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Yr 2 Pharm + Therapeutics > 2+3: Drug Mechanisms + Receptor Interactions > Flashcards

2+3: Drug Mechanisms + Receptor Interactions Flashcards

(62 cards)

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1
Q

Define pharmacodynamics

A

the effect of the drug on the body (responses produced, mechanism of action)

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2
Q

Defime pharmacokinetics

A

the effect of the body on the drug (e.g. absorption, distribution, metabolism, excretion).

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3
Q

Define drug

A

chemical substance that interacts with a biological system to produce a physiological effect.

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4
Q

4 main drug target sites

A

Receptors
Ion channels
Transport systems
Enzymes

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5
Q

What do all 4 drug target sites have in common

A

proteinacious binding sites

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6
Q

What are receptors activated by

A

NTs + hormones

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7
Q

Example of agonist and what it stimualtes

A

ACh - nonselective agonist stimulating nicotiic + muscarinic

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8
Q

Example of antagonist and what it blocks

A

Atropine - muscarinic antagonist

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9
Q

Uses of atropine

A

used as anaesthetic premediation to dry up secretions

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10
Q

2 types of ion channels

A

Voltage-sensitive (VGCC) - affected by memb potential

Receptor-linked (nicotine-ACh receptor is linked with cation channels)

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11
Q

How do local anaesthetics work

A

Block VGSCs in sensory axons, blocking Na passage. Fewer APs propagated along these axons so pain perception reduced
Nocicpetor neurons are also inhibited

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12
Q

How do ca channel blockers work

A

Block VGCCs stop Ca influx into SM of vasculature which relaxes muscle, reducing TPR thus BP

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13
Q

What is amlodipine

A

Ca channel blocker

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14
Q

What are transport systems

A

Systems of carrier proteins and molecules using ATP to carry substances against conc grad. They’re specific for certain species. They dont mediate a response

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15
Q

Examples of transport systems

A

Na/K ATPase transports Na out and K into cells.

NA and Uptake 1 - SNS releases NA into synapse, binds postsynaptic adrenoreceptors. Main uptake when inactivating NA is into presynpatic nerve terminal via Uptake 1

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16
Q

How do tricyclic anti-depressants work

A

Interfers w NA Uptake 1 system. Downregulate NA and 5HT transmission in the brain. transmission in brain. TCAs bind NA transporter and slow transporter. This increases NA conc in synapse = enhanced NA effect postsynaptically in brain. (Same w 5HT)

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17
Q

What are cardiac glycosides

A

cardiac stimulant drugs increase heart contractility: interferes w Na/K ATPase

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18
Q

What is digoxin and how it works

A

Cardiac glycoside.
Used to treat HF
Binds to the Na/K ATPase on the cardiac myocytes and slows it so there is a slightly increased intracellular Na concentration which has a knock on effect on the intracellular Ca in the cardiomyocyte. Thus improved contraction and cardiac output. Gives an increased force of contraction too.

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19
Q

3 ways that drugs interact w enzymes

A
  1. Enzyme inhibitors
  2. False Substrates
  3. Prodrug
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20
Q

Example of enzyme inhibitor

A

Anticholinesterases like neostigmine. Increase [ACh] in synapsen by slowing acetylcholinesterase by binding it.
Used to treat muscle disorders

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21
Q

Example of false substrate

A

methyldopa takes place of DOPA - taken into S neurons, folows same S pathway as NA but generates methyl NA. Less effective alpha-1 receptor action causing less effective vasoconstriction

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22
Q

Example of prodrug

A

Chloral hydrate w is converted to trichloroethanol in the liver. This has hypnotic effects
It’ds a sleeping pill.

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23
Q

Unwanted effects of paracetamol

A

If too much, can saturate microsomal enzymes so another set of enaymes, P450, have to metabolise and this generates toxic substances = irreversible damage to liver + kidney

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24
Q

How do gnereal anaesthetics work

A

dampen synaptic transmission but dont interact w specific transport system/receptor.

