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CEP > WEEK 2 > Flashcards

WEEK 2 Flashcards

1
Q

What is a drug?

A

Any substance that interacts with a biological system and changes it

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2
Q

What are two types of drugs?

A

Low-molecular-weight drugs and Biologic

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3
Q

What is pharmacology good for?

A

knowing what drugs exist and their benefits and side effects, drug categorisation, quantifying drug action (proper dosing)=good prescription practise

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4
Q

Why do drugs that cause their effects by their physiochemical properties tend to need higher concentrations?

A

Due to non-specific effects

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5
Q

Give examples of drugs that produce their effects via their physiochemical properties

A 
Antacids (Sodium Bicarbonate)
Laxatives
Heavy metal antidotes
Osmotic diuretics
General anaesthetics
Alcohol
Li+ ions
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6
Q

What are common drug characteristics?

A

effects occur at very low concentrations with high potency and can be very specific (biological or chemical specificity)

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7
Q

What is biological specificity?

A

specificity relating to the side of the receptor/biological system (receptor or target)

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8
Q

What is chemical specificity?

A

specificity relating to the substance added to the biological system (ligand or agonist)

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9
Q

Give an example of drug stereo-specificity

A

Thalidomide-two racemic forms->given as R form for pain relief but experienced in vivo racemisation to S form which had terrible side effects

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10
Q

What is an organoid?

A

A small and simplified version of an organ which is used to model a human disease

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11
Q

What is an organoid used for?

A

Monitoring disease development and drug testing

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12
Q

Give an example of organoid formation

A

Embryonic stem cell+skin fibroblast->Pluripotent stem cell culture-endoderm differentiation->sphenoid culture->matrigel culture->intestinal epithelial mesenchymal organoid

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13
Q

What is the receptor concept?

A

That drugs produce their effect by combining with specific receptor sites in cells and the response correlates to the number of occupied receptors

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14
Q

What is the lock and key hypothesis?

A

The shape of the drug is complementary to the shape of the receptor (chemical specificity)

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15
Q

What is drug affinity?

A

The binding ‘strength’ of the drug-receptor interaction or the ‘likelihood’ of binding

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16
Q

Equation for the drug-receptor interaction

A

A+R⇌AR->active AR
A=drug
R=receptor

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17
Q

What is an agonist?

A

A substance that binds to a receptor and produces a response-produces affinity and efficacy

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18
Q

What is an antagonist?

A

A substance that binds to a receptor but doesn’t produce a response and blocks agonist binding and response-possesses affinity but not efficacy

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19
Q

Equation for antagonist-receptor interaction

A

Ant+R⇌AntR-X->effect

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20
Q

What is quantitative pharmacology?

A

The assumption that drugs act by entering into a simple chemical relation with certain receptors in cells and that there is a simple relation between the amount of drug fixed by these receptors and the action produced (A+R⇌AR->active AR)

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21
Q

Relationship between drug concentration and response is:

A

continuous, saturating (hyperbolic curve, sigmoidal when log[agonist]) and exhibits threshold

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22
Q

What is EC50?

A

The drug concentration that produces half the maximum response/efficacy->model-free equivalent of Kd

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23
Q

What is specificity?

A

The capacity of a drug/receptor to manifest only one kind of action

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24
Q

What are two assumptions made when mapping the relationship between drug concentration and response?

A

1) ‘response’ scales with concentration of drug-receptor complexes
2) fixed number of receptors

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25
Q

Equation relating to law of mass action/drug-receptor interaction

A 
A+R⇌ AR
Kd=[A].[R]/[AR]
units of Kd=mol/litre
[A]=agonist conc.
[R]=receptor conc.
Kd=dissociation constant
26
Q

What does the Kd (dissociation constant) equation derive to?

A

p(constant of response)=[A]/Kd+[A]

27
Q

How do signalling cascades result in lower doses of the drug required?

A

Large signal amplification meaning low dose has larger effect than expected

28
Q

What are the different natures of drug receptors?

A

Enzymes
Ion channels
Transporters (pumps, transport proteins)
‘Physiological’ receptors

29
Q

Give two obscure natures of drug receptors

A

DNA/RNA and the ribosome

targets of monoclonal antibodies

30
Q

What are “dirty drugs”?

A

Drugs that have many targets causing unwanted/unplanned effects

31
Q

How are steroid hormones a type of “dirty drug”?

A

They bind to intracellular nuclear receptors but also activate membrane-bound GPCRs-effect is often the result of the interplay between the two mechanisms

32
Q

Give an example of a “dirty drug” having different effects at different dosings

A

Aspirin:
lower dose=blood thinner (anti-thrombotic)
higher dose=pain killer

33
Q

What are the ways of regulating cell function?

