14. Drugs and Receptors Flashcards Preview

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Flashcards in 14. Drugs and Receptors Deck (21)
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1
Q

Order the following in decreasing size: molar, micro molar, picomolar, nanomolar and millimolar.

A

Molar, millimolar, micro molar, nanomolar, picomolar.

2
Q

Why are drugs concentrations considered in molar?

A

To show how many molecules are at the site of action.

3
Q

What is drug binding governed by?

A

Association and dissociation.

4
Q

What is the difference between agonists and antagonists?

A

Agonists activate the receptor, antagonists block the binding of an endogenous agonist.

5
Q

What is receptor activation governed by?

A

Intrinsic efficacy, how good an agonist is at generating the activated state of the receptor.

6
Q

What is the difference between intrinsic efficacy and efficacy?

A

Intrinsic efficacy is just activation of the receptor, efficacy I how good it is at generating a response from that activation.

7
Q

Describe agonists and antagonists in terms of affinity, intrinsic Africans and efficacy.

A

Agonists have all three.

Antagonists only have affinity.

8
Q

How can drug-receptor interactions be measured?

A

By binding radioactive labelled ligand (radioligands) to cells or membranes prepared from cells. Low [ligand] = low binding, high [ligand] = high binding.

9
Q

What is Kd/ dissociation constant a measure of?

A

Affinity. It’s the concentration of ligand needed to bind to 50% of the receptors.

10
Q

What does a high or low Kd value tell you about affinity?

A

High Kd = low affinity.

Low Kd = high affinity.

11
Q

What is EC50?

A

Effective concentration giving 50% of the maximal response of a drug.

12
Q

What happens to the shapes of plotted graphs with drugs when [drug] is converted to [drug]log10?

A

The graph changes from a rectangular hyperbole to a sigmoidal curve.

13
Q

What is the difference between concentration and dose?

A

Concentration is the known concentration of drug at the site of action. Dose is where the concentration at the site of action is unknown.

14
Q

What is EC50 a measure of?

A

Potency.

15
Q

What does EC50 depend on?

A

Affinity and intrinsic efficacy and efficacy.

16
Q

On a [Drug]Log10 (M) vs binding/response curve of two drugs, how would two drugs of equal affinities but different efficacies appear?

A

Their binding curve would be in the same position, with the same sigmoidal curve. The difference between the binding and response curve shows the efficacy, a bigger difference is a bigger efficacy. So the drug with a greater efficacy will have a response curve further to the left, and further away from the binding curve than the lower efficacy drug.

17
Q

What is the problem of treating asthma with adrenaline on B2-adrenoceptors?

A

The treatment can act on other B-adrenoceptors elsewhere, like on B1-adrenoceptors in the heart. This will increase the force and rate of contraction.

18
Q

How is salbutamol a selective treatment for asthma?

A

It has poor selectivity for B1 and B2-adrenoceptors but it has a much higher B-selective efficacy. So the drug may bind to all the receptors but it only produces a big response on the B2-adrenoceptors, and so is selective.

19
Q

How is salmeterol a selective treatment for asthma?

A

It has a good Kd selectivity for B2-adrenoceptors over B1-adrenoceptors. Once it has bound, it does not have a selective efficacy. So it is selective but only based on affinity, it won’t bind easily to heart B1-adrenoceptors.

20
Q

Why do spare receptor exist?

A

Because of amplification in the signal transduction pathway. Also response is limited by a post-receptor event.

21
Q

Rearrange the following equation to calculate molarity. MWt (molecular weight) X molarity = g/L.

A

M = (g/L)/MWt.