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4BBY1040 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Definition of pharmacology

A

The science of drugs, their mechanisms, how the effects are measured, discovery, development, and actions on the organism.
Three branches of pharmacology are toxicology, pharmacy and therapeutics

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2
Q

Definition of pharmacy

A

How drugs are formulated and dispersed for use a s medicines

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3
Q

Definition of therapeutics

A

Medicinal use of drugs to treat symptoms and diseases

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4
Q

Definition of toxicology

A

Branch of pharmacology that focuses on harmful effects of chemicals

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5
Q

Definition of a drug

A

‘A chemical substance of known structure other than a nutrient or an essential dietary ingredient, which, when administrated to a living organism, produces a biological effect’

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6
Q

What are the three names a drug has?

A

Chemical name
Common name
Trade name (company’s given name to drug when its sold commercially)

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7
Q

How is drug useful therapeutically?

A

It needs to be selective in its actions so it treat symptoms and reduces side effects

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8
Q

What is pharmacokinetics?

A

What the body does to the drug
(ADME)
Absorption- how much and how quickly the drug enters the system
Distribution- Where does the drug go after its been absorbed
Metabolism and Excretion- factors that determine how long the drugs effects last for (determined by half-life)

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9
Q

What is pharmacodynamics?

A

What the drug does to the body

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10
Q

Key dates?

A

Does it really need to be known?

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11
Q

What are considerations during drug development?

A

Whether the drug actually works
The safety of the drug (for patient and the environment)
The cost of development and later production
Intellectual property (patents)
Ethical issues

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12
Q

Describe the drug development process

A

Potential drugs are formulated from various sources, where they then go through an assay system to be measured. A hypothesis is developed which dictates what the assay will be. Chemical optimization of the active chemical in the drug occurs to try to make the drug better at what its being measured for by the assay.
Eventually animal models will be used

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13
Q

What is an assay/ assay system?

A

The analysis of a drug to determine the potency of the active chemical.

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14
Q

Where do potential drugs come from?

A

Natural products like plants
Compound libraries of pharmaceutical companies, which is a collection of stored chemicals and chemical compounds
Combinatory chemistry (combining chemicals)

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15
Q

What is high-throughput screening?

A

Screening of the drug to see if it attaches to the target receptor. A lot of drugs are screened at the same time

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16
Q

What are the types of ‘throughput screening’?

What is the purpose of each type?

A

High (Up to 50,000 in a day), medium (Up to 100 in a day), low (Up to 10 in a day) throughput screening.
High tests whether the drug binds or not, not affinity necessarily, just whether it binds or not.
Medium uses the drugs that bind and tests its affinity and selectivity for receptor.
Low tests if the drug actually does what the hypothesis hypothesizes it does.

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17
Q

Structure activity relationships (SARs)

A

.

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18
Q

What happens during the ‘animal model’ portion of drug development?

A

Analysis of pharmacokinetics and subsequent chemical optimization in order to try to improve the potency of the drug.
Toxicology testing to see if the drug is even safe.
If drug is ‘safe’ and the chemical optimization is at its peak, it becomes a drug candidate.

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19
Q

In terms of pharmacokinetics, how can chemical optimization improve a drugs potency?

A

Try to make the drug be absorbed more readily (or easier or whatever)
Try to increase the drugs half life so that the drugs metabolism is reduced and it stays in the body for longer.

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20
Q

How long do pre-clinical trials last for?

How long do patents last for?

A

5-10 years
20 years typically. The 20 years starts early in the pre-clinical trials, not once the drug is finished for distribution.

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21
Q

What is Phase I of clinical trials?

A

Small group of healthy volunteers used to test if the drug is safe.
Includes placebos, double-blind trails and may involve specific demographic groups.

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22
Q

What is Phase II of clinical trials?

A

Used to determine the clinical effects of the drug in patients. Safety and tolerability is also analysed.
Phase IIa (Exploratory)
- ‘Small group’ of subjects (50-200)
- Placebos and double-blind trials used

Phase IIb (Confirmatory)

  • ‘Large group’ of subjects (200-500)
  • Test drug safety and efficacy against current treatment
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23
Q

What is Phase III of clinical trials?

A

Full scale confirmatory evaluation of efficacy and safety of drug compared to current treatment

  • Involves a relatively large group of subjects (2,000-10,000 patients)
  • Phase lasts for years and data is collected to support registration of drug to be used/sold post-market
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24
Q

What is Phase IV of clinical trials?

