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Medicine Year 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is pharmacology?

What are some of its uses?

A

Study of drugs and how they interact with the body.

Used in diagnosing, curing and preventing disease.

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2
Q

What is pharmacodynamics?

What is pharmacokinetics?

A

What drug does to the body.

What body does to the drug.

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3
Q

What is a drug?

What is a placebo?

Different types of drug?

A

Drug contains an active substance that has a direct effect.

Placebo contains inactive substance and has no direct therapeutic effect. Unethical uses except in drug trials where patient aware of its uses.

Natural, semi-synthetic and synthetic drugs. One not better than other.

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4
Q

Describe Salicylic acid

A

Found in bark of willow tree. Had to be purified as dose unknown and many other ingredients. Purified was toxic and not effective. Modified acetyl Salicylic acid which is aspirin. Not toxic and more effective.

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5
Q

What is homeopathy?

A

Like cures like. To enhance activity of drug have to dilute it. Smaller doses are more effective.

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6
Q

Define efficacy?

A

How big max response is.

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7
Q

Define potency?

A

Dose needed to produce the desired response.

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8
Q

Define variability?

A

How many patients. will have the desired response

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9
Q

Define selectivity?

A

How well the drug binds to a molecular target or other target and vice versa.

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10
Q

Define safety?

A

How many patients have U/E.

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11
Q

Define bioavailability?

A

The proportion of drug dose administered that reaches the general circulation unchanged.

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12
Q

Define cost?

A

How much the drug costs.

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13
Q

What does it mean that body is an open system?

A

Means that drug transiently affects functions of a system.

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14
Q

What does CACs do?

A

Command and control molecules. Drugs chemically inert usually. Bind transiently to CAC as complementary shapes. Lock and key model.

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15
Q

What are different types of CAC?

A

Membrane receptors - neurotransmitters.
Ion channels - nerve impulses, local anaesthetics.
Enzymes - produce or degrade messenger molecules.
Nuclear receptors - control gene activation.
Plasma and tissue proteins also but no major physiological effects.

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16
Q

What are agonists?

A

Drugs that transiently bind to receptors and activate them. May be endogenous or drugs binding to receptors, e.g. insulin to insulin receptors or salbutamol to beta 2 adrenergic receptors. Affinity is how well they bind.

17
Q

ED50 - how to plot it?

A

Plot it logarithmically then get a sigmoid relationship. If you have a low ED50 then a more potent drug, can do more with it. If curves are parallel then they are acting on the same receptors.

18
Q

What is pharmacovigilance?

A

It is the detection, assessment, understanding and preventing ADR.

19
Q

How to quantify safety?

A

Looking at TI. If wide TI then means patient taking the effective dose very unlikely to also get U/E. Narrow TI then more likely to get U/E. TI = TD50/ED50.

20
Q

What does alpha 1, beta 1 and beta 2 adrenergic receptors do?

A

Increases blood pressure by constricting blood vessels.

Increases heart rate by increasing blood flow.

Increases bronchodilation by increasing oxygen.

21
Q

How would you make agonist more selective for bronchodilation?

A

Add CH3 to increase selectivity for beta-adrenergic receptors.

22
Q

What adrenaline binds to each receptor?

A

Noradrenaline for alpha 1, isoprenaline for beta 1 and 2. Salbutamol just for beta 2.

23
Q

What are antagonists?

Give 2 examples

A

Drugs with affinity but no intrinsic activity.
Diabetes Mellitus - insulin is an antagonist
Schizophrenia dopamine excess - dopamine antagonist

24
Q

Describe how competitive anatgonists work.

A

Reversible, no direct biologicla effect. Compete agonist for receptor space. More antagonist less likely to get agonist binding - not getting response agonist would catalyse.

25
Q

Give an example of a competitive antagonist.

A

Atropine.

Increases heart rate by blocking the activity of muscarinic acetylcholine receptors.

26
Q

How could you overcome the effect of antagonist?

When do effects wear off?

A

By increasing the concentration of agonist.

Wear off when drug cleared from the body by metabolism or excretion.

27
Q

Describe how non-competitive antagonists work.

A

Irreversibly bind to receptor active sites which stops agonist binding and getting a max response. Also bind to allosteric sites and cause a conformational change of receptors, so agonist can’t bind.

28
Q

When do effects of non-competitive antagonist wear off?

A

Only wear off when receptor recycled or replaced.

29
Q

Difference between pharmacokinetic and physiological antagonism.

A

Pharamcokinetic is where antagonist reduces conc of agonist, decreases absorption and distribution and increases metabolism or excretion. Whereas physiological, 2 drugs which have opposing actions which tend to cancel each other out, via different receptors.

30
Q

What are spare receptors?

A

They are any receptors left over after agonist has bound and caused a max effect.

31
Q

What are partial agonists?

A

If they occupy all receptors still don’t cause a max effect. Low efficacy.

32
Q

What happens in presence of full agonist with a partial agonist?

A

Partial agonist acts as a partial antagonist by stopping affinity of a full agonist.

33
Q

Example of partial agonist

A

Pindolol.
Prevents HR from falling too low or rising too high. Adrenaline released it competes for active site on the receptor along with adrenaline. Occupies some of the receptors reducing the potency of adrenaline.

34
Q

What is a physiological antagonism example?

A

Adrenaline bind to B1 receptor and increases heart rate, acetylcholine agonist binds to M2 and decreases heart rate. Antagonist also binds to M2 receptor which stops ACh from binding and HR increases.

35
Q

What is tolerance?

Example of drug?

A

Where using a drug for a long time increases the dose needed to get the same effect. The decrease is slow.
Morphine.

36
Q

What is tachyphylaxis?

A

Where decrease of effect occurs over minutes.

Medicine Year 1 (7 decks)

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