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medical pharmacology > how drugs work > Flashcards

how drugs work Flashcards

1
Q

what is chemical signalling

A

the main mechanism by which biological function is controlled at all levels, from the single cell to the whole organism

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2
Q

what is the function of receptors

A

chemical recognition

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3
Q

what did Langley J.N 1905 do

A

he came up with the idea of ‘receptive substance’ to explain the actions of nicotine and curare on skeletal muscle

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4
Q

what are drug targets

A

critical drug binding site

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5
Q

what are the most drug targets

A

proteins

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6
Q

exceptions of drug target

A

-any antimicrobial and antitumor drugs interact with DNA

–bisphosphonates used to treat osteoporosis bind Ca2+ salts

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7
Q

what are the main types of regulatory proteins (4)

A

-receptors (classical signalling)
•ion channels
•enzymes
•carrier molecules (transporters)

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8
Q

define the term receptor in pharmacology

A

it is used for protein molecule whose function is to recognise and respond to endogenous chemical signals

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9
Q

what are the other molecules with which drugs interact with called

A

drug target

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10
Q

how do receptors work (when agonist occurs)

A
  • agonist activates receptor e.g. acetylcholine cytokine, steroid, growth factor receptors and then it can move directly through ion channel which closes/opens
  • it can also go through a transduction mechanism which are three mechanisms:
  • enzyme activation/ inhibition
  • ion channel modulation
  • DNA transcription
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11
Q

what are the two types of ion channels and what do they do

A
  • blocker- permeation blocker

- modulator- increased or decreased opening probability

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12
Q

what did Hill A.V. 1909 do

A

he came up with the quantitative expression of the receptors

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13
Q

what did Langmuir 1916 do

A

he independently derived the same equation as Hill which is why the equation is now known as Hill- Langmuir equation

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14
Q

Clark A.J. 1926 experiment

A
  • actions of acetylcholine and atropine on the frog’s isolated heart
  • as the acetylcholine increases heart rate increases
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15
Q

Gaddum J.H. 1926 experiment

A

-actions of adrenaline and ergotamine on the rabbit uterus

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16
Q

what are inhibitors and where are they sat

A

sat on the active site and block the binding site

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17
Q

what does B max mean

A

binding capacity

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18
Q

what does K mean

A

equilibrium constant

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19
Q

what does E max mean

A

maximum response

20
Q

describe transporter carrier molecule

A
21
Q

draw the binding curve

A

..

22
Q

describe the receptors in physiological systems and what do they do

A

-adrenaline (epinephrine) binds b-adrenoceptor in the heart (vascular smooth muscle)
•increase in force
•increase in heart rate

23
Q

what is non- uniform distribution of the drug

A

drug molecules must be bound to particular constituents (receptors) of cells and tissues in order to produce an effect

24
Q

what does pharmacological effects require

A

it requires non-uniform distribution of the drug

25
Q

agonist vs antagonist

A
  • agonist activates receptor through signal transduction

- antagonist combines with the receptor without causing activation (no effect as the endogenous meditators are blocked)

26
Q

what is reciprocal

A

it is when individual classes of drugs bind only to certain targets and when individual targets recognise only certain classes of drug

27
Q

what will happen by increasing the dose of a drug

A

it will cause it to affect targets other than the principal one
–can lead to side effects

28
Q

what is difference between agonist and antagonist regarding the efficacy and affinity

A

1) drug agonist bind to a receptor the affinity is K+1 and K-1 and then the efficacy is alpha and beta so therefore there is a response
2) dug antagonist bind to a receptor and has the same affinity however there is no efficacy as it is 0 therefore there is no response

29
Q

what does affinity mean

A

tendency of a drug to bind to a receptor

30
Q

what does efficacy mean

A

ability of a drug to activate the receptor–For antagonists, efficacy is zero (b = 0;

31
Q

partial vs full agonist

A

-partial agonists have intermediate efficacy, tissue response submaximal
•Full agonists, efficacy is sufficient to elicit maximal tissue response

32
Q

what does a binding curve look like

A

…

33
Q

what does a logistic curve look like

A

….

34
Q

what does EC50 mean

A

concentration required to produce a 50% maximal response

35
Q

what does ED50 mean

A

dose required to produce a 50% maximal response

36
Q

what is a sigmoidal curve

A

when the mid portion of a curve is linear

37
Q

concentration-effect curve vs binding curve

A

concentration-effect curve cannot normally be used to measure affinity of a drug to a receptor
•Response produced is not directly proportional to receptor occupancy

38
Q

where does a competitive antagonist bind too

A

it binds to the same site as an agonist

39
Q

what can happen if you raise agonist concentration

A

it can restore agonist occupancy

40
Q

explain dose ratio

A

ratio by which the agonist concentration has to be increased in the presence of antagonist to restore a given level of response

41
Q

difference between irreversible and reversible

A

…

42
Q

give an example of an irreversible enzyme inhibitor

A

aspirin (acetylsalicylic acid)
•prolonged inhibition of platelet cyclooxygenase 1 (COX-1) and reduction of aggregation
•irreversible acetylation of COX enzymes

43
Q

what does concentration effect demonstrate

A

relationship between drug concentration and the biological response

44
Q

what are the drug targets

A

receptors, Ion channels, enzymes, transporters

45
Q

what does partial agonist bring out

A

submaximal response

46
Q

what does inverse agonist reduce

A

the level of constitutive activation

47
Q

what does the two- state model take in account

A

constitutive activation

medical pharmacology (6 decks)

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