PHARM 3: Drug Receptor Interactions Flashcards
What id the difference between pharmacokinetics + pharmacodynamics?
pharmacokinetics = effect of body on the drug
(absorption, distribution, metabolism, excretion)
pharmacodynamics = effect of drug on the body
(responses, mechanism of action)
Define Drug
Drug = a chemical substance that interacts with a biological system to produce a physiological effect
What are the 4 main drug target sites?
- receptors
- ion channels
- transport systems
- enzymes
What are the 2 types ion channel?
- voltage sensitive (e.gVSCC)
- receptor linked (e.g nAChR)
What are the 3 ways in which drugs interact with enzymes?
- enzyme inhibitors
e.g anticholinesterases
bind to enzyme –> slows down metabolism of Ach –> elevation of Ach in synaptic cleft –> effects - false substrates
e. g methyldopa - -> anti hypertensive drug
- -> nerve fibre thinks methyldop is DOPA
- -> converts to methyldopamine –> then forms false substrate
- ->which is a less good vasoconstrictor
- prodrugs
e. g chloral hydrate - -> Chloral hydrate needs to interact with enzyme to form active component –> trichloroethanol
What are the 2 different mechanisms of drug action?
- full agonist
2. partial agonist
Explain the difference between full + partial agonist
FULL AGONIST
- reaches maximal tissue response eventually
- as you increase against conc
PARTIAL AGONIST
- can NEVER generate maximal response because it doesn’t have sufficient efficacy.
Why is log dose response curve useful?
- you can see more easily where the maximal response is.
Describe the difference between FULL + PARTIAL agonist in a log dose response curve.
FULL AGONISTS with lower affinity still generates maximal response, but requires higher conc
PARTIAL AGONISTS will peak before reaching maximal tissue response.
NOTE:
- antagonists have affinity but no efficacy.
-
What are the 2 main types of antagonists?
- competitive
- binds to same site as agonist on the receptor
- so their responses = surmountable
by increasing conc of agonist –> you can overcome competitive antagonist.
e.g atropine
- irreversible –> causes insurmountable antagonism
- binds more tightly to same site as agonist with covalent forces
OR
- binds to diff site
e.g hexamethonium.
What is the effect of COMPETITIVE + IRREVERSIBLE antagonists?
COMPETITIVE:
- surmountable
(you need higher conc of agonist to generate maximal response)
IRREVERSIBLE:
- curve falls away
- cannot generate maximal response regardless of agonist conc
What are receptors?
proteins within cell membs
activated by neurotransmitters or hormone
Give example of a drug that is an agonist
Ach (non selective agonist)
Give an example of a drug that is an antagonist
atropine (muscarinic antagonist)
What are ion channels
- selective pores that allow transfer of ions does electrochemical gradient
Give examples of ion channel drugs
-Local anesthetics (lidocaine)
vgsc is targeted - reduces influx of na+ ions –> less + slower propagation of AP –> less pain perceived
-Calcium channel blockers
give examples of drugs that target transport systems
- Cardiac glycosides
- Tricyclic anti depressants (TCA)
What is PPB ?
what does it do?
- drug binds to albumin or other protein
- creates a reservoir
- e.g warfarin, aspirin
what is meant by an agonist
drug that stimulates receptor
e.g Ach, nicotine
what is meant by an antagonist?
drug that interacts with the receptor and inhibits access to the receptor
e.g atropine,
potency of drug depends on 2 properties :
- AFFINITY
- EFFICACY
- -> ability to create conformational change in receptor
partial + full agonist combination results in:
antagonist activity against full agonist
NOTE: selective activity -
in pharmacology, usually there is no drug that interact with only one receptor type so rather than specific, it is selective
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