gq?

A

Gs

35
Q

Are α2 receptors activated by Gs, Gi, or Gq?

A

Gi

36
Q

Is desensitization reversible or irreversible?

A

Reversible, a second exposure to agonist will produce the response again

37
Q

Stimulation of G-protein receptors either stimulate or inhibit the formation of

A

cAMP

38
Q

Polyphosphoinositide signaling uses ___ proteins to activate ___

A

Gq

PLC

39
Q

Polyphosphoinositide signaling and Gq proteins have what effect on Ca and kinases?

A

Increase Ca

DAG activates protein kinase C (PKC)

40
Q

Are α1 receptors activated by Gs, Gi, or Gq?

A

Gq

41
Q

Cyclic GMP uses nitric oxide (NO) because

A

it is diffusible and can be synthesized in one cell and exert its effect in another cell

42
Q

If a system has spare receptors then

  1. The dose response curve shifts to the right
  2. The dose response curve does not change
  3. The dose/response curve shifts to the left
  4. The maximal binding (Emax) decreases
  5. The EC50 and Kd are the same
A

The dose/response curve shifts to the left

43
Q

An agonist has:

  1. High efficacy but low affinity
  2. Intrinsic activity of zero
  3. Both efficacy and affinity
  4. High affinity but no efficacy
A
  1. Both efficacy and affinity
44
Q

A drug is a competitive antagonist. Therefore:

  1. It has low affinity for the receptor
  2. It binds irreversibly to the receptor
  3. It has higher efficacy than a partial agonist
  4. It can be displaced by a large enough concentration of agonist
A
  1. It can be displaced by a large enough concentration of agonist
45
Q

In the presence of a partial agonist, why doesn’t the dose response curve start at zero?

A

Because the partial agonist itself causes some stimulation of the receptor

46
Q

Desensitization is generally mediated by what?

A

Phosphorylation

47
Q

What does it mean if a biological effect is amplified?

A

The biological response is greater than the degree of receptor occupancy (g proteins)

48
Q

What does cGMP cause?

A

Relaxation of smooth muscle

Pharmacology (25 decks)

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