Drug-Receptor Interactions Flashcards Preview

Y2 LCRS 1 - Pharmacology and Therapeutics - Laz > Drug-Receptor Interactions > Flashcards

Flashcards in Drug-Receptor Interactions Deck (21)
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1
Q

Define Pharmacokinetics and Pharmacodynamics.

A

Pharmacokinetics – the effect that the body has on the drug
Pharmacodynamics – the effect of the drug on the body

2
Q

Define the word ‘drug’.

A

A chemical substance that interacts with a biological system to produce a physiological response

3
Q

State the four main target sites for drugs.

A

Receptors
Ion Channels
Transport Systems
Enzymes

4
Q

What are the two types of ion channels?

A

Voltage-Gated

Receptor Linked

5
Q

Give an example of a group of drugs that act on ion channels.

A

Local anaesthetics – they block the voltage gated sodium channels of nociceptor neurons to prevent the conduction of pain signals to the CNS

6
Q

Give an example of a drug that acts on transport systems.

A

Tricyclic antidepressants
Cardiac glycosides – it slows down the Na+/K+ pump thereby increasing the intracellular calcium ion concentration, which leads to an increased force of contraction

7
Q

What are the three ways in which drugs can interact with enzymes?

A
Enzyme inhibitors (e.g. anticholinesterases) 
False transmitter (e.g. methyldopa) 
Prodrugs (e.g. chloral hydrate)
8
Q

What is a common example of the unwanted effects of drug interaction with enzymes?

A

Paracetamol overdose – this will saturate the microsomal enzymes in the liver so the paracetamol is then broken down by another set of enzymes (P450) which generates toxic metabolites

9
Q

Name three groups of drugs that are exceptions to the four target site rule.

A

General anaesthetics – reduce synaptic transmission without interacting with transport systems or receptors
Antacids – these are basic so they simply neutralize some of the stomach acid
Osmotic purgatives – draw water into the bowel due to its physicochemical properties

10
Q

Define agonist.

A

A molecule that binds to a receptor and generates a response

11
Q

Define antagonist.

A

A molecule that binds to a receptor but do NOT generate a response

12
Q

Define potency. What is it dependent on?

A

How powerful the drug is
It depends on affinity (how willingly the drug binds to the receptor) and efficacy (the ability of a drug to generate a response once bound)

13
Q

What is a full agonist?

A

An agonist that generates a maximum response

14
Q

What is a partial agonist?

A

An agonist that generates a less than maximum response

15
Q

What is selectivity?

A

Drugs have a preference for binding to certain receptors (it is rarely specific – they normally bind to a few different receptors)

16
Q

What is the difference between full agonists with a high affinity and full agonists with a lower affinity?

A

Full agonists with a lower affinity can still generate a maximum response but requires a higher dose than the full agonist with lower affinity

17
Q

Describe antagonists in terms of affinity and efficacy.

A

Antagonists have affinity but NO efficacy

18
Q

What are the two types of antagonist?

A

Competitive – they bind to the same site as the agonist on the receptor – they are surmountable
Irreversible – could bind to the same site as the agonist but will bind more tightly with covalent forces so that they can’t be moved – some irreversible antagonists will bind to sites different to the site that the agonist binds to – insurmountable

19
Q

What effect do these two types of antagonist have on dose-response curves?

A

Competitive – shifts the D-R curve to the RIGHT
Irreversible – shifts the D-R curve to the RIGHT and LOWERS the response elicited (it can no longer generate a full response)

20
Q

What is receptor reserve?

A

In some tissues, not all the receptors need to be stimulated to generate a maximum response (sometimes as little as 1% of receptors may need to be activated)
This increases the sensitivity of the tissue to the agonist

21
Q

True or false: full agonists that are selective for a given receptor will have the same efficacy.

A

True

They are full agonists so they all elicit a maximum response hence they have the same efficacy