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YR2 LCRS Pharmacology > 2. Drug-receptor interactions > Flashcards

2. Drug-receptor interactions Flashcards

1
Q

what is a drug?

A

a chemical substance that interacts with a biological system to produce a physiological effect

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2
Q

what are the 4 drug target sites and what do they have in common?

A
  1. receptors
  2. ion channels
  3. transport systems
  4. enzymes

all drug target sites are proteins

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3
Q

what is the only instance when receptors are intracellular instead of within cell membranes?

A

steroid receptors

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4
Q

what are receptors activated by?

A

neurotransmitters or hormones - namely agonists (which stimulate receptors) or antagonists (which inhibit receptor-mediated responses)

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5
Q

what are the 4 main groups of receptors defined by?

A

similarities in structure and transduction systems

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6
Q

give 2 examples of drugs acting on receptors

A

ACh which is a non-selective agonist that acts on nicotinic and muscarinic receptors

atropine which is a muscarinic antagonist

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7
Q

what are the 2 types of ion channels and how do they differ?

A

voltage sensitive e.g. voltage sensitive calcium channel

receptor-linked (ligand gated) e.g. nicotinic acetylcholine receptor (nAChR)

they differ in their gating methods

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8
Q

give 2 examples of drugs that act on ion channels

A
  1. local anaesthetics

2. calcium channel blockers

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9
Q

how do local anaesthetics act on ion channels?

A

block VGSCs in the sensory axons -> reduced sodium influx -> fewer action potentials are propagated along those axons -> perception of pain is reduced

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10
Q

how do calcium channel blockers act on ion channels?

A

block VGCCs -> cause relaxation of smooth muscle -> reduces resistance to blood flow and decreases BP

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11
Q

what are transport systems?

A

systems of carriers that transport substances against their concentration gradients (glucose, ions, NTs) which show specificity for certain species

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12
Q

give 2 examples of transport systems

A
  1. Na+/K+ATPase

2. noradrenaline ‘uptake 1’

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13
Q

give an example of a drug that acts on transport systems and describe how it works

A

tricyclic anti-depressants (TCAs) bind to and inhibit NA uptake 1 to slow down reuptake into the presynaptic fibre, prolonging the action of NA in the synaptic cleft

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14
Q

what is digoxin and how does it work?

A

cardiac glycoside

interacts with the Na+/K+ pump and slows it down, which results in a knock on effect that increases the concentration of intracellular calcium and increases the force of contraction of cardiomyocytes

used to treat heart failure

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15
Q

what are the 3 ways that drugs can interact with enzymes?

A
  1. enzyme inhibitors
  2. false substrates
  3. prodrugs
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16
Q

give an example of an enzyme inhibitor and describe how it works

A

anticholinesterases

decreases ACh breakdown by inhibiting ACh-esterase

17
Q

give an example of a false substrate and describe how it works

A

methyldopa

messes up normal NA production pathway -> reduces amount of dopamine production -> methylNA produced which is a worse vasoconstrictor so tone of blood vessel is not maintained -> increased relaxation -> reduced TPR -> decreased BP

18
Q

give an example of a prodrug and what it requires to be activated

A

prodrugs need to interact with enzymes in the body before they are activated

e.g. chloral hydrate is metabolised into trichloroethanol in the liver where it then becomes effective as a sleeping drug

19
Q

describe the unwanted effects of paracetamol

A

paracetamol overdose occurs when you saturate the liver’s microsomal enzymes so another set of enzymes (P450) start metabolising the paracetamol. the different metabolites produced interact with the liver and kidneys and damage them

20
Q

which drugs produce responses due to their physiochemical properties and what responses do they produce?

A

general anaesthetics - dampen synaptic transmission but don’t interact with a specific transport system/receptor

antacids - reduce acidity of stomach contents

osmotic purgatives - stimulate voiding of gut contents by drawing water into the stomach which softens stool

21
Q

why are plasma proteins not a drug target site?

A

they do not generate a physiological response, they are just a reservoir of the drug and the drug remains inactive

22
Q

what is an agonist?

A

ACh; nicotine

a molecule that binds to a receptor and stimulates it to generate a response, usually involving a conformational change in the receptor

23
Q

what is an antagonist?

A

atropine; hexamethonium

interacts with receptors, doesnt produce a response

24
Q

what is potency and what does it depend on?

A

the powerfulness of a drug

it depends on

  1. affinity - how willingly the drug binds to its receptor
  2. efficacy - the ability of a drug to generate a response once receptor bound (ability to cause a conformational change of receptor)
25
Q

what is selectivity?

A

preference for interacting with a particular receptor site

26
Q

what is a structure-activity relationship?

A

emphasises the relationship between the structure of a drug and its activity

you can take an agonist and make a structural change to make it an antagonist

27
Q

what does the log dose-relationship curve show about full agonists with low affinity compared to partial agonists?

A

they show that they will still generate a maximal response, just need a much higher concentration whereas the partial agonist curve will peak before it gets to maximal tissue response

28
Q

what are the 2 types of receptor antagonist?

A
  1. competitive - binds to the same site as the agonist on the receptor therefore their responses can be overcome by increasing the concentration of the agonist (e.g. atropine and propranolol)
  2. irreversible - bind to the same site as the agonist, more tightly with covalent forces so the agonist cannot displace the antagonist. may also bind to a different site to the agonist, downstream so the antagonist cannot be overcome. (e.g. hexamethonium blocks the ion channel rather than the receptor)
29
Q

what is receptor reserve?

A

you dont have to occupy 100% of receptors to generate a maximal response in some tissues

this increases the sensitivity of the tissue to the agonist and increases the speed of response

30
Q

what is the effect of competitive antagonists on the dose-response curve?

A
  • parallel displacement to the right

- surmountable

31
Q

what is the effect of irreversible antagonists on the dose-response curve?

A
  • the curve falls away

- a lot of receptors are essentially being knocked out so less response can be generated

YR2 LCRS Pharmacology (32 decks)

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