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Membranes and Receptors > Session 8 - Drugs and Receptors > Flashcards

Session 8 - Drugs and Receptors Flashcards

0
Q

What is the equation for molarity?

A

-M=g/L divided by Mwt

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1
Q

What is the main factor in determining drug action?

A

-The concentration of drug molecules around the receptors (site of action)

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2
Q

Do most drugs bind reversibly or irreversibly to receptors?

A

-Reversibly

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3
Q

Define Ligand

A

-A molecule which interacts specfically with a receptor

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4
Q

What two factors dictate drug-receptor interactions?

A
  • Affinity

- Intrinsic Efficacy

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5
Q

What is meant by affinity of a ligand?

A

-The ability of the ligand to bind to the receptor

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6
Q

What is meant my intrinsic efficacy?

A

-The ability to convert the bound receptor to its active form

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7
Q

With regards to receptors, what must a ligand do to be an agonist?

A
  • Cause a response

- Have both affinity and intrinsic efficacy

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8
Q

Define drug efficacy

A

-The ability to generate a biological response, with respect to the receptor itself and tissue/cell dependent factors (eg cellular machinery)

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9
Q

With regards to receptors, what makes antagonists different from agonists?

A

-Antagonists have affinity but no intrinsic activity. ie they bind the receptor but do not activate it

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10
Q

How do antagonists effect agonist action?

A

-Antagonists bind to the receptor but do not activate it. This means that they are blocking the receptor so an agonist cannot bind and thus prevent activation

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11
Q

How is drug-receptor binding usually measured?

A

-Radioligand binding

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12
Q

Define Bmax

A

-The maximum binding capacity, ie when all receptors are filled (100% occupancy)

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13
Q

Define Kd

A

-The concentration of ligand required to occupy 50% of the available receptors, ie it is a measure of affinity

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14
Q

What has a higher affinity, a lower or higher Kd?

A

-The lower the Kd the higher the affinity (the less conc it takes to fill 50% of available receptors)

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15
Q

Define Emax

A

-The maximum response which can be produced from a cell/tissue

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16
Q

define EC50

A

-The concentration of drug which gives 50% of the maximum response

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17
Q

What is the difference between concentration and dose?

A
  • Concentration is the known concentration of drug at the site of action
  • Dose is when the concentration at the site of action is unknown
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18
Q

What is EC50 a measure of?

A

-Potency

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19
Q

What factors effect the potency of a drug?

A
  • Affinity
  • Intrinsic efficacy
  • Efficacy
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20
Q

What 5 factors are important when assessing a drug?

A
  • Affinity
  • Efficacy
  • Selectivity
  • Drug metabolism
  • Physiochemical properties
21
Q

How can drug selectivity produce side-effects?

A

-Drug binds off-target and produces other unwanted effects in the body

22
Q

What is meant by specificity/selectivity of a drug?

A
  • Specificity= drug only binds and activates one receptor subtype
  • Selectivity= drug prefers to bind and activate to one receptor subtype but can effect others
23
Q

How is specificity/selectivity achieved with salbutamol in asthma?

A
  • Salbutamol has affinity for both B-adrenoreceptors in the heart (b1) and bronchi (b2) so binds to both
  • Has high intrinsic efficacy for b2 receptors in the bronchi, but low intrinisic efficacy for b1 in heart -> this makes it selective as only b2 predominantly activated
24
Q

Regarding the selectivity for b2-adrenoreceptors of salbutamol, why can high doses cause increased force and heart rate?

A

-Repeated high use allows enough receptors to be activated to generate a sufficient response

25
Q

What are ‘spare’ receptors?

A

-Receptors which are unoccupied in cells where less than 100% receptor occupancy produces maximal response.

26
Q

Where are spare receptors often seen?

A

-Catalytically active receptors such as receptor tyrosine kinases or GPCRs

27
Q

Why is it possible to get maximal response with less than 100% occupancy?

A
  • Amplification within the signal tranduction pathway means activation of one receptor can lead to multiple secondary messenger activation -> small number of receptors activated produces a large response
  • Response may be limited by a post-receptor event
28
Q

Why are ‘spare’ receptors beneficial?

A

-Increase the sensitivity of cells, allowing responses to be generated at low concentrations of drug (ie less % occupancy has to be reached before a response is generated)

29
Q

How does changing the receptor number effect agonist potency?

A
  • Increasing the receptor number, increases the potency of the agonist as a smaller %occupancy of the total receptor number has to be reached to generate a full response
  • Decreasing the receptor number will decrease the potency of an agonist as a higher % occupancy of the total receptor number has to be reached to generate a full response
30
Q

How can decreasing the receptor number affect the maximal response?

