Flashcards in Drug-Receptor Interactions Deck (24)
Define Pharmacokinetics and Pharmacodynamics.
Pharmacokinetics – the effect that the body has on the drug
Pharmacodynamics – the effect of the drug on the body
Define the word ‘drug’.
A chemical substance that interacts with a biological system to produce a physiological response
State the four main target sites for drugs.
What are the two types of ion channels?
Give an example of a group of drugs that act on ion channels.
Local anaesthetics – they block the voltage gated sodium channels of nociceptor neurons to prevent the conduction of pain signals to the CNS
Give an example of a drug that acts on transport systems.
Cardiac glycosides – it slows down the Na+/K+ pump thereby increasing the intracellular calcium ion concentration, which leads to an increased force of contraction
What are the three ways in which drugs can interact with enzymes?
What is a common example of the unwanted effects of drug interaction with enzymes?
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
Name three groups of drugs that are exceptions to the four target site rule.
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
A molecule that binds to a receptor and generates a response
A molecule that binds to a receptor but do NOT generate a response
Define potency. What is it dependent on?
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)
What is a full agonist?
An agonist that generates a maximum response
What is a partial agonist?
An agonist that generates a less than maximum response
What is selectivity?
Drugs have a preference for binding to certain receptors (it is rarely specific – they normally bind to a few different receptors)
What is the difference between full agonists with a high affinity and full agonists with a lower affinity?
Full agonists with a lower affinity can still generate a maximum response but requires a higher dose than the full agonist with lower affinity
Describe antagonists in terms of affinity and efficacy.
Antagonists have affinity but NO efficacy
What are the two types of antagonist?
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
What effect do these two types of antagonist have on dose-response curves?
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)
What is receptor reserve?
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
True or false: full agonists that are selective for a given receptor will have the same efficacy.
They are full agonists so they all elicit a maximum response hence they have the same efficacy
Effect of partial agonist on dose response curve
Has a lower maximum
Effect of agonist with lower affinity on log dose response curve
Shifted to right