A

Ongoing investigation of drug to monitor consequences of increasing exposure of drug, in case there’s any long term adverse effects of the drug. Investigation can also be used to compare efficacy in different groups of people.

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25
Q

What shape is the drug ‘concentration-response’ curve?

What shape is the drug ‘log concentration-response’ curve?

A

Hyperbola

Sigmoidal curve

26
Q

What are pharmacological experiments in virto?

A

A piece of tissue is dissected from an animal (humans included) and it is kept alive outside of the body.
Experiments are done on this tissue and it is the most most common way to do pharmacological experiments.

‘Responses that might be measured include changes in the tension of a muscle; changes in the activity of an enzyme; or changes in the secretion of a hormone or neurotransmitter’

27
Q

What are pharmacological experiments in vivo?

A

Drug effects are measured whilst the animal is still alive.
It is tightly regulated by the Home Office in the UK.

‘Responses that might be measured include increase in blood pressure; reduction in pain threshold; reduction in allergen-induced bronchoconstriction…….’

28
Q

What are pharmacological experiments ex vivo?

A

Animals tissues/organs are harvested, where the drug effects are measured.
It is tightly regulated by the Home Office in the UK.

‘Examples might include experiments to see whether long-term treatment with a drug induces liver damage or alters some aspect of brain biochemistry.’

29
Q

Why is it not possible to use molar concentrations for experiments in vivo?

A

The volume of solvent (blood) is not known, so we have to use the ‘weight of the drug’ per ‘weight of animal’.
mg/kg for example.

30
Q

What is Emax?

A

The maximal response able to be produce by a drug.

On a graph, as there’s the plateau, the Emax is the asymptote.

31
Q

What is EC50?

A

The molar concentration that produces half of the maximum response for that drug.

32
Q

What is EC80?

A

The molar concentration that produces 80% of the maximum response for that drug.

33
Q

What is the potency of a drug?

A

The concentration at which a drug is effective.
Quantified as the EC50.
A drug with a low EC50 is a drug which is more potent than a drug with a relatively higher EC50.

34
Q

What is the potency ratio?

A

A way of comparing potency of two drugs. Potency ratio = ‘M’

M= EC50 (test) / EC50 (standard)
LogM= log[EC50(test)] - log[EC50(standard)]
35
Q

What does the value of a potency ratio mean?

A

M = 1 means the potency of the test drug is the same as the standard.
M < 1 means the potency of the drug is higher than the standard.
M > 1 means the potency of the drug is lower than the standard.

36
Q

What is a bioassay?

A

“A bioassay is any techniques where the potency of a drug is determined by measuring the biological response it produces.”

37
Q

What is the 2+2 bioassay?

A

Makes use of the fact that the middle portion of the log conc-response is ALMOST linear. If the drugs work by the same mechanism, then the ‘linear’ parts of the curve should be parallel.
‘M’ can be obtained by comparing two doses of standard with two doses of unknown.

38
Q

What is the Therapeutic Index?

A

Therapeutic index = LD50/ED50
LD50 = lethal dose in 50% of population
ED50 = Effective dose in 50% of the population

The ratio between the toxic dose of a drug and the dose producing the desired therapeutic effect.
The higher the therapeutic index, the less chance of the drug producing toxic side-effects in therapeutic use.

39
Q

What is the function of a receptor?

A

Recognition of a ligand (drug, neurotransmitter, hormone)

Transduction (transferring the message of the ligand)

40
Q

What is the shape of a graph showing drug concentration and the percentage of drugs binding to it?

A

Rectangular hyperbola

41
Q

What feature do all clinically useful drugs have?

A
  • High affinity.

- They must be able to reversibly bind to the receptor. Every single clinically useful drug has to have this feature.

42
Q

How is affinity for a drug measured?

A

Measured by KD (D is subscript)
KD is the known as the molar concentration of a drug needed to occupy 50% of the available receptors AT EQUILIBRIUM.
The lower the KD, the higher the affinity.

43
Q

What is KD?

A

KD (D is subscript)
KD is the dissociation rate, and defines affinity
D + R ↔ DR (↔ as in reversible reaction)

Rate of FORWARD reaction = (k{+1})*([D][R])
Rate of BACKWARD reaction = (k{-1})*([DR])
Equilibrium is (forward reaction = backward reaction)

KD = (k{-1}) / (k{+1}) = [D][R] / [DR]

44
Q

What are agonists?

