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Pharmacology > Introduction > Flashcards

Introduction Flashcards

(58 cards)

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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 (i.e. is bioactive)​

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3
Q

Where do drugs come from

A

-Natural products
-Serendipity (by accident)
-Changing structures of existing molecules
-Existing drugs on new diseases
-Computer aided design
-Studying disease processes

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4
Q

When was the first antibiotic discovered

A

Penicillium - 1928 (Flemming)
Isolated in 1938

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5
Q

Where does aspirin come from

A

Willow tree

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6
Q

What is Bothrops jararaca

A

Peptide which lowers BP- forerunner of ACE inhibitors
(comes from snake)

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7
Q

What is sildenafil

A

Drug re-purposed to create viagra

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8
Q

What are the types of drug names

A

Chemical
Generic
Proprietary

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9
Q

What is the ‘code-name’

A

Name given to drugs in development to disguise their identity

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10
Q

What is Pharmacokinetics

A

“what the body does to the drug”

Typically used as a generic term to describe the fate of a drug molecule following administration to a living organism or how a drug molecule is affected by exposure to living cells​

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11
Q

What is Pharmacodynamics

A

“what the drug does to the body”​

Typically used as a generic term to describe the mechanism of drug action or what happens to cells, organs, systems, etc., as a result of drug exposure​

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12
Q

What are the different routes of drug penetration into cells

A

Diffusion through lipid membrane
Diffusion through aqueous
channels
Carrier mediated transport
Pinocytosis

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13
Q

How does insulin reach the brain

A

Pinocytosis

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14
Q

What is the major transport route for lipophilic drugs

A

Diffusion through lipid membrane

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15
Q

How do water soluble drugs/hydrophilic drugs enter cells

A

Carrier-mediated transport

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16
Q

Can drugs pass through aqueous channels

A

Most are too large

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17
Q

What is lipinski’s rule of 5

A

A molecular mass less than 500 Daltons​

No more than 5 H-bond donors (total number of N-H and O-H bonds)​

No more than 10 H-bond acceptors (all nitrogen or oxygen atoms)​

An octanol-water partition coefficient log P not greater than 5

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18
Q

What is lipinski’s rule of 5 based on

A

Observation that most orally administered drugs are relatively small and moderately lipophilic molecules

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19
Q

What is AUC

A

Measure of the total exposure to the drug

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20
Q

How do drugs act

A

-Drugs are typically small chemical molecules
-Drug molecules exert a chemical influence on constituents of cells to produce a pharmacological response
-Drug molecules must get close enough to cellular constituents in order that they can interact chemically
-This interaction leads to an alteration in molecular / cellular function

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21
Q

Where must drug molecules bind to on cells

A

Drug Targets

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22
Q

What is Paul Ehrlich famous for

A

Nobel prize for Medicine in 1908

First treatment for syphilis; popularised the concept of the ‘magic bullet’

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23
Q

What does an antagonist drug do

A

Enters the binding site but will not have any effect however it prevents the agonist from entering and producing the normal signal

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24
Q

Why do we have receptors

Study These Flashcards
A

For cell to cell communication

25
What is a receptor
A recognition molecule for a chemical mediator through which a response is transduced Often a protein or complex of two or more proteins and often expressed on the surface of cells (with some exceptions) Histamine → histamine receptor(s) Many drugs act to either mimic or block the effects of endogenous molecules at their receptors Histamine receptor → blocked by anti-histamine drugs
26
What is the basic receptor structure
1. Extracellular domain Contains ligand binding sites Comprised of hydrophilic amino acids 2. Transmembrane domain Anchors protein in membrane Comprised of hydrophobic amino acids Typically has α-helical structure 3. Intracellular domain Interacts with effector mechanisms Comprised of hydrophilic amino acids
27
What are the steps of signal transduction
Signal Reception Transduction Response
28
What is a very fast signalling receptor
Nicotinic acetylcholine
29
What receptor may take days for signal transduction
Oestrogen
30
What is a fast receptor
Muscarinic acetylcholine
31
What receptor may be classified as slow due to the rate of signal transuction
Cytokine
32
What is an agonist
a drug that binds to a specific site on a receptor, mimics the effect of the endogenous ligand for that site
33
What is a ligand
Any chemical that binds to a receptor
34
What is an antagonist
a drug that binds to a specific site on a receptor, blocks the effect of the endogenous ligand (same or different binding site as ligand)
35
What is the difference between an agonist and antagonist drug
An agonist drug fits into the lock; mimics the action of the key; can be used to pick the lock and activate the receptor An antagonist drug also fits into the lock; gets stuck and prevents opening of the lock (i.e. activation of the receptor) by either endogenous ligand or agonist
36
What does an antagonist drug lack
Efficacy
37
What would a low affinity drug mean
Binds briefly or is displaced by one with a higher affinity
38
What does a low efficacy, high affinity drug result in
binds very strongly but ability to switch receptor on is very poor
39
What is affinity
A measure of the strength of association between ligand and receptor
40
What is efficacy
A measure of the ability of an agonist to evoke a (cellular) response
41
What are the main causes of pharmacological variability
Age Genetics Disease state Drug interactions Environment
42
What is pharmacological variability
Drug response is not always the same Responses vary between people (i.e. inter-individual variability) Responses vary within the same person (i.e. intra-individual variability)
43
What is the difference between general and local anaesthetics
GENERAL -Sedates entire body -Loss of conciousness LOCAL -Sedates localised area -No loss of conciousness
44
What are the three main states of Na+ channels
Resting Open Inactivated
45
How do local anaesthetics work
-Bind to target site on the intracellular side of the Na+ channel -Prevents Na+ influx - prevents depolarisation - prevents action potential propagation-prevents perception of pain -Prevents Na+ influx by blocking channel and stabilising it in inactivated conformation -Causes REVERSIBLE BLOCK of nerve conduction
46
What do LAs need to do to be effective
Diffuse from the site of administration, across the nerve cell membrane to the intracellular side Bind to the LA target site
47
What is the difference between ester and amide linked anaesthetics
ESTER -rapidly metabolised by the tissue and plasme cholinesterases -t1/2< 3 mins AMIDE -primarily metabolised slowly in the liver by P450 enzymes -t1/2 1-3 hours
48
What occurs when the pKa of the LA =pH of the solution
50% will be in its ionised form and 50% in its un-ionised form
49
What is the range of LA pKa's
7.6-9
50
When do both ionised and neutral forms of the LA exist
pH 7.4
51
Which anaesthetics are weak bases
Local anaesthetics
52
What causes side effects of LAs
The escapeinto the systemic circulation from localised point
53
What is usually administered along with a LA
Vasoconstrictor (adrenaline)
54
Examples of LA
Cocaine Procaine Lidocaine Tetracaine Prilocaine
55
What are the uses of different LAs
Epidural - Lidocaine, bupivacaine Nerve block - Most LAs Spinal anaesthia - Lidocaine Topical - (mucous membranes only not skin) Lidocain, tetracaine, benzocaine
56
What are the three things we should knowabout a drug
What it does - the response to the drug Its potency Its selectivity
57
What is potency
A measure of the dose (or concentration) of a drug at which it is effective A potent drug is one that is effective in low doses (concentrations)
58
When is a drug selective
A DRUG IS SELECTIVE IF IT WORKS ON ONE RECEPTOR BUT NOT ON OTHERS

Pharmacology (3 decks)

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