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BAMS > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is pharmacology?

A

The study of the action of drugs on the function of living systems

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2
Q

What is a drug

A

A chemical substance or natural product that affects the function of cells, organs, systems or the whole body

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3
Q

Where do drugs come from

A
  • natural products
  • serendipity (accident)
  • changing the structure of an existing molecule
  • using an existing drug
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4
Q

What are the three types of names for drugs

A
  • chemical (named after the structure)
  • generic (non proprietary name given to a molecule)
  • proprietary (trade name)
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5
Q

What is pharmacokinetics

A

What the body does to the drug

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6
Q

What is pharmacodynamics

A

What the drug does to the body

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7
Q

Describe the process of drugs entering the body and then getting excreted

A

Absorption, distribution, metabolism and then excretion

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8
Q

What ways are drugs absorbed

A

Absorbed through the gastrointestinal transport, gastrointestinal metabolism and hepatic first pass effect

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9
Q

Describe drug distribution

A

Distributed in the intravascular space, extravascular space and through protein binding

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10
Q

Where are drugs metabolised

A

In the liver

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11
Q

What are the routes of drug penetration into cells

A
  • diffusion through the lipid membrane
  • diffusion through aqueous channels
  • carrier mediated transport
  • pinocytosis
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12
Q

What is the major route for lipophilic drugs

A

Diffusion through the lipid membrane

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13
Q

What is the major route for hydrophilic drugs

A

Carrier mediated transport

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14
Q

What is pinocytosis

A

Transport of insulin into the brain

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15
Q

What is lipinskis rule of 5

A
  • a molecular mass less than 500 daltons
  • no more than 5 H- bond donors
  • no more than 10 H- bond acceptors
  • an octanol water partition coefficient log P no greater than 5
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16
Q

Describe phase 1 of drug metabolism

A

Phase 1
Reaction - oxidation, reduction, hydrolysis
Effect - functionalisation (adding new functions), addition or unmasking of reactive group

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17
Q

What is the consequence of phase 1 metabolism of a drug

A

Small decrease in lipophilicity
Slight increase in excretion
Change in pharmacological effect

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18
Q

Describe phase 2 metabolism of a drug

A

Reaction
Effect - conjugation, addition of large and often charged group
Consequences - large decrease in lipophilicity, large increase in excretion, usually a decrease in pharmacological effect

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19
Q

At Cmax rate of … equals rate of …

A

At cmax rate of absorption equals rate of elimination

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20
Q

What are the drug effects at a cellular level

A

Drugs can have an effect on receptors, ion channels, enzymes, transporters and DNA ect

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21
Q

What are the sites that drugs usually act upon

A

Many drugs mimic or block the action of endogenous molecules (eg. Hormones and neurotransmitters) they act at specific sites : receptors, ion channels, enzymes and transporters (all of which are proteins)

22
Q

How do drugs act

A

Drugs are typically small chemical molecules, they exert a chemical influence on constituents of cells to produce a pharmacological response, they get close enough to cellular constituents in order that they can interact chemically

23
Q

What are the protein targets for drug binding called

A

Receptors

24
Q

What is the direct effect of an agonist binding to a receptor

A

Ion channel opening or closing

25
Q

What are the transduction mechanisms when an agonist binds to a receptor

A
  • enzyme activation/inhibition
  • ion channel modulation
  • DNA transcription
26
Q

What is the effect of an antagonist binding

A

No effect

27
Q

Why are receptors important

A

They are used for cell to cell communication

28
Q

What is the basic receptor structure

A

1) extracelllar domain (contains ligand binding sites comprised of hydrophilic amino acids)
2) transmembrane domain (anchors proteins in membrane , comprised of hydrophobic amino acids)
3) intercellular domain (interacts with effectors mechanisms compromised of hydrophilic amino acids)

29
Q

What kind of signal transduction would a ligand gated ion channel be used for

A

Very fast signal transduction (milliseconds)

30
Q

What signal a G protein coupled receptor transduce

A

A fast signal transduction (seconds)

31
Q

What signal would a kinase linked receptor be used to transduce

A

A slow signal transduction (hours)

32
Q

What signal would a nuclear receptor be used to transduce

A

Very slow signal transduction (hours to days)

33
Q

What is an agonist

A

A drug that binds to a specific site on a receptor mimics the effect of the endogenous ligand for that site

34
Q

What is an antagonist

A

A drug that binds to a specific sit on a receptor, blocks the effect of the endogenous ligand (same or different binding site as ligand)

35
Q

Agonists posses both …. and ….

A

Agonists posses both affinity and efficacy

36
Q

What is efficacy

A

Can cause a response

37
Q

Antagonists have …. but not …..

A

Antagonists posses affinity but not efficacy

38
Q

What is affinity

A

A measure of the strength of association between ligand and receptor

39
Q

What is pharmacological variability

A

Drug response is not always the same, different people react to drugs differently due to age, sex ect

40
Q

What is general anaesthetic

A
  • sedates entire body
  • loss of consciousness

Block presynaptic calcium entry therefore no neurotransmitter release.

Increases post synaptic hyperpolarisation (Cl- influx or K+ efflux)

41
Q

What is local anaesthetic

A
  • sedates localised area
  • no loss of consciousness

Block conduction axonal Na+ entry
Block sodium channels

42
Q

Why are esters used rather than amides for short term use anaesthetic

A

Esters are metabolised quickly which means they have a shorter effect than amides, amides have a longer half life because they are metabolised in the liver therefore have a longer effect

43
Q

What are do anaesthetic drugs generally consist of

A

Typically weak bases

44
Q

What are the three states that sodium channels can exist in

A

Resting, open and inactivated

45
Q

Describe the mechanism of action of local anaesthetics

A
  • LAs bind to a target site on the intercellular side of the Na+ channel
  • LAs prevents sodium influx > prevents depolarisation > prevents action potential propagation > prevents perception of pain
  • LAs prevents Na+ influx in 2 ways, both blocks channel and stabilises it in its inactivated conformation

Causes reversible block of nerve conduction

46
Q

To be effective LAs need to:

A

1) Diffuse from site of administration, across the nerve cell membrane to the intercellular side
2) Bind to LA target site

Their ability to do this is related to their chemical structure

47
Q

Describe ester linked anaesthetics

A

Rapidly metabolised by tissue and plasma cholinesterase
Lasts <3mins

48
Q

Describe amide linked anaesthetics

A

Primarily metabolised slowly in the liver last about 1-3 hours

49
Q

What is the use of topical anaesthetics

A

They affect mucous membranes only, not effective on the skin

50
Q

What is potency of a drug

A

A measure of the dose (or concentration) of a drug at which it is most effective

A potent drug is one that is effective in low doses

51
Q

What does it mean if a drug is selective

A

A drug is selective if it works on one receptor but not on other

BAMS (41 decks)

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