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Pharmacology 785 > Mechanism of Drug Action > Flashcards

Mechanism of Drug Action Flashcards

1
Q

What is a drug?

A

A drug is a chemical or substance that causes changes in the structure or function of living organisms

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2
Q

What is a medicine?

A

A medicine is the vehicle for administration of the duyge (active ingredient) to the human or animal e.g. tablet, capsule, injection, ointment, inhaler, suppository etc.

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3
Q

What is the Greek word for a drug

A

Pharmakon

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4
Q

What is the generic name/INN of a drug?

A

International Nonproprietary name

Standardised internally recognised name for a drug e.g. omeprazole, salbutamol

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5
Q

What is the trade/brand name of a drug?

A

Name given by the original manufacturers e.g. Ventolin, Losec

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6
Q

How long is a drug on patent?

A

10 years

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7
Q

What happens when a drug comes off patent?

A

Anyone can make the drug

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8
Q

What is pharmacology?

A

The science of drugs actions and uses, but has a number of sub-disciplines

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9
Q

What are the sub-disciplines?

A

Pharmacodynamics, pharmacokinetics,m therapeutics, toxicology, pharmacoepidemiology, pharmacogenetics, pharmacoeconomics

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10
Q

What is pharmacodynamics?

A

Focus on mechanism of drug action “what the drug does to the body”

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11
Q

What is pharmacokinetics?

A

Movement of the drug within the body “what the body does to the drug”

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12
Q

What does the mechanism of action of drugs mean?

A

Specific molecular processes by which drugs work

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13
Q

What does the mode of action of drugs mean?

A

General description of the type of action e.g. antihypertensive, antidepressant

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14
Q

What is the site of action of drugs?

A

Specific organs, tissues or cells affected by the dru ge.g. Bronchi, sensory neurons

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15
Q

What is a risk versus benefit assessment?

A

Every decision to use a drug requires an assessment of risk versus benefit - knowing how a drug achieves its action allows us to predict both its beneficial and unwanted effects

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16
Q

What are the rules of cellular society?

A

Each cell has its own specific function
It accepts communication (signals) from its own and other organs
It interprets those signals correctly
It responds to those signals appropriately
It transmits its own signals to other cells

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17
Q

What are signal molecules also known as?

A

Ligands

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18
Q

What do signal molecules include?

A

Neurotransmitters (noradrenaline, dopamine)
Local hormones or autocoids (histamine, prostaglandins)
Cytokines (interprefons, interleukins)
Hormones (thyroxine, insulin)

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19
Q

What is the second-messenger system?

A

Ligand-receptor binding causes further signalling within the cell and alteration in cell function (eg. myocardial cell contracts)

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20
Q

Do ligands bind reversibly or irreversibly with receptors?

A

Reversibly

21
Q

What drugs do not have a specific receptor?

A

Antacids and diuretics

22
Q

What are drug targets or receptors?

A

Proteins that have a specific chemical configuration or ‘shape’ that is recognised by the appropriate logan or drug

23
Q

Where are drug targets/receptors found?

A

Cell membrane receptors, cell nucleus receptors, ion channels, enzymes, carrier molecules (transporter)

24
Q

What are the mechanisms that cease ligand effects?

A

Enzymatic degradation of drug or ligand (e.g. acetylcholine broken down by cholinesterase)
Reuptake back into cells from which released (e.g. serotonin)

25
Q

What happens if the enzyme membrane is blocked?

A

If the enzyme is blocked/inhibited then the effects of the drug/ligand will be increased/prolonged

26
Q

What happens if the reuptake transporter is blocked?

A

If the reuptake transport is inhibited/blocked, then the neurotransmitter effects will be increased/prolonged e.g. SSRIs, by increasing serotonin and noradrenaline at receptors in the brain these agents act as antidepressants

27
Q

What is receptor diversity?

A

There is a wide range of receptor types and subtypes
Histamine (H1, H2)
Adrenergic (a1, a2, b1, b2)
Dopamine D1, D2, D3, D4)
Serotonin (5-HT1 tp 5-HT7) with subtypes
Receptors and their subtypes are differently distributed throughout the body

28
Q

How can chemical structure affect receptor selectivity?

A

Small changes in chemical structure can change the receptor selectivity. Meaning we can target drugs toward particular subtypes of receptors

29
Q

What is affinity?

A

A measure of the strength of interaction between the ligand and receptor (e..g how readily or easily they bind together)

30
Q

What is efficacy/intrinsic activity?

A

A measure of the ability of the ligand-receptor interaction to cause a change in function (i.e. produce an effect).

31
Q

What are agonists?

A

Are agents with good affinity for the receptor and also have intrinsic activity (the drug-receptor interaction results in a change in function)

32
Q

What are antagonists?

A

Have good affinity for the receptor but no (or very little) intrinsic activity
Work by preventing access to the receptors for endogenous ligands e.g. beta-blockers

33
Q

What is a competitive antagonist?

A

The drug with the highest concentration will bump off the other drugs
E.g. naloxone is an opioid antagonist - if administered to a patient who has overdosed on an opioid agonist the naloxone will displace the opioid by competitive antagonist

34
Q

What is a partial agonist?

A

A drug that in small concentrations acts as agonists i.e. they trigger a response by their intrinsic activity is less than a full agonist (i.e. there is a ceiling effect).
In higher concentrations they can act as ‘antagonists’ blocking further access to the receptor for other agonists or endogenous substances
E.g. buprenorphine - used as an opioid analgesic and in opioid dependence

35
Q

What is an inverse agonist?

A

An inverse agonist binds to the same receptor as an endogenous agonist but it induces a pharmacological response opposite to that agonist.
E.g. loratadine

36
Q

What is a dose-response/concentration curve?

A

This describes the relationships between the amount of drug a tissue is exposed to (i.e. the concentration at the receptor) and the level of response that occurs at the receptor sites

37
Q

Why is there a plateau?

A

There is only a finite number of receptors

38
Q

On a log-dose response curve what is a Emin?

A

Minimal dose

A certain minimum number of receptor sites must be activated before a response can occur

39
Q

On a log-dose response curve what is Emax?

A

Maximum dose
There comes a point when all available receptor sites have been activated, at this point the response is ‘maximal’ - no matter how much the dose increases you cannot get a bigger response.

40
Q

On a log-dose response curve what is EC 50?

A

There is the effective concentration in 50% of subjects

41
Q

What does a shift to the right of a log-dose curve mean?

A

E.g. Morphine & naloxone. Naloxone is a competitive antagonist

42
Q

What is tachyphylaxis?

A

Some receptors can lose responsiveness after repeated exposure to the same concentration (Dose) of a particular drug

43
Q

What is desensitisation?

A

To a decrease in the response of receptor second messenger systems, associated with chronic exposure to a particular drug

44
Q

What is drug tolerance?

A

Desensitisation and tachyphylaxis can contribute to the development of tolerance to a particular drug (requiring high doses to get the same effect).

45
Q

What is down-regulation?

A

The number of membrane receptors decrease in response to strong signals at these receptors

46
Q

What is up-regulation?

A

The number of membrane receptors increase in response to weak signals

47
Q

How does receptor dependence occur?

A

Withdrawal symptoms when drug removed

48
Q

Why do you wean down medication that causes up-regulation of receptors?

A

Abrupt cessation can lead to severe rebound

Pharmacology 785 (9 decks)

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