A

Alteration of membrane potential, alteration of enzyme activity, alteration of gene expression->most drugs affect cell function via (physiological) receptors, acting ‘hormone-like’

34
Q

How are receptors classified?

A

On the basis of the selective action of drugs, they are named according to the transmitter/hormone with which they interact (eg. AChRs)

35
Q

What are the 5 receptor super-families?

A

Integral ion channels (eg. nicotinic/glycine receptors)
Integral tyrosine kinases (eg. insulin receptor)
Steroid receptors (eg. oestrogen receptor)
GPCRs (eg. muscarinic receptors)
Cytokine receptors (eg. prolactin/EPO receptor)

36
Q

What is the action of integral ion channels?

A

They transport ions causing a change in the voltage across the membrane

37
Q

What is the action of integral tyrosine kinases?

A

They have a large extracellular domain which is busy in ligand binding and dimerisation, signal is transduced by conformational change which brings intracellular domain closer, phosphorylation of intracellular part=activation

38
Q

Where do steroid receptors usually act?

A

In the nucleus, but are located in the cytoplasm

39
Q

What are the two defining features of a steroid receptor?

A

DBD=DNA-binding domain->mediates receptor binding to genomic sites
LBD=ligand-binding domain->where ligand binds, functions like a folding sensor: without ligand=unfolded, with ligand=folded

40
Q

What is the action of steroid (nuclear) receptors?

A

as long as domain hasn’t bound to ligand it’s unfolded, makes it a substrate to folding helper enzyme (heat shock protein-HSP), grabs and holds tightly, forms HSP/NR complex, hormone (ligand) binds to LBD, HSP removed, NR/hormone complex, dimerisation of NR, moves into nucleus, DBD binds NR to target gene

41
Q

Why do GPCRs have multiplicity?

A

homo- and heterodimers and several G subunits with different effects

42
Q

What is agonism?

A

Various ways drugs produce effects by binding to receptors

43
Q

What is antagonism/desensitisation?

A

Various ways drugs block effects by binding to receptors

44
Q

What is the % agonist response of a full agonist?

A

100%

45
Q

What is the % agonist response of a super agonist?

A

> 100%

46
Q

What is the % agonist response of a partial agonist?

A

0%>x>100%

47
Q

What is the % agonist response of an antagonist/no agonist?

A

0%-binds and does nothing, doesn’t alter spontaneous openings

48
Q

What is the % agonist response of partial/full inverse agonists?

A

<0%-reduces spontaneous activity

49
Q

What is an allosteric effect?

A

The binding of a ligand to one site on a protein molecule in such a way that the properties of another site on the same protein are affected

50
Q

Give an example of allosteric effects on receptors

A

benzodiazepine agonists bind to GABAaRs on a different site on the protein channel and increase GABA affinity to GABAaRs, increase channel opening, increasing Cl- ion influx

51
Q

What is the allosteric effect of benzodiazepine antagonists/inverse agonists on GABAaRs?

A

their binding doesn’t cause Cl- ion efflux but will prevent the ion channel opening-reduced/no influx of Cl-

52
Q

What are ‘super agonists’?

A

Highly efficacious agonists that produce a maximal response from the cell without binding to all the available receptors

53
Q

What are partial agonists?

A

Low efficacy agonists that cannot produce the cell’s maximal response, even when they have bound to all available receptors

54
Q

What is a competitive antagonist?

A

A substance with a relatively similar shape to the agonist, so binds reversibly to the same site as the agonist

55
Q

What effect does a competitive antagonist have on agonist dose/response curves?

A

Parallel shift to the right due to a slower rate of response but no change in Emax

56
Q

What is an irreversible antagonist?

A

A substance that binds irreversibly at the same site as the agonist, forming a covalent bond or binding tightly

57
Q

What effect does an irreversible antagonist have on agonist dose/response curves?

A

Downward shift due to decreased maximal response to agonists so Emax is lower

58
Q

What happens to a membrane receptor once it’s inactivated by an irreversible antagonist?

A

antagonist binds, signalling (or lack of), internalisation, receptors move into cell and fuse with lysosomes, receptor degradation, recycled

59
Q

What is an allosteric antagonist?

A

A substance that binds irreversibly at a different site to the agonist and decreases agonist affinity by inducing inhibitory protein conformation

60
Q

What is a channel blocker?

A

A substance that binds inside the channel (‘plug’) and prevents ion passage which tends to be increased by receptor activation (eg. local anaesthetics)

61
Q

What is a ‘Physiological’ antagonist?

A

A substance that antagonises the physiological effect of some agonists

62
Q

What is desensitisation?

A

A reduction in agonist response due to prolonged or repeated exposure to the agonist

CEP (9 decks)

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