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25
How do antacids work
reduce stomach acidity as they are basic so can neutralise stomach acid
26
How do osmotic purgatives work
they stimulat voiding of gut contents - they draw water into stomach contents and this softens stool and stimualtes voiding.
27
Define potency
how powerful the drug is. It depends on affinity and efficacy
28
Define affinity
how willingly the drug binds to its receptor (refers to avidity)
29
What does affinity of drug to receptor depend on?
``` Electrostatic forces intermolecular forces H-bonding VDWs Hydrophobic interactions ```
30
Define efficacy
also called intrinsic activity - the ability of a drug to generate a response once it has bound to the receptor - usually involves some sort of conformational change
31
Define full agonist
Full Agonist: an agonist that generates the maximal response
32
Define partial agonist
Partial Agonist: an agonist that generates less than the maximal response
33
What happens when you administer partial agonist w full agonist
you will get an effect similar to an antagonist because the partial agonist interferes with the ability of the full agonist to generate a response
34
Antagonists have ____ but no ____
Affinity | Efficacy
35
2 main types of antagonist
Competitive | Irreversible
36
Competitive antagonists
bind to same site as agonist on receptor = responses are surmountable (they can be overcome by increasing agonist)
37
What do competitive antagonists do to D-R curve
shift to right
38
Irreversible antagonists
binds tightly w covalent bonds. They could also bind at diff sites which = responses are insurmountable so cant be overcome by increasing agonist as no competition.
39
Example of irreversible antagonist
Hexmethonium - irreversible nicotinic cholinoceptor antagonist (blocks ion channel rather than recepto)
40
4 main families of receptors:
Type 1: Ionotropic Type 2: G-protein coupled Type 3: Tyrosine kinase-linked Type 4: Intracellular Steroid Type receptors
41
Location of the diff receptor families
Types 1-3: membrane | Type 4: intracellular
42
Structure of ionotropic receptors
4/5 subunits Defining feature: transmemb sections have alpha helices There's an external binding domain which will stimulate and open ionchannels
43
Structure of type 2 receptors
1 subunit | 7 transmemb domains (7 alpha helices
44
Type 3 receptor structure
Single protein 1 transmemb domain. Inside the cell is intracellular domain.
45
Type 4 receptor structure
The DNA binding domain is called zinc fingers. When receptor stimulated, zinc fingers uncovered = DNA binding and increased transcription
46
Effectors of the receptor families
Type 1 - channel Type 2- enzyme/channel Type 3: enzyme Type 4: gene transcription
47
Example of type 1 receptor
nicotnic acetylcholine receptor | GAB A
48
Eg of Type 2 recpetor
B1 adrenoreceptor in heart | muscarinic acetylcholine receptor
49
Eg of Type 3 receptor
insulin receptor | Growth factor + cytokine receptors
50
Eg of type 4 receptor
steroid/thyroid receptors
51
4 types of drug antagonism
* Receptor Blockade * Physiological Antagonism * Chemical Antagonism * Pharmacokinetic Antagonism
52
How does receptor blockade work
An antagonist binds receptor and prevents the binding of an agonist. 'Use Dependency' - this refers to ion channel blockers; more the tissue on which drug is acting is being used (more active they are), more effective this type of blocker will be. E.g. local anaesthesia
53
What is physical antagonism
When 2 drugs act at different receptors to have opposite effects in the same tissue. E.g. NA on the vasculature binds to adrenoreceptors = vasoconstriction, increasing BP. If we coadminister histamine - it acts on different receptors (H1 receptors) on vasculature = vasodilation, reducing BP.
54
What is pharmacokinetic antagonism
When one drug reduces the concentration of the other drug at the site of its action. It may reduce the absorption, increase the metabolism or increase the excretion of another drug.
55
Eg of pharmacokinetic antagonism
Repeated administration of barbiturates increases production of microsomal enzymes so if we administer another drug that is metabolised by the same enzymes then it is going to be metabolised more quickly and its effect will be reduced
56
Define drug tolerance
the gradual decrease in responsiveness to a drug w repeated administration E.g. benzodiazepines
57
5 potential causes of drug intolerance
* Pharmacokinetic Factors * Loss of Receptors * Change in Receptors * Exhaustion of Mediator Stores * Physiological Adaptation
58
Describe how pharmacokinetic factors cause drug intolerance
Metabolism of the drug increases when it is given repeatedly over a period of time. Barbiturates and alcohol are good examples
59
Describe how loss of receptors cause drug intolerance
The cell takes receptors off its membrane via membrane endocytosis. If the cell repeatedly stimulated by agonist, the cell will endocytose some receptors so there are fewer available on the cell surface – aka receptor downregulation.
60
Describe how change in receptors cause drug introlerance
number of receptors on the cell surface doesn't change but the receptors themselves undergo desensitisation due to continued stimulation over a long period of time. This method involves a conformational change so a proportion of the receptors are no longer effective.
61
Describe how exhaustion of mediator stores causes drug intolerance
Amphetamine is an example - is a CNS stimulant and acts on noradrenergic neruosn in brains.
62
Describe how physiological adaptation causes drug introlerance
Homeostatic response - body atempts to maintain stable internal env by developing tolerance to drug side effects

Yr 2 Pharm + Therapeutics (9 decks)

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