A

Drugs with affinity and efficacy for a receptor

45
Q

What are antagonists?

A

Drugs with which act to produce an antagonistic effect for an agonist

46
Q

What is efficacy?

A

A drugs ability to activate its desired receptor

47
Q

What is a full and partial agonist?

A

A full agonist is a drug that has a high efficacy for a receptor. They produce a maximal response for a receptor despite not binding to all receptors.
A partial agonist has a relatively lower efficacy for the same receptor in comparison to a full agonist. They are unable to produce a full response even if they bind to all receptors.

If a new drug is produced that produces a higher than maximal response, the new drug will be labelled as a full agonist and the previously full agonist will be labelled as a partial agonist.

48
Q

What are the forms of antagonism?

A

Chemical- Using one drug to inactivate the other
Pharmacokinetic- Drug alters the way the body deals with another drug
Physiological- Two drugs act to produce opposing effects so that the effects cancel out. (This technically makes both drugs agonist, because the drug that produces the effect have efficacy and the drug that produces the opposing effect also has efficacy)

49
Q

What is reversible competitive antagonism?

A

When antagonist compete with agonists for the same receptors. The antagonist has affinity but no efficacy.

Because the antagonist is reversibly able to bind to the receptor, the antagonist eventually unbinds if it is ‘out-competed’ by the agonist. To out-compete the antagonist, concentration of the agonist must be high / increased.

50
Q

What is reversible non-competitive antagonism?

A

When the antagonist bind to a different receptor to the agonist, but still produce some form of antagonism (reducing the maximal response of the agonist). The antagonist has affinity and efficacy.

Because the agonist and antagonist effect different receptors, the antagonist can not be ‘out-competed’ which means that regardless of concentration of agonist, the antagonists effects can not be overcome by the agonist.
The antagonist will eventually be metabolized as it is reversibly bound to the receptor, so the half-life of the antagonist dictated how long the antagonism lasts for. Eventually all the antagonist will be unbound and the agonist will be able to produce a maximal response.

51
Q

What is irreversible non-competitive antagonism?

A

When the antagonist binds to a different receptor to the agonist, but still produce some form of antagonism. The antagonist has affinity and efficacy.

The effect of the antagonist is permanent because it irreversibly binds to the receptor. The maximal response able to be produced by the agonist will eventually reduce if more antagonist is added.

52
Q

What is irreversible competitive antagonism?

A

When antagonist compete with agonists for the same receptors. The antagonist has affinity but no efficacy.
Because the antagonist irreversibly binds to the receptor, the agonist will be unable to bind to the receptor. The effect is permanent and the maximal response able to be produced by the agonist will eventually reduce if more antagonist is added.

53
Q

Graphs of different antagonists effects on an agonist.

A

https://image.slidesharecdn.com/introductoryreceptorpharmacology2014-15jap-170125150550/95/introductory-receptor-pharmacology201415jap-19-638.jpg?cb=1485356977

NOTE: The non-competitive irreversible and competitive reversible are both the purple curve

54
Q

What is the structure of local anaesthetics?

A

They have an amide group bound to an aromatic ring or an ester group bound to an aromatic ring. (They are weak bases)

55
Q

How are local anaesthetics metabolised?

A

The drug is metabolised by the bonds between ring and either the ester or amide (depending on local anaesthetic chemical structure).
Amine ester is hydrolysed.
Amino amide is metabolised by enzymes in the liver.

56
Q

Where do local anaesthetics bind to?

A

They bind to and inactivate Na+ channels reversibly.

the cytoplasmic receptors, so the local anaesthetic has to diffuse into cell first

57
Q

What is use-dependence?

A

Drug binding increases and so Na+ channels are blocked at a faster rate. Tissues that are frequently depolarised have a grater degree of blockage so cells that depolarise at a high rate can be blocked.

58
Q

What if the happens to local anaesthetics if pH of extracellular fluid is (relatively) high?

A

The weak base will dissociate less, so the local anaesthetic can enter the cell by diffusion because it is not an ion. Therefore it can enter the cell to bind to inactivated ion channels.

59
Q

What if the happens to local anaesthetics if pH of extracellular fluid is (relatively) low?

A

The weak base will dissociate more, so the local anaesthetic will not be able to enter the cell so cant diffuse. Therefore it can not enter the cell to bind to inactivated ion channels.

60
Q

What is the effect of local anaesthetics?

A

They block the nerve that carry signals to CNS about pain, but not pressure.

4BBY1040 (6 decks)

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