A

-If the receptor number is decreased beyond the amount of receptors needed to generate a full response

31
Q

When do receptor numbers tend to change?

A
  • Increase with low-activity (up-regulation)

- Decrease with high activity (down-regulation)

32
Q

What is tachyphylaxis?

A

-Desensitisation/tolerance to the drug

33
Q

Why does tachyphylaxis occur?

A

-The drugs administered produce high-activity on the receptors which then down-regulate and thus the cell becomes tolerant/tachyphylactic

34
Q

What is a partial agonist?

A

-An agonist which, when all receptors are occupied, does not produce the maximal response

35
Q

With regards to partial agonists, how is the maximal response related to intrinsic efficacy?

A

-Even with high affinity, the agonist may not fully activate the receptor/activate it in a different way, and thus the full response is not generated

36
Q

Why might buprenorphine be advantageous over morphine in some clinical settings

A
  • Using morphine for pain relief there is a risk of respiratory depression, buprenorphine can be used which is a partial agonist of the opioid receptor, so does not generate a full response, however generates an adequate pain relief response with a decreased risk of respiratory depression.
  • NB. Buprenorphine is a partial agonist with higher affinity for the receptor but decreased intrinsic efficacy
37
Q

Why is buprenorphine used in the treatment of heroin addicts?

A
  • Buprenorphine is an opioid so binds to the same opioid receptors as heroin, however buprenorphine is a partial agonist and heroin is a full agonist, so does not deliver the same level of euphoria as efficacy is insufficient
  • Buprenorphine binds to the receptors and becomes an antagonist to heroin effects as the drug blocks the receptor site so heroin cannot bind, even if injected.
  • This enables the gradual withdrawal from heroin
38
Q

Why is a partial agonist said to be compound and system dependant?

A
  • If the receptor number is increased, the agonist can change from a partial agonist to a full agonist
  • The low intrinsic efficacy at each receptor becomes sufficient enough to produce a full response
39
Q

Do full agonists with the same intrinsic efficacy have the same efficacy?

A

-No, the drugs can have the same affinity and intrinsic efficacy but different efficacy as this takes into account how the drug causes a response with regards to the tissue-dependant factors

40
Q

What are the three types of receptor antagonists?

A
  • Reversible competitive
  • Irreversible competitive
  • Non-competitive
41
Q

Describe reversible competitive receptor antagonists

A
  • Relies on the dynamic equilibrium between ligands and receptors
  • Increasing the concentration of antagonists will overcome the agonist and increase the inhibition
  • The inhibition is surmountable by increasing the agonist
42
Q

What is IC50?

A

-The concentration of antagonist needed to reduce the maximal response to 50%

43
Q

What happens to the agonist concentration-response curve with increasing antagonist?

A
  • The curve shifts to the right as more agonist needed to produce the same response
  • The Emax stays the same
44
Q

What is naxolone, and when is it clinically useful?

A
  • A high affinity competitive antagonist of u-opioid receptors
  • Useful to reverse opioid-induced respiratory depression as the high affinity competes effectively with other opioids
45
Q

Describe irreversible competitive inhibition

A
  • The antagonist dissociates very slowly or non at all so the antagonist cannot be competed off.
  • Increasing the antagonist, increases inhibition
  • The inhibition is non-surmountable
46
Q

How do irreversible competitive antagonists effect the agonist concentration-response curve?

A
  • Shift to right with increasing antagonist concentration

- Emax begins to decrease as surpass a point where not enough receptors are available to mount a full response

47
Q

How are irreversible competitive antagonists used in pheochromocytoma?

A
  • phenoxybenzamine is a non-selective irreversible competitive a1-adrenoreceptor antagonist
  • Used in hypertensive episodes of pheochromocytoma
  • tumour of adrenal chromaffin cells which produce excess adrenaline and act on a1 adrenoreceptors causing vasoconstriction
  • phenoxybenzamine blocks receptors and reduces vasoconstriction
48
Q

Describe non-competitive antagonism

A
  • Antagonist binds to an allosteric site rather than orthosteric site of receptor
  • alters the activity of the receptor (can be increased or decreased through altering efficacy or affinity
49
Q

How is ketamine a non-competitive antagonist?

A
  • Ketamine binds to allosteric site of NMDA receptors (glutamate receptors found in nerve cells)
  • It antagonises the normal effects of the receptor when an agonist binds, and results in analgesia by reducing central excitation

Membranes and Receptors (13 decks)

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